A Practical Approach to Neurology

for the Small Animal Practitioner

A Practical Approach
­
to Neurology for
the Small Animal
Practitioner
Paul M. Freeman MA, VetMB, Cert SAO, DipECVN, MRCVS
EBVS® European Specialist in Veterinary Neurology
RCVS Specialist in Veterinary Neurology
Queen’s Veterinary School Hospital
University of Cambridge
Cambridge, UK

Edward Ives MA, VetMB, DipECVN, MRCVS

EBVS® European Specialist in Veterinary Neurology
RCVS Specialist in Veterinary Neurology
Anderson Moores Veterinary Specialists
Winchester, UK
This edition first published 2020
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Library of Congress Cataloging‐in‐Publication Data

Names: Freeman, Paul M., author. | Ives, Edward, author.
Title: A practical approach to neurology for the small animal practitioner /
Paul M. Freeman, Edward Ives.
Other titles: Rapid reference series (John Wiley & Sons)
Description: Hoboken, NJ : Wiley-Blackwell, 2020. | Series: Rapid reference
| Includes bibliographical references and index.
Identifiers: LCCN 2020017108 (print) | LCCN 2020017109 (ebook) | ISBN
9781119514589 (paperback) | ISBN 9781119514664 (adobe pdf) | ISBN
9781119514701 (epub)
Subjects: MESH: Dog Diseases | Nervous System Diseases–veterinary | Cat
Diseases | Handbook
Classification: LCC SF992.N3 (print) | LCC SF992.N3 (ebook) | NLM SF
992.N3 | DDC 636.089/68–dc23
LC record available at https://lccn.loc.gov/2020017108
LC ebook record available at https://lccn.loc.gov/2020017109
Cover Design: Wiley
Cover Image: Courtesy of Paul M. Freeman and Edward Ives
Set in 9.5/13pt MeridienLTStd by SPi Global, Chennai, India

10 9 8 7 6 5 4 3 2 1
’To all of my teachers, past and present, and to my mother Claire Ives,
­
the kindest teacher of all.’
Edward Ives
April 2020
Contents

Preface, ix

Acknowledgements, xi

­About the Companion Website, xiii

1 ‘Is it Neurological?’, 1

2 Clinical History and Signalment, 25

3 The ‘Stress‐free’ Neurological Examination, 45

4 Lesion Localisation, 99

5 Constructing the List of Differential Diagnoses, 121

6 A Practical Approach to Common Presentations in General Practice, 133

7 Neurological Emergencies, 329

Index, 371

vii

Preface

Neurology is still perceived by many students as one of the more difficult areas
of veterinary medicine to understand. In clinical practice, neurological cases can
also cause much anxiety, particularly in regard to clinical decision making when
referral is not an option. Ed and I wanted to write a book for students and gen-
eral practitioners that represents the way we feel neurology should be taught
and understood, and one which would simplify a complex topic. There are many
wonderful textbooks on the subject already in existence, and this text is in no
way designed to compete with those excellent volumes, but rather we hope that
it might prove to complement them as an approachable and useful companion
for those looking for a better grasp of a complex subject. We have tried to design
and produce a practical book full of hints and tips taken from our personal col-
lective experience, which would be accessible as a quick reference guide for use
in general practice, as well as hopefully being an easy‐to‐read textbook for final‐
year veterinary students. We have tried to include as many photographs and
diagrams as possible to illustrate and simplify some of the more complex subject
areas, and we are sure that the videos on the accompanying website will aid rec-
ognition of some of the less common clinical presentations. We have also included
video clips of a normal neurological examination as a reference. This has been a
labour of love for us and we are indebted to the many colleagues, both past and
present, who have inspired, taught, and assisted us, and are still doing so. The
book represents the product of many hours of study, conversation, observation,
and clinical practice, and we hope that it may be used and enjoyed by many.

Paul M. Freeman and Edward Ives

ix

Acknowledgements

The authors are Board‐certified neurologists with a combined total of more than
30 years in general practice before entering full‐time specialist practice. This has
given us a great insight into the needs of general practitioners when it comes to
dealing with neurological cases. We have both benefited from excellent teaching
through the University of Cambridge, both for our veterinary degrees and later
our residency training. We would like to acknowledge the support and advice of
our current and past colleagues, as well as that of family and friends.
The original drawings for the book were created by Paul’s son Jack Freeman,
with digital images produced by Edward himself. We are grateful also to our
clients, past and present, especially those of the Queen’s Veterinary School
Hospital, University of Cambridge, and Anderson Moores Veterinary Specialists,
whose images and videos bring this text to life.
Finally, thanks to Tick, star of the neurological examination videos and Paul’s
long‐time but now sadly deceased Border Collie, whose presence in the neurol-
ogy office in Cambridge was a source of education and comfort for students and
staff alike.

xi

­ bout the Companion
A
Website

Don’t forget to visit the companion website for this book:

www.wiley.com/go/freeman/neurology

There you will find valuable material designed to enhance your learning,
including:
• videos of the normal neurological examination and specific disease presentations

Scan this QR code to visit the companion website.

xiii

Chapter 1 ‘Is it Neurological?’
Paul M. Freeman

The first step to any neurological evaluation of a veterinary patient, and proba-
bly the most common question we are asked by practitioners (in a variety of
different ways), is whether the problem facing them is partially or completely
neurological. In order to answer this question, it is important to understand the
nature of the problem from the point of view of both the animal and the owner,
and furthermore to understand what is meant by the question ‘Is it neurologi-
cal?’. For example, when presented with a dog that is showing signs of exercise
intolerance, one possible reason may be a neuromuscular disorder, such as
myasthenia gravis. However, this dog may present with a completely normal
neurological examination, and the clue may be in the presenting clinical signs or
medical work‐up. Therefore, in such a case the initial answer may have to be ‘It
might be’. A dog whose problem is intermittent ‘episodes’ of abnormal behav-
iour may be having seizures, but might also be suffering from syncope, a com-
pulsive behavioural disorder, or a movement disorder. All of these possibilities
may in some way be classified as ‘neurological’ problems, but with very different
aetiologies, treatment possibilities, and prognoses. The goal of this book is to
allow practising vets to feel confident that they are approaching potentially neu-
rological problems in a reasonable and evidence‐supported way. The first step in
this process is learning how to recognise when a particular presentation may be
caused by a disease process somewhere within the central nervous system (CNS)
or the peripheral nervous system (PNS).

1.1 ­What Is the Problem?

One of the key skills to be developed in general practice, as well as referral prac-
tice, is learning how to control the consultation in order to establish what the
client’s primary concern is, what they hope to achieve from their visit with you
as the veterinarian, and how their expectations match up to their ability and/or

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

1

2 A Practical Approach to Neurology for the Small Animal Practitioner

willingness to afford and allow potential investigations and/or treatments to be

performed. This is not an easy skill, especially for the GP vet who may have very
limited time in which to carry out the initial consultation. It is, however, key to
both ultimate client satisfaction and to providing the most effective service to the
animal patient. Without establishing these essential facts, much time can be
wasted. In the worst case the client’s real concerns may not be addressed at all,
meaning that they may leave the practice dissatisfied, perhaps with good
reason.

Top tip: Always ask the client directly why they have come to see you today.

Don’t make this mistake: Take care not to become side‐tracked by a problem which
may be very interesting to you, but is possibly chronic and completely unrelated to the
reason for the visit!

1.2 ­Is this Problem Neurological?

There are many possible manifestations of neurological disease, some of which

are much easier to recognise as neurological than others. There are also many
non‐neurological diseases which can mimic a problem involving the nervous
system. In this section, we will look at the scope of neurological disease manifes-
tations that the clinician may be presented with and we will aim to provide some
clues as to the correct recognition of neurological disorders.

1.3 ­Neuroanatomy

When attempting to decide whether the problem is neurological, it is important

to be aware of the different parts of the nervous system and how disease pro-
cesses may affect them. Broadly we are concerned with the CNS (the brain and
spinal cord) and the PNS (consisting of the peripheral nerves and muscles and
the neuromuscular junctions between them). In the brain we can generally dis-
tinguish clinical signs referable to the forebrain, the brainstem, and the
cerebellum.
The forebrain is known as the prosencephalon, and can be further divided
into the telencephalon, which consists of the cerebral hemispheres, and dien-
cephalon, containing the thalamus and the hypothalamus. The group of clinical
signs which are commonly caused by lesions affecting the forebrain are some-
times referred to as a prosencephalic syndrome, and include behavioural change,
central blindness, and seizure disorders in particular.
The brainstem consists of the midbrain (mesencephalon), the pons (ventral
metencephalon), and the medulla (myelencephalon). Disease of the brainstem
 Chapter 1 ‘Is it Neurological?’ 3

also leads to characteristic signs, which can be used to anatomically localise the
problem, including proprioceptive deficits and ataxia, sometimes clusters of cra-
nial nerve signs, vestibular syndrome, and mentation change associated with
dysfunction of the ascending reticular activating system.
The third major division of the brain is the cerebellum (dorsal metencepha-
lon), and lesions in this region can lead to some of the most recognisable abnor-
malities in the neurological examination, including hypermetria and intention
tremor.
The medulla is contiguous with the spinal cord, which can be divided into a
series of segments from which a pair of spinal nerve roots arises, one pair for
each segment. For neuroanatomical localisation purposes, the spinal cord seg-
ments are grouped together according to their motor function, and whether or
not they contain the cell bodies of the nerves which directly supply the skeletal
muscles of the limbs (known as lower motor neurons, LMNs). In this regard, the
first five cervical spinal segments (C1–C5) contain only the so‐called upper
motor neurons (UMNs) which run from the gait‐generating centres of the cer-
ebral cortex and brainstem to the LMNs innervating the limbs and other struc-
tures. Spinal cord lesions affecting segments in this region lead to a characteristic
set of neurological examination findings involving UMN effects in all four limbs.
The sixth, seventh, and eighth cervical segments, along with the first two
thoracic segments, C6–T2, contain the LMN cell bodies supplying the thoracic
limbs, as well as UMNs to the pelvic limbs; lesions here cause a so‐called LMN
paresis or plegia (paralysis) of thoracic limbs and an UMN paresis/plegia of the
pelvic limbs.
Lesions in spinal segments caudal to the second thoracic segment will gener-
ally only affect the pelvic limbs, and the division between UMN and LMN here
occurs between the third and fourth lumbar segments. Hence, lesions affecting
the T3–L3 spinal cord segments lead to UMN paresis of pelvic limbs, whereas
lesions caudal to L3 (L4–S3) cause LMN paresis/plegia of the pelvic limbs.
As well as the descending motor tracts within the spinal cord, there are of
course ascending sensory tracts including those carrying proprioceptive infor-
mation from the limbs and trunk; therefore, a spinal cord disorder will usually
lead to variable degrees of ataxia and proprioceptive dysfunction, as well as the
paresis associated with the loss of motor function.
The final part of the nervous system within which we can make an anatomi-
cal localisation consists of the peripheral nerves, neuromuscular junctions, and
muscles. Lesions affecting this neuromuscular system tend to lead to more obvi-
ous weakness and LMN paresis/plegia affecting all limbs. Therefore, syndromes
such as weakness, stiffness, exercise intolerance, and collapse may all arise as a
result of disease affecting this PNS.
The neurological examination and neuroanatomical localisation of specific
lesions will be explored and explained in more detail in Chapters 3 and 4, but an
understanding of the anatomical structures involved in neurological disorders is
4 A Practical Approach to Neurology for the Small Animal Practitioner

Forebrain

Cerebellum
C1
–C
5
C6 – T2 T3 – L3 L4 – S3
Brainstem

Bladder & perineum

Thoracic limb Pelvic limb
Figure 1.1 Neuroanatomical regions. The aim of the neurological examination is to localise
the site of a lesion into the brain, the spinal cord, or peripheral (neuromuscular) regions.
Functionally, the brain is separated into the forebrain, brainstem, and cerebellum; the spinal
cord into sections containing the segments 1st cervical – 5th cervical (C1–C5), 6th
cervical – 2nd thoracic (C6–T2), 3rd thoracic – 3rd lumbar (T3–L3), and 4th lumbar – sacral
(L4–S3); and the peripheral nervous system consists of peripheral nerves, with the neuromus-
cular junctions and muscles also considered as a potential neuroanatomical localisation.

an essential part of the ability to recognise when one is facing a neurological

problem (see Figure 1.1).

1.4 ­Manifestations of Diseases of the Nervous

System

Disorders that affect different parts of the nervous system may manifest them-
selves in a wide variety of ways. In this section, we will briefly look at each of
these, with the most important and more common problems being examined in
greater detail in Chapter 6. The majority of nervous system disease will result in
one or more of the following clinical presentations, some of which can be more
easily defined and recognised than others. Where relevant, non‐neurological
disorders that can mimic or also result in these clinical presentations will also be
mentioned:

• seizures
• collapse
• movement disorder/dyskinesia
• mentation change
• behaviour change
• blindness
• deafness
• tremor
• paresis/plegia
• ataxia
 Chapter 1 ‘Is it Neurological?’ 5

• abnormality of head position (head tilt/turn)

• abnormality of eye position or movements
• hypaesthesia
• lameness
• pain
• disorders of micturition/urination.

1.4.1 Seizures
For the purposes of this text, an epileptic seizure will be defined as an acute
onset of excessive and hypersynchronous brain activity that results in transient
visible motor activity; this description does not allow for so‐called ‘absence sei-
zures’, where a person may become transiently ‘absent’, since no motor activity
is seen in such a seizure. However, such seizures, although they may occur in
cats and dogs, are very difficult to diagnose without the help of an electroen-
cephalogram (EEG).
It is rare that an affected animal will seizure during the consultation, so usu-
ally we rely on owner description and often video evidence when trying to
decide if a problem is truly an epileptic seizure or some kind of seizure mimic. A
generalised seizure is normally easily recognisable (see Video 1); the seizure may
begin with a focal contraction of, for example, the facial muscles, but this rapidly
spreads to cause loss of conscious state and tonic contraction of all the anti‐grav-
ity muscles leading to recumbency. There follows a period of tonic and clonic
muscle activity causing running‐like movements, and there may be vocalising,
hypersalivation, jaw champing, and often urination or defecation. The tonic‐
clonic movements gradually subside and the animal will frequently adopt pad-
dling movements as consciousness returns and attempts are made to stand.
There will usually then follow a post‐ictal period, which may last for minutes or
hours, when the animal may show varying levels of altered behaviour, circling,
ataxia, blindness, and other neurological abnormalities.
Focal seizures may involve simple focal muscle twitching, commonly of the
orofacial muscles (see Video 2), but may also include more complex patterns of
movement and/or behaviour – leading to apparent loss of consciousness and
awareness. Such activity can be very difficult to distinguish from obsessive behav-
ioural abnormalities and movement disorders for instance, but there are some key
indicators which may be helpful in recognising when a problem is a true focal epi-
leptic seizure (see below). A specific form of focal seizure is the myoclonic seizure,
characterised by jerky twitches resembling the dog being fearful of a sudden stimu-
lus, and seen especially in the genetic storage disease of Miniature Wire‐haired
Dachshunds, Beagles, and Bassett Hounds known as Lafora Disease (see Video 3).
Epilepsy implies a tendency for seizures to recur and can be further classified
as ‘reactive/metabolic’, when there is an extracranial cause, ‘structural’, when
there is an abnormality of brain structure such as an inflammatory or neoplastic
lesion, and ‘idiopathic’, when brain structure is normal.
6 A Practical Approach to Neurology for the Small Animal Practitioner

It is important to try to ascertain whether the abnormal event described by

the owner or captured on video is an epileptic seizure or not. This is because the
occurrence of true seizures implies a possible prosencephalic or forebrain lesion
and dictates a certain path of investigation. The initiation of antiepileptic medi-
cation is always a subject for discussion and consideration, since all antiepileptic
drugs (AEDs) can have undesirable side‐effects, and their use in non‐seizure
disorders is usually contraindicated.
The description above contains some clues to the features of epileptic seizures
that can be used in order to ascertain whether the event described is truly an
epileptic seizure or represents a ‘seizure mimic’. These include:

1. Presence of post‐ictal signs. This is common and can include ataxia, blindness,
polyphagia, or a temporary character change such as becoming aggressive.
2. Presence of autonomic signs during the event. In itself this is not necessarily
pathognomonic for an epileptic seizure, but involuntary salivation, urination,
and/or defecation is more common in seizure events than syncope, and is
rarely observed for movement disorders.
3. Absence of consciousness during the event. It can be difficult to be sure about this,
especially in mild focal seizures. However, the ability to rouse an animal from
the behaviour, as is the case for idiopathic head‐bobbing for instance, is an
indication that the event is probably not a seizure.
4. Presence of some form of tonic muscular activity, twitching, or stiffness.

There are many other causes of paroxysmal transient events, or ‘seizure

mimics’, and these should always be considered when trying to decide whether
or not we are dealing with an epileptic seizure. These include:

• Syncope, which may have a cardiovascular or respiratory cause. Most cases of syn-
cope result in a flaccid collapse, but this is again not always the case, and there
is a significant ‘grey zone’ of signs seen with seizures and syncope which can
make them difficult to distinguish. This is also the case in human medicine,
with a significant percentage of people being diagnosed with epilepsy when in
fact they are suffering syncopal attacks.
• Dyskinesia or movement disorder. These paroxysmal disorders of movement are
being increasingly described, often with specific breed associations. Examples
include the epileptoid cramping syndrome of Border Terriers (which has been
associated with a gluten sensitivity and recently renamed paroxysmal gluten‐
sensitive dyskinesia, see Video 4) and episodic falling in Cavalier King Charles
Spaniels (CKCSs), which has a known genetic mutation associated with it.
Although these syndromes are fairly well described, the fact that the CKCS
also suffers with idiopathic epilepsy can make this an even more complicated
picture in this breed.
 Chapter 1 ‘Is it Neurological?’ 7

• Behavioural events. These are often described as obsessive compulsive or OCD

behaviours, such as some cases of so‐called ‘fly‐catching’. The latter can also
be a focal seizure, and has even been associated with floating bodies within
the anterior chamber of the eye, or gastrointestinal pain (see Video 5).
• Transient vestibular events. Perhaps associated with transient ischaemic attacks
or TIAs.
• Narcolepsy/cataplexy. This is a rare condition with a suspected genetic basis in
certain breeds, but can look very much like the so‐called ‘drop seizures’
described in humans (see Video 6).
• Idiopathic generalised tremor syndrome or so‐called ‘little white shaker disease’
(see Video 7). This is an inflammatory condition of the CNS leading to a gen-
eralised tremor. The tremor can wax and wane, worsens with excitement, and
is potentially confusable with an animal suffering with a prolonged seizure or
status epilepticus, such as may be seen following exposure to certain toxic
substances (e.g. aflatoxins or mouldy food).
• Episodic pain, such as that associated with some cervical intervertebral disc
herniations, may cause episodic, short‐lived behavioural and physical changes.
The French Bulldog in particular seems prone to such manifestations (see
Video 8).
• Episodic collapse, which may have a neuromuscular, metabolic, or orthopaedic
cause; if recovery is rapid; such events may be mistakenly diagnosed as
seizures.
• Rapid eye movement (REM) sleep disorder. This is a condition where affected dogs
may suffer violent episodes of paddling and limb movement during periods of
REM sleep (see Video 9). It has recently been shown to have a higher inci-
dence in dogs recovering from tetanus (Shea et al. 2018).

Top tip: Seizures can have multiple causes but also have multiple mimics.

Careful observation of video footage, together with accurate history taking, is key to
defining whether the presenting problem is truly a seizure.

Ultimately, the only sure way to define a seizure (currently categorised as a

Tier 3 level of diagnostic confidence for idiopathic epilepsy) is by making EEG
recordings of abnormal brain activity during the abnormal event. Even in spe-
cialist referral practice this is rarely an option, and therefore we are usually
working at a lower level of confidence.

1.4.2 Collapse
Collapse implies a loss of extensor motor tone, and may be either intermittent or
permanent. When an owner describes a problem of collapsing, usually they are
referring to episodic collapse, since a permanent collapse is immediately ­obvious!
8 A Practical Approach to Neurology for the Small Animal Practitioner

Differential diagnoses for intermittent collapse include seizures, syncope, narco-

lepsy/cataplexy, and metabolic disorders (such as hypoglycaemia). More perma-
nent collapse may be caused by musculoskeletal and orthopaedic problems,
inflammatory conditions such as polyarthritis or polymyositis, as well as medical
conditions involving weakness, anaemia, or pain. Neurological causes of loss of
extensor muscle tone or strength may include brain, spinal cord, and PNS disor-
ders. The neurological examination is therefore key to identifying, firstly,
whether the problem is neurological, and then obtaining a correct neuroana-
tomical localisation.
Care must be taken in interpretation of the findings of the neurological
examination in cases of collapse; an animal which is suffering from shock,
trauma, or acute pain may well show apparent neurological deficits without any
neurological disease or pathology. Examples include animals in shock which
apparently have poor proprioception and spinal reflexes, lack of menace
response, and even absent deep pain response. Once the shock and pain has
been appropriately managed, the neurological abnormalities may disappear.

Top tip: Be careful with interpretation of the neurological examination in severely

shocked or traumatised animals.

Don’t make this mistake: Diagnosing severe spinal trauma due to apparent loss of
deep pain perception post‐trauma, especially in cats following a road traffic accident.
Once stabilised, the neurological examination may change, indicating a less severe injury.

1.4.3 Movement Disorders

Movement disorders are an increasingly recognised group of conditions which
affect many dog breeds. These conditions involve abnormal muscular move-
ments, occasionally episodes of collapse, but no change of consciousness or
autonomic signs that may be seen in focal epileptic seizure events (see Video 10).
Well‐documented examples include episodic falling in CKCSs (‘Collapsing
Cavaliers’), paroxysmal gluten‐sensitive dyskinesia of Border Terriers (epileptoid
cramping syndrome or ‘Spikes disease’, see Video 4), ‘Scotty cramp’ in Scottish
Terriers and ‘dancing Dobermann’ disease.
Some of these conditions have a known genetic cause, and a specific test may be
available (e.g. episodic falling in Cavaliers), but for many there is no specific diagnos-
tic test. Dancing Dobermann disease is suspected to be a polyneuropathy, Spike’s
disease has been shown to be caused by a hypersensitivity to gluten in the diet, and
it may be that some so‐called movement disorders are in fact focal seizures.
In all of these conditions, the neurological examination should be normal,
and in general all investigations are likely to be unremarkable (with the excep-
tion of specific genetic tests for example). The diagnosis is often one of exclusion
and pattern recognition, and for many of the conditions there is no specific treat-
ment available.
 Chapter 1 ‘Is it Neurological?’ 9

Further discussion of movement disorders and how they may present in

practice can be found in Section 6.2 ‘Movement Disorders’.

1.4.4 Mentation and Behaviour

Observation and recognition of changes in either behaviour or mentation can be
crucial in recognising that one is dealing with a neurological problem. Mentation
concerns the level of general alertness and is sometimes referred to as the level of
mentation (as opposed to the quality of mentation, which may be better be
understood as behaviour). Mentation levels can be categorised as:

1. Normal
2. Obtundation. A generalised reduction in level of alertness or interaction with
the environment; an animal which appears to show an absence of the usual
anxiety and stress associated with a visit to the veterinarian, a lack of normal
interaction with the owner, a ‘can’t be bothered’ or ‘couldn’t care less’ atti-
tude. There can clearly be a marked difference between mild and severe
obtundation, and milder levels may be variously described as lethargy or
depression, although these terms should be used with caution in animal
species.
3. Stupor. This implies a level of mentation in which the animal is basically
asleep or semi‐asleep, and only arousable by a noxious stimulus.
4. Coma. An animal which is not rousable even by a noxious stimulus.

A change in the level of mentation frequently implies neurological disease;

stupor and coma are most commonly seen in moderate to severe brainstem dis-
orders where the ascending reticular activating system is affected. This causes a
reduction in sensory input to the cerebral cortex. Forebrain disease may also
cause altered mentation, and in particular pituitary macroadenomas can present
with obtundation as the only neurological sign.
Focal cerebrocortical lesions more rarely present with obviously altered menta-
tion although larger lesions may, including compulsive pacing or circling behav-
iour. Animals with generalised encephalopathies, such as those seen in portosystemic
shunting for instance, often show an altered level of mentation, sometimes inter-
mittently. Another important observation is that raised intracranial pressure (ICP)
can affect mentation, and serial observation and monitoring of mentation level in
animals with suspected head trauma or with other reasons for potentially raised
ICP (usually as part of the modified Glasgow Coma Scale) is extremely important
in allowing recognition of a deteriorating situation/rising ICP.

Top tip: Altered mentation may be the only sign of severe intracranial pathology.

It is also important to be aware that altered mentation can occur as a result

of non‐neurological disease. Animals which have significant medical disorders,
10 A Practical Approach to Neurology for the Small Animal Practitioner

pyrexia, anaemia, or pain may in some situations show moderate to severe

obtundation without any primary neurological disease. As already mentioned,
animals which have suffered significant trauma or stress, for example after a
road traffic accident, may also show an apparently reduced level of mentation.
In these situations, mentation may be expected to improve if the underlying
problems are corrected, and this should allow a reduced suspicion of the pres-
ence of a primary neurological disorder.
Changes in behaviour or the quality of mentation usually imply involvement
of the cerebral cortex. Behavioural changes can be caused by many things,
including ageing, stress, change of environment or home situation, metabolic
disease, chronic pain, dietary change, etc. Therefore, taking a careful clinical his-
tory is crucial in cases where a change of behaviour forms part of the presenting
complaint. If a more subtle behavioural change is reported during the history‐
taking related to the investigation of a problem for which altered behaviour was
not immediately apparent, then this may raise the level of suspicion for a possi-
ble intracranial disease.
Altered behaviour is less commonly the primary clinical sign reported for
neurological disease, possibly due to our relative lack of sensitivity as veterinar-
ians and owners in being able to identify more subtle changes. However, there
are occasions when an owner will have recognised a loss of learned behaviour,
or a change in demeanour or willingness to play in their pet, and this may be
significant. As already stated, neurological disease leading to behavioural change
usually implies a prosencephalic lesion and, in such situations, careful perfor-
mance and interpretation of the neurological examination may identify other
abnormalities consistent with a lesion affecting the cerebral cortex.

1.4.5 Blindness
An acute onset of blindness is usually noticed by pet owners, since it may be
extremely disorientating for the affected animal, and may lead to behavioural
changes as well as more obvious signs such as bumping into objects. It is often
the case that vision is lost progressively rather than acutely, but in these situa-
tions owners frequently do not notice the more subtle changes brought about in
their pet by a reduction in the quality of their vision, and it is only when the
problem has progressed to complete or near‐complete blindness that the owner
becomes aware. When presented with an animal with reduced vision, it is there-
fore important to question the owner carefully in order to elucidate whether the
visual loss may in fact have occurred progressively rather than acutely.
A blind cat or dog may be reluctant to move around, become ‘clingy’ or fearful
in situations where they were previously relaxed and confident, and may even
develop obsessive or phobic behaviours. For neuroanatomical evaluation, the
important thing to establish is whether the blindness appears peripheral or cen-
tral. Central blindness implies dysfunction of the central visual pathways and/or
visual cortex; this is usually rare in the absence of other signs of intracranial
 Chapter 1 ‘Is it Neurological?’ 11

disease. More commonly, vision may be lost in one eye as a result of a lesion
affecting the contralateral visual cortex, but as vision remains normal in the other
eye, the owner either may not be aware of the vision loss or may have noticed
the animal bumping into objects on only one side. The menace response will be
absent in the affected eye, but the pupillary light reflex (PLR) (as well as palpebral
reflex and other cranial nerves) are likely to be normal. Use of the so‐called
‘cotton‐­ball’ test (see Chapter 3) may also help to identify visual loss in one eye.
In general, animals that present as completely or almost completely blind
with no other neurological abnormalities, will have lesions affecting either the
optic nerves or the eyes themselves. In the case of ocular disease, if there are no
grossly obvious abnormalities such as cataracts, then the retina is the region
most likely to be affected. A fundic examination should be performed and may
reveal evidence of retinal disease or detachment. In the absence of an obvious
cause for sudden blindness, then the two conditions which must be considered
are sudden acquired retinal degeneration syndrome (SARDS) and optic nerve
disease; optic nerve disease can have a number of possible causes (see Section 6.4
‘Blindness’).
SARDS is a syndrome that usually presents as an apparent acute onset of
complete blindness, although careful history taking may reveal evidence that
vision has deteriorated over a period of weeks. There is frequently an accompa-
nying history of polyphagia, polydipsia, and polyuria and sometimes behav-
ioural changes. Menace responses are absent bilaterally, and PLRs are reduced
although may still be present to some degree. Routine biochemistry can reveal
increased alkaline phosphatase and cholesterol, and there is often a high suspi-
cion of hyperadrenocorticism although this is rarely confirmed. Despite the
problem being associated with retinal degeneration of an unknown cause, fun-
dic examination is usually normal at least in the early stages. Diagnosis can be
made with a high degree of certainty from the history, physical examination,
and biochemistry findings, but confirmation requires the presence of a bilater-
ally abnormal electroretinogram. The prognosis for return of sight is poor,
although other systemic signs may improve over time.
The optic nerves can be affected by neoplastic disease that either infiltrates
the nerves, such as lymphoma, or that compresses the optic chiasm, such as
pituitary macroadenomas. Inflammatory disease affecting the optic nerves is
more common and can be either confined to the optic nerves as the condition
‘optic neuritis’, or present as part of a more generalised inflammatory condition
of the CNS (such as meningoencephalitis of unknown origin, MUO). In optic
neuritis cases, it is sometimes possible to visualise swollen optic nerve heads dur-
ing the fundoscopic evaluation. Other neurological abnormalities may be
observed in cases with MUO, such as postural reaction deficits or other cranial
nerve abnormalities. Cerebrospinal fluid analysis frequently confirms the pres-
ence of inflammation.
12 A Practical Approach to Neurology for the Small Animal Practitioner

Top tip: Acute blindness with reduced or absent PLRs and no other physical or
neurological abnormalities usually indicates either SARDS or optic neuritis. In both
cases, the prognosis is guarded but diagnosis is worth pursuing because some cases of
optic neuritis are responsive to immunosuppressive therapy.

1.4.6 Deafness
Deafness is a rare presentation in isolation, but owners may report behavioural
changes which could imply that deafness or reduced hearing may be present.
Bilateral hearing loss may be very significant to the lifestyle and behaviour of
individual animals, and its effects should not be underestimated. Unilateral deaf-
ness is more challenging to detect and may be more debilitating than is currently
thought as a result of an inability to localise the source of sounds. Deafness is a
difficult neurological deficit to confirm clinically, but careful testing may lead to
a high index of suspicion. As with other conditions, careful clinical history tak-
ing may provide some clues as to the origin of the deafness. Physical examina-
tion should obviously include an examination of the external ear canals.
Neurological examination may reveal other abnormalities which can give clues
as to the origin of the deafness (e.g. vestibular signs, facial nerve paralysis, and
Horner syndrome may all be associated with otitis media/interna).
Confirmation of deafness requires electrodiagnostic evaluation through the
recording of brainstem auditory evoked responses (BAER). Deafness may be
either conductive, associated with abnormalities of conduction of sound waves
to the receptors in the inner ear (e.g. accumulation of debris in the external ear
canal or fluid accumulation in the tympanic bulla), or sensorineural, associated
with a problem in the cochlea of the inner ear or the cochlear nerve itself.

1.4.7 Tremor
Tremor associated with neurological disease can be broadly divided into head
tremor and whole‐body tremor. Head tremor is most commonly associated with
cerebellar disease (see Video 11), when it may be permanent, but tremor often
becomes more severe when an affected animal attempts to perform some action
involving the head, such as eating or drinking (termed an ‘intention tremor’).
The tremor may be very mild and subtle, and occasionally has not been appreci-
ated by the owner. If a head tremor is observed in the consultation, then a full
neurological examination should be performed, particularly to look for other
signs consistent with cerebellar disease.
A slower head ‘tremor’ known as idiopathic head bobbing is occasionally
seen, particularly in young Boxers and English Bulldogs (see Video 12). The
cause is unknown, the problem is intermittent, and is generally self‐limiting. All
investigative and diagnostic tests tend to be normal in affected dogs, and the
head‐bobbing movements may be vertical (‘Yes’) or horizontal (‘No’). Affected
dogs can usually be distracted during an episode; when distracted the head
 Chapter 1 ‘Is it Neurological?’ 13

­ obbing will cease, and this can be used to distinguish this paroxysmal occur-
b
rence from a focal seizure.
Whole‐body tremor is an uncommon presentation, but when seen can be
severe and debilitating. The two most common forms of whole‐body tremor are
that associated with toxin ingestion (particularly tremorgenic mycotoxins found
in mouldy food, metaldehyde, chocolate, and some prescription medications)
and idiopathic generalised tremor syndrome (see Section 6.2 ‘Movement
Disorders’ and Video 7). Tremors resulting from toxicity usually affect the whole
body, can be severe and unremitting, do not subside with recumbency, and may
occasionally progress to generalised seizures. This is a neurological emergency
and requires emergency treatment to prevent hyperthermia and hypoglycaemia.
Diagnosis generally relies on thorough history taking and the clinical
presentation.
Another type of tremor that may be encountered is orthostatic tremor. This
type of tremor predominately affects the limbs in large and giant breed dogs
(particularly Great Danes) and is present only when the limbs are weight‐bear-
ing (see Video 13). The condition is benign and there is no treatment. Occasionally,
a limb tremor may be associated with orthopaedic disease, especially if there is
significant muscle atrophy or pain. It can also occur in some older dogs, appar-
ently as part of an ageing process, and this is termed an ‘essential’ or ‘senile’
tremor (see Video 14).
There are a few conditions affecting the myelination of axons which present
as whole‐body tremors in young puppies around 6–8 weeks of age. Breeds that
are typically affected include the English Springer Spaniel, Chow, Samoyed,
Weimaraner, and Dalmatian.

Top tip: The major differential diagnoses for an acute onset of generalised tremor in
an adult dog are toxin ingestion and idiopathic generalised tremor syndrome (‘little
white shaker’ disease); in the former the tremor is persistent and severe, in the latter
it may wax and wane and disappears when the dog is at rest.

1.4.8 Paresis/Plegia
Paresis can be defined as a reduced ability to initiate or maintain motor activity.
It may manifest as a reduced ability to support weight (LMN paresis) or a reduced
ability to generate gait (UMN paresis). Plegia is defined as an absence of volun-
tary movement (i.e. paralysis). A plegic animal usually indicates that severe CNS
injury has occurred, either at the level of the brainstem or neck for tetraplegia or
caudal to the T2 spinal segment for paraplegia. Paraplegia, involving only the
pelvic limbs, is far more common than tetraplegia, partly because any lesion in
the CNS that is capable of causing tetraplegia may be accompanied by other
severe effects which may include respiratory failure and death. When an animal
is presented in such a condition, particularly if there is a history of possible or
14 A Practical Approach to Neurology for the Small Animal Practitioner

definite trauma, great care should be taken when moving the patient in case
there is instability of the vertebral column and the potential for further spinal
cord damage.
In an animal that is plegic (and only in these animals), it is necessary to
include the testing of so‐called ‘deep pain perception’ (DPP), which is the ability
of the animal to recognise a noxious stimulus applied to the deep structures of
the foot or toe (see Chapter 3). The loss of DPP is a poor prognostic indicator in
many situations, since the sensory fibres that convey this information are carried
in many tracts which are located deep within the spinal cord. Their loss may
therefore indicate spinal cord damage at the deepest level. However, DPP is not
likely to be lost in animals which have less severe spinal cord injury and remain
paretic; testing for DPP therefore need not be performed in such animals.
The neurological examination is critical to being able to localise the likely
anatomical location of any lesion causing paresis or plegia. This particularly
includes an understanding of the spinal reflexes. It is still a common mistake to
interpret the presence of a normal pedal withdrawal reflex as an indicator that
DPP is present, and this can lead to overly optimistic prognosis being given to
owners of animals with severe spinal cord injury (see Chapter 3 and Video 15).

Don’t make this mistake: In paralysed animals, make sure you understand the
difference between testing spinal reflexes and testing for deep pain perception (see
Chapter 3).

Disorders affecting the PNS can present as a relatively acute onset of tetraple-
gia or severe tetraparesis. In this situation, the differentiation from a spinal cord
lesion can usually be made by the fact that the neurological deficits cannot be
explained by a single, focal CNS lesion as the spinal reflexes are reduced in all
limbs. The major differentials for acute onset severe tetraparesis/tetraplegia
localising to the PNS are acute canine polyradiculoneuritis, fulminant myasthe-
nia gravis, and botulism.
Milder forms of paresis may be much more difficult to identify and a degree
of paresis affecting one or more limbs may be the only sign of a neurological
problem. Close observation of gait, including retrospective and slow‐motion
video analysis, may be helpful in identifying a reduction in the quality of move-
ment. UMN paresis occurs when the control or initiation of movement is affected
by a lesion that is affecting either the gait‐generating regions of the cerebral
cortex or brainstem or the spinal cord pathways containing the UMNs descend-
ing to synapse with the LMNs in the brachial or lumbosacral plexi. UMN paresis
may lead to a long‐strided gait, toe dragging, and postural reaction deficits, but
the affected limbs retain normal spinal reflexes and are not weak. LMN paresis,
by contrast, causes a paresis like that seen in PNS diseases, characterised by
weakness, an inability to support weight, and a short‐strided, choppy gait. For
 Chapter 1 ‘Is it Neurological?’ 15

lesions affecting the C6–T2 spinal cord segments, this can lead to the so‐called
‘two‐engine’ gait, with short, choppy thoracic limbs and long‐striding, ataxic
pelvic limbs.
Paraparesis can be misinterpreted as bilateral pelvic limb lameness of orthopae-
dic origin, and vice versa. Some conditions, such as hip dysplasia and ­bilateral cra-
nial cruciate ligament disease, can present in a very similar way to a paraparesis
caused by a spinal cord disorder. A knowledge of orthopaedic disease and a famili-
arity with basic orthopaedic examination is therefore important for the neurologist
to avoid unnecessary investigative procedures resulting from a failure to recognise
potential orthopaedic problems. Testing of postural reactions may allow recognition
of a genuine neurological problem, but significant orthopaedic disease involving
pain and a reluctance to bear weight may also complicate the interpretation of pos-
tural reaction testing. When in doubt, it may be wise to consult the opinion of an
orthopaedic surgeon in these cases before assuming a neurological problem.

Don’t make this mistake: An acute onset of bilateral cranial cruciate ligament
failure can appear surprisingly similar to an acute T3–L3 myelopathy!

1.4.9 Ataxia
Ataxia is frequently, but not always, associated with paresis. Ataxia implies some
disorder of coordination of movement, and there are three recognisable forms of
ataxia that each suggest a lesion involving different parts of the nervous system.
The observation of ataxia is highly suggestive of a neurological problem.
However, as for paresis, some non‐neurological problems can mimic ataxia if
they significantly interfere with an animal’s gait (e.g. bilateral cruciate ligament
disease). The hallmark of ataxia is an unpredictability of limb placement, which
is usually different to the predictable gait abnormalities observed in cases with
lameness or orthopaedic disease.
The form of ataxia that is most commonly associated with paresis is a general
proprioceptive ataxia (or ‘spinal’ ataxia, see Video 16). This occurs when a lesion
disrupts the proprioceptive pathways in the spinal cord or brainstem, and is
invariably therefore seen in conjunction with paresis. It may be symmetric or
asymmetric, depending on the precise location of the lesion and, as for paresis,
may affect all limbs or just the pelvic limbs. Attempting to differentiating between
ataxia and paresis for lesions affecting the brain or spinal cord is neither neces-
sary nor particularly useful; the most important thing is being able to recognise
mild forms of either, which may give a clue to the possibility of a neurological
condition as opposed to, for instance, an orthopaedic problem.
Lesions affecting the vestibular system result in a vestibular ataxia. This has
a different quality to general proprioceptive ataxia, being caused in part by a
loss of extensor muscle tone on the side of the lesion due to a reduction in the
level of activity in the ipsilateral vestibulospinal tracts. This leads to a tendency
16 A Practical Approach to Neurology for the Small Animal Practitioner

to collapse or fall towards the affected side, and sometimes tight circling towards
that side; there is also a loss of balance associated with the vestibular distur-
bance, which increases the tendency to fall or lurch towards the affected side
(see Video 17).
The third form of ataxia is caused by lesions of the cerebellum, resulting in a
cerebellar ataxia (see Video 18). The cerebellum is intimately involved in the
coordination of gait and movement, receiving proprioceptive information from
the limbs and body, as well as from the vestibular system; this involves feedback
loops with the gait‐generating centres of the forebrain and brainstem, as well as
having a significant inhibitory function on the vestibular nuclei of the brainstem.
All of this explains the signs seen with cerebellar disease, including the intention
tremor described above, the classical hypermetric gait, and the potential for ves-
tibular signs. The gait of a dog with a cerebellar lesion may therefore have quali-
ties of both vestibular and cerebellar ataxia, sometimes termed ‘cerebellovestibular
ataxia’. The hypermetria seen in cerebellar ataxia can affect all limbs but may also
be confined to one side of the body, or even just one limb, depending on the pre-
cise location of the lesion. The other confusing aspect of cerebellar disorders,
which can cause problems when trying to decide if the neurological deficits can
be explained by a single lesion, is its involvement with the vestibular system;
because the cerebellum receives some direct input from the peripheral vestibular
system bilaterally, some cerebellar lesions will cause vestibular signs (such as a
head tilt) on the same side as the lesion (ipsilateral). However, since the cerebel-
lum itself has a primarily inhibitory influence on the vestibular nuclei of the
brainstem, cerebellar lesions in specific locations may result in a so‐called para-
doxical vestibular syndrome, where the vestibular signs would suggest a lesion on
the opposite side of the body to that of the actual lesion (see Chapter 4 and
Section 6.8 ‘Cerebellar Dysfunction’ for a fuller explanation, and Video 19). If
this is not appreciated, then it may lead to the incorrect assumption that there
must be a multifocal localisation, potentially suggesting a different set of differen-
tial diagnoses to a problem explained by a single (focal) lesion.

Top tip: Learn to recognise the three common forms of ataxia, as this provides a short
cut to lesion localisation and assists with forming the list of differential diagnoses.

Don’t make this mistake: Remember, pure cerebellar lesions may cause variable
hypermetria, and either ipsilateral or contralateral vestibular signs.

1.4.10 Abnormalities of Head Position and Eyeball Position

and Movement
1. Head tilt
Rotation of the head about the long axis of the body is known as a head tilt and is
typically associated with disorders of the vestibular system or cerebellum (see
above). The head is rotated so that the affected side is down relative to the midline,
 Chapter 1 ‘Is it Neurological?’ 17

such that the ear on the affected side lies at a lower level than that of the unaf-
fected side (see Figure 1.2). This is indicative of a reduction in the influence of the
vestibular system on the affected side. This also explains the so‐called paradoxical
head tilt seen with certain unilateral cerebellar lesions, where the head is tilted in
the opposite way due to relative increase in influence of the vestibular system on
the affected side brought about by a loss of inhibitory input from the cerebellum.

2. Head turn
Some unilateral forebrain lesions can cause a phenomenon known as a head
turn. This occurs when the head remains level about its central long axis, but is
turned to right or left, usually towards the affected side. It may also be associated
with compulsive circling in the same direction and is thought to be caused by the
loss of sensory input being perceived from the contralateral environment (i.e.
the animal turns and circles towards the side from which it still perceives sensory
information).

Figure 1.2 A Cavalier King Charles Spaniel with a left head tilt associated with a left
peripheral vestibular syndrome caused by otitis media/interna.
18 A Practical Approach to Neurology for the Small Animal Practitioner

3. Strabismus
This indicates an abnormal position of one or both eyes and may be either static
or positional. In a static strabismus, the eye is permanently positioned incor-
rectly, and this indicates a lesion affecting either the extraocular muscles or one
or more of the cranial nerves supplying them (III, IV, or VI, see Chapter 3). The
direction of the strabismus is governed by the precise loss of muscle function. A
bilateral ventrolateral strabismus (so‐called ‘sunset sign’) is seen in certain cases
of severe hydrocephalus, and is thought to occur as a result of either changes in
skull morphology or pressure on the oculomotor nuclei in the midbrain.
Positional strabismus occurs when an eye moves into an abnormal position
only when the head position is changed. When there is a suspicion of vestibular
syndrome it is necessary to elevate the head so that the affected animal is look-
ing directly up at the observer. In this position, the eye on the affected side often
assumes an abnormal ventrolateral position. This occurs due to loss of the ability
to determine the new correct position of the eye when the head has been moved
(see Section 6.7 ‘Vestibular Syndrome’ for a fuller explanation).

4. Nystagmus
This is the phenomenon of rapid involuntary eye movements. Physiological nys-
tagmus is seen in response to head movement, and is a normal phenomenon
requiring the vestibular system and extraocular muscles to all be functioning
normally (see Chapter 3). Pathological nystagmus occurs most commonly when
there is an imbalance between the two sides of the vestibular system. This usu-
ally implies a unilateral vestibular lesion, and in this situation the movements
are commonly described as a jerk nystagmus, with fast and slow phases in oppo-
site directions. The direction of the movements may be horizontal, rotatory, and
occasionally vertical. When it is possible to define the direction of each phase,
the slow phase of movement tends to be directed towards the side of the vestibu-
lar lesion (see Video 20).
Pendular nystagmus is seen in some oriental cat breeds, especially Siamese
cats. Affected animals show rhythmic, usually horizontal, eye movements at
rest, with no fast or slow phase. This is considered normal in these cats, and does
not appear to affect their quality of life. It is thought to occur as a result of an
abnormal degree of crossing over of optic nerve fibres at the optic chiasm during
embryological development (see Video 21).

Top tip: Be prepared to move an affected animal’s head into abnormal positions to
induce nystagmus or strabismus when there is a suspicion of vestibular disease; any
abnormality of eye position or movement which occurs when the head is at rest is
likely to be pathological and usually indicative of vestibular dysfunction.

Don’t make this mistake: Pendular nystagmus can be a ‘normal’ phenomenon in

certain pedigree oriental cats and is not always an indicator of vestibular disease.
 Chapter 1 ‘Is it Neurological?’ 19

1.4.11 Reduced Sensation (Hypaesthesia)

The skin is supplied with sensory receptors that are sensitive to pressure and
deformation (mechanoreceptors), heat (thermoreceptors), and pain (nocicep-
tors). These are relatively specific and respond only to the source of energy for
which they are adapted. Each spinal cord segment receives information from
sensory neurons that enter via the dorsal horn from a region of skin known as
the dermatome. Along most of the trunk, this information is carried in cutane-
ous nerves which arise in a largely segmental fashion and form an important
part of the cutaneous trunci reflex (see Chapter 3). Skin sensation in the limbs is
transmitted via sensory neurons carried in the major peripheral nerves of the
limb, most of which are mixed nerves carrying both motor and sensory fibres. In
the limbs, much of the skin is supplied by more than one peripheral nerve. The
area of skin supplied by a single nerve is divided into overlap zones around the
edges; the specific regions in the centre supplied by just that nerve are known as
autonomous zones (see Figure 1.3). A knowledge of these zones is important to
allow for the identification of damage to individual spinal nerves or segments,
for instance in the case of brachial or lumbosacral plexus injury.
Skin sensation from the face and head is carried largely within the different
branches of the trigeminal nerve (V), including from the surface of the cornea.
Identification of hypaesthesia on one side of the face can be indicative of a
trigeminal neuropathy, sometimes in the absence of other signs. The only excep-
tion is the skin of the outer (concave) surface of the pinna, which is supplied by
the auricular branch of the facial nerve (VII).
Loss of sensation from the inner medial surface of the nose (nasal planum
sensation) may be useful in recognising the presence of a focal forebrain lesion.
Touching the nasal planum induces a conscious reaction in the normal dog or
cat, and lesions either of the ipsilateral trigeminal nerve or of the contralateral
forebrain may lead to a loss of this response (see Chapter 3).

1.4.12 Lameness
Lameness represents a reluctance to bear weight on a limb. Lameness resulting
from neurological disease (neurogenic lameness) can be very difficult to distin-
guish from orthopaedic lameness. Monoparesis may also appear very similar to
a true lameness in many cases. Clues to the lameness having a neurogenic origin
may include rapid muscle atrophy, reduced proprioception, toe dragging, and
reduced spinal reflexes (particularly the pedal withdrawal reflex). However, in
many cases electrodiagnostic testing and imaging are required for certainty of
diagnosis. Neurogenic lameness can arise from a variety of causes, such as a lat-
eralised disc herniation, peripheral nerve sheath tumour, neuritis, nerve trauma,
and degenerative lumbosacral stenosis (DLSS).
DLSS is a common condition with a variety of causes in which the nerves of
the cauda equina are variably compressed by adjacent structures at the level of
the lumbosacral disc and intervertebral foraminae. These structures include the
20 A Practical Approach to Neurology for the Small Animal Practitioner

intervertebral disc, bony structures, such as the articular facets, pedicle, and arch
of the sacrum, and other soft tissue structures, including the interarcuate liga-
ment and joint capsules. Because of the different functions supplied by the
nerves of the cauda equina at this level, the presentations associated with DLSS
can be variable and also similar to orthopaedic diseases such as hip dysplasia.
Unilateral lameness may occur if there is significant foraminal stenosis leading to
compression of the L7 nerve root which exits the vertebral canal at this level.
Bilateral lameness, paresis, and stiffness, as well as pain, are also commonly
seen. Ataxia is usually mild or non‐existent in these cases.

1.4.13 Pain (Hyperaesthesia)

Pain can be very severe in neurological disease and may be the only presenting
sign in some conditions. Pain is defined as the conscious awareness of a noxious
stimulus, and requires a conscious response to stimulation of nociceptors.
Detecting, interpreting, and localising the source of pain, even when one is rea-
sonably certain it is present, can be a challenge. In some conditions, the pain
may be focal but so severe that the animal responds to palpation in multiple
regions of the body. At other times, multiple regions of the body may be genu-
inely painful, but this again may make the examination difficult to interpret.
In the authors’ experience, when an animal presents with a history of crying
or screaming in pain, a neurological cause should always be considered. There are
very few conditions which will induce this reaction in an animal. Orthopaedic
conditions, even including fractures, will rarely cause an animal to vocalise unless
a peripheral nerve is involved in the fracture site. Visceral pain can be severe, but
affected animals usually become dull and depressed rather than vocalise. The pain
associated with mechanically pinching or stretching a peripheral nerve is extreme
and acute, and is often associated with specific or sudden movements; this history
should therefore lead to a high index of suspicion for a neurogenic origin.

Sciatic n.
Musculocutaneous n.

Ulnar n.
Radial n. Saphenous n.

Peroneal n. Tibial n.

Figure 1.3 The cutaneous autonomous zones of the distal parts of the thoracic limb and the
distal parts of the pelvic limb. A knowledge of these zones may assist the clinician in deter-
mining which peripheral nerves may be involved in a traumatic injury for instance.
 Chapter 1 ‘Is it Neurological?’ 21

Other potential sources of severe neurogenic pain include inflammation of

the meninges, as seen in conditions such as steroid responsive meningitis arteri-
tis (SRMA), stretching of the meninges and/or compression of the nerve roots in
intervertebral disc herniation, atlantoaxial instability, certain spinal neoplastic
conditions, and inflammation/infection of the intervertebral disc in discospon-
dylitis. The nerves of the cauda equina and tail can be the source of severe pain
associated with DLSS or other compressive or inflammatory lesions. In these
situations, the presenting signs can be limited to behavioural change or extreme
reluctance to lift the tail. An animal presenting with severe pain when defecat-
ing may have tail‐base pain, which can be associated with intervertebral disc
disease at this level. Severe inflammation of the epidural fat and meninges, such
as in epidural empyema, may also cause severe pain.
Certain intraparenchymal spinal cord conditions such as syringohydromyelia
can present with signs of intermittent crying in pain. In this situation, there
appears to be an association with larger lesions and those affecting the dorsolat-
eral horns of the spinal cord. In susceptible breeds, this diagnosis should be con-
sidered in an animal presenting with pain only.
When faced with a potentially painful animal, the physical examination
becomes crucial in trying to locate the source of the pain, but as already stated
this can easily be misinterpreted or misleading. Great care should be taken, and
the examination initially performed gently and with minimal movements of head
and/or limbs. The amount of movement and pressure applied by palpation can
then gradually be increased. If a potentially painful region is identified (e.g. in the
thoracolumbar region), the examination should focus on other parts of the body
before returning to the suspected region in order to try to elucidate if this is really
the source of the pain. Even with this approach, mistakes will be made!

Top tip: Always look for a neurogenic cause when presented with an animal with a
history of vocalising in pain.

Don’t make this mistake: Be prepared to repeat imaging when an animal remains
persistently in pain and a cause of the pain has not been found. Non‐displaced verte-
bral fractures can be missed!

1.4.14 Disorders of Micturition

The ability to pass urine can be affected by many neurological problems, although
rarely in isolation. Spinal cord lesions (myelopathies), particularly severe lesions
associated with intervertebral disc extrusion, are commonly associated with
problems of micturition, and the anatomical level of the myelopathy dictates the
nature of the dysfunction. It is necessary to have an understanding of the inner-
vation of the bladder and urethral sphincters in order to appreciate why this is
the case.
22 A Practical Approach to Neurology for the Small Animal Practitioner

The bladder is innervated by the pelvic nerve which arises from the sacral
spinal cord segments. This provides motor (parasympathetic) innervation to the
smooth muscle of the detrusor as well as carrying sensory information from
stretch receptors in the bladder wall. The external urethral sphincter (striated
muscle) is supplied by the pudendal nerve arising also from S1–S3 spinal cord
segments. This is also motor to the anal sphincter and carries sensory informa-
tion from the perineum. These LMNs receive modulation from the UMNs arising
from the micturition centre in the medulla (see Figure 1.4). Problems affecting
the spinal cord segments cranial to S1 usually lead to a so‐called UMN bladder,
whereas problems caudal to L7 normally lead to a LMN bladder.
In the UMN bladder, loss of modulation of the LMNs leads to an increase in
tone in both detrusor and external urethral sphincter. The result is a bladder
which over‐fills to the point at which the pressure from inside the bladder is
enough to force leakage through the spastic urethral sphincter. The detrusor
muscle can be stretched and, if not treated, irreversible detrusor muscle damage
can occur, and this leads to irreversible incontinence.
In the LMN bladder, damage to the LMNs supplying both the detrusor and
sphincter muscles leads to a flaccid bladder and sphincter, so that urine leaks out
easily and the bladder remains small and flaccid. Lesions that cause this type of
presentation usually also cause loss of anal tone, loss of perineal sensation, and,

Upper motor neuron

L1–L4 S1–S3

Pudenal nerve
Micturition centre Hypogastric nerve
of the brain stem Pelvic nerve

External urethral sphincter

Internal urethral sphincter
Figure 1.4 The innervation of the urinary tract. The bladder detrusor muscle is innervated
mainly by the pelvic nerve (parasympathetic supply) originating in the sacral spinal cord
segments (S1–S3), but also by the sympathetic nervous system via the hypogastric nerve,
which originates in the lumbar spine. The pelvic nerve carries both motor fibres responsible
for contraction of the detrusor muscle in micturition and sensory fibres responsible for
detecting bladder wall stretching. In young animals, there is a simple reflex arc involving
these fibres, meaning the bladder empties when it is full; in older animals, higher centres in
the brainstem and forebrain lead to voluntary control of micturition and the possibility of
‘toilet‐training’. The external urethral sphincter is a skeletal muscle sphincter innervated by
the pudendal nerve, arising from the sacral spinal cord (S1–S3); this nerve also receives upper
motor neuron input, as well as carrying sensory information back from the sphincter. The
internal urethral sphincter is a smooth muscle thickening of the urethral wall innervated by
the sympathetic fibres of the hypogastric nerve.
 Chapter 1 ‘Is it Neurological?’ 23

sometimes, loss of tail function. The prognosis for return to function with this
type of injury may be more guarded than for an UMN lesion. A common pres-
entation of LMN bladder that does not always behave in this way is the so‐called
‘tail‐pull’ injury seen in cats, when a traumatic incident results in fracture/luxa-
tion of sacral or caudal vertebrae. In this situation, the bladder often becomes
over‐full, as in the UMN bladder, and is difficult to express. This is believed to
result from on‐going innervation of the internal urethral smooth muscle
sphincter by the hypogastric (sympathetic) nerve which arises from more
cranially in the lumbar spine. Interestingly, this phenomenon is rarely seen in
dogs with fractures of the sacrum for instance.
Reflex dyssynergia is a disorder of micturition where the coordination
between contraction of the detrusor muscle and relaxation of the urethral
sphincters is lost. This leads to an inability to empty the bladder; the usual pres-
entation is of an over‐full bladder with no urethral obstruction and a history of
straining and sometimes urine leakage or dripping. The cause of this problem is
unknown, and treatment can be challenging.

1.5 ­Summary

It is clear that diseases of the nervous system may present in a wide variety of
different ways, and this presents the first challenge to their diagnosis and treat-
ment. Once it has been decided that a problem is likely to have a neurological
origin, the next step is to use the neurological examination to decide where the
lesion may be located within the CNS or PNS. It is only at this stage that further
investigations should be planned. In the following chapters we shall attempt to
present a logical and methodical approach to neurological disease, which should
enable the practitioner to develop a good differential diagnosis list when faced
with such problems. We also attempt to give sensible, practical advice to owners
of animals affected by neurological conditions.

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Chapter 2 Clinical History
and Signalment
Paul M. Freeman

The ultimate goal of the consultation in the investigation of any neurological

problem is to come up with a sensible and reasonably short list of differential
diagnoses. This short list can then be used to focus and direct the diagnostic
approach, dependent on the client’s expectations and budget. To that end, the
starting point is taking an appropriate and complete clinical history. The animal’s
signalment can then be incorporated with this information to formulate a ranked
list of differential diagnoses once the general physical and neurological examina-
tions have been performed.

2.1 ­General Medical History

It is important not to neglect the general medical history when approaching a

neurological case. This is particularly relevant when the problem appears to
clearly represent a neurological disease, such as generalised seizures. In acute
and severe presentations, where time may be important, detailed client ques-
tioning should be tempered by the need to start investigations and treatment,
such as in cases of status epilepticus or suspected head or spinal trauma.
However, important facts pertaining to the ultimate diagnosis may be missed if
certain information is not gathered, and the clinician must always be aware of
these potentially conflicting demands. Furthermore, many general practitioners
will be expected to complete the consultation in a relatively short period of
time. The taking of a complete general medical history as well as the specific
neurological history, in addition to performing a physical and neurological
examination, can therefore put severe time pressures on the consultation. In a
non‐emergency situation, the option of admitting the animal for a more detailed
examination and to allow a longer time for client questioning should always be
considered.

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

25

26 A Practical Approach to Neurology for the Small Animal Practitioner

Potentially important questions from the general medical history may include
the following.

a. How long has the animal in question been in the owner’s possession?
For any suspected neurological disease, one of the key factors to be looked at
in the neurological history will be the onset of the problem; if an animal has
been ‘rescued’ or has been owned for a relatively short period of time, and
the problem is intermittent, it may not be possible to establish precisely how
long the presenting problem has been ongoing. In a case of behavioural
change, a knowledge of how this has developed may be very important, and
an animal which has not been with the current owner since a puppy or a kit-
ten may exhibit behavioural changes which are due to an alteration in envi-
ronment or other factors, rather than reflecting a primary brain disorder.
b. Vaccination status
There are a number of viral diseases which are largely preventable by appro-
priate vaccination, but which may be responsible for neurological disease.
Canine distemper virus (CDV) was once a major cause of neurological dis-
ease, causing a variety of signs including blindness, vestibular syndrome, sei-
zures, and, in particular, myoclonus. In the UK, the frequency of CDV has
been greatly reduced by vaccination, although cases are still seen in environ-
ments where there are a large number of unvaccinated dogs. It may also
cause neurological disease in vaccinated animals, although this is unusual,
and signs may be reduced in severity and often not accompanied by systemic
disease. Feline leukaemia virus (FeLV) may be associated with lymphoma,
which is a relatively common cause of neurological dysfunction in cats, with
signs dependent on the specific lesion location. However, FeLV has also been
reported to have direct neurotoxic effects, and has been associated with pro-
gressive central nervous system (CNS) signs (Hartmann 2012). Feline immu-
nodeficiency virus (FIV) has been associated with an inflammatory
encephalopathy as well as polymyositis (Hartmann 2012). Feline panleuko-
penia virus infection in utero can lead to a syndrome of cerebellar hypoplasia
in newborn kittens and is another potential diagnosis which may be sus-
pected simply by knowing the vaccination status.
c. Anti‐parasite treatment
This has a specific bearing on the likelihood of vascular neurological disease
associated with Angiostrongylus vasorum infection but may also be important
due to the possibility of overdose or adverse reactions. Permethrin toxicity in
cats associated with the use of proprietary ‘pet‐shop’ antiparasiticides is well
recognised, and certain dog breeds may be at significant risk of neurological
signs following treatment with products containing ivermectins. Many
Border Collies and some other breeds are affected with a mutation of the
MDR gene, leading to a dysfunctional P‐glycoprotein complex; this forms an
important part of the blood–brain barrier by pumping substances out of the
 Chapter 2 Clinical History and Signalment 27

CNS, and may lead to acute toxicity when such dogs are treated with iver-
mectins due to accumulation of drug within the CNS.
d. Travel history (outside and within the country)
Certain parasite‐transmitted diseases that may have neurological manifesta-
tions should be included as possible differential diagnoses in animals with a
known travel history to regions where these infections are common (e.g.
Ehrlichia canis, Leishmania spp., and Babesia spp.). When the affected animal
has an unknown travel history, or has been imported or ‘rescued’ from a
country or region where such infections are endemic, their likelihood should
also be considered. There is an increasing tendency in the United Kingdom
(UK) for canine rehoming centres to import dogs from countries such as
Spain and Romania, and these animals may be important as carriers of infec-
tious diseases that may potentially lead to neurological syndromes.
Other diseases may be more common in certain parts of the UK. For
example, the canine lungworm Angiostrongylus vasorum, which is transmitted
through molluscs, may be present in as many as 50% of foxes in the south-
east of the UK (Taylor et al. 2015), but appears less common in other parts of
the country. This parasite may cause a coagulopathy in affected dogs, which
can present as an acute onset of neurological signs. The tick‐borne infection
Borrelia burgdorferi, which results in the condition Lyme disease, is known to
be more common in the south and southwest of England and the Scottish
Highlands. Although an uncommon cause of neurological disease, exposure
to the appropriate environment may increase consideration of this disease as
a possible cause of certain presenting signs.
e. Toxin exposure
Known, suspected, or potential exposure to neurotoxins is a key part of the
clinical history taking for any acute syndrome, particularly for presentations
such as whole‐body tremor and status epilepticus with no previous seizure
history. Mouldy food may contain mycotoxins, which are a common source
of tremorgenic toxicity in dogs and can lead to severe and difficult to control
tremors, or even status epilepticus. Clues, such as being walked off‐lead in
areas where food may have been discarded or going missing for a period of
time when on a walk, may increase the suspicion of such toxicity. Tremor
may also be induced by other toxins including permethrins, organophos-
phates, hexachlorophene (used as a disinfectant), and bromethalin (a neuro-
toxic rodenticide). Other potential excitatory neurotoxins include chocolate,
caffeine, and amphetamines. Exposure to potential human recreational drugs
should also be considered, with many cases of cannabis toxicity being reported
in dogs, usually resulting in depression, hypersalivation, mydriasis, and
hypermetria; signs may be variable and hyperexcitability and seizures can
also be seen. Bear in mind that owners may be reluctant to admit to the pos-
session of illegal recreational drugs, and therefore this line of questioning
must be carried out in a careful and sensitive manner. There are many other
28 A Practical Approach to Neurology for the Small Animal Practitioner

reported neurotoxic substances to which dogs in particular may be exposed.

These include lead, metaldehyde, alphachloralose, and avermectins. The
widely used antibiotic metronidazole may cause an acute onset of central
vestibular signs, especially at higher or p ­ rolonged doses (see Section 6.7
‘Vestibular Syndrome’). This may be overlooked if the animal is seen by a
different veterinary surgeon to the individual who originally prescribed the
drug, or if the animal has been taking the drug for a long period of time (e.g.
for chronic diarrhoea). Diagnosis may be difficult or impossible in many cases
of intoxication, and therefore careful history taking may be crucial in identi-
fying potential cases of toxic disease.
f. Previous and concurrent illness
Cases of neurological disease may present with previous or concurrent sys-
temic disease that could also predispose the animal to the development of
neurological signs. Examples include hyper‐ and hypoadrenocorticism; the
former can occasionally present as a myopathic syndrome, or can lead to
hypertension and hypercoagulability, which may in turn predispose to cere-
brovascular disease. Hypoadrenocorticism (‘Addison’s disease’) may lead
to a variety of clinical signs, including episodic weakness or collapse.
Hypothyroidism has been linked to a variety of cranial neuropathies, poly-
neuropathies, and polymyopathy (Bertalan et al. 2013); however, it is fre-
quently difficult to prove a definitive association. Chronic renal disease may
lead to hypertension and/or urinary protein loss, the former predisposing to
haemorrhagic stroke and the latter to thromboembolic disease, including
stroke and aortic thromboembolism. Vascular diseases, such as vasculitis, sys-
temic inflammatory conditions, and non‐neurological neoplasia may all
either directly or indirectly predispose to neurological disease of some kind.
There are some specific, well‐documented associations between certain neu-
rological conditions and diseases affecting other body systems which clini-
cians should also be aware of, such as that between myasthenia gravis and
the presence of a thymoma (Robat et al. 2013). In other cases, a paraneoplas-
tic syndrome should be considered when investigating certain generalised
conditions, such as a suspected polyneuropathy.
g. Trauma
A history of trauma will be known at the time of presentation in the majority
of cases; however, this may only be suspected in outdoor cats and in some
dogs the animal may have disappeared before presenting with neurological
signs. Moderate to severe trauma is usually required to cause signs associated
with CNS damage, since both the brain and spinal cord are well protected by
the skull, vertebral column, cerebrospinal fluid, and other soft tissues. For
this reason, trauma is an uncommon cause of neurological signs in animals
which are confined to the house and garden. Whenever trauma is suspected,
great care should be taken in moving the animal, since there may be instabil-
ity of the vertebral column that could lead to further damage to the spinal
 Chapter 2 Clinical History and Signalment 29

cord. In cases of head trauma, there may also be a depressed fracture and/or
raised intracranial pressure. Acute traumatic injury to the CNS will be consid-
ered in more detail in Chapter 7. Peripheral nerve trauma may occur in a
variety of ways and should always be considered when an animal presents
with a severe monoparesis or single limb neuropathy.
In humans, head trauma can lead to a delayed onset of epilepsy known as
post‐traumatic epilepsy, and this phenomenon is also thought to occur in
dogs and cats (Steinmetz et al. 2013). It can be difficult, if not impossible, to
prove a definitive association between prior trauma and a latter diagnosis of
‘idiopathic’ epilepsy. However, if an animal presents with a history of seizures
then asking the question about whether there has been any history of head
trauma in the recent or more distant past is a sensible consideration. Vertebral
or appendicular trauma can, in rare cases, lead to delayed nerve root or
peripheral nerve compression due to callus formation. More often, delayed
or malunion limb bone fractures may lead to muscular contracture which can
be very difficult to resolve.
h. General questions regarding the household from which the animal comes from
General questions may occasionally yield some useful pieces of information
that may end up being the clue to unravelling the disease process. In a multi‐
cat household, viral infection is more likely; in a home with young children,
inadvertent trauma may be a consideration. If an infectious disease or toxin
ingestion is suspected, a knowledge of whether other animals in the house-
hold are similarly affected may be important.

2.2 ­Specific History of the Neurological Problem

2.2.1 Onset
‘When and how did the problem begin?’ is one of several key questions, the
answers to which provide important information that enables the clinician to
draw up the most likely differential diagnoses. Depending on the problem, this
may or may not be an easy question for the owner to answer. For instance, in
the case of acute onset paraplegia the owner is likely to have a good idea of the
day and even the hour that the problem started. However, for other conditions
it may not be so easy or so certain. In the case of seizures, the owner may not
have been present when the first seizure occurred but may have a suspicion, due
to returning home and finding their pet in some sort of distress, or having unu-
sually urinated or defecated in the house. This can be significant, especially
when an animal is presented after what is apparently a ‘first’ seizure event. If,
after careful questioning, it appears likely that the event in question may not
have been the first, this can affect the decision‐making process (see Chapter 6).
In cases with a history of mentation or behaviour change, it may be very difficult
to establish the precise time of onset, since these may frequently be waxing and
30 A Practical Approach to Neurology for the Small Animal Practitioner

waning or may not be obvious until they have become quite severe. Thorough
history taking could lead to the realisation that some changes may have been
present for longer than the owner initially was aware. This can also be the case
with an apparent acute onset of blindness where, as discussed in Chapter 1,
visual deterioration may in fact have gone unnoticed until complete blindness
occurred.
The nature of the onset of signs is at least as important as the timing of the
onset. Disease onset may be either acute (the syndrome developed within min-
utes to hours), subacute (onset over a few days), or chronic (onset over several
days to several weeks). Further subdivision into peracute (instantaneous onset)
and acute may also be possible. Frequently, it is difficult to truly categorise the
onset of a syndrome, especially when attempting to distinguish between suba-
cute and chronic onset. However, this is less important than establishing the
truly acute and peracute onset syndromes, as outlined below.
In Chapter 5, we will discuss in more detail the use of the differential diag-
nosis mnemonic VITAMIND or DAMNITV; these mnemonics break down
potential differential diagnoses into categories of disease, where V is for vascu-
lar diseases, I is inflammatory/infectious, T is traumatic/toxic, A is anomalous,
M is metabolic, I is idiopathic, N is neoplastic (and nutritional), and D is degen-
erative. Most diseases fit into a single category although some, such as interver-
tebral disc disease, may occur either as a degenerative or traumatic process. An
understanding of how the different categories of disease behave is crucial in
constructing the differential diagnosis list, and the information derived from
this part of the history taking is specifically intended to allow certain groups of
disease to be eliminated from the differential list of likely causes of the present-
ing syndrome.
For the categories mentioned above, vascular diseases (such as ischaemic
stroke and fibrocartilaginous embolism, FCE) normally have an acute or pera-
cute onset; an exception would be aortic thromboembolism in the dog where
signs often develop in a more chronic manner. Inflammatory and infectious dis-
eases (such as meningoencephalomyelitis of unknown origin, MUO) are nor-
mally subacute or occasionally acute in onset. Discospondylitis (intervertebral
disc infection) may have a more chronic onset, and the protozoal infections of
toxoplasmosis and neosporosis may also be more chronic in onset. Trauma
should be peracute, and toxic diseases are usually acute in onset. The anomalous
disease category includes anatomical abnormalities, both congenital and devel-
opmental, and encompasses problems such as hydrocephalus, vertebral anoma-
lies (e.g. hemivertebrae), arachnoid space disorders (e.g. diverticuli and fibrosis),
and syringohydromyelia. Onset of signs is usually subacute or chronic, but occa-
sionally may appear to be acute. Metabolic diseases (such as portosystemic
shunt, hypoglycaemia, and endocrine disorders) will usually have a subacute
onset of signs, although again there can be exceptions to this such as might be
 Chapter 2 Clinical History and Signalment 31

the case with an insulinoma where the first sign may be one of collapse or an
epileptic seizure due to hypoglycaemia. Idiopathic disease encompasses idio-
pathic epilepsy and some cranial neuropathies, with onset usually being acute.
Neoplastic disease characteristically has a subacute or chronic onset, although
spinal neoplasia is often an exception to this rule and may present acutely due
to sudden decompensation or even pathological fracture. Finally, degenerative
diseases (such as lysosomal storage diseases, cerebellar abiotrophy, and degen-
erative polyneuropathies) normally have a chronic onset of signs; the exception
is Hansen type 1 intervertebral disc disease, where onset of neurological signs is
often apparently acute.

2.2.2 Progression
The next key question is: ‘How has the problem developed since the onset?’
Assuming that the condition has been present for long enough to tell, then a
distinction needs to be made between disease states which are improving, dete-
riorating, static, or waxing and waning. As with the disease onset, this is impor-
tant for establishing which diseases or categories of disease are more or less
likely in the given situation. Most owners will be able to answer this question
with reasonable certainty, although differentiating between a static and slowly
progressive condition or between a slowly progressive and waxing and waning
condition may be more difficult. In a case of suspected seizures, the use of a
seizure diary may allow a more objective analysis of disease progression, and
video clips taken by the owner at different stages of the disease may also be
helpful in establishing the progress of a syndrome. Some conditions may pro-
gress from affecting just one or two limbs to affecting all limbs for instance, or
an animal may have progressed from paresis to plegia, or vice versa. If a condi-
tion is considered to be waxing and waning, then some discussion of the details
of when the problem appears better or worse may be helpful in elucidating the
underlying cause.
Vascular conditions, which, as stated above, normally have an acute onset,
are usually either static or improving by the time the animal is seen by the
veterinarian.
Inflammatory and infectious conditions are usually deteriorating, especially
if no treatment has been instigated, and a history of acute or subacute onset and
relatively rapid deterioration is typical for the inflammatory CNS diseases that
are grouped under the term MUO. Some inflammatory diseases, such as steroid
responsive meningitis arteritis (SRMA), however, may take a more waxing and
waning course.
Traumatic conditions will usually be static or occasionally improving, but
rarely deteriorating. Trauma involving either the CNS or PNS will likely produce
a peracute onset of deficits which either remain static until there is some inter-
vention, or very gradually improve due to recovery of nervous tissue. Exceptions
32 A Practical Approach to Neurology for the Small Animal Practitioner

include unstable fractures, where there may be some deterioration associated

with movement, and head trauma, where deterioration may occur due to the
development of haematoma and raised intracranial pressure. The so‐called trau-
matic intervertebral disc extrusion, also known as a hydrated nucleus pulposus
extrusion or acute non‐compressive nucleus pulposus extrusion (ANNPE), may
be improving more rapidly than would be expected for other types of traumatic
spinal cord injury, and this needs to be borne in mind when considering this dif-
ferential diagnosis. As will be discussed below, there are other factors that can
help to distinguish between a traumatic disc extrusion and bony trauma involv-
ing the nervous system, in particular the presence or absence of pain.
Anomalous conditions may be static or deteriorating, dependent on whether
they are congenital or developmental. Congenital hydrocephalus, for example,
may be expected to lead to static signs, whereas syringomyelia is a progressive
condition with an expected progression following diagnosis due to gradual
enlargement of the syrinx within the spinal cord. These individual conditions
will be discussed in more depth in Chapter 6.
Metabolic diseases often have a waxing and waning disease progression.
Hepatic encephalopathy associated with a portosystemic shunt often becomes
severe after eating but may improve following a period of relative starvation.
Detailed questioning around paroxysmal, intermittent, or waxing and waning
conditions may help to elucidate the likely underlying aetiology, or at least pro-
vide some clues. With a suspected seizure disorder, asking the owner specifically
when the ‘seizures’ occur and whether anything appears to predispose the ani-
mal to an attack may be very important. As mentioned in Chapter 1, true epilep-
tic seizures involve a prodrome and aura that owners may recognise. It has also
recently been shown that many owners are able to identify seizure ‘triggers’ in
epileptic dogs (Forsgård et al. 2019), and so‐called feline audiogenic reflex sei-
zures have been well described (Lowrie et al. 2016). If an animal only suffers its
apparent ‘seizure’ when excited or exercising, it may be that the episodes are in
fact cardiorespiratory syncopal attacks rather than epileptic seizures. Whilst
these details are not strictly part of the disease progression, they are important in
establishing likely differential diagnoses, which is the primary goal of the
consultation.
Neoplastic diseases should have a deteriorating progression with a few excep-
tions; the only presenting sign of brain neoplasia may be seizures, with the ani-
mal being normal in between. The course of progression with CNS neoplasia can
be quite rapid, with animals going downhill over a period of days in many cases.
Degenerative conditions also should usually have a progressive deteriorating
disease course, although this is usually more slowly progressive over weeks to
months. Once again, the exception to this rule is the Hansen type 1 interverte-
bral disc extrusion, where progression may be more rapid.
 Chapter 2 Clinical History and Signalment 33

2.2.3 Presence or Absence of Pain

The identification of pain as part of the presenting syndrome is another key
aspect of arriving at the definitive differential diagnosis list. The clinical and neu-
rological examinations may allow the clinician to determine the presence/
absence and potential location of any pain, but this is only part of the process. It
can also be surprisingly difficult to be certain whether an animal is painful from
examination alone. Dogs may have altered pain sensation when examined due
to stress; they may react to palpation or head or limb movements in a way which
is very inconsistent and variable, and so leave the clinician wondering whether
a particular reaction was an indication of pain or not. Cats, on the other hand,
tend to become depressed or even aggressive when in pain; they can be difficult
or impossible to examine and making any sort of judgement about the presence
of pain from the examination can be very difficult.
In these situations, the clinical history may provide important informa-
tion that can suggest that the animal is in pain. Depression can be an indica-
tor of pain, particularly head pain, in both cats and dogs. Changes in
behaviour, such as a reluctance to play, increasing levels of fear and anxiety
especially around other people and animals, and even uncharacteristic
aggressive behaviour, may all be caused by the presence of pain. Typically,
cats want to be left alone, not touched or picked up, and may scratch or bite
when handling is attempted. If these sorts of behaviours are reported as a
new syndrome in conjunction with the presence of potential neurological
signs, then pain should always be suspected. Dogs may exhibit similar behav-
ioural changes, but often will also vocalise when affected by neurogenic pain.
Vocalising due to pain in dogs is rare except in neurological disease.
Orthopaedic disease, even when severe such as in the case of fractures, luxa-
tions, and osteosarcoma, rarely leads to persistent or episodic spontaneous
vocalisation. Any condition which causes inflammation or stretching of the
meninges, stretching or entrapment of spinal nerve roots or peripheral
nerves, or distortion of the dorsal horn of the spinal cord may result in inter-
mittent crying or screaming in pain. An owner reporting this type of behav-
iour should always lead the clinician to consider the possibility of neurological
disease.
When considering the categories of disease in relation to the presence/
absence of pain, there are again some generalisations which can be made.
Vascular conditions are in general not painful. Exceptions may be conditions
such as subdural haemorrhage, where there may be meningeal stretching or
inflammation, and aortic thromboembolic (ATE) disease in cats, which leads to
an ischaemic neuromyopathy that can be very painful. By contrast, ATE in dogs,
as mentioned previously, tends to present as a more chronic and non‐painful
syndrome associated with partial obstruction to blood flow in the distal aorta.
34 A Practical Approach to Neurology for the Small Animal Practitioner

Inflammatory and infectious diseases are often associated with pain due to
the presence of inflammatory cytokines and other factors. Bacterial discospon-
dylitis is typically very painful on spinal palpation, but is less commonly associ-
ated with vocalisation because it rarely causes meningeal inflammation or nerve
root entrapment. Steroid‐responsive meningitis arteritis can be extremely pain-
ful, leading to a very depressed animal, although the pain may wax and wane
with this condition. Inflammatory conditions of the CNS may be painful, espe-
cially when involving the spinal cord. Protozoal infections such as toxoplasmosis
and neosporosis are rarely associated with obvious pain, despite the presence of
oocysts in multiple tissues provoking often significant inflammation (Barber
et al. 1996).
Trauma may often present with pain, as would be expected. The exception
here is the acute, traumatic intervertebral disc extrusion of non‐degenerate
nucleus pulposus material that is not resulting in spinal cord compression. In
this condition, the onset is often peracute and associated with some kind of
physical activity such as jumping for a ball; the affected animal often vocalises at
the time the intervertebral disc extrudes, and may exhibit some signs of pain for
up to 24 hours, but beyond this usually appears relatively comfortable. Toxic
disease is rarely painful, and the same is true for metabolic diseases. Anomalous
conditions vary with respect to pain. Many, such as vertebral anomalies and
arachnoid space disorders, may be relatively pain‐free, whereas others, such as
syringohydromyelia, can be associated with significant pain, discomfort, and
vocalising. Atlantoaxial instability often presents with a history of significant
intermittent vocalisation.
Neoplasia affecting the central or peripheral nervous systems is commonly
painful. Tumours of the brain are often associated with significant depression;
much of this may be due to severe headache, although this can only be extrapo-
lated from human reports and clinical improvement following administration
of analgesics and corticosteroids. Tumours of the spinal cord may be extradural
(e.g. vertebral body osteosarcoma), intradural (e.g. meningioma), or intramed-
ullary (e.g. glioma). Extradural and intradural masses are commonly painful,
whereas some intramedullary tumours may not be associated with pain.
Neoplasia of the peripheral nerves, such as malignant nerve sheath tumours,
commonly present with lameness that is thought to result from pain. However,
in these situations vocalising is rare and response to analgesics is often poor.
Degenerative conditions, with the exception of intervertebral disc disease,
are rarely painful. Hansen type 1 intervertebral disc extrusions, especially in the
cervical region, can be associated with significant pain and vocalisation. Hansen
type 2 disc protrusions, on the other hand, may be less painful, being more asso-
ciated with chronic progressive compression of the spinal cord and minimal
inflammation. Unless such a protrusion is lateralised and impinging on a spinal
nerve root, these disc protrusions often are accompanied by little or no apparent
back pain.
 Chapter 2 Clinical History and Signalment 35

2.2.4 Response to Medication

If an animal has previously been presented to you or another veterinary surgeon
for the same presenting problem, then careful attention to the owner’s reporting
of their pet’s response to any medications administered or prescribed may fur-
ther help to refine the list of differential diagnoses. This type of questioning
needs to be carried out in a thorough manner, often with reference to the
patient’s records. Owners may require some prompting to recollect any response
to medication given historically. Furthermore, many owners will reply that a
medication was not beneficial if the improvement was not permanent, even if
there was an initial improvement following its administration.
A response to analgesics may support a suspicion that the condition is painful;
however, understanding whether the apparent response was real by taking into
account all of the medications that were administered and the possibility of a
placebo effect is also important. A positive response to corticosteroid administra-
tion may indicate that the disease is inflammatory or has an inflammatory com-
ponent. Many of the inflammatory diseases of the CNS already discussed may
initially respond to anti‐inflammatory doses of corticosteroid, even if they ulti-
mately require immunosuppressive therapy to achieve remission. Again, it is
important to remember that corticosteroids have a wide variety of effects.
Temporary improvement may therefore be seen following their administration
for many neoplastic conditions, where they may reduce peri‐tumoural oedema
or have a specific anti‐neoplastic effect (e.g. lymphoma). Corticosteroids may
also lead to improvement in Hansen type 2 intervertebral disc protrusion through
a reduction in spinal cord oedema, and may also lead to improvement in some
anomalous conditions such as hydrocephalus and syringomyelia due to their
ability to reduce the rate of production of cerebrospinal fluid.
An improvement following the administration of a non‐steroidal anti‐­
inflammatory drug (NSAID) may be seen in many painful conditions, as well as
for some inflammatory conditions. Conditions such as SRMA are commonly
associated with pyrexia, and NSAIDs may assist in reducing the fever and thereby
improving the condition of the affected animal.
Bacterial infections such as discospondylitis may show a response to antibi-
otic administration. A relatively common history in such cases may be of a par-
tial response to a standard course of broad‐spectrum antibiotics followed by
relapse, since this condition typically requires prolonged administration of a
suitable antibiotic to achieve a permanent cure.

2.2.5 History of Asymmetry

As for the presence or absence of pain, the presence or absence of asymmetry in
the presenting neurological signs can assist with formulating the list of differen-
tial diagnoses. The neurological examination should establish whether or not
the presenting animal shows asymmetry in some way and this may form part of
the neuroanatomical localisation. However, it is also important to question the
36 A Practical Approach to Neurology for the Small Animal Practitioner

owner about this, as the condition may have changed and evolved with time
since the onset. What we are concerned with here is whether there is a signifi-
cant difference in the level of paresis, ataxia, or proprioceptive dysfunction
affecting the limbs on one side of the body relative to the other, or whether there
is more obvious or severe hypermetria on one side relative to the other. Many
cranial nerve presentations will be asymmetrical due to them having an idio-
pathic or inflammatory cause. It is worth remembering that the presence of sym-
metrical cranial nerve deficits, in the absence of other neurological deficits such
as a change in the level of mentation, tetraparesis, ataxia, or even breathing
difficulties, makes a central (brainstem) lesion unlikely and makes a peripheral
cranial neuropathy more likely (see Chapter 4).
The reason why the symmetry of the neurological deficits can be important
is that we would generally expect toxic, metabolic, and many degenerative con-
ditions to present with largely symmetrical signs as they do not typically target
specific, lateralised regions of the nervous system. Of course, there are always
exceptions to every rule, and the presence of asymmetric vestibular signs may be
observed for some toxic, metabolic, or degenerative conditions.
In contrast, vascular causes of neurological dysfunction, such as FCE and
stroke, usually have a markedly asymmetric presentation. This is due to the
bilateral nature of the blood supply to most parts of the brain and spinal cord; it
would be uncommon for an FCE to affect both left and right spinal arteries
equally and, consequently, it is more common for these cases to present with a
significant degree of asymmetry. Inflammatory lesions can occur anywhere in
the CNS and there may be multiple lesions affecting different regions; it is there-
fore common for a degree of asymmetry to be present on the neurological exam-
ination for such conditions.
Intervertebral disc disease can be very variable in presentation; in general, the
extruded material associated with a Hansen type 1 extrusion lies more to one side
of the spinal cord than the other, and the neurological deficits will show a degree
of asymmetry to reflect this (e.g. proprioceptive deficits). However, because the
spinal cord injury caused by such an extrusion reflects a mixture of initial contu-
sion followed by compression and a cascade of secondary effects, it is also common
for the clinical signs to appear quite symmetrical even with a markedly asymmet-
ric extrusion. It has also been documented that the most severely affected side on
the neurological examination does not always correlate with the side of the disc
extrusion (Smith et al. 1997). For Hansen type 2 disc protrusions, the clinical signs
are usually fairly symmetrical because most of these protrusions are relatively
midline. However, it is again possible to have a very lateralised, focal protrusion
leading to markedly lateralised signs such as monoparesis or unilateral lameness.
Table 2.1 provides a summary of the information regarding the evolution and
expected presentations expected with the major categories of neurological dis-
ease that are described in more detail above.
 Chapter 2 Clinical History and Signalment 37

Table 2.1

Onset Progression Pain Symmetrical signs

Vascular Acute/peracute Static/improving Usually no Often marked asymmetry

Inflammatory/ Acute/subacute Deteriorating Usually yes
infectious
Toxic Acute Usually yes
Traumatic Peracute Static/improving Usually yes
Anomalous Usually chronic Variable
Metabolic Variable Often waxing/waning Usually no Usually yes
Idiopathic Variable, often Usually no
acute
Neoplastic Usually chronic Deteriorating Variable
Degenerative Usually chronic Deteriorating Variable

2.3 ­Signalment

2.3.1 Breed‐specific Conditions

Many conditions have been shown to have a significant predilection for a par-
ticular breed of dog or cat, and a knowledge of these predilections may be help-
ful when considering potential differential diagnoses. For some problems, a
definite mode of inheritance has been identified within the breed, and genetic
testing to confirm the presence of a specific mutation known to predispose to
the problem may be available. In other cases, there may be a known over‐­
representation of a certain breed, but the exact cause remains unknown. Tables
listing these breed predilections tend to become out of date, even by the time
they are ready for production. Genetic testing is a rapidly growing area in vet-
erinary neurology, with new tests becoming available relatively frequently. All
of this information is readily available online and we have included links to
some of the important genetic testing centres below. What we have attempted
to include in the table in ‘Appendix : Common breed-associated neurological
conditions in cats and dogs’ is a list of the more commonly seen problems which
have a known breed predilection. This is in order to assist the general practi-
tioner with the recognition of such problems. The list is by no means exhaustive
and should not be used to rule out the possibility that a disease may be inher-
ited; it is intended to provide a quick reference of the more common and well‐
recognised conditions. It is also important to remember that a specific condition
should never be excluded just because it has never been reported in that par-
ticular breed.
Useful links for genetic testing:
www.ahtdnatesting.co.uk/test‐category/canine#
http://www.caninegeneticdiseases.net
38 A Practical Approach to Neurology for the Small Animal Practitioner

2.3.2 Sex‐linked Conditions

There are few common neurological diseases which show a significant sex pre-
dilection. Probably the most widely known is X‐linked muscular dystrophy of
male golden retrievers. Feline infectious peritonitis (feline coronavirus) infec-
tion is a common cause of neurological disease in the cat, and this has a strong
predilection for male cats (Crawford et al. 2017). Spinal nephroblastoma, a
tumour which is found in the thoracolumbar region of the spinal cord in young
dogs, appears to have a significantly higher occurrence in female dogs as opposed
to males (Brewer et al. 2011). However, in general the patient’s sex is unlikely
to provide much help when considering the list of differential diagnoses.

2.3.3 Age
The age of an animal at presentation clearly has a bearing on the likely differen-
tial diagnoses. In general terms, younger animals are more likely to suffer with
congenital and inflammatory conditions, whereas neoplastic conditions are
more commonly seen in older animals. However, there are many exceptions to
these rules, and the practitioner should always be aware of this.
For specific diseases and categories of disease, there are certain observations
which can be made.

• Vascular disease
FCE is associated with the presence of an at least partially degenerate interverte-
bral disc. Therefore, this will be unlikely in very young animals (less than 1 year
of age). Most cases of FCE occur in middle‐aged larger breeds, although the min-
iature schnauzer also appears to be a commonly affected breed (Bartholomew
et al. 2016). Neither haemorrhagic nor ischaemic stroke has been shown to have
a significant age distribution, which may be surprising considering that these
conditions are often associated with underlying disease such as hypertension.
Some studies have shown a breed association with Cavalier King Charles Spaniels
and Greyhounds being overrepresented (Wessmann et al. 2009).
• Inflammatory/infectious disease
SRMA is usually seen in younger dogs and very rarely occurs in dogs over
3 years of age. MUO is generally a disease of younger dogs, although it may be
seen at any age. Infectious diseases are more common in younger animals,
with feline infectious peritonitis virus being the most common cause of spinal
cord disease in cats <2 years of age (Marioni‐Henry et al. 2004). However, this
virus can also cause neurological disease in much older cats, with the oldest
being 10 years in a recent study (Crawford et al. 2017).
• Anomalous disease
Congenital anomalies such as hydrocephalus usually manifest themselves
early in life, as would be expected. However, occasionally a diagnosis of hydro-
cephalus may be made in an older animal, either due to an obstruction to the
flow of cerebrospinal fluid caused by a neoplastic or inflammatory lesion, or
 Chapter 2 Clinical History and Signalment 39

due to the progression of a case of congenital hydrocephalus, possibly associ-

ated with inflammation or trauma. Many other anatomical abnormalities are
developmental and, as such, lead to signs later in life. In some instances, a
degenerative process such as an intervertebral disc herniation may occur in
association with a congenital vertebral anomaly.
• Metabolic disease
Congenital portosystemic shunts usually lead to signs of hepatic encephalopa-
thy in young, growing animals. However, portosystemic shunts may also be
acquired and therefore lead to similar signs in adult dogs or cats.
• Neoplastic disease
As would be expected, most neoplastic disease is seen in older animals.
Exceptions include spinal cord nephroblastoma, which is seen in young dogs
between 5 months and 4 years, and lymphoma in young dogs and cats
(Marioni‐Henry et al. 2004).
• Degenerative disease
Lysosomal storage diseases are caused by genetic defects leading to abnor-
malities of metabolism, with CNS signs often being the earliest to present due
to the inability of the CNS neurons to regenerate. As would be expected,
signs are usually seen in young animals <1 year of age. However, there are
also exceptions with the most significant being Lafora disease; this is a late‐
onset storage disease occurring in the Miniature Wire‐haired Dachshund and
Bassett Hound, where the onset of signs occurs later in life. Hansen type 1
intervertebral disc disease can occur at any age from 1 to 2 years, whereas
Hansen type 2 disc disease typically occurs in middle‐aged and older
animals.

2.4 ­Summary

All of these signalment features are merely guides to the clinician, enabling sen-
sible use of what is currently known from the literature and from our own expe-
rience. There will always be exceptions to any rule, and when faced with a
neurological disease it is wise to keep an open mind when it comes to differential
diagnoses. However, by following the basic guidelines set out in this text and
combining these with the neuroanatomical localisation resulting from the neu-
rological examination (see Chapters 3 and 4), it will usually be possible to come
up with a relatively short, rational, and evidence‐based list. This should then
allow a sensible dialogue with the pet’s owner regarding an investigation and
treatment plan. The aim of this book is to provide the general practitioner with
an uncomplicated and logical approach to veterinary neurology, and not a com-
prehensive list of disease descriptions for which much information already
exists. However, many of the individual conditions mentioned above will be
discussed in greater detail in Chapter 6.
40 A Practical Approach to Neurology for the Small Animal Practitioner

Appendix: Common breed‐associated neurological

conditions in cats and dogs
Breed Disease Signs Genetic
test

Abyssinian cat Myasthenia gravis Weakness No

Airedale Cerebellar degeneration Cerebellar signs 3 months No
Alaskan Malamute Hereditary polyneuropathy Tetraparesis 11–18 months No
Basset Hound Cervical spondylomyelopathy Progressive tetraparesis, No
(wobbler syndrome) neck pain
Hansen type 1 intervertebral disc Depends on location No
extrusion
Beagle Idiopathic epilepsy Seizures 6 months to 6 years No
Steroid responsive meningitis Pain and pyrexia <3 years No
arteritis
Hansen type 1 intervertebral disc Depends on location No
extrusion
Bernese Mountain Steroid‐responsive meningitis Pain and pyrexia <3 years No
Dog arteritis
Degenerative myelopathy Progressive paraparesis and Yes
ataxia >5 years
Border Collie Idiopathic epilepsy Seizures 6 months to 6 years No
Sensory neuropathy Progressive ataxia 2–6 months Yes
Fibrocartilage embolism Acute asymmetrical No
myelopathy
Border Terrier Paroxysmal gluten‐sensitive Cramping +/− GI or skin No
dyskinesia (Spike’s disease) signs 1–8 years
Boxer Steroid‐responsive meningitis Pain and pyrexia <3 years No
arteritis
Immune‐mediated polymyositis Generalised weakness, No
myalgia, atrophy
Degenerative myelopathy Progressive paraparesis and Yes
ataxia >5 years
Idiopathic head‐bobbing Episodic head bobbing No
<2 years
Idiopathic epilepsy Seizures 6 months to 6 years No
Primary brain tumour Depends on location No
Cavalier King Syringomyelia/Chiari‐like Pain, pruritis 2–6 years No
Charles Spaniel malformation
Episodic falling Episodic hypertonicity and Yes
collapse <1 year
Idiopathic epilepsy Seizures 6 months to 6 years No
Stroke Acute brain signs No
Chihuahua Hydrocephalus Forebrain signs, usually No
congenital
Necrotising meningoencephalitis Brain signs, usually young No
Atlantoaxial instability Neck pain, tetraparesis, No
<1 year
Cocker Spaniel Hansen type 1 intervertebral disc Depends on location No
extrusion
 Chapter 2 Clinical History and Signalment 41

Breed Disease Signs Genetic

test

Dachshund Hansen type 1 intervertebral disc Depends on location No

extrusion
Idiopathic epilepsy Seizures 6 months to 6 years No
Lafora disease Progressive myoclonic Yes
seizures >3 years
Narcolepsy/cataplexy Sudden episodic collapse/ Yes
sleep
Congenital myasthenia gravis Episodic weakness 1–2 months No
Dalmatian Congenital deafness Deafness No
Cervical spondylomyelopathy Progressive tetraparesis, No
(wobbler syndrome) neck pain
Laryngeal paralysis polyneuropathy Stridor, weakness No
complex 4–6 months
Dobermann Cervical spondylomyelopathy Progressive tetraparesis, No
(wobbler syndrome) neck pain
Congenital deafness and vestibular Deafness/vestibular No
disease syndrome
Dancing Dobermann disease Intermittent pelvic limb gait No
abnormality
English Bulldog Vertebral malformation Often asymptomatic No
Idiopathic head bobbing Episodic head bobbing No
<2 years
Cerebellar degeneration Cerebellar signs 3 months No
French Bulldog Vertebral malformation Paraparesis, ataxia, No
incontinence
Hansen type 1 intervertebral disc Depends on location No
extrusion
Idiopathic head bobbing Episodic head bobbing No
<2 years
German Shepherd Degenerative myelopathy Progressive paraparesis and Yes
Dog ataxia >5 years
Cervical spondylomyelopathy Progressive tetraparesis, No
(wobbler syndrome) neck pain
Idiopathic epilepsy Seizures 6 months to 6 years No
Gracilis muscle contracture Non‐painful pelvic limb No
lameness
Immune‐mediated polymyositis Generalised weakness, No
myalgia, atrophy
Acquired myasthenia gravis Episodic weakness, No
megaoesophagus
Hansen type 2 intervertebral disc Depends on location No
herniation
Golden Retriever Idiopathic epilepsy Seizures 6 months to 6 years No
X‐linked muscular dystrophy Stiffness, muscle atrophy Yes
2–3 months males
Acquired myasthenia gravis Episodic weakness, No
megaoesophagus
Gordon Setter Cerebellar degeneration Cerebellar signs 3 months Yes
42 A Practical Approach to Neurology for the Small Animal Practitioner

Breed Disease Signs Genetic

test

Great Dane Cervical spondylomyelopathy Tetraparesis 6–18 months No

(osseous wobbler syndrome)
Orthostatic tremor Weight‐bearing tremor of No
limbs
Inherited myopathy Generalised weakness No
6 months
Distal symmetrical polyneuropathy Paraparesis or tetraparesis No
1–5 years
Greyhound Steroid‐responsive meningitis Pain and pyrexia <3 years No
arteritis
Stroke Acute brain signs No
Jack Russell Terrier Hereditary (spinocerebellar) ataxia Progressive cerebellar ataxia Yes
>2 months
Labrador Retriever Idiopathic epilepsy Seizures 6 months to 6 years No
Exercise‐induced collapse Weakness after strenuous Yes
exercise
Acquired laryngeal paralysis/ Progressive dysphonia, No
polyneuropathy stridor, cough >6 years
Leonberger Inherited polyneuropathy Tetraparesis and typical gait Yes
1–2 years
Maltese Terrier Idiopathic tremor (‘little white Generalised tremor No
shaker’)
Syringomyelia/Chiari‐like Pain, pruritis 2–6 years No
malformation
Miniature Myotonia congenita Stiffness and collapse Yes
Schnauzer
Nova Scotia Duck Steroid‐responsive meningitis Pain and pyrexia <3 years No
Tolling Retriever arteritis
Newfoundland Immune‐mediated polymyositis Generalised weakness, No
myalgia, atrophy
Old English Cerebellar degeneration Cerebellar signs 3 months Yes
Sheepdog
Pembroke Welsh Degenerative myelopathy Progressive paraparesis and Yes
Corgi ataxia >8 years
Poodle Idiopathic epilepsy Seizures 6 months to 6 years No
Hansen type 1 intervertebral disc Depends on location No
extrusion
Pug Vertebral malformation and Paraparesis, ataxia, No
arachnoid space disorder incontinence
Necrotising meningoencephalitis Brain signs, usually young No
Rottweiler Adult onset and juvenile Weakness, tetraparesis No
polyneuropathies +/− stridor
Several congenital/juvenile Weakness, stiffness, paresis No
myopathies
Spinal arachnoid diverticulum Progressive tetraparesis and No
ataxia, adult
St Bernard Idiopathic epilepsy Seizures 6 months to 6 years No

Polyneuropathy Weakness, laryngeal paralysis Yes

 Chapter 2 Clinical History and Signalment 43

Breed Disease Signs Genetic

test

Springer Spaniel Hypomyelination Congenital tremor No

Siamese cat Congenital pendular nystagmus Permanent pendular eye No
tremor
Staffordshire Bull L‐2‐Hydroxyglutaric aciduria Progressive ataxia, seizures, Yes
Terrier encephalopathy
Hungarian Vizsla Idiopathic epilepsy Seizures 6 months to 6 years No
Weimaraner Steroid‐responsive meningitis Pain and pyrexia <3 years No
arteritis
Hypomyelination Generalised tremor from No
3 weeks
West Highland Idiopathic tremor (‘little white Generalised tremor No
White Terrier shaker’)
Yorkshire Terrier Necrotising leukoencephalitis Brain signs, usually young No
Atlantoaxial instability Neck pain, tetraparesis, No
<1 year
Syringomyelia/Chiari‐like Pain, pruritis 2–6 years No
malformation
Portosystemic shunt/hepatic Waxing/waning No
encephalopathy encephalopathy, young

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Chapter 3  he ‘Stress‐free’
T
Neurological
Examination
Edward Ives

The neurological examination can strike fear in the hearts of many practitioners,
often due to a lack of confidence in its interpretation or the belief that it is a
confusing and time‐consuming process. However, the neurological examination is
a simple, focused assessment that, with practice, can be approached with the same
confidence as for the general clinical examination. This should make neurology
more approachable and encourage you to perform repeated examinations in more
animals. The primary goal of this process is to make the neurological examination
as ‘stress‐free’ as possible for the veterinarian, the owner, and the animal involved.
This is particularly true for nervous or aggressive animals, when the most useful
information can often be gleaned from simple observation in a calm environment.

3.1 ­Why Perform a Neurological Examination?

In contrast to diseases affecting other body systems, in which specific tissues and
organs can be palpated, auscultated, or directly visualised, the majority of disor-
ders affecting the nervous system can only be identified by recognising their
impact on normal neurological function. This almost invariably represents
abnormal, reduced neurological function, termed a neurological deficit; an
exception being the excessive, involuntary movements observed during epilep-
tic seizures or certain forms of movement disorder. In order to recognise neuro-
logical deficits, the spectrum of normal neurological function between individuals
and species must be known, which underlies the importance of regularly per-
forming a complete neurological examination.
The neurological deficits identified on examination reflect the location of the
lesion and not the cause. It is therefore essential to identify this location before

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

45

46 A Practical Approach to Neurology for the Small Animal Practitioner

considering what type of disease process could result in a lesion at that location.
The most common error is jumping straight to possible causes and planning fur-
ther investigations without first performing a full neurological examination.
The aim of the neurological examination is to answer two questions:

1. Does this animal have a disorder affecting the nervous system?

As discussed in Chapter 1, answering this question will ensure that conditions
affecting other body systems (e.g. orthopaedic, cardiovascular, metabolic) are
also considered. These conditions can mimic neurological disease and their
early identification will ensure that the most appropriate further investiga-
tions are chosen in the first instance.
2. Where is the lesion?
This is termed the neuroanatomic localisation. The aim is to identify the site
of a single lesion that could explain all of the neurological deficits found on
examination. Less commonly, diseases may present with multiple lesions
scattered throughout the nervous system (e.g. inflammatory diseases), whilst
others may cause diffuse and symmetrical dysfunction (e.g. toxic or meta-
bolic disorders). The possibility of a multifocal or diffuse disease should always
be considered in cases that present with a combination of neurological deficits
that cannot be explained by a single, focal lesion.

The neuroanatomic localisation can then be used in combination with the

clinical history (e.g. signalment, onset, and progression of the clinical signs) to
achieve the following:

• Formulate a problem list and a ranked list of differential diagnoses. This process is
discussed in Chapter 5.
• Estimate disease severity and potential prognosis. As clinicians we are often focused
on achieving a definitive diagnosis; however, one of the most important pieces
of information for an owner is the anticipated prognosis for their pet.
• Plan and guide the most appropriate diagnostic investigations to rule in/out the differ-
ential diagnoses. As an example, deciding whether spinal radiography would be
useful prior to referral for advanced imaging (if possible) is entirely dependent
upon your differential diagnoses. Spinal radiography would be an excellent
choice if your lesion localises to the vertebral column and your differential
diagnoses include a vertebral malformation (e.g. atlantoaxial subluxation),
discospondylitis, or an osteolytic lesion (Figure 3.1). However, spinal radiog-
raphy may be unrewarding if your top differential diagnoses include interver-
tebral disc disease or degenerative myelopathy.

The neuroanatomic localisation is also vital for deciding where to focus

any subsequent diagnostic imaging. Imaging the entire spine, particularly
using radiography or magnetic resonance imaging (MRI), is a time‐consuming
 Chapter 3 The ‘Stress‐free’ Neurological Examination 47

Right Left

Figure 3.1 A ventrodorsal radiograph of the pelvis and lumbosacral region in a 12‐year‐old,
male neutered Labrador retriever with a 4‐week history of weight loss and progressive right
pelvic limb lameness and paresis. There was marked discomfort on palpation of the
lumbosacral spine and radiography demonstrated an osteolytic and proliferative lesion
affecting the right side of the sacrum at the level of the sacroiliac joint (arrow). A neoplastic
process was suspected in this case, but further investigations would be required to definitively
characterise the lesion.

and inefficient process that is costly for the owner unless completely necessary.
Focusing your imaging to the region of interest also means that it is easier to
determine the clinical significance of any observed abnormalities (e.g.
spondylosis deformans, in situ intervertebral disc mineralisation, or disc space
narrowing).

3.2 ­When to Perform a Neurological Examination

A neurological examination should be performed in every animal that presents

with clinical signs that could reflect a lesion affecting the nervous system. This
48 A Practical Approach to Neurology for the Small Animal Practitioner

decision may be easy in animals with a convincing history of epileptic seizures

or marked neurological dysfunction (e.g. pelvic limb paralysis). However, the
possibility of a neurological disorder can be overlooked in animals with condi-
tions that mimic disorders affecting other body systems, or in those that present
with subtle or vague clinical signs (e.g. lethargy, lameness, collapsing episodes).
Performing the neurological examination on a regular basis should increase
your confidence in its interpretation and will assist in the appreciation of the
broad spectrum of normal variation between different breeds and individuals.
Therefore, taking the time to perform a full neurological examination is always
valuable and should be carried out in every case if time allows. However, as one
gains in confidence a smaller number of more focused examinations can often
be chosen.

3.3 ­Where to Perform a Neurological Examination

The neurological examination should ideally be performed in a quiet, unre-

stricted environment that allows adequate time and space for observation of the
animal’s demeanour, gait, and interaction with the environment. This initial
observation can usually be performed when taking the history from the owner.
Other basic screening tests can be performed in the consultation room, but often
this is not the ideal environment for a more thorough examination. Therefore,
if the clinical history is suggestive of neurological disease, an owner should be
reassured that admitting their pet into the hospital for further assessment is the
most important first step and by far the best use of their money before perform-
ing other clinical investigations.
The ideal environment for a neurological examination would be an unclut-
tered, enclosed room that allows for unrestricted movement of the dog or cat,
and that does not have potential hiding places or escape routes. A non‐slip floor
is most useful for assessing gait and performing proprioceptive testing but is
often impractical for most hospitals in terms of hygiene and allowing deep clean-
ing. A roll of rubber matting can be stored for this purpose and used at the time
of examinations. Observation of the gait on both smooth and non‐slip surfaces
can sometimes assist in the identification of more subtle proprioceptive deficits,
which will be more obvious on surfaces with less grip. Black out blinds, or a
room without external windows, can be useful when performing retinal exami-
nation and for the assessment of pupil abnormalities.
For dogs that present with a history of lameness, gait abnormalities, or exer-
cise intolerance, lead walking on a concrete surface at various speeds of gait can
be extremely informative. An audible ‘scuff’ may be heard in animals that do not
flex their limbs sufficiently during protraction; this could indicate either a
mechanical resistance to flexion, reluctance to flex the limb, or a proprioceptive
deficit. Encouraging an animal to perform tight circles, figure‐of‐eight walking,
 Chapter 3 The ‘Stress‐free’ Neurological Examination 49

or walking up and down a kerb can also reveal more subtle gait abnormalities.
Stair climbing can be used to accentuate the excessive limb flexion associated
with cerebellar lesions (hypermetria).

3.4 ­How to Perform the Neurological Examination

As previously discussed, the aim of the neurological examination is to determine

whether an animal may have a neurological disorder, and the location of the
lesion(s) responsible if this is the case. Performing a complete neurological exami-
nation should always be encouraged; however, this may not be possible in all ani-
mals. The choice of the most appropriate tests in an individual animal is dependent
on the presenting clinical signs, the tolerance of the dog or cat to handling, and the
presence of significant pain or a history of trauma that would limit the ability to
perform certain tests. For example, the gag reflex or pupillary light reflex (PLR)
may be difficult to perform and interpret in a stressed or aggressive animal, with the
results unlikely to influence your neuroanatomic localisation in many cases.
The neurological examination can be broadly divided into a number of parts,
involving assessment of:

1. mentation
2. gait and posture
3. cranial nerves
4. postural reactions (proprioceptive testing)
5. spinal reflexes
6. palpation and assessment for regions of apparent discomfort.

When performing the neurological examination, the clinician should further

consider two distinct phases:

• an initial period of observation (‘hands‐off’ assessment)

• followed by a more ‘hands‐on’ assessment to screen different regions of the
nervous system in a logical manner.

It cannot be overstated how important the initial period of observation is, but
this is often overlooked in favour of immediately performing more focused tests.
This initial period of observation allows for a broad assessment of the animal,
time to process that information, and can reveal subtle deficits that would be
missed if the animal were restrained for other tests. A preliminary neuroana-
tomic localisation can be formed on the basis of the history and observation of
the animal alone, which can then be further interrogated by the choice of spe-
cific ‘hands‐on’ tests. This approach allows for an efficient and rewarding exami-
nation that is as stress‐free as possible for all involved.
50 A Practical Approach to Neurology for the Small Animal Practitioner

If abnormalities are identified at any stage of the examination, then they

should be added to the problem list and both neurological and non‐neurological
causes should be considered for each abnormality in turn.

3.4.1 Observation: ‘Hands‐Off’ Assessment

This vital part of the examination can usually be performed whilst taking the
clinical history and involves observation of the animal as it roams around the
consultation room without the restriction of its lead or owner.
The key questions to consider when observing the patient are:

• Is this animal interacting with the owner and environment as expected?

• Are the limbs, head, and body held in a normal position?
• If the animal can walk, is the gait normal?
• Are there any involuntary movements or muscle contractions?
• Does the face look symmetrical?
• Can the animal blink voluntarily?

1. Level of alertness and interaction with the environment

The level of alertness or wakefulness is primarily determined by diffuse stimula-
tion of the cerebral cortex from an extensive neuroanatomical structure residing
within the brainstem called the ascending reticular activating system (ARAS).
Focal lesions affecting the ARAS in the brainstem, or more diffuse lesions affect-
ing its cortical projections via the thalamus or the cerebral cortex itself, may result
in a diminished level of alertness (Box 3.1). This can range from mild obtunda-
tion to coma, dependent on the severity, extent, and location of the lesion.

• Obtundation. A subjectively quiet state in which the animal is less responsive

to commands, interaction, or stimulation. As discussed in Chapter 1, the term
‘depressed’ has also been used in veterinary medicine to describe a similar
reduced level of alertness. However, this term should be used with caution in

Box 3.1 Level of Alertness and Interaction with the Environment

• Non‐neurological: primary behavioural disorder, pain, systemic disease, adverse effects

of medications.
• Neurological: brainstem or forebrain lesion.

Top tip: Animals will often, but not exclusively, circle towards the side of a forebrain
lesion.

Don’t make this mistake: Some animals may be particularly sensitive to certain medi-
cations (e.g. methadone, buprenorphine, apomorphine). This can result in significant
short‐term changes in the level of mentation and mimic primary intracranial disease or a
deteriorating mental status. Serial examinations are advised if this is suspected.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 51

animal species due to its association with specific mental health conditions in
human medicine.
• Stupor. Unconscious but responsive to painful stimuli.
• Coma. Unconscious and no response to painful stimuli.

Lesions affecting other regions of the forebrain, particularly those involving

the limbic system, can result in various behaviour changes that appear inappro-
priate in a given situation or environment, such as:

• Compulsive pacing around the consultation room.

• Becoming stuck in corners or confined spaces.
• Circling in a particular direction. Compulsive circling often indicates a unilateral
lesion affecting the forebrain or brainstem (see Video 22). It may also be seen
in association with a head tilt and ataxia in cases with vestibular dysfunction.
Whether the circling appears wide or tight does not appear reliable for deter-
mining the specific location of a lesion.
• Bumping into furniture.
• Sleeping throughout the consultation or appearing disinterested.
• Reduced interaction with the owner.

Judging how appropriate an animal’s behaviour appears to be at the time of

examination is complicated by the wide range of normal variation between dif-
ferent individuals. This will therefore always represent a subjective impression
rather than an objective assessment. An owner is often the best source of infor-
mation regarding their pet’s normal behaviour and response to veterinary assess-
ment, and this information can be very useful in determining the significance of
a subjectively quiet or withdrawn animal.
The apparent level of alertness and interaction with the environment can
also be influenced by other factors, which should always be considered when
interpreting these findings:

• visual deficits (e.g. cataracts, progressive retinal atrophy, sudden acquired reti-
nal degeneration, optic nerve lesions, cortical blindness)
• pain (e.g. abdominal, orthopaedic, spinal)
• pyrexia or systemic disease (e.g. hypovolaemia, sepsis)
• cardiorespiratory disease
• medications (e.g. sedatives, analgesics, anti‐epileptic medications).

The behaviour of cats can be particularly difficult to interpret as many become

nervous, are reluctant to walk, or seek hiding places when placed into a foreign
environment. However, a general impression as to how appropriate their behav-
iour appears can usually be determined throughout the examination and inter-
preted in the light of other examination findings.
52 A Practical Approach to Neurology for the Small Animal Practitioner

2. Abnormal posture
Abnormal postures can be divided into those affecting the head, limbs, individ-
ual joints, the entire body, spine, or tail.

a. Head position
Head tilt. This posture is characterised by rotation of the head in the trans-
verse plane so that one ear is held lower than the other (Figure 3.2 and Box 3.2).
Head turn. This posture is characterised by a lateral turn of the head to one
side with the ears remaining horizontal (Box 3.3).

Figure 3.2 Left head tilt in a cat with otitis media/interna.

 Chapter 3 The ‘Stress‐free’ Neurological Examination 53

Box 3.2 Head Tilt

• Non‐neurological: aural irritation, aural haematoma.

• Neurological: vestibular syndrome (central or peripheral).

Top tip: Whilst uncommon, bilateral vestibular syndrome will not result in a head tilt
as the output from the vestibular nuclei on each side remains balanced. This syndrome
is often characterised by wide head excursions from side to side.

Don’t make this mistake: Previous episodes of vestibular syndrome may leave a
residual head tilt. This has the potential to confuse future neurological examinations if
this history is not available.

Box 3.3 Head Turn

• Non‐neurological: paraspinal cervical mass resulting in mechanical deviation of the

head.
• Neurological: forebrain lesion, vertebral malformation (scoliosis), neck pain.

Top tip: As for circling, the direction of a head turn is most commonly towards the
side of a forebrain lesion.

b. Limb and joint position

Abnormal positioning of one or more limbs when standing, excessive joint flex-
ion, or excessive joint extension can be the result of many different neurological
and non‐neurological causes (Box 3.4). A thorough general clinical examina-
tion, orthopaedic assessment, and neurological examination are therefore
required to distinguish between these different causes.
Wide‐based stance. Often observed secondary to lesions affecting the knowl-
edge of where the affected limbs are in space (proprioceptive deficit), or as an
attempt to correct for balance loss in cases with vestibular and/or cerebellar
dysfunction.
Narrow‐based stance. Animals with proprioceptive deficits may variably adopt
a narrow‐ or wide‐based stance when standing, or if they abruptly stop when
walking.
Poor joint extension. An inability to extend a joint can be caused by mechanical
disruption to the structures involved in maintaining joint stability (ligaments,
tendons), or a weakness of the extensor muscles associated with that joint. The
most commonly affected joints are the elbow (triceps muscle innervated by the
radial nerve), stifle (quadriceps muscle innervated by the femoral nerve – see
Figure 3.3), and hock (gastrocnemius muscle innervated by the tibial branch of
the sciatic nerve).
54 A Practical Approach to Neurology for the Small Animal Practitioner

Box 3.4 Limb and Joint Position

Poor elbow extension:

• Non‐neurological: triceps tendon rupture.

• Neurological: C7–T2 spinal cord segments, C7–T2 nerve roots, radial nerve injury.

Poor stifle extension:

• Non‐neurological: cruciate ligament rupture (unilateral or bilateral), patellar frac-

ture, patellar tendon injury.
• Neurological: L4–L6 spinal cord segments, L4–L6 nerve roots, femoral nerve injury.

Poor hock extension:

• Non‐neurological: Achilles tendon rupture, calcaneal fracture.

• Neurological: L6–S1 spinal cord segments, L6–S1 nerve roots, sciatic‐tibial nerve injury.

Top tip: Carpal hyperextension is most commonly the result of palmar carpal ligament
insufficiency (chronic or acute) rather than representing a primary neuropathy (Figure 3.4).
This posture can also be observed in some dogs with congenital myopathies.

Don’t make this mistake: Dogs with bilateral cruciate ligament rupture show reluc-
tance to walk and a crouched pelvic limb posture that can be easily confused with
paraparesis as a result of spinal cord disease. However, proprioception will be normal
in the pelvic limbs and orthopaedic examination in these cases will reveal stifle swell-
ing, discomfort on stifle extension, and joint instability.

Figure 3.3 Reduced extension of the stifle joints in a 10‐year‐old boxer dog with chronic
degenerative radiculomyelopathy (CDRM). Note also the wide‐based pelvic limb stance and
worn nails of both pelvic limbs, suggestive of bilateral proprioceptive dysfunction.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 55

Figure 3.4 Bilateral carpal hyperextension in a cat with palmar carpal ligament insufficiency
that was exacerbated after jumping out of a window.

c. Body and spinal postures

A number of terms are used to describe different body or spinal postures, some
of which may help guide the neuroanatomic localisation.
Decerebrate rigidity. A body posture that is characterised by rigid extension of
all limbs and extension of the neck (opisthotonus). This posture results from
lesions at the level of the midbrain, or can be seen secondary to severe, diffuse
forebrain lesions. Animals presenting in this posture will have a markedly
reduced level of mentation (stupor or coma) and should be treated as a neuro-
logical emergency.
Decerebellate rigidity. Severe dysfunction of the rostral cerebellum can result in
a posture that is similar in appearance to decerebrate rigidity; however, impor-
tant differences are that the pelvic limbs are often held flexed at the hips and the
animal remains alert and responsive to external stimuli (Figure 3.5).
Schiff–Sherrington posture. This posture is characterised by increased extensor
muscle tone in the thoracic limbs following an acute T3–L3 spinal cord lesion,
such as an intervertebral disc extrusion, fibrocartilaginous embolism (FCE), or
vertebral fracture (see Video 23). The increased extensor tone is the result of
interruption to inhibitory pathways that run from cells in the lumbar spinal cord
segments (known as ‘Border cells’) up to the cell bodies of the nerves that inner-
vate the thoracic limb extensor muscles. Loss of inhibition following damage to
these pathways results in increased extensor muscle tone in the thoracic limbs.
The increased extensor muscle tone in the thoracic limbs can restrict an animal’s
ability to rise into sternal recumbency, and affected animals may therefore be
suspected of having a cervical spinal cord lesion. However, once these animals
56 A Practical Approach to Neurology for the Small Animal Practitioner

Figure 3.5 A decerebellate posture in a 2‐year‐old Jack Russell terrier with meningoen-
cephalitis of unknown origin. Note the increased extensor muscle tone in the thoracic limbs
and extended neck posture (opisthotonus). This dog remained responsive to visual and
auditory stimuli.

are assisted to stand it becomes clear that voluntary movement and propriocep-
tion are normal in the thoracic limbs. This would not be expected for a cervical
spinal cord lesion that is severe enough to result in recumbency. It is important
to remember that whilst this posture is commonly associated with extensive
T3–L3 spinal cord lesions that result in non‐ambulatory paraparesis or paraple-
gia, it has no prognostic significance (Box 3.5).
Kyphosis. A dorsal curvature of the spine resulting in a more convex dorsal
aspect.

• Non‐neurological causes: intra‐abdominal pain, polyarthritis resulting in joint

pain and shifting of the limbs under the body to reduce loading.

Box 3.5 Schiff–Sherrington Posture

Don’t make this mistake: Schiff–Sherrington posture is most commonly associated

with acute, severe T3–L3 spinal cord lesions that result in non‐ambulatory paraparesis
or paraplegia. However, this posture has no prognostic significance and should not be
used to guide an owner as to the prognosis for return of pelvic limb function.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 57

• Neurological causes: spinal pain, vertebral malformation, neuromuscular

weakness.

Lordosis. A ventral curvature of the spine resulting in a more concave dorsal

aspect.

• Non‐neurological causes: intra‐abdominal pain (prayer positioning).

• Neurological causes: spinal pain, vertebral malformation, neuromuscular
weakness.

Scoliosis. A lateral curvature or twisting of the spine.

• Non‐neurological causes: mechanical deviation by a paraspinal mass.

• Neurological causes: vertebral malformation, damage to spinal cord dorsal
horn (e.g. syringomyelia).

d. Tail postures
Elevated tail posture. Many dogs and some cats may have a naturally elevated tail
carriage or adopt this posture appropriately during excitement or greeting.
However, cats with vestibular dysfunction will often elevate their tails to assist
with balance (Figure 3.6).

Figure 3.6 Elevated tail posture in a cat with left‐sided peripheral vestibular dysfunction.
Note also the wide‐based stance, left head tilt, and leaning to the left side displayed by this cat.
58 A Practical Approach to Neurology for the Small Animal Practitioner

Low tail carriage. A low tail carriage may simply reflect the nervous demean-
our of an animal, or a reluctance to elevate the tail as a result of pain in the
region of the tail base (e.g. coccygeal intervertebral disc disease, acute caudal
myopathy, cat bite abscess, neoplasia). The tail tone should be normal in these
cases and a degree of voluntary movement will be present. In contrast, lesions
affecting the caudal spinal cord segments or caudal nerves will result in a flaccid
tail with minimal or no voluntary movement (Box 3.6). The adjacent sacral spi-
nal cord segments or nerve roots (S1–S3) may also be affected, resulting in defi-
cits in anal tone, bladder tone, and/or a poor perineal reflex.

3. Gait
Disorders affecting many different regions of the nervous system can result in an
abnormal gait and careful gait analysis is vital to ensure an accurate neuroana-
tomic localisation. Objective methods for gait analysis are increasingly reported;
however, these techniques are time consuming and impractical for general prac-
tice. Therefore, a logical approach to subjective gait analysis is important,
together with careful consideration of non‐neurological conditions that may
also affect gait. Choice of the most appropriate further tests can then be made to
identify the underlying cause for an abnormal gait and to refine the differential
diagnoses (e.g. cardiac auscultation, focused orthopaedic examination, hands‐
on neurological assessment).
A number of specific terms are used to describe gait abnormalities (e.g. ataxia,
paresis, hypermetria); however, the authors recommend simply describing what
appears to be abnormal about the way the limbs are moving, before reaching for
a specific term. This will help to avoid making incorrect assumptions about a
particular gait that may result in mislocalisation and an inappropriate choice of
further investigations.
The key points to consider when assessing the gait are:

• How many limbs are affected?

• What is the stride length in the affected limbs?
• Is the limb placement predictable on each stride?
• Does the animal appear exercise intolerant or is the gait abnormality exacer-
bated by exercise?

Box 3.6 Aortic Thromboembolism in Cats

Aortic thromboembolism is a common cause of acute pelvic limb paralysis in cats and
can sometimes be mistaken for a spinal cord lesion. However, a spinal cord lesion that
is severe enough to cause pelvic limb paralysis would also be expected to affect the
voluntary motor function of the tail. The tail function may be normal in cats with
aortic thromboembolism, as the blood supply to the muscles and nerves of the tail can
be preserved.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 59

How many limbs are affected?

• All limbs
• Thoracic limbs only
• Pelvic limbs only
• Thoracic and pelvic limbs on one side of the body
• Single thoracic or single pelvic limb

Stride length of the affected limbs

• A short stride length suggests that the animal is either prematurely shifting
weight away from a painful limb (i.e. a reluctance to weight bear on the limb)
or is shifting weight away from a weak limb to avoid collapsing through the
affected limb.
• A long stride length is most commonly seen in association with disruption to
the spinal cord upper motor neuron (UMN) tracts that run from the motor
centres in the brain to the cell bodies of the peripheral motor neurons that
directly innervate the limb muscles. These UMN tracts are involved in the
initiation and termination of the stride. Disruption to these messages will
therefore delay both the onset and termination of limb movements, resulting
in a long or ‘over‐reaching’ stride.

Is the limb placement predictable for each stride?

When evaluating the gait of a dog or cat it is important to assess whether the
placement of a limb (or limbs) is predictable with each stride, as a limb may be
placed into an abnormal position for numerous reasons. If this abnormal place-
ment is identical for every stride, then a mechanical cause (e.g. orthopaedic
disease) should always be considered before assuming a neurological deficit. If
limb placement is erratic and unpredictable then a neurological disorder is more
likely; the term ‘ataxia’ is often used to describe this incoordination (see below).
Further tests during the ‘hands‐on’ assessment can be used to provide support
for this initial impression (e.g. proprioceptive testing).
Exercise intolerance
If there is an apparent deterioration of the gait as an animal is exercised, then
conditions affecting oxygen delivery to the muscles (e.g. cardiorespiratory dis-
ease, anaemia, polycythaemia, thromboembolic disease [Box 3.7]), the neuro-
muscular junction, or the muscles themselves (e.g. myopathies) should be
considered. This will often present as an increasingly short‐strided gait, or the
animal choosing to sit or lie down during exercise. Spinal cord disorders typically
result in static clinical signs that are not influenced by exercise unless there is
significant discomfort or vertebral instability.
Specific terminology
Specific terms that can be used to describe gait abnormalities include ‘ataxia’
and ‘paresis’. The correct use of these terms and understanding their meaning is
60 A Practical Approach to Neurology for the Small Animal Practitioner

Box 3.7 Aortic Thromboembolism in Dogs

Aortic thromboembolism may also occur in dogs (see Video 24). In contrast to the
acute embolisation seen in cats, this more commonly presents as a chronic aortic
thrombosis resulting in progressive pelvic limb weakness. Affected dogs may present
with marked exercise intolerance as the blood flow becomes insufficient to meet the
increased muscle demand during exercise, and this can mimic spinal cord disease or
myasthenia gravis. Taking time to feel for adequate femoral pulses in any dog present-
ing with a pelvic limb gait abnormality will ensure that this unusual but easily diag-
nosed condition is not overlooked.

important, particularly when describing an animal’s gait in the clinical records or

to another clinician.

a. Ataxia
This term is used to describe an incoordination of limb movement and place-
ment that is secondary to dysfunction of the complex neurological pathways and
structures involved in gait coordination. These structures include the proprio-
ceptive receptors in the joints and muscles, the spinal cord proprioceptive tracts,
the vestibular system, and the cerebellum. Lesions affecting these components
will result in forms of ataxia with different characteristics. Recognition of ataxia
on examination is useful to support the presence of a neurological disorder.
However, the distinction between these different forms of ataxia can be difficult
and should not be used to form a definitive neuroanatomic localisation without
considering the presence of other consistent deficits.
Spinal (or proprioceptive ataxia). This form of ataxia is characterised by unpre-
dictable limb placement when walking, crossing of the affected limbs, scuffing of
the dorsal aspect of the nails or paws, and circumduction of the affected limbs
during the swing phase of the stride (see Video 16). All limbs, the limbs on one
side, or only the pelvic limbs may be affected, dependent on the lesion location
and distribution along the spinal cord.
Vestibular ataxia. Animals with vestibular dysfunction may drift or fall to one
side when walking or may stumble after sudden changes in head position (e.g.
turning to look upwards, shaking of the head) (see Video 17). All limbs will be
affected by disorders of the vestibular system, but the pelvic limbs may appear
more noticeably affected as they lie further away from the centre of gravity.
Cerebellar ataxia. This gait abnormality is characterised by an abnormal rate,
range, and force of movement. This is clinically apparent as excessive flexion of
all limbs during the swing phase of the stride (‘hypermetria’), erratic limb place-
ment, and rapid limb extension at the time of placement resulting in a ‘bouncing’
nature to the gait (see Video 18). Dependent upon the precise location of the
lesion within the cerebellum, it is possible for just the thoracic and pelvic limbs
on the side of the lesion to be affected, and occasionally even just a single limb.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 61

Components of the central vestibular system also reside within the cerebellum;
therefore, a gait with a vestibular nature, or a combination of vestibular and
cerebellar characteristics, may also be observed in cerebellar disorders.

b. Paresis
The use of this term can cause much confusion and does not simply relate to
‘muscle weakness’. It should be used more broadly to suggest an inability to
generate normal voluntary movements, and therefore a normal gait. This can be
the result either of the skeletal muscles being too weak to support the weight
of the body against gravity and to perform voluntary movements, or disruption
to the messages from the brainstem motor centres, via the descending spinal
cord UMN tracts, to the peripheral motor nerves that innervate the limbs.
Paretic animals may therefore present with a long‐strided gait if the lesion
responsible is affecting the brainstem motor centres or spinal cord UMN tracts
(e.g. in all four limbs for a C1–C5 spinal cord lesion). This gait results from a
delay in the onset and termination of the stride. Limb strength will be preserved,
as the peripheral motor nerves to the limb muscles and the limb muscles them-
selves are unaffected. This is termed ‘upper motor neuron paresis’ and is usually
accompanied by concurrent ataxia, as any pathology affecting the spinal cord
UMNs will commonly affect the adjacent, ascending spinal proprioceptive tracts.
If a lesion involves the cell bodies or axons of the peripheral motor nerves,
the neuromuscular junction, or the limb muscles themselves then the UMN
messages for initiation and termination of the stride will be unaffected. However,
the muscles of the affected limb(s) will be less able to support the animal’s weight
against the effects of gravity. This will be clinically apparent as a short‐strided
gait due to shifting of weight away from a ‘weak’ limb to avoid collapse.
If an animal is reluctant or unable to walk at all, then gait evaluation is obvi-
ously not possible. However, it is still very important to determine why the animal
is unable to walk, and to assess the degree of any voluntary movement that is pre-
sent in the affected limbs. A diminished degree of voluntary movement is termed
‘paresis’ and an absence of voluntary movement is termed ‘plegia’ or ‘paralysis’.

4. Involuntary movements
Spontaneous muscle contractions that result in involuntary movements of the
limbs, face, or body are more commonly reported by owners as part of the clini-
cal history than they are directly observed in the consultation. As previously
discussed in Chapters 1 and 2, it is essential to obtain a detailed description of
these movements from an owner as the nature of such movements may be mis-
interpreted by owners, potentially resulting in the incorrect use of terms such as
‘seizure’ or ‘fit’. Access to video footage of any abnormal events observed in the
home environment can be extremely useful for further classification of
involuntary movements or episodes of collapse, guiding the choice of the most
appropriate diagnostic investigations.
62 A Practical Approach to Neurology for the Small Animal Practitioner

Involuntary movements arise from the spontaneous contraction of skeletal

muscles, with the nature and appearance dependent on their origin and the
number and location of muscles involved. These spontaneous muscle contrac-
tions can arise secondary to disorders affecting the skeletal muscles, the periph-
eral motor nerves, the spinal cord, or motor centres within the brain (including
the motor cortex, basal nuclei, and cerebellum). Therefore, a number of possible
neuroanatomic localisations need to be considered when presented with an ani-
mal showing involuntary movements. Disorders of involuntary movement,
including seizures, tremors, peripheral nerve hyperexcitability, myoclonus, and
dyskinesias, are further discussed in Chapter 6.

5. Basic cranial nerve functions

A number of basic cranial nerve functions can be assessed during the ‘hands‐off’
assessment, before a more‐focused cranial nerve examination is performed dur-
ing the ‘hands‐on’ assessment. This is particularly useful in animals that will not
tolerate handling.

a. Facial asymmetry
Non‐neurological causes to consider for facial asymmetry include congenital
skull malformations, cranial neoplasia, nasal disease, and abscesses/cellulitis.
Dysfunction of the facial (VII) nerve will result in loss of tone to the muscles
of facial expression on the same side as the affected nerve. Clinical signs of facial
paralysis include drooping of the ipsilateral lip, an inability to retract the lip com-
missure when panting, deviation of the nasal philtrum (initially away from the
affected side in acute cases, and then towards the affected side following atrophy
and fibrosis of the affected muscles in chronic cases), a narrow palpebral fissure
on the affected side, or an inability to move the auricular cartilage (Figure 3.7).

b. Voluntary blinking
The absence of voluntary blinking in one or both eyes is consistent with dys-
function of the facial (VII) nerve. Animals with facial paralysis will still protract
the third eyelid across the globe, which is often commented on by owners as
appearing unusual.

c. Strabismus
Strabismus is the term used to describe an abnormal position of the eyeball
within the orbit. A resting strabismus (i.e. when the head is in a normal posi-
tion) can be caused by:

• mechanical deviation or distortion of the eyeball (e.g. retrobulbar abscess, ret-

robulbar mass, intra‐ocular mass)
• imbalance in the tone of the extra‐ocular muscles responsible for maintaining
a normal eyeball position.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 63

Figure 3.7 Right‐sided facial paralysis in a Chihuahua with inflammatory brain disease. Note
the narrow palpebral fissure on the right side and the inability to voluntarily retract the right
ear against the head compared to the normal left side. The palpebral reflex and menace
response were absent on the right side, but the vision and facial sensation remained normal.

The position and movement of each eye is determined by six extra‐ocular

muscles that act as three agonist–antagonist pairs:

• lateral rectus (LR) and medial rectus (MR) for movement in the horizontal
plane
• dorsal rectus (DR) and ventral rectus (VR) for the vertical plane
• dorsal oblique (DO) and ventral oblique (VO) for torsional movements
(Figure 3.8).

These muscles are innervated by motor neurons of three separate cranial

nerves: the oculomotor (III) nerve innervating the MR, DR, VR, and VO, the
trochlear (IV) nerve innervating the DO, and the abducent (VI) nerve innervat-
ing the LR. The muscles are innervated in yoked pairs to allow conjugate move-
ments of the eyeballs (e.g. right MR and left LR, left DO and right VO).
Denervation of one or more of the extra‐ocular muscles will result in loss of tone
in the affected muscles and deviation of the eyeball by unopposed contraction of
the unaffected muscle(s).

• Oculomotor (III) nerve dysfunction results in denervation of the MR, DR, VR,
and VO. Unopposed contraction of the LR and DO will result in a lateral or
ventrolateral strabismus.
• Trochlear (IV) nerve dysfunction is rarely seen in isolation but would result in
loss of tone in the DO and rotation of the eyeball secondary to unopposed
contraction of the VO muscle. This is clinically apparent in the cat as the verti-
64 A Practical Approach to Neurology for the Small Animal Practitioner

Dorsal rectus
(Oculomotor nerve)

Dorsal oblique
(Trochlear nerve)

Lateral rectus Medial rectus

(Abducent nerve) (Oculomotor nerve)

Ventral oblique
(Oculomotor nerve)

Ventral rectus
(Oculomotor nerve)

Figure 3.8 The extraocular muscles and their innervation in the right eye of a dog.

cally orientated, slit‐shaped pupil becomes diagonally orientated, with lateral

deviation of the dorsal aspect of the pupil away from the nose. The presence
of a round pupil in dogs means that this is not immediately appreciable; how-
ever, retinal examination reveals lateral deviation of the dorsal retinal vein
away from its normal vertical position.
• Abducent (VI) nerve dysfunction results in denervation of the LR and a medial
strabismus in the affected eye secondary to unopposed contraction of the MR.

d. Jaw tone and position

Reduced jaw tone is clinically apparent as an inability to close the mouth
(‘dropped jaw’). This results from dysfunction of the motor axons in the man-
dibular branches of both trigeminal (V) nerves.

Top tip: A unilateral lesion affecting the motor component of one trigeminal (V)
nerve will not result in a dropped jaw, as sufficient muscle strength will be present
on the unaffected side to maintain a normal jaw position and function.

An important differential diagnosis to consider for an inability to close the

mouth is a reluctance to close the mouth. This can be seen with temporoman-
dibular joint disease or intraoral lesions. However, in contrast to cases with bilat-
eral trigeminal neuropathy, evidence of discomfort is frequently found on clinical
examination in these cases.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 65

e. Tongue symmetry and tone

This can be assessed if a dog is panting or licks its nose in the consultation.
Deviation of the tongue to one side, tongue atrophy, or reduced tone of the
tongue suggests dysfunction of the hypoglossal (XII) nerve and/or its nucleus in
the caudal brainstem. Acute lesions result in deviation of the tongue away from
the affected side as a result of unopposed contraction of muscles on the unaf-
fected side. With time, denervation atrophy of the affected tongue muscles will
slowly deviate the tongue back towards the affected side.

3.4.2 ‘Hands‐On’ Assessment

The ‘hands‐on’ part of the neurological examination involves performing specific
tests to screen certain regions or components of the nervous system. A wide array
of different tests is described and it is important to appreciate that some of these
tests simply represent different ways to screen the same components of the nerv-
ous system, whilst others may not add further information to that already acquired
from the clinical history and simple observation of demeanour, gait, and posture.
It is always important to perform a number of basic tests in every case to
ensure that neurological deficits are not missed, particularly those that could
suggest the presence of more than one lesion (e.g. concurrent disease processes
or multifocal disease). Familiarity with performing and interpreting these differ-
ent tests is vital as there is a wide range of normal variation that can only be
appreciated with practice and experience. However, once a practitioner gains in
confidence a selection of ‘hands‐on’ tests can often be chosen, tailored to each
case, to refine the preliminary neuroanatomic localisation based upon the clini-
cal history and ‘hands‐off’ assessment.
A number of the tests performed during the ‘hands‐on’ assessment involve
the application of a tactile stimulus to the skin of a specific region of the body,
followed by observation of an appropriate response. This is most commonly in
the form of a reflexive muscle contraction resulting in movement of a body part.
An abnormal test result can therefore be the result of an inability to detect or
transmit the initial sensory information and/or an inability to perform the appro-
priate motor response. For example, the corneal reflex involves gently touching
the surface of the cornea and observing for an appropriate blink in response. The
absence of an appropriate blink could therefore result from:

• An inability to feel the stimulus following the application of topical local

anaesthetic drops.
• A lesion affecting the ophthalmic branch of the trigeminal nerve, resulting in
an inability to detect and transmit the sensory information to the level of the
brainstem.
• Damage to connections between the trigeminal sensory nucleus in the brain-
stem and the motor nucleus of the facial nerve, or damage to the nuclei
themselves.
66 A Practical Approach to Neurology for the Small Animal Practitioner

• Dysfunction of the facial nerve innervating the periocular muscles required

for blinking.
• A disorder affecting the neuromuscular junction or periocular muscles, result-
ing in reduced muscle tone and facial paresis.

If each test that you perform is approached in a similar manner, from start to
finish in terms of its sensory and motor arms, then the interpretation of each test
should hopefully be more logical and approachable. Combinations of tests that
share common sensory or motor pathways can then be used to determine the
most likely reason for an abnormal test result.
The ‘hands‐on’ part of the examination can be divided into the following parts:

1. Cranial nerve examination

2. Limb palpation
3. Assessment of postural reactions (proprioceptive testing)
4. Spinal reflex testing
5. Spinal palpation and neck manipulation
6. Testing for pain perception (nociception)

1. Cranial nerve examination

The cranial nerve examination can be approached in an efficient and logical
manner if it is separated into different parts according to the regions of the head
being assessed. This also means that several tests can be performed concurrently
to provide complementary information and assist in determining the neuroana-
tomic localisation (e.g. the palpebral reflex and menace response).

a. Eyes
With the animal sitting or standing to face you, use the fingers of one hand to
gently hold the muzzle and stabilise the head. The following tests can then be
performed:

• Palpebral reflex and menace response testing

• Assessment of pupil size and symmetry
• Observation of any abnormal spontaneous eye movements (e.g. nystagmus)
• Elevation of the head towards the ceiling to look for a positional strabismus or
positional nystagmus
• Vestibulo‐ocular reflex testing
• Pupillary light reflexes and dazzle reflexes

Palpebral reflex testing. Gently cover one of the animal’s eyes with the fingers
of one hand (i.e. cover the right eye with your left hand) and touch the medial
canthus of the exposed eye (see Video 1a). This should induce a reflex contrac-
 Chapter 3 The ‘Stress‐free’ Neurological Examination 67

tion of the muscles of the upper and lower eyelids, resulting in a blink. This test
screens the integrity of the sensory fibres in the ophthalmic branch of the
trigeminal nerve, the motor fibres in the facial nerve, and the interneurons in
the brainstem that connect the sensory nucleus of the trigeminal nerve to the
motor nucleus of the facial nerve. Touching the lateral canthus of the eye will
stimulate sensory nerves in the maxillary branch of the trigeminal nerve, with
the remainder of the pathway being the same as described for medial canthus
stimulation.
An abnormal palpebral reflex therefore implies one or more of the following:

• ipsilateral trigeminal (sensory) nerve lesion resulting in an inability to feel the

stimulus
• ipsilateral facial (motor) nerve lesion resulting in an inability to blink (i.e.
facial paresis/paralysis)
• brainstem lesion
• mechanical inability to blink (e.g. marked exophthalmos)

The precise cause for the abnormal reflex can be determined by considering
the following:

• A trigeminal nerve lesion should result in loss of sensation to other regions of

the face innervated by the branch affected (e.g. nasal septum for the ophthal-
mic branch or lateral muzzle for the maxillary branch). Concurrent involve-
ment of the motor fibres residing in the mandibular branch of the trigeminal
nerve would result in masticatory muscle atrophy on the affected side.
• A facial nerve lesion will result in an inability to voluntarily blink on the
affected side or blink in response to a menacing gesture (absent menace
response). In these cases, the animal will still be able to retract the eyeball and
protract the third eyelid when performing the palpebral reflex, confirming an
intact sensory arm of the reflex.
• A brainstem lesion that results in an abnormal palpebral reflex will commonly
affect adjacent neuroanatomical structures in addition to the trigeminal and/
or facial nuclei. This will result in other neurological deficits on examination,
which will be dependent on the structure or tract affected: altered mentation
(ARAS), paresis (descending UMN tracts), proprioceptive deficits (ascending
proprioceptive tracts), other cranial nerve deficits (other cranial nerve nuclei).

Menace response. The menace response can be performed concurrently with

the palpebral reflex by alternately touching the medial canthus of the eye and
moving your hand towards the eye in a ‘menacing gesture’ (see Video 1a). This
provides a visual stimulus for blinking, but care should be taken to avoiding
creating a waft of air when moving your hand towards the face as this could also
provide a tactile stimulus. This is to ensure that only visual stimulation for blink-
68 A Practical Approach to Neurology for the Small Animal Practitioner

ing is tested by the menace response. Alternating between actually touching the
face (palpebral reflex testing) and performing a menacing gesture can be particu-
larly useful when testing the menace response of cats. The nature of this species
means that they may not blink in response to a visual stimulus unless they think
that it may actually touch their face! A study assessing the menace response in
50 neurologically and ophthalmologically healthy cats concluded that the major-
ity of cats showed a strong menace response when the untested eye remained
uncovered, but 40% failed to show a complete menace response when the con-
tralateral eye was covered (Quitt et al. 2018). The most reliable examination
appeared to be achieved when the examiner was positioned behind the cat and
each eye was tested without covering the contralateral eye.
As the name suggests, the menace response is not a true reflex and is classi-
fied as a ‘response’ because the pathway tested includes areas of the cerebral
cortex. This is a learned response that is absent in dogs and cats before about
12 weeks of age. The sensory arm of the pathway involves recognition of an
object approaching the eye via the retina, optic nerve, optic chiasm, optic tracts,
and central visual pathways (thalamus, contralateral visual cortex in the occipi-
tal lobe). Initiation and coordination of an appropriate blink in response to this
visual information involves the cerebral motor cortex, cerebellum, brainstem,
and facial nerve (Figure 3.9). Therefore, there are several lesion locations that
can result in an absent menace response:

Menacing gesture

Motor cortex

Facial nerve

Visual cortex

Cerebellar cortex Pontine nucleus

Motor nucleus of facial nerve

Figure 3.9 The menace response. An object approaching the eye is interpreted as a potential
threat to the health of the eye by the brain, resulting in a coordinated response to blink and
protect the surface of the eye (see Video 1a).
 Chapter 3 The ‘Stress‐free’ Neurological Examination 69

• Ipsilateral retina or optic nerve. The direct PLR may be absent in the affected eye.
If vision is intact in the opposite eye, then the pupil of the affected eye will
passively dilate if the visual eye is covered.
• Contralateral visual and/or motor cortex. The PLR will be normal in the affected
eye.
• Ipsilateral cerebellar lesion (rare). Vision will be normal in both eyes and other
signs of cerebellar disease will usually be present (e.g. ataxia, intention tremor,
hypermetria, head tilt).
• Ipsilateral facial nerve lesion resulting in an inability to blink (facial paresis/paralysis).
The palpebral reflex will also be absent but eyeball retraction in response to
the menacing gesture will still occur if vision is present in the eye being tested.

As the palpebral reflex and menace response both require normal function of
the facial nerve, they are complementary tests that can be used to screen for
potential lesions involving the trigeminal (sensory) nerve, facial nerve, and vis-
ual pathways. For example, the most likely reason for the following neurological
deficits would be:

• intact palpebral reflex, absent menace response – visual deficit in the affected eye
• absent palpebral reflex, intact menace response – absent facial sensation (trigeminal
nerve lesion)
• absent palpebral reflex, absent menace response – facial paralysis (facial nerve
lesion) or multiple cranial nerve deficits (e.g. blindness and absent facial
sensation).

Pupil size and symmetry. Pupil size is determined by two main factors:

1. The external light levels

2. The emotional status of the animal.

Pupil size is controlled to ensure optimum vision; the brighter the light level,
the more constricted the pupil will become to avoid becoming dazzled. Light is
detected by the retina, and this information is transmitted to the parasympa-
thetic nucleus of the oculomotor nerve in the brainstem to reflexively control
pupil constriction. This is the pathway that is tested by the PLR. The pupil will
passively dilate as the light levels fall to ensure that enough light enters the eye
for optimum vision.
The emotional status of the animal is determined by the sympathetic nervous
system, with stimulation of the sympathetic nervous system (‘fight or flight’
response) resulting in active pupil dilation.
Abnormal or excessive pupil dilation is termed ‘mydriasis’, and abnormal or
excessive pupil constriction is termed ‘miosis’. Asymmetry of pupil size is
termed ‘anisocoria’ and may result from unilateral autonomic lesions affecting
70 A Practical Approach to Neurology for the Small Animal Practitioner

the ability of the pupil to either dilate or constrict on the affected side.
Application of topical medications and non‐neurological diseases are also com-
mon causes for anisocoria and should always be considered before neurological
disease. Further discussion on the approach to pupil abnormalities can be found
in Chapter 6.

Top tip: Always consider stress during examination as a common cause for apparent
bilateral mydriasis: the PLR may also appear reduced due to sympathetic stimulation.
However, vision should be normal in both eyes and the menace responses will be
intact bilaterally.

Spontaneous eye movements. If the head is in a static position and the animal is
not tracking objects in their visual field or attempting to look for their owner,
then the eyeballs should be stationary within the orbits and pointing in the same
direction as the head.
The presence of abnormal, spontaneous eye movements is most commonly
encountered in the form of rhythmic eyeball oscillations that have a slow drift
phase, followed by a fast corrective phase. This distinctive form of involuntary
eye movement is termed a jerk nystagmus (see Video 20). Nystagmus results
from dysfunction of the vestibular system and disruption to its important role in
coordinating the position of the eyes relative to the position and movement of
the head. Therefore, a jerk nystagmus is often observed concurrently with other
clinical signs of vestibular dysfunction, such as a head tilt or ataxia of all limbs.
The characteristics of a jerk nystagmus may be useful to guide the neuroana-
tomic localisation. However, they are not definitive and should always be used
in combination with other consistent neurological deficits.

• Direction of the fast ‘jerk’ phase

The fast phase of a nystagmus represents the attempt by the body to correct for
the slow drift phase that results from the underlying pathology. The fast phase
is most commonly directed away from the side of the lesion, and a tip to remem-
bering this is that it can be thought of as ‘running away from the problem’!
A nystagmus can be horizontal, vertical, or torsional (rotatory). A true vertical
nystagmus may suggest the presence of a lesion affecting the central rather
than peripheral vestibular system. However, lesions affecting the peripheral
vestibular system can result in a diagonal nystagmus that is almost vertical and
difficult to distinguish from a true vertical nystagmus, particularly in an ani-
mal with a head tilt and loss of balance. Disorders of the central vestibular
system can also result in horizontal and torsional nystagmus, therefore whilst
the presence of a true vertical nystagmus is supportive of a central lesion, its
absence does not exclude disease of the central vestibular system. It has also
been suggested that a lesion affecting the central vestibular system is more
 Chapter 3 The ‘Stress‐free’ Neurological Examination 71

likely if the fast phase of the nystagmus changes in direction when the head is
placed into different positions (e.g. in dorsal recumbency or following head
elevation). Further discussion of the approach to vestibular disease can be
found in Chapter 6.
• Rate of nystagmus (beat frequency)
It has been suggested that acute disorders affecting the peripheral vestibular
system may result in a more rapid nystagmus compared to those affecting the
central vestibular system, with a beat frequency >66 beats per minute being
more suggestive of a peripheral lesion (Troxel et al. 2005).
• Positional nystagmus
By adjusting the position of the head, a nystagmus can sometimes be induced
in animals that do not have a spontaneous nystagmus when the head is in its
normal position. This may be observed in animals with central vestibular dis-
ease or in those that are compensating for more chronic peripheral vestibular
dysfunction. The easiest way to assess for positional nystagmus is by elevating
the head so that it points towards the ceiling, or by placing the animal in dor-
sal recumbency with the neck extended if it will allow. Positional nystagmus
is often observed in cats, which appear to be able to compensate more rapidly
for vestibular dysfunction compared to dogs (see Video 25). Recognition of a
positional nystagmus in an animal that otherwise appears normal is useful for
determining the neuroanatomic localisation as it is a distinctive sign of ves-
tibular dysfunction.

In animals that do not have a resting strabismus (see above), a ventral stra-
bismus may also be observed when elevating the head to assess for positional
nystagmus. This positional strabismus is not related to pathology affecting the
cranial nerves innervating the extraocular muscles but is consistent with a lesion
to the vestibular system on the same side as the affected eye. It results from an
inability of the vestibular system to detect the change in head position and
appropriately alter the eyeball position to point in the direction of the head.
Disorders affecting the cranial nerves innervating the extra‐ocular muscles (III,
IV, VI) will result in a static strabismus that is present in all head positions, and
not only when the head position is changed.
Other forms of spontaneous eye movement. In addition to disorders affecting the
vestibular control of eye movement, other forms of involuntary eye movement
are rarely observed secondary to disorders affecting the control of saccadic eye
movements. Saccadic eye movements occur in the normal way to rapidly shift
the direction of gaze from one object of interest to another when the head is in
a static position. Disorders affecting their control result in involuntary, rapid eye
movements that lack the initial drift phase characteristic of a nystagmus. These
involuntary eye movements are called saccadic oscillations. Saccadic oscillations
are rarely reported in small animals, but recognition of these unusual eye move-
ments may help to guide a specific neuroanatomic localisation.
72 A Practical Approach to Neurology for the Small Animal Practitioner

• Convergence–retraction pulses. This form of abnormal, spontaneous eye move-

ment is characterised by rhythmic convergence and retraction of both eyeballs
into the sockets and has been reported in dogs with lesions in the dorsal mid-
brain (Crawford et al. 2016).
• Opsoclonus. This distinctive form of spontaneous eye movement is character-
ised by rapid, multi‐directional eye movements without a drift phase (see
Video 26). The recognition of opsoclonus may suggest a cerebellar neuroana-
tomic localisation. Opsoclonus has been reported in a dog with neuronal
ceroid lipofuscinosis and in dogs and a cat with idiopathic generalised tremor
syndrome (Ives et al. 2018).

Vestibulo‐ocular reflex testing. Movement of the head from side‐to‐side, or up‐

and‐down, should result in coordinated, conjugate eyeball movements that rea-
lign the direction of gaze with that of head position. This is called the
vestibulo‐ocular reflex. The eyeballs initially appear to remain in a fixed position
as the head is moved, but this actually represents a slow eyeball movement in an
equal and opposite direction to head movement. This ensures that the gaze can
remain fixed and stable on an object of interest in spite of small head movements
during normal activity. As the head is moved further from the midline, there
follows a fast corrective eye movement in the direction of head movement that
realigns the head and eyeball position.
These movements are initiated and coordinated by the vestibular system,
which includes parts of the cerebellum. Therefore, in addition to resulting in
abnormal spontaneous eye movements, disorders of the vestibular system can
also interfere with the normal vestibulo‐ocular reflex. This may be clinically
apparent with a vestibular lesion as an absent, incomplete, or slow corrective eye
movement when the head is moved towards the side of the lesion (see Video 2a).
Disorders affecting the vestibular system equally on both sides (e.g. bilateral otitis
media/interna) may result in an absent vestibulo‐ocular reflex when moving the
head in any direction. Animals with bilateral vestibular dysfunction will not have
a head tilt but may show wide head excursions, a crouched posture, ataxia of all
limbs, and drifting to both sides when walking (Figure 3.10 and Video 27).
Lesions affecting the brainstem that involve the vestibular nuclei in the
medulla oblongata can result in a poor vestibulo‐ocular reflex when moving the
head from side‐to‐side. This clinical sign will also be accompanied by other indi-
cations of severe brainstem dysfunction, such as a reduced level of mentation
(stupor or coma), tetraparesis, and other cranial nerve deficits (e.g. poor gag
reflex, miosis, or anisocoria). An absent or incomplete vestibulo‐ocular reflex
may be observed in association with brainstem compression secondary to
increased intracranial pressure and herniation of brain parenchyma under the
tentorium cerebelli or through the foramen magnum. The vestibulo‐ocular
reflex therefore forms an important part of the serial assessment of animals with
 Chapter 3 The ‘Stress‐free’ Neurological Examination 73

Figure 3.10 A transverse T2‐weighted MRI at the level of the tympanic bullae in a 20‐year‐
old, female neutered, domestic shorthair cat with a 4‐week history of a crouched posture and
progressive loss of balance. Neurological examination revealed ataxia of all limbs, drifting to
both sides when walking, wide head excursions, an absent vestibulo‐ocular reflex, and a mild
right head tilt. Proprioception was normal in all limbs and withdrawal reflexes were strong in
all limbs. The neuroanatomic localisation was bilateral peripheral vestibular system. Note the
hyperintense material filling both tympanic bullae (arrows). The tympanic bullae should
normally be gas‐filled and appear black on MRI. Bilateral bacterial otitis media/interna was
diagnosed following myringotomy; this was medically managed in the first instance in light of
the cat’s advanced age.

suspected elevated intracranial pressure (e.g. following head trauma) to allow

early identification of a deteriorating clinical status and rapid intervention. The
neurological assessment and monitoring of animals following head trauma is
discussed further in Chapter 7.
Pupillary light reflex and dazzle reflex. The PLR and dazzle reflex can be assessed
at the same time but may not significantly influence your neuroanatomic locali-
sation in an animal that appears to be visual and does not have any pupil abnor-
malities (e.g. anisocoria). Therefore, if there is no history to suggest visual
deficits, if the menace responses are intact, and if the pupils appear symmetrical
and an appropriate size for the light levels and emotional state of the animal, it
may not be necessary to perform these tests.
The PLR and dazzle reflex both rely upon a strong light source to allow accu-
rate assessment. The most common reason for a subjectively poor PLR is use of
a light that is not bright enough, particularly when trying to overcome increased
sympathetic tone in a stressed patient.
74 A Practical Approach to Neurology for the Small Animal Practitioner

• Dazzle reflex
This is a subcortical reflex that tests the integrity of the visual pathways to the
level of the midbrain, together with the facial nerve. It involves observing for
a narrowing of the palpebral fissure in response to a bright light source.
• Pupillary light reflex
As previously discussed, active pupil constriction is mediated by the para-
sympathetic component of the oculomotor nerve and is dependent on the
environmental light levels. This information is transmitted via the optic
nerve to the parasympathetic nucleus of the oculomotor nerve in the mid-
brain. Decussation of this information at both the level of the optic chiasm
and between the pre‐tectal nucleus and the oculomotor nuclei, means
that light entering one eye will result in constriction of both pupils
(Figure 3.11). Constriction of the pupil receiving the light is termed the
‘direct PLR’ and constriction of the contralateral pupil is termed the ‘con-
sensual PLR’.

This concept explains why blindness in one eye will often result in little
appreciable anisocoria, that is until the visual eye is covered and there is passive
dilation of the blind pupil. If light is shone into the blind eye there will be no
change in the size of either pupil (no direct or consensual PLR). However, if light
is shone into the visual eye then this will result in constriction of both pupils
(intact direct and consensual PLRs).
If there is no anisocoria observed, then assessing for a normal direct PLR in
each eye is all that is required. An indication that the PLR is likely to be normal
can also be acquired by simply closing both eyes when in a bright environment,

Optic nerve
Oculomotor nerve
(parasympathetic) Optic chiasm

Optic tract

Pretectal nucleus

Parasympathetic
nucleus of the
oculomotor nerve

Figure 3.11 The pupillary light reflex. Light directed into either eye will stimulate the
parasympathetic nuclei of the oculomotor nerves which will, in turn, result in reflex
constriction of the pupils of both eyes.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 75

followed by opening each eye in turn to observe for appropriate pupil constriction.
Observing for a consensual PLR is primarily useful if there is anisocoria
present:
Unilateral miosis. If this is the result of loss of sympathetic innervation to the
affected eye (as part of a Horner syndrome), then the affected pupil will constrict
further in response to light shone into either eye (assuming that the optic and
oculomotor nerves are not affected).
Unilateral mydriasis. The most common neurological cause for unilateral
mydriasis is a lesion affecting the parasympathetic component of the oculomotor
nerve, resulting in an inability to constrict the pupil. Assuming that the optic
nerve is unaffected, vision will still be present in this eye and the menace
response will be intact. The affected pupil will not constrict when light is shone
into it (absent direct PLR), but there will still be active constriction of the con-
tralateral pupil (intact consensual PLR). Light shone into the unaffected eye will
result in a direct PLR in this eye, but no change in the size of the mydriatic pupil
(absent consensual PLR).

b. Mouth and jaws

Jaw tone. Jaw tone can be assessed by appreciating the resistance to opening
of the mouth. This reflects the function of the motor component of the trigemi-
nal nerve (mandibular branch). Bilateral loss of function is required before a
reduced jaw tone is clinically apparent, as there is sufficient strength from the
masticatory muscles on one side to result in normal jaw function.
Tongue symmetry and tone. This can be assessed when the mouth is open (see
‘Hands-Off’ Assessment).
Gag reflex (see Video 3a). If the animal is amenable, then the gag reflex can
be assessed by gently placing one or two fingers to the back of the throat and
feeling for reflexive contraction of the pharyngeal muscles around your fin-
gers. Animals with a poor gag reflex will show little reluctance to this exami-
nation and the pharynx will not contract as expected around your fingers.
Care should be taken so that you are not inadvertently bitten when perform-
ing this examination. This is particularly important as the results may add
little to your neuroanatomic localisation if there is no history to suggest dys-
phagia or difficulty swallowing. Therefore, appropriate case selection is
advised before performing the gag reflex. Individual variation in the interpre-
tation of this test also needs to be considered, both in terms of the examiner
and the patient. The gag reflex may appear subjectively poor in docile, large
breed dogs such as Labrador Retrievers that do not appear to have a genuine
neurological deficit.
Palpation of the masticatory muscles. The temporalis and masseter muscles
should be assessed for atrophy or swelling (Figure 3.12). See Chapter 6 for fur-
ther discussion regarding the different causes of masticatory muscle atrophy and
the approach to these cases.
76 A Practical Approach to Neurology for the Small Animal Practitioner

Figure 3.12 Marked, unilateral (right‐sided) masticatory muscle atrophy in a 10‐year‐old

Labrador Retriever with a peripheral nerve sheath tumour affecting the mandibular branch of
the right trigeminal nerve. Note the prominent zygomatic arch and contours of the skull on
the affected side compared to the normal left side.

c. Nose
Nasal septum nociception (see Video 4a). The end of a pair of closed haemostats can
be used to gently apply a mild noxious stimulus to the inside of the nostril on each
side of the nasal septum. This stimulus should elicit a conscious response of irrita-
tion, indicated by withdrawal or shaking of the head to avoid the stimulation. As
for the menace response, this test screens both cranial nerve and cerebrocortical
functions: the ipsilateral trigeminal nerve (sensory–ophthalmic branch) and the
contralateral sensory cortex. If the ipsilateral palpebral reflex is intact then it can
be assumed that the trigeminal (sensory) component of this test is functional.
Therefore, a deficient response to stimulation on one side of the nasal septum
compared to the other would be more consistent with a lesion involving the con-
tralateral forebrain (see Video 5a). This would be further supported by the pres-
ence of other compatible neurological deficits, such as an absent menace response
or proprioceptive deficits on the same side as the abnormal nasal nociception.

2. Limb palpation
The limbs should be examined in turn for focal or generalised muscle atrophy,
for the general impression of limb muscle tone, and for any swellings or foci of
 Chapter 3 The ‘Stress‐free’ Neurological Examination 77

discomfort. This is most easily performed in each limb with the animal standing
and immediately prior to performing the proprioceptive tests described below.
Further examination can then be performed, if required, at the time of with-
drawal reflex testing.

• Focal atrophy of individual muscles is most consistent with denervation atro-

phy secondary to a lesion affecting the motor fibres in the peripheral nerve
that innervates the affected muscle (e.g. suprascapular nerve for the supraspi-
natus and infraspinatus muscles – see Figure 3.13).
• Generalised atrophy of the muscles in a single limb could result from chronic
disuse of that limb, a lesion affecting multiple nerve roots, or a lesion affecting
the individual peripheral nerves innervating the affected muscles (e.g. bra-
chial plexus lesion).
• Generalised atrophy of the muscles of all limbs could be consistent with a gen-
eralised neuromuscular disorder (primary myopathy or generalised motor
polyneuropathy); however, cachexia related to a systemic disease process
should always be considered (malnutrition, malabsorption, maldigestion, pro-
tein‐losing conditions, heart failure, neoplasia).
• Reduced muscle tone in one or more limbs is clinically apparent as a reduced
resistance to flexion and extension of the limb, and a general impression of
flaccidity and increased joint mobility when the limb is moved. This is most
often noticeable in the carpi and hocks.

3. Assessment of postural reactions (proprioceptive testing)

Proprioception can be defined as the perception of the relative position and
movement of different parts of the body at any point in time. This information is
important for adopting a normal posture and for planning and coordinating
movements. Receptors called ‘proprioceptors’ are associated with the muscles
and joints of the body and provide information about the current state of play
(e.g. joint position, muscle stretch). This information is transmitted to the level
of the spinal cord in peripheral sensory nerves. Large, myelinated axons within
the spinal cord transmit this information up to the regions of the brain con-
cerned with coordination and proprioception (forebrain and cerebellum).
Dysfunction of the receptors, the pathways transmitting this information, or the
areas of the brain involved with processing proprioceptive information can
therefore result in abnormal postures and gaits. The vestibular system and its
control of equilibrium and balance is also intimately involved in proprioception.
This is termed ‘special proprioception’ and is grouped together with the other
special senses of hearing, smell, taste, and vision.
Proprioceptive testing is a sensitive way to increase suspicion for an underly-
ing neurological disorder and a proprioceptive deficit would not be expected for
a primary orthopaedic condition. However, as normal proprioception relies upon
78 A Practical Approach to Neurology for the Small Animal Practitioner

the integrity of multiple neuroanatomic structures and long pathways from the
limbs to the brain, identification of a proprioceptive deficit is poorly specific for
a particular neuroanatomic localisation. A lesion anywhere between the limb
being tested and the brain can result in a proprioceptive deficit on examination.
Therefore, whilst identification of abnormal proprioception supports the pres-
ence of a neurological lesion, other tests that screen more specific regions of the
nervous system are required to narrow down the neuroanatomic localisation.
Proprioception is a sensory modality; however, testing for proprioception
also relies upon normal motor function to perform the corrective movements
that we use to define a normal test result. Therefore, these tests will naturally
be absent in a paralysed dog or cat even if the sense of proprioception is com-
pletely unaffected by the lesion responsible. Proprioceptive testing is unreward-
ing in these cases and does not need to be performed in limbs that are truly
paralysed. Proprioceptive testing is extremely useful in animals with some
degree of voluntary motor function (i.e. paresis) and it is vital that the animal’s

Figure 3.13 Marked, focal atrophy of the left supraspinatus and infraspinatus muscles in a
dog following traumatic damage to the left suprascapular nerve. Note the prominent spine of
the underlying scapula in this case.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 79

weight is adequately supported when performing these tests. This is so that any
attempt to initiate a corrective movement is observed, even if the movement is
weak or incomplete. If the weight is not supported then an animal with neuro-
muscular weakness, for example, in which the proprioception may in fact be
normal, will collapse through the limb being tested; this will give the impres-
sion of absent proprioception. It is the attempt to correct for a change in limb or
joint position that tells you whether an animal knows where the limbs are in
space (i.e. has normal proprioception) and not the strength of the corrective
movement itself.
There are several different tests, known as postural reactions, that can be
performed to assess an animal’s proprioception, but it is important to appreciate
that performing all of these tests is not required in the majority of cases. Paw
replacement is often the most useful first test and is easy to perform in most
dogs.

a. Paw replacement
The animal being examined should be standing as squarely as possible, with
their weight evenly distributed across all limbs (see Video 6a). A tabletop can be
used for small dogs and cats, but larger dogs will feel more relaxed when exam-
ined on the floor. With the animal facing away from you, place your hand under
the sternum to support some of the animal’s weight. As previously discussed,
providing this support is important to ensure that the animal does not collapse
through the limb if it is weak, or that the animal does not shift their weight away
from the limb during testing. This can result in the false impression that replace-
ment of the paw is delayed. One front paw should be gently lifted and turned
over so that the dorsal skin surface is in contact with the ground. The paw should
be rapidly replaced into its normal position in a clean and coordinated manner.
If you are unable to place the dorsal aspect of the paw onto the ground without
the animal starting to replace it, then this test can be assumed as normal. The
pelvic limbs can be assessed in an identical manner by supporting the weight
under the abdomen during testing.
A delayed or absent paw replacement should be considered abnormal
(Figure 3.14). However, considerations should also include:

• Reluctance to replace the paw secondary to limb or joint pain rather than a
true proprioceptive deficit
• An inability to perform the replacing movement secondary to severe motor
dysfunction (e.g. paralysis) rather than a lack of knowledge of abnormal paw
position.
• Uneven weight bearing (i.e. shifting of weight away from the limb being
tested).
• Severe systemic illness resulting in lethargy, generalised weakness, and a sub-
jectively delayed paw replacement.
80 A Practical Approach to Neurology for the Small Animal Practitioner

Figure 3.14 Absent paw replacement in the right pelvic limb of a dog with a spinal cord
lesion affecting the T3–L3 spinal cord segments on the right side.

If paw replacement testing is convincingly abnormal, then other tests of pro-

prioception may not be required to further refine your neuroanatomic localisa-
tion. If paw replacement testing is equivocal, then further proprioceptive testing
should be performed. Hopping is the most useful test to perform next, particu-
larly in cats for which paw replacement can be difficult to interpret and may
appear normal unless a severe neurological deficit is present.

b. Hopping
Hopping requires more complex movements and coordination when compared
to paw replacement. It therefore represents a complementary test and may
reveal subtle proprioceptive deficits that are not apparent using paw replace-
ment alone. Hopping can be performed on a tabletop for small dogs and cats, but
it can be easier to interpret when the limb being examined is viewed from above
and the animal is on the ground for testing.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 81

Thoracic limbs. With the animal facing away from you, the thoracic limb on
one side can be gently lifted away from the ground by holding the humerus
immediately proximal to the elbow (see Video 7a). Your other arm should be
placed under the abdomen just in front of the pelvic limbs so that the pelvic
limbs can be lifted a small distance above the ground. This means that the animal
is now bearing weight on a single thoracic limb. It is very important to take the
majority of the animal’s weight at this stage and not force the dog or cat to take
its full weight on only a single limb. If the animal has neuromuscular weakness
or is reluctant to bear weight on the limb due to pain, then it may collapse
through the limb, which could be misinterpreted as a true proprioceptive
deficit.
The body of the dog or cat should now be moved in a slow and steady man-
ner towards the side of the limb being tested. This will move the shoulder of the
tested limb lateral to the paw that is in contact with the ground. The normal
response is for the animal to compensate for this change in body position by
performing a small, coordinated hop that is initiated the moment you lose sight
of the paw under the shoulder. This hop should result in the paw coming to rest
on the ground immediately underneath the shoulder again. Several consecutive
hops can be assessed on one side before assessment of the other limb in an iden-
tical manner. Repeated cycles of testing should be performed in each limb to gain
an overall impression as to whether hopping is normal and symmetrical.
Observing the limb being tested from above makes it easier to appreciate a subtle
delay in the initiation of the hop when you start to lose sight of the paw. With
practice, this test can be performed very quickly and with minimal stress to the
patient.
Pelvic limbs. The easiest way to test hopping in the pelvic limbs is to stand at
the side of the animal with their head facing either to your left or to your right.
If the head is facing to your left, then the animal’s right pelvic limb can be tested
first by passing your left hand under the sternum to lift the thoracic limbs away
from the ground. Your right arm can then be used to lift the left pelvic limb
away from the ground, as this limb is closest to you. As for hopping the thoracic
limbs, it is important that the animal’s weight is adequately supported during
testing. The animal’s body can then be moved away from you so that you start
to lose sight of the right hind paw as the hip moves laterally. At this stage, the
animal should hop to replace the paw immediately under the new position of
the hip. The initiation of the hop in the pelvic limbs is often slightly slower than
for the thoracic limbs but it should still be a brisk and coordinated movement.
The left pelvic limb can then be tested in an identical manner but with the ani-
mal facing to your right.
See Video 8a for an example of abnormal paw replacement and hopping in
the pelvic limbs. In addition to a delay in the initiation of the hop, other abnor-
malities that can be appreciated when performing hopping include:
82 A Practical Approach to Neurology for the Small Animal Practitioner

• Wide and inappropriate replacement of the paw to a new position that is further
lateral than that of the hip or shoulder joint. This is often accompanied by a delay
in the initiation of the hop and is consistent with abnormal proprioception.
• Excessive flexion of the limb during hopping and/or excessive force used to
replace the paw on the ground. This inappropriate rate, range, and force of
movement is termed ‘dysmetria’ and can be seen in association with disorders
affecting the cerebellum. However, certain breeds such as pugs may also show
apparent dysmetria when hopping as a normal breed variation.

c. Hemi‐walking
Hopping can be difficult to perform and interpret in large or heavy dogs. If this
is the case, then the thoracic and pelvic limbs on the same side can be assessed
at the same time using hemi‐walking. This is performed in a similar manner to
pelvic limb hopping but instead of lifting both thoracic limbs away from the
ground, only the thoracic and pelvic limbs on the side closest to you are lifted up.
The animal’s body is then moved away from you to assess the ‘hopping’ of the
thoracic and pelvic limbs on the opposite side. The animal can then be moved to
face in the other direction to test the contralateral limbs.

d. Wheelbarrow testing
This test can be useful to accentuate any subtle proprioceptive deficits that are
suspected following gait assessment, paw replacement, and hopping. With the
animal facing away from you, place your arms under the abdomen and lift both
pelvic limbs a small distance above the ground. The dog or cat is then encour-
aged to walk forwards using only their thoracic limbs for weight support.
Elevating the head using one hand placed under the muzzle can also help to
accentuate any abnormal limb movements or positioning. Possible abnormalities
that may be observed on wheelbarrow testing include:

• Scuffing of the thoracic limbs or erratic limb placement suggestive of a pro-

prioceptive deficit in the affected limb(s).
• Excessive flexion of the limbs during protraction (hypermetria) in animals
with cerebellar dysfunction.
• Animals with lower motor neuron paresis of the thoracic limbs (e.g. general-
ised neuromuscular disease or a C6–T2 spinal cord lesion) may struggle to
perform wheelbarrow testing. This is clinically apparent as buckling of the
affected limb(s) under the animal’s weight, sometimes together with a low
head carriage and performing a ‘forward roll’ in those with generalised neuro-
muscular weakness.

e. Extensor postural thrust

This test is most useful in cats or small dogs to further evaluate the pelvic limb
proprioception. Place both hands around the thorax, just caudal to the shoulders,
 Chapter 3 The ‘Stress‐free’ Neurological Examination 83

and hold the animal upright so that it is elevated from the ground. The animal is
then lowered towards the ground and encouraged to walk backwards. The nor-
mal response should be for the dog or cat to extend the pelvic limbs in anticipa-
tion of them reaching the ground, followed by even and coordinated backward
steps.
Animals with lower motor neuron weakness of the pelvic limbs (e.g. gener-
alised neuromuscular disease or an L4–S1 spinal cord lesion) will show poor
extension of the pelvic limb joints (stifles and/or hocks) and may collapse when
trying to perform the stepping movements. Proprioceptive deficits in the pelvic
limbs are apparent as a delay in the onset and termination of the corrective step-
ping movements, resulting in long steps with erratic placement of the affected
limb(s).

f. Other tests of proprioception

Other tests that can be used to assess proprioception include the paper slide test
and tactile placing. These tests need not be performed if a convincing proprio-
ceptive deficit has already been identified using paw replacement or hopping.
Paper slide test. With the animal standing squarely and distributing weight
evenly across all limbs, a piece of paper is placed under the paw of the limb being
tested. This piece of paper is then pulled slowly in a lateral direction and the
normal response is for the animal to briskly correct the position of the limb so
that it lies underneath the body (e.g. under the shoulder for the thoracic limb,
or under the hip for the pelvic limb). A proprioceptive deficit is suggested if there
is a delay in the replacement of the paw back to its normal position. This test
assesses proprioception in a similar way to hopping but in reverse, with the limb
being moved lateral to the body rather than the body being moved lateral to the
limb. It can therefore be useful for large or giant breed dogs, or for nervous ani-
mals, in which hopping may be difficult to perform and interpret.
Tactile placing. This test of proprioception can be useful in cats or small dogs,
particularly within the confines a small consultation room (see Video 9a). The
animal is held with one hand under the abdomen or thorax, and the other hand
gently covering the eyes so that the dog or cat cannot see the examination table
in front of them (see Video 10a). The thoracic and pelvic limbs are then tested in
turn by moving the animal towards the edge of the table so that the dorsal
aspects of the paws being tested contact the table edge. Contact with the table
edge should induce a coordinated stepping movement so that the paws are
placed onto the table. If there is a proprioceptive deficit, then there will be a
delay in the initiation of the stepping action and the dorsal aspect of the paw will
drag along the table edge before a corrective movement is observed. The results
of this test should be confirmed using other tests of proprioception (e.g. hopping
or paw replacement). Tactile placing can appear abnormal in animals that are
nervous as they may be tense and hold their limbs in an extended position. It is
also prudent to perform this test when holding the animal on each side of your
84 A Practical Approach to Neurology for the Small Animal Practitioner

body (e.g. alternating between using your right and left arm to cover the eyes),
as the limb closest to your body can sometimes appear to show an abnormal
response. This should only be interpreted as abnormal if repeatable with the
animal held on both sides of your body.

4. Spinal reflex testing

Gait evaluation and proprioceptive testing are most useful to confirm the pres-
ence of a neurological problem and to determine which limbs are affected.
However, they are non‐specific in terms of localising the site of the lesion respon-
sible. This is because numerous neuroanatomical structures, including compo-
nents of the brain, spinal cord, and peripheral nervous system, are required for
normal proprioception and to generate a normal gait. Other tests are therefore
required, which assess the integrity of more limited regions of the nervous sys-
tem, to determine a specific neuroanatomical localisation. This includes assess-
ment of the local spinal reflexes in all limbs.
Similar to the cranial nerve examination, spinal reflex testing involves appli-
cation of a tactile stimulus to a region of the body and the observation of an
appropriate motor reaction to this stimulus. In doing so, these tests screen the
function of three main components.

1. The peripheral sensory nerves that detect and transmit the sensory informa-
tion to the level of the spinal cord.
2. The peripheral motor nerves that innervate the muscles responsible for the
reflex movement.
3. The region of the spinal cord that contains both the cell bodies of the periph-
eral motor neurons involved in the reflex and the interneurons that connect
the sensory component to these cell bodies.

A spinal reflex will be abnormal if there is dysfunction of one or more of

these three components and spinal reflexes can therefore be affected by lesions
involving the spinal cord or peripheral nervous system. It is important to remem-
ber that these local spinal reflexes do not require input from the brain or spinal
cord UMNs to be normal. They will therefore be intact as long as the peripheral
nerves and spinal cord segments required for reflex activity are functional, irre-
spective of brain or spinal cord lesions at distant sites. For example, the spinal
reflexes in the pelvic limbs will appear normal even if the spinal cord is severed
at a site cranial to the L3 spinal cord segment. This concept underlies the impor-
tance of separating the interpretation of spinal reflex testing and assessment for
nociception (‘deep pain sensation’) in the limb being tested. Otherwise, confu-
sion may arise regarding both the lesion localisation and the severity of the clini-
cal signs. If the peripheral sensory nerve responsible for detecting a tactile or
noxious stimulus is damaged, then both the flexor withdrawal reflex and nocic-
eption may be absent in the limb being tested. However, the flexor withdrawal
 Chapter 3 The ‘Stress‐free’ Neurological Examination 85

reflex may be reduced or absent in a dog with a generalised peripheral motor

polyneuropathy whilst nociception will remain normal as the sensory nervous
system and spinal cord are not affected in these cases. In contrast, a severe thora-
columbar spinal cord lesion may result in loss of nociception in the pelvic limbs
but the pelvic limb withdrawal reflexes will remain normal as the spinal cord
segments responsible for the reflex are spared (L4–S1 spinal cord segments).
Spinal reflex testing is therefore most useful for:

• localising the site of a spinal cord lesion by screening the function of specific
regions of the spinal cord
• assessing the integrity of the peripheral nerves required for reflex function.

a. Flexor withdrawal reflex

The flexor withdrawal reflex is the most useful spinal reflex to perform in the
majority of cases (see Video 11a). It is particularly useful for refining the neuro-
anatomic localisation in an animal with a suspected spinal cord lesion. It should
be assessed in both the thoracic and pelvic limbs and can initially be performed
in a standing animal at the same time as proprioceptive testing (see Videos 12a
and 13a). If there is any suspicion that the reflex is abnormal, then this should
be confirmed by repeating the test with the patient in lateral recumbency.
The interdigital skin of the limb being tested is held between your thumb and
forefinger, with the limb in extension. A gradually increasing pressure is then
applied, which should induce flexion of the limb to pull it away from the stimulus;
all of the joints in the limb being tested should flex at this time (shoulder, elbow,
carpus, and digits for the thoracic limb, and the hip, stifle, hock, and digits for the
pelvic limb). The animal should still be able to withdraw the limb even if you apply
mild resistance to flexion by keeping hold of the interdigital skin between your
fingertips. If there is no response to fingertip pressure, then fingernails can be used
to apply a stronger stimulus. If no attempt is subsequently made to withdraw the
limb, then artery forceps can be used to apply gentle pressure to the interdigital
skin or nail bed of one digit. This pressure should be increased very gradually to
avoid local trauma to the digit. If the animal does not withdraw the limb but dem-
onstrates apparent discomfort at any time during testing (e.g. vocalisation, dis-
tress, trying to bite, or move away), then it can be assumed that the motor
component of the reflex is abnormal and increasing pressure should not be applied.
The most important considerations when performing this test are:

• the strength of limb withdrawal

• whether all joints are adequately flexed at the time of withdrawal.

There is significant individual variation regarding the force required to elicit

a withdrawal reflex between different animals. Therefore, an apparent delay in
86 A Practical Approach to Neurology for the Small Animal Practitioner

the onset of withdrawal or the fact that more force was required to elicit the
reflex compared to another animal is not significant. The most important thing
is whether the animal is able to perform normal limb flexion at any point during
testing.
Other important factors to consider are:

• Is there a mechanical resistance to joint flexion that could influence interpre-

tation of the test (e.g. marked osteoarthritis and reduced range of joint
motion)?
• Is there a focus of limb pain that may make an animal reluctant (rather than
unable) to withdrawal the limb?

Do not make this mistake: A strong withdrawal reflex does not mean that the
animal is consciously aware of the stimulus being applied to the distal limb, only
that the peripheral nerves and local spinal cord segments required for the reflex are
functional. This is therefore not the same as having intact ‘deep pain perception’
(nociception) (see Video 15).

Thoracic limb withdrawal reflex. This test screens the integrity of the C6–T2
spinal cord segments, C6–T2 dorsal and ventral nerve roots, and the peripheral
nerves that innervate the flexors of the shoulder (axillary nerve), elbow (mus-
culocutaneous nerve), carpus, and digits (median and ulnar nerves). The sen-
sory nerves responsible for detecting the stimulus reside within the radial nerve
(dorsal aspect of the paw) and median and ulnar nerves (palmar aspect of the
paw) if the second or third digits are stimulated (see Video 12a).
This test is most useful to refine the neuroanatomic localisation in an animal
with tetraparesis/tetraplegia and a suspected spinal cord lesion between the C1
and T2 spinal cord segments. Strong thoracic limb withdrawal reflexes would be
consistent with a lesion affecting the C1–C5 spinal cord segments, whereas weak
thoracic limb withdrawal reflexes would imply a lesion involving the C6–T2 seg-
ments (or peripheral nerves).
Pelvic limb withdrawal reflex. This test primarily screens the integrity of the
L6–S1 spinal cord segments, L6–S1 nerves roots, and the sciatic nerve that inner-
vates the flexors of the stifle, hock, and digits. The hip flexors are innervated by
the femoral nerve (L4–L6 spinal cord segments and nerve roots) and the lumbar
spinal nerves. The sensory nerve responsible for detecting the stimulus depends
on which digit is used to perform the test, with this being the sciatic nerve if the
stimulus is applied to the fifth (lateral) digit and the femoral nerve for the first
(medial) digit (see Video 13a).
This test is most useful for refining the neuroanatomic localisation in an ani-
mal with paraparesis/paraplegia and a suspected spinal cord lesion between the
 Chapter 3 The ‘Stress‐free’ Neurological Examination 87

T3 and S1 spinal cord segments. Strong pelvic limb withdrawal reflexes would
be consistent with a lesion affecting the T3–L3 spinal cord segments, whereas
weak pelvic limb withdrawal reflexes would imply a lesion involving the L4–S1
segments/nerve roots (or sciatic nerves) (see Video 14a).
A diffuse or multifocal spinal cord lesion affecting both the C6–T2 and L4–
S1 spinal cord segments would be required to affect the withdrawal reflexes in
both the thoracic and pelvic limbs concurrently. Such conditions are rare, and
the scenario of reduced/absent withdrawal reflexes in all limbs is more com-
monly observed in association with generalised neuromuscular disorders that
affect the peripheral nerves required for reflex function away from the spinal
cord.

b. Patellar reflex
The patellar reflex is the most commonly performed tendon reflex in veterinary
medicine, and familiarity with the same reflex in human medicine means that
owners often find it entertaining to see it performed in their pet! However, this
test may be of little use for refining the neuroanatomic localisation in many
cases and there are several considerations to bear in mind when interpreting the
results. The patellar reflex is most useful in animals that have an abnormal pelvic
limb gait, show apparent pelvic limb weakness, or show poor stifle extension
when standing.
The patellar reflex is most easily assessed with the animal in lateral recum-
bency and the limb being tested held partially flexed (see Video 15a). It may also
be tested when the animal is standing, by holding the femur just proximal to the
stifle and allowing the distal limb to hang beneath (see Video 16a). However,
the limb should always be relaxed at the time of testing as increased extensor
tone in the limb can complicate interpretation of a subjectively weak reflex. The
patellar tendon that runs between the patella and the tibial tuberosity is struck
briskly using a tendon hammer to elicit a reflex extension of the stifle. The
handle of a pair of scissors or forceps can also be used to apply the blunt stimulus
to the patellar tendon.
Striking the patellar tendon results in stretching of small, specialised
myofibres called muscle spindles that lie within the quadriceps muscle. This
results in firing of nerve endings associated with the muscle spindles, and this
information is relayed to the spinal cord via sensory nerve fibres within the
femoral nerve. These sensory axons connect directly (monosynaptically) to
the cell bodies of motor nerve fibres that reside within the ventral grey matter
of the L4–L6 spinal cord segments. These motor axons leave the spinal cord in
the L4, L5, and L6 ventral nerve roots and form the motor component of the
femoral nerve which innervates the quadriceps muscle responsible for stifle
extension.
88 A Practical Approach to Neurology for the Small Animal Practitioner

Important considerations when performing the patellar reflex are:

• The reflex may appear reduced/absent in animals with pre‐existing stifle dis-
ease (e.g. cruciate ligament rupture, osteoarthritis).
• The reflex may appear reduced/absent if there is increased muscle tone in the
limb being tested. This can often be the case for nervous animals or those that
are intolerant of being held in lateral recumbency.
• The reflex will also appear absent if the patellar tendon is not struck cleanly,
or if the patella or tibial tuberosity are inadvertently struck instead.
• The patellar reflex may appear reduced/absent in older dogs as an inciden-
tal finding. Interpretation of the reflex in this subset of animals therefore
needs careful consideration. If an animal has a normal pelvic limb gait and
is able to stand with a normal stifle posture, then femoral nerve function
(motor) can be assumed to be adequate. A reduced/absent patellar reflex
in these cases is unlikely to be significant and should not be used to guide
the neuroanatomic localisation unless there are other neurological deficits
consistent with abnormal sensory nerve function (e.g. reduction of other
tendon reflexes, poor flexor withdrawal reflexes, proprioceptive deficits).

Top tip: If the animal is in lateral recumbency, the patellar reflex may appear
reduced in either the recumbent or uppermost limb; if this is the case, then the reflex
should be repeated with the animal in the opposite recumbency. If the patellar reflex
is normal in one recumbency, then this does not need to be confirmed in the other
recumbency.

A subjectively exaggerated patellar reflex could reflect:

• A spinal cord lesion rostral to the L4 spinal cord segment resulting in loss of
UMN inhibition on reflex function. This can be apparent as clonus of the
patellar reflex in which there is repetitive extension of the stifle in response to
a single stimulus.
• Sciatic nerve dysfunction resulting in loss of tone in the antagonist stifle flexor
muscles that would normally provide resistance to stifle extension. This is
termed ‘pseudo‐hyperreflexia’.
• The patellar reflex may also appear exaggerated in a stressed or excited dog,
therefore a subjectively ‘strong’ reflex should always be interpreted with cau-
tion. Given the degree of natural variation between animals it is more reliable
to simply think of this reflex as being either normal or reduced/absent.

c. Other limb reflexes

In addition to the patellar reflex, other tests of reflex function include the exten-
sor carpi radialis, biceps brachii, triceps, cranial tibial, and gastrocnemius reflexes.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 89

These tests aim to assess the integrity of the specific spinal cord segments, their
associated nerve roots, and the peripheral nerves involved in each reflex.

• Extensor carpi radialis: C7–T2 spinal cord segments and nerve roots; radial nerve
(see Video 17a).
• Biceps brachii: C6–C8 spinal cord segments and nerve roots; musculocutaneous
nerve.
• Triceps: C7–T1 spinal cord segments and nerve roots; radial nerve.
• Tibialis cranialis: L6–S1 spinal cord segments and nerve roots; peroneal nerve
(see Video 18a).
• Gastrocnemius: L7–S1 spinal cord segments and nerve roots; tibial nerve.

The authors rarely perform these tests in practice as they are less reliable than
the patellar reflex and their interpretation is complicated by the fact that they
may be absent in the normal animal. Recent studies have also questioned the
clinical utility of the cranial tibial and extensor carpi radialis reflexes as they can
still be elicited in cats after anaesthetic blockade of the brachial and lumbosacral
plexi (Tudury et al. 2017). This suggests that these reflexes are not strictly myo-
tactic, as they appear independent of the reflex arc and are more likely to repre-
sent local muscle contraction in response to percussion of the muscle belly itself.

d. Perineal reflex, anal tone, tail tone, and bladder function

Perineal reflex and anal tone. The perineal reflex can be performed at the same time
as assessment of anal tone and tail tone (see Video 19a). These tests are used to
screen the integrity of the first sacral (S1) to fifth caudal (Cd5) spinal cord seg-
ments, the S1–Cd5 nerve roots, the pudendal nerves for anal sphincter tone, and
the caudal nerves for tail tone and movement. The S1–S3 and Cd1–Cd5 spinal
cord segments reside within the spinal canal of most dogs in the region of the L5
and L6 vertebrae, respectively. Their associated nerve roots then course caudally
as part of the cauda equina to exit the spinal canal via their respective foramina.
Pathology affecting the L5 and L6 vertebrae or their associated intervertebral
discs may therefore affect these adjacent spinal cord segments, resulting in poor
tail or anal tone. The termination of the spinal cord in cats is located more cau-
dally within the spinal canal, typically at the level of the L7 to sacral vertebrae.
To assess the perineal reflex, artery forceps are used to gently pinch the skin
either side of the anus. This should elicit a reflex contraction of the anal sphincter
and flexion of the tail. Reduced or absent anal tone, indicating a lesion involving
the S1–S3 spinal cord segments/nerve roots or the pudendal nerve, will be appar-
ent as a relaxed anal sphincter that does not constrict around your finger when
digital rectal examination is performed. There will also be little or no resistance to
gentle opening of the anus using the ends of a pair of artery forceps.
Tail carriage. A low tail carriage can be the result of both neurological and
non‐neurological conditions.
90 A Practical Approach to Neurology for the Small Animal Practitioner

• A flaccid tail that lacks voluntary movement and hangs limp would be most
consistent with a lesion affecting the Cd1–Cd5 spinal cord segments, nerve
roots, or caudal nerves. It is important to note that the flaccid tail may pas-
sively swing from side to side when the animal is walking, which may be
mistaken for a voluntary tail wag.
• A spinal cord lesion involving the descending UMN tracts between the first
cervical (C1) and seventh lumbar (L7) spinal cord segments may result in a
low tail carriage and reduced voluntary tail function if the messages informing
the tail to move are interrupted (e.g. an absent tail wag when greeting the
owner). However, the muscle tone in the tail should be normal and reflex
flexion should still be observed on perineal reflex testing.
• A low tail carriage with normal tail tone can be seen in nervous animals, or
secondary to discomfort in the region of the tail base (e.g. lumbosacral disease,
caudal disc extrusion, cat bite abscess).
• Reduced tone in the distal tail concurrent with firm, painful swelling of the tail
base that is held rigidly extended can be seen in dogs with acute caudal myo-
pathy (often colloquially called ‘limber tail’ or ‘swimmer’s tail’). This condition
is more commonly seen in working dogs, with swimming being a risk factor.
Recent research has suggested a possible genetic predisposition in Labrador
Retrievers (Pugh et al. 2016). This condition is likely to reflect a form of com-
partment syndrome in which excessive use or trauma to the tail muscles
results in swelling and an increase in pressure within muscles that are con-
strained by a tight fascia. This increased pressure can result in ischaemia of the
caudal muscles and nerves.

Bladder function and palpation. If there is a history of urinary incontinence

(either urine leakage or an inability to pass urine), then assessment of bladder
size, tone, and ease of expression can help to guide the neuroanatomic localisa-
tion if a neurological lesion is responsible. However, non‐neurological causes of
urinary incontinence should always be considered first, as these are likely to be
more common in general practice compared to neurological lesions, particularly
in the absence of other neurological deficits such as paraparesis, paraplegia, or
poor tail or anal tone. Non‐neurological conditions to consider in these cases
include urolithiasis and urethral obstruction (particularly in male cats), feline
lower urinary tract disease, bacterial cystitis, bladder or urethral neoplasia, and
urethral sphincter mechanism incompetence in spayed female dogs.
The detrusor muscle of the bladder and the urethral sphincters are primarily
innervated by the autonomic nervous system (sympathetic and parasympathetic
components). Contraction of the detrusor muscle for urination is mediated by the
parasympathetic nervous system via the pelvic nerve, which has cell bodies in the
S1–S3 spinal cord segments. Contraction of the striated muscle of the external
urethral sphincter is mediated by the pudendal nerve, which also has cell bodies
in the S1–S3 spinal cord segments (Figure 3.15). Therefore, a lesion that damages
 Chapter 3 The ‘Stress‐free’ Neurological Examination 91

the S1–S3 spinal cord segments/nerve roots, or the pelvic and pudendal nerves
themselves, can result in a flaccid bladder that is easy to express. Incomplete
urine voiding will occur as the animal is unable to contract the detrusor muscle,
and urine leakage may occur secondary to loss of tone in the external urethral
sphincter. This is often termed a ‘lower motor neuron’ bladder and is frequently
accompanied by poor tail and anal tone and/or a weak perineal reflex.
There is also an internal urethral sphincter that is made up of smooth muscle
and is innervated by sympathetic nerve fibres in the hypogastric nerve. This
nerve originates from cell bodies in the cranial lumbar spinal cord segments (L1–
L4 in the dog) and can therefore be spared by lesions that affect the S1–S3 seg-
ments in the low lumbar/lumbosacral spine. Intact tone in the internal sphincter
may therefore provide some resistance against bladder expression in animals
with an otherwise flaccid ‘lower motor neuron’ bladder. The hypogastric nerve
can be damaged, together with the pelvic and pudendal nerves, by lesions in the
region of the pelvic plexus in the caudal abdomen (e.g. pelvic fracture, neopla-
sia). This will result in complete loss of internal and external urethral sphincter
competence, and a leaking bladder that is very easy to express.
Voluntary control of urination is mediated by spinal cord UMNs that travel
from the micturition centres in the brainstem to the cell bodies of the hypogas-
tric, pelvic, and pudendal nerves that directly control bladder function
(Figure 3.15). Spinal cord lesions between C1 and L7 may damage these UMN
fibres, resulting in loss of the voluntary control of urination. In affected cases,
the bladder will fill until the pressure inside it exceeds the tone of the urethral
sphincters, and it starts to overflow. It is therefore very important to distinguish
between voluntary urination and an overflowing ‘upper motor neuron’ bladder
in animals with spinal cord lesions. This is to avoid the bladder becoming over‐
stretched and non‐functional. The pelvic nerves and pudendal nerves are unaf-
fected in these cases, meaning that the bladder remains tonic and is often difficult
to express against a contracted urethral sphincter. Loss of voluntary urination is
usually observed with spinal cord lesions that are severe enough to result in

Micturition
centres of the
brainstem Upper
motor
L1–L4 spinal S1–S3 spinal
neuron
cord segments cord segments

Pelvic nerve Pudendal nerve

Hypogastric nerve

Bladder External urethral

sphincter
Internal urethral
sphincter

Figure 3.15 The innervation of the bladder.

92 A Practical Approach to Neurology for the Small Animal Practitioner

paraplegia. It is therefore unusual (but not impossible) to see a loss of voluntary

bladder function in animals that still have voluntary movement in their pelvic
limbs (i.e. ambulatory or non‐ambulatory paraparesis). Likewise, voluntary uri-
nation frequently returns at roughly the same time as pelvic limb movements in
animals that are recovering from severe spinal cord injury. See Sections 6.10
‘Paresis, Paralysis and Proprioceptive Ataxia’ and 7.3 ‘Acute Spinal Cord Injury’
in Chapters 6 and 7 respectively for further discussion regarding bladder man-
agement in animals with spinal cord lesions.

e. Cutaneous trunci reflex

The cutaneous trunci reflex is most useful when used to more accurately localise
a suspected spinal cord lesion between the T3 and L3 spinal cord segments (see
Video 20a). Assessment of this reflex in a dog or cat with a normal gait and nor-
mal proprioception in all limbs is not usually required. The term ‘panniculus
reflex’ has been used for this test but is a misnomer as the word ‘panniculus’
refers to the layer of subcutaneous fat that is not involved in this reflex arc.
This test is performed by pinching the skin of the dorsum on either side of the
vertebral spinous processes, which should elicit reflex contraction of the cutane-
ous trunci muscle on both flanks (Figure 3.16a). This is a bilateral reflex and
pinching on one side of the dorsum should elicit contraction of the cutaneous
trunci muscles on both sides. The cutaneous trunci reflex should be present in
the majority of dogs from the level of the L5–L6 vertebrae. Testing should there-
fore start at this level and can be stopped if the reflex is present; further testing
at more cranial levels is only required if no contraction of the cutaneous trunci
is observed. Stimulation should be repeated sequentially at the level of each
spinous process, moving forwards until contraction is observed.
If the cutaneous trunci reflex can only be elicited at a level more cranial than
the L5–L6 vertebrae, then this would be consistent with a spinal cord lesion that
is blocking the ascending sensory information travelling to the cell bodies of the
lower motor neurons that innervate the cutaneous trunci muscle (Figure 3.16b).
These cell bodies reside in the C8 and T1 spinal cord segments, with their associ-
ated axons forming the lateral thoracic nerve. A spinal cord lesion that interrupts
the cutaneous trunci reflex may lie up to four vertebrae cranial to the level of
reflex loss but is most commonly around two vertebrae cranial to the level of
interruption (Gutierrez‐Quintana et al. 2012). For example, if the cutaneous
trunci reflex is absent caudal to the level of the L2 spinous process then this
would be most consistent with a spinal cord lesion in the vicinity of the T13 ver-
tebra (e.g. T13–L1 disc extrusion).
A bilateral lesion involving the C8–T1 spinal cord segments, C8–T1 nerve
roots, or lateral thoracic nerves would result in an absent cutaneous trunci reflex
at all levels of stimulation. However, it is important to note that this reflex may
be difficult to elicit in some dogs and cats. An absent cutaneous trunci reflex at
all levels of stimulation should therefore be interpreted with caution unless
 Chapter 3 The ‘Stress‐free’ Neurological Examination 93

(a)
C8
Lateral thoracic nerve
T1

Cutaneous trunci muscle Cutaneous trunci muscle

Sensory nerve fibres

(b)
C8
Lateral thoracic nerve
T1

Cutaneous trunci muscle Cutaneous trunci muscle

Intact
cutaneous Spinal cord lesion
trunci reflex

Absent
cutaneous
trunci reflex

Figure 3.16 (a) The cutaneous trunci reflex. Stimulation of the skin overlying the dorsum
results in reflex contraction of the cutaneous trunci muscle on both sides. (b) A spinal cord
lesion that blocks the ascending sensory information from reaching the C8–T1 spinal cord
segments will interrupt the cutaneous trunci reflex at a level roughly two vertebrae caudal to
the level of the spinal cord lesion.

there are other neurological deficits consistent with a lesion affecting the C8–T1
spinal cord segments or nerve roots.
A unilateral lesion that involves the C8–T1 spinal cord segments, nerve roots, or
lateral thoracic nerve will result in an ipsilateral loss of cutaneous trunci muscle
contraction. This will be clinically apparent as contraction of the cutaneous trunci
94 A Practical Approach to Neurology for the Small Animal Practitioner

muscle on only one side (opposite to the side of the lesion) in response to stimula-
tion of either side of the dorsum at any level. Other clinical signs that could be asso-
ciated with a unilateral lesion affecting the C8–T1 spinal cord segments or nerve
roots include lower motor neuron paresis of the ipsilateral thoracic limb, propriocep-
tive deficits in the ipsilateral pelvic limb, or Horner syndrome in the ipsilateral pupil.

5. Spinal palpation and neck manipulation

Tests that may be uncomfortable for the animal or that involve the application
of a noxious stimulus should only be performed if the information is essential for
determining the prognosis or to refine the neuroanatomic localisation (see
Videos 21a and 22a). They should also be performed at the end of the examina-
tion so that the dog or cat remains cooperative.
Identification of a focus or foci of apparent discomfort when moving the neck
or applying pressure to the vertebral column can greatly assist in supporting
your lesion localisation. This can be performed by working from head to tail.

• Direct palpation of the cervical spine. This is most easily performed by apply-
ing pressure from laterally using your fingers on either side of the paraspinal
muscles, working from the wings of the atlas to in front of the scapulae.
• Direct pressure applied to the transverse processes that protrude from the ven-
trolateral aspect of the C6 vertebra at the level of the thoracic inlet.
• Ventral flexion, dorsal extension, and lateral movement of the neck to the left
and right sides. A normal dog or cat should allow the head to be moved so that
the nose touches each flank. Resistance to such movement may imply discom-
fort, but mechanical restriction by a paraspinal mass should also be consid-
ered. Flexion of the neck in a young toy breed dog with suspected neck pain
and/or neurological deficits in all limbs should be avoided due to the risk of
exacerbating possible atlantoaxial instability.
• Direct palpation of the dorsal spinous processes from the first thoracic vertebra
(T1) to the lumbosacral junction. Light pressure should be used initially, fol-
lowed by cycles of palpation using increasing force to identify any foci of
apparent discomfort.
• Lordosis testing of the lumbosacral junction can be performed by extending
both hips and applying direct pressure to the lumbosacral region from dorsally
using either your other hand or chin.
• Tail elevation may elicit discomfort in dogs with lumbosacral discomfort or
tail pain.
• Digital rectal examination can be performed to assess for prostatic enlarge-
ment or discomfort, anal sac disease, intrapelvic mass lesions, or discomfort on
direct pressure to the ventral aspect of the sacrum.

All innervated anatomical structures in the region of discomfort should be

considered as a possible origin for any apparent pain that is elicited. This approach
 Chapter 3 The ‘Stress‐free’ Neurological Examination 95

is particularly useful to guide further investigations if there are no other neuro-

logical deficits on examination (e.g. in an animal that presents with neck pain as
the sole clinical finding). These anatomical structures include vertebrae, verte-
bral facet joints, paraspinal muscles, outer annulus fibrosus of the intervertebral
disc, ligaments (e.g. dorsal longitudinal ligament), meninges, and nerve roots.
The spinal cord itself is comprised of many sensory nerve fibres but does not
contain nociceptive nerve endings, therefore lesions affecting the spinal cord in
isolation do not typically result in overt discomfort (e.g. intramedullary
tumours). However, meningeal or nerve root involvement can result in severe
pain, and parenchymal lesions that affect the processing of nociceptive infor-
mation at the level of the dorsal horn may also result in apparent discomfort
(e.g. syringomyelia).

6. Testing of pain perception (nociception)

Nociception is the response of the nervous system to a harmful or potentially
harmful stimulus. This process involves the transmission of sensory informa-
tion from the site of stimulation to the forebrain in order to determine the
potential for harm. A conscious response to such stimulation therefore needs to
be observed when testing for nociception, which could include vocalisation,
turning to look at the site of stimulation, or attempting to bite. This is often
termed ‘deep pain perception’ and involves applying firm pressure using a pair
of artery forceps to the nail bed or digit of the limb being tested. Application of
a noxious stimulus using artery forceps is of course not required if a conscious
response to more gentle stimulation using your fingertips or fingernails is
observed first.
This conscious response to stimulation is not the same as the reflex movement
of a limb in response to the stimulus being applied, as described for the flexor
withdrawal reflex (see Video 15). Reflex testing only screens the peripheral
nerves and spinal cord segments involved in the reflex action and will remain
present even if the spinal cord is transected away from the segments involved.
The presence of a conscious response to a noxious stimulus requires integrity
of the axons within the spinal cord that transmit this information to the sensory
cortex in the forebrain. These are small, unmyelinated axons that lie deep within
the spinal cord on both sides, making them more resilient to injury compared to
the more superficial, larger, myelinated proprioceptive and motor fibres. This is
of clinical importance as it means that there is always an ordered loss of neuro-
logical function with increasing severity and extent of spinal cord injury:

• Loss of proprioception
• Loss of voluntary motor function (ranging from paresis to paralysis)
• Loss of nociception only when proprioception and voluntary motor function
have both been lost (i.e. nociception will only be lost once the affected limb is
paralysed).
96 A Practical Approach to Neurology for the Small Animal Practitioner

The fact that a severe, transverse lesion to the spinal cord is required to stop
the nociceptive messages being able to reach the brain, means that it is
extremely useful for predicting lesion severity and likely prognosis in a para-
lysed animal. However, this also means that nociceptive testing is only required
in animals with no appreciable voluntary movement in the limb(s) being
tested. Performing this test in an animal that has voluntary movement or, even
worse, that can still walk only adds unnecessary pain and distress. The inter-
pretation of nociceptive testing can also be difficult in stressed or stoic animals,
particularly in those that have another focus of pain or that have received
recent analgesia, and this makes appropriate case selection even more
important.
Testing for nociception in the thoracic and/or pelvic limbs in a tetraplegic
animal is not inappropriate; however, it is unusual for a cervical spinal cord
lesion to result in deep pain negative tetraplegia without also affecting the
descending axons for respiration, resulting in death.

3.5 ­Summary of the Neurological Examination

As previously discussed, performing a complete neurological examination in every

animal that presents to you with a possible neurological problem is always good
practice. However, a more refined neurological examination can often be per-
formed in the majority of patients and should take about 10 minutes to perform.

3.5.1 Observation
• Alertness and interaction with the environment (‘mentation and behaviour’).
• Posture of the head, limbs, joints, body, and tail.
• Gait: Is it normal? Which limbs are affected? What is the stride length in the
affected limbs? Is limb placement predictable?
• Presence of any involuntary movements.
• Facial symmetry, voluntary blinking, eyeball position, jaw tone and position.

3.5.2 Hands‐On Assessment

• Cranial nerve examination:
• Eyes: palpebral reflexes, menace responses, observation for involuntary
eye movements (spontaneous and positional), pupil size and symmetry.
• Mouth and jaws: jaw tone, tongue symmetry, masticatory muscle bulk.
• Nose: nasal septum nociception.
• Limb palpation: muscle atrophy, muscle tone.
• Postural reactions: paw replacement in all limbs, followed by hopping if paw
replacement is normal or equivocal.
• Spinal reflex testing: withdrawal reflexes in all limbs, patellar reflexes if abnor-
mal pelvic limb gait or posture.
 Chapter 3 The ‘Stress‐free’ Neurological Examination 97

• Perineal reflex and assessment of tail tone, anal tone, and bladder function.
• Spinal palpation and neck manipulation: for spinal hyperaesthesia.

The choice of additional tests will depend upon the presenting complaint,
how tolerant the patient is of examination, and how confident you are of a neu-
rological deficit(s) after performing the tests above. These tests could include the
following:

• Turning the patient into dorsal recumbency to look for positional nystagmus. This is
particularly useful to confirm vestibular dysfunction if there is a suspicion of
intracranial disease, or if there are subtle signs of possible vestibular dysfunc-
tion (e.g. slight head tilt or drifting when walking) but no spontaneous nystag-
mus on cranial nerve examination.
• Vestibulo‐ocular reflex. This test can be used to add support for a vestibular dis-
order but may offer little extra information if a head tilt, positional strabismus,
or abnormal spontaneous nystagmus has already been identified. This test is
most useful in animals with bilateral vestibular dysfunction or as part of a
modified Glasgow Coma Scale (MGCS) to monitor trends in brainstem
function.
• Pupillary light reflex. This test should be performed if anisocoria is present or if
visual deficits are suspected in one or both eyes.
• Gag reflex. If it is safe to perform, this test is most useful in animals with a his-
tory of dysphagia, gagging, regurgitation, or difficulty swallowing. As for the
vestibulo‐ocular reflex, it is also useful to monitor trends in brainstem
function.
• Hemi‐walking. This test is only required if an animal is too large to perform
hopping in individual limbs.
• Wheelbarrow testing. This test can be useful if there is a suspicion of neuromus-
cular weakness (e.g. generalised motor polyneuropathy). Animals with gener-
alised weakness may find it difficult to support their head and can collapse on
the thoracic limbs as if performing a forward roll. Elevating the head when
performing wheelbarrow testing can also accentuate hypermetria in animals
with cerebellar dysfunction.
• Extensor postural thrust. This test can be very useful in cats to assess for proprio-
ceptive deficits in the pelvic limbs.
• Tactile placing. This is an additional test of proprioception that can be used to
confirm or refute the findings of hopping or paw replacement if the results of
these tests are equivocal.
• Cutaneous trunci reflex. This should be performed in all cases for which there is
a suspicion of a spinal cord lesion between C6–L3 to further guide the neuro-
anatomic localisation.
• Nociceptive testing. This test should only be performed if there is no voluntary
movement observed in one or more limbs (paralysis/plegia).
98 A Practical Approach to Neurology for the Small Animal Practitioner

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Chapter 4 Lesion Localisation
Edward Ives

As discussed in Chapter 3, the neurological deficits identified on examination

reflect the lesion location and not the underlying cause. This location is called the
neuroanatomic localisation. It is essential that the neuroanatomic localisation is
determined before you consider individual diseases and perform further tests. This
is because some disorders will be more likely to affect certain regions of the nerv-
ous system and others less likely to do so. Conditions affecting different regions of
the nervous system can also result in similar clinical signs. For example, an abnor-
mal gait in all limbs could result from a lesion affecting the brain (e.g. cerebellar
infarct), or the cervical spinal cord (e.g. intervertebral disc disease), or any part of
the neuromuscular system (e.g. peripheral neuropathy, myasthenia gravis). If the
neuroanatomic localisation is not considered before tests are performed, then the
diagnostic approach is likely to become confused and expensive for the owner,
with unnecessary tests being performed that are difficult to interpret.
The subjective nature of the neurological examination, together with the wide
range of individual variation, means that it may be difficult to determine the sig-
nificance of an individual examination finding. Therefore, after performing the
full neurological examination it can be useful to classify your findings as follows:

• Tests that you feel confident were normal.

• Tests for which a clear neurological deficit was present (e.g. absent palpebral
reflex, paraplegia, absent paw replacement).
• Equivocal findings (e.g. subjectively weak withdrawal reflex, poor patellar
reflex, incomplete PLR in a stressed animal).

The tests for which a clear neurological deficit was present should then be
used to determine the site of a single lesion that could explain all of these deficits.
It can then be decided whether the equivocal findings:

a. support this localisation

b. are more likely to be insignificant or unrelated to the current problem
c. suggest a multifocal disease process.

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

99
100 A Practical Approach to Neurology for the Small Animal Practitioner

Many neurological tests involve the same test being performed on both sides
of the body. This means that there is an internal control, and by comparing the
results for the left and right sides, the potential significance of a subtle or equivo-
cal finding may be determined. If there is clear asymmetry in the test results,
then a subtle deficit is more likely to be significant than if your findings are simi-
lar for both the left and right sides.
As discussed in Chapter 3, if it is not possible to determine the site of single
lesion to explain all of the neurological deficits, then a multifocal or diffuse neuro-
anatomic localisation should be considered.
It is always important to consider the clinical history and the owner’s primary
concerns when determining the neuroanatomic localisation. This ensures that
unrelated, pre‐existing neurological deficits are flagged up that could have oth-
erwise complicated the interpretation of the current examination. These could
include:

• a head tilt in an animal with a prior history of vestibular disease

• pelvic limb proprioceptive deficits in a dog that has had previous spinal sur-
gery for intervertebral disc disease
• dysphonia, poor hock flexion on withdrawal reflex testing, or pelvic limb pro-
prioceptive deficits in an old Labrador Retriever with a degenerative
polyneuropathy.

4.1 ­Principles of Lesion Localisation

The nervous system can be broadly divided into two parts (Figure 4.1).

• Central nervous system: the brain and spinal cord.

• Peripheral nervous system: peripheral sensory nerves, peripheral motor nerves,
the skeletal muscles responsible for movement, and the neuromuscular
junction between the motor axons and skeletal muscles. It is important to
remember that the cell bodies of the peripheral motor nerves reside within
the central nervous system (ventral horn of the spinal cord grey matter),
with the axons leaving the spinal cord in the ventral nerve roots before
forming the individual, named, peripheral nerves (e.g. femoral nerve, radial
nerve).

The first step in every case should be to decide whether the lesion responsible
for the presenting clinical signs is most likely to be affecting the:

• brain
• spinal cord
• neuromuscular system.
 Chapter 4 Lesion Localisation 101

Brain Central
nervous
Spinal cord system

Peripheral nerves Peripheral

nervous
system
Neuromuscular junction
Skeletal muscles

Thoracic limb Pelvic limb

Figure 4.1 The anatomic division of the nervous system into central and peripheral
components.

This will ensure that a large category of neurologic disease is not overlooked
and aims to make the localisation process more approachable by limiting the
initial choice to one of three broad regions.
In some instances, particularly for neuromuscular disorders, it may be diffi-
cult to refine the neuroanatomic localisation further based upon the neurologi-
cal examination alone. However, the final goal of the neuroanatomic localisation
should be to localise the lesion to one of the following 10 possibilities (Figure 4.2).

• Brain (intracranial)
• forebrain
• brainstem
• cerebellum
• Spinal cord
• C1–C5 spinal cord segments
• C6–T2 spinal cord segments
• T3–L3 spinal cord segments
• L4–caudal (Cd) spinal cord segments

Forebrain
Cerebellum

Spinal cord

C1–C5 C6–T2 T3–L3 L4–Cd

Brainstem Peripheral motor

nerves

Neuromuscular junction
Skeletal muscles

Thoracic limb Pelvic limb

Figure 4.2 The nervous system divided into the regions that are used for lesion localisation.
102 A Practical Approach to Neurology for the Small Animal Practitioner

• Neuromuscular system
• peripheral neuropathy
• neuromuscular junction disorder (junctionopathy)
• myopathy

Any lateralisation of neurological deficits, if present, should also be consid-

ered to determine your final neuroanatomic localisation (e.g. left forebrain, right
brainstem, or diffuse cerebellum if there is no lateralisation and the clinical signs
are symmetric). This localisation can then be used to formulate a list of differen-
tial diagnoses, before planning further investigations.

4.1.1 Cranial Nerve Deficits

The neuroanatomic localisation for animals presenting with single (or multiple)
cranial nerve deficits should also be mentioned, as where they fall within the 10
subcategories listed above is sometimes unclear. A cranial nerve deficit may
result from damage to either the neuronal cell bodies that lie within the brain-
stem nuclei, or to the peripheral, axonal component of the cranial nerve. The
neuroanatomic localisation relating to dysfunction at the level of the neuronal
cell bodies would be brain (brainstem). In this scenario, other neurological defi-
cits will usually be observed that would support this lesion location, such as
tetraparesis or hemiparesis, ataxia of all limbs, other cranial nerve deficits, and
an altered level of mentation. Dysfunction of the peripheral component of the
cranial nerve outside the central nervous system is a common cause of cranial
nerve dysfunction, and usually presents as an isolated deficit in the absence of
other clinical signs (e.g. idiopathic facial paralysis, trigeminal neuropathy). The
neuroanatomic localisation in these cases falls best within the neuromuscular
(peripheral nerve) category, even if there are no other deficits found to support
a generalised neuromuscular disorder affecting the rest of the body.
Junctionopathies and myopathies may also result in clinical signs of cranial
nerve dysfunction, including facial weakness, dysphagia, and megaoesophagus.
The deficits in these cases usually reflect bilateral dysfunction. This should raise
the index of suspicion for a neuromuscular localisation unless there are other
neurological deficits to support an extensive/bilateral brainstem lesion.

A logical approach to the neuroanatomic localisation should start by consider-

ing if any of the presenting clinical signs or neurological deficits are consistent with
a disease affecting the brain. If an intracranial lesion localisation appears unlikely,
then a spinal cord lesion or neuromuscular disorder should be considered next.

4.2 ­Intracranial Lesions

The brain is an extremely complex neuroanatomical structure that processes

sensory information from within and outside the body, before initiating and
 Chapter 4 Lesion Localisation 103

coordinating appropriate motor responses via the spinal cord and peripheral
nervous system. Functions of the brain that can be screened by the neurological
examination include:

• level of alertness
• behaviour and interaction with the environment
• conscious response to noxious stimuli
• cranial nerve functions, including vision and vestibular function (balance)
• proprioception
• initiation and coordination of movements.

Different regions of the brain are responsible for different functions and the
brain can be divided into three broad regions when considering the neuroana-
tomic localisation: the forebrain, brainstem, and cerebellum. Classical clinical
signs that would add support for a lesion involving these regions are discussed
next.

1. Forebrain
• A history of epileptic seizures.
• Behavioural abnormalities (e.g. loss of house training, restlessness, pacing,
altered interaction with the owner or other dogs).
• Change in the level of mentation (depression to stupor).
• Circling, most commonly towards the side of a forebrain lesion (see Video 22).
• Proprioceptive deficits affecting the thoracic and pelvic limbs on the opposite
side to a lateralised forebrain lesion (Box 4.1).
• Visual deficits (e.g. an absent menace response in the eye on the opposite side
to a lateralised forebrain lesion, see Video 28). A forebrain lesion that affects
the central visual pathways at the level of the thalamus or visual cortex will
result in blindness without affecting the pupillary light reflex.

Box 4.1

Top tip: The motor centres that are responsible for the initiation of movement in
dogs and cats reside predominately within the brainstem. Therefore, whilst a
forebrain lesion may result in reduced/absent paw replacement in the contralateral
thoracic and pelvic limbs, the gait may appear subjectively normal if the animal is on
an even surface as the brainstem motor centres are not affected.

2. Brainstem
The brainstem contains many important nuclei and neuronal pathways. Disease pro-
cesses that affect these structures can result in profound neurological signs dependent
on the extent of the lesion and the speed of onset. These structures include:
104 A Practical Approach to Neurology for the Small Animal Practitioner

• nuclei of cranial nerves III (oculomotor) to XII (hypoglossal)

• ascending reticular activating system (ARAS), responsible for level of wakefulness
by diffuse stimulation of the cerebral cortex
• central components of the vestibular system
• basal motor nuclei responsible for the initiation and control of movement
• respiratory and cardiac centres
• descending upper motor neuron tracts destined to the travel down the spinal cord
to initiate movement by stimulating the cell bodies of the peripheral motor
nerves that innervate the skeletal muscles
• ascending sensory and proprioceptive tracts travelling from the periphery to the
forebrain and cerebellum via the spinal cord.

A brainstem neuroanatomic localisation should be considered if one or more

of the following neurological deficits is observed on examination.

• Change in the level of mentation (depression to coma).

• Cranial nerve deficits (cranial nerves III–XII): see Box 4.2. Further discussion of
individual cranial nerve deficits can be found in Chapter 6.
• Vestibular syndrome (e.g. head tilt, spontaneous nystagmus, ataxia of all limbs
with drifting or rolling). Further discussion regarding the distinction between
peripheral and central vestibular disorders can be found in Chapter 6.
• Tetraparesis or ipsilateral hemiparesis. Interruption to the descending upper
motor neuron tracts will result in a long stride length in the affected limbs
(delay in the onset and termination of the stride).
• General proprioceptive ataxia of all limbs or the ipsilateral thoracic and pelvic limbs for
a lateralised brainstem lesion.
• Proprioceptive deficits in all limbs or in the ipsilateral thoracic and pelvic limbs for a
lateralised lesion.

Seizures, loss of learned behaviours and visual deficits would not be expected
for a lesion that is isolated to the brainstem. Therefore, a forebrain lesion or a

Box 4.2 Bilateral Cranial Nerve Dysfunction

Cranial nerve deficits that affect the same nerve on both sides (e.g. bilateral facial
paralysis, or a dropped jaw as a result of bilateral loss of trigeminal [motor] nerve func-
tion) are more likely to reflect a disorder affecting these nerves outside the brainstem.
This is particularly likely if the level of mentation is unaffected. A lesion that is exten-
sive enough to result in dysfunction of the cranial nerve nuclei on both sides of the
brainstem would also be expected to affect adjacent nuclei and pathways. This would
result in a change to the level of mentation (stupor/coma), tetraparesis, proprioceptive
deficits in all limbs, or even death secondary to interruption of the descending cardi-
orespiratory pathways.
 Chapter 4 Lesion Localisation 105

multifocal disease process should be considered if these are observed or reported

in the clinical history.
A lesion that involves the upper cervical spinal cord will also affect the
ascending proprioceptive pathways and the descending upper motor neuron
tracts to and from the brain. This means that it can sometimes be difficult to
distinguish a brainstem lesion from a lesion affecting the cervical spinal cord.
The concurrent presence of an altered level of mentation, vestibular syndrome,
or ipsilateral cranial nerve deficits would be most consistent with a brainstem
lesion in these cases.

3. Cerebellum
The cerebellum plays a vital role in coordinating the rate, range, and force of
movements. This also includes learned responses, such as the coordination of
blinking in response to objects approaching the eyes (menace response). The
initiation of these movements originates in the forebrain and brainstem and
does not involve the cerebellum. Therefore, a lesion that is isolated to the
cerebellum may result in marked ataxia (see Video 18) and proprioceptive
deficits (hopping in particular), but it will not result in appreciable upper or
lower motor neuron paresis (‘weakness’). In contrast to lesions that affect the
ARAS in the brainstem or that diffusely affect the forebrain, cerebellar lesions
also do not influence the level of mentation and animals will remain alert and
responsive.
The cerebellum contains regions that are intimately associated with the con-
trol of balance and forms part of the central vestibular system. These regions exert
a tonic inhibitory influence on the vestibular nuclei in the brainstem. Unilateral
cerebellar lesions may reduce this inhibitory influence on one side, resulting in
uneven output from the vestibular nuclei on each side of the brainstem and clini-
cal signs of a head tilt or nystagmus. A disease process that affects the peripheral
vestibular system or the brainstem vestibular nuclei will reduce the output from
the ipsilateral vestibular nuclei, resulting in a head tilt towards the side of the
lesion. In contrast, a unilateral cerebellar lesion will result in an increased output
from the ipsilateral vestibular nuclei due to the loss of inhibition. This results in a
‘paradoxical vestibular syndrome’ in which the direction of the head tilt is away
from the side of the lesion (see Video 19). Other regions of the cerebellum are
usually also affected in these cases, resulting in additional neurological deficits
that assist in the recognition of a cerebellar neuroanatomic localisation:

• ipsilateral proprioceptive deficits (particularly hopping)

• ipsilateral hypermetria (excessive flexion of the thoracic and pelvic limbs during
protraction)
• head and neck tremors that are exacerbated by intention to perform movements
• reduced/absent menace response in the ipsilateral eye, without loss of visual
tracking.
106 A Practical Approach to Neurology for the Small Animal Practitioner

In summary, a cerebellar neuroanatomic localisation should be considered if a

combination of the following neurological deficits is observed on examination:

• ataxia of all limbs without apparent paresis – normal stride length but inappropri-
ate rate, range, and force of movement (see Video 18)
• hypermetria (excessive limb flexion during protraction) affecting all limbs or
the ipsilateral thoracic and pelvic limbs for a lateralised lesion
• head and neck tremors – most noticeable with intention to perform a movement
(e.g. lowering the head to a food or water bowl) (see Video 11)
• central vestibular syndrome, with a head tilt either towards or away from the side
of the lesion
• absent menace response(s) with normal vision.

4.3 ­Spinal Cord Lesions

The spinal cord contains the descending upper motor neuron pathways that
connect the motor centres in the brain to the cell bodies of the peripheral motor
nerves that innervate the skeletal muscles of the limbs and trunk (Figure 4.3).
These peripheral motor nerves, termed ‘lower motor neurons’, have cell bodies
that reside within the ventral grey matter of the spinal cord. The spinal cord is
also comprised of ascending sensory and proprioceptive pathways that transmit
information from the peripheral sensory nerves to the cerebellum and sensory
cortex of the forebrain. Other than rare, degenerative disease processes that may
selectively affect certain tracts, a structural lesion to the spinal cord will indis-
criminately affect the function of both the ascending (sensory) and descending
(motor) pathways. Lesions affecting the ventral grey matter in certain regions of

Motor centres
of the brain

Upper motor neuron

Peripheral motor
nerves

Skeletal muscles

Thoracic limb Pelvic limb

Figure 4.3 The upper motor neurons descend the spinal cord and connect the motor centres
in the brain to the cell bodies of the peripheral motor nerves that innervate the skeletal
muscles of the body and limbs.
 Chapter 4 Lesion Localisation 107

the spinal cord can also damage the cell bodies of the lower motor neurons
innervating the limb muscles. Disease processes that affect the spinal cord are
termed ‘myelopathies’ and will result in a spectrum of clinical signs dependent
on the location, severity, and extent of the lesion.

• An inability to initiate movement or support weight in one or more limbs – this is

termed ‘paresis’ and results from damage to the spinal cord upper motor neu-
ron tracts and/or the cell bodies of the lower motor neurons in the ventral
grey matter.
• Proprioceptive ataxia in one or more limbs (‘incoordination’).
• Proprioceptive deficits in one or more limbs.
• Reduced nociception caudal to the level of an extensive spinal cord lesion – this will
only be observed once all voluntary motor function is lost (i.e. in cases with
paralysis/plegia).
• Apparent discomfort on spinal palpation if adjacent innervated structures are affected
(e.g. meninges, nerve roots, vertebrae, muscles, ligaments, intervertebral facet
joints, outer annulus fibrosus).

As previously discussed, whilst lesions affecting the brain can also result in an
abnormal gait, ataxia, and proprioceptive deficits, there are some important fac-
tors to consider.

a. Animals presenting with a single, focal spinal cord lesion should not have
any cranial nerve deficits. The main exception to this rule is Horner syn-
drome secondary to a spinal cord lesion affecting the C1–T3 spinal cord
segments (see Chapter 6).
b. Animals with spinal cord lesions may appear ‘dull’ secondary to pain or
distress at being recumbent; however, their level of mentation should be
alert and appropriate. The presence of seizure activity, visual deficits,
behaviour change, or an abnormal level of mentation should alert you to
the presence of a multi‐focal or diffuse disease process if the lesion other-
wise localises to the spinal cord.
c. An intracranial lesion will only affect the gait and/or proprioception in all
limbs, or in the thoracic limbs and pelvic limbs on one side if there is a
lateralised lesion. Therefore, a lesion residing outside the brain should be
suspected if only a single limb is affected, or if the pelvic limbs are affected
without thoracic limb involvement.

The spinal cord can be divided into individual segments, each with an associ-
ated pair of peripheral sensory and motor nerves (one on each side). In the dog
and cat, there are 8 cervical spinal cord segments, 13 thoracic segments, 7 lum-
bar segments, 3 sacral segments, and a variable number of caudal segments
related to tail innervation.
108 A Practical Approach to Neurology for the Small Animal Practitioner

The aim of the neuroanatomic localisation in an animal with a suspected spinal

cord disorder is to localise the lesion to one of four broad regions (see Figure 4.2):

• C1–C5 spinal cord segments

• C6–T2 spinal cord segments
• T3–L3 spinal cord segments
• L4–Cd spinal cord segments.

These regions are chosen as we have a limited number of examinations that

can be used to screen the function of specific spinal cord segments. The basis of
these tests is that the cell bodies of the lower motor neurons to the thoracic limbs
reside within the C6–T2 spinal cord segments, and those for the pelvic limbs and
tail reside within the L4–Cd spinal cord segments. Therefore, tests which assess
the muscle strength in the thoracic and pelvic limbs will screen both the integrity
of the peripheral nerves innervating the muscles being tested, together with the
spinal cord segments involved in the reflex activity (Figure 4.4). These tests are
called segmental spinal reflexes and are further discussed in Chapter 3.
Having first excluded an intracranial neuroanatomic localisation, the first ques-
tion to consider when assessing the gait and proprioception of an animal with a
suspected spinal cord lesion is: ‘How many limbs are affected?’ Answering this ques-
tion will assist in deciding which spinal cord segments are most likely to be affected.

• C1–T2 spinal cord segments: all limbs are affected, or the thoracic and pelvic limbs
on one side are affected.
• T3–Cd spinal cord segments: only the pelvic limbs +/− tail are affected, or only
one pelvic limb is affected.

C6 C7 C8 T1 T2 L4 L5 (L6) L6 L7 S1

Thoracic limb Patellar Pelvic limb

withdrawal reflex reflex withdrawal reflex

Figure 4.4 The thoracic limb withdrawal reflex tests the integrity of the C6–T2 spinal cord
segments/ventral nerve roots and the peripheral motor and sensory nerves of the thoracic
limb. The patellar reflex tests the integrity of the L4–L6 spinal cord segments/ventral nerve
roots and the femoral nerve. The pelvic limb withdrawal reflex tests the integrity of the L6–S1
spinal cord segments/ventral nerve roots and the sciatic nerve. These reflexes do not require
input or involvement of any other parts of the nervous system to be normal; they can
therefore be intact even if the spinal cord is severed at a distant site.
 Chapter 4 Lesion Localisation 109

The lesion can then be localised further, based on observation of the gait and
posture, and on the use of neurological tests that screen certain regions of the
nervous system. As discussed in Chapter 1, if the gait is abnormal in one or more
limbs but the proprioception appears normal then non‐neurological disease
should always be considered (e.g. orthopaedic disease, reduced vascular
perfusion).

1. All limbs are affected

If there are no neurological deficits to suggest an intracranial lesion, then the
neuroanatomic localisation is most likely to involve one of following three
regions (Figure 4.5):

• C1–C5 spinal cord segments

• C6–T2 spinal cord segments
• generalised neuromuscular disease.

Assessment of the thoracic limb withdrawal reflexes and thoracic limb muscle
tone can now be performed to screen the integrity of the C6–T2 spinal cord seg-
ments, which contain the cell bodies of the lower motor neurons to the thoracic
limbs. These lower motor neurons are responsible for extensor muscle tone to
support the weight against gravity, and for flexor muscle strength that we can test
using the withdrawal reflex. The thoracic limb withdrawal reflexes and muscle
tone should be normal for a lesion affecting the C1–C5 spinal cord segments, as
the lower motor neuron cell bodies will be unaffected. The gait associated with a
C1–C5 lesion will also be long‐strided in all limbs, with a characteristic ‘over‐
reaching’ of the thoracic limbs at the end of protraction, as there is a delay in onset
and termination of the swing phase of the stride secondary to interruption of the
upper motor neuron messages from the motor centres in the brainstem (see Video
29). In contrast, a lesion affecting the C6–T2 spinal cord segments would result in:

C1–C5 C6–T2 T3–L3 L4–Cd

Thoracic limb Pelvic limb

Figure 4.5 The potential locations for a neurological lesion (‘lightning bolt’ symbol) that
could result in an abnormal gait in all limbs.
110 A Practical Approach to Neurology for the Small Animal Practitioner

• reduced/absent thoracic limb withdrawal reflexes

• reduced muscle tone (flaccidity) in the thoracic limb muscles
• neurogenic atrophy of the affected thoracic limb muscles
• an inability to support weight against gravity for the thoracic limbs.

The inability to support weight on the thoracic limbs will result in a short‐
strided thoracic limb gait +/− collapse through the thoracic limbs when hopping
is performed. This short‐strided thoracic limb gait will contrast with the long‐
strided, ataxic pelvic limb gait that results from disruption of the upper motor
neuron signals running down to the pelvic limbs via the C6–T2 spinal cord. This
discrepancy between the thoracic and pelvic limb stride lengths for a C6–T2 spi-
nal cord lesion is termed a ‘two‐engine’ gait (see Video 30).
Assessment of the withdrawal reflexes will always be associated with a degree
of subjectivity, and there can be a wide range of natural variation between indi-
viduals of different species, breeds, and temperaments. Therefore, it is not unrea-
sonable to have a final neuroanatomic localisation of C1–T2 spinal cord segments
if the tests above appear equivocal. This broader localisation can still be used to
plan further investigations, such as diagnostic imaging, and remains far superior
to deciding on further tests without a neurolocalisation at all.
The pelvic limb withdrawal reflexes and the patellar reflexes only involve the
L4–S1 spinal cord segments, femoral nerve, and sciatic nerve. They will therefore
be normal if there is a focal spinal cord lesion between the C1–T2 spinal cord seg-
ments. The muscle tone in the pelvic limbs will also be normal. A generalised
neuromuscular disorder resulting in weakness of all limbs should be suspected if
the withdrawal reflexes are weak in the thoracic and pelvic limbs. Unless there is
a history of significant trauma, this would be more likely than the presence of a
multifocal or diffuse spinal cord lesion that is concurrently affecting the C6–T2 and
L4–Cd spinal cord segments (see below for further discussion of neuromuscular
disease).

2. The thoracic and pelvic limbs on only one side are affected
(‘hemiparesis’)
If there are no neurological deficits to suggest an intracranial lesion, then the
neuroanatomic localisation is most likely to be:

• lateralised (ipsilateral) C1–C5 spinal cord segments

• lateralised (ipsilateral) C6–T2 spinal cord segments.

In exactly the same manner as for all limbs being affected, assessment of the
thoracic limb withdrawal reflexes and thoracic limb muscle tone should be per-
formed to further localise the lesion. These tests should be normal for a C1–C5
spinal cord lesion and reduced/absent if the lesion is affecting the lower motor
neuron cell bodies in the C6–T2 segments. In contrast to the situation when all
 Chapter 4 Lesion Localisation 111

limbs are affected, a generalised neuromuscular disorder would be highly unlikely

to only affect one side of the body whilst sparing the limbs on the other side.

3. The thoracic limbs appear normal but both pelvic limbs are affected
(‘paraparesis’)
If the voluntary motor function, gait, and proprioception appear normal in the
thoracic limbs, then we can reasonably assume that both the brain and the spi-
nal cord down to the level of the T2 spinal cord segment are functioning nor-
mally. The neuroanatomic localisation in this situation is most likely to involve
one of the following three regions (Figure 4.6):

• T3–L3 spinal cord segments

• L4–Cd spinal cord segments/nerve roots
• femoral nerves and/or sciatic nerves (bilateral).

The following neurological tests should be performed to distinguish between

these scenarios:

• the patellar reflexes, testing the L4–L6 spinal cord segments and femoral nerves
• the pelvic limb withdrawal reflexes, testing the L6–S1 spinal cord segments
and sciatic nerves
• the perineal reflex, anal tone, and tail tone, screening the S1–Cd spinal cord
segments
• the pelvic limb flexor and extensor muscle tone, reflecting the integrity of
lower motor neuron cell bodies in the L4–S1 spinal cord segments, the femo-
ral nerves and the sciatic nerves.

All of these tests should be normal for a lesion affecting the T3–L3 spinal cord
segments but may be reduced/absent for a lesion affecting the L4–Cd spinal cord
segments. Lesions that affect the L4–Cd spinal cord segments may also result in
weakness of the extensor muscles in the affected limbs. This will be clinically

C1–C5 C6–T2 T3–L3 L4–Cd

Thoracic limb Pelvic limb

Figure 4.6 The potential locations for a neurological lesion (‘lightning bolt’ symbol) that
could result in an abnormal gait in the pelvic limbs only (i.e. normal thoracic limbs).
112 A Practical Approach to Neurology for the Small Animal Practitioner

apparent as an inability to support the weight against gravity and poor joint
extension (e.g. dropped hock for a sciatic nerve lesion). The animal may also
appear ‘lame’ as they rapidly shift weight away from the affected limb(s) to
avoid collapse. This can mimic shifting weight away from a painful limb or limb
weakness secondary to vascular compromise. Therefore, aortic thromboembo-
lism, orthopaedic, and neurologic conditions should all be considered in animals
with a short‐strided or ‘lame’ gait in the pelvic limbs. This is in contrast to the
gait typically observed for lesions affecting the T3–L3 spinal cord segments. In
these cases, there is good tone in the pelvic limbs together with a long‐strided,
ataxic gait secondary to interference with the ascending proprioceptive tracts
and descending upper motor neurons to the pelvic limbs (see Video 16).
It can be difficult to distinguish a lesion that is affecting the L4–Cd spinal
cord segments at the level of the spinal canal, from the less common scenario of
a bilateral lesion involving the femoral and/or sciatic nerves outside the verte-
bral column. The latter may be observed in trauma cases or in the early stages
of a generalised neuromuscular condition, before clinical involvement of the
thoracic limbs is observed. However, the tail function and perineal reflex will
frequently be normal in cases with bilateral femoral and/or sciatic nerve
involvement, as the sacral and caudal spinal cord segments and nerves are
unaffected. This is in contrast to lesions at the level of the spinal canal, which
typically also affect the sacral/caudal spinal cord segments or nerve roots in
addition to the causing paraparesis (e.g. intervertebral disc disease, neoplasia).
It may be possible to further refine the location of a T3–L3 spinal cord lesion
by using the cutaneous trunci reflex or by identification of a focus of spinal pain
(see Chapters 3 and 6).

4. A single pelvic limb is affected (‘monoparesis’)

If only a single pelvic limb is affected, then non‐neurological disease should
always be considered as a cause of lameness that is mimicking a true monopare-
sis. Common underlying causes for this presentation include hip dysplasia, cru-
ciate ligament disease, and patellar luxation. If non‐neurological disease is
excluded on the basis of the clinical history and good physical and orthopaedic
examinations, then this situation can be approached in a similar manner to
when both pelvic limbs are affected. A convincing proprioceptive deficit in the
affected limb compared to the normal contralateral limb would also add support
for an underlying neurologic cause:

• lateralised (ipsilateral) T3–L3 spinal cord segments

• lateralised (ipsilateral) L4–S1 spinal cord segments
• ipsilateral femoral and/or sciatic nerve lesion in the affected limb.

The most useful examinations that can be used to distinguish between these
options would be:
 Chapter 4 Lesion Localisation 113

• the patellar reflex testing the L4–L6 spinal cord segments and femoral nerve
• the pelvic limb withdrawal reflex testing the L6–S1 spinal cord segments and
sciatic nerve
• the pelvic limb flexor and extensor muscle tone, reflecting the integrity of
lower motor neuron cell bodies in the L4–S1 spinal cord segments, the femo-
ral nerve, and the sciatic nerve.

These tests should be normal for a lesion residing within the T3–L3 spinal
cord segments and may be reduced/absent in the case of a lateralised lesion
affecting the L4–S1 spinal cord segments, L4–S1 nerve roots, femoral nerve, or
sciatic nerve. A lesion affecting the L4–L6 spinal cord segments, L4–L6 nerve
roots, or femoral nerve will affect the patellar reflex. A lesion affecting the L6–S1
spinal cord segments, L6–S1 nerve roots, or sciatic nerve will affect the with-
drawal reflex. The perineal reflex, anal tone, and tail tone may be affected if the
sacral and caudal spinal cord segments or nerve roots are also affected.

5. A single thoracic limb is affected (‘monoparesis’)

As for when a single pelvic limb is affected, non‐neurological disease should
always be considered as a cause for lameness rather than true paresis (e.g. ortho-
paedic disease affecting the shoulder or elbow, paw injury, nail bed infection). If
local disease affecting the limb itself is excluded, then an intracranial or primary
spinal cord localisation is highly unlikely in these cases. If this were the case,
then the tracts to the ipsilateral pelvic limb should also be affected as they pass
via the site of injury, resulting in hemiparesis. The most likely neuroanatomic
localisation for thoracic limb monoparesis is therefore the ipsilateral peripheral
nerve(s) to the affected thoracic limb.

6. Both thoracic limbs are affected but the pelvic limbs appear normal
Whilst uncommon, if both thoracic limbs are affected (e.g. proprioceptive deficits
and weak withdrawal reflexes in both thoracic limbs) but the pelvic limbs appear
normal, then the following rare clinical presentations could be considered:

• isolated damage to the peripheral nerves innervating both thoracic limbs (e.g.
traumatic avulsion of the nerve roots to both brachial plexi, bilateral brachial
plexus neuritis, bilateral nerve infiltration by lymphoma)
• a spinal cord lesion that damages the grey matter of the C6–T2 spinal cord seg-
ments with relative sparing of the surrounding white matter tracts to and from
the pelvic limbs, termed a ‘central cord syndrome’ (e.g. traumatic spinal cord
injury, intramedullary spinal neoplasia, spinal cord ischaemia).

See Boxes 4.3–4.6 for a summary of the most common clinical signs observed
secondary to spinal cord lesions affecting the C1–C5, C6–T2, T3–L3, and L4–Cd
spinal cord segments.
114 A Practical Approach to Neurology for the Small Animal Practitioner

Box 4.3 C1–C5 Spinal Cord Segments

• Tetraparesis/tetraplegia or ipsilateral hemiparesis/hemiplegia: interruption to the

descending upper motor neuron tracts resulting in a long stride length (delay in the
onset and termination of the stride) (see Video 29).
• Proprioceptive ataxia in all limbs, or in the ipsilateral thoracic and pelvic limbs for a
lateralised lesion.
• Proprioceptive deficits in all limbs, or in the ipsilateral thoracic and pelvic limbs.
• Normal flexor withdrawal reflexes in all limbs.
• Normal patellar reflexes.
• Normal tail and anal tone, intact perineal reflex.
• Cutaneous trunci reflex present at the level of L5.
• Possible neck pain.
• Possible Horner syndrome.

Box 4.4 C6–T2 Spinal Cord Segments

• Tetraparesis/tetraplegia or ipsilateral hemiparesis/hemiplegia: damage to the

descending upper motor neuron tracts to the pelvic limbs results in a long pelvic
limb stride length (delay in the onset and termination of the stride), and damage to
the cell bodies of the lower motor neurons innervating the thoracic limb skeletal
muscles results in a short thoracic limb stride length (extensor muscle weakness
and inability to support weight). This is termed a ‘two engine gait’ as the short
thoracic limb gait appears faster than the long pelvic limb gait (see Video 30).
• Proprioceptive ataxia in all limbs: this is more noticeable in the pelvic limbs as the
weakness of the thoracic limbs and short stride length masks underlying ataxia.
• Proprioceptive deficits in all limbs, or in the ipsilateral thoracic and pelvic limbs.
• Weak thoracic limb withdrawal reflexes.
• Reduced thoracic limb muscle tone.
• Denervation atrophy of thoracic limb muscles.
• Normal pelvic limb withdrawal reflexes.
• Normal patellar reflexes.
• Normal tail and anal tone, intact perineal reflex.
• Cutaneous trunci reflex may be absent if the C8–T1 spinal cord segments or C8–T1
nerve roots are affected.
• Possible neck pain.
• Possible Horner syndrome.

7. Potential pitfalls in the localisation of spinal cord lesions

Two interesting phenomena that may complicate the localisation of spinal cord
lesions are discussed below. These should always be considered in animals that
present with acute spinal cord injury.
 Chapter 4 Lesion Localisation 115

Box 4.5 T3–L3 Spinal Cord Segments

• Normal thoracic limb voluntary motor function, proprioception, and withdrawal

reflexes.
• Paraparesis/paraplegia, or ipsilateral pelvic limb monoparesis/monoplegia: interrup-
tion to descending upper motor neuron tracts resulting in a long stride length (delay
in the onset and termination of the stride).
• Proprioceptive ataxia in the pelvic limbs.
• Proprioceptive deficits in the affected pelvic limb(s).
• Normal pelvic limb withdrawal reflexes.
• Normal patellar reflexes.
• Normal tail and anal tone, intact perineal reflex.
• Cutaneous trunci reflex may be interrupted approximately two vertebrae caudal to
the level of a transverse spinal cord lesion.
• Possible thoracolumbar spinal discomfort.

Box 4.6 L4–Cd Spinal Cord Segments

• Normal thoracic limb voluntary motor function, proprioception, and withdrawal

reflexes.
• Paraparesis/paraplegia, or ipsilateral pelvic limb monoparesis/monoplegia. Damage
to the cell bodies of the lower motor neurons innervating the pelvic limb skeletal
muscles resulting in a short pelvic limb stride length and poor joint extension
(extensor muscle weakness and inability to support weight).
• Proprioceptive deficits in the affected pelvic limb(s).
• Weak pelvic limb withdrawal reflexes (L6–S1).
• Reduced/absent patellar reflexes (L4–L6).
• Reduced pelvic limb muscle tone (L4–S1).
• Reduced hock and/or stifle extension.
• Denervation atrophy of pelvic limb muscles.
• Reduced/absent tail and anal tone, reduced/absent perineal reflex (S1–Cd).
• Cutaneous trunci reflex present at the level of L5.
• Possible lumbosacral spinal discomfort.

a. Schiff–Sherrington posture
The distinctive Schiff–Sherrington posture (see Video 23) has already been dis-
cussed in Chapter 3 and is characterised by increased extensor muscle tone in
the thoracic limbs following an acute lesion affecting the T3–L3 spinal cord seg-
ments. The increased extensor tone may restrict an animal’s ability to rise into
sternal recumbency, meaning that they often present in lateral recumbency.
This can mimic a lesion affecting the C1–T2 spinal cord segments. However,
unlike an animal with a C1–T2 lesion, those with Schiff–Sherrington posture
will have normal thoracic limb voluntary movement and proprioception when
assisted to stand. This posture is commonly associated with acute, severe lesions
116 A Practical Approach to Neurology for the Small Animal Practitioner

to the T3–L3 spinal cord segments, but it has no prognostic significance and
should not be used to guide an owner as to the prognosis for a functional
recovery.

b. Spinal shock phenomenon

This is a poorly understood phenomenon that is observed in both humans and
animals following experimental or natural spinal cord injuries (Smith and Jeffery
2005). It is characterised by a counterintuitive loss of local spinal reflexes (e.g.
reduced/absent withdrawal reflexes +/− patellar reflexes) following an acute,
often severe, lesion affecting the spinal cord segments lying rostral to those
involved in the reflex arcs being tested. This is most commonly observed as a loss
of pelvic limb withdrawal reflexes following an acute lesion affecting the T3–L3
spinal cord segments. The patellar reflexes may be lost for between minutes and
hours following spinal cord injury in domestic animals but have often returned
to normal by the time of presentation. In the author’s experience, the pelvic limb
withdrawal reflexes may remain weak for up to 5–7 days following an acute
T3–L3 lesion if spinal shock is present.
This syndrome is thought to represent an acute loss of upper motor neuron
input to interneurons involved in the local reflexes being tested. This results in
a transient loss of reflex function and reduced muscle tone in the affected limbs.
As for Schiff–Sherrington posture, whilst spinal shock is often associated with
severe neurological deficits (e.g. paraplegia) it has not been shown to have indi-
vidual prognostic significance. Therefore, the primary clinical significance is the
possibility for an incorrect neuroanatomic localisation. A lesion affecting the L4–
Cd spinal cord segments would sensibly be your first thought in a dog or cat that
presents with:

• normal forelimb voluntary motor function and proprioception

• non‐ambulatory paraparesis or paraplegia
• reduced muscle tone in the pelvic limbs
• weak pelvic limb withdrawal reflexes.

However, a lesion affecting the T3–L3 spinal cord segments with associated
spinal shock should always be considered in cases with the same clinical presen-
tation but that also have:

• intact patellar reflexes

• a cutaneous trunci reflex that is interrupted at or rostral to the level of L2–L3
• focal spinal discomfort in the region of the T3–L3 vertebrae.

This differentiation is very important in terms of deciding where to focus

further imaging (e.g. radiography or MRI) and how to interpret any changes
observed on these images.
 Chapter 4 Lesion Localisation 117

4.4 ­Neuromuscular Disease

Disorders that affect the peripheral nerves, skeletal muscles, or the neuromuscular
junction are less commonly encountered in general practice compared to condi-
tions involving the central nervous system (Figure 4.7). A lack of familiarity with
these conditions, coupled with the fact that the clinical signs may mimic disorders
affecting the brain or spinal cord, may lead to misdiagnosis. As a result, there may
be an inappropriate choice of further investigations (e.g. spinal radiography or
advanced imaging) that delays reaching a diagnosis and can be costly for an owner.
Disorders that affect the peripheral motor nerves, neuromuscular junction,
or skeletal muscles will cause variable degrees of lower motor neuron weakness
in the affected body parts, resulting in one or more of the following clinical signs
(see Video 31).

• Poor extensor muscle tone (flaccidity) and an inability to support weight

against gravity. If the animal has enough strength to stand and walk, this
results in a stiff, short‐strided gait in the affected limbs as the animal shifts its
weight away from a weak limb to avoid collapse. Poor extension of the joints
when standing/walking may also be observed (e.g. tarsi, stifles, elbows).
• Weakness of the flexor muscles resulting in reduced/absent withdrawal reflexes.
• Reduced/absent tendon reflexes (e.g. patellar reflex).
• Muscle atrophy. This atrophy could reflect damage to the peripheral motor
nerves and denervation of the affected muscle(s), or be the result of primary

Upper motor neuron

Interneuron

Peripheral motor neuron

Cell body of peripheral motor neuron
in ventral horn of spinal cord

Neuromuscular junction Acetylcholine

Skeletal muscle
Figure 4.7 The motor arm of the peripheral nervous system comprises the peripheral motor
nerves (with their cell bodies in the ventral horn of the spinal cord), the neuromuscular
junction, and the skeletal muscles themselves. Disorders that affect any of these components
are grouped under the broad term of ‘neuromuscular disease’.
118 A Practical Approach to Neurology for the Small Animal Practitioner

muscle damage in the case of generalised myopathies. Some animals with

generalised neuromuscular disease may present with a primary clinical his-
tory of weight loss as a result of significant muscle atrophy.
• Exercise intolerance. Animals with disorders affecting the neuromuscular
junction or skeletal muscles may present with exercise intolerance and/or
exacerbation of their clinical signs during exercise. This results from an inabil-
ity to meet the increased demand put on the muscles at the time of activity.
This is in contrast to disorders affecting the brain, spinal cord, or peripheral
motor nerves, for which the clinical signs are usually persistent and independ-
ent of exercise.
• The cranial nerves, masticatory muscles, and oesophageal muscles may be
affected by neuromuscular disorders. These deficits are often bilateral and
symmetric, and the most commonly affected nerves include the facial (VII)
nerve resulting in facial paralysis, and the glossopharyngeal (IX) and/or vagus
(X) nerves resulting in dysphagia, dysphonia, or megaoesophagus. The brain
is not affected by neuromuscular disorders, therefore the mentation will
remain alert and appropriate at all times. This is in contrast to animals with
cranial nerve deficits secondary to a brainstem lesion. Animals with neuro-
muscular disease may also have other neurological deficits that would be
incompatible with a brainstem neurolocalisation (e.g. weak withdrawal
reflexes in all limbs).

The skeletal muscles and neuromuscular junction form part of the common
motor pathway for movement and play no role in sensory functions such as
proprioception or nociception. The same applies for the peripheral motor nerves.
Therefore, unless a neuromuscular disorder affects the peripheral sensory
nerves, which is uncommon for many of the disorders observed in general prac-
tice, the sensory function will be preserved. This means that in contrast to brain
or spinal cord lesions, the proprioception remains normal for most neuromuscu-
lar cases. As long as there is sufficient motor function present for a small degree
of limb movement, the animal will still attempt to initiate a corrective move-
ment when performing proprioceptive testing, even if this movement is very
‘weak’ (see Video 31). For the same reason, if an animal with a neuromuscular
disorder is able to walk then it will not be ataxic. The gait may appear stiff or
short‐strided secondary to generalised weakness, but limb placement should be
predictable for each step. The relative sparing of sensory function in the majority
of neuromuscular cases can be extremely useful to allow differentiation between
these disorders from lesions affecting the brain or spinal cord that can also result
in an abnormal gait in all limbs. Unless neuromuscular disease is considered, the
proprioception in affected animals may appear ‘confusingly’ good given how
weak the animal appears on examination.
A neuromuscular lesion localisation should therefore be considered in any
animal presenting with an abnormal gait in all limbs. These animals will have a
 Chapter 4 Lesion Localisation 119

short‐strided gait, may be exercise intolerant, and show generalised muscle

atrophy, weak withdrawal reflexes in all limbs, and have possible cranial nerve
deficits. However, the proprioception is often normal as long as the body weight
is sufficiently supported during testing to avoid collapse (see Chapter 3). There
will be no clinical signs to suggest an intracranial localisation (e.g. seizures,
visual deficits, altered level of mentation), and the relative sparing of proprio-
ception, absence of ataxia, and lower motor neuron weakness affecting all limbs
would not be consistent with a focal spinal cord lesion. Further discussion
regarding the diagnostic approach to neuromuscular disease can be found in
Chapter 6.
Neuromuscular disorders are most commonly generalised conditions that
concurrently affect all limbs. The appendicular muscles can be preferentially
affected by some conditions (e.g. idiopathic polyradiculoneuritis), whilst others
may also affect the cranial nerves and tail (e.g. botulism). In some instances, the
pelvic limbs are initially affected before the disease progresses over days/weeks
to involve the thoracic limbs. These cases can therefore be difficult to distinguish
from a spinal cord lesion affecting the L4–S1 spinal cord segments before disease
progression is observed. However, the presence of concurrent cranial nerve defi-
cits (e.g. dysphonia, megaoesophagus, bilateral facial paresis), or exacerbation of
the clinical signs by exercise, may help to increase suspicion for a neuromuscular
disorder.
The clinical differentiation between peripheral neuropathies, junctionopa-
thies, and myopathies may not be possible without performing further investiga-
tions. Therefore, a broader neuroanatomic localisation of ‘neuromuscular
disease’ is a good starting point for planning these investigations. The following
observations may be useful to refine your localisation but are not always
reliable.

• Myopathies and junctionopathies only affect the motor component of the

neuromuscular system, therefore proprioception will always be normal. It is
unusual for these conditions to result in such severe weakness that an animal
is unable to perform any corrective movement when proprioception is
assessed.
• Peripheral neuropathies may also affect the peripheral sensory nerves, and the
proprioception can therefore also be affected. However, the most common
forms of peripheral neuropathy observed in general practice appear to pre-
dominately affect the motor nerves, with the proprioception being normal in
these cases (e.g. idiopathic polyradiculoneuritis).
• Peripheral neuropathies more frequently progress to the point at which the
animal is unable to walk compared to myopathies and junctionopathies.
Exceptions to this include necrotising myopathies, fulminant myasthenia
gravis, and botulism. In a similar manner, animals with absent withdrawal
reflexes in all limbs and marked flaccidity of the trunk and limbs are more
120 A Practical Approach to Neurology for the Small Animal Practitioner

likely to be affected by a generalised polyneuropathy than by a myopathy or

junctionopathy, with botulism being the exception to this rule.
• Peripheral neuropathies usually present with persistent clinical signs that are less
influenced by exercise or rest compared to myopathies and junctionopathies.

Chapter 5 will discuss how the neurological examination and final neuroana-
tomic localisation can be used, in conjunction with the clinical history, to formu-
late a meaningful list of differential diagnoses. It is always vital to consider the
reported onset and progression of the clinical signs at this stage. Only then
should further investigations be planned to rule in or out the most likely differ-
ential diagnoses.

­Bibliography
Añor, S. (2014). Acute lower motor neuron tetraparesis. Vet. Clin. North Am. Small Anim. Pract.
44: 1201–1222.
Atkinson, P.P. and Atkinson, J.L. (1996). Spinal shock. Mayo Clin. Proc. 71: 384–389.
Berg, J. (1989). Problems in neurolocalisation. Probl. Vet. Med. 1: 358–365.
Brooks, N.P. (2017). Central cord syndrome. Neurosurg. Clin N. Am. 28: 41–47.
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Farrow, B.R., Murrell, W.G., Revington, M.L. et al. (1983). Type C botulism in young dogs. Aust.
Vet. J. 60: 374–377.
Garosi, L., de Lahunta, A., Summers, B. et al. (2006). Bilateral hypertrophic neuritis of the bra-
chial plexus in a cat: magnetic resonace imaging and pathological findings. J. Feline Med. Surg.
8: 63–68.
Glass, E.N. and Kent, M. (2002). The clinical examination for neuromuscular disease. Vet. Clin.
North Am. Small Anim. Pract. 32: 1–29.
Henke, D., Vandevelde, M., Doherr, M.G. et al. (2013). Correlations between severity of clinical
signs and histopathological changes in 60 dogs with spinal cord injury associated with acute
thoracolumbar intervertebral disc disease. Vet. J. 198: 70–75.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Lorenz, M.D., Coates, J., and Kent, M. (2011). Handbook of Veterinary Neurology, 5e. St Louis,
MO: Elsevier Saunders.
Parent, J. (2010). Clinical approach and lesion localization in patients with spinal diseases. Vet.
Clin. North Am. Small Anim. Pract. 40: 733–753.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
Smith, P.M. and Jeffery, N.D. (2005). Spinal shock – comparative aspects and clinical relevance.
J. Vet. Intern. Med. 19: 788–793.
Sprague, J.M. (1953). Spinal border cells and their role in postural mechanism (Schiff–
Sherrington phenomenon). J. Neurophysiol. 16: 464–474.
Thomas, W.B. (2010). Evaluation of veterinary patients with brain disease. Vet. Clin. North Am.
Small Anim. Pract. 40: 1–19.
Thomsen, B., Garosi, L., Skerritt, G. et al. (2016). Neurological signs in 23 dogs with suspected
rostral cerebellar ischaemic stroke. Acta Vet. Scand. 58: 40–48.
Chapter 5 Constructing the List
of Differential
Diagnoses
Edward Ives

The aim of this chapter is to bring together all of the information from the previ-
ous four chapters and to summarise how this can be used to construct a concise
and appropriate list of differential diagnoses, upon which the most useful diag-
nostic investigations can be planned.
As discussed in the previous chapters, the primary goal of taking a complete
clinical history and performing the general physical examination and a neuro-
logical examination is to answer two key questions:

1. Does this animal have a lesion affecting its nervous system?

2. What is the location of that lesion?

Only at this stage of the diagnostic process should specific categories of dis-
ease or individual disease processes be considered. This involves constructing a
ranked list of conditions that could potentially result in a lesion in that location
(from most likely to least likely). This is termed the ‘list of differential diagnoses’.
It is vital that other aspects of the clinical history and general physical examina-
tion findings are also considered at this stage in order to determine the most
likely differential diagnoses (see Chapter 2). Dependent on the clinical history
and neurological deficits, a list of three to five differential diagnoses can usually
be chosen. This list can then be modified on the basis of focused further investi-
gations, which aim to rule in or rule out your most likely diagnoses first.
Adopting this approach to every case is important. This is because diagnostic
tests perform best when they are targeted to answering a specific clinical ques-
tion – the limitations of the test are known and it is therefore easier to interpret the
significance of a positive or negative test result. If you perform a test for a specific
condition without first considering how common that condition is in the popula-

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

121
122 A Practical Approach to Neurology for the Small Animal Practitioner

tion of interest, or how likely it is to explain the clinical signs observed, then it is
very difficult to know what to do if the test result is equivocal or ‘positive’. This
is particularly true for serum antibody testing, in which a high titre could represent
active infection or incidental, historic exposure. Achieving an accurate diagnosis in
the most efficient way possible means that treatment can be started promptly, more
funds will be available for treatment, and the outcome is likely to be better.
Formulating the list of differential diagnoses relies upon the concept of clini-
cal reasoning. This problem‐orientated approach involves consideration of sev-
eral aspects of the clinical history and presentation, together with how common
certain diseases are in the population that the individual comes from. This will
depend upon geographical location, travel history, and vaccination status. The
most important aspects to consider when constructing the list of differential
diagnoses are as follows:

1. The signalment of the animal (species, breed, age, and gender)

As discussed in Chapter 2, some conditions are more common in (or specific
to) a particular species or certain breed of dog or cat. Different disease pro-
cesses will also be more common in animals of certain age groups, such as
congenital anomalies in young animals or neoplastic disease in middle‐aged
and older animals. Gender is an important factor to consider for genetic dis-
orders that may have different modes of inheritance (e.g. X‐linked disorders
in males) or in metastatic diseases from certain organs (e.g. prostatic adeno-
carcinoma in males, mammary gland adenocarcinoma in females).
2. Signs of systemic disease from the clinical history and general physical examination
These clinical signs could include gastrointestinal disease (vomiting, regurgi-
tation, diarrhoea), respiratory signs, pyrexia, or weight loss. Certain catego-
ries of disease will more commonly result in pyrexia or may affect other
organ systems in addition to the nervous system. The index of suspicion for
these categories will therefore be higher if systemic clinical signs are reported
in the clinical history or are identified on the general physical examination.
This is particularly relevant for infectious, neoplastic, and certain inflamma-
tory conditions. The travel history and vaccination status of the affected ani-
mal are also important factors in deciding the relative likelihood of certain
diseases to explain the presenting problem(s) (see Chapter 2).
3. The reported onset and progression of the clinical signs
The speed of onset of clinical signs and how these signs progress over time
may vary considerably dependent on the disease process responsible
(Figure 5.1). This information is particularly useful to refine the list of differ-
ential diagnoses and makes disease onset and progression a vital part of clini-
cal reasoning in veterinary neurology. For example, obstruction of blood flow
to the brain or spinal cord will result in a sudden onset of clinical signs that
may remain static or show a gradual improvement dependent on the collat-
eral circulation and damage caused. In contrast, neoplastic and infectious dis-
 Chapter 5 Constructing the List of Differential Diagnoses 123

Infectious,
Inflammatory,
Neoplastic

Degenerative

Severity Metabolic

Traumatic
Vascular

Time
Figure 5.1 The speed of onset of clinical signs, and how these signs progress over time, may
vary considerably, dependent on the disease process responsible.

orders would be expected to show a progressive clinical course unless treated

and may have a more insidious onset. Further consideration of disease onset
and progression in relation to different disease categories is discussed below.
As discussed in Chapter 2, considering how the clinical course has, or has not,
been influenced by previously administered medications, such as analgesics,
antibiotics, or corticosteroids, can also help to refine the list of differential
diagnoses.
4. The neuroanatomic localisation, including lesion distribution and any lateralisation of
neurological deficits
Certain disorders will only affect specific regions of the nervous system (e.g.
myasthenia gravis for the neuromuscular junction, intervertebral disc disease
for the spinal cord), whereas other conditions can affect any region (e.g.
neoplasia, inflammation). Some disease processes are also more likely to present
with focal, asymmetric clinical signs and lateralisation of neurological deficits
compared to others (e.g. vascular disorders). Inflammatory and infectious con-
ditions may result in multifocal clinical signs. The neurological deficits observed
secondary to toxic or metabolic disorders tend to be diffuse and/or symmetric as
there is even distribution of affected blood to all regions of the nervous system.
5. The presence or absence of discomfort
Apparent discomfort may be reported in the clinical history, or be identified
on examination, for many disease processes. It therefore represents a non‐
specific finding with many possible origins, including the meninges, nerve
roots, peripheral nerves, vertebrae, muscles, joints, or ligaments. However,
an absence of discomfort on examination may increase the index of suspicion
for certain disorders, such as those involving the parenchyma of the brain or
spinal cord that spare adjacent innervated structures (e.g. ischaemic lesions).
124 A Practical Approach to Neurology for the Small Animal Practitioner

In summary, the five key areas that should be considered before formulating
the list of differential diagnoses are:

1. Signalment
2. Clinical history and presence/absence of non‐neurologic signs
3. Onset and progression of clinical signs
4. Neuroanatomic localisation, including any lateralisation of deficits
5. Presence/absence of discomfort

As an example, consider the most likely differential diagnosis for a 5‐year‐

old, male, neutered Border Collie dog that is otherwise well and presents with
a peracute onset of pelvic limb ataxia after running for a ball. There has been
no progression of clinical signs over the last 48 hours, the lesion localises to the
T3–L3 spinal cord segments, with the left pelvic limb being more affected than
the right pelvic limb, and there is no apparent discomfort on spinal palpation.
An ischaemic vascular event (e.g. fibrocartilaginous embolism) would be a
common differential diagnosis to explain this peracute, non‐progressive, non‐
painful, lateralised T3–L3 spinal cord lesion. This differential diagnosis would
be highly unlikely if there had been progression of the clinical signs after the
first 24 hours or if the dog appeared markedly painful on spinal palpation, even
if the presentation was otherwise identical. Other differential diagnoses to con-
sider in this case would include an acute non‐compressive nucleus pulposus
extrusion, an acute compressive nucleus pulposus extrusion, extrusion of a
degenerate intervertebral disc, and possibly acute decompensation of underly-
ing neoplasia.

5.1 ­Categories of Disease

In order to simplify the approach to formulating a list of differential diag-

noses, broad categories of disease should be considered before individual
conditions. This is similar to determining the neuroanatomic localisation,
when three broad regions of the nervous system are initially considered
(brain, spinal cord, or neuromuscular), before refining the localisation fur-
ther. This ensures that an entire category of disease is not overlooked and
that the most appropriate diagnostic investigations are chosen first. These
broad categories of disease can be easily remembered using the mnemonic
VITAMIN D:

• Vascular
• Inflammatory, Infectious
• Toxic, Traumatic
• Anomalous
 Chapter 5 Constructing the List of Differential Diagnoses 125

• Metabolic
• Idiopathic
• Neoplastic, Nutritional
• Degenerative

These categories may be further subdivided before specific conditions are

chosen as possible differential diagnoses (Box 5.1).
When formulating the list of differential diagnoses, each broad category of
disease should be considered in turn and a specific category chosen if there is a
consistent clinical picture for the individual case. This process is made easier by
the fact that the different categories may typically affect animals of different
ages, show a different onset and progression, affect different regions of the nerv-
ous system, or be more or less likely to result in discomfort on examination
(Box 5.2). However, this should only be seen as a general guide and is unfortu-
nately not a strict set of rules that every case will follow.

5.1.1 Vascular
Interruption of the normal blood supply to the nervous system is most com-
monly the result of vascular obstruction. This leads to ischaemia of the tissues
within the territory of the affected vessel. The typical presentation for an ischae-
mic vascular event would be:

• acute onset (minutes to hours)

• static or improving clinical signs (over hours to weeks)
• focal neuroanatomic localisation
• lateralisation of neurological deficits is commonly observed, as a single vessel
on one side of the brain or spinal cord is affected
• non‐painful on spinal palpation or neck manipulation.

An animal of any species, age, or breed can theoretically be affected by

ischaemic events, dependent on the nature of the occluding material. However,
vessel obstruction by blood clots is more commonly observed in older animals
and systemic diseases that predispose to clot formation may also result in non‐
neurologic clinical signs on examination (e.g. chronic renal disease,
hyperadrenocorticism).
Haemorrhagic vascular events are a less common cause of neurological dys-
function when compared to ischaemia. They typically have an acute onset but
may show progressive clinical signs if there is continued haemorrhage and an
enlarging haematoma. Haemorrhage may also be associated with pain on exam-
ination as a result of mass effect, nerve root compression, or meningeal irrita-
tion. If there is a systemic disease process that has predisposed to vessel leakage
or hypocoagulability, then haemorrhage may occur in multiple locations result-
ing in a multifocal neuroanatomic localisation.
126 A Practical Approach to Neurology for the Small Animal Practitioner

Box 5.1 Subdivision of the categories of disease that are used to formulate a list of
differential diagnoses

Vascular
• ischaemic/blood vessel obstruction (e.g. ischaemic stroke, fibrocartilaginous
embolism)
• haemorrhagic/blood vessel rupture or leakage (e.g. coagulation disorder, Angiostrongylus
vasorum)

Inflammatory
• sterile/non‐infectious (e.g. meningoencephalitis of unknown origin)
• infectious: bacterial, viral, fungal, protozoal, rickettsial, algal

Traumatic
• external trauma (e.g. road traffic accident, kick, fall)
• internal trauma (e.g. acute non‐compressive nucleus pulposus extrusion)

Toxic
• topical exposure (e.g. permethrin in cats)
• ingestion (e.g. metaldehyde)

Anomalous
• primary (e.g. hydrocephalus)
• secondary (e.g. vertebral malformation)

Metabolic
• excess (e.g. hepatic encephalopathy, uraemia, hypernatraemia)
• deficit (e.g. hypoglycaemia, hypocalcaemia, hyponatraemia)

Idiopathic

Neoplastic
• primary central nervous system neoplasia (e.g. glioma, meningioma)
• local extension (e.g. nasal adenocarcinoma invading the cranial vault)
• metastasis from a distant site (e.g. haemangiosarcoma)

Nutritional
• excess (e.g. vitamin A)
• deficiency (e.g. thiamine)

Degenerative
• primary degeneration of neurons (e.g. motor neuron disease)
• degeneration of structures that secondarily affect the nervous system (e.g. interver-
tebral disc disease)
 Chapter 5 Constructing the List of Differential Diagnoses 127

Box 5.2 Here the different disease categories are divided according to their most
common clinical presentation.

Onset
• Acute: vascular, inflammatory, infectious, traumatic, toxic, idiopathic, (neoplastic,
nutritional)
• Chronic: inflammatory, anomalous, metabolic, neoplastic, nutritional, degenerative
Clinical Course
• Static: vascular, traumatic, (anomalous), idiopathic
• Improving: vascular, traumatic, toxic, idiopathic
• Waxing‐waning: inflammatory, metabolic
• Progressive: inflammatory, infectious, anomalous, metabolic, neoplastic, nutritional,
degenerative
Lesion Distribution
• Focal: vascular, traumatic, anomalous, idiopathic, neoplastic, degenerative
• Multi‐focal: inflammatory, infectious, (traumatic), (neoplastic)
• Diffuse and symmetrical: toxic, metabolic, nutritional, degenerative
Apparent Discomfort
• Non‐painful: vascular, toxic, anomalous, metabolic, idiopathic, degenerative
• Painful: inflammatory, infectious, traumatic, neoplastic, degenerative

Typical presentation: Acute, non‐progressive, non‐painful, lateralised clinical

signs.

5.1.2 Inflammatory/Infectious
Inflammatory or infectious diseases can have an acute or chronic onset but tend
to be progressive over time without treatment. The severity of clinical signs asso-
ciated with sterile inflammatory conditions, which are currently thought to rep-
resent autoimmune disorders, may also wax and wane over time.
Dependent on the specific disease process, inflammatory or infectious dis-
eases can present with focal clinical signs (e.g. single abscess, granuloma, or
discospondylitis) or produce lesions that are scattered throughout the nervous
system, resulting in a multifocal lesion localisation.
In contrast to ischaemic events, inflammatory or infectious disease can result
in foci of pain on examination and may also present with concurrent pyrexia,
dependent on the disease process. However, inflammatory disorders should
never be excluded on the basis of an absence of pyrexia or pain on
examination.
Typical presentation: Acute or subacute, progressive, focal or multi‐focal, pos-
sible discomfort on examination.
128 A Practical Approach to Neurology for the Small Animal Practitioner

5.1.3 Traumatic
Traumatic events that result in neurological dysfunction will have an acute onset
and are usually accompanied by a consistent clinical history or other examina-
tion findings suggestive of trauma. The severity of clinical signs may progress
over 1–3 days secondary to oedema formation and expansion of the primary
injury into the adjacent parenchyma. This process is termed secondary injury.
The clinical signs will then remain static or show gradual improvement, depend-
ent on the nature and severity of the injury. A traumatic event that results in
instability of the vertebral column would be an exception to this rule, as progres-
sive clinical signs may be observed secondary to recurrent spinal cord injury at
the site of instability.
Traumatic events may affect a single region of the nervous system, resulting
in a focal neuroanatomic localisation. However, the presence of multiple sites of
injury should always be considered, particularly following blunt force trauma
such as road traffic accidents. Pain is a common feature of trauma cases, second-
ary to direct neuronal injury (e.g. nerve roots) and/or damage to adjacent soft
tissues and bones.
Typical presentation: Acute, non‐progressive, painful, consistent clinical history.

5.1.4 Toxic
External toxins typically result in an acute onset of neurological signs following
ingestion or topical administration, usually within minutes to hours of exposure.
There may be a high suspicion of toxin exposure from the clinical history; young
animals are often affected, given their inquisitive nature. If there is no further
exposure to the toxin and the initial dose is not fatal, then the clinical signs
should improve over time as the levels of toxin within the body and nervous
system decline. As for metabolic disorders, toxicity most commonly results in
symmetric neurological deficits as the toxin is distributed diffusely via the
bloodstream.
Typical presentation: Acute, diffuse/symmetric clinical signs, non‐painful, con-
sistent clinical history.

5.1.5 Anomalous
As discussed in Chapter 2, anomalous disorders include congenital or develop-
mental anatomic abnormalities. Congenital anomalies are present from birth
and should always be considered in young, growing animals. However, an
anomaly should never be excluded in middle‐aged or older animals as decom-
pensation may occasionally occur in later life. The clinical signs will typically be
chronic in onset unless the anomaly predisposes to acute instability (e.g. atlan-
toaxial subluxation). These clinical signs can remain static, or they may show
gradual progression if there is lesion expansion and secondary effects on the
 Chapter 5 Constructing the List of Differential Diagnoses 129

adjacent neuronal tissue (e.g. hydrocephalus, intradural spinal arachnoid

diverticulum).
Typical presentation: Highly variable (see above).

5.1.6 Metabolic
Metabolic disorders can have an acute onset but may also present with a
waxing‐waning or episodic clinical history due to fluctuation in the levels of
electrolytes, nutrients, or internal toxins. The index of suspicion for certain met-
abolic disorders may be higher in animals of certain ages or breeds (e.g.
portosystemic shunting and hepatic encephalopathy in a young Yorkshire Terrier
with poor growth). Non‐neurologic signs may also be reported in the clinical
history, such as gastrointestinal signs or polyuria/polydipsia.
Both toxic and metabolic disorders occur secondary to an excess or deficit of
certain substances within the bloodstream. This blood is distributed to the entire
nervous system and most commonly results in diffuse, symmetric neurological
deficits reflecting involvement of the brain or neuromuscular system. A focal
spinal cord neuroanatomic localisation would be unlikely to result from a meta-
bolic or toxic disease process. It is also uncommon for metabolic disorders to
present with apparent discomfort on examination.
Typical presentation: Concurrent non‐neurological signs, diffuse/symmetric
deficits, non‐painful.

5.1.7 Idiopathic
An idiopathic disorder should only be suspected if there is a known condition
(for which the underlying cause is currently unknown) that could result in the
specific neurological signs displayed in an individual animal. A good example
would be idiopathic facial paralysis in a dog that has had an extensive work up
to exclude other possible causes for facial paralysis. The term should not be used
as a ‘diagnostic dustbin’ simply because a definitive diagnosis has not been
reached or when a reported idiopathic condition does not exist that would
explain the presenting neurological signs.
The onset, progression, and lesion distribution for idiopathic disorders are
specific to each condition. However, they frequently result in an acute onset of
non‐progressive or improving clinical signs. This most commonly reflects
involvement of the peripheral nervous system, particularly individual cranial
nerves, but an important exception is idiopathic epilepsy. It is uncommon for
idiopathic disorders to present with a history of discomfort or pain on
examination.
Typical presentation: Variable dependent on condition but typically acute, non‐
painful, and non‐progressive.
130 A Practical Approach to Neurology for the Small Animal Practitioner

5.1.8 Neoplastic
Neoplasia is typically associated with focal mass lesions that enlarge over time.
Therefore, it would appear reasonable to assume that the associated clinical signs
should have a chronic onset and be progressive in nature. Whilst this may be the
case, the clinical signs associated with spinal neoplasia can have an acute onset
secondary to pathological fracture, sudden haemorrhage, or vascular decompen-
sation as the mass reaches a critical size. An acute onset of seizure activity is also
a common presenting sign for intracranial neoplasia.
The index of suspicion for a neoplastic process should be higher in older
animals, but certain forms of neoplasia may also be seen in young to middle‐
aged dogs (e.g. medulloblastoma, glioma) and cats (e.g. lymphoma). A focal
neuroanatomic localisation is most common for neoplastic disorders; how-
ever, multi‐focal or diffuse lesions can be seen for metastatic disease or in
association with round cell neoplasms such as lymphoma or histiocytic sar-
coma. Invasion of surrounding tissues and/or meningeal stretching or nerve
root compression often result in pain on examination. However, an absence
of discomfort should not be used to exclude a neoplastic process. Non‐neuro-
logic signs may be reported in the clinical history and abnormalities identified
on general physical examination in cases with systemic involvement or meta-
static neoplasia.
Typical presentation: Acute or chronic, progressive, middle‐aged or older
animals.

5.1.9 Nutritional
Nutritional disorders are rare in domestic species but may be observed in animals
fed on an imbalanced, home‐cooked diet or if there has been a manufacturing
fault for commercial diets. The clinical signs can have an acute or chronic onset,
dependent on the nutritional excess or deficiency, and are often progressive over
time until treated. As for metabolic and toxic disorders, the lesion distribution is
most commonly multifocal or diffuse unless there is susceptibility of certain
regions of the nervous system to a particular nutritional deficiency (e.g.
thiamine).
Typical presentation: Progressive, multi‐focal or diffuse, non‐painful, concur-
rent non‐neurologic signs.

5.1.10 Degenerative
Disorders resulting from primary neuronal degeneration typically present with
a chronic onset of progressive clinical signs. Certain disorders may be seen in
specific breeds, with different ages at onset dependent on the individual condi-
tion. Degenerative disease should always be considered in a young animal that
presents with chronic, progressive neurological signs, particularly if there is no
apparent discomfort on examination. However, other degenerative conditions
 Chapter 5 Constructing the List of Differential Diagnoses 131

may not present until later in life and they should therefore still be considered
in older animals (e.g. degenerative myelopathy, laryngeal paralysis‐polyneu-
ropathy, certain cerebellar abiotrophies). Different disorders may preferentially
affect neurons in different regions of the nervous system, particularly the cer-
ebellum, and the clinical signs tend to have a symmetric distribution as neurons
on both sides are equally affected. If a degenerative disorder is suspected, then
a literature search should be performed to look for reported conditions in the
same breed that could explain the clinical history and examination findings.
Degeneration of anatomical structures that lie in close association with the
nervous system, such as the intervertebral discs or articular facet joints, can
result in neurological signs secondary to compression and neuronal injury.
Whether this category should be classified as degenerative or fall within a sub-
category of internal trauma is arguable (see Box 5.1). These disorders can have
an acute onset (e.g. intervertebral disc extrusion) or a more chronic, progressive
course, dependent on the pathology and nature of the injury. Clinical signs are
typically progressive over time and discomfort may be present on examination
secondary to meningeal or nerve root compression.
Typical presentation: Chronic, progressive, non‐painful (the primary exception
being degenerative intervertebral disc disease – see above).

5.2 ­Summary

The construction of a meaningful list of differential diagnoses for any given neu-
rological problem relies upon a systematic and logical approach, with considera-
tion of the following factors:

• Signalment
• The clinical history – onset and progression of the clinical signs, owner‐perceived dis-
comfort, response to previous medications, concurrent non‐neurologic signs
• The neuroanatomic localisation – lesion location, distribution, and symmetry
• Presence/absence of apparent pain on examination

In the following chapter, we will discuss how to use this approach when
managing the most common neurological presentations in general practice.

­Bibliography
Armasu, M., Packer, R.M., Cook, S. et al. (2014). An exploratory study using a statistical
approach as a platform for clinical reasoning in canine epilepsy. Vet. J. 202: 292–296.
Cardy, T.J., De Decker, S., Kenny, P.J., and Volk, H.A. (2015). Clinical reasoning in canine spinal
disease: what combination of clinical information is useful? Vet. Rec. 177: 171.
132 A Practical Approach to Neurology for the Small Animal Practitioner

da Costa, R.C. and Moore, S.A. (2010). Differential diagnosis of spinal diseases. Vet. Clin. North
Am. Small Anim. Pract. 40: 755–763.
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester,
UK: British Small Animal Veterinary Association.
Stanciu, G.D., Packer, R.M.A., Pakozdy, A. et al. (2017). Clinical reasoning in feline epilepsy:
what combination of clinical information is useful? Vet. J. 225: 9–12.
Chapter 6  Practical Approach
A
to Common
Presentations
in General Practice
Edward Ives and Paul M. Freeman

The previous five chapters have summarised the initial approach to any case
with suspected neurological disease, including how to determine if there is likely
to be a lesion affecting the nervous system, where that lesion is located, and how
to formulate a list of appropriate differential diagnoses. The next step is to decide
whether urgent referral is indicated, or whether diagnostic tests can initially be
performed in general practice. For those cases in which referral is not an option,
the decision regarding which tests should be performed is particularly impor-
tant. The aim of this chapter is to provide a logical approach to the diagnosis and
treatment of the most common neurological presentations in general practice.
The reader is referred to the many excellent ‘disease‐orientated’ texts for more
in‐depth discussion regarding the pathophysiology, diagnosis, and treatment of
the individual diseases mentioned. The neurologic syndromes discussed in this
chapter are as follows:

• epileptic seizures
• movement disorders
• altered mentation
• blindness
• abnormalities of pupil size
• cranial nerve dysfunction
• vestibular syndrome
• cerebellar dysfunction
• neck and/or spinal pain

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

133
134 A Practical Approach to Neurology for the Small Animal Practitioner

• paresis, paralysis, and proprioceptive ataxia

• monoparesis and lameness
• neuromuscular weakness.

6.1 ­Epileptic Seizures

Edward Ives

The term ‘seizure’ can refer to any sudden attack or paroxysmal event. It is
therefore a non‐specific term but one that is frequently used to describe a seizure
of neurological origin, or an ‘epileptic seizure’. Owners may also use other non‐
specific terms for epileptic seizures, such as a ‘fit’ or ‘convulsion’.
Epileptic seizures represent one of most common neurological presentations
in small animal general practice. A logical and systematic approach is essential to
achieve an accurate diagnosis and to plan the most appropriate treatment. Client
communication is also vital, as expectations may differ greatly, management is
frequently lifelong, and factors such as the requirement for daily medications
and regular monitoring all depend upon good owner compliance.

6.1.1 What Is an Epileptic Seizure?

An epileptic seizure is not a disease entity itself but represents a clinical sign
resulting from excessive and often hypersynchronous neuronal activity in the
cerebral cortex (Berendt et al. 2015). This is most commonly apparent as tran-
sient, involuntary motor activity affecting a part or parts of the body, together
with an altered level of mentation. Neurons are excitable cells that are con-
stantly held in check, with the normal activity of neural networks reflecting a
balance between excitatory and inhibitory connections between neurons. Each
neuron has a threshold for excitation dependent on the environment surround-
ing it. This environment includes neighbouring neurons, supporting cells (e.g.
astrocytes), neurotransmitter levels, electrolyte levels, and oxygen levels.
Alterations to this environment, such as genetically determined factors, inflam-
mation, oedema, or adjacent mass lesions, can result in a decrease in the neu-
ronal threshold of activation that is sufficient to result in a seizure. Put simply,
epileptic seizures are the result of either excessive excitation (via neurotransmit-
ters such as glutamate) or inadequate inhibition (via neurotransmitters such as
gamma‐aminobutyric acid [GABA] or glycine). The initial seizure focus may
involve only a small number of unstable neurons. However, this can induce sur-
rounding neurons to discharge, resulting in seizure activity that affects a local
region of the cerebral cortex, or that propagates to involve both cerebral hemi-
spheres. The specific manifestation of a seizure will depend upon the area(s) of
brain affected. For this reason, any unusual, involuntary phenomena that are
episodic and recurrent should be investigated as possible epileptic seizures.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 135

The term ‘epilepsy’ is used to describe recurrent seizure activity (i.e. the occur-
rence of more than one confirmed or highly suspected epileptic seizure, irrespec-
tive of the underlying cause). Epilepsy is therefore a clinical sign and should not
be confused with the condition ‘idiopathic epilepsy’, which is a specific diagnosis
of exclusion.

6.1.2 Seizure Classification

1. Classification by clinical presentation
a. Focal seizures
Focal seizures occur when the excessive, hypersynchronous neuronal activity
remains localised to a specific region of the cerebral cortex. This typically results
in lateralised clinical signs, such as rhythmic contraction of the facial muscles on
one side of the face or flexion of a single limb (see Video 2 and 32). These signs
should be contralateral to the side of the seizure focus and are often accompa-
nied by autonomic signs such as salivation. Structural brain lesions may present
as focal seizures if they stimulate excessive neuronal activity in surrounding
cerebral tissue (e.g. a neoplastic mass). However, focal seizures are also recog-
nised in dogs for which no identified cause of the seizures can be found. These
dogs will have a diagnosis of idiopathic epilepsy or ‘epilepsy of unknown cause’.
A study of 404 dogs with seizures of intracranial origin reported that the seizure
pattern (focal versus generalised versus mixed) could not be used to differentiate
dogs with asymmetric structural lesions (n = 135) from those with symmetric
structural lesions (n = 11) or epilepsy of unknown cause (n = 258) (Armas˛u et al.
2014).
Focal seizures may secondarily generalise to involve both cerebral hemi-
spheres if the abnormal neuronal activity propagates across the midline.
Generalisation of focal seizures is frequently observed in certain breeds of dog
with idiopathic epilepsy (IE), such the Belgium Shepherd Dog.

b. Generalised seizures
Generalised seizures are the most common form of epileptic seizure observed in
general practice. They are a manifestation of excessive neuronal activity that is
affecting both cerebral hemispheres. This results in a loss of consciousness, bilat-
erally symmetric involuntary motor activity, rhythmic jaw movements, and
recumbency (see Video 1). Generalised seizures are frequently accompanied by
autonomic signs such as mydriasis, urination, defecation, and hypersalivation.
Generalised seizures frequently follow a set pattern, with each event having
a similar appearance in an individual animal. This stereotypical nature is likely
to reflect the same seizure focus being responsible for each recurrent seizure
event. A generalised epileptic seizure can be divided into four main parts.

1. The prodrome: the period of abnormal behaviour that may be observed hours
to days before a seizure occurs (e.g. restlessness, seeking the owner).
136 A Practical Approach to Neurology for the Small Animal Practitioner

2. The aura: the sensory signs that occur seconds or minutes before a seizure.
In humans, this may involve an unusual metallic taste or visual hallucina-
tions. A genuine aura may therefore be difficult to appreciate in veterinary
patients. However, the owners of dogs with recurrent seizures will often
recognise when their pet is about to have a seizure as the dog may appear
agitated, and either hide away or seek their owner immediately prior to
the event.
3. The ictus: this is the seizure event itself. The majority of generalised epileptic
seizures are self‐limiting, with a duration between 30 seconds and 3 minutes.
4. The post‐ictal phase: this is the period of abnormal behaviour that follows a
seizure. This may last for several hours, up to several days, and typical
signs include disorientation, ataxia, proprioceptive deficits, blindness, pac-
ing, and polyphagia. If an animal is examined shortly after a seizure, then
the potential influence of post‐ictal signs on the findings and interpretation
of your neurological examination should always be considered. For this
reason, it is prudent to repeat the examination after a few hours, or the
following day, to ensure that any neurological deficits are interpreted
correctly.

Acute repetitive seizures, also termed ‘cluster seizures’, refers to when two or
more individual seizures occur over a 24‐hour period, with a complete recovery
between events.
Status epilepticus is the term used to describe a seizure that is not self‐limiting.
It is specifically used if a single seizure is greater than 5 minutes in length, or if
two or more seizures occur over a 30‐minute period without a complete recov-
ery between them. The emergency management of status epilepticus and acute
repetitive seizures is discussed in Chapter 7.

Box 6.1.1 Reflex Seizures

Epileptic seizures are classified as ‘reflexive’ if they are triggered by certain stimuli.
Reflex epilepsy is widely reported in humans but rarely described in veterinary medi-
cine. It has been reported in dogs with stimulus‐specific seizures, such as in response
to certain sounds (e.g. lawnmower engine, doorbell ringing), exercise, car journeys,
and visits to the vets or groomers (Forsgård et al. 2019; Shell et al. 2017). Some dogs
may have multiple triggers for their seizures. A condition named ‘audiogenic reflex
seizures’ has also been reported in older cats (median age 15 years) (Lowrie et al.
2016). These events are associated with high‐pitched noises, such as crinkling of tin
foil, chinking of glass, keys jangling, or metal spoon contact with a ceramic food bowl.
Birman Cats appear over‐represented and levetiracetam appears to provide good sei-
zure control when compared to phenobarbitone (Lowrie et al. 2017).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 137

2. Classification by underlying aetiology

See Figure 6.1.1 for a summary.

a. Extracranial disorders (reactive seizures)

Reactive seizures result from abnormal blood being pumped to a normal brain.
This change in blood composition alters the neuronal environment in favour of
excitation. Extracranial disorders usually present with generalised seizures +/−
symmetric neurological deficits as there is equal delivery of abnormal blood to
both cerebral hemispheres. Examples of extracranial causes of epileptic seizures
include:

1. Metabolic disorders – hypoglycaemia, hepatic encephalopathy, uraemic enceph-

alopathy, hypoxia, electrolyte abnormalities (e.g. hypocalcaemia, hyper-
natraemia, hyponatraemia)
2. External toxin exposure – lead, ethylene glycol, organophosphates, metalde-
hyde (found in slug pellets), chocolate, strychnine, illegal drugs, permethrin
(in cats).

b. Intracranial disorders
If the blood being pumped to the brain is normal, then epileptic seizures may
reflect a structural brain lesion that is detectable on diagnostic investigations, or
may reflect a functional disorder that lowers the threshold for neuronal
excitation.

Vascular

Toxic Infectious/
Inflammatory

Extracranial Metabolic Traumatic

Anomalous
Epileptic seizure

Neoplastic
Functional
Intracranial
(idiopathic)
Nutritional

Structural Degenerative

Figure 6.1.1 Classification of epileptic seizures according to their underlying cause.

138 A Practical Approach to Neurology for the Small Animal Practitioner

i. Structural epilepsy
A structural brain lesion may sufficiently alter the neuronal environment to
favour excessive neuronal excitation. Advanced imaging +/− cerebrospinal fluid
(CSF) analysis is usually required for the diagnosis of these conditions.

• Vascular – cerebrovascular disease (haemorrhage or ischaemic stroke).

• Infectious/inflammatory – e.g. bacterial, viral, fungal or protozoal meningoen-
cephalitis, meningoencephalitis of unknown origin (MUO).
• Traumatic – seizures may occur at the time of head trauma, or the onset can be
delayed by weeks to months. Post‐traumatic epilepsy has been reported to
affect 6–10% of dogs following significant head trauma (see Chapter 7).
• Anomalous – e.g. hydrocephalus, porencephaly, meningoencephalocele.
• Neoplastic – primary (e.g. glioma, meningioma), metastatic, locally invasive
(e.g. nasal adenocarcinoma) (Figure 6.1.2).
• Degenerative – e.g. neuronal ceroid lipofuscinosis (NCL), Alaskan Husky
encephalopathy.

Figure 6.1.2 A parasagittal image (left side) from a brain MRI of a 12‐year‐old, male
neutered Labrador Retriever with a clinical history of intermittent sneezing and eight
generalised epileptic seizures over a 4‐day period. Neurological examination revealed a
depressed level of mentation, circling to left, and a left head turn. The neuroanatomic
localisation was the left forebrain. The MRI demonstrated a large mass lesion occupying the
caudal nasal cavity that had invaded through the cribriform plate, resulting in compression of
the olfactory and frontal lobes of the brain (white arrow). Note also the accumulation of fluid
in left frontal sinus secondary to obstruction of drainage by the nasal mass (arrow head). A
nasal adenocarcinoma was suspected in this case, but histopathology was not performed to
confirm the diagnosis.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 139

ii. Idiopathic epilepsy (‘epilepsy of unknown cause’)

Idiopathic epilepsy (IE) is a functional intracranial disorder in which the lowered
seizure threshold is likely to result from a combination of genetic, environmen-
tal, and developmental factors. A genetic component is supported by the fact
that IE appears to be more common in certain breeds of dog, with evidence to
suggest inheritance in breeds such as the Border Collie, Labradors Retriever, and
German Shepherd Dog (Hülsmeyer et al. 2015).
Idiopathic epilepsy is the most common diagnosis for recurrent seizures in
dogs, with a prevalence of 0.62% reported by a study of over 87 000 dogs from
a UK general practice population (Kearsley‐Fleet et al. 2013). It appears to be
less common in cats, likely related to their more diverse genetic background.
However, IE is increasingly recognised in this species and has been reported as
the underlying cause of recurrent seizures in 20–60% of cats (Barnes Heller
2018; Pakozdy et al. 2013; Pakozdy et al. 2014; Stanciu et al. 2017; Wahle et al.
2014).
Idiopathic generalised epilepsy represents a group of epileptic disorders in
humans, with specific subtypes that differ in relation to seizure type, age at
onset, and whether a known genetic mutation is responsible. The term ‘idio-
pathic epilepsy’ is currently used in veterinary medicine as an umbrella‐term to
describe all seizure disorders for which an underlying cause cannot be identified.
However, there are also likely to be specific subtypes of idiopathic epilepsy in
different species and breeds of animal. This is supported by the fact that epilep-
sies of unknown cause may have a specific presentation in certain breeds of dog
(e.g. juvenile myoclonic epilepsy in Rhodesian Ridgeback dogs [Wielaender
et al. 2018]), and that the disease progression may differ dependent on the breed
of dog; some breeds will typically show a relatively benign clinical course of IE
(e.g. Finnish Spitz, Belgian Shepherd), whereas other breeds may present with
a more severe phenotype and seizures that are difficult to control in spite of
multiple medications (e.g. Italian Spinone, Australian Shepherd dog, Border
Collie). Knowledge of these breed‐specific differences is important when plan-
ning treatment and for managing owner expectations.
The onset of seizures in dogs with IE most commonly occurs between
6 months and 6 years of age. In spite of this, IE should never be excluded from
the list of differential diagnoses in older dogs; between 13% and 45% of dogs
with a seizure onset at >7 years old were diagnosed with IE in two studies
(Ghormley et al. 2015; Schwartz et al. 2013). However, a study of over 400 dogs
with recurrent seizures reported that the odds of an asymmetric structural brain
lesion compared to IE increased by 1.6‐fold for each additional year of age
(Armas˛u et al. 2014). Therefore, performing further investigations to exclude
structural epilepsy is always advised in dogs with an onset of seizures at >6 years
of age. A diagnosis of structural epilepsy is more likely in cats that are >7 years
old at the time of seizure onset (Stanciu et al. 2017). However, the lower inci-
dence of IE in cats compared to dogs means that further investigations should
140 A Practical Approach to Neurology for the Small Animal Practitioner

ideally be performed in all cats that present with a history of seizures (see
Box 6.1.2).
The clinical course of IE can be extremely variable dependent on the indi-
vidual. Many dogs will initially present with infrequent single seizures; however,
some dogs may show cluster seizures or status epilepticus as their first presenta-
tion of IE. The occurrence of cluster seizures has been associated with a worse
long‐term prognosis in dogs with IE. This unpredictable clinical course should
always be discussed with the owner at the time of diagnosis.
Dogs and cats with IE should have a normal neurological examination during
the inter‐ictal period. One study reported that dogs with an abnormal neurologi-
cal examination were 16.5 times more likely to have an asymmetric structural
brain lesion and 12.5 times more likely to have a symmetric structural brain
lesion (e.g. hydrocephalus) compared to a diagnosis of IE (Armas˛u et al. 2014).
A structural brain lesion is also more likely in cats with an abnormal neurologi-
cal examination (Stanciu et al. 2017). However, the possibility of pre‐existing
neurological deficits, post‐ictal deficits, and the influence of recently adminis-
tered antiepileptic medications on the neurological examination should also be
considered. These deficits may mimic those associated with a structural brain
lesion and the examination should be repeated if there is any uncertainty.
Idiopathic epilepsy is currently a diagnosis of exclusion, with no abnormali-
ties being found on diagnostic investigations. Inter‐ictal electroencephalography
(EEG) does not appear to be a useful screening method to distinguish dogs with
IE from those with structural epilepsy (Brauer et al. 2012). Recent guidelines for
the diagnosis of IE in dogs have defined 3 tiers of diagnosis in practice.

Box 6.1.2 Epilepsy in Cats

The diagnostic approach to epileptic seizures in cats is broadly similar to that for dogs.
However, there are some important considerations in this species which include:

• Third‐degree AV block resulting in cerebral hypoxia is an important differential

diagnosis for episodic, seizure‐like episodes in cats.
• Idiopathic epilepsy is an increasingly recognised cause for recurrent seizures in cats,
particularly in young cats with a normal inter‐ictal neurological examination
(Stanciu et al. 2017). However, structural epilepsy remains more common in cats
than dogs and performing further investigations is always advised in this species.
• Phenobarbitone is currently the first‐line treatment of choice for the majority of cats
with recurrent seizures. Other treatment options include levetiracetam, imepitoin,
and zonisamide (Bailey et al. 2008; Engel et al. 2017).
• Levetiracetam is reported to be the treatment of choice for audiogenic reflex seizures
in older cats (Lowrie et al. 2017).
• Potassium bromide should not be used in cats as it has the potential to cause severe,
potentially fatal, bronchial irritation.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 141

Tier I
• Two or more unprovoked seizures at least 24 hours apart.
• Age at onset between 6 months and 6 years old.
• Normal inter‐ictal physical and neurological examination.
• No abnormalities on haematology, serum biochemistry and urinalysis.

Tier II
• As for Tier I, together with negative findings on serum bile acid stimulation
testing, magnetic resonance imaging (MRI) of the brain, and CSF analysis.

Tier III
• As for Tiers I and II, together with consistent EEG abnormalities.

6.1.3 Diagnostic Approach to Epileptic Seizures

The diagnostic approach to epileptic seizures should be logical and systematic so
that the most appropriate investigations are performed in the first instance, and
so that the management can be individualised to each case.

1. Establish if the events described are likely to represent

epileptic seizures
This is vital before pursuing further investigations as owners may describe vari-
ous forms of abnormal event as a ‘seizure’ (Box 6.1.3). The widespread popular-
ity of smartphones has made access to videos of abnormal events much easier.
This can be incredibly useful to further characterise an event, particularly if they
are short, do not occur during veterinary visits, or if the clinical examination is
normal between events. EEG during an episode can be used to confirm an

Box 6.1.3 Seizure Mimics

• Syncope or cardiorespiratory disease (e.g. third‐degree AV block in cats)

• Vestibular syndrome
• Systemic disease resulting in weakness or collapse (e.g. hypoadrenocorticism)
• Narcolepsy/cataplexy (see Video 6)
• Pain (e.g. cervical disc disease resulting in pain and cervical muscle spasm, see
Video 8)
• Stereotypical behaviours or obsessive compulsive behaviour disorders (e.g. tail chas-
ing, fly catching)
• Rapid eye movement (REM) sleep disorders (see Video 9)
• Movement disorders (e.g. paroxysmal dyskinesia) (see Video 10, 33 and 37)
• Neuromuscular weakness (e.g. myasthenia gravis)
• Tetanus.
142 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.1.4 When to Suspect an Epileptic Seizure

• Acute, often unexpected onset.

• Frequently occurring at times of rest, particularly when associated with idiopathic
epilepsy. However, seizures associated with structural brain disease can occur at any
time.
• A stereotypical pattern for each event in an individual cat or dog.
• Involuntary motor activity lasting <5 minutes. Unless representing status epilepti-
cus, or if the owner has included the post‐ictal period in the total duration of an
event, generalised seizures most commonly last between 30 seconds and 3 minutes.
A movement disorder should be considered if the abnormal motor activity lasts for
more than 5–10 minutes, particularly if the animal has a normal level of mentation
during the event.
• Increased muscle tone during the event, usually accompanied by rhythmic limb
movements and facial muscle contractions (see Video 1).
• The presence of autonomic signs during the event (salivation, urination,
defecation).
• A reduced level of mentation or a lack of response to the owner during the event.
• The presence of a distinct post‐ictal phase (e.g. ataxia, disorientation, hyperactivity,
polyphagia, visual deficits).

epileptic seizure. However, access to this equipment is currently limited in vet-

erinary medicine and there are practical considerations regarding its use in dogs
and cats, particularly for infrequent events. A positive response to an antiepilep-
tic medication may suggest that previously observed events did represent epilep-
tic seizures. However, a temporal association between starting a medication and
a reduction in episode frequency does not always imply causation, and naturally
regressive or waxing/waning disorders should also be considered. A general
guide for when to suspect an epileptic seizure can be found in Box 6.1.4. Further
discussion regarding the distinction between epileptic seizures and other parox-
ysmal events can be found in Chapter 1.

2. Formulate a list of differential diagnoses

As discussed in Chapter 5, a list of differential diagnoses should always be made
before planning further tests. This list will depend upon the neuroanatomic local-
isation, the signalment of the animal, the clinical history, the disease onset, and
the clinical progression.
Neuroanatomic localisation: an epileptic seizure is a manifestation of abnormal
neuronal activity in the cerebral cortex, irrespective of whether the inciting
cause is extracranial or intracranial in origin. Therefore, the neuroanatomic
localisation for any animal with epileptic seizures is the forebrain. However,
epileptic seizures may also be accompanied by other neurological deficits that
could indicate a multi‐focal or diffuse disease process.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 143

Signalment: certain disorders are more common in animals of a particular age,

breed, or sex. Therefore, the signalment can be used to rank the list of differen-
tial diagnoses (see Chapters 2 and 5).

• Female animals – decreased seizure threshold during oestrous in intact female

dogs, metastatic mammary adenocarcinoma.
• Young animals (<1 year of age) – portosystemic shunt, hydrocephalus, hypogly-
caemia, infectious diseases (e.g. canine distemper virus [CDV] encephalitis).
• Middle‐aged animals (1–6 years of age) – idiopathic epilepsy (particularly in
breeds with known heritability such as Border Collies and Labradors), menin-
goencephalitis of unknown origin (MUO).
• Older animals (>6 years of age) – intracranial neoplasia (particularly in brachy-
cephalic breeds of dog), hypoglycaemia secondary to insulinoma, MUO, idio-
pathic epilepsy.

Clinical history: Important questions to ask when taking the clinical history
should include:

• The age at the time of the first seizure.

• The seizure frequency and the presence or absence of cluster seizures.
• If there are any known or suspected trigger factors, such as seizures after eat-
ing in the case of a portosystemic shunt.
• The vaccination status and travel history of the affected animal.
• Concurrent medical conditions and any medications being administered.
• The diet and any known or suspected toxin exposure.
• A history of seizures in the parents or siblings would increase the index of
suspicion for idiopathic epilepsy; a contagious disease or intoxication should
also be considered if there is an acute onset of seizures in multiple animals at
the same time.

The general clinical examination: a thorough general clinical examination is

important to assess for signs of systemic disorders that could cause seizures (i.e.
extracranial disease), mimic seizures, or that would affect the prognosis or risks
associated with sedation/general anaesthesia.
The neurological examination: the neurological examination should ideally be
performed in the inter‐ictal period to avoid overlap of post‐ictal deficits, such as
ataxia, circling, vision loss, and proprioceptive deficits. Antiepileptic medications
may also cause sedation and ataxia, which could influence the interpretation of
the examination findings.
The inter‐ictal neurological examination should be normal for all animals
with IE but may also be normal for other diseases. These include waxing/waning
metabolic conditions or intracranial neoplasia in ‘silent’ brain regions (e.g. the
olfactory lobe) (Figure 6.1.3). Structural epilepsy should therefore never be
144 A Practical Approach to Neurology for the Small Animal Practitioner

R L

Figure 6.1.3 A T1‐weighted MRI in the dorsal plane following the administration of
intravenous contrast media in an 8‐year‐8‐month‐old, female neutered, German Shepherd
Dog with a history of three generalised epileptic seizures over the last 6 weeks. There were no
neurological deficits at the time of examination in the inter‐ictal period, and haematology,
serum biochemistry, and urinalysis were normal. Magnetic resonance imaging of the brain
demonstrated a 1.5 × 1.5 × 1 cm, ovoid, broad‐based, contrast‐enhancing, extra‐axial mass in
the right olfactory lobe (white arrow). These imaging characteristics were most consistent
with a meningioma as the cause of structural epilepsy in this case.

excluded on the basis of a normal neurological examination. A previous study of

dogs with a normal inter‐ictal neurological examination identified a cause for
the observed seizures on brain MRI in 3% of dogs that were <6 years old and in
25% of dogs that were >6 years old (Smith et al. 2008). Very similar findings
were reported for epileptic cats with a normal inter‐ictal neurological examina-
tion; a detectable lesion was observed on MRI in 5% of cats between 1 and
6 years old and in 23% of cats >6 years old (Raimondi et al. 2017). Neurological
deficits that would be consistent with an asymmetric structural brain lesion
include a contralateral menace response deficit (see Video 28), contralateral pro-
prioceptive deficits, reduced nasal septum nociception in the contralateral nos-
tril, a head turn, circling (see Video 22), an altered level of mentation, and
possibly neck pain.

3. Perform further investigations in general practice

The decision whether to perform further investigations in general practice, and
when to perform them, will depend on many factors. These include the nature
and frequency of the episodes, the inter‐ictal examination findings, the list of
differential diagnoses, the degree of owner concern, and the funds available for
referral or further investigations.
If an animal has had a single episode that is suspected to represent an epilep-
tic seizure, if it has fully recovered by the time of assessment, and it has a normal
physical and neurological examination, then it is not unreasonable to monitor
 Chapter 6 A Practical Approach to Common Presentations in General Practice 145

for further episodes. The owner should be encouraged to video any future events
and should always be made aware that the option of performing further investi-
gations is available at any time.
If an animal has had two or more isolated epileptic seizures, a cluster of sei-
zures, or status epilepticus, then performing further investigations is advised (De
Risio et al. 2015). In general practice, this should start by excluding extracranial
disorders as referral for advanced imaging is generally required to diagnose
intracranial disease. The specific investigations to perform will depend upon the
signalment and list of differential diagnoses.

• Haematology, serum biochemistry, and urinalysis should be performed in all cases.

• Blood pressure testing, particularly in geriatric cats.
• Bile acid stimulation testing +/− serum ammonia, particularly if a portosystemic
shunt is suspected.
• Thyroid function testing – total thyroid hormone (T4), free T4, thyroid stimulat-
ing hormone (TSH).
• Fructosamine and insulin levels if an insulinoma is suspected.
• A coagulation profile if a disorder of blood clotting is suspected (e.g. rodenticide
ingestion or petechiae or ecchymoses on clinical examination).
• Infectious disease testing dependent on the species and relative risk of expo-
sure – Toxoplasma gondii in cats and dogs, Neospora caninum or CDV in dogs,
feline leukaemia virus (FeLV), feline immunodeficiency virus (FIV), and feline
coronavirus in cats.
• Urine metabolic screening if an inborn error of metabolism is suspected (e.g.
young animal with seizures and progressive neurological disease).
• Toxicology for known or suspected toxin exposure.
• Thoracic radiography, abdominal ultrasonography, or thoracic and abdominal com-
puted tomography (CT) – if metastatic neoplasia or an extracranial cause of sei-
zures is suspected, particularly if referral for further investigations is not
possible.

It is not unreasonable to make a presumptive diagnosis of idiopathic epi-

lepsy in general practice on the basis of the clinical history, signalment, a nor-
mal inter‐ictal neurological examination, and normal blood/urine tests (Tier I
classification). This diagnosis becomes extremely likely if the seizures remain
infrequent and the neurological examination remains normal over a period of
6–12 months. However, the animal’s owner should always be made aware that
this is not a definitive diagnosis and the option of referral for further investiga-
tions should be discussed. This is particularly relevant if the seizures are diffi-
cult to control, or if the subsequent disease progression is incompatible with a
diagnosis of idiopathic epilepsy (e.g. the appearance of inter‐ictal neurological
deficits).
146 A Practical Approach to Neurology for the Small Animal Practitioner

4. Refer for further investigations

Referral to a veterinary neurologist should be offered to the owner of any animal
that has had one or more suspected epileptic seizures. Further investigations
may not necessarily be performed at this time, but the consultation gives the
opportunity for further neurological assessment and an in‐depth discussion
regarding the causes and management of epilepsy.
If an extracranial cause for the events has been excluded, and if funds are
available, then advanced imaging of the brain and CSF sampling may be advised.
This is to achieve a diagnosis of either a structural brain lesion or idiopathic epi-
lepsy (Tier II classification). MRI of the brain is the gold standard imaging modal-
ity in light of its superior soft tissue resolution compared to CT. A general guide
as to when advanced imaging of the brain would be recommended is as
follows:

• All cats with a history of epileptic seizures given the higher incidence of struc-
tural epilepsy in this species.
• Dogs with a seizure onset at <6 months or >6 years of age for which an extrac-
ranial cause has not been identified.
• Any animal with a history of cluster seizures or status epilepticus.
• Animals with inter‐ictal neurological deficits that are consistent with a fore-
brain neuroanatomic localisation.
• Animals with a presumptive diagnosis of idiopathic epilepsy that appear
refractory to antiepileptic drug (AED) therapy despite adequate serum drug
levels.

6.1.4 Management of Epileptic Seizures

1. Owner communication
Good owner communication is vital throughout every step in the diagnosis and
management of their pet’s condition. This is to ensure that they are well‐
informed regarding the diagnosis, treatment options, and likely prognosis. The
owner should also be made aware of the potential requirement for lifelong daily
medication, regular monitoring of treatment, and the associated costs. This can
be a big responsibility and one that may not be appropriate for all owners. It is
always better to discuss these factors and to manage an owner’s expectations
prior to starting treatment, rather than have the owner feel misinformed at a
later date.
Encouraging an owner to keep a record of their pet’s seizures in the form of
a seizure diary will assist in the monitoring of disease progression and the
response to treatment. It may also help to keep the owner motivated, allow
them to feel involved with the management of their pet’s condition, and help to
de‐emotionalise the seizures for them at the time of an event. There are some
 Chapter 6 A Practical Approach to Common Presentations in General Practice 147

recent smartphone applications that some owners may find useful for this
purpose.

2. Goals of seizure management

The primary goal of seizure management is a reduction in the frequency and
severity of seizures, with minimal adverse effects of treatment (Bhatti et al.
2015; Potschka et al. 2015). The overall quality of life for the animal should be
prioritised, with the aim of reducing seizure‐related morbidity and mortality.
Whilst seizure freedom is the ideal management goal, this is rarely achieved in
veterinary patients. Some studies have estimated that only 15–25% of epileptic
dogs may become seizure‐free on medication. A commonly used definition of a
‘responder’ is if a > 50% reduction in seizure frequency is seen following the
introduction of a medication or other intervention. Whether this is a satisfactory
result for an individual animal (and owner) will obviously depend upon the
seizure frequency before starting treatment. A reasonable goal to discuss with
the owner of an animal with IE would be to achieve a single, short, self‐limiting
seizure every 3 months.

3. When to start treatment

The decision when to start treatment will depend upon:

• the underlying cause for the seizures

• seizure type and frequency
• the effects of the seizures on the owner
• the effects of the seizures on the animal’s quality of life and its brain
• the adverse effects and costs of medication.

It has been suggested that long‐term management of idiopathic epilepsy in

dogs may be more successful if treatment is started early in the course of the
disease, particularly in dogs with a high seizure density (i.e. a short time interval
between seizures). However, several questionnaire studies have also docu-
mented that the adverse effects of medications have a large impact on owner‐
perceived quality of life for their pet (Chang et al. 2006). This is important, as
dogs with epilepsy have an increased risk of premature death as a result of
euthanasia, which is driven in part by a combination of economic burden and
the emotional stress on the owner (Podell et al. 2016). Chronic behaviour
changes are increasingly reported in dogs with recurrent seizures, including fear
and anxiety‐related behaviours (Packer and Volk 2015; Shihab et al. 2011;
Watson et al. 2018; Winter et al. 2018). These can also contribute to owner‐per-
ceived poor quality of life for their pet and drive a decision to euthanasia. A
general guide as to when to start medical management of epileptic seizures can
be found in Box 6.1.5.
148 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.1.5 When to Start Treatment

‘No?’
• A single, self‐limiting seizure‐like event and a normal neurological examination – monitor
the animal closely for further events or abnormalities.
• Infrequent, short, self‐limiting seizures in an animal with suspected idiopathic epilepsy
(i.e. one seizure every 2–3 months).
• Seizures that are affecting an animal’s quality of life less than the expected adverse effects of
medications (e.g. infrequent, short, or focal seizures).
• Seizures following toxin exposure, after their initial management.

‘Yes?’
• >2 seizures over a 6‐month period, or an increasing frequency or severity of seizures.
• Cluster seizures or status epilepticus.
• An underlying progressive disease (i.e. structural epilepsy).
• Owner distress or a desire to treat when aware of the expected adverse effects of medications and
responsibilities required.
• Severe post‐ictal signs (e.g. aggression or blindness).

4. How to manage epileptic seizures

a. Correct the underlying disease
This could include medical management or surgical attenuation of a portosys-
temic shunt, medical or surgical management of an insulinoma, radiotherapy or
surgery for intracranial neoplasia, or medical management of meningoencepha-
litis. Antiepileptic medications are commonly used as an adjunctive treatment
for these conditions until the underlying disease is deemed to have resolved.
Long‐term medical management is frequently required for conditions such as
meningoencephalitis of unknown origin or intracranial neoplasia, for which a
cure is not often possible.

b. Antiepileptic medications
Antiepileptic drugs (AEDs) are most commonly used for the long‐term manage-
ment of idiopathic epilepsy and in the palliative treatment of structural epi-
lepsy. They exert their clinical effect by reducing neuronal excitability and
increasing the threshold of neuronal excitation. There are three AEDs that are
currently licensed in the United Kingdom (UK) for use in dogs: phenobarbi-
tone, potassium bromide, and imepitoin. The choice of medication to use in an
individual animal will depend upon multiple factors, including tolerability, effi-
cacy, whether concurrent diseases are present (e.g. hepatic dysfunction, renal
disease), and owner‐related factors (e.g. financial, lifestyle). A flow diagram
summarising a suggested approach to the management of idiopathic epilepsy in
dogs using imepitoin, phenobarbitone, and/or potassium bromide can be found
in Figure 6.1.4.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 149

Isolated History of
epileptic seizures cluster seizures
or Continue to monitor serum
level +/– reduce dose to
Continue same Start imepitoin Start phenobarbitone achieve a level <30 mg/L
dose (10–20 mg/kg BID) (2–3 mg/kg BID)
> 30–35 mg/L

Increase dose Measure serum drug

< 30 mg/L Monitor serum drug
to 30 mg/kg BID level 2 weeks after
level at 6 weeks and
starting or changing
then every 6–12 months
the dose

Key
< 25 mg/L 25–35 mg/L > 35 mg/L
= adequate seizure control
= poor seizure control
Increase dose up Start potassium Reduce dose aiming
to serum level bromide (KBr) for a serum level
25–30 mg/L (15 mg/kg BID) 25–30 mg/L and start KBr

Increase dose up < 2000 mg/L

Refer for Measure serum drug Monitor serum drug
to serum level
specialist opinion level after 3 months level every 6–12 months
2000 mg/L

Figure 6.1.4 A flow diagram summarising a suggested approach to the management of

idiopathic epilepsy in dogs using imepitoin, phenobarbitone, and/or potassium bromide.

Phenobarbitone
License: Phenobarbitone is licensed in the UK as a first‐line medication for the
management of epileptic seizures in dogs.
Mechanism of action: Poorly understood but likely works by enhancing the
effects of the inhibitory neurotransmitter GABA, reducing the excitatory effects
of glutamate, and decreasing calcium flow into neurons.
Clinical indications: First‐line medication for dogs with generalised seizures,
licensed treatment of choice for dogs with cluster seizures, first‐line medication
of choice in cats with epileptic seizures. Phenobarbitone is also useful in the
emergency management of cluster seizures and status epilepticus (see Chapter 7).
Contraindications: Pre‐existing hepatic dysfunction. If used, the hepatic param-
eters and drug serum levels should be carefully monitored.
Metabolism and excretion: Hepatic metabolism by microsomal enzymes, taking
7–14 days to reach a steady‐state serum concentration (15–35 mg/l). Phenobarbitone
auto‐induces the hepatic cytochrome p450 system, resulting in a decreased half‐life
with chronic therapy. Gradually increasing oral doses are therefore often required
over the life of an animal to maintain an adequate serum level.
Starting dose: 2–3 mg/kg per os twice daily in dogs and cats. Smaller dogs often
require higher oral doses to achieve the same serum level when compared to
larger dogs. Administration every 8 hours can be considered in dogs with inad-
equate seizure control on twice daily administration and a phenobarbitone elim-
ination half‐life of less than 20 hours (estimated by measuring peak and trough
serum concentrations) (Stabile et al. 2017).
Serum level monitoring: 14 days after starting treatment or a change in the
dose. Then at 6 weeks, 6 months, and every 6–12 months if the seizures are
well‐controlled.
150 A Practical Approach to Neurology for the Small Animal Practitioner

The blood sample should be taken into a plain serum tube (not a serum gel
tube) and can be taken at any time after the last dose in the majority of animals.
However, it should ideally be taken at a similar time of day for each blood test to
allow a fair comparison with previous levels. A trough serum drug concentration
(i.e. one that is taken immediately before the next dose) can be considered in
animals that show seizures close to when their next dose is due, or if a drug reac-
tion is suspected.
The therapeutic range should be determined on an individual basis; toxicity
may occur in some animals below the upper limit of the reference range, and
some animals may be well controlled with a serum level below the lower limit
(Bhatti et al. 2015, Podell et al. 2016).

• Adequate seizure control at a serum level <25–30 mg/l. No change in oral dose
required (even if the serum level is below the lower limit of the ‘therapeutic
range’, i.e. <15 mg/l).
• Adequate seizure control but the serum level is >30 mg/l. Continue to monitor the
serum level and if it remains >30–35 mg/l then reduce the oral dose, aiming
for seizure control at a level of <30 mg/l.
• Inadequate seizure control and the serum level is <30 mg/l. Increase the oral dose
and recheck the serum level after 14 days, aiming for a level of 25–30 mg/l
before considering other treatment options.
• Inadequate seizure control with a serum level 25–35 mg/l. Introduce potassium bro-
mide (see below).

Adverse effects: Common adverse effects include polydipsia, polyuria, polypha-

gia, sedation, and ataxia. Significant sedation and ataxia will usually be self‐lim-
iting and markedly improve after the first 1–2 weeks. Less common adverse
effects include superficial necrotising dermatitis, blood dyscrasias (e.g. anaemia,
thrombocytopenia, or pancytopenia), and hepatotoxicity (Bersan et al. 2014;
Charalambous et al. 2016). Hepatotoxicity may be seen as an idiosyncratic reac-
tion that is independent of the oral dose. It can also be associated with chronic
phenobarbitone therapy, but this is rare if the serum levels are kept below
35 mg/l.
Adverse effect monitoring: A complete blood cell count, biochemical profile, bile
acid stimulation test at 3 months and then every 6–12 months.
Phenobarbitone induces alkaline phosphatase (ALP) in dogs and this param-
eter is frequently elevated as a ‘normal’ finding on serum biochemistry in
treated dogs. Alanine aminotransferase (ALT) may also be mildly elevated in
dogs, but the levels of both ALP and ALT should be monitored for further
increases over time. Both aspartate aminotransferase (AST) and gamma gluta-
myltransferase (GGT) are useful for hepatic monitoring in dogs as their levels
are not directly induced by phenobarbitone. Liver enzymes do not appear to be
influenced by phenobarbitone use in cats at serum levels between 15 and 45 mg/l
 Chapter 6 A Practical Approach to Common Presentations in General Practice 151

(Finnerty et al. 2014). Phenobarbitone does not affect adrenocortical assess-

ment (e.g. adrenocorticotropic hormone [ACTH] stimulation testing) but may
alter the levels of total thyroid hormone (T4) and TSH, complicating the inter-
pretation of thyroid function testing in dogs receiving phenobarbitone.

Potassium bromide
License: Potassium bromide (KBr) is licensed in the UK as an adjunctive medi-
cation in dogs with seizures that are refractory to phenobarbitone alone.
Mechanism of action: Incompletely understood but likely involves hyperpolari-
sation of the neuronal cell membrane and elevation of the seizure threshold as
negatively charged bromide ions compete with chloride to enter via anion
channels.
Clinical indications: Most commonly used as an add‐on medication to pheno-
barbitone in dogs that continue to show a high seizure frequency in spite of an
adequate phenobarbitone serum level (25–30 mg/l). KBr has been reported to be
less effective when used as a monotherapy compared to phenobarbitone in dogs
with idiopathic epilepsy (Boothe et al. 2012). Its use may also be associated with
more severe adverse effects. However, KBr can be a useful first‐line medication
in dogs that cannot tolerate phenobarbitone (e.g. hepatic disease or previous
idiosyncratic reaction).
Contraindications: Potassium bromide should not be used in cats due to the
risk of potentially fatal eosinophilic bronchitis. Use with care in dogs with a his-
tory of pancreatitis. Serum levels should be monitored closely in dogs with renal
disease.
Metabolism and excretion: Excreted unchanged via the kidneys, with a long
serum half‐life of 24–36 days. KBr takes 3–4 months to reach a steady state
serum concentration (1000–2500 μg/ml in dogs) and the levels will fall slowly
after a dose reduction.
The salt content of the diet should be kept constant in animals receiving KBr
(Larsen et al. 2014; Shaw et al. 1996). Bromide and chloride compete for reab-
sorption by the kidneys, therefore a high dietary salt content (e.g. urinary diet)
will result in reduced bromide reabsorption, increased renal excretion, and the
potential for low KBr serum levels. Conversely, a low dietary salt content (e.g.
cardiac diet) will result in increased bromide reabsorption, reduced renal excre-
tion, and higher KBr serum levels. The use of loop diuretics (e.g. furosemide)
can also increase KBr excretion, potentially resulting in loss of seizure control.
Renal insufficiency may result in reduced renal excretion, an increase in the KBr
serum level, and the potential for bromide intoxication if the dose is not appro-
priately adjusted.
Starting dose: 20–40 mg/kg/day per os. The long serum half‐life means that
KBr can be administered as a single daily dose; however, twice daily administra-
tion with food is recommended to reduce the incidence of gastrointestinal
irritation.
152 A Practical Approach to Neurology for the Small Animal Practitioner

Oral loading regimes have been described to achieve therapeutic serum levels
more rapidly in dogs with frequent seizures (e.g. 125 mg/kg/day divided into
four to six daily doses for 5 days). The use of loading doses may be associated
with significant sedation, ataxia, and/or vomiting, therefore loading should only
be performed if absolutely required and hospitalisation of the animal should be
considered over the loading period. This is particularly recommended if rapid
loading regimes are used (e.g. 625 mg/kg over 2 days divided into 8–12 separate
doses).
Serum level monitoring: 3 months after starting treatment or a change in the
dose, then every 6–12 months if the seizures are well controlled. The level can be
checked after 1 month if a loading regime is used.
Adverse effects: The adverse effects of KBr are similar to those for phenobarbi-
tone and include polydipsia, polyuria, polyphagia, sedation, and ataxia. Nausea,
vomiting, irritability, restlessness, and erythematous dermatitis may also be
observed (Baird‐Heinz et al. 2012; Rossmeisl and Inzana 2009). Intravenous
administration of sodium chloride (0.9%) can be used to increase renal excre-
tion and reduce serum bromide levels more rapidly in the event of severe adverse
effects or overdose.
Adverse effects monitoring: A complete blood cell count and serum biochemistry
should be checked every 6–12 months in dogs on chronic therapy. KBr will arte-
factually elevate the chloride level on serum biochemistry as the laboratory
machines cannot distinguish between chloride and bromide ions. Elevated
serum canine pancreatic lipase immunoreactivity (cPLI) concentrations may
also be observed in dogs receiving KBr; however, clinically significant pancreati-
tis is reported as a rare adverse reaction affecting less than 1 in 10 000 animals.

Imepitoin
License: Imepitoin is licensed in the UK for the reduction of the frequency of
generalised seizures due to idiopathic epilepsy in dogs after evaluation of alter-
native treatment options. It has also recently been licensed for the reduction of
anxiety and fear associated with noise phobia in dogs.
Mechanism of action: Imepitoin is a low affinity partial agonist at the benzodi-
azepine receptor and potentiates GABA‐mediated inhibition, whilst also having
a weak Ca‐channel blocking effect.
Clinical indications: Imepitoin represents a first‐line medication for dogs with
isolated generalised seizures and highly suspected or confirmed idiopathic epi-
lepsy (Rundfeldt et al. 2015; Tipold et al. 2015). The rapid onset of action, lack
of serum monitoring requirements, and the possibility of milder adverse effects
makes it an attractive option in these cases. However, its use is not recommended
in dogs with a history of cluster seizures or status epilepticus. Dogs that are cur-
rently stable on an alternative AED should not be transitioned onto imepitoin
unless there is evidence of poor efficacy or severe adverse effects associated with
the other medication(s).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 153

Imepitoin appears to be well tolerated in cats but its efficacy for seizure con-
trol remains unknown in this species (Engel et al. 2017).
Contraindications: Severe renal, hepatic, or cardiac disease.
Metabolism and excretion: Imepitoin reaches a maximum blood concentration
2 hours after oral dosing, followed by rapid blood clearance via the faecal route.
Starting dose: 10–30 mg/kg per os twice daily, with a constant timing of dosing
in relation to food recommended (e.g. always with food, or always on an empty
stomach).
There is currently limited data on the use of imepitoin in combination with
other AEDs; however, it has been used in combination with phenobarbitone,
potassium bromide, and levetiracetam without reported harmful clinical interac-
tions (Neßler et al. 2017; Royaux et al. 2017). If seizure control is inadequate in
dogs receiving 10–20 mg/kg of imepitoin twice daily, then the oral dose should be
increased to 30 mg/kg twice daily (Bhatti et al. 2015). If seizure control remains
inadequate, then phenobarbitone or potassium bromide can be added to the treat-
ment regime. The addition of an adjunctive medication was reported to improve
seizure control in 79% (phenobarbitone) and 69% (potassium bromide) of dogs
with idiopathic epilepsy that was refractory to imepitoin monotherapy (Royaux
et al. 2017). If the epilepsy is subsequently well controlled, then imepitoin with-
drawal over 3 months can be considered (20 mg/kg twice daily for 1 month, 10 mg/
kg twice daily for 1 month, 10 mg/kg once daily for 1 month). This did not result in
an increase in monthly seizure frequency in one study, and also improved the
adverse effects experienced by the dogs (Stee et al. 2017). Conversely, the addition
of imepitoin may improve seizure control in dogs with idiopathic epilepsy that is
resistant to treatment with phenobarbitone, with or without other adjunctive
medications (Neßler et al. 2017). A lower starting dose of 5 mg/kg twice daily is
recommended in these cases to reduce the incidence of adverse effects.
Serum level monitoring: No serum level monitoring is required as the blood
levels correlate poorly with clinical effect.
Adverse effects: Potential adverse effects are similar to other AEDs but are gen-
erally mild and transient. These may include ataxia, polydipsia, polyuria, poly-
phagia, sedation, apathy, hyperactivity, vomiting, diarrhoea, anorexia, and
hypersalivation. Aggression has been uncommonly reported and the use of
imepitoin should therefore be carefully considered in dogs with a history of
aggressive behaviour.
Adverse effects monitoring: Imepitoin does not induce hepatic enzyme eleva-
tion; however, a complete blood cell count and serum biochemistry is recom-
mended every 6–12 months in any dog receiving daily, long‐term medication.

c. Antiepileptic drug withdrawal

If an animal with idiopathic epilepsy becomes seizure‐free on medication, then
it can be difficult to know whether or when to attempt AED withdrawal. This
can be considered if the animal has been in remission (seizure‐free) for greater
154 A Practical Approach to Neurology for the Small Animal Practitioner

than 12 months. However, there will be an associated risk of seizure recurrence

and it can be difficult to regain seizure freedom if AEDs are subsequently re‐
introduced. A small study reported seizure recurrence in 7 out of 11 dogs in
which treatment had been stopped after a period of remission (Gesell et al.
2015). Only three of the seven dogs regained seizure freedom after resuming
AED therapy. Seizure recurrence after cessation of treatment also appears to be
common in cats that were previously in remission (Pakozdy et al. 2013). These
considerations should therefore always be discussed with the owner before the
decision is made to withdraw treatment.

d. Other antiepileptic medications

In recent years, there has been a trend in veterinary medicine towards the use
of novel AEDs from human medicine, particularly in cases that are refractory to
the veterinary licensed drugs discussed above. Examples of these medications
include felbamate, zonisamide, gabapentin, and levetiracetam. The original
branded formulations of these AEDs were often prohibitively expensive in the
majority of veterinary cases. However, the increased availability of generic for-
mulations means that their use is more feasible for many owners. It is important
to consider that, at the time of writing, there are no veterinary‐licensed versions
of these medications. Their use is therefore off‐label and the prescribing cascade
should be adhered to at all times. Owners should always be made aware when
any off‐label medication is prescribed to their pet, an information sheet regard-
ing the medication should be provided, and a disclaimer signed by the owner.
Potential advantages of these medications over phenobarbitone, potassium
bromide, and imepitoin include a reduced incidence of adverse effects and the
potential for a novel mechanism of action. This latter advantage may be useful
for treating seizures that are refractory to drugs with other common mecha-
nisms of action (e.g. GABA‐mediated inhibition). However, the short half‐life of
several medications (e.g. levetiracetam) means that they ideally need to be
administered three times a day to maintain adequate serum concentrations. This
may not be feasible for some owners in terms of both lifestyle and cost.

Levetiracetam
License: No authorised veterinary formulation in the UK.
Mechanism of action: Levetiracetam is thought to exert its anti‐seizure activity
via binding to a synaptic vesicle glycoprotein called SV2‐A and inhibiting the
release of excitatory neurotransmitters.
Clinical indications: Levetiracetam is most commonly used as a third‐line
adjunctive medication in dogs that have poor seizure control in spite of adequate
serum levels of phenobarbitone and potassium bromide (Volk et al. 2008). A
randomised, placebo‐controlled, crossover trial of levetiracetam for the treat-
ment of idiopathic epilepsy in 34 dogs that were refractory to phenobarbitone
and potassium bromide did not demonstrate a significant reduction in seizures
 Chapter 6 A Practical Approach to Common Presentations in General Practice 155

compared to placebo (Muñana et al. 2012). However, this study had a low power
and a number of dogs had levetiracetam plasma drug concentrations that were
below the lower limit of the suggested therapeutic range.
The efficacy of levetiracetam as an off‐label monotherapy in dogs is cur-
rently unknown. A small, single‐blinded, randomised, phenobarbitone‐con-
trolled trial of levetiracetam as a monotherapy for dogs with newly diagnosed
epilepsy did not report a significant difference in the monthly number of sei-
zures before and after treatment for the levetiracetam group (Fredsø et al.
2016). Five of the six dogs in the phenobarbitone group showed a >50% reduc-
tion in seizures per month, whilst none of the dogs treated with levetiracetam
fulfilled this definition of a responder. The use of levetiracetam as a monother-
apy in dogs with idiopathic epilepsy is therefore not currently advised. However,
the favourable adverse effect profile of levetiracetam means that its use has
been suggested for dogs with structural brain disease to avoid the additional
sedation and ataxia that may be associated with phenobarbitone administration
(Kelly et al. 2017).
Levetiracetam has been used anecdotally as a pulse treatment to reduce the
number of seizures per cluster in dogs with a tendency to experience cluster
seizures (Packer et al. 2015). The suggested regime, in addition to the dog’s daily
maintenance medications, is to administer a single 60 mg/kg oral dose immedi-
ately following a seizure. The drug is then continued at a lower dose of 20–30 mg/
kg per os three times a day until there have been no seizures for 48 hours. The
administration of levetiracetam is then stopped until further seizures are
observed.
Levetiracetam is well tolerated in cats (Bailey et al. 2008; Carnes et al. 2011),
and appears particularly effective in the management of audiogenic reflex sei-
zures (Lowrie et al. 2017). It has been suggested that the extended release for-
mulation can be used once daily in cats if three times daily dosing of the standard,
intermediate‐release formulation is not practical or feasible (Barnes Heller et al.
2018).
The intravenous formulation of levetiracetam is expensive but can be useful
in the management of acute cluster seizures and status epilepticus (Hardy et al.
2012) (see Chapter 7).
Contraindications: Severe renal disease.
Metabolism and excretion: Levetiracetam does not undergo hepatic metabolism
and 70–90% is excreted unchanged in the urine.
Starting dose: 20–30 mg/kg per os every 8 hours (every 12 hours for the
extended release formulation). Concurrent administration of phenobarbitone
has been shown to increase levetiracetam clearance in epileptic dogs, meaning
that increased oral doses of levetiracetam may be required in these cases
(Muñana et al. 2015).
Serum level monitoring: Infrequently performed but can be measured in ani-
mals with a poor response to treatment or if toxicity is suspected.
156 A Practical Approach to Neurology for the Small Animal Practitioner

Adverse effects: A serious adverse event has been reported following the rapid
intravenous administration of undiluted levetiracetam; therefore, care should be
taken during its preparation and administration (Biddick et al. 2018). Adverse effects
associated with oral administration are generally mild and include sedation or ataxia.
Adverse effects monitoring: A complete blood cell count and serum biochemistry
is recommended every 6–12 months in any dog receiving daily, long‐term
medication.

Zonisamide
License: No authorised veterinary formulation in the UK.
Mechanism of action: Numerous suggested mechanisms of action, including
blockade of voltage‐gated sodium and T‐type calcium channels, facilitation of
dopaminergic and serotonergic neurotransmission, enhancement of GABA
activity in the brain, and inhibition of glutamate‐mediated neuronal excitation.
Clinical indications: Zonisamide is primarily used as an adjunctive medication
in dogs or cats with seizures that are refractory to licensed AEDs (phenobarbi-
tone, imepitoin, and/or KBr).
Contraindications: Severe hepatic impairment and pregnancy.
Metabolism and excretion: Zonisamide is metabolised by the liver and primarily
excreted by the kidneys. The elimination half‐life is 15–17 hours in the dog.
Zonisamide is metabolised by the same hepatic microsomal enzymes that metab-
olise phenobarbitone, therefore the elimination half‐life is likely to be shorter in
dogs that are receiving both medications.
Starting dose: 5 mg/kg per os twice daily (monotherapy in dogs and cats),
10 mg/kg per os twice daily (add‐on therapy to phenobarbitone in dogs).
Serum level monitoring: Infrequently performed but can be measured in ani-
mals with a poor response to treatment or if toxicity is suspected.
Adverse effects: Adverse effects include sedation, ataxia, anorexia, and vomit-
ing. Uncommon adverse effects include hepatotoxicity and renal tubular acidosis
in dogs, and lymphadenopathy, hyperglobulinaemia, and cytopaenia in one
feline case report (Collinet and Sammut 2017).
Adverse effects monitoring: A complete blood cell count and serum biochemistry
is recommended after 1 month and then every 6–12 months if the animal is oth-
erwise well and the seizures are well controlled. Blood tests should be performed
immediately if the animal is unwell and there is a suspicion of an adverse
reaction.

e. Non‐pharmacological treatment options

Non‐pharmacological treatment options for canine and feline epilepsy include
dietary modification (Larsen et al. 2014; Law et al. 2015), and the implantation
of deep brain electrodes or vagus nerve stimulators (Long et al. 2014; Martlé
et al. 2016).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 157

A randomised trial of a commercially available, ketogenic, medium‐chain

triglyceride (MCT) diet was performed in 21 dogs that were on chronic AED
drug therapy for idiopathic epilepsy (Law et al. 2015). A reduction in seizure
frequency was reported in the dogs receiving the trial diet compared to those
receiving a standardised placebo diet. This study had low power but suggested a
potential role for MCT diets in the management of dogs with idiopathic
epilepsy.
The use of surgically implanted vagus nerve stimulators and deep brain elec-
trodes has been reported for the management of drug‐resistant epilepsy in cer-
tain human cases (Martlé et al. 2014). The high cost and complexity of implant
placement currently limits the use of these implants in veterinary medicine.
However, studies have demonstrated that their implantation appears to be safe
and feasible in dogs, and the availability of these interventions may become
more widespread in the future (Long et al. 2014, Martlé et al. 2016).

6.1.5 Refractory Epilepsy

Epilepsy is deemed to be refractory to treatment if an animal’s quality of life is
compromised by severe adverse effects of medication and/or frequent or severe
seizures in spite of appropriate drug therapy (i.e. drug serum levels at the upper
end of the therapeutic range). An estimated 25–30% of dogs with idiopathic
epilepsy may be refractory to treatment and owners should always be warned of
this possibility at the time of diagnosis. A history of cluster seizures appears to be
a risk factor for refractory epilepsy.
The underlying basis of refractory epilepsy is likely to be multifactorial and
will vary from case to case. Factors to consider should include:

• inadequate/inappropriate drug choice or dose

• poor owner compliance regarding administration of medications
• seizures related to changes in oestrogen and/or progesterone levels in entire
female dogs
• a change in patient size or weight
• an incorrect diagnosis (e.g. idiopathic epilepsy in a dog with a non‐epileptic
movement disorder or intracranial neoplasia)
• natural progression of an underlying disease (e.g. meningoencephalitis, intrac-
ranial neoplasia)
• dietary changes
• newly developed systemic disease.

The approach to these cases should include a review of the diagnosis and
previous investigations, measurement of serum drug levels if applicable (e.g.
phenobarbitone and potassium bromide), the addition of adjunctive AEDs if
appropriate, dietary modification, or referral for a specialist opinion.
158 A Practical Approach to Neurology for the Small Animal Practitioner

6.1.6 Seizure Management in the Home Environment

A small supply of rectal diazepam can be dispensed to the owner of any animal
that has a history of epileptic seizures. This can be administered per rectum at a
dose of 1–2 mg/kg in the event of a seizure lasting for longer than 2–3 minutes.
This ensures that medications are administered in the home environment before
the potential onset of status epilepticus. Owners will also feel reassured and
more in control of their pet’s condition if they have this medication at home or
in the car. As summarised above, levetiracetam can also be used as a pulse ther-
apy in animals with a history of cluster seizures.

6.2 ­Movement Disorders

Edward Ives

Involuntary motor activity is a hallmark of epileptic seizures, but there are a

number of other disorders that are also characterised by involuntary movement.
These ‘movement disorders’ are also known as dyskinesias, derived from ‘dys’
meaning abnormal, and ‘kinesia’ meaning movement. Movement disorders are
increasingly recognised in veterinary medicine and it is therefore important that
a general practitioner is aware of their existence. This ensures that they are not
mistaken for epileptic seizures and that the most appropriate tests and treatment
are chosen in the first instance. As discussed in Chapter 1, there are certain char-
acteristics of a movement disorder that can be useful to distinguish them from
epileptic seizures.

• An alert level of mentation throughout an episode, even if the involuntary

motor activity is affecting multiple limbs and/or both sides of the body (see
Video 33). If both sides of the body were affected by epileptiform seizure
activity, then this would imply involvement of both cerebral hemispheres
and it is highly unlikely that the level of mentation would remain normal.
• An absence of autonomic signs (e.g. salivation, urination, defecation).
• An episode duration that may be longer than expected for epileptic seizure
activity (e.g. >5–10 minutes).
• The absence of a post‐ictal phase, despite a long episode duration.

There are still many unanswered questions regarding movement disorders in

veterinary medicine, including the precise terminology that should be used to
describe them, how they should be classified, and how they may relate to similar
conditions in human medicine. Different forms of involuntary movement may
also occur concurrently, further complicating a simple framework for c­ lassification.
The aim of this section is to provide a basic summary of the different forms of
 Chapter 6 A Practical Approach to Common Presentations in General Practice 159

involuntary movement that may be encountered in dogs and cats. It is hoped that
this will allow the reader to more easily recognise a potential movement disorder
if an animal presents with a history of constant or episodic abnormal motor activ-
ity. The reader is referred to the Bibliography section for more in‐depth discus-
sion regarding this complex subject in both human and veterinary medicine
(Lowrie and Garosi 2016, 2017a,b; Urkasemsin and Olby 2015; Vanhaesebrouck
et al. 2013).
Involuntary movements of the limbs, head, or body can be classified accord-
ing to either their appearance (e.g. tremor, myoclonus) or their origin (e.g. mus-
cle, peripheral nerve, or central nervous system [CNS]). The broad categories of
involuntary movement that will be covered in this section are:

• tremors
• disorders of peripheral nerve hyperexcitability (fasciculations, myokymia,
neuromyotonia, tetanus, and tetany)
• myoclonus
• paroxysmal dyskinesias.

6.2.1 Tremors
A tremor can be defined as an involuntary, rhythmic, oscillatory movement of a
body part. These movements may vary in amplitude, but often have a specific
frequency for each disorder. Resting tremors, as observed in Parkinsonian move-
ment disorders in humans, have not been described in veterinary medicine. The
pathologic tremors observed in animals are therefore ‘action‐related’ and are
termed ‘kinetic tremors’ if they affect body parts involved in active movements,
or ‘postural tremors’ if they affect body parts involved in the maintenance of
posture against gravity (Lowrie and Garosi 2016).
Examples of kinetic tremors reported in veterinary medicine include:

• Intention tremors secondary to diffuse conditions affecting the cerebellum (e.g. degenera-
tive disorders, inflammatory or infectious diseases) – intention tremors predomi-
nately affect the head and are most noticeable during attempts to perform a
purposeful movement, such as eating or drinking from a bowl (see Video 11).
Further discussion regarding the approach to cerebellar disorders can be found
in Section 6.8 ‘Cerebellar Dysfunction’.
• Abnormalities of myelin production or development (hypomyelination or dysmyelina-
tion) – affected dogs typically show clinical signs of generalised body tremors
and ataxia when they first start to walk at 2–6 weeks of age. Any breed may
theoretically be affected but commonly reported breeds include the Springer
Spaniel, Samoyed, Chow Chow, Dalmatian, Weimaraner, and Bernese
Mountain Dog. If myelin development is delayed, and not absent, then a
spontaneous clinical improvement may be observed over the first year of life.
160 A Practical Approach to Neurology for the Small Animal Practitioner

• Idiopathic generalised tremor syndrome (see Video 7) – this condition results in an

acute onset of generalised body tremors that are exacerbated by excitement,
stress, or exercise (Wagner et al. 1997). It predominately affects young
(<2‐year‐old), small breed dogs and was previously known as ‘little white
shaker syndrome’ given its frequent occurrence in small, white dogs such as
Maltese Terriers. However, it may be observed in dogs of any breed and coat
colour and has also been reported in cats (Mauler et al. 2014). It is assumed to
represent an autoimmune inflammatory disorder, predominately affecting the
cerebellum, with an unknown trigger. MRI of the brain is usually normal but
CSF analysis may reveal an elevated protein and a mildly increased white
blood cell count. Infectious disease testing should be negative. The response to
immunosuppressive treatment using prednisolone is usually favourable (1 mg/
kg twice daily, tapering over weeks/months to the lowest dose required to
control the clinical signs).

Examples of postural tremors reported in veterinary medicine include:

• Orthostatic tremor – this condition most commonly affects young, giant breed
dogs (e.g. Great Danes) and results in high frequency tremors that are trig-
gered by standing and predominately affect the limbs (Garosi et al. 2005).
These tremors may result in difficulty standing or lying down but disappear
when the affected limbs are not bearing weight (see Video 13).
• Benign, idiopathic postural tremor – this condition affects the pelvic limbs of older
dogs when they are standing (see Video 14). These tremors are not visible dur-
ing movement and no treatment is advised. They may become more severe
with increasing age.
• Canine idiopathic head tremor syndrome – this condition is characterised by epi-
sodes of involuntary side‐to‐side or up‐and‐down head tremors that start and
stop spontaneously (see Videos 12 and 34). Affected animals are typically
young at the time of the first episode and are otherwise normal between
events. The condition can be observed in any breed, but English Bulldogs,
Dobermans, and French Bulldogs appear over‐represented (Guevar et al.
2014). Animals remain alert during the episodes, which can last for seconds,
minutes, or hours. Stress has been reported as a potential trigger factor for
some dogs. In contrast to typical epileptic seizures, animals with idiopathic
head tremors can be distracted at the time of an episode and the episodes will
often abate if the animal is given a toy or food. These episodes appear benign
and do not usually require treatment. Over 50% of affected dogs are reported
to show a spontaneous resolution over time and antiepileptic medications do
not appear effective in controlling the episodes. Episodic head tremors have
also been reported secondary to structural brain lesions (particularly those
involving the thalamus) and advanced imaging of the head should be always
 Chapter 6 A Practical Approach to Common Presentations in General Practice 161

be considered in these cases, particularly in dogs that are older at the time of
onset (e.g. >6 years old).

A tremor can be often recognised by its distinctive rhythmic, oscillatory

nature. If a tremor is suspected in general practice, then a high suspicion for a
specific disorder can often be made on the basis of the animal’s signalment, the
region of the body affected, and the onset of the tremors. A clinical approach to
tremors in dogs should therefore include the following considerations:

–– The part of the body that is predominately affected – head (intention tremors, idio-
pathic head tremors), limbs (orthostatic tremor, benign postural tremor), or
whole‐body tremors (hypomyelination, idiopathic generalised tremor
syndrome).
–– The age of the animal – hypomyelination in puppies, benign postural tremor in
older dogs.
–– Whether the tremors are unpredictable and episodic (e.g. idiopathic head tremors),
or only present at specific times (e.g. when standing for orthostatic tremor, or
when performing a purposeful movement for intention tremors).

6.2.2 Peripheral Nerve Hyperexcitability

Hyperexcitability of the peripheral motor nerves results in sustained or intermit-
tent contraction of the skeletal muscles. The level of mentation remains normal,
even if the entire body is affected, as the areas of brain responsible for wakeful-
ness are not involved. In contrast to the characteristic rhythmic, oscillatory
nature of a tremor, peripheral nerve hyperexcitability results in less regular
involuntary muscle activity that has a variable frequency, may be sustained, and
does not typically result in movement of the affected body part (Lowrie and
Garosi 2017). Different phenotypic variants have been described, each with their
own clinical and electrophysiological characteristics.

• Fasciculations – a flicker movement under the skin as a result of brief contrac-

tion of a small number of myofibres.
• Myokymia – rippling of the skin overlying a muscle that is affected by continu-
ous muscle contractions at a rate of 5–150 Hz.
• Neuromyotonia – generalised muscle stiffness, with delayed relaxation, that
persists during sleep or general anaesthesia and is seen as a consequence of
high frequency (150–300 Hz) motor nerve activity. Myokymia and neuromyo-
tonia are often observed concurrently as they generally represent a contin-
uum of the same underlying pathology (Vanhaesebrouck et al. 2013).
• Tetanus and tetany – sustained muscle contraction without relaxation, predomi-
nately affecting the extensor muscles. The term ‘tetanus’ is most commonly
162 A Practical Approach to Neurology for the Small Animal Practitioner

used to describe the increased extensor muscle tone seen following Clostridium
tetani infection, whilst the term ‘tetany’ is most commonly used to describe the
clinical signs resulting from hypocalcaemia.

The clinical signs associated with peripheral nerve hyperexcitability may be

restricted to a single cranial nerve or appendicular muscle(s), or they can be
generalised and affect the whole body.
Focal hyperexcitability may result from:

• local irritation to a peripheral nerve (e.g. following radiotherapy or compres-

sion by an adjacent vascular structure) (Rogatko et al. 2016)
• loss of central inhibition to peripheral nerve firing secondary to a focal brain
or spinal cord lesion (Holland et al. 2010).

Generalised clinical signs can occur secondary to a number of different

aetiologies:

• intoxications
• electrolyte disturbance (acute dehydration, hypocalcaemia)
• endocrine disorders (hypothyroidism, hypoadrenocorticism)
• neurodegenerative diseases
• hereditary or acquired disorders affecting the peripheral nerves and their asso-
ciated ion channels; voltage‐gated potassium channel dysfunction, disrupting
repolarisation and termination of the action potential, is postulated to be the
most frequent cause of generalised peripheral nerve hyperexcitability in
humans (Gilliam et al. 2014; Vanhaesebrouck et al. 2013).

The most widely described syndrome of generalised peripheral nerve

hyperexcitability in veterinary medicine is myokymia and/or neuromyotonia
affecting young Jack Russell Terriers (onset <3 years old) (Bhatti et al. 2011;
Vanhaesebrouck et al. 2010). These dogs are commonly also affected by the
hereditary condition spinocerebellar ataxia (SCA), reported in 84% of Jack
Russell Terriers with generalised myokymia and/or neuromyotonia in one
study. Spinocerebellar ataxia results in characteristic clinical signs of cerebel-
lar dysfunction, including hypermetria, truncal ataxia, head tremors, and
reduced menace responses. The myokymia that may be observed in these
dogs presents as rippling of the skin overlying affected muscles, and the neu-
romyotonia presents as transient episodes of severe generalised muscle stiff-
ness which may be fatal. This disorder should therefore be highly suspected in
a young Jack Russell Terrier that presents with this distinctive combination of
cerebellar signs and abnormal muscle activity. Generalised myokymia and/or
neuromyotonia has also been reported in two Yorkshire Terriers, one
Dachshund, a crossbreed dog, a Border Collie and one adult cat, with concur-
 Chapter 6 A Practical Approach to Common Presentations in General Practice 163

rent SCA only reported in the Dachshund (Galano et al. 2005; Vanhaesebrouck
et al. 2013).
If a disorder of peripheral nerve hyperexcitability is suspected from the clini-
cal history or physical examination, then a previous history of radiotherapy for
focal cases or toxin exposure in generalised cases should be excluded. Additional
investigations should include haematology, serum biochemistry, and endocrine
testing to exclude a metabolic disorder. Tetanus is usually a clinical diagnosis
made on the basis of identification of a wound or anaerobic focus of infection,
together with consistent clinical signs of focal or generalised increased extensor
muscle tone. Further investigations are often limited in general practice as they
rely upon complex electrophysiological testing, with or without advanced imag-
ing. Contacting a specialist centre for advice or referral is therefore advised in
these cases if possible.

6.2.3 Myoclonus
Myoclonus is the term used to describe a sudden, brief, involuntary, shock‐like
movement or ‘jerk’, which usually results in gross movement of the affected
body part(s) (Lowrie and Garosi 2017). Whilst rhythmic myoclonic movements
may appear similar to a tremor, tremors do not have an interval between move-
ments and lack the ‘shock‐like’ nature of a myoclonus. Disorders resulting from
peripheral nerve hyperexcitability also lack this brief and sudden nature, and
more commonly result in muscle rippling or sustained muscle contraction that
does not move the affected body part. The classification of myoclonus is complex
and remains controversial. A recent review on this subject in veterinary medi-
cine attempted to classify myoclonus as either ‘epileptic’ or ‘non‐epileptic’ based
upon the association with concurrent epileptic seizures or degenerative enceph-
alopathy (Lowrie and Garosi 2017).

1. Epileptic myoclonus
Myoclonic movements can be observed in association with several disorders that
also result in generalised epileptic seizures and/or progressive intracranial signs.

a. Lafora disease
Lafora disease is a late‐onset myoclonic epilepsy that is most widely recognised
in the Miniature Wire‐haired Dachshund, but has also been reported in Beagles,
Basset Hounds, and several other breeds (Swain et al. 2017). The median age at
the time of onset is 7 years old and dogs typically present with sudden jerking
head and neck movements in response to visual or auditory stimuli (see Video
3). It is a progressive disease that may also be accompanied by intermittent gen-
eralised tonic‐clonic seizures. A mutation in the EPM2B (NHLRC1) gene has
been demonstrated in Miniature Wire‐haired Dachshunds and a Beagle with
this condition. A gene test to confirm the presence of this causative mutation is
now commercially available.
164 A Practical Approach to Neurology for the Small Animal Practitioner

b. Neuronal ceroid lipofuscinosis

NCL is one of a group of lysosomal storage disorders that can result in myoclonic
seizures, in addition to other multifocal signs of neuronal degeneration such as
blindness, behaviour change, and cerebellar dysfunction. Breed‐specific gene
testing is commercially available for many NCL subtypes.

c. Feline audiogenic reflex seizures

This recently described condition predominately affects older cats and is com-
monly associated with myoclonic seizures triggered by high‐frequency sounds
(see Section 6.1 ‘Epileptic Seizures’) (Lowrie et al. 2016).

d. Myoclonic epilepsy of unknown origin in older dogs

Intermittent myoclonic movements, particularly affecting the head, may be
observed in older dogs that otherwise appear normal. Cavalier King Charles
Spaniels (CKCSs) are anecdotally over represented (see Video 35). Some dogs
may show a gradual cognitive decline over months to years, but it remains
uncertain as to whether this is related to the myoclonic episodes or is reflective
of an unrelated, age‐related canine cognitive dysfunction. Cardiac disease result-
ing in partial syncope, or structural epilepsy resulting in focal seizure activity,
should always be considered in these cases.

2. Non‐epileptic myoclonus
Constant, repetitive myoclonic movements of the limbs or facial muscles may be
observed in dogs that have recovered from CDV encephalomyelitis (see Video 36).
These movements can persist under general anaesthesia or during sleep. This
condition is most commonly encountered in the United Kingdom as a static
clinical sign in rescue dogs that have been imported from countries in which
routine CDV vaccination is less common. Affected dogs do not show associated
epileptic seizures, and an alternative cause for any reported seizure activity
should always be investigated in these cases.
A condition called ‘hemi‐facial spasm’ may also represent a form of
non‐epileptic myoclonic disorder. This condition is most commonly idiopathic
and results in spontaneous, intermittent, and sudden contraction of the facial
muscles on one side of the face. This is observed in the absence of facial paresis
or paralysis, and the palpebral reflex is therefore intact between episodes of con-
traction. This is in contrast to cases of chronic facial nerve paralysis with dener-
vation atrophy of the affected facial muscles. Referral for further assessment and
advanced imaging of the head is advised in these cases to exclude an underlying
structural cause for this unusual clinical sign.

6.2.4 Paroxysmal Dyskinesias

The paroxysmal dyskinesias are a large group of self‐limiting, episodic movement
disorders that, in light of their clinical presentation and episodic nature, are the
 Chapter 6 A Practical Approach to Common Presentations in General Practice 165

most likely of all movement disorders to be mistaken for epileptic seizures (De
Risio et al. 2015). Important differences between paroxysmal dyskinesias and an
epileptic seizure include the absence of autonomic signs during an episode of
dyskinesia, the maintenance of an alert mentation in spite of involuntary move-
ments affecting multiple limbs, and the fact that episodes may last significantly
longer than expected for an epileptic seizure (>5–10 minutes) (see Video 33).
The onset and cessation of involuntary movements are frequently abrupt for
dyskinesias, which also lack the post‐ictal disorientation, ataxia, restlessness, or
visual disturbance that typically follow epileptic seizures. The neurological
examination should be normal between episodes, as for idiopathic epilepsy.
A paroxysmal dyskinesia should therefore be considered in any animal that
is not responding as expected to treatment for epileptic seizures and the diagno-
sis reviewed at this time. Conversely, it is important to consider that movement
disorders and epilepsy can potentially co‐exist as separate conditions, without
the requirement for a shared pathophysiology. This may rarely be observed in
breeds with an apparent genetic predisposition for both idiopathic epilepsy and
paroxysmal dyskinesia (e.g. Labrador Retrievers), or in dogs with a long‐term
dyskinesia that acquire a new structural cause for epilepsy in later life (e.g.
intracranial neoplasia).
A number of different paroxysmal dyskinesias have been reported in veteri-
nary medicine, with their names frequently including the breed of dog in which
the condition was first recognised (Lowrie and Garosi 2017; Urkasemsin and
Olby 2014). However, irrespective of the breed, a paroxysmal dyskinesia should
be considered in any dog that presents for self‐limiting episodes of involuntary
muscle activity, without a loss of consciousness during the events.
Paroxysmal dyskinesias appear less common or poorly recognised in cats.
Drug‐induced dyskinesias have been rarely reported following the administra-
tion of phenobarbitone and propofol, underlying the importance of a complete
clinical history in these cases.
The diagnosis of a paroxysmal dyskinesia is often made on the basis of the
clinical history and the characteristics of an observed episode. With a few nota-
ble exceptions, further diagnostic testing is often unrewarding and expensive,
being primarily aimed at excluding other potential causes. Differential diagnoses
are similar to those listed for seizures in Section 6.1 ‘Epileptic Seizures’. In light
of the low diagnostic yield of investigations such as MRI and CSF analysis, it is
not unreasonable to make a presumptive diagnosis of a paroxysmal dyskinesia if
there is a consistent clinical history, a known disorder in that particular breed, a
normal neurological examination between episodes, and blood tests have
excluded a metabolic or endocrine cause for involuntary motor activity. However,
referral to a veterinary neurologist for further assessment and discussion regard-
ing the suspected diagnosis should always be offered to the owners of these dogs.
A short summary of the most common paroxysmal dyskinesias that may be
encountered in general practice is given below. The reader is referred to the
166 A Practical Approach to Neurology for the Small Animal Practitioner

Bibliography for more in‐depth discussion regarding the numerous paroxysmal

dyskinesias that are increasingly reported in veterinary medicine.

1. Paroxysmal gluten‐sensitive dyskinesia in the Border Terrier

This condition has been formerly referred to as ‘Spike’s disease’ and ‘canine
epileptoid cramping syndrome’. It can affect Border Terriers of any age (from
6 weeks to over 7 years old) but the majority of dogs have their first episode
before 3 years of age. The episodes typically present as stiffness, difficulty walk-
ing, apparent ataxia, tremors, abnormal muscle tone, and contraction of the
muscles of the neck or limbs (see Video 4). These episodes most frequently
affect all four limbs and last for between 5 and 30 minutes; however, they may
last for several hours in some cases. Gastrointestinal signs, such as vomiting,
diarrhoea, and borborygmi, may also be observed in around 50% of dogs, either
in close association with an episode or between episodes (Black et al. 2014).
A recent study demonstrated anti‐canine gliadin IgG and anti‐canine trans-
glutaminase‐2‐IgA antibodies in affected Border Terriers (Lowrie et al. 2015).
It was therefore concluded that this disorder represents a manifestation of glu-
ten sensitivity in the breed. This hypothesis was supported by a clinical
improvement and reduction in serum antibody levels after institution of a
strict gluten‐free diet. Testing for anti‐canine gliadin IgG and anti‐canine trans-
glutaminase‐2‐IgA antibodies is therefore recommended in Border Terriers
that present with episodic clinical signs consistent with a dyskinesia. However,
careful interpretation of these results is required. Antibody testing appears
highly specific for this condition, but false positive results can be seen in dogs
with other clinical manifestations of gluten sensitivity, such as gastrointestinal
disease or dermatological signs (Lowrie et al. 2016). These tests also lack sen-
sitivity, as in a study of 45 Border Terriers with presumed paroxysmal dyskine-
sia 16% of dogs had anti‐canine gliadin IgG levels within the control range and
9% had levels of anti‐canine transglutaminase‐2‐IgA antibodies within the
control range (Lowrie et al. 2018). Differential diagnoses for this condition
should include other causes of intermittent discomfort or reluctance to walk,
with or without gastrointestinal signs, such as spinal pain, pancreatitis, gastro‐
oesophageal reflux, or hypoadrenocorticism.

2. Episodic hypertonicity syndrome in Cavalier King Charles Spaniels

This condition has also been termed ‘episodic falling syndrome’ (Herrtage and
Palmer 1983). Clinical signs are usually first observed between 3 months and
4 years of age. Episodes are typically triggered by excitement, stress, or exercise
and are characterised by increased muscle tone in the pelvic and/or thoracic
limbs. This results in a crouched posture, difficulty walking, falling over, or lift-
ing of the thoracic limbs above the level of the head. These clinical signs abate at
times of rest and affected individuals appear otherwise normal. A mutation of
the brevican gene (BCAN) has been identified as the cause of this condition in
 Chapter 6 A Practical Approach to Common Presentations in General Practice 167

the Cavalier King Charles Spaniel (Gill et al. 2012). This gene encodes a proteo-
glycan complex that is required for normal axonal conduction and synaptic sta-
bility. The commercial availability of a gene test for this condition simplifies the
diagnosis in suspected cases, with further testing for alternative diagnoses rec-
ommended if the results are negative. The use of acetazolamide and clonazepam
has been reported as treatment for this condition, particularly if episodes are
adversely affecting the quality of life in an individual dog.

3. ‘Scottie cramp’ in Scottish Terriers

‘Scottie cramp’ is a form of paroxysmal dyskinesia that affects young Scottish
Terriers, with the majority of dogs showing their first episode at less than 1 year of
age (Urkasemsin and Olby 2015). Female dogs were over‐represented in one
study. Episodes are triggered by excitement, stress, or exercise and typically last for
between 5 and 20 minutes. Clinical signs vary in severity between individual dogs,
and range from skipping, bunny‐hopping, and kicking of the pelvic limbs during
exercise, to progressive lowering of the neck, arching of the spine, and increasing
spasticity of the limbs until the dog is unable to walk or falls over. The frequency
and duration of these episodes may spontaneously decrease over time, with or
without reduced exposure to known trigger factors. Fluoxetine has been used to
treat more severely affected cases with some reported success (Geiger and Klopp
2009). Patellar luxation and hip dysplasia are important differential diagnoses in
any young dog that presents with a skipping pelvic limb gait or bunny hopping. A
thorough orthopaedic examination should therefore always be performed in these
cases. A similar, milder form of exercise‐induced dyskinesia may be responsible for
the intermittent pelvic limb ‘skipping’ observed in some other small breed dogs in
which orthopaedic examination is normal (e.g. Jack Russell Terriers).

4. Paroxysmal nonkinesigenic dyskinesia in Labrador Retrievers and Jack

Russell Terriers
Affected dogs are typically young at the time of the first episode, with a reported
median age at onset of 2 years old for Labrador Retrievers and 4 years old for
Jack Russell Terriers (Lowrie and Garosi 2016). In some cases, the episodes may
not be observed until 8–10 years of age, potentially related to acquired condi-
tions acting as secondary trigger factors. The episodes of dyskinesia are charac-
terised by an acute onset of involuntary limb movements in the absence of
mentation change, autonomic signs, post‐ictal signs, or inter‐ictal abnormalities
(see Video 37). These episodes are self‐limiting and typically last for 2–10 min-
utes. They are most commonly observed in the home environment and may be
triggered by excitement, sudden movements, or being startled (Labrador
Retrievers), or by extremes of temperature (Jack Russell Terriers). The results of
extensive diagnostic investigations are unremarkable in these dogs. The natural
history of this condition appears to be regressive, with 75% of dogs showing
improvement and 32% entering spontaneous remission over a median follow‐
168 A Practical Approach to Neurology for the Small Animal Practitioner

up of 7.5 years in one study (39% of Labradors and 22% of Jack Russell Terriers).
Dogs showing clusters of episodes appear less likely to achieve remission (Lowrie
and Garosi 2016).
Similar forms of paroxysmal dyskinesia have been reported in other breeds
of dog (e.g. Chinook Dogs) and it is likely that many breeds are affected by these
under‐recognised disorders (Packer et al. 2010; Urkasemsin and Olby 2014).

6.3 ­Altered Mentation

Paul M. Freeman

Changes in mentation are common with neurological disease, and in some

situations may be the only abnormality seen. Any animal presenting with a his-
tory of altered mentation immediately provides both a diagnostic and manage-
mental challenge, and a careful, methodical, and logical approach is required to
ensure a successful outcome.

6.3.1 Definitions and Terminology

There are a plethora of terms associated with the field of mentation and behav-
iour, and this alone can lead to confusion and potential complications, particu-
larly when conversations between colleagues are required for in‐house or
external referral of patients. The term mentation may be used to describe the
animal’s level of consciousness as well as the appropriateness of its behaviour.
Some neurologists prefer the terms ‘consciousness’ and ‘behaviour’ rather than
mentation per se, and some like to divide mentation into the level of mentation
(consciousness) and the quality of mentation (behaviour).
For the purposes of this text, we will consider that the term mentation
describes both the level of consciousness and the behaviour of the animal. We will
look at consciousness and behaviour in turn, although in many situations both
may be affected, and an abnormality of mentation may be considered to include
either or both of these.

1. Consciousness (level of mentation)

There are also many terms used to describe an animal’s state of consciousness. In
general terms, what we are talking about is the animal’s awareness of its sur-
roundings and its responsiveness to external stimuli. An animal with a normal
level of consciousness may be described as being alert and the acronym BAR,
standing for ‘bright, alert, and responsive’, is the first entry in many consultation
notes. This is very reasonable, and in fact may be considered a part of the neu-
rological examination as well as the physical examination; an alert animal with
a normal level of consciousness should be bright and responsive to normal
 Chapter 6 A Practical Approach to Common Presentations in General Practice 169

external stimuli such as sounds, visual stimuli, touch, smell, people, and other
animals in the vicinity.
An animal that is able to walk, has generally normal reflexes and voluntary
movement, but which exhibits reduced responsiveness to external stimuli, may
be described as obtunded. Obtundation implies a reduced awareness or willing-
ness to respond to stimuli, although some response is still seen. The state of
obtundation may describe a wide range of reduced consciousness, from an ani-
mal that is just a bit ‘quiet’, through to an animal which prefers to lie in a corner
sleeping. The latter is still considered obtunded if it can be woken by noise or
touch. The term ‘depressed’ may be applied to animals in this state, but is best
avoided since its use has connotations of certain behavioural changes in humans
which may not strictly apply to an obtunded animal.
An animal whose level of mentation is so severely depressed that they are
only rousable with a noxious stimulus may be described as stuporous. Stupor
describes a very severely reduced level of mentation, where the animal does not
respond to touch, visual stimulation, or sound stimulation. However, the appli-
cation of a painful stimulus will rouse the animal at least for a short time.
Finally, animals may enter the state of coma, where their mentation is so
reduced that they are not rousable even with a noxious stimulus. Coma implies
severe pathology, often intracranial, and immediately demands a high level of
monitoring and urgent investigation. Comatose animals may show altered car-
diorespiratory parameters associated with brain lesions and/or raised intracra-
nial pressure (ICP), increasing the level of care required in the hospital
environment.

2. Behaviour (quality of mentation)

Behaviour may simply be classified as normal or abnormal for any individual ani-
mal in their current situation. This may be difficult to determine, since an animal’s
behaviour may be affected by stress and anxiety, and reference to the owner and
careful history taking may help the clinician to decide whether any observed
apparent behavioural abnormality is genuine or normal for the individual.
Behaviour consists of an animal’s normal performance of day‐to‐day func-
tions, and abnormalities may include changes in temperament, changes in sleep-
ing or eating pattern, excessive chewing or grooming, abnormal levels of anxiety
(especially in novel situations), excessive vocalisation, abnormal autonomic
activity (including sexual activity), and compulsive pacing, amongst other
things. Obsessive compulsive behavioural activities can be episodic, such as ‘fly
catching’ and tail chasing, and may also be described as part of an altered, abnor-
mal behaviour.
Whenever a behavioural abnormality is encountered as part of the present-
ing complaint, an attempt must be made to establish whether the particular
change(s) in question are part of a true neurological syndrome, or whether they
may be more correctly considered a purely ‘behavioural’ abnormality. For the
170 A Practical Approach to Neurology for the Small Animal Practitioner

purposes of this text, we are concerned only with genuine neurological disease,
and not with primary behavioural disease. However, it is often difficult to be
sure whether an observed or reported abnormality of behaviour could have an
underlying neurological cause. Once again careful history taking may give clues
regarding the development of a behavioural problem, and perhaps the reasons
why it has developed, and in many situations the advice of a properly trained
animal behaviourist can be helpful.
Episodic behavioural abnormalities, especially obsessive or compulsive
behaviours such as ‘fly catching’ (see Video 5), can in some instances be a mani-
festation of a focal seizure disorder. A simple test that can be applied to deter-
mine whether a behaviour pattern is more likely to be behavioural or potentially
neurological in origin, is whether the behaviour can be interrupted in any way
once started. Focal seizure activity should not be interruptible, whereas obses-
sive compulsive behaviours often are (see also Section 6.1 ‘Epileptic Seizures’).
Furthermore, it is also common for primary behavioural issues to have a more
distinct pattern in terms of when they occur, such as in response to certain stim-
uli or in the presence (or absence) of a specific person. In contrast, neurological
behavioural disturbances are more commonly random and unpredictable.
A very specific form of behavioural disturbance is the so‐called rapid eye move-
ment (REM) sleep disorder, in which dogs can develop abnormal behaviour pat-
terns during REM sleep (see Video 9). This may include violent movements,
barking and growling, chewing, biting, or howling. These episodes can develop
at any age and may occur during daytime naps as well as during night‐time
sleep. In one study, 78% of cases responded to oral potassium bromide adminis-
tration, indicating the possibility that this may be a seizure disorder (Schubert
et al. 2011). A recent paper found an association between REM sleep disorder
and dogs recovering from tetanus (Shea et al. 2018).

6.3.2 Neuroanatomic Localisation

An animal’s level of consciousness and behaviour are governed by both intrinsic
and extrinsic factors to the CNS. For a normal level of consciousness, neurons in
the ascending reticular activating system (ARAS) of the brainstem and the thala-
mus (processing centre) must all be functioning normally. The ARAS lies deep
within the brainstem and receives all kinds of sensory information from the
body, before projecting this information into the thalamus. The thalamus is then
responsible for diffusely stimulating the entire cerebral cortex. Therefore, lesions
affecting the deeper parts of the brainstem or the thalamus may cause a reduced
level of consciousness.
An animal’s behaviour is governed more by the cerebral cortex, with the
sensory cortex being responsible for the animal’s perception of its environment.
This explains why animals with unilateral cerebral cortical lesions may circle or
turn their heads towards the side of the lesion; the cerebral cortex receives infor-
mation from the contralateral side of the body, therefore the animal will circle or
 Chapter 6 A Practical Approach to Common Presentations in General Practice 171

turn towards the side of its environment which it is still able to perceive (see
Chapter 4). The limbic system, consisting of regions within the thalamus, the
deep cerebral cortex, and parts of the brainstem such as the amygdala, hip-
pocampus, and hypothalamus, is responsible for emotional and visceral responses
and behaviour, and perhaps the more ‘hard‐wired’ behaviours such as copula-
tion and sleep/wake cycles.

6.3.3 Diagnostic Approach to Altered Mentation

A reduced level of consciousness indicates a potential intracranial lesion, most
often affecting the brainstem (ARAS) or thalamus. However, it is very impor-
tant to remember that extracranial disease may also result in reduced con-
sciousness. A recent, large retrospective study of dogs and cats that presented
to an emergency clinic because of stupor or coma revealed that although the
commonest cause was head trauma, a significant percentage of these animals
were suffering from some kind of systemic disease, in particular hypoglycae-
mia (Parratt et al. 2018). For this reason, the initial approach to any animal
presenting with altered mentation should consider both intracranial and
extracranial possibilities.

1. Clinical history
As in most situations, the first step should be acquiring a relevant clinical history.
Depending on the degree of concern, this may be more or less shortened accord-
ing to time available. However, several key questions must be answered.

a. General history
Apart from the usual questions concerning appetite, drinking, vaccination, travel
status, antiparasitic treatments, and so on, there are a number of key questions
relating to the presentation of altered mentation.

1. Is there any possibility of trauma? If the patient involved is feline, the answer
may be ‘possibly’ or ‘not sure’. For most canines, the owner can be more cer-
tain that this is not the case. In either case, if the patient is obtunded rather
than stuporous or comatose then it is reasonable to allow time for a complete
history taking and examination. If the patient is presented with a more
severely depressed mentation and a history of possible head trauma, action
may need to be taken more rapidly to deal with the possibility of brain injury.
2. Is there any possibility of intoxication? In any case of altered mentation, consid-
eration must be given to the possible ingestion of recreational drugs such as
cannabis. Careful questioning around the owners’ dog‐walking habits may
reveal the possibility that the dog has scavenged discarded cannabis‐contain-
ing material. Owners may be reluctant to admit to the possession of illegal
recreational drugs in the home, so this line of questioning must be carried out
in a sensitive way in order to gain maximum information.
172 A Practical Approach to Neurology for the Small Animal Practitioner

3. Is the animal in otherwise good health, or is it currently receiving medications? In

particular, care should be taken with animals which are diabetic and receiv-
ing insulin, as an overdose leading to hypoglycaemia may lead to a presenta-
tion of altered mentation. Endocrine disorders, such as hypothyroidism and
hypoadrenocorticism, may also lead to an obtunded level of mentation. An
animal which is in significant pain may occasionally present in an apparent
state of mild obtundation (e.g. orthopaedic pain from osteosarcoma or severe
osteoarthritis, visceral pain secondary to pancreatitis, spinal pain from chronic
intervertebral disc disease).

b. Specific neurological history

1. Onset – When did the problem start? Was it an acute onset of mentation
change, or has it come on more gradually? Did anything specifically seem to
precipitate the change (such as possible trauma or toxin ingestion)? Did the
owner notice any other changes accompanying the change of mentation
which may indicate systemic disease?
2. Progression – Since the owner first noticed their pet’s reduced consciousness, has
the problem remained static, got worse, improved, or does it wax and wane?
3. Pain – Does the owner perceive their animal to be in pain? Determining
whether an animal has a headache, particularly from physical examination,
can be very difficult. In many cases of intracranial disease, it is likely that a state
of obtundation may be brought about by head pain rather than specific effects
on the anatomical structures responsible for maintaining alertness. Therefore,
gaining the owner’s insight, questioning whether there has been any vocalisa-
tion for instance, or any anorexia or even nausea, may assist the veterinarian
in understanding the presence or absence of pain in this situation.
4. Response to medication – If the animal has been seen before, did it receive any
medications and, if so, did they lead to any improvement? Again, this ques-
tion must be phrased correctly in order to gain the appropriate response,
since owners will often reply that a medication was not beneficial because,
even if there was an obvious initial improvement, the effect was not perma-
nent. In particular, a response to corticosteroids may indicate the presence of
brain oedema or inflammation, or even that the animal may be hypoglycae-
mic or suffering from hypoadrenocorticism. A response to analgesics may
support a suspicion of headache or some other pain leading to the animal’s
mentation change.

2. Signalment
The age of the animal may give a clue that a certain disease category is more
likely to explain the clinical presentation than another, for example increasing
age leading to an increased suspicion of intracranial neoplasia. Animals which
 Chapter 6 A Practical Approach to Common Presentations in General Practice 173

present with obtundation at a very young are more likely to be suffering from a
metabolic disease or perhaps even a congenital problem.
An awareness of certain breed predilections is always helpful when trying to
establish an appropriate list of differential diagnoses (see Chapter 2). In the case
of obtundation, the Cavalier King Charles Spaniel and Greyhound have been
shown to be over‐represented in cases of stroke; smaller terrier breeds are more
commonly affected by immune‐mediated inflammatory disease of the brain
(meningoencephalitis of unknown origin, MUO), with Chihuahuas, Yorkshire
Terriers and Pugs suffering from specific forms such as necrotic meningoen-
cephalitis (NME) in the case of Pugs and Chihuahuas, and necrotic leucoen-
cephalitis (NLE) in the case of Yorkshire Terriers; Chihuahuas are predisposed to
hydrocephalus; Yorkshire Terriers are prone to portosystemic shunting and
hepatic encephalopathy; and Boxers are predisposed to intracranial neoplasia.
There are also many other breed‐specific degenerative conditions which may
lead to an altered mentation, although rarely in the absence of other neurological
signs.

3. Physical examination
A full general physical examination should be performed in all cases of altered
mentation. Specific attention should be paid to the cardiorespiratory system,
since raised ICP may lead to changes in breathing patterns and/or cardiovascular
parameters. These changes are rare, however, and usually only occur in extreme
states. More importantly, examining for evidence of systemic disease such as
anaemia, pyrexia, and abdominal pain may give vital clues as to the cause of the
patient’s altered mental state. Checking for evidence of lymphadenopathy, for
any signs of unknown trauma, and at the same time observing the animal’s
response to being examined can also be rewarding. Careful examination for evi-
dence of petechiae or ecchymoses, or overt bruising, is also important, since
coagulopathy or trauma may have led to intracranial haemorrhage. Where pos-
sible and when time allows, fundoscopic examination should be performed to
look for signs of retinal haemorrhage, which could indicate hypertension or a
coagulopathy, and optic disc swelling, which can occur with raised ICP.

4. Neurological examination
A complete neurological examination is ideal in all cases of suspected neurologi-
cal disease, but the clinician will sometimes need to modify this approach
because the animal is uncooperative, is unable to perform all aspects of the
examination, or due to time constraints. This rarely limits the possibility of mak-
ing at least some sort of neuroanatomical localisation, which is the purpose of
the examination. As stated in Chapter 3, an understanding of the possible and/
or likely neuroanatomical localisations for any given presentation means that
the examination can, if needed, be tailored towards identifying the presence or
absence of key deficits.
174 A Practical Approach to Neurology for the Small Animal Practitioner

In cases of altered mentation, as already stated, the potential neuroanatomi-

cal localisations for primary neurological disease are intracranial and may
involve either the brainstem or forebrain. Therefore, the focus of the neurologi-
cal examination should be on performing tests which may identify potential
disease in these locations.
Mentation: This is the reason for the presentation. However, the clinician
should continuously observe the patient throughout the consultation in order to
form an opinion about the true state of the animal’s mentation, allowing for the
effects of stress and anxiety.
Gait and posture: The animal may have normal posture or may have low head
carriage, or potentially head tilt or turn. An attempt should be made to observe
the animal’s gait. Most obtunded animals should be physically able to walk,
although many will refuse to do so (especially cats). Owners often have video
clips of their animal taken in the home environment, which may be helpful in
these situations. Many cases of forebrain disease have a surprisingly normal gait,
even in the presence of relatively large lesions, but there may be evidence of
tetra‐ or hemiparesis, compulsive pacing, or circling. In brainstem disease, there
is often moderate to severe ataxia, again with hemi‐ or tetraparesis. Circling may
also be apparent, especially if there is any vestibular involvement. Generalised
weakness may be present in cases of systemic disease, which may be difficult to
distinguish from genuine tetraparesis.
Postural reactions: The author finds the paw replacement test to be the most
consistent and reliable when looking for evidence of proprioceptive deficits.
However, other tests, such as hopping, can also be very useful when looking for
subtle deficits (see Chapter 3). Remember that proprioceptive responses require
the entire nervous system to be functioning, and therefore they are a sensitive
but non‐specific part of the neurological examination. In general, with asym-
metrical brain lesions, forebrain disease will lead to contralateral postural reac-
tion deficits, whereas brainstem disease causes ipsilateral deficits. As with other
parts of the examination, great care must be taken when interpreting postural
reaction testing, since a severely obtunded or painful animal may show apparent
deficits which are not caused by a proprioceptive failure, but by a reluctance to
perform the test.
Cranial nerves: The reader should refer again to Chapter 3 for a full explana-
tion of how to perform a cranial nerve examination with the minimum of stress
and ‘hands‐on’ testing. For obtunded animals in particular, maximum use of
observational skills should be made to gain information regarding the cranial
nerves. If forebrain disease is suspected, the menace response and nasal planum
nociception tests should always be performed if possible, since these are both
conscious responses that require forebrain involvement. All other cranial nerve
tests involve brainstem reflexes, and abnormalities may therefore point to a
structural brainstem lesion. In the case of structural disease, one may see deficits
in consecutive cranial nerves on the same side of the brain; deficits which point
 Chapter 6 A Practical Approach to Common Presentations in General Practice 175

to isolated cranial nerve problems, particularly if bilateral, are more likely to

indicate peripheral nerve disease.
Spinal reflexes: In cases of altered mentation, this is potentially the least useful
part of the neurological examination. One would not expect deficits of spinal
reflexes in cases of intracranial disease, unless the disease is multifocal and also
involves the spinal cord intumescences. However, if an animal appears genu-
inely weak then the pedal withdrawal reflexes should always be assessed, since
occasionally a peripheral localisation (such as botulism or acute fulminating
myasthenia gravis) may present with an apparently obtunded mentation.
Palpation: In the majority of cases, palpation for the presence of pain will be
unrewarding, but it should always be carried out in order to exclude the possibil-
ity that the animal’s altered mentation is actually caused by chronic or severe
pain.

6.3.4 Obtundation
1. Neuroanatomical localisation
As already stated, the two possible neuroanatomic localisations for primary neu-
rological causes of altered mentation are the forebrain and the brainstem. The
results of the neurological examination may confirm the likelihood of one of
these locations, but it is also possible, particularly in the case of forebrain disease,
that the remainder of the neurological examination is normal. In this case, the
clinician must remain open to the possibility of extracranial disease, whilst also
being aware that intracranial disease is not ruled out by such a neurological
examination.

2. Differential diagnoses
Broadly speaking, the possible causes of intracranial disease are similar for both
forebrain and brainstem, and therefore the differential diagnoses will be similar in
the case of either neuroanatomical localisation. Additional information from the
clinical history and signalment should allow the clinician to formulate a list of likely
and possible differential diagnoses for intracranial disease. These may include
vascular disorders (e.g. stroke), inflammatory or infectious disease (e.g. menin-
goencephalitis of unknown origin), head trauma, anomalies (e.g. hydrocephalus),
metabolic (e.g. hepatic encephalopathy, hypoglycaemia, shock), neoplastic disor-
ders, and degenerative disorders (e.g. storage diseases).

3. Formulating a plan
The decision whether to start with in‐house investigations or to immediately
refer for further investigation by a specialist is one which requires discussion
with the owner, and in many cases referral may not be an option for financial or
logistical reasons. Immediate referral should be considered, if possible, in cases
where the neurological examination reveals clear evidence for an intracranial
structural lesion. The one exception to this may be in situations where a vascular
176 A Practical Approach to Neurology for the Small Animal Practitioner

cause (e.g. stroke) is highly suspected from the clinical history and/or physical
examination findings, in which case further in‐house investigation of potential
underlying cases may be justified.
If the remainder of the neurological examination is normal, it is certainly
reasonable to consider further investigations in‐house, which may be similar to
those recommended in cases of seizures (see Section 6.1 ‘Epileptic Seizures’).
Investigations that could be performed might include:

• Haematology, serum biochemistry, and urinalysis.

• Blood pressure testing. If this is persistently elevated, an ACTH stimulation test
may be justified, especially with supporting clinical and biochemical features
of hyperadrenocorticism.
• Bile acid stimulation testing +/− serum ammonia, particularly if hepatic encepha-
lopathy and a portosystemic shunt is suspected.
• Thyroid function testing – total thyroid hormone (T4), free T4, TSH.
• Fructosamine, glucose, and insulin levels if an insulinoma is suspected.
• A coagulation profile and testing for Angiostrongylus vasorum if a disorder of blood
clotting is suspected.
• Infectious disease testing dependent on the species and relative risk of expo-
sure – T. gondii in cats and dogs, N. caninum or canine distemper virus in dogs,
FeLV, FIV, and feline coronavirus in cats.
• Urine metabolic screening if an inborn error of metabolism is suspected (e.g.
young animal with progressive neurological disease).
• Toxicology for known or suspected toxin exposure.
• Thoracic radiography, abdominal ultrasonography, or thoracic and abdominal
CT – particularly if neoplasia is likely.

If a diagnosis of systemic disease is confirmed, then treatment should be

directed at resolving the underlying disease and then assessing whether this
leads to an improvement in the animal’s mentation. Where in‐house investiga-
tions do not reveal the diagnosis, referral for potential advanced imaging of the
brain and CSF analysis should always be offered, since it is possible to have a
large intracranial structural lesion in the forebrain with minimal effects on the
neurological examination.

4. Raised intracranial pressure (ICP)

In any case with an obtunded level of mentation, consideration should be given
to the possibility of raised ICP; signs may include a reduced level of conscious-
ness, altered brainstem reflexes (especially pupillary light reflexes and vestibulo‐
ocular reflexes), and altered motor function. This topic will be covered more
extensively in Chapter 7, but it is important to be aware that mild rises in ICP
may only lead to obtundation with minimal other signs. Direct or indirect meas-
urement of ICP is difficult and in a first‐opinion practice without access to
 Chapter 6 A Practical Approach to Common Presentations in General Practice 177

advanced imaging and specialist monitoring equipment, diagnosis may only

ever be presumptive. If advanced imaging is not available, treatment should ide-
ally be directed at correcting the underlying disease suspected to be responsible
for the abnormal mentation. However, careful monitoring should be performed,
particularly in cases of suspected stroke, head trauma, or inflammatory disease,
and if the animal’s neurological status appears to be deteriorating then specific
treatment may normally be safely instigated with the purpose of reducing a sus-
pected ICP elevation. In emergency or rapidly deteriorating situations, this
entails administering a bolus of either hypertonic saline or mannitol. Dose rates
may be found in the Chapter 7 section on head trauma; it is always important to
follow administration with adequate crystalloid fluid therapy to avoid systemic
dehydration.

Animal presented with OBTUNDATION

obtundation

History and signalment to

create list of differentials

Rest of neurological Abnormal

examination normal neurological Refer for advanced
examination imaging
Perform in-house
tests to look for
systemic illness
No diagnosis made

Diagnosis confirmed

Treat systemic illness

Approach to cases of obtundation in practice.

The following section is aimed at providing advice and guidance in situations where
further referral is not an option and where the diagnosis is unclear or can only be
suspected.
For treatment of specific medical conditions, the reader is directed to consult
an appropriate textbook on internal medicine.

5. Treatment of specific suspected causes of obtundation

a. Stroke
Cerebrovascular disease (ischaemic stroke) most commonly presents as an acute
onset of cerebellar/vestibular dysfunction resulting from involvement of the vas-
178 A Practical Approach to Neurology for the Small Animal Practitioner

cular supply to the cerebellum. However, if a cerebral artery is occluded and the
forebrain is affected, then stroke may result in a peracute onset of altered menta-
tion and frequently asymmetrical neurological deficits. If referral for advanced
imaging to confirm the diagnosis is not possible, then investigations and treat-
ment should be directed at identifying and correcting any underlying predispos-
ing factors. If the animal has presented with significant obtundation, the
possibility of raised ICP should always be considered.
Correction of underlying factors:

1. Coagulopathy: If the animal has an unknown antiparasiticide status and/or

tests positive for the presence of A. vasorum, an appropriate antiparasitic treat-
ment should be administered. If rodenticide ingestion is suspected, this should
be further investigated and treated with administration of vitamin K as appro-
priate. Other suspected coagulopathies, such as immune‐mediated thrombo-
cytopenia, will require further investigations for diagnosis and instigation of
immunosuppressive therapy if confirmed.
2. Hypertension: In cases where significant systemic hypertension is identified
(MAP persistently greater than 180 mmHg), use of an antihypertensive medi-
cation such as amlodipine should be considered. Factors predisposing to
hypertension include chronic renal disease and hyperadrenocorticism, and
these should be appropriately investigated and treated if identified.

It is important to bear in mind that hypertension can affect the brain in

two ways; firstly, it may predispose to haemorrhagic stroke, but secondly it
can also lead to a specific hypertensive encephalopathy which may present
with obtundation as the main or only clinical sign. Diagnosis of hypertensive
encephalopathy can be difficult, and in some cases the diagnosis is presump-
tive based on response to antihypertensive medication. Animals usually
improve rapidly with resolution of the hypertension, and the prognosis is
relatively favourable.

b. Hydrocephalus
If hydrocephalus is suspected to be the most likely cause of altered mentation
based upon the physical appearance, age, and breed of the animal, and if sys-
temic illness has been excluded and advanced imaging for confirmation is not
possible, then starting medical treatment may be appropriate. The focus of such
treatment is reduction in the production of CSF. The most effective medication
at achieving this, and the only one with good evidence for efficacy, is corticoster-
oid. Therefore, initiating treatment with prednisolone at a starting dose of
0.5 mg/kg twice daily may be reasonable. In mild cases, the prognosis can be
good, with significant improvement in the animal’s demeanour following initia-
tion of steroid therapy. A recent paper found little difference in outcome between
dogs treated medically and surgically for congenital hydrocephalus, with roughly
 Chapter 6 A Practical Approach to Common Presentations in General Practice 179

half of dogs having a positive outcome in both the medically and surgically
treated groups (Gillespie et al. 2019).
It is important to remember that corticosteroids have multiple effects, and in
cases where diagnosis is presumptive and not confirmed by advanced imaging
+/− CSF analysis, there is always the possibility that one may be dealing with a
different disease process (e.g. sterile inflammatory brain disease). Infectious dis-
ease of the CNS is rare and therefore, whilst still a risk, deterioration due to the
potentially immunosuppressive effect of corticosteroid is unlikely. It should also
be considered that the use of corticosteroid may complicate or even preclude the
possibility of making a diagnosis if referral were subsequently pursued; the pres-
ence of inflammatory cells in the CSF may be reduced or altered, and previous
corticosteroid administration may alter the changes observed on brain MRI.

c. Cannabis intoxication
If intoxication with cannabis, or a similar recreational drug, is suspected from
the clinical history and presenting signs, treatment is largely supportive. A large
recent study found that ataxia and obtundation were the most common present-
ing signs in dogs with a known history of marijuana intoxication, with almost
half of cases also showing acute dribbling urinary incontinence (Meola et al.
2012).
As for most suspected intoxications, treatment involves reducing exposure
by inducing emesis if it is considered safe and ingestion has occurred within
30–60 minutes. Administration of activated charcoal to reduce further absorp-
tion, and potentially administration of intravenous lipid emulsion can be per-
formed as cannabinoids are extremely lipophilic. Supportive care involves the
use of intravenous fluid therapy and general nursing to ensure animals are kept
clean, dry, and warm. Specific medications which may be helpful can include
anxiolytics, such as acepromazine or butorphanol, and antiepileptic medications
if seizures occur, such as diazepam or phenobarbitone. The prognosis is generally
good, with most affected animals recovering within 1–2 days.

d. Neoplasia
If intracranial neoplasia is suspected based upon the signalment, history, and
neurological examination but cannot be confirmed with advanced imaging,
owners must be aware of the potential for a guarded prognosis (for example, a
10‐year‐old Boxer Dog with seizures and slowly progressive intracranial signs,
including obtundation). Extracranial disease (e.g. insulinoma) should always be
excluded first, and thoracic radiographs +/− abdominal ultrasound can be per-
formed to look for evidence of primary neoplastic or metastatic disease. If these
investigations are normal and it is firmly established that referral is not possible,
then palliative treatment with corticosteroids can be considered. Prednisolone at
a dose of 0.5 mg/kg twice daily may be effective in the short to medium term by
reducing any peritumoural oedema and may also provide some analgesic effect
180 A Practical Approach to Neurology for the Small Animal Practitioner

if a structural intracranial lesion is present. In addition, specific analgesics such

as paracetamol, gabapentin, and tramadol may also be useful. Antiepileptic
medications should be used if there is a history of epileptic seizures. Prognosis
remains guarded, with the median survival time for dogs with intracranial neo-
plasia treated symptomatically being around 2 months (Hu et al. 2015).

6.3.5 Coma and Stupor

1. Differential diagnoses
Any animal that presents in a state of coma or stupor represents a clinical and
neurological emergency. It is therefore important to have an understanding of
the potential causes of coma and stupor. A relatively large study published in
2018 provided an overview of the causes that were identified in one emergency
referral centre (Parratt et al. 2018); the most common identified cause was head
trauma, with hypoglycaemia, shock, and systemic disease also being relatively
common.
The general approach to achieving a list of differential diagnoses is the same
as described above for obtundation. However, for animals presenting in a state
of stupor or coma, the clinical history taking may need to be more rapid due to
the potential emergency nature of the situation, and the performance of a com-
plete neurological examination may be more difficult since assessment of gait
and postural reactions is unlikely to be possible. A complete physical examina-
tion should always be performed to investigate the potential for systemic disease
and since cardiorespiratory abnormalities are more likely in cases of significant
head trauma.

2. Formulating a plan
Initial patient assessment using the modified Glasgow Coma Scale (MGCS), as
described in (Box 6.3.1), has been proposed as a means to provide an initial
objective assessment and to provide a baseline from which monitoring can be
performed.
One study has correlated the MGCS on admission with survival in dogs suf-
fering from head trauma, with a 50% survival to 48 hours in dogs with a score
of 8 (Platt et al. 2001). However, there are some considerations with the use of
this scale: there is clearly a degree of subjectivity regarding the brainstem
reflexes, and even the motor activity may be difficult to consistently categorise
since it may be variable, and true decerebrate rigidity (mentioned in level 5)
could also be described well by the situation corresponding to level 2 of motor
activity. Furthermore, the use of the terms ‘depression’, ‘delirium’, and ‘semi‐
comatose’ does not fit well with the terminology and descriptions currently
accepted within veterinary neurology and, again, an allowance for observer
interpretation must be made. The scale does, however, provide some level of
objectivity in the monitoring of animals presented with suspected head trauma
and is a method of monitoring response to treatment interventions.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 181

Box 6.3.1 Modified Glasgow Coma Scale.

Score

Motor activity
Normal gait and spinal reflexes 6
Hemiparesis, tetraparesis, or decerebrate activity 5
Recumbent, intermittent extensor rigidity 4
Recumbent, constant extensor rigidity 3
Recumbent, constant extensor rigidity with opisthotonus 2
Recumbent, hypotonia, depressed, or absent spinal reflexes 1
Brainstem reflexes
Normal PLR and vestibulo‐ocular reflexes 6
Slow PLR and normal to reduced vestibulo‐ocular reflexes 5
Bilateral unresponsive miosis with normal to reduced vestibulo‐ocular reflexes 4
Pinpoint pupils with reduced to absent vestibulo‐ocular reflexes 3
Unilateral, unresponsive mydriasis with reduced/absent vestibulo‐ocular reflexes 2
Bilateral unresponsive mydriasis with reduced/absent vestibulo‐ocular reflexes 1
Level of consciousness
Occasional periods of alertness and responsive to environment 6
Depression or delirium, capable of responding but response may be inappropriate 5
Semi‐comatose, responsive to visual stimuli 4
Semi‐comatose, responsive to auditory stimuli 3
Semi‐comatose, responsive only to repeated noxious stimuli 2
Comatose, unresponsive to repeated noxious stimuli 1

In‐house investigations that may be considered in cases with stupor or coma

are very similar to those described for obtundation. It should be remembered
that cases of coma and stupor caused by primary intracranial disease are more
likely to be suffering from elevated ICP, and therefore controlling this in order to
maintain cerebral blood flow may be vital to the prognosis. Management of head
trauma in dogs and cats is described in Chapter 7 and the reader is referred to
this chapter for a more detailed understanding of the approach to traumatic
brain injury.
For other possible causes of coma and stupor, the major differential diagnoses
are the same as for obtundation, with systemic illness being a major considera-
tion. Therefore, routine blood tests, urinalysis, and blood pressure measurement
should be performed in every case. Supportive care, restoration of circulating
blood volume in cases of shock, maintaining systemic blood pressure, and occa-
sionally the use of hyperosmolar solutions aimed at reducing ICP may all be
important in such cases. Ultimately, the prognosis is dependent on the underly-
ing aetiology, but successful management of cases presenting as stuporous or
comatose requires both an understanding of possible aetiologies and a recogni-
tion of the physiological factors which can play a role in maintenance of adequate
182 A Practical Approach to Neurology for the Small Animal Practitioner

cerebral blood flow. Referral to an establishment where adequate critical care

can be provided, alongside advanced imaging and monitoring, should always be
considered when possible, as long as the animal is considered stable enough to
travel.

6.3.6 Behavioural Abnormalities

If an animal presents with an abnormal quality of mentation or behaviour there
are some key considerations, as previously discussed. There must be an attempt
to evaluate whether the problem is primarily neurological or is actually behav-
ioural (i.e. a psychological or obsessive compulsive disorder which may have
causes and treatments lying outside of the scope of experience of the neurologist
or general practitioner). If this is thought likely or possible, and the rest of the
physical and neurological examination is normal, then referral to a suitably
qualified veterinary behaviourist may be the best solution.
If the behavioural abnormality is episodic or paroxysmal in nature, then
there may be the possibility that it is a manifestation of focal seizure activity. In
this case, the same approach as for seizure investigation should be followed (see
Section 6.1 ‘Epileptic Seizures’). Videos of the episodes may also be particularly
useful in such cases.
However, if the behavioural abnormality is thought to represent a true neu-
rological disorder then this may imply forebrain disease. In this situation, the
diagnostic approach to obtundation is appropriate and should be pursued. If the
neurological examination is consistent with a structural forebrain lesion, then
an attempt should always be made to refer the animal for further investigations
and advanced imaging.

Animal presented with behavioural BEHAVIOURAL ABNORMALITY

abnormality

Suspect brain disease

History & signalment

Suspect behavioural disorder

Follow obtundation flow-
Suspect focal seizure
chart

Normal rest of Abnormal Follow seizure investigation

neurological neurological flow-chart
examination examination

Refer for advanced imaging

Seek behaviourist advice

Approach to cases of behavioural abnormality in practice.

 Chapter 6 A Practical Approach to Common Presentations in General Practice 183

6.4 ­Blindness

Edward Ives

Blindness can be defined as complete, or near complete, vision loss that results
in an inability to perceive objects within the field of view. It may affect one or
both eyes and can be caused by a multitude of disorders affecting the eyeball
itself, or the neuroanatomic structures that transmit visual information from the
retina to the visual cortex in the occipital lobe of the brain. Animals often pre-
sent with a history of sudden onset blindness. However, it may be difficult to
judge from the clinical history whether the vision loss was genuinely acute, or
whether it was a culmination of a chronic, progressive process that was only
apparent to the owner once all vision was lost.

6.4.1 Is Vision Loss the Cause of the Presenting Complaint?

When an animal presents with a history of suspected vision loss, the first consid-
eration should always be whether the animal is genuinely blind or whether the
clinical signs represent a different cause. Dogs or cats may bump into objects or
stumble when walking for reasons other than vision loss, and it is therefore
essential that vision loss is confirmed before formulating a diagnostic plan.
Mimics of vision loss may include:

• Ataxia of all limbs resulting in falling, stumbling and bumping into objects. This
may be observed secondary to vestibular disease, cerebellar disease, or spinal
cord lesions.
• A reduced level of mentation secondary to a brainstem lesion, diffuse forebrain
disease, or severe systemic disease.
• Reduced or absent menace responses, without vision loss, as a result of facial paral-
ysis or cerebellar disease; menace responses may also appear reduced in ani-
mals that are stressed at the time of examination and can be particularly
difficult to elicit in some normal cats (see Chapter 3) (Quitt et al. 2018).

6.4.2 How to Assess Vision

As summarised in Chapter 3, vision can be assessed in a number of ways.

• Observation of the animal navigating an unfamiliar environment.

• Setting up an obstacle course for a dog or cat to walk around.
• Visual tracking of an object that is dropped within the field of view, such as a
small piece of cotton wool (see Video 38). This object should not have a strong
smell or make a sound when it is dropped.
• Menace response testing (see Video 1a) – if the palpebral reflex is normal, con-
firming an ability to blink, then an absent menace response would be most
184 A Practical Approach to Neurology for the Small Animal Practitioner

consistent with a complete, or near complete, vision loss in the eye being
tested. This is particularly appreciable if the vision loss is unilateral, as the
response in the blind eye can be compared to the normal response in the vis-
ual eye (see Video 28).

The pupillary light reflex (PLR) and dazzle reflex are subcortical reflexes that
screen the function of the retina and optic nerves, but their integrity does not
rely upon cerebrocortical perception of the visual image. These reflexes can,
therefore, be normal in an animal that is clinically blind if the lesion responsible
is restricted to the thalamus or visual cortex and spares the optic nerves. The
reader is referred to Chapter 3 for further discussion of these reflex tests.

6.4.3 Lesion Localization

If blindness is confirmed or highly suspected, based upon the tests summarised
above, then the site of the lesion responsible should be determined before a
diagnostic plan is made. The first consideration should be whether there are any
abnormalities on ophthalmic examination that could explain the vision loss.

1. Ophthalmic disease
Normal vision relies upon light reaching the surface of the eye, passing through
the transparent structures of the eyeball, and stimulating the retinal photorecep-
tors. Passage to the visual cortex then occurs for processing and perception of this
visual information. From a clinical perspective, the retina will be included in the
ophthalmic category and post‐retinal blindness will be considered separately.
Ophthalmic disease can result in vision loss as a consequence of the following.

• Light being unable to reach the retina (i.e. loss of transparency of the cornea,
aqueous humour, lens, or vitreous humour):
–– corneal ulceration and oedema
–– cataract formation and lens opacification
• Retinal damage, detachment, or degeneration:
–– post‐traumatic retinal detachment
–– hypertensive retinopathy
–– toxic retinopathy (e.g. fluoroquinolones, ivermectin in cats)
–– glaucoma‐induced retinal damage
–– progressive retinal atrophy (PRA)
–– sudden acquired retinal degeneration syndrome (SARDS) (see Box 6.4.1).

Referral to a veterinary ophthalmologist should be considered in any animal

with suspected vision loss, even if your ocular and retinal examinations appear
generally unremarkable. This ensures that an ophthalmic condition is not missed
before the possibility of neurologic disease is considered. Normal functioning of
the retina can also be confirmed using electroretinography (ERG) if indicated.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 185

Box 6.4.1 Sudden Acquired Retinal Degeneration Syndrome (SARDS)

SARDS is an acute retinal disorder that results in sudden vision loss, initially without
abnormalities on fundoscopic examination (Komáromy et al. 2016). It can therefore
mimic a central nervous system (CNS) lesion that is resulting in post‐retinal blindness.
An abnormal electroretinogram is required to differentiate SARDS from causes of post‐
retinal blindness (e.g. optic neuritis), reinforcing the importance of referral to an oph-
thalmologist with access to such equipment before assuming the presence of a CNS
lesion. The pathogenesis of SARDS is poorly understood and up to 40% of dogs will
show concurrent systemic signs of polyuria, polydipsia, polyphagia, and weight gain
(Komáromy et al. 2016). Some dogs will also show abnormalities on haematology,
serum biochemistry, and urinalysis, such as a stress leucogram, thrombocytosis, hyper-
cholesterolaemia, elevated hepatic enzymes, isosthenuria, and proteinuria. The pres-
ence of these signs may increase the index of suspicion for SARDS; however, they are
very similar to the changes observed in association with hyperadrenocorticism.
Therefore, a hormonally active pituitary macroadenoma that is compressing the adja-
cent optic chiasm/tracts should also be considered. The median age of dogs with SARDS
is reported to be 9 years old, with an over‐representation of female dogs, smaller dog
breeds (<10 kg), Dachshunds, and Miniature Schnauzers (Heller et al. 2017). The pres-
ence of conjunctival hyperaemia and retinal vascular attenuation on ophthalmic exam-
ination can also be suggestive of SARDS (Montgomery et al. 2008). A previous study
did not find a statistical difference in the age or sex distribution between dogs with
SARDS and those with neurologic disease as a cause for acute blindness (Montgomery
et al. 2008). However, an acute onset of blindness in a young dog may reduce the index
of suspicion for SARDS and increase suspicion for optic neuritis. Assessment of the
pupillary light reflex using both red and blue light can also be helpful to distinguish
SARDS from disorders involving the optic nerve and/or chiasm. This test is termed the
chromatic pupillary light reflex (cPLR). The cPLR will be absent using both red and blue
light in dogs with acute blindness secondary to an optic nerve lesion. This is in contrast
to dogs with SARDS, in which the pupils will remain dilated in response to red light but
will constrict when a blue light source is used (Grozdanic et al. 2007).

Retinal examination, or more specifically assessment of the optic nerve head, is

unique in that it is the only non‐invasive test that allows direct visualisation of
the CNS. The index of suspicion for neurological disease can therefore be
increased on the basis of a thorough retinal examination. However, retinal
examination may be normal, even in the presence of significant optic nerve or
CNS disease, if the affected region is post‐retinal.
If the eyeball itself appears normal and retinal examination is unremarkable,
then a lesion affecting the neuroanatomic structures between the back of the eye-
ball and the visual cortex is most likely. This is termed ‘post‐retinal blindness’ or
‘amaurosis’. The term ‘central blindness’ has been used to suggest a cortical lesion
that results in vision loss, in which the PLR should be intact. However, this term
can be misleading as the optic nerves also form part of the CNS. Therefore, a
‘central blindness’ could more accurately be thought of as anything post‐retinal.
186 A Practical Approach to Neurology for the Small Animal Practitioner

2. Post‐retinal blindness
The visual pathway between the retina and visual cortex is summarised in
Figure 6.4.1. A lesion affecting one or more of the following structures can
therefore result in reduced or absent vision in one or both eyes:

• Optic nerves.
• Optic chiasm – the majority of optic nerve fibres cross at the optic chiasm (c.75%
in dogs, c.65% in cats), with a smaller proportion continuing to the ipsilateral
thalamic nuclei.
• Optic tracts between the optic chiasm and the lateral geniculate nuclei in the
thalamus.
• Lateral geniculate nuclei in the thalamus.
• Optic radiation travelling in the white matter tracts of the cerebral hemispheres
(corona radiata).
• Visual cortices in the occipital lobes of the forebrain – the occipital lobes form the
caudodorsal part of the cerebral cortex, lying immediately rostral and dorsal to
the cerebellum. The right visual field is predominately represented within the
left visual cortex, and vice versa.

In order to localise a post‐retinal lesion further, the following questions

should be considered:

• Is the vision loss unilateral or bilateral?

• Is the PLR normal in the affected eye(s)?
• Are there any other neurological deficits consistent with a forebrain lesion?

Optic nerve

Optic chiasm
Optic tract
Lateral geniculate nucleus
Optic radiation

Visual cortex

Figure 6.4.1 The visual pathway in dogs and cats. The right visual field is predominately
represented within the left visual (occipital) cortex, and vice versa. The degree of decussation
of the optic nerve fibres at the optic chiasm varies between species (dog c.75%, cat c.65%).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 187

a. Is the vision loss unilateral or bilateral?

Unilateral vision loss would most commonly result from either:

• an optic nerve lesion on the same side as the blind eye (ipsilateral)
• a forebrain lesion (thalamus, optic radiation, and/or visual cortex) on the con-
tralateral side to the blind eye (as the majority of optic nerve fibres decussate
at the optic chiasm).

Bilateral vision loss could result from:

• a disease process affecting both optic nerves concurrently (e.g. optic neuritis,
ischaemic optic neuropathy)
• a lesion or mass in the region of the optic chiasm where the visual pathways from
both eyes are in close association (e.g. meningioma, pituitary macroadenoma)
• diffuse or bilateral forebrain disease (e.g. hepatic encephalopathy, hydroceph-
alus, inflammatory brain disease, cerebrocortical hypoxia).

b. Is the PLR normal in the affected eye(s)?

The neurologic pathway tested by the PLR is summarised in Figure 6.4.2. There is a
common pathway for vision and the PLR up the level of the optic tracts. At this point,
the pathway for vision continues to the lateral geniculate nuclei in the thalamus (see
Figure 6.4.1) and the PLR pathway branches off to the pretectal nuclei in the midbrain.
A lesion affecting the common pathway before this branching point will result in both
blindness and an absent direct PLR in the blind eye. A lesion that affects the visual
pathway after this point may result in blindness, but the PLR will remain normal in both
eyes. This pathway is discussed further in Section 6.5 ‘Abnormalities of Pupil Size’.

Optic nerve
Oculomotor nerve
(parasympathetic) Optic chiasm

Optic tract

Lateral geniculate nucleus

Pretectal nucleus

Parasympathetic
nucleus of the
oculomotor nerve

Figure 6.4.2 The pathway tested by the pupillary light reflex (PLR).
188 A Practical Approach to Neurology for the Small Animal Practitioner

By using the PLR, post‐retinal blindness can therefore be separated into

lesions that affect the following.

• Optic nerve(s), optic chiasm and proximal optic tract(s):

–– Menace response absent in the affected eye(s).
–– Direct PLR absent in the affected eye(s).
–– Dazzle reflex absent in the affected eye(s).
–– For bilateral blindness, both pupils will be fully dilated.
–– In the case of unilateral blindness, both pupils may appear similar in size as enough
light will enter the visual eye to result in constriction of the contralateral pupil. If the
visual eye is covered then the pupil of the blind eye will passively dilate to full
­mydriasis (see Section 6.5 ‘Abnormalities of Pupil Size’ for further discussion).
• Forebrain (thalamic or cortical):
–– Menace response absent in the affected eye(s).
–– PLR and dazzle reflex normal in the affected eye(s) and both pupils will be an
appropriate size for the external light level.

Unfortunately, not all cases conform to our attempts to understand and over-
simplify the neurological system; some animals will appear clinically blind and
have an intact PLR on examination, but further investigations will reveal a lesion
affecting the retina, optic nerves, or optic chiasm. This is most likely to be caused
by an incomplete lesion that is damaging a sufficient number of optic nerve
axons to result in near complete vision loss, but enough axons remain functional
to elicit reflexive pupil constriction in response to bright light.

c. Are there any other neurological deficits consistent with a forebrain

lesion?
Neurological deficits that would add support for a lesion at the level of the thala-
mus, subcortical white matter, or visual cortex include:

• Compulsive circling: most frequently towards to side of the lesion, and therefore
away from the side of the blind eye (i.e. absent menace response in the right
eye, circling to the left).
• Proprioceptive deficits in the thoracic and pelvic limbs ipsilateral to the side of the
blind eye.
• Reduced nasal nociception in the nostril ipsilateral to the side of the blind eye.
• An onset of seizures coincident with the onset of blindness.
• A reduced level of mentation, particularly in cases of bilateral cortical blindness.

6.4.4 Clinical Approach

The clinical approach to an animal presenting with suspected vision loss is sum-
marised below:
 Chapter 6 A Practical Approach to Common Presentations in General Practice 189

1. Confirm unilateral or bilateral vision loss as the cause

for the presenting complaint
• Vision appears normal in the consultation – consider other causes for the pre-
senting complaint (e.g. lethargy, ataxia), or a waxing/waning disease process
(e.g. hepatic encephalopathy).
• Blindness confirmed on clinical assessment (obstacle course, visual tracking,
menace response testing) – go to step 2.

2. Perform a full ophthalmic and retinal examination

• Ophthalmic examination reveals a possible cause for reduced vision (e.g. cor-
neal ulceration/oedema, cataract formation, retinal lesions):
○ investigate and manage in practice if appropriate

○ consider referral to a veterinary ophthalmologist if possible.

• Ophthalmic examination appears normal – go to step 3.

3. Perform a full neurological examination

a. Neurological examination otherwise normal
Refer to a veterinary ophthalmologist to further exclude ophthalmic disease before
considering referral to a veterinary neurologist for advanced imaging of the head.
If an animal presents with a clinical history of acute, bilateral vision loss and
there are no abnormalities found on ophthalmic or neurological examinations,
then two possibilities should be considered:

• This animal suffers from SARDS – see Box 6.4.1.

• There is a post‐retinal lesion that is currently sparing other neurological func-
tions. This is most commonly seen with disorders that affect the optic nerves/
optic chiasm. In a case series of four dogs and three cats with acute blindness as
the only neurological deficit at presentation, a lesion was observed on MRI in
six out of seven cases (Seruca et al. 2010). All of these cases had a normal oph-
thalmic examination and electroretinogram prior to advanced imaging of the
head. One case was diagnosed with bilateral optic neuritis and five cases with
intracranial neoplasia (two meningiomas in the region of the optic chiasm, two
nasal tumours with intracranial extension, and one pituitary tumour). CNS dis-
ease should therefore always be considered as a cause for blindness, even in the
absence of other neurologic deficits, and this study emphasises the importance
of advanced imaging to achieve a definitive diagnosis if referral is an option.

If referral is not an option, then a diagnostic approach to these cases in gen-

eral practice could include:

• Haematology, serum biochemistry and urinalysis to further investigate possible

inflammatory, metabolic, or systemic disease. As summarised in Box 6.4.1,
certain biochemical changes may also be seen in dogs with SARDS.
190 A Practical Approach to Neurology for the Small Animal Practitioner

• Blood pressure testing.

• Thyroid hormone testing, particularly in cats.
• Infectious disease testing (e.g. T. gondii serology in dogs and cats, FeLV and FIV
testing in cats, and N. caninum serology and CDV testing in dogs).
• Ultrasound of the retrobulbar space through a closed eyelid.
• Nasal radiography to screen for a nasal tumour with possible intracranial exten-
sion, particularly if there is a history of epistaxis or reduced nasal airflow on
examination.
• Thoracic radiography and abdominal ultrasonography to screen for neoplastic disease
in other body cavities (e.g. lymphoma, metastatic disease). This can be particu-
larly useful in cats, for which lymphoma is an important differential diagnosis.
• Computed tomography (CT) is increasingly available in general practice and can
be used to image the head and other body cavities. However, magnetic reso-
nance imaging (MRI) remains preferred over CT for imaging of the optic
nerves and brain in light of its superior soft tissue resolution. Referral for
assessment by a neurologist, and MRI +/− CSF analysis if indicated, should
therefore always be offered to an owner prior to performing CT in practice.
This ensures that funds are available to perform the test that is most likely to
achieve a definitive diagnosis. The lower cost of CT means that it can be a use-
ful test if the costs associated with referral and MRI are prohibitive.
• Monitoring the clinical course of the disease without treatment. The appearance of
neurological deficits over time would support a progressive intracranial lesion
as a cause for blindness. If the clinical signs remain static and the animal is
suspected as having SARDS, then many dogs can still live a good quality of life
in the long‐term.

b. Additional neurological deficits are found on examination that

support an intracranial lesion as a cause for blindness
Refer to a veterinary neurologist if possible.
The list of differential diagnoses in these cases will depend upon the species,
the signalment, and whether the vision loss is unilateral or bilateral.

• Unilateral blindness in an older dog or cat that has a concurrent history of

altered mentation, circling, or seizures: this would be most consistent with a
focal asymmetric, intracranial lesion (e.g. neoplastic mass).
• Unilateral or bilateral blindness in a young or middle‐aged, small breed dog
with concurrent neurological deficits (e.g. Pug, Yorkshire Terrier, Chihuahua,
Boston Terrier, French Bulldog): this could indicate an underlying inflamma-
tory disorder, with meningoencephalitis of unknown origin (MUO) being
most common if infectious disease testing is negative.
• Bilateral blindness in a young animal with a dull mentation, domed skull, and
bilateral ventrolateral strabismus: this could indicate underlying hydroce-
phalus, but hepatic encephalopathy should also be considered in these cases.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 191

• Post‐anaesthetic cortical blindness may be observed in dogs or cats following

anaesthetic complications that result in cerebral hypoxia (e.g. cardiorespira-
tory arrest). However, it has also been reported in cats following routine
anaesthesia during which a spring‐loaded mouth gag was used, such as den-
tistry or endoscopy. It has been hypothesised that use of a mouth gag results
in compression of the maxillary arteries which, unlike in the dog, provide the
majority of cerebral blood flow in cats (Martin‐Flores et al. 2014). In a study
of 20 cats with post‐anaesthetic cortical blindness, a mouth gag had been used
in 16 cases; 85% had other neurological deficits in addition to blindness, 70%
of cats had a documented recovery of vision, and 59% of the cats that had
additional neurological deficits showed a full recovery (Stiles et al. 2012).

If referral to a veterinary neurologist is not possible, then the same tests listed
above for animals with a normal neurological examination should be consid-
ered. The choice of which tests to perform will depend upon the list of differen-
tial diagnoses. If the clinical signs are progressive, and further investigations
have been unrewarding or cannot be performed for economic reasons, then the
option of starting a prednisolone trial could be considered. The limitations of this
approach should always be thoroughly discussed with the owner before starting
treatment, particularly regarding the possibility of clinical deterioration if an
undiagnosed infectious disease is present, or the likelihood of a poor response to
treatment. An initial dose of 0.5–1 mg/kg prednisolone once or twice daily could
be used, dependent on the ranked list of differential diagnoses (e.g. 0.5 mg/kg
once or twice daily for neoplasia, 1 mg/kg twice daily for meningoencephalitis of
unknown origin). Concurrent seizures, if present, should always be managed
using antiepileptic medications, as discussed in Section 6.1 ‘Epileptic Seizures’.

6.5 ­Abnormalities of Pupil Size

Edward Ives

In the healthy dog or cat, pupil size is determined by the environmental light
levels and emotional status of the individual. Both pupils should be equal in size
and respond in the same manner to these stimuli.

• A bright environment will stimulate active pupil constriction to optimise

vision and avoid being dazzled. This is mediated via the parasympathetic nerv-
ous system.
• The pupils will passively dilate in low environmental light levels to maximise
the amount of light reaching the retina.
• Stimulation of the sympathetic nervous system in response to stress, pain, or
exercise will result in active pupil dilation as part of the ‘fight or flight
response’.
192 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.5.1 Terminology

• Pupil dilation is termed ‘mydriasis’ and pupil constriction is termed ‘miosis’.

• A dilated pupil is therefore termed ‘mydriatic’ and a constricted pupil ‘miotic’.
• The term ‘anisocoria’ is used to describe unequal pupil size, with one pupil being
either inappropriately miotic or mydriatic.
• Internal ophthalmoparesis/ophthalmoplegia refers to weakness/paralysis of the iris
sphincter and ciliary body muscle secondary to loss of parasympathetic innervation
by the oculomotor nerve. This results in a mydriatic pupil.
• External ophthalmoparesis/ophthalmoplegia refers to weakness/paralysis of the
extraocular muscles that are responsible for eyeball movement.

1. Active pupil constriction in response to light

As discussed in Section 6.4 ‘Blindness’, there is a common neurological pathway
for both vision and pupil constriction up to the level of the optic tracts
(Figure 6.5.1). The majority of optic tract fibres are destined for the visual area
of the cerebral cortex, via the lateral geniculate nuclei of the thalamus. However,
around 20% of the optic tract fibres branch away to the pretectal nuclei, which
reside at the boundary of the thalamus and midbrain. Axons from the pretectal
nuclei stimulate the parasympathetic nuclei of the oculomotor (III) nerves.
These parasympathetic fibres leave the midbrain to join the motor fibres of the
oculomotor nerve. The oculomotor nerves run along the floor of the skull
through the middle cranial fossa, either side of the pituitary gland, and leave the
skull via the orbital fissures. The pre‐ganglionic parasympathetic fibres con-
tained within the oculomotor nerve synapse with post‐ganglionic ciliary nerve
axons at the ciliary ganglion in the retrobulbar space. These post‐ganglionic
parasympathetic fibres innervate the constrictor muscles of the pupil.

Optic nerve
Oculomotor nerve
(parasympathetic) Optic chiasm

Optic tract

Lateral geniculate nucleus

Pretectal nucleus

Parasympathetic
nucleus of the
oculomotor nerve

Figure 6.5.1 The pathway for active pupil constriction in response to light. This is the same
pathway that is tested by the pupillary light reflex (see Section 6.4 ‘Blindness’).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 193

This is the entire pathway that is tested by the pupillary light reflex (PLR). Partial
decussation at both the optic chiasm and pretectal nuclei means that there is
bilateral representation of information at the level of the optic tracts, pretectal
nuclei, and oculomotor nuclei. This results in constriction of both pupils, even if
light only enters one eye. Constriction of the pupil of the stimulated eye is termed
the ‘direct PLR’ and constriction of the contralateral pupil is termed the ‘consen-
sual PLR’. However, the use of the terms ‘direct’ and ‘consensual’ can sometimes
be confusing when reading clinical records, as it can be unclear as to which eye
is being stimulated and which pupil is being referred to. For this reason, the
results of PLR testing should be described in terms of which eye is receiving light
and which pupil constricts. For example, the left pupil constricts when light is
shone into both the left and right eyes, but the right pupil does not constrict
when light is shone into either eye – this situation would be most consistent with
a lesion affecting the parasympathetic fibres in the right oculomotor nerve.
Lesions affecting a multitude of anatomical structures (transparent structures
of the eyeball, retina, optic nerves, optic chiasm, optic tracts, midbrain, para-
sympathetic fibres of the oculomotor nerves, iris constrictor muscles) could all
result in a failure of pupil constriction, a pathological mydriasis, and/or an
abnormal PLR. However, by careful assessment of vision, menace responses,
and PLR testing in both eyes, the most likely site of the lesion can be identified.
A list of differential diagnoses can then be formulated, and the decision regard-
ing whether to refer, who to refer to (e.g. ophthalmologist or neurologist), or
what further investigations would be most useful in practice can be made.
2. Active pupil dilation in response to sympathetic stimulation
The sympathetic innervation to each eye represents a long, ipsilateral path-
way that can be divided into three main sections (Figure 6.5.2).

= Upper motor neurons (1st order)

= Pre-ganglionic neurons (2nd order)
= Post-ganglionic neurons (3rd order)
Pupil dilator
muscles Tectotegmental
spinal tract

T1 T2 T3

Tympanic bulla
Thoracic
Vagosympathetic sympathetic trunk
Cranial cervical trunk
ganglion

Figure 6.5.2 The neurologic pathway for active pupil dilation in response to sympathetic
stimulation (‘fight or flight response’).
194 A Practical Approach to Neurology for the Small Animal Practitioner

• The upper motor neurons (also termed ‘first‐order’ neurons) originate in the hypo-
thalamus and midbrain. They travel down the brainstem and cervical spinal
cord in an ipsilateral bundle of nerve fibres called the ‘tectotegmental spinal
tract’. These axons synapse with the cell bodies of the pre‐ganglionic sympa-
thetic neurons in the grey matter of the T1–T3 spinal cord segments.
• The pre‐ganglionic (‘second‐order’) neurons originate in the intermediolateral grey
matter of the T1–T3 spinal cord segments and leave the spinal cord in the
T1–T3 ventral nerve roots. The sympathetic fibres separate from the ventral
nerve roots before the level of the brachial plexus and ascend through the
cranial thorax as the thoracic sympathetic trunk. They then join the vagus
nerve to form the vagosympathetic trunk within the carotid sheath. Synapse
with the post‐ganglionic sympathetic neurons occurs in the cranial cervical
ganglion, which lies adjacent to the tympanic bulla.
• The post‐ganglionic (‘third‐order’) neurons are the final neurons in the pathway.
The precise route that these fibres take to the smooth muscles of the eyelids,
iris, and periorbita has not been fully elucidated, and may involve multiple
routes. However, it is thought that they travel in close association with the
tympanic bulla, before running with the ophthalmic branch of the trigeminal
nerve via the retrobulbar space.

This long sympathetic pathway to the eye means that lesions affecting the
brain, cervical spinal cord, cranial thorax, neck, tympanic bulla, and/or retrobul-
bar space can all result in a failure of pupil dilation and unopposed pupil con-
striction (miosis).

6.5.1 Bilateral Mydriasis

Bilateral pupil dilation would be appropriate in a dark environment; however, if
both pupils appear inappropriately dilated for the external light levels then it is
important to consider both non‐neurological and neurological causes for patho-
logic mydriasis. Increased sympathetic stimulation (e.g. excitement, stress, or
fear) is a very common cause of bilateral, symmetric pupil dilation during clini-
cal examination. The PLR may also appear bilaterally reduced unless a very
bright light is used. Examination in bright sunlight can help to demonstrate
appropriate pupil constriction in these cases, but care should always be taken
when interpreting the clinical significance of bilateral, symmetric mydriasis in a
stressed animal that otherwise appears normal.

1. Non‐neurological causes
• Bilateral glaucoma – The index of suspicion should be increased by concurrent
ophthalmic abnormalities such as scleral congestion or discomfort on gentle
retropulsion of the eyeballs.
• Previous application of a topical parasympathetic blocking agent into both eyes (e.g.
atropine, tropicamide) – This should be supported by a history of such application.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 195

• Bilateral iris atrophy – The application of 0.1% pilocarpine eye drops can
help to differentiate age‐related atrophy of the iris constrictor muscles
from denervation secondary to an oculomotor nerve lesion. This direct
parasympathomimetic agent will stimulate pupil constriction if there is
denervation hypersensitivity of the iris constrictor muscles. In the case of
iris atrophy, these muscles will remain mechanically unable to contract
even when stimulated pharmacologically, and the pupils will therefore
remain dilated.
• Bilateral blindness resulting from an ophthalmic lesion (e.g. bilateral cataract for-
mation, bilateral retinal lesion such as SARDS).

2. Neurological causes
• Bilateral blindness involving the visual pathway between the retina and the branching
of the optic tracts to the pretectal nuclei – Affected animals will have difficulty navi-
gating around obstacles, will not visually track objects dropped silently in
front of them, and the PLR, dazzle reflex, and menace response will be absent
in both eyes. Assuming that there are no concurrent trigeminal or facial nerve
lesions, the palpebral reflexes should be normal and spontaneous blinking
should be observed. Differential diagnoses could include a bilateral optic nerve
lesion (e.g. optic neuritis) or a lesion affecting the optic chiasm (e.g. pituitary
macroadenoma). A lesion that affects the visual pathway from the level of the
lateral geniculate nuclei to the visual cortex, sparing the earlier components
(e.g. retina, optic nerves, optic chiasm, optic tracts), can result in blindness but
will not affect the pupil size or PLR.
• A disorder that affects both parasympathetic oculomotor nuclei in the midbrain (e.g.
thiamine deficiency, increased intracranial pressure [ICP]), or that affects the parasym-
pathetic fibres in both oculomotor nerves (e.g. mass situated in the middle cranial fossa,
dysautonomia, botulism) – The PLR will be absent in both eyes, but the vision
should be normal and the menace responses intact bilaterally unless there is
concurrent involvement of the optic nerves. Affected animals may appear
dazzled in a bright environment as a result of excessive light entering via the
inappropriately dilated pupils.
• Ingestion of belladonna plant species containing atropine – This will block the effect
of acetylcholine released from the parasympathetic oculomotor nerve fibres,
resulting in bilateral mydriasis. The PLR will be absent in both eyes, but vision
will be normal.

6.5.2 Bilateral Miosis

1. Non‐neurological causes
• Bilateral corneal lesions resulting in reflex pupil constriction (e.g. ulceration).
• Bilateral uveitis.
196 A Practical Approach to Neurology for the Small Animal Practitioner

• Previous application of a topical parasympathomimetic agent into both eyes (e.g. pilo-
carpine) – This should be supported by a history of such application.
• Following opioid administration in dogs (e.g. buprenorphine, methadone, fenta-
nyl) – This is particularly apparent following high doses of opiates, or in ani-
mals that are individually sensitive to such agents (Stephan et al. 2003).
Opiate administration can also result in sedation and cardiorespiratory depres-
sion which, in conjunction with bilateral miosis, could mimic primary intrac-
ranial disease and increased ICP.

2. Neurological causes
• Appropriate response to a bright environment.
• Bilateral stimulation of the parasympathetic oculomotor nuclei (e.g. increased ICP or
diffuse forebrain lesions that result in disinhibition of the oculomotor nerves) – This
will be accompanied by other neurological deficits reflecting significant intrac-
ranial pathology, such as an altered level of mentation, tetraparesis, a poor gag
reflex, or a reduced vestibulo‐ocular reflex.
• Organophosphate or carbamate toxicity – These agents inhibit the enzyme acetyl-
cholinesterase, resulting in an increased level of acetylcholine at the neuro-
muscular junction (NMJ) and stimulation of the pupil constrictor muscles.
• Bilateral loss of sympathetic innervation to the pupil dilator muscles (bilateral Horner
syndrome) – This is rarely observed but has been reported in association with
extensive cervical spinal cord lesions, diabetes mellitus, bilateral trigeminal
nerve disorders, and as an idiopathic condition (Carpenter et al. 1987; Holland
2007). Concurrent bilateral enophthalmos, third eyelid protrusion, and ptosis
should allow bilateral Horner syndrome to be distinguished from other causes
of bilateral miosis.

6.5.3 Anisocoria
Anisocoria is the term used to describe a difference in the size of the left and
right pupils. The most common reason for this difference is that one pupil
remains normal whilst the contralateral pupil is either inappropriately dilated
(unilateral mydriasis) or inappropriately constricted (unilateral miosis).
Therefore, the first step in the approach to anisocoria should be to identify which
pupil is the abnormal one. This differentiation can be more difficult than it ini-
tially sounds, but a simple and effective way is to assess pupil size in both dark
and bright environments:

• An inappropriately dilated pupil will be most obvious in a bright environment.

This will accentuate the difference between the abnormal pupil, which fails to
appropriately constrict, and the normal pupil, which will still constrict in
response to light.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 197

• An inappropriately constricted pupil will be more obvious in a dark environ-

ment, as it will fail to dilate when compared to the normal contralateral pupil.

Other important tests to perform include assessment of vision, menace

responses, pupillary light reflexes, and observation for other neurological deficits
that would indicate dysfunction of either the oculomotor nerve or sympathetic
nerve supply to the eyes (e.g. abnormal strabismus, eyelid position).
In simple terms, an inappropriately dilated pupil (mydriasis) will result from
either:

• a loss of the ability to constrict the pupil (i.e. a parasympathetic oculomotor

nerve lesion)
• or, increased activity of the pupil dilator muscles (i.e. stimulation or disinhibi-
tion of the sympathetic innervation to the eye).

Likewise, an inappropriately constricted pupil (miosis) will result from either:

• an inability to dilate the pupil (i.e. loss of sympathetic innervation to the eye)
• or, increased activity of the pupil constrictor muscles (i.e. stimulation or disin-
hibition of the parasympathetic fibres of the oculomotor nerve).

Other than the notable exceptions of epileptic seizures and certain movement
disorders (see Sections 6.1 ‘Epileptic Seizures’ and 6.2 ‘Movement Disorders’), clini-
cal neurology most commonly deals with loss of function in the form of neurological
‘deficits’. This is also true for anisocoria, in which unilateral mydriasis most com-
monly results from loss of parasympathetic innervation to the pupil constrictor mus-
cles, and unilateral miosis results from loss of sympathetic innervation to the pupil
dilator muscles. A logical approach to these two scenarios is summarised below.

1. Unilateral mydriasis
As for bilateral mydriasis, it is essential to consider non‐neurological causes for
unilateral mydriasis as these may be commonly encountered in general practice.
Such conditions include unilateral glaucoma, iris atrophy (Grahn and Cullen
2004), and previous application of a mydriatic agent into the affected eye (e.g.
atropine or tropicamide).
Unilateral blindness results in only mild anisocoria as sufficient light will enter
the visual eye to elicit a consensual PLR. This will maintain a near‐normal pupil
size in the blind eye. If the visual eye is covered, then the blind eye will passively
dilate and become mydriatic. Light directed into the visual eye will result in
constriction of both pupils, whereas neither pupil will change in size if light is
directed into the blind eye.
In the absence of a non‐neurological cause, unilateral mydriasis most com-
monly results from ipsilateral dysfunction of the oculomotor nerve
198 A Practical Approach to Neurology for the Small Animal Practitioner

(parasympathetic fibres). This is termed internal ophthalmoparesis/ophthalmo-

plegia and presents as a visual eye with a dilated pupil that fails to constrict when
light is shone into either eye. The contralateral pupil should, however, still con-
strict when light is shone into the affected eye.
In addition to parasympathetic fibres, the oculomotor nerve also has a motor
component. These fibres innervate the levator palpebrae superioris muscle con-
tributing to elevation of the upper eyelid and innervate the extraocular muscles
responsible for eyeball movement. The motor fibres can be affected at the same
time as the parasympathetic fibres, resulting in ptosis, a resting ventrolateral
strabismus, and an inability to move the eyeball dorsally, ventrally, or medially
(O’Neill et al. 2013). These signs of motor dysfunction are termed external oph-
thalmoparesis/ophthalmoplegia. The parasympathetic fibres lie superficial to the
motor fibres in their course to the eye, meaning that they can be affected in
isolation before motor involvement is observed. This may be seen in association
with slowly expanding masses within the middle cranial fossa.
Differential diagnoses to consider for a suspected, unilateral parasympathetic
oculomotor nerve lesion should include:

• A unilateral midbrain lesion that is affecting the ipsilateral parasympathetic

nucleus of the oculomotor nerve (e.g. neoplasia, infarction, focal inflamma-
tory lesion, head trauma) (Webb et al. 2005). In light of the small size of this
nucleus, adjacent neuroanatomic structures are likely to also be affected,
resulting in concurrent neurological deficits, such as ipsilateral hemiparesis,
proprioceptive deficits, and a reduced level of mentation.
• A lesion in the middle cranial fossa that is compressing the oculomotor nerves
as they run along the floor of the cranial vault towards the eye (e.g. pituitary
macroadenoma, meningioma, germ cell neoplasia, lymphoma, abscess/granu-
loma) (Larocca 2000) (Figure 6.5.3). Lesions in this location may affect other
cranial nerves that run in close association with the oculomotor nerves,
including the trochlear nerve, abducens nerve, and all three branches of the
trigeminal nerve. This will result in a combination of ipsilateral clinical signs
termed ‘cavernous sinus syndrome’, such as loss of facial sensation, mastica-
tory muscle atrophy, and complete paralysis of all extra‐ocular muscles
(Guevar et al. 2014; Jones et al. 2018).
• A primary oculomotor nerve lesion (e.g. lymphoma, malignant nerve sheath
tumour).
• A retrobulbar lesion (e.g. neoplasia, abscess, trauma) – lesions in this location
may also affect the optic nerve, resulting in blindness of the affected eye, an
absent menace response, and absent constriction of the contralateral pupil
when light is shone into the affected eye.
• Idiopathic oculomotor neuropathy – unilateral mydriasis, with or without
external ophthalmoplegia, has been reported as an idiopathic condition in
dogs (Tetas Pont et al. 2017). Flat‐coated Retrievers appear over‐represented.
MRI can reveal enlargement and contrast enhancement of the affected oculo-
 Chapter 6 A Practical Approach to Common Presentations in General Practice 199

Figure 6.5.3 A transverse T1‐weighted MRI at the level of the pituitary gland and inter‐tha-
lamic adhesion following the administration of intravenous contrast media in a 12‐year‐old,
male neutered Border Terrier with a clinical history of lethargy and unilateral, right‐sided
mydriasis. The neurological examination was otherwise normal. The lesion localised to the
parasympathetic component of the right oculomotor nerve. Magnetic resonance imaging of
the brain demonstrated a large, strongly contrast‐enhancing, extra‐axial mass in the region of
the pituitary fossa that was suspected to represent a pituitary macroadenoma. The mydriasis
observed in this case was secondary to compression of the adjacent right oculomotor nerve as
it ran rostrally through the middle cranial fossa on its way to the eye.

motor nerve, prompting suggestion that this may represent an idiopathic ocu-
lomotor neuritis. This condition is non‐progressive and is associated with a
good prognosis. A retrospective study of 14 dogs with suspected idiopathic
oculomotor neuropathy reported an improvement in 50% of dogs over a
median follow‐up time of 25 months (five dogs without treatment and two
dogs with systemic corticosteroid treatment) (Tetas Pont et al. 2017).

Rare neurological causes for unilateral mydriasis:

• Cerebellar lesions can result in ipsilateral or contralateral mydriasis dependent

on the cerebellar nucleus affected (Figure 6.5.4). The vision and palpebral
reflexes will be normal in these cases, but the menace response may be absent.
Additional signs to indicate cerebellar dysfunction will usually be present,
such as hypermetria, ataxia, an intention tremor, or central vestibular
syndrome.
• Overstimulation/irritation of the sympathetic nerve supply to the eye. This is
termed ‘Pourfour du Petit syndrome’ and has been reported in cats with otitis
media and in cats following mild, iatrogenic trauma to the middle ear cavity
(Boydell 2000). In these cases, the pupil should still be able to constrict to some
degree in response to a bright light source as the optic and oculomotor (para-
sympathetic) pathways remain intact. This condition may precede a loss of
sympathetic function that will result in Horner syndrome in the affected eye.
200 A Practical Approach to Neurology for the Small Animal Practitioner

(a) (b)

Right Left

Figure 6.5.4 (a) Anisocoria with left mydriasis in an 8‐year‐old, female neutered Greyhound
with a clinical history of acute onset, non‐progressive ataxia of all limbs and a left head tilt.
(b) A transverse T2‐weighted MRI at the level of the cerebellum and medulla oblongata in the
affected dog demonstrating a well‐defined, ‘wedge‐shaped’ hyperintensity affecting the
cerebellar cortex and fastigial nucleus on the left side (white arrow). The clinical history and
imaging findings in this case were consistent with a cerebrovascular accident (ischaemic stroke).
With thanks to Joe Fenn DipECVN, Royal Veterinary College, UK, for the photo and MRI.

Box 6.5.2 Oculomotor Nerve Dysfunction in Cats

Isolated oculomotor nerve dysfunction is a rare clinical sign in cats, with neoplastic
disease being the most common cause. A recent retrospective study from a referral
institution reported 12 cats with internal ophthalmoparesis/ophthalmoplegia (unilat-
eral in 9 cats and bilateral in 3 cats) (Hamzianpour et al. 2018). An abnormal menta-
tion was recorded in 9 cats and additional neurologic deficits were present in 10 of the
12 cats. A mass lesion was observed on advanced imaging of the head in all 10 cases in
which it was performed, and the remaining 2 cats were diagnosed with multicentric
lymphoma following abdominal ultrasound and biopsy. The prognosis was poor in all
cases, with a median time from diagnosis to euthanasia of 3.5 days (range 0–80 days).

Clinical approach to unilateral mydriasis

1. Confirm that the mydriatic pupil is the abnormal pupil by examination in a
bright environment and PLR testing.
2. Have any topical medications been recently applied that could cause mydria-
sis (e.g. atropine, tropicamide)?
3. Perform an ophthalmic examination to assess for primary ocular disorders
that could result in mydriasis (e.g. glaucoma, iris atrophy), or evidence of
retrobulbar disease that could be affecting the oculomotor nerve.
–– Refer to an ophthalmologist or further work‐up in practice as appropriate.
4. If the eye otherwise appears normal, then a neurological cause for unilateral
mydriasis is most likely:
 Chapter 6 A Practical Approach to Common Presentations in General Practice 201

–– Perform a menace response to assess vision in the affected eye.

–– If vision is normal, then an ipsilateral parasympathetic oculomotor nerve
lesion is most likely. The affected pupil will not constrict when light is shone
into either eye, but the normal pupil will still constrict when light is shone
into the affected eye. Clinical signs consistent with external ophthalmople-
gia may also be present (e.g. ptosis, resting ventrolateral strabismus).
–– A pilocarpine response test (0.1% pilocarpine eye drops) can be per-
formed to further exclude iris atrophy. Constriction of the pupil follow-
ing pilocarpine application would be consistent with oculomotor nerve
dysfunction and denervation of the pupil constrictor muscles.
5. Perform a full neurological examination:
–– Assess for other neurological deficits that would be consistent with a
lesion affecting the parasympathetic nucleus of the oculomotor nerve in
the midbrain (e.g. tetraparesis or hemiparesis, proprioceptive deficits,
reduced level of mentation, other cranial nerve deficits).
–– Concurrent involvement of cranial nerves IV, V, and VI, with or without
other neurologic deficits, could indicate a lesion in the region of the mid-
dle cranial fossa.
–– Idiopathic oculomotor neuropathy should be considered in dogs with
unilateral mydriasis and no other neurologic deficits on examination.
However, internal ophthalmoplegia may be the sole clinical sign in the
early stages of progressive disease (e.g. neoplasia) and, if funds allow,
idiopathic oculomotor neuropathy should never be assumed without
exclusion of other causes.
6. Refer for advanced imaging of the head – MRI is the gold standard due to its
superior soft tissue resolution when compared to CT. However, CT may reveal
the underlying cause if an extra‐axial middle cranial fossa mass is highly sus-
pected (e.g. meningioma, pituitary macroadenoma, nasal adenocarcinoma
with intracranial extension).
7. If referral is not an option, then further investigations can be performed in
practice:
–– Screening for involvement of other body systems or body cavities: hae-
matology, serum biochemistry, urinalysis, thoracic radiography, abdomi-
nal ultrasonography. This is recommended in cats due to the relatively
high incidence of lymphoma in this species compared to dogs; this is
frequently a systemic disease process that may be diagnosed by sampling
other, more accessible, regions of the body (e.g. lymph nodes, liver,
spleen).
–– Infectious disease testing: T. gondii serology in dogs and cats, N. caninum
serology in dogs, FeLV, FIV and feline coronavirus testing in cats.
–– Monitoring of the clinical course without treatment, particularly if there
is a high clinical suspicion of idiopathic oculomotor neuropathy in a dog.
202 A Practical Approach to Neurology for the Small Animal Practitioner

Owners should always be warned of the possibility of an underlying pro-

gressive disease process and that the prognosis may be poor if additional
neurological deficits are subsequently observed.

2. Unilateral miosis
If non‐neurological causes are excluded (e.g. uveitis, painful ocular conditions),
then the most common cause for unilateral miosis is loss of sympathetic inner-
vation to the smooth dilator muscles of the pupil. This results in unopposed
pupil constriction and a miotic pupil that fails to dilate fully in a dark environ-
ment. The affected pupil may constrict further in response to bright light as the
parasympathetic fibres in the oculomotor nerve are unaffected.
In addition to the dilator muscles of the pupil, the sympathetic nervous sys-
tem also provides innervation to the smooth muscles of the eyelids, periorbita,
and blood vessels of the head. Therefore, a combination of clinical signs termed
‘Horner syndrome’ is commonly observed following loss of sympathetic inner-
vation to the eye (Kern et al. 1989; Morgan and Zanotti 1989) (Figure 6.5.5):

• ipsilateral miosis
• a narrow palpebral fissure – drooping of the upper eyelid (ptosis) and decreased
smooth muscle tone in the lower eyelid

Figure 6.5.5 Horner syndrome in a 5‐year‐old cat with left‐sided otitis media. Note the
narrow palpebral fissure in the left eye, protrusion of the left third eyelid, and left‐sided miosis
relative to the normal right eye.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 203

• third eyelid protrusion – observed secondary to loss of tone in the periorbital

smooth muscle and subsequent passive retraction of the eyeball
• enophthalmos – often mild or clinically inapparent
• loss of sympathetic vascular smooth muscle tone on the affected side of the head, result-
ing in peripheral vasodilation, hyperaemia, warmth of the ipsilateral pinna,
and mild scleral congestion.

Partial Horner syndrome, associated with miosis alone, is uncommon but can
occur following partial avulsion of the roots of the brachial plexus (e.g. avulsion
of the T1 nerve root sparing the T2 and T3 nerve roots).
Unilateral Horner syndrome is rarely a problem for the affected animal, but
it should alert the clinician to the presence of a sympathetic lesion somewhere
in the long and convoluted pathway from the brain to the eye. This syndrome
represents a prime example of why a thorough clinical history, general clinical
examination, and neurological examination are essential to correctly localise the
site of the lesion. The presence of concurrent clinical signs or neurological defi-
cits can greatly assist in achieving an accurate neuroanatomic localisation, which
can then be used to guide further investigations. The neuroanatomic localisation
can be divided into the three parts of the sympathetic pathway described above.

a. Upper motor neuron (first‐order) lesion: brain and C1–C8 spinal cord
segments (Figure 6.5.6)
Concurrent neurological deficits will be present in cases with a first‐order lesion
as adjacent neuroanatomical structures are invariably affected. These deficits
will depend upon the lesion location but could include a change in the level of
mentation, seizures, other cranial nerve deficits, a change in drinking (e.g. hypo-
thalamic lesions), tetraparesis, ipsilateral hemiparesis/hemiplegia, and ipsilateral
proprioceptive deficits.
Differential diagnoses to consider in these cases should include head trauma, neo-
plasia, meningoencephalomyelitis (infectious or sterile), fibrocartilaginous embolic
myelopathy, cervical intervertebral disc extrusion, and spinal fracture/luxation.

Upper motor neuron

(1st order)

T1 T2 T3

Post-ganglionic fibres
(3rd order)
Pre-ganglionic fibres
(2nd order)

Figure 6.5.6 Lesion localisation for an upper motor neuron (first‐order) Horner syndrome.
204 A Practical Approach to Neurology for the Small Animal Practitioner

b. Pre‐ganglionic (second‐order) lesion: T1–T3 spinal cord segments,

T1–T3 nerve roots, cranial thorax, and neck (Figure 6.5.7)
A lesion that affects the cell bodies of the second‐order neurons residing within
the grey matter of the T1–T3 spinal cord segments will result in Horner syn-
drome, together with lower motor neuron paresis of the ipsilateral thoracic limb
(reduced limb muscle tone, weak withdrawal reflex), and upper motor neuron
paresis of the ipsilateral pelvic limb (delayed/absent proprioception, normal
muscle tone, intact patellar and withdrawal reflexes). Horner syndrome and
concurrent lower motor neuron paresis of the ipsilateral thoracic limb, without
involvement of the pelvic limbs, can be seen secondary to disorders affecting the
T1–T3 ventral nerve roots (e.g. avulsion of the roots of the brachial plexus,
peripheral nerve sheath tumour [PNST]).
Horner syndrome is frequently the only neurological deficit observed in cases
with lesions affecting the thoracic sympathetic trunk or vagosympathetic trunk
in the neck. Thorough cervical palpation should always be performed in these
cases, assessing for bite wounds, evidence of previous venepuncture, or masses
(e.g. thyroid adenocarcinoma, lymphoma) (Melián et al. 1996). Thoracic radiog-
raphy may also be useful to assess for cranial mediastinal masses. Iatrogenic
trauma to the pre‐ganglionic sympathetic fibres can be seen as a post‐surgical
complication following thyroid surgery, ventral slot surgery, thoracotomy, or
chest drain placement (Boydell et al. 1997).

c. Post‐ganglionic (third‐order) lesion: from the level of the tympanic

bulla to the eye, via the trigeminal nerve (Figure 6.5.8)
Recognition of concurrent vestibular syndrome and/or facial paralysis, without
other neurological deficits, would be highly suggestive of a lesion in the region
of the tympanic bulla (e.g. otitis media, neoplasia). Horner syndrome may also
be observed as a post‐surgical complication following total ear canal ablation or
ventral bulla osteotomy (Spivack et al. 2013).

Upper motor neuron

(1st order)

T1 T2 T3

Post-ganglionic fibres
(3rd order)
Pre-ganglionic fibres
(2nd order)

Figure 6.5.7 Lesion localisation for a pre‐ganglionic (second‐order) Horner syndrome.

 Chapter 6 A Practical Approach to Common Presentations in General Practice 205

Upper motor neuron

(1st order)

T1 T2 T3

Post-ganglionic fibres
(3rd order)
Pre-ganglionic fibres
(2nd order)

Figure 6.5.8 Lesion localisation for a post‐ganglionic (third‐order) Horner syndrome.

Retrobulbar disease that damages the sympathetic nerve fibres behind the eye is
often accompanied by exophthalmos or mechanical strabismus (e.g. abscess, neo-
plasia). The optic and oculomotor nerves can also be affected in these cases, resulting
in blindness and/or a mid‐range pupil that can neither dilate nor constrict.
Disorders affecting the trigeminal nerve may result in concurrent damage to
the sympathetic fibres that run in close association with this nerve to the eye
(Carpenter et al. 1987). Clinical signs of trigeminal nerve dysfunction include
ipsilateral masticatory muscle atrophy, weak/absent palpebral reflex in the ipsi-
lateral eye as a result of loss of facial sensation, and a dropped jaw in the case of
bilateral lesions.

Box 6.5.3 Idiopathic Horner Syndrome

This is a relatively common condition that has been estimated to affect up to 55% of
dogs and 40% of cats presenting with Horner syndrome (Kern et al. 1989, Morgan and
Zanotti 1989). Male Golden Retrievers appear to be over‐represented (Boydell 2000).
It is a diagnosis of exclusion with no identifiable cause being found on diagnostic
investigations. This syndrome was previously reported as an idiopathic pre‐ganglionic
(second‐order) lesion; however, a recent publication reported a post‐ganglionic (third‐
order) lesion in 8 of 10 Golden Retrievers assessed (Simpson et al. 2015). This conclu-
sion was made on the basis of pharmacologic testing using topical phenylephrine. All
of these cases were unilateral and showed complete resolution over 11–20 weeks. The
aetiopathogenesis of idiopathic Horner syndrome remains unknown but suggestions
include autoimmune demyelination, direct trauma to the pre‐ganglionic axons as they
ascend the neck, or a vascular aetiology related to the close proximity of the internal
carotid artery and sympathetic axons.

Clinical approach to unilateral miosis

1. Confirm that the miotic pupil is the abnormal pupil by examination in light
and dark environments.
206 A Practical Approach to Neurology for the Small Animal Practitioner

2. Have any topical medications be recently applied that could cause miosis (e.g.
pilocarpine)?
3. Perform an ophthalmic examination to assess for retrobulbar disease or primary
ocular disorders that could result in miosis (e.g. uveitis, ocular discomfort).
• Refer to an ophthalmologist or further work‐up in practice as appropriate.
4. If the eye otherwise appears healthy, then a neurological cause for miosis is
most likely. Horner syndrome is the most common neurological cause for
unilateral miosis and would be supported by concurrent ptosis, third eyelid
protrusion, and enophthalmos.
5. Perform a full clinical and neurological examination
• Assess for other neurological deficits that would be consistent with either
an upper motor neuron (first‐order) Horner syndrome, or damage to the
T1–T3 spinal cord segments/nerve roots (e.g. reduced level of mentation
for brainstem lesions, tetraparesis, hemiparesis, proprioceptive deficits,
ipsilateral thoracic limb monoparesis).
• In the absence of other neurological deficits to indicate a brainstem locali-
sation, a lesion in the region of the tympanic bulla would be most likely if
there is a Horner syndrome with concurrent vestibular syndrome and/or
facial paralysis. Otitis media is a common cause of Horner syndrome with
concurrent vestibular syndrome and/or facial paralysis in cats.
6. If other neurological deficits are present, then referral for further neurological
assessment and advanced imaging is advised. If referral is not possible, then
the options for further diagnostic investigations and management in general
practice will depend upon the neuroanatomic localisation and your differen-
tial diagnoses. The reader is referred to Sections 6.10 ‘Paresis, Paralysis, and
Proprioceptive Ataxia’ and 6.11 ‘Monoparesis and Lameness’ for further dis-
cussion on the approach to spinal cord lesions and monoparesis. Tympanic
bulla radiography and/or myringotomy could be performed if there is a high
clinical suspicion of a tympanic bulla lesion (e.g. otitis media).
7. If the neurological examination is otherwise normal, then a pre‐ganglionic
lesion in the cranial thorax / neck or a post‐ganglionic lesion are most likely.
• Perform thorough palpation of the cervical region for any lesions that could
affect the sympathetic nerve fibres as they ascend the neck.
• A phenylephrine response test could be used to guide whether a pre‐ or
post‐ganglionic lesion is most likely (Box 6.5.4).
8. If a pre‐ganglionic lesion is suspected, then appropriate further investigations
could include thoracic radiography, ultrasound examination of the neck, or
advanced imaging (e.g. CT) of the thorax and neck. Referral for further neu-
rological examination, with a view to advanced imaging if indicated, should
always be discussed with an owner at this time.
9. Monitoring the clinical course without treatment is not an unreasonable
option if funds are not available for further investigations and the animal is
otherwise well. This is particularly the case if there is a high clinical suspicion
 Chapter 6 A Practical Approach to Common Presentations in General Practice 207

Box 6.5.4 The Phenylephrine Response Test

Phenylephrine is a direct sympathomimetic agent that can be used to confirm sympa-

thetic denervation of the pupil dilator muscles by stimulating dilation of the affected
pupil. The time to pupil dilation following topical application of 1% phenylephrine eye
drops into the affected eye has been suggested to guide the distinction between a pre‐
ganglionic and post‐ganglionic lesion:

• pupil dilation in <20 minutes most consistent with a post‐ganglionic lesion

(<5–8 minutes if 10% drops are used)
• pupil dilation in 20–45 minutes more consistent with a pre‐ganglionic lesion.

This test is not required if there are concurrent neurological deficits that would con-
firm either an upper motor neuron (first‐order) lesion or damage to the T1–T3 spinal
cord segments/nerve roots (e.g. hemiparesis, ipsilateral thoracic limb monoparesis).

The phenylephrine response test should only be used as a guide to the neuroanatomic
localisation and the results should always be combined with other clinical findings and
the results of further investigations. The test requires denervation hypersensitivity of
the pupil dilator muscles to have occurred, which may take 7–14 days, therefore the
results may not be reliable before this time.

of idiopathic Horner syndrome (e.g. in a male Golden Retriever) (see

Box 6.5.3). In this instance, owners should always be warned of the possibil-
ity of an underlying disease process that may have a poor prognosis if clinical
progression is subsequently observed.

6.6 ­Cranial Nerve Dysfunction

Edward Ives

Cranial nerve deficits are frequently encountered in general practice and can
have a multitude of clinical presentations from unilateral dysfunction of a single
cranial nerve, to involvement of multiple cranial nerves +/− the lower motor
neurons to the limbs and trunk. A logical approach is therefore essential in order
to accurately localise the lesion and plan further investigations.
There are 12 pairs of cranial nerves that, with the exception of the olfactory
(I) and optic (II) nerves, have cell bodies that lie within corresponding brainstem
nuclei. A peripheral, axonal component connects each nucleus to either the
receptor organ for sensory functions, or to the effector muscle or gland for motor
functions. Cranial nerve dysfunction can therefore be termed ‘central’ if a lesion
affects the neuronal cell bodies in a brainstem nucleus, or ‘peripheral’ if it affects
208 A Practical Approach to Neurology for the Small Animal Practitioner

the receptor organ, effector muscle, NMJ, or the cranial nerve axons after they
have left the brainstem. As will be discussed for vestibular dysfunction in
Section 6.7 ‘Vestibular Syndrome’, this distinction is important as different dis-
ease processes, with potentially different treatments and prognoses, will be more
likely to affect the central component compared to peripheral component.
The initial considerations in the approach to any case with cranial nerve dys-
function should be:

1. Is only one cranial nerve affected, or are multiple nerves affected?

• The involvement of multiple cranial nerves on the same side, particularly if
their nuclei reside close to each other in the brainstem, should increase the
index of suspicion for a central lesion (e.g. trigeminal (V), facial (VII), and
vestibulocochlear (VIII) nerves).
• However, there are also regions outside the brain where specific cranial
nerves lie in close anatomical association. A certain combination of cranial
nerve deficits may therefore be highly suggestive a particular peripheral
localisation, such as in the region of the tympanic bulla if the facial nerve,
vestibulocochlear nerve, and sympathetic fibres to the head are affected, or
the middle cranial fossa if there is concurrent involvement of the oculomo-
tor (III), trochlear (IV), trigeminal (V), and abducens (VI) nerves.
2. Are the clinical signs unilateral or bilateral?
• Unilateral paresis or paralysis of a single muscle is most likely to reflect a
lesion affecting the cranial nerve (nucleus or axons), rather than the NMJ
or muscle itself. Whilst individual cranial muscles can be affected by myo-
pathies or junctionopathies, this involvement is usually bilateral and
symmetric.
• Bilateral dysfunction of one or more cranial nerves should increase the
index of suspicion for a peripheral lesion, particularly if the level of menta-
tion remains bright and there are no proprioceptive deficits. A central
lesion that is large enough to damage the brainstem nuclei on both sides
would be expected to affect adjacent neuronal pathways, resulting in con-
current neurological deficits (e.g. stupor/coma, tetraparesis, proprioceptive
deficits in all limbs).
3. Are there any other neurological deficits that would be consistent with a
brainstem neuroanatomic localisation (e.g. tetraparesis, hemiparesis, propri-
oceptive deficits, an abnormal level of mentation)?
4. Are there any other clinical signs to suggest a generalised neuromuscular
disorder?
• Dependent on whether this represents a peripheral neuropathy, myopathy,
or junctionopathy, other clinical signs could include exercise intolerance, a
stiff gait in all limbs, generalised muscle atrophy, reduced limb muscle tone,
and reduced/absent spinal reflexes. The approach to neuromuscular dis-
ease is further discussed in Section 6.12 ‘Neuromuscular Weakness’.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 209

This section will focus on an approach to disorders affecting the two most
commonly affected cranial nerves in general practice: the trigeminal (V) and
facial (VII) nerves. Dysfunction of the olfactory (I) nerve results in an inability to
smell, termed anosmia. However, this is difficult to appreciate clinically, particu-
larly if partial or unilateral, and would rarely occur or be recognised in isolation.
Dysfunction of the optic (II) and oculomotor (III) nerves is discussed further in
Sections 6.4 ‘Blindness’ and 6.5 ‘Abnormalities of Pupil Size’, respectively.
Deficits relating to trochlear (IV) or abducens (VI) nerve dysfunction are rarely
observed in isolation, resulting in different forms of resting strabismus as dis-
cussed in Chapter 3. The reader is referred to Section 6.7 ‘Vestibular Syndrome’
for a summary of the approach to vestibulocochlear (VIII) nerve dysfunction.
Dysfunction of the vagus (X) nerve, resulting in megaoesophagus or laryngeal
paralysis, and the hypoglossal (XII) nerve, resulting in paresis of the tongue, are
also discussed at the end of this section.

6.6.1 Trigeminal Nerve

The trigeminal nerve is the fifth cranial nerve and contains both motor and sen-
sory fibres. It is comprised of three main branches.

• The ophthalmic branch, providing sensory information from the skin overly-
ing the medial canthus of the eye, cornea, nasal septum, and frontal region.
• The maxillary branch, providing sensory information from the skin overlying
the muzzle, upper lips, lateral canthus of the eye, and top of the head.
• The mandibular branch, providing sensory information from the skin overly-
ing the mandible, and motor innervation to the muscles of mastication
(temporalis, masseter, pterygoids, and rostral digastricus).

From a clinical perspective, dysfunction of the trigeminal nerve may result in

two primary abnormalities on the neurological examination.

• Loss of facial sensation, with the region affected dependent on the branches
involved (e.g. medial canthus of the eye if the ophthalmic branch is affected).
This is most frequently recognised as a reduced/absent palpebral reflex in an
animal that can still voluntarily blink, assuming that there is normal facial
nerve function. Marked neurogenic keratitis may occur following loss of
sensory innervation to the cornea, and this can be the primary reason for pres-
entation in some cases.
• Denervation of the masticatory muscles if either the trigeminal motor nucleus
in the pons or the motor axons in the mandibular branch are affected. If the
lesion is unilateral, this will be clinically apparent as rapid denervation atrophy
of the masticatory muscles on the affected side (Figure 6.6.1). These animals
will still be able to close their mouth and eat normally, as sufficient strength
will remain in the masticatory muscles on the unaffected side. An inability to
210 A Practical Approach to Neurology for the Small Animal Practitioner

keep the mouth closed against the force of gravity (‘dropped jaw’) will only be
seen if the motor components in both trigeminal nerves are affected (i.e.
bilateral denervation).

1. Unilateral trigeminal nerve dysfunction

The most common cause of unilateral trigeminal nerve dysfunction in dogs is a
trigeminal peripheral nerve sheath tumour (PNST). A presumptive trigeminal
PNST was diagnosed in 48% of dogs presenting with unilateral masticatory mus-
cle atrophy in one study (Milodowski et al. 2018). The degree of unilateral mas-
ticatory muscle atrophy observed in these cases is often marked (Figure 6.6.1).
This asymmetric involvement of the masticatory muscles would not be expected
for a primary myopathy, which usually result in bilateral and symmetric muscle
loss. Ipsilateral loss of facial sensation may also be observed if the trigeminal
sensory fibres are affected. Trigeminal PNSTs can be relatively slow‐growing
neoplasms, but they will frequently progress along the nerve to invade the
brainstem at the level of the pons. Additional neurological deficits can be
observed at this stage, including involvement of other cranial nerve nuclei in the
near vicinity (e.g. facial, vestibulocochlear, glossopharyngeal, vagus), a reduced
level of mentation, ipsilateral hemiparesis, and ipsilateral proprioceptive
deficits.
Differential diagnoses for a unilateral trigeminal PNST are listed below.

• A brainstem lesion involving the motor nucleus of the trigeminal nerve (e.g.
inflammatory/infectious, another form of extra‐axial mass lesion, intra‐axial

Figure 6.6.1 Marked, right‐sided atrophy of the masseter and temporalis muscles in a 10‐
year‐old Labrador Retriever with a peripheral nerve sheath tumour affecting the motor fibres
of the right trigeminal nerve. Note the prominent zygomatic arch secondary to loss of the
surrounding musculature.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 211

neoplasia). The presence of additional neurological deficits that are consistent

with a brainstem lesion should alert the clinician to the possibility of a central
rather than peripheral lesion.
• Trauma to one or more branches of the trigeminal nerve (external or
iatrogenic).
• A different form of neoplasia that is involving the peripheral component of
the trigeminal nerve (e.g. lymphosarcoma, particularly in cats).
• Unilateral inflammation of the trigeminal nerve (trigeminal neuritis). This
diagnosis would require biopsy confirmation as it may be difficult to distin-
guish inflammation from neoplastic infiltration as the cause for nerve enlarge-
ment on advanced imaging. A study has reported that dogs with trigeminal
neuritis are more likely to show diffuse nerve enlargement without a mass
effect, compared to the solitary or lobulated masses with displacement of the
adjacent neuropil observed in cases with PNST (Schultz et al. 2007).

Diagnosis of a trigeminal PNST, and the other less common causes of uni-
lateral masticatory muscle atrophy, requires advanced imaging of the head
(Figure 6.6.2). This can also be used to evaluate the proximity of a suspected
PNST to the brainstem, which may guide the likely rate of clinical progression.
A recent association between trigeminal nerve lesions on MRI and the pres-
ence of asymptomatic, ipsilateral middle ear effusion has also been reported

R L

Figure 6.6.2 A transverse T1‐weighted MRI at the level of the caudal midbrain/pons
following the administration of intravenous contrast media in a 7‐year‐2‐month‐old, female
neutered Staffordshire Bull Terrier with a 4‐week history of progressive, right‐sided mastica-
tory muscle atrophy. The neurological examination was otherwise normal. Note the marked,
right‐sided masticatory muscle atrophy with fibrous and fat replacement (white arrow). The
right trigeminal nerve is strongly contrast‐enhancing, enlarged (4 mm compared to 1.5 mm on
the contralateral side) and is exerting a mild mass effect on the pons (arrow head).
212 A Practical Approach to Neurology for the Small Animal Practitioner

(Kent et al. 2013; Wessmann et al. 2013). This is suggested to result from den-
ervation of the tensor veli palatini muscle, failure of dilation of the Eustachian
tube, and reduced drainage of the middle ear (Kent et al. 2015). Thoracic and
abdominal imaging can be performed in general practice to screen for neopla-
sia elsewhere in the body, particularly if there is a high clinical suspicion of
lymphoma. However, this may be unrewarding as metastasis is uncommon for
primary tumours of the trigeminal nerve.
Surgical resection of trigeminal PNST is performed in humans and has been
reported in dogs (Bagley et al. 1998; Schmidt et al. 2013). However, the location
of these neoplasms deep within the head means that primary surgical manage-
ment is rarely performed in veterinary medicine at the current time. Trigeminal
PNSTs also appear to be poorly responsive to chemotherapy. Palliative medical
management may therefore be chosen until an animal’s quality of life becomes
adversely affected. This is usually observed when the brainstem becomes com-
pressed by the expanding mass, or if there are complications associated with loss
of facial sensation (e.g. keratitis, self‐trauma). A survival time ranging from 5 to
21 months was reported for untreated dogs with a presumptive diagnosis of
trigeminal PNST in one study (Bagley et al. 1998).
Two recent studies have reported the use of focused stereotactic radiation
therapy for trigeminal nerve sheath tumours in dogs. The median disease‐spe-
cific survival was 745 days in one study (range 99–1375 days, n = 6), with no
acute adverse effects reported (Hansen et al. 2016). The second study compared
15 dogs treated with stereotactic radiation therapy to 10 dogs not receiving treat-
ment (Swift et al. 2017). All dogs in this study had neoplastic extension into the
brainstem at the time of diagnosis. Of the 15 dogs treated with stereotactic radia-
tion therapy, one had improved masticatory muscle atrophy, and six had poor
ocular health after treatment. Neurologic signs improved in 4/5 dogs with intrac-
ranial signs. The difference in mean survival time between the two groups was
not statistically significant but the study was limited by both sample size and
selection bias (mean 95% CI for unirradiated dogs was 44–424 days and mean
95% CI for dogs receiving stereotactic radiation therapy was 260–518 days).

2. Bilateral trigeminal nerve dysfunction

Bilateral dysfunction of the trigeminal motor fibres presents as a loss of mastica-
tory muscle tone and an inability to close the mouth, colloquially known as a
‘dropped jaw’. Animals will often have a history of drooling and abnormal pre-
hension of food, but they remain able to move their tongue and swallow if food
can get to the pharyngeal region. An important differential diagnosis for a
dropped jaw is an unwillingness to close the mouth rather than an inability to
close to the mouth. This may be observed secondary to painful conditions such
as masticatory myositis, temporomandibular joint disease, craniomandibular
osteopathy, retrobulbar lesions, dental disease, oropharyngeal foreign bodies, or
tongue lesions.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 213

If an unwillingness to close the mouth is excluded, then a full neurological

examination should be performed to localise the lesion to either the peripheral,
axonal component of both trigeminal nerves, or to the trigeminal motor nuclei
in the brainstem (pons). As discussed previously, a central lesion that is large
enough to affect both trigeminal motor nuclei should be accompanied by other
neurological deficits, such as tetraparesis, ataxia of all limbs, proprioceptive defi-
cits, a reduced level of mentation, or other cranial nerve deficits.
In the absence of other neurological deficits, bilateral trigeminal dysfunction
most commonly represents a peripheral lesion. Horner syndrome may be
observed in some cases if the sympathetic fibres that run in close association
with the trigeminal nerves are also affected. In a retrospective study of 29 dogs
that were unable to close their mouths due to flaccid paresis/paralysis of the
masticatory muscles, an idiopathic trigeminal neuropathy was diagnosed in
26 dogs based on complete resolution of the clinical signs and a lack of any long‐
term neurological disease (Mayhew et al. 2002) (see Box 6.6.1). The remaining
three dogs were diagnosed with lymphosarcoma, N. caninum infection, and poly-
neuritis of unknown origin following post‐mortem examination. Lymphosarcoma
should always be considered in cats as idiopathic disease appears to be less com-
mon in this species. Bilateral trigeminal neuropathy has also been reported sec-
ondary to immune‐mediated inflammation of the dura mater (pachymeningitis)
(Roynard et al. 2012). This likely represents involvement of the trigeminal
nerves as they exit the brainstem via its surrounding meninges. Dogs with this
condition usually present with additional neurological deficits, such as blindness
and mentation change. Obtaining a full travel history is also important in all
cases, as the early stages of rabies may rarely present as a dropped jaw if there
has been a bite to the face.

Box 6.6.1 Idiopathic Trigeminal Neuropathy

This condition is suspected to represent an autoimmune demyelinating neuritis. The

extent of bilateral masticatory muscle atrophy observed in these cases depends on the
degree of axonal loss but is usually mild. Idiopathic trigeminal neuropathy is the most
common cause of flaccid paresis/paralysis of the masticatory muscles in dogs, and
Golden Retrievers appear to be over‐represented (Mayhew et al. 2002). Loss of facial
sensation has been reported in around a third of cases, concurrent Horner syndrome
in 10% of cases, and facial nerve deficits in 10% of cases as part of a suspected inflam-
matory cranial polyneuropathy. Idiopathic trigeminal neuropathy should self‐resolve
without treatment over 3–4 weeks, with a mean time to recovery of 22 days reported
by one study (Mayhew et al. 2002). Assisted feeding with balls of wet food is often
required over this time, or an oesophagostomy tube can be placed in more severely
affected cases. Ocular lubrication should be used in cases with sensory dysfunction.
Corticosteroid therapy has not been reported to influence the clinical course of this
condition.
214 A Practical Approach to Neurology for the Small Animal Practitioner

a. Clinical approach to bilateral trigeminal neuropathy

1. Exclude an unwillingness to close the mouth and confirm an inability to close
the mouth as a result of loss of jaw tone.
2. Perform a full neurological examination. Referral for advanced imaging
would be advised if there are concurrent neurological deficits consistent with
a central lesion.
3. If there are no additional neurological deficits, then the option of referral
should still be discussed. If referral is not an option, then further investiga-
tions that could be performed in general practice would include serological
testing for N. caninum in dogs, and screening for lymphoma affecting other
body systems (especially in cats). It is not unreasonable to make a presump-
tive clinical diagnosis of idiopathic trigeminal neuropathy in a dog that is
otherwise well. However, further investigations should always be advised if
there is no clinical improvement over 2–4 weeks, or if other neurological defi-
cits are observed at any time.

b. Bilateral masticatory muscle atrophy

A disorder that affects the motor fibres in both trigeminal nerves may result in
bilateral masticatory muscle atrophy, but this is invariably accompanied by loss
of jaw tone and an inability to close the mouth (see above). Bilateral masticatory
muscle atrophy without a loss of jaw function most frequently occurs secondary
to disorders affecting the masticatory muscles themselves. This can present as an
isolated masticatory myopathy, or as part of a more generalised polymyopathy
(Evans et al. 2004).
The masticatory muscles appear particularly susceptible to atrophy resulting
from systemic disease processes or secondary to corticosteroid excess. This is
often more noticeable than the accompanying atrophy of the appendicular mus-
cles. Therefore, hyperadrenocorticism, exogenous steroid therapy, and systemic
conditions that result in cachexia (e.g. neoplasia, cardiac failure, systemic inflam-
matory disease, malnutrition, maldigestion, malabsorption) should always be
considered in cases with bilateral masticatory muscle atrophy. Age‐related atro-
phy of the masticatory muscles, termed sarcopenia, can also be observed and
may be related to enhanced autophagocytosis with ageing (Pagano et al. 2015).
In the absence of systemic disease or corticosteroid excess, the most common
cause of bilateral masticatory muscle atrophy (without loss of jaw tone) is
inflammation and destruction of the masticatory muscles. This may form part of
a generalised myopathy affecting skeletal muscles throughout the body (e.g. idi-
opathic polymyositis, N. caninum myositis (Figure 6.6.3)). However, it is more
commonly observed as an isolated, sterile inflammatory condition called masti-
catory myositis (Evans et al. 2004; Paciello et al. 2007; Shelton et al. 1987) (see
Box 6.6.2).
Chapter 6 A Practical Approach to Common Presentations in General Practice 215

Box 6.6.2 Masticatory Myositis

This is a suspected autoimmune condition that results in damage to the Type II‐M
myofibres that are unique to the masticatory muscles (Paciello et al. 2007, Shelton
et al. 1987). This results in two phases.

• An acute phase – swollen painful masticatory muscles, raised submandibular lymph

nodes, reluctance to eat/open mouth +/− exophthalmos secondary to swelling of
the masticatory muscles behind the eyes.
• A chronic phase – bilateral masticatory muscle atrophy with fibrous replacement,
often in conjunction with enophthalmos and third eyelid protrusion secondary to
loss of muscle mass behind the eyes.

Masticatory myositis is most frequently observed in young adult, large breed dogs,
with the German Shepherd Dog and Hungarian Vizsla appearing over‐represented
(Tauro et al. 2015). An atypical form has been reported in three 12‐week‐old Cavalier
King Charles Spaniel littermates (Pitcher and Hahn 2007). Masticatory myositis has
also been reported in a mixed breed cat presenting with trismus (Blazejewski and
Shelton 2018).

Diagnosis:

• Clinical signs – bilateral masticatory muscle swelling or atrophy dependent on

whether the animal presents in the acute or chronic phase. The acute phase may be
mild and short and can be missed by some owners. Therefore, masticatory myositis
should not be excluded if there is no prior history of muscle swelling or
discomfort.
• Exclusion of other causes for bilateral masticatory muscle atrophy (cachexia, mal-
nutrition, hyperadrenocorticism, exogenous corticosteroid therapy).
• Serum biochemistry – elevated serum muscle enzymes may be observed (creatine
kinase [CK], AST, ALT).
• Serum Type II‐M antibody titre – this test will result in a definitive diagnosis if ele-
vated; however, the serum titre may be normal during the chronic phase or after
steroid therapy. One study reported a positive result in 65% of affected cases (Evans
et al. 2004).
• Muscle biopsy – this can confirm the diagnosis by demonstrating inflammatory infil-
trates (primarily lymphocytes), muscle necrosis, and by excluding the presence of
infectious agents.
• Infectious disease testing – N. caninum (Figure 6.6.3), T. gondii, Leishmania infantum
(Vamvakidis et al. 2000).
• Magnetic resonance imaging – symmetric, heterogeneous hyperintensity within the
masticatory muscles is observed in the acute phase, followed by atrophy and T1W
muscle hyperintensity in the chronic phase (Cauduro et al. 2013). The computed
216 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.6.2 (Continued)

tomographic appearance of masticatory myositis has also been reported in dogs

(Reiter and Schwarz 2007).
• Electromyography – abnormal spontaneous myofibre activity in the affected mus-
cles under general anaesthesia. This test is most useful to assess for involvement of
other skeletal muscle groups in the case of a generalised polymyopathy.

Treatment:

• Immunosuppressive doses of prednisolone are the most common treatment for mas-
ticatory myositis, starting at 1 mg/kg per os twice daily for 2–4 weeks, followed by a
steady tapering to 0.5 mg/kg per os every other day. Relapsing clinical signs may be
observed as the dose is reduced.
• The use of adjunctive immunosuppressive agents, such as cyclosporine or azathio-
prine, can be used in dogs that do not adequately respond to prednisolone alone.
These can also be useful as steroid‐sparing agents, particularly in large dogs that may
not tolerate high oral doses of prednisolone.
• Chronic muscle loss may result in permanent muscle atrophy and dysphagia. It is
therefore advised to encourage jaw movements to minimise the risk of fibrosis and
restricted jaw movements in the long term (e.g. chew toys).

Figure 6.6.3 A transverse T2‐weighted MRI at the level of the thalamus in a dog with myositis
of the masticatory muscles resulting from Neospora caninum infection. Note the multifocal
hyperintense lesions throughout the masticatory muscles, particularly affecting the temporalis
muscles bilaterally. This dog also presented with hypermetria and ataxia of all limbs secondary to
protozoal meningoencephalitis affecting the cerebellum (see Section 6.8 ‘Cerebellar Dysfunction’).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 217

6.6.2 Facial Nerve

The facial nerve is the seventh cranial nerve and it has three primary functions:

1. motor innervation to the muscles of facial expression

2. parasympathetic innervation to the mandibular and sublingual salivary
glands, lacrimal glands, and lateral nasal glands
3. special sensation of taste from the rostral two thirds of the tongue – loss of
this function is difficult to appreciate clinically.

Clinical signs of facial nerve dysfunction can therefore include:

• Ipsilateral drooping of the upper and lower lips. The lip commissure on the
affected side will be lower than the normal side when a dog is panting.
• Drooping of the ear on the affected side in dogs without a rigid auricular car-
tilage. Animals with a rigid auricular cartilage will be unable to move the
affected ear back against the head when excited or nervous (Figure 6.6.4).
• Drooling from the affected side of the mouth, food and salivation accumula-
tion, and secondary halitosis.
• Absent spontaneous blinking, an absent palpebral reflex, and absent menace
response on the affected side. Retraction of the eyeball and subtle third eyelid
protrusion may still be observed at the time of palpebral reflex and menace
response testing. This confirms intact facial sensation and vision, respectively.
• Exposure keratitis secondary to loss of spontaneous blinking, especially in
brachycephalic breeds.

Figure 6.6.4 Right‐sided facial paralysis in a Chihuahua with inflammatory brain disease.
Note the narrow palpebral fissure on the right side and the inability to voluntarily retract the
right ear against the head compared to the normal left side.
218 A Practical Approach to Neurology for the Small Animal Practitioner

• Ipsilateral neurogenic keratoconjunctivitis sicca (KCS) secondary to loss of

tear production if the parasympathetic fibres to the lacrimal glands are affected
(Box 6.6.3).
• Hyperkeratosis of the ipsilateral nasal planum (xeromycteria) if the parasym-
pathetic fibres to the lateral nasal glands are affected (Figure 6.6.5).

These clinical signs can be unilateral or bilateral and result from a lesion at
any point along the course of the facial nerve(s), from the motor and parasym-
pathetic nuclei in the brainstem to the target muscles/glands. Junctionopathies
and myopathies may also result in facial paresis, which will usually be bilateral
and associated with other clinical signs of generalised neuromuscular weakness.
As for trigeminal nerve dysfunction, a full neurological examination is impor-
tant to distinguish between a central and peripheral lesion localisation.

1. Central lesions
Central (brainstem) lesions resulting in facial paralysis are less frequently observed
in practice compared to peripheral lesions. Differential diagnoses include vascular
events (e.g. ischaemic stroke), neoplasia, and inflammatory or infectious disorders.
These lesions will usually be accompanied by other neurological deficits, such as an
altered level of mentation, other cranial nerve deficits, tetra‐/hemiparesis, or ataxia
of all limbs. However, it is important to remember that whilst the presence of these
signs confirms a central lesion, their absence does not exclude one. Extra‐axial,

Box 6.6.3 Neurogenic Keratoconjunctivitis Sicca (Neurogenic ‘Dry Eye’)

This condition may be observed in combination with facial nerve paralysis or it can
occur in isolation as an idiopathic disorder (Matheis et al. 2012). Tear production is
often markedly reduced, with Schirmer tear test values in the range of 1–5 mm/min in
the affected eye(s) (normal >15 mm/min). Ipsilateral hyperkeratosis of the nasal pla-
num (xeromycteria) may also be seen secondary to denervation of the lateral nasal
glands in cases with concurrent facial paralysis (Figure 6.6.5). An important differen-
tial diagnosis for neurogenic keratoconjunctivitis sicca (KCS) should always be
immune‐mediated KCS, as the pathogenesis and treatment of these conditions differ.
Firstly, immune‐mediated KCS should not be associated with a concurrent facial nerve
paralysis. Secondly, treatment of immune‐mediated KCS involves the application of
topical cyclosporine to restore tear production by regulating immune‐mediated
destruction of the lacrimal glands. This treatment will not be effective for neurogenic
KCS other than by providing a very expensive lubricant. Treatment of neurogenic KCS
involves the regular application of ocular lubrication to avoid keratitis and corneal
ulceration. Administration of 1% pilocarpine eye drops by mouth has also been reported
to treat neurogenic KCS, starting with one drop per 10 kg body weight twice daily until
either restoration of tear production is observed or there are adverse effects of treat-
ment (vomiting, diarrhoea, salivation). The idiopathic form of neurogenic KCS may
self‐resolve over a period of 3–4 months (Matheis et al. 2012).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 219

Figure 6.6.5 Left‐sided xeromycteria in a dog with left‐sided facial paralysis and peripheral
vestibular syndrome. Note the hyperkeratosis of the left side of the nasal planum (arrow)
compared to the normal right side, and also the mild left head tilt and drooping of the left
upper lip.

intracranial masses in the region of the internal acoustic meatus can sometimes
result in facial paralysis and/or vestibular dysfunction without other signs of brain-
stem involvement. A definitive diagnosis of central disease requires referral for
advanced imaging of the head +/− CSF analysis. Screening of the thorax and abdo-
men for distant neoplasia can also be performed, particularly if there are progressive
clinical signs and/or referral is not an option. Blood pressure testing, haematology,
serum biochemistry, and urinalysis should be performed to investigate possible pre‐
disposing factors for cerebrovascular disease if there is consistent clinical history (e.g.
an acute, non‐progressive, non‐painful, lateralised central lesion).

2. Peripheral lesions
Disorders that affect the peripheral component of the facial nerve(s) are more
commonly observed in general practice compared to central lesions. These con-
ditions may result in unilateral or bilateral clinical signs, with possible differen-
tial diagnoses including:

• Infectious: Otitis media/interna is a common cause of facial paresis/paralysis,

particularly in cats. Concurrent vestibular syndrome and/or Horner syndrome
may be observed (Figure 6.6.6).
220 A Practical Approach to Neurology for the Small Animal Practitioner

Right Left

Figure 6.6.6 A transverse T2‐weighted MRI at the level of the tympanic bullae in an 8‐
year‐5‐month old, male neutered Pyrenean Mountain Dog with a 1‐week history of right
facial paralysis, a right head tilt, and pain on opening the mouth. The MRI demonstrates
heterogeneous, hyperintense material filling the right tympanic bulla (arrow), focal osteolysis
of the bulla wall, and extension into the para‐aural soft tissues. Note the difference when
compared to the normal, gas‐filled, hypointense tympanic bulla on the left side. A final
diagnosis of bacterial otitis media and para‐aural abscessation was made following myringot-
omy and the dog was treated surgically by total ear canal ablation (TECA) and lateral bulla
osteotomy.

• Traumatic: External trauma (e.g. petrous temporal bone fracture) or iatrogenic

trauma (e.g. following bulla osteotomy surgery).
• Metabolic: Hypothyroidism has been associated with facial paralysis in dogs but
the evidence to support this association remains inconclusive (Jaggy and
Oliver 1994).
• Neoplasia: PNST, lymphosarcoma, local invasion by adjacent neoplasia (e.g.
affecting the tympanic bulla).
• Idiopathic facial neuropathy: This is a diagnosis of exclusion that is further
described in Box 6.6.4.
• As part of a generalised neuromuscular disorder, such as polyneuropathy (e.g.
polyradiculoneuritis) or junctionopathy (e.g. botulism, myasthenia gravis).
Bilateral facial paresis/paralysis will be apparent in these cases.

The option of referral for further assessment should always offered to the
owner of an animal with facial paralysis. MRI is the imaging modality of choice
 Chapter 6 A Practical Approach to Common Presentations in General Practice 221

Box 6.6.4 Idiopathic Facial Neuropathy

Idiopathic facial neuropathy is the most common cause of facial paralysis in dogs,
reported in up to 75% of cases (Kern and Erb 1987). Cocker Spaniels and Cavalier
King Charles Spaniels appear over‐represented. There is usually an acute onset of
unilateral or bilateral clinical signs, and the neurological examination is consistent
with a peripheral lesion localisation. In unilateral cases, the contralateral side may
subsequently become affected. Studies have reported that 40–70% of dogs may show
concurrent vestibular signs (head tilt, ataxia, nystagmus), which is suggested to reflect
the close proximity of the facial and vestibulocochlear nerves where they enter and
exit the skull via the internal acoustic meatus (Smith et al. 2012). This condition has
been termed ‘facial and vestibular neuropathy of unknown origin’ (FVNUO). A recent
study of dogs with FVNUO reported that only 31% of dogs showed complete resolu-
tion of clinical signs: 38% showed long‐term vestibular signs, 15% had permanent
facial paralysis, 46% developed hemifacial contracture, and 15% showed relapse
(Jeandel et al. 2016).
Idiopathic facial neuropathy may be analogous to a condition called Bell’s Palsy in
humans, in which a link has been found to human herpes simplex virus infection.
There has been no definitive association found between idiopathic facial neuropathy
and viral infection in dogs to date. However, it has been suggested that canine herpes
virus‐1 infection may be associated with idiopathic vestibular disease and other ‘idio-
pathic’ cranial neuropathies (Parzefall et al. 2011). The clinical signs of idiopathic facial
neuropathy may self‐resolve over 1–3 months, but this may simply reflect fibrosis and
restoration of a more normal facial symmetry (hemifacial contracture), rather than a
true return of voluntary motor function. Frequent ocular lubrication may be required
to reduce the risk of exposure keratitis in an animal that cannot blink. There is cur-
rently no evidence to support the use of corticosteroids to accelerate the rate of recov-
ery or to improve the chance of a functional recovery in affected dogs. Further work is
required to assess whether a sub‐set of dogs may benefit from this treatment and how
these cases can be distinguished at the time of diagnosis from those that are unlikely
to benefit.

as it can be used to exclude a central lesion and can also be used to support a
diagnosis of idiopathic facial neuropathy. Enlargement and/or contrast enhance-
ment of the affected facial nerve may be observed in idiopathic cases, with the
presence of contrast enhancement potentially associated with a reduced chance
of self‐resolution (Varejão et al. 2006). Volumetric interpolated breath‐hold
examination magnetic resonance imaging (VIBE‐MRI) has been shown to offer
better visualisation of the facial nerve when compared to routine MRI sequences
for the investigation of idiopathic facial neuropathy (Smith et al. 2012). A CT
scan of the head could be performed if there is a high clinical suspicion of middle
ear pathology. Electromyography and nerve conduction studies can be per-
formed if there are other neurological deficits that are consistent with a general-
ised neuromuscular disorder.
222 A Practical Approach to Neurology for the Small Animal Practitioner

In cases with a suspected peripheral cause for facial nerve paralysis, diagnos-
tic investigations that could be performed in general practice include:

• otoscopic examination +/− myringotomy for cytology, culture, and

sensitivity
• tympanic bulla radiography
• serum biochemistry, including total thyroid hormone (T4) and TSH concen-
trations in dogs
• if referral is not possible and further investigations are unrewarding, then a
presumptive diagnosis of idiopathic facial neuropathy could made in a dog
with consistent clinical signs, non‐progressive disease, and that is otherwise
well (Box 6.6.4).

6.6.3 Vagus Nerve

The vagus nerve is the tenth cranial nerve and has sensory, motor, and auto-
nomic functions:

• sensory innervation from the larynx, pharynx, and thoracic and abdominal
viscera
• motor innervation to the oesophagus, larynx (recurrent laryngeal branch),
and pharynx (together with motor fibres of the glossopharyngeal [IX] nerve)
• parasympathetic innervation to all of the thoracic and abdominal viscera,
other than those of the pelvic region.

The most common clinical signs associated with vagus nerve dysfunction are
laryngeal paralysis, dysphagia, and regurgitation associated with oesophageal
dysmotility (megaoesophagus).

1. Laryngeal paralysis
Laryngeal paresis/paralysis can be a congenital or an acquired condition
(Box 6.6.5). It may be the sole clinical sign in some cases but often reflects a
more generalised disease process. Typical clinical signs of laryngeal dysfunction
include:

• dysphonia – most commonly reported by the owner as a change in the tone or

strength of the bark
• inspiratory stridor – secondary to a failure to abduct the laryngeal cartilages dur-
ing inspiration
• exercise intolerance, particularly during periods of hot weather – this may be
severe enough to result in collapse
• coughing, particularly when drinking, secondary to an inability to adduct the
laryngeal cartilages to protect the upper airway; these animals are at risk of aspi-
ration pneumonia, particularly if there is concurrent pharyngeal weakness.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 223

Box 6.6.5 Congenital Laryngeal Paralysis

Congenital laryngeal paralysis has been reported in a number of dog breeds and should
be suspected in animals presenting at <1 year of age. Commonly affected breeds
include Bouvier des Flandres, Siberian Huskies, Rottweilers, Pyrenean Mountain
Dogs, Dalmatians, Russian Black Terriers, Bull Terriers, and Miniature Schnauzers
(Braund et al. 1994; Gabriel et al. 2006; Mahony et al. 1998; von Pfeil et al. 2018).
Laryngeal paralysis may also present in young animals as part of a more widespread
degenerative disease process (e.g. inherited encephalomyelopathy‐polyneuropathy in
Rottweiler puppies) (Granger 2011). The clinical signs of laryngeal dysfunction in
these cases may precede those of progressive tetraparesis and ataxia. Therefore, the
possibility of a progressive, degenerative disease process should always be considered
in puppies with laryngeal paralysis, and owners should be counselled accordingly
before arytenoid lateralisation is performed (de Lahunta et al. 2015). A late‐onset form
of hereditary laryngeal paralysis, which is also associated with generalised neuropathic
signs, has been reported in the Leonberger (Granger 2011; Shelton et al. 2003).

An important differential diagnosis for laryngeal paresis/paralysis is local

structural disease affecting the larynx and/or pharynx, such as trauma, neopla-
sia, inflammation, infection, or obstruction by a foreign body. This possibility
should always be excluded by thorough cervical palpation and laryngoscopic
examination prior to performing further investigations. Confirmation of laryn-
geal paresis/paralysis can be made by direct observation of laryngeal function
under a light plane of sedation or anaesthesia. Abnormal movement of the
laryngeal cartilages can also be observed using ultrasound.
Laryngeal paralysis may result from:

• A central lesion that is affecting the motor nucleus of the vagus nerve (nucleus ambiguus)
in the caudal brainstem – neoplastic and inflammatory lesions are most com-
monly responsible, with advanced imaging of the brain +/− CSF analysis usu-
ally required for a diagnosis.
• A disorder that is affecting the vagus nerve and/or its recurrent laryngeal branch – the
vagus nerve is a long nerve that exits the back of the skull through the tympano‐
occipital fissure and runs to the larynx via the neck and cranial mediastinum.
Potential causes of vagal nerve dysfunction include trauma (e.g. bite wound),
iatrogenic damage during cervical surgery, retropharyngeal infections, thyroid
neoplasia, and neuronal degeneration. A detailed clinical history and examina-
tion of the cervical region can assist in the exclusion of these possible causes.
• A primary myopathy or junctionopathy that is affecting the skeletal muscles of the lar-
ynx – this may be observed as focal laryngeal involvement, but more com-
monly forms part of a generalised neuromuscular disease. Differential
diagnoses include idiopathic polymyositis, myasthenia gravis, and botulism.
The clinical suspicion for each condition will depend upon the concurrent
clinical signs and biochemical changes (e.g. elevated muscle enzymes for
224 A Practical Approach to Neurology for the Small Animal Practitioner

polymyositis). Electrodiagnostic testing may be useful to confirm involvement

of other muscle groups in these cases.

Laryngeal paralysis is most commonly encountered in middle‐aged or older,

large breed dogs. It can present in isolation but is more frequently associated
with additional neurological deficits that reflect a diffuse polyneuropathy, termed
‘laryngeal paralysis‐polyneuropathy syndrome’ (LPP) (Bookbinder et al. 2016;
Braund et al. 1989; Jeffery et al. 2006; Thieman et al. 2010). Labrador Retrievers
appear to be over‐represented with this condition. Laryngeal paralysis‐polyneu-
ropathy (LPP) results in clinical signs of laryngeal paralysis and sciatic nerve
dysfunction, including a plantigrade posture, poor hock flexion when walking,
reduced pelvic limb withdrawal reflexes, and pelvic limb proprioceptive deficits.
The oesophagus may also be affected, resulting in megaoesophagus (see below).
It is postulated that the long length of the recurrent laryngeal and sciatic nerves
predisposes them to this condition, as the neuronal cell bodies become unable to
maintain such a long axon in later life.
Idiopathic laryngeal paralysis is a diagnosis of exclusion in adult dogs that
present without other neurological deficits. The early stages of LPP, before the
onset of sciatic nerve dysfunction, should always be considered in these cases.
Hypothyroidism has been anecdotally associated with laryngeal paralysis in
dogs, and thyroid function testing (total T4 and TSH levels) can be performed to
exclude this potentially treatable condition (Jaggy and Oliver 1994).
Laryngeal paralysis appears to be rare in cats but has been reported as a uni-
lateral or bilateral condition (Macphail 2014). Unilateral laryngeal paralysis may
remain subclinical, and therefore undiagnosed, in cats given their relatively
inactive nature compared to dogs. Idiopathic laryngeal paralysis has been
reported in cats but neoplastic infiltration, particularly by lymphoma, should
always be considered in this species.
Treatment of laryngeal paralysis is required if the clinical signs of stridor,
coughing, and exercise intolerance are impacting significantly on an animal’s
quality of life. This involves surgical lateralisation of the arytenoid cartilage to
improve air flow through the larynx (Monnet 2016). Owners should always be
warned of the increased risk of aspiration following surgery, particularly in cases
with concurrent pharyngeal dysphagia or megaoesophagus (Wilson and Monnet
2016). They should also be made aware that pre‐operative exercise intolerance
may persist following surgery, particularly in those with a progressive polyneu-
ropathy; dogs with LPP will show an inevitable decline in their pelvic limb gait
secondary to sciatic nerve dysfunction over a period of months to years.
A logical approach to a case with suspected laryngeal paralysis should include
the following considerations. A short list of differential diagnoses can usually be
formulated by combining the clinical history and signalment of the animal
together with the results of a thorough general physical examination and neu-
rological examination.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 225

1. Exclude a local structural cause for the clinical signs and confirm laryngeal
paralysis.
2. What was the age of the animal at the onset of clinical signs (see Box 6.6.5)?
3. Is there a history of toxin exposure? Laryngeal paralysis has been reported
following lead or organophosphate intoxication. Additional clinical signs,
specific to the particular toxin, would be expected in these cases, such as
weight loss, gastrointestinal signs, seizures, ataxia, and blindness for lead tox-
icity, and miosis, salivation, gastrointestinal signs, muscle fasciculations, rest-
lessness, or weakness for organophosphate exposure.
4. Is there a history of recent cervical surgery (e.g. thyroid surgery, ventral slot
decompression)?
5. Are there any other neurological deficits that would be consistent with a brain-
stem neuroanatomic localisation? These would include a depressed level of men-
tation, hemiparesis/tetraparesis, proprioceptive deficits, and other cranial nerve
deficits such as facial paralysis, vestibular syndrome, or pharyngeal dysphagia.
6. Are there any other neurological deficits that would be consistent with a gen-
eralised neuromuscular disorder? These could include generalised muscle
atrophy, exercise intolerance, megaoesophagus, lower motor neuron tetrapa-
resis, and reduced/absent spinal reflexes.

2. Megaoesophagus
Megaoesophagus is the term used to describe oesophageal dilatation, which is
frequently accompanied by reduced oesophageal motility and regurgitation of
undigested food. As for laryngeal paralysis, megaoesophagus may be secondary to
local structural disease, or it may be non‐structural resulting from abnormal inner-
vation of the oesophageal musculature. The canine oesophagus is predominately
comprised of striated skeletal muscle, meaning that it may be affected by general-
ised neuromuscular disorders such as polymyopathies and myasthenia gravis.

a. Classification
Local structural disorders resulting in megaoesophagus include intra‐ and extra‐
luminal masses, obstruction by foreign bodies, oesophageal strictures, hiatal her-
nia, vascular ring anomalies, and oesophagitis. These disorders frequently result
in focal dilation of the oesophagus cranial to the level of obstruction. This is in
contrast to non‐structural causes, which more frequently result in generalised
dilation and dysmotility.
Non‐structural megaoesophagus can be classified as:

• Congenital, idiopathic megaoesophagus in animals presenting within 6 months

of weaning (at less than around 8 months of age) and for which an underlying
cause cannot be found (Boudrieau and Rogers 1985).
• Acquired megaoesophagus – this category can be further subdivided into:
–– Idiopathic acquired megaoesophagus in animals first displaying clinical
signs at >8 months of age for which an underlying cause cannot be
226 A Practical Approach to Neurology for the Small Animal Practitioner

found. An idiopathic disorder affecting the sensory innervation of the

oesophagus is suspected in these cases. This condition may account for
up to 75% of all canine cases with acquired, non‐structural megaoe-
sophagus (Boudrieau and Rogers 1985; Nakagawa et al. 2019). However,
the incidence of idiopathic disease may be overestimated in older studies
as recent advances in both knowledge and the diagnostic tools available
mean that an underlying disease process may now be identified in many
of these cases.
–– Secondary acquired megaoesophagus in animals presenting at any age for
which an underlying cause is identified on diagnostic investigations. These
animals frequently present with other neurological deficits and/or clinical
signs consistent with the presence of an underlying disease process.

b. Clinical signs
The classical clinical sign associated with megaoesophagus is regurgitation of
undigested food. This process involves minimal abdominal effort and is usually
observed shortly after eating. However, it may be delayed by minutes to several
hours in some cases. In order to distinguish regurgitation from gagging or vom-
iting, it is vital to obtain a thorough clinical history from the owner or observe
an episode first‐hand. Gagging is typically associated with pharyngeal abnor-
malities and is observed at the time of swallowing. Vomiting most commonly
occurs in association with gastrointestinal disease and is an active process
involving abdominal effort. It is also frequently associated with nausea, the
vomitus may be partially or completely digested, and often contains bile.
However, it can be difficult to distinguish vomiting from regurgitation in many
cases, as some animals with oesophageal disorders may appear nauseous and
salivate profusely at the time of regurgitation. Weight loss is commonly observed
in dogs with megaoesophagus, secondary to frequent regurgitation and reduced
calorie intake.

c. Diagnosis and neuroanatomic localisation

The presence of megaoesophagus can be confirmed on conscious, plain thoracic
radiography, with a left lateral view being preferred (Figure 6.6.7). Oesophageal
dilation may be observed as an incidental finding in animals that have received seda-
tion or a general anaesthetic for imaging. Therefore, care should always be taken in
the interpretation of thoracic radiographs in these cases. The use of a barium swal-
low to highlight oesophageal dilation is not recommended, as animals with megaoe-
sophagus are prone to aspiration, potentially resulting in a chemical pneumonitis.
The neuroanatomic localisation for secondary acquired megaoesophagus can
be divided as follows:

• A central lesion that is affecting the motor nucleus of the vagus nerve (nucleus
ambiguus) in the caudal brainstem – this is an uncommon cause of acquired
 Chapter 6 A Practical Approach to Common Presentations in General Practice 227

Figure 6.6.7 Left lateral thoracic radiograph in a dog with generalised acquired megaoesoph-
agus secondary to myasthenia gravis. Note the well‐defined, linear, soft tissue opacity created
by summation of the ventral oesophageal wall and dorsal tracheal wall, termed a ‘tracheal
stripe sign’ (black arrow). Note also the sharp, soft tissue interface from the thoracic inlet to
the ventral aspect of the T6 vertebra created by the dorsal wall of the dilated oesophagus
contacting the paired longus colli muscles under the vertebral column, and the pair of thin,
parallel, soft tissue opacity stripes that converge at the diaphragm representing the dorsal and
ventral walls of the dilated oesophagus (white arrows).

megaoesophagus as bilateral vagal dysfunction is typically required to result in

clinically significant oesophageal dilation. This would require a large lesion
that involves the motor nuclei on both sides of the brainstem, with potentially
fatal involvement of other neuroanatomical structures.
• Bilateral dysfunction of the peripheral component of the vagus nerves – meg-
aoesophagus rarely occurs in isolation in these cases and is more commonly
seen together with dysfunction of the pharynx, larynx, and/or appendicular
muscles (e.g. paraneoplastic polyneuropathy, LPP syndrome).
• A primary myopathy or junctionopathy that is affecting the striated muscles of
the oesophagus – this is the most common neuroanatomic localisation for sec-
ondary acquired megaoesophagus in dogs and cats. Myasthenia gravis is the
most common diagnosis in dogs, which may be focal to the oesophagus or
present as a generalised form (Haines 2019; Nakagawa et al. 2019; Yam et al.
1996). Other differential diagnoses include idiopathic polymyositis, infectious
myopathies, hypoadrenocorticism, hypothyroidism, and botulism (Bartges and
Nielson 1992; Fracassi and Tamborini 2011; Gaynor et al. 1997; Haines 2019;
228 A Practical Approach to Neurology for the Small Animal Practitioner

Whitley 1995). The clinical suspicion for each condition will depend upon the
concurrent clinical signs and biochemical changes (e.g. elevated muscle
enzymes for myopathies). Electrodiagnostic testing may be useful for the diag-
nosis of generalised myopathies.

d. Diagnostic approach
The diagnostic approach to megaoesophagus is very similar to that for laryngeal
paralysis:

1. Confirm the presence of megaoesophagus and exclude a local structural cause.

2. What was the age of the animal at the onset of clinical signs? Congenital idiopathic
megaoesophagus is the most common cause of non‐structural megaoesophagus in
young animals, but a structural cause should always be considered first (e.g. vascu-
lar ring anomaly). Congenital myasthenia gravis should also be considered as a
cause for secondary acquired megaoesophagus in a young animal.
3. Is there a history of toxin exposure? Megaoesophagus has been reported as a
rare clinical sign associated with lead or organophosphate intoxication.
4. Are there any other neurological deficits that would be consistent with a
brainstem neuroanatomic localisation?
5. Are there any other neurological deficits that would be consistent with a gen-
eralised neuromuscular disorder?
6. Are there any other clinical signs that could be consistent with an underlying
endocrine disorder? These could include gastrointestinal signs and intermit-
tent weakness/collapse for hypoadrenocorticism, or non‐pruritic hair loss,
weight gain, lethargy, and bradycardia for hypothyroidism.

If megaoesophagus is confirmed on conscious thoracic radiography, local

structural disease has been excluded, and there are no additional neurological
deficits to suggest a central lesion, then further investigations should include a
complete blood cell count, serum biochemistry, and endocrine testing (total T4,
TSH, basal cortisol). An ACTH stimulation test should be performed in animals
for which hypoadrenocorticism cannot be excluded using a basal cortisol level
alone (i.e. those with a basal cortisol <55 nmol/l) (Bovens et al. 2014). Serum
muscle enzymes (CK, AST, ALT) can be used to investigate the possibility of a
polymyopathy. This can be further excluded using electrodiagnostic testing +/−
muscle biopsy. Myasthenia gravis is the most common cause of secondary
acquired megaoesophagus in dogs, therefore nicotinic acetylcholine receptor
(nAchR) antibody testing is a useful test in general practice. However, false neg-
ative results are possible in cases with focal or generalised disease and this should
always be considered if there is otherwise a high clinical suspicion for this condi-
tion. Repeat testing can be performed after 2–4 weeks in these cases. Radiographic
measurements do not appear useful in distinguishing dogs with megaoesopha-
gus secondary to myasthenia gravis from those with megaoesophagus due to
other causes (Wray and Sparkes 2006).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 229

e. Management
The management of megaoesophagus should focus on correction of the underlying
cause if possible. Megaoesophagus may be reversible in certain cases, such as those
with hypothyroidism, hypoadrenocorticism, and in some cases of myasthenia gravis.
However, megaoesophagus is frequently permanent, particularly in idiopathic cases.
Management of these cases involves careful feeding and provision of water to
reduce the risk of aspiration and secondary pneumonia (Mace et al. 2012):

• Feed a high‐quality, calorific food in small portions, multiple times a day. This
reduces the volume of food eaten at any one time. Access to other sources of
food and water away from meal times should ideally be prevented. The ideal
consistency of food to reduce the risk of aspiration varies with the individual;
some dogs tolerate balls of wet food best, whereas others cope better with
soaked kibble or a slurry of food.
• Mild cases may be fed from a height using elevated food and water bowls. The
animal can also be taught to stand with their front paws on a block to increase
the height of the mouth relative to the stomach.
• More severe cases benefit from being held vertically for 20–30 minutes after
eating, either in an owner’s arms or by using a specially designed ‘Bailey chair’
for bigger dogs.
• A permanent gastrostomy tube can be placed for longer‐term feeding in
severely affected cases.
• Intermittent, at‐home suctioning of oesophageal content has been reported to
reduce the incidence of regurgitation and recurrent aspiration pneumonia in
dogs with megaoesophagus (Manning et al. 2016).

A recent study has suggested that sildenafil citrate could represent a novel
treatment option for dogs with congenital idiopathic megaoesophagus
(Quintavalla et al. 2017).

6.6.4 Hypoglossal Nerve

The hypoglossal nerve is the twelfth cranial nerve. It provides motor innervation
to geniohyoideus and to the intrinsic and extrinsic muscles of the tongue (stylo-
glossus, hyoglossus, genioglossus). The neuronal cell bodies reside within a
motor nucleus in the medulla oblongata of the caudal brainstem, and the axons
exit the caudal aspect of the skull via the hypoglossal canal.
Hypoglossal nerve dysfunction presents as ipsilateral atrophy of the tongue. In
chronic cases, the tongue may deviate towards to the affected side following den-
ervation and contracture of the intrinsic tongue muscles. Bilateral lesions result in
an inability to withdraw the tongue into the mouth and associated difficulty in the
prehension of food and water. An important differential diagnosis for bilateral
hypoglossal nerve dysfunction is tongue paresis/atrophy secondary to a primary
myopathy affecting the tongue. This condition has been reported sporadically in
Pembroke Welsh Corgis (Ito et al. 2009; Toyoda et al. 2010). The intrinsic tongue
230 A Practical Approach to Neurology for the Small Animal Practitioner

muscles may also be affected in dogs with generalised polymyositis; however,

these dogs will typically show other clinical signs consistent with a generalised
disease process (e.g. weight loss, generalised muscle atrophy, stiff gait, exercise
intolerance, elevated muscle enzymes). Dysphagia secondary to a focal inflamma-
tory myopathy and consequent dorsiflexion of the rostral part of the tongue has
been recently reported as an isolated case in a young, female Pitbull Terrier cross-
breed dog (Strøm et al. 2018). The tongue may also be affected as a component of
the generalised neuromuscular weakness observed in cases with botulism.
The hypoglossal nerve is rarely affected in isolation and is more frequently
affected by lesions that also involve adjacent cranial nerves. This may occur at
the level of the brainstem nuclei, or where the individual nerves are closely
associated as they exit the skull. These cranial nerves include the vestibulococh-
lear nerve (VIII), glossopharyngeal nerve (IX), and vagus nerve (X). Tongue
atrophy and paresis may therefore be observed in combination with other neu-
rological deficits, such as vestibular syndrome, pharyngeal dysphagia, laryngeal
paralysis, or megaoesophagus. A depressed level of mentation, ipsilateral hemi-
paresis, tetraparesis, and/or ataxia of all limbs may be observed if the lesion
involves the brainstem nuclei (Figure 6.6.8). These additional deficits would be
absent if the lesion is situated outside the skull and is affecting the cranial nerve
axons as they exit from their respective foramina. Radiography and/or ultra-
sonography of the caudal aspect of the skull can be performed in general practice

Figure 6.6.8 A mid‐sagittal T2‐weighted MRI in an 8‐year‐1‐month old, female neutered

Labrador Retriever with a 2‐week history of lethargy, pacing, a low head carriage, dysphagia,
and drooling from the left side of the mouth. Neurological examination revealed a depressed
level of mentation, compulsive pacing, mild tetraparesis and ataxia of all limbs, delayed
proprioception in all limbs, intact withdrawal reflexes in all limbs, a positional vertical
nystagmus on head elevation, a poor gag reflex, and reduced tongue tone. The neuroanatomic
localisation was to the brainstem. The MRI demonstrates an ovoid, broad‐based, extra‐axial
mass lesion with a cystic component that is lying ventral to the medulla oblongata and is
resulting in marked, dorsal deviation of the brainstem. This mass was suspected to represent a
meningioma, but histopathology was not performed in this case to confirm the diagnosis.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 231

if unilateral tongue paresis/atrophy is noted, with or without concurrent involve-

ment of other cranial nerves. Referral for advanced imaging of the head and CSF
analysis is recommended in animals with a suspected brainstem lesion. In con-
trast to the trigeminal and facial nerves, an idiopathic cause of hypoglossal nerve
dysfunction has not been reported in dogs or cats, therefore a structural cause
should always be investigated in these cases if possible.

6.7 ­Vestibular Syndrome

Paul M. Freeman

The vestibular system broadly consists of the sensory organs located in the inner
ear (semi‐circular canals, utricle, and saccule), the vestibulocochlear nerve, and
the vestibular nuclei of the brainstem. A detailed description of the anatomical
structures of the vestibular system is beyond the scope of this book but is
available in many other texts for the interested reader. What is required for the
general practitioner is an understanding of the functional anatomy and how this
affects the clinical approach to vestibular disease (see Figure 6.7.1). For the
purposes of formulating a sensible approach to differential diagnoses and
prognosis, the vestibular system may be divided into peripheral and central
components; the sensory organs of the inner ear and the vestibulocochlear nerve
comprise the peripheral vestibular system, and the brainstem vestibular nuclei
and associated cerebellar projections form the central vestibular system.
The vestibular nuclei in the brainstem project axons rostrally via the medial
longitudinal fasciculus (MLF) to the nuclei of cranial nerves III, IV, and VI in
order to control eyeball position and movement. Axonal projections also pass via
the thalamus to the cerebral cortex to enable conscious perception of head and
body position. Deeper fibres project to the vomiting centre of the medulla oblon-
gata. Caudally, fibres from the vestibular nuclei form the medial and lateral ves-
tibulospinal tracts, which are motor tracts that predominantly facilitate the
ipsilateral extensor muscles. Through these fibres, they are responsible for main-
taining weight‐bearing and posture of the limbs, neck, and trunk.
In addition, the vestibulocochlear nerve projects directly to the cerebellum,
and there are further connections between the cerebellum and the brainstem ves-
tibular nuclei. The cerebellum is largely responsible for coordinating movement,
and it also has a mainly inhibitory effect on the vestibular nuclei via ipsilateral
projections. Finally, there are afferent fibres which travel from the dorsal nerve
roots of the first three cervical spinal cord segments (C1–C3) to the vestibular
nuclei that are thought to play a role in maintaining head and neck position. The
basic anatomy and important connections to be aware of in order to understand
the common reasons behind vestibular dysfunction are illustrated in Figure 6.7.1.
232 A Practical Approach to Neurology for the Small Animal Practitioner

Eye

III IV VI

Cerebellum

Vestibulocochlear nerve (CN VIII)

al
Rostr
MLF Medulla
Ear canal

Vestibular nuclei

Semicircular canals

al
Vestibulospinal tract

Caud
Figure 6.7.1 Anatomy of the vestibular system.

6.7.1 Clinical Signs of Vestibular Disease

In order to adequately assess and approach vestibular cases, it is important to
understand the potential presenting signs of vestibular disease. An understanding
of the functional anatomy of the vestibular system allows for a better apprecia-
tion of the various signs of vestibular dysfunction, and the possible neuroana-
tomical localisations when faced with such a case. The major signs of vestibular
disease, some or all of which may be present in any case, are summarised below.
Head tilt (Figure 6.7.2) – This is when the horizontal axis of the head (through
the eyes) is rotated relative to the sagittal plane of the animal. It must be differ-
entiated from head turn, which is when the head is turned towards the body, but
the horizontal axis remains perpendicular to the sagittal plane, as may be seen
in forebrain disease. A head tilt almost always implies vestibular disease, although
in some instances of painful otitis externa an animal may hold the head tilted to
one side because of pain.
Vestibular ataxia – Vestibular ataxia involves the tendency to drift or fall
towards the affected side, due to loss of normal extensor muscle tone. There may
also be tight circling to that side (see Video 17). In cases of bilateral vestibular
 Chapter 6 A Practical Approach to Common Presentations in General Practice 233

Figure 6.7.2 Head tilt. This cat is suffering from a left central vestibular syndrome and is
displaying a particularly severe left head tilt. The gait was also severely affected, although the
severity of the signs does not always correlate with the prognosis in vestibular syndrome.

disease, animals tend to crouch low and often show wide excursions of the head
from side to side. The tail is often carried high in cats as a means of improving
balance (see Video 27 and Figure 3.6).
Nystagmus – Nystagmus is involuntary or uncontrolled eye movement and is
seen frequently as part of vestibular syndrome. Nystagmus can be induced in a
normal animal by moving the head from side to side (the vestibulo‐ocular reflex,
or physiologic nystagmus). This ensures that the eyes are kept centrally positioned
to maximise visual acuity. In cases with vestibular dysfunction, reduced vestibular
output on the affected side when the head is not moving is ‘interpreted’ as move-
ment of the head, causing the eyes to drift slowly towards the affected side, and
then ‘run away’ rapidly from the side of the lesion. This is termed a ‘jerk nystagmus’
as it consists of these fast and slow phases (see Video 20). In bilateral disease, both
the vestibulo‐ocular reflex and any pathological nystagmus are absent, since there
is symmetric loss of vestibular information bilaterally.
Nystagmus may be horizontal, rotatory, or vertical. When horizontal or rota-
tory, the slow phase is typically directed towards the affected side. The loss of
unilateral vestibular signal that causes nystagmus is often rapidly superseded by
visual compensation, and this can lead to resolution of the spontaneous nystagmus.
234 A Practical Approach to Neurology for the Small Animal Practitioner

When vestibular disease is suspected but signs are subtle, an abnormal ‘positional’
nystagmus can sometimes be induced by placing the animal in an abnormal posi-
tion (e.g. lying on its back looking up [see Figure 6.7.3], or by elevating the head)
(see Video 25). Similarly, blindfolding an animal with vestibular disease will
remove the ability to visually compensate and will often cause a marked deteriora-
tion in signs. See Chapter 3 for further discussion of how different characteristics
of a nystagmus (e.g. direction or rate) can be used to guide the distinction between
a suspected peripheral or central vestibular syndrome.
Strabismus – Strabismus is defined as an abnormal position of an eye. It may
be either ‘fixed’, where the eye is permanently displaced, or ‘positional’, where
the strabismus is elicited by changing the position of the head. In vestibular dis-
ease, animals will not have a fixed strabismus but may show a ventrolateral
positional strabismus when the head is elevated (see Figure 6.7.4).

6.7.2 Diagnostic Approach to Vestibular Disease

In terms of producing the differential diagnosis list for cases with vestibular syn-
drome, an important distinction must first be made between a central and a
peripheral neuroanatomic localisation. To this end, the neurological examina-
tion is of critical importance, and should be considered ahead of the signalment
and clinical history in cases of vestibular syndrome.

1. Neurological examination
Mentation: In cases of peripheral vestibular disease, the level of mentation should
be normal. The exception is in situations where the animal feels so disorientated
and/or nauseous that they may become apparently depressed. In cases of central

Figure 6.7.3 Attempting to induce nystagmus in an animal with subtle vestibular signs.
Visual compensation means that many animals with a vestibular syndrome may lose the
spontaneous nystagmus within a day or two; however, it is often possible to induce nystagmus
in such cases by elevating the head or placing the affected animal on their back, as in this case.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 235

Figure 6.7.4 Strabismus. Animals with vestibular syndrome will often demonstrate a ventral
or ventrolateral strabismus when the head is elevated, as in this case where the right eye is in
an abnormal position associated with a right‐sided vestibular syndrome.

disease, it is possible that any lesion which affects the vestibular nuclei of the
brainstem may also affect the ascending reticular activating system (ARAS),
leading to a reduced level of consciousness and genuine obtundation.
Gait and posture: A head tilt towards the affected side and vestibular ataxia (see
Video 17) may be features of both peripheral and central vestibular disease. In
some cerebellar lesions, the head tilt (and nystagmus) may point towards a lesion
on the opposite side to that of the actual cerebellar lesion. This is termed a ‘para-
doxical vestibular syndrome’ (see Section 6.8 ‘Cerebellar Dysfunction’). This is
due to a loss of inhibition to the vestibular nuclei on the side of the cerebellar
lesion, leading to a relatively reduced vestibular output on the opposite (contralat-
eral) side to the lesion. It is usually obvious that there is a cerebellar lesion on the
truly affected side due to the presence of asymmetrical hypermetria and/or other
signs of cerebellar disease or postural reaction deficits (see Video 19). The veteri-
narian only needs to be aware of the possibility of a paradoxical vestibular syn-
drome to avoid a mistaken assumption that there may be multifocal lesions, which
can lead to problems regarding formulating the list of differential diagnoses.
Postural reactions: These should be normal in cases with peripheral vestibular
disease but can be abnormal in cases of central disease due to concurrent disrup-
tion of the ascending proprioceptive pathways within the brainstem. Deficits are
usually ipsilateral to the side of the central lesion.
Cranial nerves: Nystagmus and/or positional strabismus may be expected in
the early stages of most cases of peripheral or central vestibular syndrome (see
above). Associated ipsilateral cranial nerve deficits, especially of those nerves that
are anatomically close to cranial nerve VIII, may indicate a central (brainstem)
localisation. However, it should be remembered that cranial nerve VII (the facial
236 A Practical Approach to Neurology for the Small Animal Practitioner

nerve) and the sympathetic nerves to the eye pass immediately adjacent to the
tympanic bulla unseparated by bone from the cavity of the middle ear. Therefore,
it is common for facial nerve paralysis and/or Horner syndrome to accompany
peripheral vestibular syndrome in cases of otitis media/interna (see Sections 6.5
& 6.6 ‘Abnormalities of Pupil Size’ and ‘Cranial Nerve Dysfunction’). The clini-
cian should take care not to misinterpret these signs as evidence of brainstem
involvement in the absence of other key indicators, such as postural reaction
deficits or changes in the level of mentation.
Spinal reflexes: Unless there is multi‐focal disease, the spinal reflexes should be
normal in cases with both peripheral and central vestibular syndrome as the
C6–T2 and L4–S3 spinal cord segments will not be affected.
Palpation for pain: This is frequently normal except in the case of otitis media/
interna, which may be a very painful condition, or in animals with inflamma-
tory brain disease and referred neck pain.
In summary, the neuroanatomic localisation may be considered central if
there is an abnormal level of mentation, multiple cranial nerve deficits, or pos-
tural reaction deficits. In the absence of these signs, or if there is concurrent
vestibular syndrome, facial paralysis +/− Horner syndrome without postural
reaction deficits, the localisation may be considered peripheral. This differentia-
tion is crucial, but not always easy! It is also vital to consider that a central lesion
is highly likely if there are concurrent postural reaction deficits or a convincingly
altered level of mentation, but a central lesion can never be excluded in the
absence of these signs (i.e. central disease can mimic peripheral disease but
rarely vice versa) (Box 6.7.1).

Box 6.7.1

Top tip: Neither the severity of signs nor the acuteness of onset have any correlation
with prognosis in vestibular disease. Some of the most acute and severe cases are
idiopathic!

2. Differential diagnoses for peripheral vestibular disease

(see also Section 6.6.2 ‘Facial Nerve’)
• Vascular: unlikely.
• Inflammatory/infectious: otitis media/interna, inflammatory nasopharyngeal
polyp, inflammatory neuritis.
• Traumatic: injury to tympanic bulla.
• Toxic: topical otitis treatments, aminoglycosides (topical or systemic).
• Anomalous: congenital vestibular syndrome; this has been described in a num-
ber of breeds including German Shepherd Dogs and Doberman Pinschers.
• Metabolic: hypothyroidism; as with facial neuropathy, the evidence that
hypothyroidism can cause vestibular nerve dysfunction is weak, but there are
 Chapter 6 A Practical Approach to Common Presentations in General Practice 237

reports of vestibular signs responding to thyroid supplementation in dogs with

a diagnosis of hypothyroidism.
• Idiopathic vestibular syndrome (see below).
• Idiopathic cranial polyneuropathy: occasionally a syndrome of apparently idio-
pathic polyneuropathy of cranial nerves is seen, where multiple cranial nerve
deficits are found either unilaterally or bilaterally and all investigations are
unrewarding. Prognosis appears good although occasionally some symptoms
such as facial paralysis and head tilt may be permanent.
• Neoplastic: lymphoma, ceruminous gland adenocarcinoma, squamous cell
carcinoma.
• Degenerative: no specific syndromes.

Hence it can be seen that if the neuroanatomic localisation is peripheral, by

far the most likely causes are idiopathic or otitis media/interna. It should often
be possible to eliminate ‘anomalous’/‘congenital’ from signalment and ‘toxic’
from history taking. Hypothyroidism is a suggested cause of peripheral vestibu-
lar syndrome but is extremely rare without other significant signs of hypothy-
roidism in the author’s experience. Neoplastic causes of peripheral vestibular
syndrome are also rare in the absence of other signs.

3. Idiopathic (geriatric) vestibular syndrome

Idiopathic vestibular syndrome is the most common cause of vestibular disease
in dogs. It may be seen in any age or breed of dog, as well as in cats, but is most
commonly seen in older dogs. Clinical signs are acute or peracute, moderate to
severe, and are consistent with a peripheral vestibular syndrome, including head
tilt, nystagmus, and vestibular ataxia. The signs may be severe enough to render
an affected animal unable to walk, and occasionally may cause nausea, vomit-
ing, and associated anorexia. The diagnosis is achieved by excluding other pos-
sible causes of vestibular disease. However, as long as the clinician is reasonably
certain from the general physical and neurological examinations that he or she
is dealing with a peripheral vestibular syndrome rather than a central lesion,
making a presumptive diagnosis of idiopathic vestibular syndrome without
advanced imaging may be reasonable.
There is no specific treatment for idiopathic vestibular syndrome. Most dogs
and cats improve within a few days, and many make a full recovery within
1–2 weeks. Occasionally, a suspected idiopathic vestibular syndrome may have a
much longer and more chronic recovery, with the acute and severe signs improv-
ing but milder signs persisting or sometimes even waxing and waning. In this
situation, referral for further investigation is advised in order to rule out a poten-
tial central vestibular disease, or a less common cause of peripheral disease such
as neoplasia. Symptomatic treatment with antiemetics, such as maropitant, and
occasionally even mild sedation with diazepam or acepromazine may prove use-
ful in the most acute, severe phase.
238 A Practical Approach to Neurology for the Small Animal Practitioner

4. Differential diagnoses for central vestibular disease

• Vascular: ischaemic or haemorrhagic stroke affecting the brainstem or
thalamus.
• Inflammatory/infectious: meningoencephalitis of unknown origin, protozoal
meningoencephalitis (Toxoplasma, Neospora), bacterial meningitis or empy-
ema (potentially secondary to chronic otitis media/interna), viral meningoen-
cephalitis (such as feline infectious peritonitis [FIP] and canine distemper
virus [CDV]).
• Traumatic: traumatic brain injury (unlikely to present with central vestibular
signs alone).
• Toxic: metronidazole toxicity (see Section 6.8 ‘Cerebellar Dysfunction’).
• Anomalous: hydrocephalus, supracollicular fluid accumulation.
• Metabolic: hypothyroidism; again, central vestibular disease has been reported
in dogs with hypothyroidism, but the mechanism for this is not understood
and the evidence remains weak.
• Neoplastic: intracranial (e.g. glioma, meningioma), extracranial (e.g.
lymphoma).
• Nutritional: thiamine deficiency; cats and dogs may occasionally be affected
with thiamine deficiency, most commonly cats fed a diet containing raw fish
which may contain thiaminase. Clinical signs include anorexia and lethargy,
as well as neurological signs such as a central vestibular syndrome (often bilat-
eral) and occasionally seizures. The onset may be acute or subacute, and diag-
nosis may be presumptive based on history and clinical signs. Blood thiamine
levels may be measured although results are difficult to interpret. Many
affected animals will show characteristic changes on brain MRI. Treatment
involves correction of the diet and thiamine supplementation, with prognosis
being good as long as treatment is initiated early enough.
• Degenerative: vestibular signs may be seen in neurodegenerative disorders,
such as the lysosomal storage diseases. The signs are typically progressive and
often multifocal, with involvement of other areas of the brain as well as in
some cases other organs. These diseases are rare in general practice, but it is
important to be aware of their existence and poor prognosis.

The most common causes of central vestibular disease are stroke, menin-
goencephalitis of unknown origin (MUO), and neoplasia, and therefore a suspi-
cion of central disease should lead to a more guarded prognosis than for
peripheral disease. In arriving at the most likely differential diagnoses, the sig-
nalment should increase the index of suspicion for the anomalous causes, and
the history may help to eliminate metronidazole toxicity. Degenerative diseases
should present as chronic progressive signs, usually in younger animals, unlike
the three more common differential diagnoses. Stroke may be expected to have
acute or peracute onset and then remain static or improve. MUO is likely to have
 Chapter 6 A Practical Approach to Common Presentations in General Practice 239

an acute or subacute onset followed by often rapidly progressive signs, which

may be multifocal. Neoplasia is usually chronic and progressive and is most com-
monly seen in older animals.
For a more detailed description of the potential conditions which may under-
lie a central vestibular syndrome please see also Section 6.8 ‘Cerebellar
Dysfunction’, since there is significant overlap between lesions that may lead to
central vestibular syndrome and lesions that may cause a cerebellar syndrome.

6.7.3 Investigation of Vestibular Syndrome

Once the differential diagnoses are established, then a decision must be made
whether to investigate further in‐house, treat empirically based on most likely
differentials, or refer for specialist examination +/− advanced imaging.
In a case of peripheral vestibular disease, this may be a relatively easy deci-
sion because the two most likely differential diagnoses are idiopathic vestibular
syndrome and otitis media/interna. The main decision is therefore whether to
investigate and/or treat for suspected otitis media/interna; this can often be
based on the clinical history and physical examination, as well as radiography or
CT of the tympanic bullae if available. If there is significant doubt regarding the
possibility of otitis media/interna, or if there is uncertainty whether this is a
peripheral or central lesion, then referral for specialist evaluation should be
considered.
When central vestibular disease is suspected on the basis of the neurological
examination, referral should always be offered to further investigate the most
common causes. These conditions are likely to require advanced imaging and
perhaps cerebrospinal fluid (CSF) analysis in order to obtain a diagnosis, and
carry a guarded prognosis. The one exception to this may be in situations where
a vascular cause (stroke) is strongly suspected from the history and/or physical
examination findings; in these cases, further in‐house investigation of potential
underlying cases may be justified.
If referral is not an option, then a basic diagnostic work‐up as for other
potential intracranial disorders should be considered. The decision whether to
initiate in‐house investigations or immediately refer for further investigation by
a specialist is, as already stated above, one which requires careful discussion with
the owner, and in many cases referral may not be an option for financial or logis-
tical reasons.
Investigations which may be performed include:

• Haematology, serum biochemistry, and urinalysis.

• Blood pressure testing – if this is persistently elevated an ACTH stimulation test
may be justified, especially with supporting clinical and biochemical features
of hyperadrenocorticism.
• Thyroid function testing – total thyroid hormone (T4), free T4, TSH.
240 A Practical Approach to Neurology for the Small Animal Practitioner

• A coagulation profile and testing for A. vasorum if a disorder of blood clotting is

suspected.
• Infectious disease testing dependent on the species and relative risk of expo-
sure – T. gondii in cats and dogs, N. caninum or CDV in dogs, FeLV, FIV, and
feline coronavirus in cats.
• Urine metabolic screening if an inborn error of metabolism is suspected (e.g.
young animal with progressive neurological disease).
• Radiography or CT of the tympanic bullae.
• Thoracic radiography, abdominal ultrasonography, or head, thoracic, and abdominal
CT – particularly if neoplasia is likely.

If a diagnosis of systemic disease is confirmed, then treatment should be

directed at resolving the underlying disease and monitoring the progression of
the vestibular signs. Where in‐house investigations do not reveal the diagnosis,
either continued monitoring or empirical treatment based on the most likely dif-
ferential diagnoses may be considered.

6.7.4 Management of Vestibular Disease

1. Symptomatic treatment
Treatment is aimed at reducing any nausea with the use of antiemetics such as
maropitant, and occasionally providing some anxiolytic therapy such as ace-
promazine or butorphanol if clinical signs are severe. It may be necessary to
hospitalise a severely affected dog or cat with suspected idiopathic vestibular
syndrome until the most severe signs have resolved and the animal is able to
ambulate and is eating. Owners are often very distressed to see their pet in an
acute severe vestibular state, and because most idiopathic cases occur in older
animals they are sometimes inclined to assume that the prognosis is poor and
request euthanasia. This should be resisted if the clinician is satisfied that the
problem is most likely to be peripheral and represent an idiopathic vestibular
syndrome.

2. Management of suspected stroke (see Section 6.3.4 ‘Obtundation’)

3. Treatment of suspected intracranial neoplasia (see also Section 6.3.4

‘Obtundation’)
The prognosis and likelihood of achieving even short‐term improvement with
neoplasia in the brainstem is less than when palliatively treating tumours in
the forebrain. If symptomatic treatment with corticosteroids is initiated in a
case of suspected brainstem neoplasia that is causing central vestibular signs,
improvement should be expected within a few days if it is going to occur at all;
if this is not seen, and referral is not an option, then euthanasia should be
considered.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 241

Animal presented with Perform full neurological VESTIBULAR SYNDROME

vestibular signs examination

Central localisation (e.g.

postural reaction deficits,
Peripheral localisation mentation change)

Consider
Investigate for otitis differentials
media/interna
Refer to specialist
if possible
Investigate
Treat suspected Treat for idiopathic and/or treat
otitis vestibular syndrome empirically if
media/interna symptomatically vascular cause
seems likely

Approach to cases of vestibular syndrome in practice.

6.8 ­Cerebellar Dysfunction

Edward Ives

The cerebellum resides within the caudal fossa of the skull and lies dorsal to the
pons and medulla oblongata of the brainstem. The primary functions of the
cerebellum are:

• coordination and refinement of movements that are initiated by the motor

centres of the cerebrum and brainstem
• regulation of posture and inhibition of extensor muscle tone
• coordination of postural reactions, such as hopping
• coordination of appropriate motor responses to visual and auditory stimuli
(e.g. blinking of the eye in response to a menacing gesture).

The cerebellum also forms part of the central vestibular system and has a
predominately inhibitory influence on the vestibular nuclei of the brainstem.
Disorders that affect the cerebellum do not influence whether a particular
movement is initiated in the first place, but result in an inappropriate rate,
range, and force of movement. This presents as unpredictable limb placement
(ataxia), truncal swaying, and exaggerated, hypermetric limb movements, par-
ticularly if an animal is encouraged to walk up a kerb or climb steps (see Video
18). These hypermetric movements are characterised by excessive flexion of
the limb during protraction, followed by forceful, erratic replacement of the
paw back to the ground. This loss of coordination is termed ‘dysmetria’ and
242 A Practical Approach to Neurology for the Small Animal Practitioner

will also be appreciated when performing hopping tests, which will be delayed
and exaggerated in the affected limbs. These clinical signs will involve all limbs
for diffuse cerebellar lesions, or the ipsilateral thoracic and pelvic limbs for
unilateral lesions. A loss of postural regulation may also result in a wide‐based
stance. In severe cases, the degree of ataxia may mean that an animal is unable
to walk. However, as the cerebellum does not play a role in the initiation of
movement, animals with cerebellar disease do not show paresis and will have
preserved strength. The spinal reflexes will also be strong as the spinal cord
segments involved in these reflexes remain unaffected.
Diffuse lesions affecting both cerebellar hemispheres may result in the oscil-
lation of goal‐orientated movements, termed an ‘intention tremor’ (Lowrie and
Garosi 2016). This is most appreciable as a tremor of the head and neck during
actions such as lowering the head towards a food bowl or reaching for a toy.
Cerebellar dysfunction may also result in reduced/absent menace responses, but
the vision, pupillary light reflexes, and palpebral reflexes will remain normal.
Severe, usually acute, lesions affecting the rostral cerebellum can result in a
complete loss of inhibition of extensor muscle tone, termed ‘decerebellate rigidity’
(see Chapter 3). Affected animals will usually present in lateral recumbency with
extended thoracic limbs, an extended neck posture (opisthotonus), and extended
pelvic limbs that may be held flexed at the hips (Figure 6.8.1). This posture appears
similar to the posture adopted by animals with diffuse cerebrocortical or midbrain
lesions (decerebrate rigidity). However, as cerebellum does not play a role in the
maintenance of wakefulness, the level of mentation will be unaffected by lesions
that are isolated to the cerebellum. Therefore, animals in decerebellate rigidity will
remain alert and responsive, whilst animals with decerebrate rigidity will have a
severely altered level of mentation (stupor or coma). The close proximity of the
cerebellum to the brainstem means that lesions affecting one of these structures
may also influence the function of the other. This can result in combinations of
neurological deficits that reflect both cerebellar and brainstem dysfunction, such as
hypermetria, ataxia, and vestibular dysfunction together with hemi‐/tetraparesis,
paw replacement deficits, and/or cranial nerve deficits.
Cerebellar dysfunction, particularly if asymmetric, may be associated with
clinical signs of vestibular syndrome (e.g. head tilt, nystagmus, drifting, and fall-
ing to one side). The underlying basis of any vestibular syndrome is an imbal-
ance in the output from the vestibular nuclei in the brainstem; reduced output
from the vestibular nuclei on one side relative to the other results in a head tilt
and slow phase of a jerk nystagmus that are towards the side with reduced output.
Unilateral disorders of the peripheral vestibular system, or those that affect the
vestibular nuclei themselves, will result in reduced output from the ipsilateral
vestibular nuclei. The direction of the resultant head tilt and slow phase of nys-
tagmus will therefore be towards the side of the lesion. Certain regions of the
cerebellum, such as the flocculonodular lobe, exert an inhibitory influence on
the brainstem vestibular nuclei. A lesion that affects these regions, or the
 Chapter 6 A Practical Approach to Common Presentations in General Practice 243

Figure 6.8.1 Decerebellate posture in a 2‐year‐old Jack Russell Terrier with meningoen-
cephalitis of unknown origin, demonstrating increased extensor muscle tone in the thoracic
limbs and an extended neck posture (opisthotonus). The pelvic limbs have more normal tone
and are held partially flexed at the hip joints. This dog remained responsive to visual and
auditory stimuli.

connections between the cerebellum and vestibular nuclei via the caudal cere-
bellar peduncle, will result in a loss of inhibition and an increased output from the
ipsilateral vestibular nuclei. The subsequent imbalance between the output from
the vestibular nuclei on each side of the brainstem will result in a head tilt and
slow phase of a jerk nystagmus that are away from the side of the lesion
(Figure 6.8.2). This is termed a ‘paradoxical vestibular syndrome’. All the other
neurological deficits that reflect cerebellar dysfunction will be ipsilateral to the
side of the lesion (e.g. hypermetria, abnormal postural reactions, menace
response deficit) (Figure 6.8.3). Dysfunction of the cerebellum does not always
result in a paradoxical vestibular syndrome as this will depend on the region
affected. Cerebellar lesions may therefore also result in a vestibular syndrome in
which the direction of the head tilt or slow phase of the nystagmus are towards
the side of the lesion.
As discussed in Chapter 3, cerebellar lesions can also disrupt the control of
saccadic eye movements. This will present as abnormal spontaneous eye move-
ments that lack the initial drift phase that is so distinctive for a nystagmus. These
pathologic eye movements are termed saccadic oscillations. Opsoclonus is a form
244 A Practical Approach to Neurology for the Small Animal Practitioner

(a)
Cerebellar nuclei

Vestibular
nuclei
Vestibular receptors
in the inner ear Vestibulocochlear nerve

(b)

Lesion

(c)

Lesion

of saccadic oscillation that is characterised by rapid, multidirectional eye move-

ments, and has been reported in animals with both cerebellar cortical degenera-
tion and inflammatory disorders affecting the cerebellum (e.g. idiopathic
generalised tremor syndrome) (Ives et al. 2018) (see Video 26).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 245

Figure 6.8.2 Paradoxical vestibular syndrome. (a) In the normal animal with a static and
horizontal head position, there is an equal and balanced input from the vestibular receptors in
the inner ears to the brainstem vestibular nuclei. The output from the vestibular nuclei on
both sides is therefore also equal (red arrows). The cerebellar nuclei exert a constant,
inhibitory influence on the vestibular nuclei in the brainstem. (b) In the case of a peripheral
vestibular lesion, there is loss of input from the vestibular receptors on the affected side
compared to the contralateral side. This results in an imbalance in the output from the
vestibular nuclei on each side of the brainstem; the reduced output on the affected side
(smaller red arrow) results in a head tilt towards the side of the lesion as the extensor muscle
tone in the ipsilateral neck muscles is reduced. (c) A cerebellar lesion may disrupt the normal
inhibitory influence on the ipsilateral vestibular nuclei. This loss of inhibition results in an
increased output from the brainstem vestibular nuclei on the affected side (large red arrow)
compared to the unaffected side. This results in a head tilt that is away from the side of the
lesion as there is a relative reduction in the extensor muscle tone in the contralateral neck
muscles compared to the affected side.

Right Left

Figure 6.8.3 A transverse T2‐weighted MRI at the level of the cerebellum and medulla
oblongata in a 2‐year‐old, male neutered Pug with a 1‐month history of a left head tilt and
progressive balance loss. Neurological examination revealed a left head tilt, vestibular ataxia
of all limbs, delayed proprioception and increased extensor muscle tone in the right thoracic
and right pelvic limbs, and a reduced menace response in right eye. The neuroanatomic
localisation was the right cerebellum, with a paradoxical vestibular syndrome explaining the
left head tilt. The MRI demonstrated an ill‐defined, intra‐axial lesion affecting the right side of
the cerebellum (arrow). Cerebrospinal fluid analysis revealed a mononuclear pleocytosis and
infectious disease testing was negative. The dog showed a clinical improvement following the
introduction of immunosuppressive medications, supporting a diagnosis of meningoencepha-
litis of unknown origin (MUO).
246 A Practical Approach to Neurology for the Small Animal Practitioner

6.8.1 Differential Diagnoses

The presence of hypermetria, intention tremors, dysmetric hopping, and/or cen-
tral vestibular dysfunction should alert the clinician to the possibility of a cere-
bellar lesion. The ranked list of differential diagnoses and subsequent clinical
approach will then depend upon the signalment of the affected animal and the
onset and progression of the disease. Disorders that may cause cerebellar dys-
function are discussed below and have been divided according to the VITAMIND
mnemonic described in Chapter 5. This list is far from exhaustive, but it repre-
sents some of the more common disorders that may be observed in general
practice.

1. Vascular
Cerebrovascular disease results from pathology affecting the blood supply to the
brain (Boudreau 2018). It manifests clinically as an acute onset of non‐progressive
clinical signs, termed a cerebrovascular accident or ‘stroke’. Cerebrovascular
accidents affecting the blood supply to the cerebellum are not uncommon in
dogs but have only been reported rarely in cats (Altay et al. 2011; Cherubini
et al. 2007; Garosi et al. 2006; McConnell et al. 2005; Negrin et al. 2009; Negrin
et al. 2018; Thomsen et al. 2016; Whittaker et al. 2018).
Cerebrovascular disease can be subdivided into the following categories:

• Ischaemia or infarction resulting from occlusion of the arterial supply to the

region of the brain affected. This may be in the form of local thrombus forma-
tion or represent blood vessel occlusion by an embolus from a distant site
(blood clot, neoplastic embolus, septic embolus, parasitic embolus).
• Haemorrhage secondary to disorders of coagulation or local disruption to the
integrity of a vessel wall (artery or vein).
• Systemic hypertension resulting in hyperperfusion and cerebral oedema.

Ischaemic stroke is the most common form of cerebrovascular disease that

affects the cerebellum, with Cavalier King Charles Spaniels and Greyhounds
being over‐represented in many case series (Kent et al. 2014; Thomsen et al.
2016). It typically presents as an acute onset of non‐progressive, lateralised cen-
tral vestibular syndrome, but ipsilateral hypermetria, loss of the menace
response, and intention tremors can also be observed (Garosi et al. 2006;
Thomsen et al. 2016). A concurrent medical condition may be identified in
50–60% of dogs with ischaemic stroke in general; the most frequently diagnosed
conditions being chronic renal disease (protein‐losing nephropathy) and hyper-
adrenocorticism (Garosi et al. 2005). Other reported conditions include diabetes
mellitus, neoplasia, and hypothyroidism in dogs, and pulmonary disease, cardio-
myopathy, and hyperthyroidism in cats (Whittaker et al. 2018). If ischaemic
stroke is confirmed or suspected, then screening for an underlying predisposing
factor is always important. This is because affected animals are significantly more
 Chapter 6 A Practical Approach to Common Presentations in General Practice 247

likely to suffer recurrent events and have a poorer prognosis compared to ani-
mals for which an underlying medical condition cannot be identified (Garosi
et al. 2005).
The diagnosis of ischaemic stroke requires advanced imaging of the brain
(Figure 6.8.4). However, a high clinical suspicion can often be formed on the
basis of the typical presentation of acute onset, lateralised, non‐progressive clini-
cal signs. Euthanasia of these animals at initial presentation may be requested by
the owner, but if referral is not an option then monitoring without treatment is
encouraged. A significant proportion of animals will show a gradual improve-
ment over days or weeks and go on to make a functional recovery, even if they
appear severely affected at initial presentation. The use of corticosteroids is not
recommended and has the potential to worsen certain underlying medical

Right Left

Figure 6.8.4 A transverse T2‐weighted MRI at the level of the cerebellum and medulla
oblongata in a 10‐year‐3‐month old, male neutered Greyhound with a clinical history of
acute onset, non‐progressive balance loss. Neurological examination revealed falling to right
side, ataxia of all limbs, and delayed and dysmetria hopping in the right thoracic and right
pelvic limbs. The neuroanatomic localisation was the right central vestibular system (brain-
stem or cerebellum). Note the well‐defined, hyperintense lesion affecting the cerebellar cortex
on the right side. The clinical history and imaging findings in this case were most consistent
with a territorial infarct involving the right rostral cerebellar artery. Urinalysis revealed a
markedly elevated urine protein : creatinine ratio, with protein losing nephropathy and loss of
antithrombin III being a likely predisposing factor for this ischaemic stroke. The dog’s clinical
signs showed a gradual improvement over a 6‐week period.
248 A Practical Approach to Neurology for the Small Animal Practitioner

conditions if present. Euthanasia should be considered if further investigations

or referral are not possible, and there is a subsequent clinical deterioration that
would suggest a progressive disease process (e.g. neoplasia).
Non‐traumatic haemorrhagic lesions may also affect the cerebellum and can
be primary or secondary in origin. Concurrent medical conditions that have
reported in these cases include A. vasorum, intracranial neoplasia, metastatic
neoplasia (e.g. hemangiosarcoma), hypertension, hypothyroidism, hyperadren-
ocorticism, and chronic kidney disease (Lowrie et al. 2012). The prognosis will
depend upon the underlying cause but can be favourable in some dogs, particu-
larly in those with A. vasorum infection or if no identifiable underlying cause is
found. Hepatic disease and nephritis have been reported as concurrent medical
conditions in cats with haemorrhagic infarcts (Altay et al. 2011).
Systemic hypertension may result in damage to susceptible organs, including
the brain, eyes, and kidneys. This is most commonly associated with sustained
elevations in systolic arterial blood pressure (>180 mmHg) or following acute
elevations from the resting level. The clinical signs associated with hypertensive
encephalopathy in animals more commonly reflect forebrain dysfunction, such
as seizures, blindness, and an altered level of mentation (Brown et al. 2005,
O’Neill et al. 2013). However, structures within the caudal fossa can also be
affected, resulting in vestibular and cerebellar dysfunction. It may be difficult to
determine whether hypertension represents the primary cause of the clinical
signs observed, or whether it is secondary to another condition or clinical sign
(e.g. stroke, neoplasia, stress, or seizures). Demonstration of persistent hyper-
tension on repeat readings is therefore recommended in these cases. If a persis-
tent hypertension is confirmed, then screening for underlying medical conditions
is recommended, such as protein‐losing nephropathy, hyperadrenocorticism,
and phaeochromocytoma in dogs, or hyperaldosteronism in cats. Cases of essen-
tial or primary hypertension, in which a concurrent medical condition cannot be
identified, are increasingly recognised in dogs and cats.

2. Inflammatory (sterile)
Inflammation of the CNS, in the absence of detectable infectious agents, is sus-
pected to be autoimmune in origin and may involve the cerebellum and its over-
lying meninges (see Figure 6.8.3) (Hoon‐Hanks et al. 2018). Definitive diagnosis
of a specific, named condition requires histopathologic assessment of brain
tissue. These conditions are therefore grouped under the broad term of
‘meningoencephalitis of unknown origin’ (MUO) pending biopsy or post‐
mortem confirmation of a specific disorder (Cornelis et al. 2019). The most com-
mon form of MUO to affect the cerebellum in dogs is called granulomatous
meningoencephalitis (GME). These conditions frequently result in multi‐focal
brain disease, with or without spinal cord involvement, and isolated cerebellar
dysfunction is uncommon. Ante‐mortem diagnosis of MUO requires consistent
findings on MRI and CSF analysis, together with exclusion of infectious diseases.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 249

Numerous treatment protocols for MUO in dogs have been reported. These most
commonly involve the use of oral prednisolone together with an adjunctive
immunosuppressive agent (e.g. cytosine arabinoside, cyclosporine, azathio-
prine). The prognosis appears highly variable, dependent on the individual case
and short‐term response to treatment.
Idiopathic generalised tremor syndrome is also suspected to represent an
autoimmune condition. It is most commonly observed in young, small breed
dogs and was previously termed ‘little white shaker syndrome’ due to the appar-
ent over‐representation of breeds such as West Highland White Terriers and
Maltese Terriers. However, this condition may be observed in dogs of any breed
or coat colour (Wagner et al. 1997). It has also been rarely reported in cats
(Mauler et al. 2014). Affected animals present with low‐amplitude, whole body
tremors that are exacerbated by excitement or handling. The term ‘idiopathic
cerebellitis’ has been used for this condition, as affected animals may also pre-
sent with clinical signs referable to cerebellar dysfunction, such as hypermetria,
vestibular dysfunction, and abnormal saccadic eye movements (opsoclonus).
Diagnosis is made on the basis of clinical presentation and exclusion of other
possible causes. Brain MRI is usually normal and CSF analysis may reveal evi-
dence of mild inflammation. Treatment involves a tapering course of predniso-
lone starting at 1 mg/kg twice daily. Some dogs may relapse as the dose is reduced
or stopped and require long‐term therapy to maintain remission. Adjunctive
immunosuppressive medications (e.g. cytosine arabinoside, azathioprine) may
be useful in these cases to allow a reduction in the dose of steroid required to
control the disease.

3. Infectious
Infectious meningoencephalitis may affect the cerebellum in both dogs and cats.
It should therefore be considered as a differential diagnosis in any animal pre-
senting with progressive signs of cerebellar dysfunction.
Feline coronavirus infection that results in feline infectious peritonitis (FIP)
commonly affects the brainstem and cerebellum in cats. Affected cats may
therefore present with clinical signs of ataxia, intention tremors, an altered
level of mentation or vestibular dysfunction. T. gondii infection is an important
differential diagnosis in any cat with CNS disease and can be screened for by
serological testing. However, false positive results that reflect previous exposure
to T. gondii rather than active infection are common, and a negative result may
be more useful to lower the index of suspicion for this parasite. Bacterial men-
ingitis resulting from cat bites over the caudal cranial fossa or extension of otitis
media into the cranial vault can also affect the cerebellum in cats (Martin‐
Vaquero et al. 2011; Sturges et al. 2006). The clinical history and general clini-
cal examination will often be supportive in these cases, with advanced imaging
(CT or MRI) required for a definitive diagnosis. Otoscopy and myringotomy to
collect samples for cytology and bacterial culture can be useful to diagnose otitis
250 A Practical Approach to Neurology for the Small Animal Practitioner

media. However, otoscopic examination may be normal in many cats with otitis
media as infection frequently ascends from the pharynx via the Eustachian
tube. This is in contrast to dogs, in which otitis media is most commonly sec-
ondary to otitis externa. Surgical management of both bacterial otitis media and
intracranial abscessation has been advocated to improve the long‐term out-
come (Sturges et al. 2006). However, successful medical management of intrac-
ranial bacterial infection has been reported in cats and should be considered in
animals for which surgery or referral are not an option (Cardy et al. 2017). See
Figure 6.8.5 for a case example of a cat with an intracranial abscess involving
the cerebellum after it was bitten on the head by another cat. Surgical

Right Left

Figure 6.8.5 A transverse T1‐weighted MRI following the administration of intravenous

contrast media in a 6‐year‐old, male neutered, Maine Coon cat with a 4‐day history of
lethargy and progressive ataxia after returning home with wounds consistent with a cat fight.
Physical examination revealed two puncture wounds on head, with the deepest being over
the left occipital region. Neurological examination revealed a depressed level of mentation,
marked ataxia of all limbs, falling to both sides, a poor menace response in the left eye, and a
positional, vertical jerk nystagmus. The neuroanatomic localisation was brainstem and left
cerebellum. The brain MRI revealed a left‐sided, intra‐axial, ring‐enhancing, cavitated
cerebellar lesion (arrow) that was exerting a mass effect on the adjacent brainstem. This lesion
was communicating through a 4 mm left occipital bone defect with another cavitated lesion
involving the soft tissues of the left temporal region (star). Other changes on the MRI scan
included two small (1–2 mm) bone fragments depressed to lie within the caudal fossa,
perilesional brain oedema, cerebellar herniation into the foramen magnum, focal meningitis,
medial retropharyngeal lymphadenitis, and left temporal and right cervical myositis secondary
to penetrating wounds. Surgical management was recommended in this case but was not
possible due to economic limitations. The cat was initially treated with mannitol, a single
injection of dexamethasone, and intravenous marbofloxacin and potentiated amoxicillin. The
antibiotics were continued for 6 weeks and the cat made a complete recovery without relapse
of clinical signs at 6‐month follow‐up.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 251

management was recommended in this case but was not possible due to eco-
nomic constraints. A complete clinical recovery was subsequently seen with
medical management alone. Clinical deterioration in spite of treatment or
relapsing clinical signs after cessation of antibiotic therapy are the primary con-
cerns in these cases.
In utero infection by feline panleukopaenia virus can affect cerebellar cor-
tical development in cats (Poncelet et al. 2013; Stuetzer and Hartmann 2014).
This results in congenital cerebellar hypoplasia and affected kittens will dis-
play non‐progressive clinical signs from the time they first attempt to walk.
These clinical signs include coarse, low frequency (2–6 Hz) tremors, ataxia,
hypermetria, and vestibular signs. Cats may compensate for this incoordina-
tion as they develop and can have a good quality of life if they are indepen-
dently mobile. Ante‐mortem diagnostic testing is usually normal and is
primarily aimed at excluding other possible causes. There is no treatment for
this congenital condition. Vaccination of pregnant queens with modified‐live
panleukopaenia virus vaccines should be avoided to reduce the incidence of
this disorder.
Any infectious meningoencephalitis can theoretically affect the cerebellum
in dogs, including bacterial, fungal, parasitic, and viral diseases (e.g. canine dis-
temper virus, CDV). However, Neospora caninum appears to have a predilection
for the cerebellum of adult dogs, resulting in progressive signs of cerebellar dys-
function (Garosi et al. 2010). This may occur in isolation or can be accompanied
by additional deficits that reflect involvement of the spinal cord, peripheral nerv-
ous system, or other regions of the brain (Parzefall et al. 2014). The life cycle of
N. caninum is incompletely understood but involves a canine definitive host and
cattle as intermediate hosts. A history of exposure to farms or cattle may there-
fore raise the index of suspicion for this parasite. However, this is not always
reported in the clinical history and dogs can harbour the parasite following
transplacental transmission from mother to puppy. Immunosuppression related
to systemic disease, or secondary to the use of immunosuppressive medications,
may predispose to recrudescence of dormant parasitic stages in some dogs.
Serological testing for N. caninum is recommended in all adult dogs that present
with a history of progressive cerebellar dysfunction. Low positive serum anti-
body titres may indicate previous exposure but high serum titres (>1:800) are
highly suggestive of active infection. Demonstration of parasite antigen by poly-
merase chain reaction (PCR) testing on CSF can confirm the diagnosis. The MRI
appearance in adult dogs with neosporosis and cerebellar involvement is distinc-
tive and is also highly suggestive for this condition (Figure 6.8.6). Clindamycin
(10–15 mg/kg per os twice daily for a minimum of 2–3 months) and/or
trimethoprim/sulphonamide can be used for treatment, but relapses are possible
when treatment is stopped. Serum antibody titres can may remain high during
and following treatment, which complicates their use for deciding when to stop
therapy.
252 A Practical Approach to Neurology for the Small Animal Practitioner

Figure 6.8.6 A mid‐sagittal T2‐weighted MRI in a 4‐year‐old, male neutered Greyhound

with a 4‐week history of progressive balance loss and a subsequent diagnosis of protozoal
meningoencephalitis secondary to Neospora caninum. Neurological examination revealed a
normal level of mentation, absent menace responses bilaterally, delayed and dysmetria
hopping in all limbs, a wide‐based stance, and hypermetria and ataxia affecting all limbs.
Withdrawal reflexes were strong in all limbs and spinal palpation did not reveal any discom-
fort. The neuroanatomic localisation was diffuse cerebellar disease. Magnetic resonance
imaging of the brain revealed marked cerebral and cerebellar atrophy, with thinning of the
cortices and enlargement of the lateral ventricles. Note the markedly reduced size of the
cerebellum, with an apparent increased volume of cerebrospinal fluid (CSF) surrounding the
cerebellar folia (arrow). CSF analysis revealed a moderate, mixed (predominantly neutro-
philic) pleocytosis. Serological testing for Neospora caninum was positive at >1:800 and PCR
testing for N. caninum antigen in the CSF was positive.

4. Traumatic
Trauma to the cerebellum is uncommon but may result from blunt force trauma
to the back of skull or bite wounds that puncture the occipital bones overlying
the caudal cranial fossa. A clinical history and thorough general clinical exami-
nation will usually support a diagnosis of head trauma. The approach to head
trauma as a potential neurological emergency is discussed in Chapter 7.

5. Toxic
Diffuse or multi‐focal CNS disease may be observed following exposure to
numerous toxins and cerebellar dysfunction is not uncommon in these cases.
A thorough clinical history is therefore always important and should include
questions regarding medications that the animal is currently receiving or other
substances in the household that the dog or cat may have had access to. The
most common neurotoxicity that presents with predominately cerebellar signs
in dogs is metronidazole intoxication.

a. Metronidazole toxicity
Metronidazole is an antibacterial, anthelmintic, and antiprotozoal medication
that is widely used in veterinary medicine, particularly in dogs with gastrointes-
tinal disease. It is highly lipid soluble, which means that it can readily gain access
 Chapter 6 A Practical Approach to Common Presentations in General Practice 253

to the CNS across the blood–CSF and blood–brain barriers. Serum concentra-
tions peak within 1–2 hours of oral administration, with an elimination half‐life
of 4–6 hours in dogs. Previously recommended oral doses of metronidazole
ranged from 10 to 25 mg/kg every 12 hours. A recently licensed veterinary for-
mulation for the treatment of gastrointestinal infections caused by Giardia and
Clostridia spp. in dogs and cats recommends a daily oral dose of 25 mg/kg every
12 hours. Clinical signs associated with metronidazole neurotoxicity include
ataxia, hypermetria, increased extensor muscle tone, tremors, convulsions, and
central vestibular syndrome (head tilt, vertical nystagmus). The pathophysiolog-
ical mechanism of neurotoxicity is unknown but may be related to modulation
of the receptor for the inhibitory neurotransmitter GABA within the cerebellum.
A recent retrospective study of 26 dogs with metronidazole‐induced neurotoxic-
ity reported a median oral dose of 21 mg/kg twice daily (range 13–56 mg/kg
twice daily) (Tauro et al. 2018). The median duration of treatment was 35 days
(range 5–180 days). The authors of this study therefore recommended caution in
administering metronidazole at oral doses >20 mg/kg twice daily. Diagnostic
testing is generally unremarkable in affected animals, but MRI may rarely reveal
symmetrical changes within the cerebellar medullary nuclei. Clinical signs
should resolve when metronidazole administration is stopped. The median time
to resolution of clinical signs was 3 days (range 1–26 days) in the study described
above. The administration of diazepam to affected dogs (0.5 mg/kg per os every
8 hours for 3 days) has been recommended to shorten the recovery time in
affected dogs; the recovery time for diazepam‐treated dogs (1.6 days) was signifi-
cantly shorter than that for untreated dogs (11 days) in a retrospective study of
21 cases (Evans et al. 2003). The mechanism of action for diazepam in these
cases is potentially related to competitive reversal of metronidazole binding at
the GABA receptor.

6. Anomalous
Anomalous disorders are most commonly observed in younger animals and
include complete or near‐complete absence of the cerebellum (aplasia), or a
congenital reduction in cerebellar volume (hypoplasia). Congenital cerebellar
hypoplasia has been reported in several breeds of dog, including Chow Chows,
Irish Setters, and Wire‐haired Fox Terriers. Clinical signs of cerebellar dysfunc-
tion are non‐progressive in these animals and will be present from the time an
animal first tries to walk. As discussed previously, in utero infection with certain
viruses may be responsible for cerebellar hypoplasia in some puppies and kittens
(e.g. feline panleukopaenia virus).
Other developmental abnormalities that may result in cerebellar dysfunction
include epidermoid and dermoid cysts (Platt et al. 2016; Steinberg et al. 2007).
These mass lesions represent entrapment of ectodermal tissue within the devel-
oping neural tube and are most commonly found in the region of the fourth
ventricle, immediately ventral to the cerebellum. Enlargement of these cystic
254 A Practical Approach to Neurology for the Small Animal Practitioner

structures as the animal grows, together with the inflammatory response to their
presence, results in progressive cerebellar disease in young to middle‐aged
animals. These cystic lesions mimic neoplasia and advanced imaging +/− biopsy
is required for diagnosis.

7. Neoplastic
Primary tumours of the cerebellar parenchyma are rare in small animals but
include medulloblastoma and gliomas. Extra‐axial tumours arising from ana-
tomical structures that are closely associated with the cerebellum are more com-
mon, such as meningiomas at the level of the cerebellomedullarypontine angle
or choroid plexus tumours of the fourth ventricle. These tumours typically result
in ipsilateral, asymmetric clinical signs of brainstem and cerebellar dysfunction.
Advanced imaging is required for diagnosis, but the clinical suspicion of a neo-
plastic lesion should be increased in an older dog or cat with progressive clinical
signs. Inflammatory or infectious diseases (e.g. neosporosis) are important dif-
ferential diagnoses in these cases. A late onset form of cerebellar cortical degen-
eration should also be considered but, in contrast to neoplasia, degenerative
disorders usually result in diffuse and symmetric cerebellar involvement (see
below).

8. Degenerative
Clinical signs of cerebellar dysfunction may occur secondary to numerous degen-
erative disorders that affect the CNS. Evidence of more widespread neurological
dysfunction is frequently observed in these cases (e.g. visual deficits, behaviour
change, seizures, tetra/paraparesis). These disorders include inborn errors of
metabolism that result in accumulation of cellular products within affected neu-
rons and abnormal neuronal function. These conditions have been termed
‘storage diseases’ and primarily affect young pure‐breed animals of specific
breeds. However, the age at onset can be highly variable dependent on the breed
and condition. Therefore, a degenerative disorder should always be considered
in animals of any age that present with a chronic, progressive history of non‐
painful clinical signs, particularly if a known disorder has been reported in the
same breed. Diagnosis may be achieved by a combination of urine metabolic
screening, blood enzymatic testing, tissue biopsy, advanced imaging findings,
and genetic testing (if available for a particular breed) (Sewell et al. 2012; Skelly
and Franklin 2002). A list of degenerative conditions that may present with
signs of cerebellar dysfunction is given below. Corneal clouding is a distinctive
finding on the general physical examination for several of these conditions and
would help to increase the index of suspicion if observed (e.g. mucopolysaccha-
ridosis [MPS] II, MPS III, and GM1 gangliosidosis).

• Mucopolysaccharidosis (MPS) II – Labrador Retriever

• MPS III – Dachshund (adult onset), New Zealand Huntaway, Schipperke
 Chapter 6 A Practical Approach to Common Presentations in General Practice 255

• Ceroid lipofuscinosis (adult and juvenile forms dependent on the

breed) – American Staffordshire Terrier, American Bulldog, Border Collie,
Chihuahua, Cocker Spaniel, Dachshund, Dalmatian, English Setter
• Glucocerebrosidosis – Silky Terrier
• Globoid cell leukodystrophy – Beagle, Cairn Terrier, Irish Setter, Poodle, West
Highland White Terrier, domestic shorthair cat
• GM1 gangliosidosis – Beagle, English Springer Spaniel, Portuguese Water Dog,
Siberian Husky, domestic shorthair cat, Siamese cat
• GM2 gangliosidosis – German Shorthaired Pointer, Japanese Chin, Burmese cat,
domestic shorthair cat, Korat cat
• Niemann–Pick – Balinese and Siamese cats (type A), domestic shorthair cat
(type C).

a. Neuroaxonal dystrophy
Neuroaxonal dystrophy is a degenerative disease that is most widely recognised
in the Rottweiler (Chrisman et al. 1984; Sisó et al. 2001; Lucot et al. 2018).
However, it has also been reported in the Papillon, Spanish Water Dog,
Chihuahua, Jack Russell Terrier, Collie, and domestic shorthair cats (Hahn et al.
2015; Nibe et al. 2007). Affected Rottweilers present with a history of chronic,
progressive ataxia, hypermetria, and a wide‐based stance at 1–2 years of age.
Clinical progression is observed over months/years to include intention tremors,
menace response deficits, and nystagmus. There is a gene test available in the
Rottweiler, Papillon, and Spanish Water Dog but a definitive diagnosis can only
be achieved post‐mortem in other breeds (Hahn et al. 2015; Lucot et al. 2018).
Diagnostic investigations are therefore primarily targeted at excluding other dif-
ferential diagnoses such as N. caninum infection, meningoencephalitis of
unknown origin, neoplasia (e.g. medulloblastoma), and anomalous conditions
(e.g. epidermoid cyst). There is no effective treatment for this condition and the
prognosis is poor.

b. Primary cerebellar cortical degeneration

Primary cerebellar cortical degeneration refers to degeneration of cerebellar
neurons that have initially developed normally. An intrinsic cellular defect
results in a reduced life span of the affected neurons, with the age at the onset
of clinical signs dependent upon the onset of neuronal loss. This typically occurs
between 3 and 12 months of age in affected dogs, but the onset of clinical signs
may not be observed until 5–8 years old in certain breeds (e.g. Old English
Sheepdog, Brittany Spaniel, Gordon Setter, Scottish Terrier, Labrador Retriever).
Important differential diagnoses in these dogs include inflammatory, infectious,
and neoplastic disorders. Primary cerebellar cortical degeneration has been
reported in numerous breeds of dog, including the Kerry Blue Terrier, American
Staffordshire Terrier, Scottish Terrier, Rough‐coated Collie, Border Collie,
256 A Practical Approach to Neurology for the Small Animal Practitioner

Labrador Retriever, Rhodesian Ridgeback, Golden Retriever, Beagle, and Cocker

Spaniel, and has also been reported in cats (Bertalan et al. 2014, de Lahunta and
Averill 1976, Urkasemsin et al. 2010, Inada et al. 1996, Olby et al. 2004). Clinical
signs of cerebellar dysfunction are progressive and there are no effective treat-
ments. Ante‐mortem diagnostic testing is usually unremarkable and primarily
aimed at excluding other differential diagnoses for which there may be a
treatment. MRI may reveal reduced cerebellar volume in some cases, and a gene
test is available for certain breeds (Henke et al. 2008; Inada et al. 1996;
Kwiatkowska et al. 2013).

6.8.2 Clinical Approach to Cerebellar Disease

The clinical approach to any animal that presents with a neurological examina-
tion consistent with cerebellar dysfunction will depend upon many factors.
These include the clinical history, the list of differential diagnoses, and the funds
available for referral or further investigations. As for all neurological syndromes,
there is no ideal ‘recipe’ for approaching these cases and some may fall between
the broad categories summarised below. However, the clinical approach can be
initially divided by onset, progression of clinical signs, and age of the affected
animal.

1. Acute, non‐progressive or improving clinical signs

• Rule out trauma using the clinical history and general clinical examination.
• Consider cerebrovascular disease, particularly if the neurological deficits are
asymmetrical: Refer for advanced imaging to confirm the diagnosis if possible.
• Screen for underlying medical conditions: blood pressure testing, urinalysis
(including urine protein : creatinine ratio), haematology, serum biochemistry,
coagulation testing, A. vasorum testing, ACTH stimulation testing, total thyroid
hormone and TSH levels, body cavity screening for neoplasia.

2. Chronic, non‐progressive clinical signs in a puppy or kitten

• Congenital cerebellar aplasia or hypoplasia is most likely. The prognosis may
be good if the animal is ambulatory and has a reasonable quality of life.

3. Acute, progressive clinical signs in an animal of any age

• Rule out intoxication (e.g. metronidazole).
• Consider infectious, inflammatory, and neoplastic disorders: Refer for further
investigations if possible.
• Perform an otoscopic examination, haematology, serum biochemistry, urinal-
ysis, body cavity screening for systemic or metastatic neoplasia, and infectious
disease testing (e.g. N. caninum serology in dogs, T. gondii serology and feline
coronavirus testing in cats).
 Chapter 6 A Practical Approach to Common Presentations in General Practice 257

4. Chronic, progressive clinical signs in a young animal

• Rule out intoxication (e.g. metronidazole).
• Consider degenerative, anomalous, infectious, inflammatory (and neoplastic)
disorders: Refer for further investigations if possible.
• Perform an otoscopic examination, haematology, serum biochemistry, urinalysis,
and infectious disease testing (e.g. N. caninum serology in dogs, T. gondii serology
and feline coronavirus testing in cats). Search for a consistent degenerative dis-
order in the same breed +/− urine metabolic screening and genetic testing.

5. Chronic, progressive clinical sigs in a middle‐aged or older animal

• Rule out intoxication (e.g. metronidazole).
• Consider neoplastic, inflammatory, infectious, and late‐onset degenerative
disorders: Refer for further investigations if possible.
• Perform an otoscopic examination, haematology, serum biochemistry, urinal-
ysis, body cavity screening for systemic or metastatic neoplasia, and infectious
disease testing (e.g. N. caninum serology in dogs, T. gondii serology and feline
coronavirus testing in cats). Search for a consistent degenerative disorder in
the same breed +/− urine metabolic screening and genetic testing. Consider a
steroid trial before euthanasia if the clinical signs are progressive, infectious
disease has been excluded, and further investigations are not possible.

6.9 ­Neck and/or Spinal Pain

Paul M. Freeman

Apparent pain is a very common presentation in general practice. This may be

the complaint of the owner, or it may be the conclusion of the veterinary sur-
geon, and such cases can prove diagnostically challenging.

6.9.1 Signs of Pain

Animals may react to pain in different locations in varied ways, but there are
some generalisations which can be made to assist the veterinarian when faced
with such a case. Cats and dogs also react in different ways to pain; the first part
of this section will be mostly concerned with canine manifestations of pain, and
we will consider cats separately.

1. Neck pain
Animals with significant cervical pain classically adopt a ‘head down’ posture
(Figure 6.9.1). They may be very reluctant to elevate the head and when tempted
with a food treat, will sometimes perform a movement that will elicit an attack
of pain. The adopted posture is evidently the most pain‐free and is likely to be a
258 A Practical Approach to Neurology for the Small Animal Practitioner

Figure 6.9.1 Low head carriage, which is commonly seen in animals with neck pain.
Affected animals may be reluctant to raise their heads even when tempted with a food treat.

protective mechanism. Cervical pain may be very severe when associated with
neurological disease, and it is not uncommon for dogs with cervical pain to yelp,
cry, or scream intermittently, which is often very distressing to owners. If the
caudal cervical region is involved, there is the possibility of a permanent or inter-
mittent thoracic limb lameness known as ‘nerve root signature’ (Figure 6.9.2).

Figure 6.9.2 Nerve root signature. Animals with compression of a spinal nerve root that
contributes to the major thoracic limb or pelvic limb peripheral nerves may show an intermit-
tent or permanent non‐weight‐bearing lameness associated with pain. Occasionally, animals
will vocalise when becoming non‐weight‐bearing on the affected limb. In most cases, an
apparent nerve root signature indicates a lateralised problem such as an intervertebral disc
extrusion affecting the C6–T2 or the L4–S3 spinal cord regions.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 259

This is caused by mechanical or inflammatory effects on a cervical nerve root

supplying the brachial plexus.
Affected animals are frequently reluctant to run, jump, or play, and may
appear quite lethargic or ‘depressed’. Appetite may be affected either because
the animal does not feel like eating because of the pain, or more often because
fully flexing the neck to eat from the ground exacerbates the pain.

2. Thoracolumbar pain
Animals with thoracolumbar pain often show a degree of kyphosis, with exag-
gerated flexion of the thoracolumbar spine (Figure 6.9.3). They may walk in a
stiff and hunched manner, and again will be reluctant to run, jump, or play. On
examination, the abdomen may feel tense due to the muscle contracture
involved with the kyphotic posture, and this commonly leads to confusion and
a suspicion of abdominal pain. Again, if the pain is caused by neurological dis-
ease, crying or yelping may occur, although far less commonly than with cervi-
cal pain. Shivering may occur when the pain is severe, and occasionally a tremor
of the pelvic limbs may be evident when the animal is standing.
Posturing to urinate and defecate can be difficult, leading sometimes to
incontinence or overfilling of the bladder, and many affected animals will choose
to urinate and/or defecate whilst walking, apparently because this is more com-
fortable than squatting in a stationary manner.

3. Lumbosacral pain
Lumbosacral pain can be the most difficult region to localise with certainty.
Animals with lumbosacral pain may walk stiffly, and again have difficulties pos-
turing to urinate or defecate. They are most commonly reported by their owners

Figure 6.9.3 Kyphosis of the spine (increased dorsal flexion at the thoracolumbar region),
such as in this case, is usually associated with marked thoracolumbar pain.
260 A Practical Approach to Neurology for the Small Animal Practitioner

to be reluctant to jump up, for example into a car or onto a bed or sofa, and have
difficulties climbing stairs. They may have problems sitting or lying and take
excessive time to change posture. Vocalising occurs occasionally, although not
commonly, and in the case of lateralised lumbosacral disease a permanent or
intermittent pelvic limb lameness or nerve root signature may be seen. All of
these signs may be mimicked to some extent by orthopaedic disease, such as hip
dysplasia and cranial cruciate ligament disease, making this a very challenging
area for diagnosis and treatment.

4. Cats in pain
Cats tend to react to pain in a different manner to dogs. Most commonly, they
will become subdued, choosing to sleep much longer than normal and reject
attention from their owner or other animals in the household. They may become
aggressive when approached, making physical and neurological examinations
very challenging. Cats rarely vocalise when in pain, but commonly become ano-
rexic and apparently lethargic. They may show a reluctance or apparent inability
to climb or jump, which can appear as weakness, and owners will often recog-
nise changes in behaviour patterns such as choosing not to go outside, upstairs,
or climb fences or trees as part of a painful syndrome. Lower back pain may
make posturing to defecate or urinate painful, as for dogs, and cats may even
present with an over‐full bladder or constipation for this reason.

6.9.2 Physical Examination for Pain

Palpation for the presence of possible pain is an important part of the neurological
examination. However, when presented with an animal with a history of sus-
pected pain, this must be carried out with great care and sensitivity. If the clini-
cian has a strong suspicion that pain may be present in a particular region of the
spine, then it is wise to leave that region until last in the examination. By the time
that many animals are presented to the veterinarian, they have become over‐
sensitised to their pain and this, combined with the stress and anxiety of being
examined by a stranger in a strange environment, may cause them to over‐react.
This can make interpretation of the examination difficult. Furthermore, once an
animal has been hurt by the examiner, they may react to palpation in many parts
of the body where pain is not in fact located, which can lead to a very confusing
examination. The basic method of palpating for pain is shown in Videos 21a and
22a of the normal neurological examination of the dog.
Where there is not a strong suspicion of neck pain (i.e. no head down pos-
ture, no frequent, spontaneous vocalisation), it is reasonable to work from head
to tail. The author prefers to begin the examination by palpating from the atlas
wings down the lateral sides of the cervical spine, followed by palpation from
dorsoventrally at the level of the caudal cervical spine. This may often reveal a
focal region of pain without the need to move the head and neck. However, if
palpation appears unremarkable it is reasonable to flex and extend the neck,
 Chapter 6 A Practical Approach to Common Presentations in General Practice 261

and also to turn the head and neck to the left and right, in order to assess whether
any of these manoeuvres appear particularly uncomfortable. Care should be
taken with full neck flexion, especially in the case of miniature and toy breeds
where atlantoaxial instability (AAI) may be a differential diagnosis.
Moving on to the thoracolumbar spine, gentle pressure should be applied
with a thumb and forefinger or the thumbs of both hands to the dorsal spinous
processes, working cranial to caudal down to the lumbosacral region. If an area
of apparent focal pain is identified (e.g. tensing of the epaxial muscles, groaning,
or crying), then this area should be re‐visited, this time by moving from caudal
to cranial in order to see if the reaction is consistent. If no area of pain is identi-
fied, the palpation should be repeated with increasing pressure. Care must be
taken to avoid compressing the abdomen during this examination, and it is a
good idea to initially palpate the abdomen in order to assess how guarded the
abdominal wall muscles are and whether in fact cranial abdominal pain (such as
from pancreatitis) may be the cause of the animal’s clinical signs.
Palpating the lumbosacral region forms a continuation of the thoracolumbar
palpation as described above. However, here it is important to be sure that the
pressure applied over the lumbosacral area is not creating pain through the hips
or stifles. Locating the lumbosacral joint is not easy since the dorsal spines of L7
and the sacrum are rarely palpable; in most dogs, the spinous process of L7 is
located in the midline just caudal to the level of the most palpable parts of the
iliac wings. In some cases, it may be possible to gently elevate the animal’s hind-
quarters while carrying out the examination in order to prevent possible misin-
terpretation of orthopaedic pain; however, it is still very easy to confuse
lumbosacral and orthopaedic pain. It is therefore wise to palpate/manipulate the
hips and stifles as a routine part of the examination in order to assess whether
they could also represent a source of pain. Remember that many animals with
lumbosacral disease may also have concurrent orthopaedic disease. The lordosis
test involves applying pressure over the lumbosacral region whilst simultane-
ously extending both hips and has been recommended as a good test for identi-
fying lumbosacral pain; however, in the author’s opinion it is a very difficult test
to carry out effectively, especially in larger dogs, and if the dog has hip pain this
may easily create a confusing reaction.
Examining cats for pain is often unrewarding and frequently dangerous!
However, there are situations where identification of a painful region may pro-
vide the clue which leads to ultimate diagnosis of the problem, and it should
therefore always be attempted, particularly in cases where pain is considered pos-
sible or likely from the history. Careful and gentle palpation with minimal
restraint is most likely to be rewarding and may need to be performed over a
period of time. Once a cat has become hypersensitised and ‘angry’, the examina-
tion is likely to be unrewarding. A quiet, calm environment with minimal people
and minimal restraint is most likely to yield the best results, and great patience is
required to get the most from the feline neurological examination in general.
262 A Practical Approach to Neurology for the Small Animal Practitioner

6.9.3 Pathophysiology of Pain

It is beyond the scope of this text to provide great detail on the pathophysiology
of pain. However, a basic understanding is necessary in order to properly man-
age chronic pain. Nociceptors are the pain receptors which are free nerve end-
ings located in high numbers in the skin, joint capsules, muscles and tendons,
periosteum, and meninges. These can be variously stimulated by pressure and
inflammatory mediators, causing nerve impulses to be transmitted to the dorsal
horns of the spinal cord via sensory neurons. Here there are synapses relying
largely on the neurotransmitters glutamate and substance P, and which also con-
tain opioid receptors capable of modulating the transmission of impulses across
these synapses. The dorsal horns project mainly to spinal cord pathways called
spinothalamic tracts that carry the pain information to the thalamus and then on
to the cerebral cortex. This pain information is thought to be carried in multiple
tracts, bilaterally within the spinal cord, and primarily in small axon fibres which
are relatively resistant to damage. Hence, the sensation of ‘deep pain’ is the last
clinical parameter to be lost in cases of severe spinal cord damage (see later).
There are also descending, modulating fibres which are capable of acting at the
opioid receptors within the dorsal horns, that can be stimulated in order to
downregulate and modulate the pain response.
Both the peripheral nociceptors and the central pain receptors within the
cerebral cortex can undergo a process of sensitisation or ‘wind‐up’. This can
occur either with significant damage to the CNS, such as a stroke, or may be the
result of chronically painful conditions. This is a well‐recognised syndrome in
people, but may be more difficult to diagnose in animals. It is, however, thought
to play a role in animals with chronic back or limb pain, and provides a potential
target for treatment.
Because of the complex and multi‐level neuropharmacology of pain, there
are many different classes of drug which may be beneficial in treating pain.
These range from non‐steroidal anti‐inflammatory drugs (NSAIDs), which tar-
get inflammatory mediators and potential sensitisation of peripheral nocicep-
tors, through opioids, which act directly at the opioid receptors along the pain
pathways, to drugs like gabapentin and amantadine, which are believed to act
centrally by targeting the central sensitisation mechanisms. Ketamine and the
alpha‐2 agonist drugs can also act at multiple levels, with the alpha‐2 drugs hav-
ing a direct effect on the descending modulating pathways of pain. The table in
Box 6.9.1 lists some of the more commonly used drugs that may be utilised in
animals with spinal pain.
For many painful spinal conditions, it is necessary to use a multimodal
approach to analgesia, and the authors will often combine an opioid with a
NSAID and/or a drug such as gabapentin in conditions such as acute interverte-
bral disc extrusion. Paracetamol may also be safely added to this combination
since its major mode of action as an analgesic is believed to be central via activa-
tion of descending serotonergic pathways.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 263

Box 6.9.1 Analgesic Drugs and Targets

Target Dose rate Side‐effects and interactions

Drug – Injectable
Methadone Opioid receptors (full 0.1–0.4 mg/kg im Respiratory depression, nausea,
agonist) or iv q 4–6 h anorexia
Buprenorphine Opioid receptors 0.01–0.02 mg/kg May antagonise full agonists such
(partial agonist) im or iv q 6–8 h as methadone
Ketamine Central action via 0.25–0.5 mg/kg Dysphoria, tachycardia, or
NMDA receptors in iv followed by cri cardiovascular and respiratory
CNS 2–5 μg/kg/min depression
Medetomidine α2 adrenoreceptor 10 μg/kg im or iv, Sedation; causes significant
agonist followed by cri reduction in dose requirement of
2–5 μg/kg/h anaesthetic drugs. Bradycardia,
peripheral vasoconstriction
Drug – Oral
Tramadol Opioid receptors, 2–5 mg/kg po q Sedation. Care in animals taking
noradrenaline and 8h tricyclic antidepressants
5‐HT reuptake (amitriptyline), monoamine
inhibition oxidase inhibitors (selegiline),
SSRIs, and other opioids
Gabapentin Complex interactions 10–20 mg/kg po Sedation and ataxia; reversible
in CNS to q 8–12 h hepatotoxicity has been seen in
downregulate pain chronic use
responses
Amantadine NMDA antagonism (as 3–5 mg/kg q 24 h None reported
ketamine)
Paracetamol Anti prostaglandin, 10 mg/kg po or iv Not for use in cats
probably other q 12 h
mechanisms also
NSAID Blockage of See individual Gastrointestinal ulceration and
prostaglandin synthesis data sheets bleeding, renal damage in
hypovolaemia

6.9.4 Differential Diagnoses for Conditions Presenting Only

with Pain
The diagnostic challenge of pain‐only conditions is exacerbated by the fact that,
by definition, there are no other significant abnormalities on the neurological
examination, and the neuroanatomic localisation relies solely on identifying the
origin of pain. Also, the classical features of the clinical history that we employ
in order to create a differential diagnosis list for other presenting complaints may
not apply as well to pain‐only conditions: onset may be difficult for the owner to
define, progression may or may not be clear, and is often confused by multiple
visits to see multiple veterinary surgeons, with multiple attempts to control the
264 A Practical Approach to Neurology for the Small Animal Practitioner

pain with different medications. Therefore, we feel that in this situation it is

important for the clinician to have a good knowledge of the specific conditions
which may present with pain, and the more common signalments for these
conditions.

1. Vascular
In general, vascular conditions are not painful, with the exception of the classic
acute aortic thromboembolic neuromyopathy of cats.

2. Inflammatory/infectious
a. Steroid‐responsive meningitis arteritis (SRMA)
Steroid‐responsive meningitis arteritis (SRMA) is an autoimmune inflammatory
condition of the meninges that is seen primarily in young dogs, with the first
presentation usually under 3 years of age. Breeds that are over‐represented for
this condition include the Beagle, Boxer, Bernese Mountain Dog, Nova Scotia
Duck Tolling Retriever, and Weimaraner. Affected dogs classically present with
neck pain and pyrexia, although pain may be present throughout the spine and
is often waxing and waning. Some affected dogs may have a chronic history,
with a partial response to previously administered NSAIDs or even apparently to
antibiotics. In the latter case, this is usually because the antibiotic was adminis-
tered alongside an analgesic, or the condition was naturally waning at the point
of treatment, which may add to confusion in diagnosis. Affected animals nor-
mally show a peripheral neutrophilia, and diagnosis requires evidence of neu-
trophilic inflammation in CSF. These animals do not have neurological deficits
such as ataxia and paresis, except in rare situations where the condition is very
chronic and has led to meningeal thickening.

b. Meningomyelitis of unknown origin (MUO)

A different form of autoimmune inflammation can cause focal lesions in the
spinal cord and meninges that may also be painful. This is usually accompanied
by neurological deficits such as paresis and ataxia. This condition may affect any
age or breed of dog, as well as cats, but is more typically seen in younger and
smaller dog breeds such as terriers. Systemic signs and changes in peripheral
blood are inconsistent, and diagnosis relies upon identification of a typical lesion
in the spinal cord on MRI, associated with a mixed, mainly mononuclear, inflam-
mation in the CSF (see Section 6.8 ‘Cerebellar Dysfunction’ for further discus-
sion of this condition).

c. Discospondylitis
Bacterial (and occasionally fungal) infections of the intervertebral disc are seen
sporadically, and usually present as a focal, painful region within the vertebral
column with minimal or no neurological deficits. Occasionally, there is an
­associated disc protrusion or significant inflammation that creates a compressive
 Chapter 6 A Practical Approach to Common Presentations in General Practice 265

myelopathy, and this may lead to signs of paresis and/or ataxia. Any age and
breed of animal can be affected, but this condition appears to be most common
in young to middle‐aged pure breeds of dog. The most commonly affected sites
are the caudal cervical, mid thoracic, thoracolumbar, and lumbosacral regions.
Presumptive diagnosis may be made by survey radiography (Figure 6.9.4),
although advanced imaging with culture of the infectious organism is required
for definitive confirmation.
Spinal radiography in cases of discospondylitis typically reveals ventral spon-
dylosis, erosion of vertebral endplates with loss of clear endplate structure, and
lytic regions within generally sclerotic endplates. The intervertebral disc space
may appear widened, although it can also be narrowed. These radiographic
signs, with accompanying physical findings, may warrant a presumptive diagno-
sis of discospondylitis if referral for advanced imaging is not possible.
Conditions such as spinal empyema (purulent inflammation in the epidural
space) and FIP in cats are rare causes of pain without neurological deficits and
will not be considered further in this section. Polyarthritis and polymyositis will
be discussed in Section 6.9.5 ‘Confounders of Spinal Pain’.

3. Traumatic
Spinal fracture and luxation will usually present with pain and often significant
neurological deficits. However, trauma may occasionally result in fracture of a
peripheral part of a vertebra that does not lead to instability, and these cases can
present with acute and severe pain only. Most commonly, these will be cervical

Figure 6.9.4 Discospondylitis in the lumbar spine. Bacterial infection of the intervertebral
disc may be diagnosed by survey radiography when the infection has been present for at least
2–3 weeks. Changes seen in affected animals include sclerosis and irregularity of vertebral
endplates at the site of the intervertebral disc infection, with lytic regions within the more
sclerotic bone of the endplates. Ventral spondylosis is usually also a feature.
266 A Practical Approach to Neurology for the Small Animal Practitioner

fractures such as those of the atlas wing, an articular facet, or even the dens of
C2 (Figure 6.9.5). In most cases, a history of suspected trauma such as running
into an object at speed will lead to a thorough radiographic investigation.
However, some fractures (particularly when small or minimally displaced) can
be difficult to identify, and CT is required for confirmation. If a spinal fracture is
identified or suspected, referral for specialist advice and possible surgical treat-
ment should always be considered.

4. Anomalous
a. Atlantoaxial instability
Some cases of AAI will present with neck pain only although in more severely
affected dogs, tetraparesis and ataxia will also be seen associated with damage to
the spinal cord parenchyma. Instability between the atlas (C1 vertebra) and axis
(C2 vertebra) is normally a congenital problem due to malformation of the dens of
the axis. In such cases, the problem is likely to present in young animals less than
a year old, and miniature and toy breeds are over‐represented. Diagnosis is made
with survey radiography, where extended and slightly flexed lateral views should
reveal a widening of the dorsal intervertebral space between C1 and C2
(Figure 6.9.6). Flexion of the neck to perform such radiography, and indeed the
sedation or anaesthesia that is usually required to perform the procedure, should
always be carried out with caution in any case where instability of the spine is
considered a possibility. This may include cases where there is a history of known
or suspected trauma, as well as in suspected cases of AAI. Clinicians should also
use caution when taking radiographs under sedation or general anaesthesia in
cases of suspected acute intervertebral disc extrusion, since flexion and extension
of the vertebral column may potentially lead to extrusion of further nucleus

Figure 6.9.5 Vertebral body fracture at the level of C3, with mild ventral displacement but
no involvement of the vertebral canal. Vertebral fractures and luxations are usually readily
diagnosed by survey radiography, but orthogonal views should always be taken since
minimally displaced fractures may only be apparent on a single view.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 267

Figure 6.9.6 Atlantoaxial instability. Diagnosis may be made by carefully flexing the neck
and comparing the dorsal space between C1 and C2 in neutral and flexed views. An obviously
increased space, as in this case, indicates instability at the atlantoaxial joint. A ventrodorsal
view may also indicate an abnormal dens, as shown. In many cases, the neutral lateral view
may be enough to make the diagnosis and flexing the neck will pose a risk to the animal.

pulposus into the vertebral canal (see below). A recent study has shown that the
degree of overlap of the cranial edge of the spine of the axis beyond the caudal
arch of the atlas in neutral lateral views may be a safer and equally valid way to
diagnose AAI in small dogs (Cummings et al. 2018).
The radiographs shown in Figure 6.9.6 illustrate the increased dorsal interver-
tebral space between C1 and C2 seen in dogs with confirmed AAI when the neck
is flexed, compared to a normal dog where the space does not change. In the
ventrodorsal radiograph the very shortened, abnormal dens is apparent.
Occasionally, AAI may be a traumatic condition, due to failure of the dorsal
interspinous ligament or fracture of the dens; in such instances, even greater
care should be taken when performing radiographs under sedation or anaesthe-
sia, especially when flexing the neck, due to the possibility of spinal cord damage
being exacerbated by instability at the region.

b. Chiari‐like malformation/syringohydromyelia (SM)

Chiari‐like malformation is defined as an overcrowding of the caudal fossa of the
skull caused by malformation of the occipital bone and leading to herniation of
the vermis of the cerebellum through the foramen magnum. It is often associ-
ated with other craniocervical junction abnormalities, such as atlanto‐occipital
268 A Practical Approach to Neurology for the Small Animal Practitioner

overlapping and kinking of the cranial cervical spine. It is hypothesised that the
changes in the flow of CSF which these abnormalities bring about are responsi-
ble for the development of syringomyelia, a condition in which CSF accumulates
within the parenchyma of the spinal cord. Therefore, these two conditions often
occur concurrently, although they may also occur independently to one another.
Chiari‐like malformation is almost ubiquitous in the Cavalier King Charles
Spaniel (CKCS) breed, with clinically relevant syringomyelia seen less fre-
quently. Syringomyelia may also be seen in association with other conditions
that alter CSF flow, such as brain tumours or chronic compressive lesions of the
spinal cord. There is an extensive literature concerning these conditions and the
interested reader is directed to the Bibliography section at the end of this chapter
for further information.
Syringomyelia is believed to be a relatively common cause of neck and spinal
pain in young to middle‐aged CKCS dogs, and also occurs frequently in Brussels
Griffons and Chihuahuas. A recent study has shown evidence that CKCS affected
with Chiari‐like malformation alone may also suffer from neuropathic pain,
casting doubt on the belief that syringomyelia is necessary to cause signs of pain
(Rusbridge et al. 2019). However, it remains the case that both Chiari‐like mal-
formation and syringomyelia can be present asymptomatically in many dogs and
other causes of acute neck pain should always be considered in susceptible
breeds, such as intervertebral disc extrusion.
Syringomyelia may also cause neurological deficits, such as paresis, and a
commonly associated clinical sign is phantom scratching, where the animal has
bouts of sometimes frenzied scratching at the neck or flank without making con-
tact with the skin (see Video 39). In the Chihuahua, phantom scratching appears
to be the most common clinical sign, reported in 75% of affected dogs in one
study (Kiviranta et al. 2017). Affected dogs will frequently scratch while walk-
ing, unlike dogs affected with skin disease. Diagnosis of Chiari‐like malformation
and syringomyelia may be strongly suspected from signalment and history but
requires advanced imaging for confirmation (Figure 6.9.7).

Syrinx

Figure 6.9.7 A T2 weighted mid‐sagittal MRI of a Cavalier King Charles Spaniel showing
Chiari‐like malformation and syringomyelia. The syringomyelia is seen as the hyperintense
(white) region on a T2 weighted scan within the parenchyma of the spinal cord.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 269

5. Metabolic, toxic, and nutritional

These disorders rarely present as pain‐only conditions.

6. Neoplastic
Most spinal tumours cause concurrent neurological deficits, and some may not
be associated with pain at all. However, a vertebral tumour may occasionally
present as a pain‐only condition (e.g. osteosarcoma, plasma cell tumour, multi-
ple myeloma). Survey radiography will usually identify such a lesion.

7. Degenerative
a. Intervertebral disc disease
Intervertebral disc disease covers a wide spectrum of disease, ranging from
intervertebral disc degeneration without herniation, through to acute severe
extrusion of non‐degenerate nucleus pulposus. A more complete discussion of
this disease, along with specific definitions, is given in Section 6.10 ‘Paresis,
Paralysis, and Proprioceptive Ataxia’. However, intervertebral disc disease is a
common cause of back and neck pain without neurological deficits and therefore
features in the differential diagnosis list for this presentation.
Pain may be caused in a number of ways by intervertebral disc disease. It is
known that degenerate discs can in themselves be a source of pain in people,
so‐called ‘discogenic pain’. Although this is less well recognised in dogs, it seems
likely that it may also occur, and should be considered in the absence of a more
definitive diagnosis of back or neck pain. Better understood is the pain caused by
a disc that has herniated (i.e. the disc outline extends into adjacent soft tissues,
which may cause compression of spinal cord or nerve roots). Direct spinal nerve
root compression may be painful, especially when associated with the inflam-
matory response that a herniated disc can cause. Spinal cord compression itself
is not inherently painful, although accompanying stretching or inflammation of
the meninges may be.
Recent work on intervertebral disc degeneration has led to some revision of
our understanding of the degenerative process, and there is now believed to be
much more overlap between the chondroid and fibroid degeneration than was
previously thought. It remains the case that the most common form of disc her-
niation, the so‐called Hansen type 1 intervertebral disc extrusion (where there is
escape of the nucleus pulposus through the ruptured annulus fibrosus), is seen
mainly in chondrodystrophic breeds such as Dachshunds, French Bulldogs,
Cavalier King Charles Spaniels, Poodles, Chihuahuas, Pekingese, Pugs, Beagles,
and Cocker Spaniels. The median age of presentation is 5 years although dogs as
young as 1 year may be affected. Intervertebral disc extrusion is very unlikely in
dogs less than a year of age. It can be seen from the previous discussion that
many of the breeds affected by Hansen type 1 intervertebral disc extrusion are
also commonly affected with other causes of neck pain, meaning that confirma-
tion of diagnosis is particularly important.
270 A Practical Approach to Neurology for the Small Animal Practitioner

Large, non‐chondrodystrophic breeds, including Labrador Retrievers,

German Shepherd Dogs, Dalmatians, and Dobermanns, may also be affected by
Hansen type 1 intervertebral disc extrusion. However, these breeds more com-
monly suffer with Hansen type 2 intervertebral disc protrusion, where there is
partial rupture and protrusion of the annulus fibrosus without escape of the
nucleus pulposus. Signs typically develop more chronically with this condition
and pain may be less apparent.
As previously stated, a more in‐depth discussion of intervertebral disc disease
will be given in Section 6.10 ‘Paresis, Paralysis, and Proprioceptive Ataxia’, but
it is important to be aware this disease is very common, affecting up to 20% of
Dachshunds in their lifetime. It should therefore be at the forefront of the clini-
cian’s mind when faced with a potential painful spinal cord lesion. Cervical
intervertebral disc extrusions are often significantly more painful than thora-
columbar extrusions, and frequently present with just pain and minimal or no
neurological deficits. This is in contrast to thoracolumbar disease in which pare-
sis and ataxia are more common.
Diagnosis of intervertebral disc disease may be suspected from the signalment
and presenting clinical signs, and survey radiography may reveal a narrowed
intervertebral disc space in the region of pain or calcified material overlying the
vertebral canal. However, advanced imaging is required for confirmation, and
other differential diagnoses should always be considered if this is not available.

6.9.5 Confounders of Spinal Pain

1. Immune‐mediated polyarthritis
Immune‐mediated polyarthritis (IMPA) may present as a painful condition, and
it is a possible cause of spinal pain due to inflammation of the intervertebral
joints. Affected animals are usually young, although any age can be affected.
One study found that 30% of dogs with IMPA showed spinal pain, and roughly
30% of these dogs also had evidence of concurrent neutrophilic inflammation in
the CSF, consistent with SRMA (Webb et al. 2002). It is therefore important to
check for joint pain in any dog presented with suspected neck or back pain, with
the distal joints (carpi and tarsi) most commonly affected. Synovial fluid analysis
is required for diagnosis, with neutrophilic inflammation being seen in more
than one joint in the absence of potential sepsis. Treatment requires immuno-
suppressive therapy (see below).

2. Immune‐mediated polymyositis
This condition more commonly presents as generalised weakness, but significant
muscular pain may be present and can mimic apparent spinal pain. Diagnosis
requires evidence of significant elevations of muscle enzymes (such as creatinine
kinase), although care must be taken when interpreting elevations of this
enzyme since it is very labile and may be also elevated non‐specifically, especially
 Chapter 6 A Practical Approach to Common Presentations in General Practice 271

in cats. Muscle biopsy is required for confirmation of polymyositis. A specific

immune‐mediated myositis affecting only the muscles of mastication also occurs,
called masticatory myositis, for which an antibody test is available (Type IIM
antibodies). This condition usually presents as pain on opening the mouth that
may occasionally be confused for neck pain. Treatment of most forms of immune‐
mediated myositis requires immunosuppressive doses of corticosteroid, although
this may exacerbate the muscle atrophy already caused by this disease.

3. Orthopaedic disease
As already stated, orthopaedic disease may present very similarly to spinal dis-
ease, and animals that suffer from chronic osteoarthritic or degenerative condi-
tions such as cranial cruciate ligament disease, elbow dysplasia, or hip dysplasia,
may frequently show generalised pain, stiffness, and apparent ‘weakness’. Such
cases require careful evaluation, since many dogs presenting with genuine spi-
nal disease, such as intervertebral disc disease and lumbosacral disease, may also
have concurrent orthopaedic problems. A thorough orthopaedic examination as
well as a neurological examination should be performed in all animals present-
ing with apparent neck or back pain, especially in cases where there are minimal
or no neurological deficits. Radiographic studies must, however, be interpreted
with some caution, since many animals can have clinically insignificant radio-
graphic joint disease.

4. Neoplasia
Many forms of neoplastic disease, including osteosarcoma and even brain
tumours, can present as painful animals that may be reluctant to move. Some
brain tumours present with apparent neck pain and this should always be a con-
sideration if the signalment is appropriate and the diagnosis is not immediately
clear. Thorough screening for evidence of neoplasia, including thoracic radiogra-
phy and abdominal ultrasound, should be performed in animals presenting with
non‐specific or difficult to localise pain, and any evidence of neoplastic disease
investigated appropriately.

5. Abdominal pain
Abdominal pain, especially acute pancreatitis, is frequently mistaken for thora-
columbar pain and vice versa. When presented with a dog with suspected thora-
columbar pain, careful abdominal palpation should be performed in order to
prevent such a mistake from being made. If there is any doubt, then a more
complete abdominal diagnostic work‐up, including imaging, should be consid-
ered. One recent study found an association between thoracolumbar interverte-
bral disc extrusion and elevations of serum canine pancreatic lipase, so it is
possible that there may be an association between these two conditions (Schueler
et al. 2018). However, pancreatic lipase is also an enzyme which is commonly
272 A Practical Approach to Neurology for the Small Animal Practitioner

elevated non‐specifically, and so this association may be clinically insignificant.

Care should be taken when making a suspected diagnosis of pancreatitis in a dog
that presents with apparent abdominal pain only, particularly in a chondrodys-
trophic breed such as the Dachshund; in the author’s experience, a significant
number of dogs referred with thoracolumbar disc extrusion were initially misdi-
agnosed as suspected acute pancreatitis, meaning strict rest was not considered
a necessary part of their treatment protocol (see Section 6.10 ‘Paresis, Paralysis,
and Proprioceptive Ataxia’).

6.9.6 Management of Pain‐only Conditions

After an attempt has been made to localise the source of pain, a knowledge
of the possible and likely differential diagnoses for any given presentation
should allow the clinician to formulate an appropriate plan to discuss with
the owner. If the animal is presenting with a first episode of pain which is
mild or moderate, then in‐house investigation and symptomatic treatment
are usually a sensible first step. Routine haematology and biochemistry to
look for evidence of neutrophilia (which might indicate SRMA, IMPA, or
bacterial infection), systemic disease, or raised muscle enzymes may be indi-
cated. Survey radiography of the painful region of the spine may provide
evidence for an increased likelihood of intervertebral disc disease (narrowed
intervertebral disc space, calcified material in vertebral canal), or even of
discospondylitis or neoplasia.
If Hansen type 1 intervertebral disc extrusion is suspected, then the reader is
referred to a more extensive discussion in Section 6.10 ‘Paresis, Paralysis, and
Proprioceptive Ataxia’. However, the basic management strategy should include
a period of confinement and appropriate analgesia.
Management strategies for other potential differential diagnoses are listed
below.

1. Steroid‐responsive meningitis arteritis (SRMA)

Whenever a true immune‐mediated inflammatory condition of the spine is
considered a significant possibility, whether it be SRMA or meningomyelitis of
unknown origin (MUO), referral for specialist advice and diagnostic work‐up
should be offered. However, if this is not possible then what are the options
for the general practitioner? Measurement of acute phase proteins such as
C‐reactive protein may add weight to the suspected diagnosis. This may be
expected to be elevated in SRMA and not in cases with MUO, but it must
always be remembered that this is a very non‐specific marker of acute inflam-
mation that can also be elevated in animals with IMPA, discospondylitis, bac-
terial meningitis, and neoplasia. It may be wise to perform serology for
infectious diseases, such as toxoplasmosis and neosporosis, before initiating
immunosuppressive therapy, although these conditions are rare compared to
the prevalence of non‐infectious meningitis; a recent study found results
 Chapter 6 A Practical Approach to Common Presentations in General Practice 273

consistent with active infection in 0.25% for toxoplasmosis and 2.25% for
neosporosis of dogs with suspected immune‐mediated meningoencephalitis
(Coelho et al. 2019).
The mainstay of treatment of SRMA (and also MUO) is prednisolone at immu-
nosuppressive doses (4 mg/kg/day for 1–2 days, followed by 2 mg/kg/day for
2 weeks, then 1 mg/kg/day for 6 weeks, 0.5 mg/kg/day for 6 weeks, then 0.5 mg/
kg on alternate days for 1–2 months). Pyrexia, neutrophilia, and C‐reactive
protein can be used for monitoring if CSF analysis is not possible, and ideally
treatment should not be discontinued until all of these parameters are normal.
However, it has been shown that C‐reactive protein may remain elevated even
after remission of disease (Lowrie et al. 2009). Relapse of SRMA is relatively com-
mon and may be more likely if the disease is not treated aggressively enough or
for long enough. If this occurs, prednisolone therapy should be reinstated. The
disease is eventually self‐limiting in most dogs by the age of 3 years, although
may rarely require longer‐term treatment.

2. Discospondylitis
If discospondylitis is suspected from survey radiographs (see Figure 6.9.4), an
attempt should be made to culture the likely causative organism. When direct
biopsy of the affected intervertebral disc is not possible, urine and blood culture
should be performed. Antibiotic choice should be based on culture and sensitiv-
ity results where possible, but in the absence of a positive culture empirical anti-
biotic use is necessary. Because most bacterial infections of the intervertebral
disc are caused by Staphylococcus spp., the author favours cephalexin (20 mg/kg
twice daily), but potentiated‐amoxycillin or clindamycin may be reasonable
alternatives. Treatment should be continued for at least 3 months and well
beyond the resolution of clinical signs.

3. Atlantoaxial instability (AAI)

If AAI is considered likely or is confirmed by radiography (see Figure 6.9.6), then
medical and surgical management options are available. In severe cases with
significant neurological deficits, specialist referral for possible surgical manage-
ment is preferred. In more mild cases, conservative management with a form of
external splinting and cage confinement may be sufficient to allow stabilisation
of the atlantoaxial joint. In most cases of confirmed or suspected AAI, referral to
a specialist for a thorough discussion of the problem and potential treatment
options should be recommended.

4. Chiari‐like malformation/syringomyelia
If these conditions are suspected from the clinical history and signalment,
then referral to a specialist neurologist for confirmation by advanced imaging
(Figure 6.9.7) and a discussion of the treatment options available is advised.
Syringomyelia is a progressive condition that is likely to require lifelong
274 A Practical Approach to Neurology for the Small Animal Practitioner

treatment, although one study showed that most dogs maintain a reasonable
quality of life following diagnosis (Plessas et al. 2012). If referral is not an
option, then it is reasonable to offer symptomatic treatment. Analgesia and
reduction in cerebrospinal fluid production are the key treatment goals.
NSAIDs may be useful in early and mild cases, but often drugs more specifi-
cally acting on neuropathic pain and central wind‐up may be more effective.
The most commonly used medications for this role in veterinary medicine
are gabapentin and amantadine, although pregabalin and topiramate may
also be useful (see Box 6.9.1). Opiates such as tramadol may also be useful,
although the evidence for the efficacy of tramadol in dogs is mixed.
Omeprazole was proposed as a potential treatment due to experimental evi-
dence showing that it may reduce CSF production via inhibition of proton
pumping; however, a more recent paper showed no effect on CSF production
following administration to Beagle dogs (Girod et al. 2016). The only drug
with good evidence for a reduction in CSF production is corticosteroid, and
due to its multiple other potentially beneficial effects such as inhibition of
the formation of pro‐inflammatory mediators and substance P, it can be a
very effective drug at treating the clinical signs of syringomyelia. The author
generally favours a stepwise approach to treatment of this condition, begin-
ning with an NSAID, then adding gabapentin and perhaps also amantadine,
before considering the use of prednisolone as a ‘last resort’. However, at anti‐
inflammatory doses prednisolone can be very effective, and the dose can be
titrated down to minimise side‐effects in the longer term. In severely affected
dogs which are poorly responsive to medical management, surgical treat-
ment options may be available, although evidence for the long‐term efficacy
of these is currently lacking.

6.9.7 When Should Referral of Pain‐only Spinal Disease

be Actively Encouraged
Indications for referral of animals presenting with neck and/or back pain include:

• diagnosis unclear, or significantly in doubt

• initial symptomatic treatment unsuccessful
• recurring, relapsing, or chronic pain
• high suspicion of inflammatory disease, potentially requiring immunosup-
pressive therapy; achieving a confirmed diagnosis before embarking on pro-
longed immunosuppression is always preferable
• possible surgical disease (e.g. suspected AAI, history of trauma, intervertebral
disc disease)
• high suspicion of syringomyelia; confirmation of diagnosis advisable since this
is likely to be a progressive and lifelong disease.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 275

6.10 ­Paresis, Paralysis, and Proprioceptive Ataxia

Paul M. Freeman

6.10.1 Neuroanatomic Basis of Paresis

As has already been discussed, paresis implies a reduction in voluntary motor
activity, which may impair an animal’s ability to weight‐bear or to initiate move-
ment. When the lower motor neurons directly innervating the skeletal muscles
of the limbs are affected, the paresis is known as ‘lower motor neuron paresis’
and the gait is characteristically short‐strided and choppy due to impaired ability
to weight‐bear. When the so‐called upper motor neurons of the brain or spinal
cord are affected, the paresis is said to be ‘upper motor neuron’ and the strides
tend to be longer due to a reduced ability to initiate movement (see Chapter 3).
Paresis in combination with proprioceptive ataxia implies brainstem or spinal
cord involvement due to the effects of the lesion on the proprioceptive tracts of
the spinal cord; generalised lower motor neuron paresis, such as occurs in disor-
ders affecting the peripheral nervous system, does not usually cause ataxia
because the sensory nerves and proprioceptive receptors are rarely involved.
Lower motor neuron paresis is considered further in Section 6.12 ‘Neuromuscular
Weakness’.
Paresis is generally divided into ‘ambulatory’ and ‘non‐ambulatory’ as a
measure of severity and for the purposes of grading spinal cord injury. The most
severe injuries will cause paralysis (or plegia), which is complete absence of vol-
untary movement.
The following discussion will be restricted to diseases affecting the spinal
cord; an approach to diseases of the brainstem, which may also result in tetrapa-
resis and proprioceptive ataxia, has already been considered in Section 6.3
‘Altered Mentation’. When faced with an animal exhibiting tetraparesis and pro-
prioceptive ataxia, it can be assumed that the neuroanatomic localisation is cer-
vicothoracic spinal cord if the level of mentation and cranial nerve examination
are normal. The reader is also referred to Section 6.9 ‘Neck and/or Spinal Pain’
on neck and spinal pain, since there is considerable overlap with the approach to
an animal presenting with paresis and ataxia.

6.10.2 Diagnostic Approach to Paresis and Proprioceptive

Ataxia
Using the approach outlined in Chapter 5, the potential differential diagnoses for
a dog or cat presenting with suspected spinal cord disease may be narrowed
down in the following way.
276 A Practical Approach to Neurology for the Small Animal Practitioner

1. Clinical history
The primary considerations regarding an animal that presents for suspected spi-
nal cord disease are the onset and progression of the clinical signs, the presence
or absence of pain, and the degree of asymmetry. A recent study evaluated the
usefulness of this approach and concluded that the only spinal disorders present-
ing as a peracute, improving, non‐painful, and lateralising myelopathy are fibro-
cartilaginous embolism (FCE) and acute non‐compressive nucleus pulposus
extrusion, so this is clearly very valuable information (Cardy et al. 2015). The
same study concluded that most cases of type 1 intervertebral disc herniation
present as an acute onset of painful, often progressive, and symmetrical clinical
signs.

a. Onset of clinical signs

i. Peracute onset
• Fibrocartilaginous embolism (FCE)
FCE is a condition in which a small piece or pieces of fibrocartilage, which are
thought to arise from an intervertebral disc, embolise into an arteriole(s) sup-
plying a focal region of the spinal cord. This causes ischaemic damage to the
parenchyma of the spinal cord and often leads to asymmetrical signs due to
the nature of the blood supply to the spinal cord. The precise route by which
this material gains entry to the vascular system is unknown but may involve
invasion of a degenerate intervertebral disc with blood vessels from the adja-
cent vertebral endplate. Most affected dogs are middle‐aged or older, large
and giant breeds, and occasionally there is a history of onset during exercise.
However, there is frequently no association with trauma and affected dogs
are found at home by their owners having suffered an acute onset of paresis
or plegia. The dog may yelp at the time of onset and there may be mild pain
on palpation over the affected region of the spine which only lasts for a few
hours, so that by the time affected dogs are seen by a veterinary surgeon
there is usually no apparent spinal pain (see below).
• Acute hydrated nucleus pulposus extrusion (compressive or non‐compressive), or
‘traumatic disc extrusion’
These terms (along with others) are used to describe the peracute extrusion
of non‐ or partially degenerate, gelatinous nucleus pulposus material from an
apparently healthy intervertebral disc. This condition is commonly referred
to as acute non‐compressive nucleus pulposus extrusion or ANNPE, or, if
spinal cord compression is seen, hydrated nucleus pulposus extrusion or
HNPE. This is presumed to be associated with forceful compression of the disc
during some kind of trauma. Such an extrusion may be associated with exter-
nal trauma, such as a road traffic accident, but is also seen in association with
vigorous exercise such as jumping and ball chasing. Affected dogs are often
heard to cry or yelp in pain at the time of a sudden onset of paresis or plegia.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 277

As for FCE, the neurological deficits are often asymmetrical, meaning that
these two conditions are very difficult to distinguish clinically. Pain on palpa-
tion may be present for up to 24 hours after the onset of signs, but again may
be absent by the time animals are presented. Neurological deficits can be
severe, with some animals presenting with tetra‐ or paraplegia. Staffordshire
Bull Terriers may be over‐represented. Most often, the extruded nuclear
material is minimally or non‐compressive and the spinal cord damage is a
result of contusion; compressive lesions have also been described, although a
recent study showed no difference in outcome between these treated surgi-
cally and non‐surgically (Nessler et al. 2018).
• Vertebral fracture/luxation
This diagnosis would normally be associated with a known trauma and would
therefore be suspected. However, a fracture of an articular process or the atlas
wing for example may occur without an obvious (to the owner at least)
trauma and can be difficult to diagnose with survey radiography. Neurological
deficits are related to the level and degree of trauma and, in some situations,
fractures may cause pain only with no apparent deficits (see Section 6.9 ‘Neck
and/or Spinal Pain’).

ii. Acute onset over minutes to hours

• Hansen type 1 intervertebral disc extrusion
See below.
• Meningomyelitis of unknown origin (MUO)
MUO affecting the brain has already been discussed in Section 6.8 ‘Cerebellar
Dysfunction’. However, autoimmune inflammation may also affect the spinal
cord, leading to focal or multifocal lesions that can present as an acute or
subacute onset of paresis and proprioceptive ataxia. These lesions may be
variably painful and can also cause a more chronic and insidious progression
of signs. Neurological deficits are usually progressive, with disease progres-
sion sometimes being quite rapid. Diagnosis requires the identification of
characteristic T2‐weighted hyperintense lesions within the parenchyma of
the spinal cord on MRI, most often associated with a mixed, mononuclear
inflammatory CSF sample. Treatment requires immunosuppression, with
corticosteroids being the most widely used and often effective treatment.
Prognosis, as for MUO affecting the brain, is guarded.
• Infectious disease
Bacterial infection causing accumulation of purulent exudate within the epi-
dural space (empyema) is an uncommon cause of acute spinal cord disease.
Such infections are frequently associated with systemic signs such as pyrexia
and may be extremely painful. They usually lead to a rapid progression of
neurological signs within a short period of time (hours to days). Many cases
are associated with an infectious focus somewhere in the body, such as a
foreign body, urinary tract infection (UTI), or skin disease, although they are
278 A Practical Approach to Neurology for the Small Animal Practitioner

occasionally spontaneous. Diagnosis may be suspected from clinical history

and physical examination but requires advanced imaging +/− sampling or
surgical exploration for confirmation. Treatment may be medical or surgical,
although if there is a rapid deterioration and significant pain then surgery
may provide more rapid resolution of clinical signs.
Toxoplasmosis and neosporosis can in theory cause focal cystic lesions
affecting the spinal cord. However, these infections are extremely rare when
compared to non‐infectious inflammatory disease as described above.

iii. Subacute onset over a few days

Conditions with a possible subacute onset of clinical signs include meningoen-
cephalomyelitis of unknown origin and infectious disease (as discussed above),
Hansen type 1 intervertebral disc extrusion (see below), and neoplasia.

iv. Chronic onset over several days to several weeks

• Hansen type 2 intervertebral disc protrusion
See below.
• Syringomyelia
See Section 6.9 ‘Neck and/or Spinal Pain’.
• Degenerative myelopathy
There are a number of chronic, progressive neurodegenerative conditions
that may affect the spinal cord of dogs and cats. These are generally rare but the
most well known and common is degenerative myelopathy in dogs. This chronic,
progressive neurodegenerative disease is seen in many large breeds of dog, most
notably the German Shepherd Dog. It is also known to affect the Corgi,
Chesapeake Bay Retriever, Siberian Husky, Boxer, Bernese Mountain Dog,
Rhodesian Ridgeback, Golden Retriever, Pug, and Standard Poodle, amongst
others. Affected dogs are typically middle‐aged or older (>8 years), but it may be
seen in dogs as young as 5 years old. In the Corgi, especially Cardigan Corgis,
disease onset is often much later.
Degenerative myelopathy is caused by a genetic mutation affecting the
superoxide dismutase (SOD) enzyme system responsible for destroying free
radicals within the body. This leads to degeneration of white matter tracts in
the spinal cord, predominantly in the thoracic region. This causes a chronic,
progressive pelvic limb paresis and ataxia, with classical signs of toe‐dragging,
scuffed nails, and significant ataxia. The condition is not painful, but over
time may progress to urinary and faecal incontinence, thoracic limb involve-
ment, and complete paraplegia. Diagnosis is by exclusion of other conditions
that may also present as a chronic, progressive T3–L3 myelopathy, such as
Hansen type 2 intervertebral disc protrusion and neoplasia. There is currently
no treatment. A genetic test is available for identification of the SOD‐1A
mutation associated with the disease in the German Shepherd Dog and prob-
 Chapter 6 A Practical Approach to Common Presentations in General Practice 279

ably most affected breeds, although an additional mutation SOD‐1B has been
identified specifically in the Bernese Mountain Dog. Affected dogs are usually
homozygous for the mutation, with heterozygous dogs being carriers of the
disease but rarely showing clinical disease. It is important to remember that a
positive genetic test result does not mean that an affected animal has degen-
erative myelopathy, only that it is at an increased risk of acquiring the condi-
tion at some point in its lifetime. The results must therefore always be
combined with other factors when forming a diagnosis, such as the signal-
ment, clinical history, and exclusion of other possible differential diagnoses by
advanced imaging.
• Arachnoid space disease
A chronic, progressive myelopathy may be seen in association with a focal
accumulation of CSF in the subarachnoid space, usually dorsal to the spinal
cord in either the cervical or thoracic regions. Such ‘arachnoid diverticuli’ are
seen mainly in young Rottweilers in the cervical region, and older Pugs in the
mid‐thoracic spine. The aetiology is uncertain in many cases but is suspected
to be related to chronic instability secondary to hypoplasia of the articular
facets in the thoracolumbar region of older Pugs. Many affected Pugs show
signs of faecal incontinence as well as paraparesis and proprioceptive ataxia.
The condition is usually non‐painful, chronic, and progressive. Diagnosis
requires advanced imaging, and treatment usually involves some form of sur-
gical drainage of the diverticulum +/− stabilisation.
• Cervical spondylomyelopathy (osseous‐ and disc‐associated ‘wobbler syndrome’)
‘Wobbler syndrome’ is caused by cervical spinal cord compression, either by
bony structures or soft tissues. Young giant breed dogs, such as the Great
Dane, Bernese Mountain Dog, and Rhodesian Ridgeback, may be affected by
osseous wobbler syndrome, in which the cervical spinal cord is compressed at
multiple levels by bony enlargement of articular processes or the vertebral
arch causing constriction of the vertebral canal. Affected dogs are typically
2–3 years old, but may present at less than 1 year of age, and show a progres-
sive tetraparesis which may be moderately painful. Diagnosis may be sus-
pected from survey radiographs but requires advanced imaging for
confirmation. Treatment usually requires surgical removal of compressive
bone, although many cases will stabilise or can be managed medically, and a
recent case report described spontaneous resolution of signs in a growing
Mastiff dog (Doran et al. 2019).
Disc‐associated wobbler syndrome is more common and is seen in
the Dobermann and other large breeds of dog such as the Labrador Retriever
and Dalmatian. Clinical signs of tetraparesis develop in middle‐aged and
older dogs and may be progressive, with variable pain. The pelvic limbs are
often more severely affected than the thoracic limbs. The disc‐associated
lesions responsible for the clinical signs are more common in the caudal
280 A Practical Approach to Neurology for the Small Animal Practitioner

c­ ervical spine, typically at the C5–C6 and C6–C7 levels. These range from a
simple intervertebral disc protrusion to more complex compressive lesions
involving the intervertebral disc and associated soft tissues, such as the
intervertebral ligaments and facet joint capsules. The location of the spinal
cord lesions within the C6–T2 intumescence can lead to the typical ‘two‐
engine’ gait, with short, choppy thoracic limb strides and long, ataxic pelvic
limb strides (see Chapter 4). Diagnosis again requires advanced imaging to
demonstrate the site and nature of the spinal cord compression. Occasionally,
dogs may suffer acute deterioration to severe, non‐ambulatory tetraparesis
or ‐plegia, potentially associated with trauma. Treatment may be surgical or
medical (see below). Many dogs will respond well to initial treatment with
anti‐inflammatory doses of prednisolone, although the long‐term prognosis
may be better with surgical treatment.
• Degenerative lumbosacral stenosis
Dogs affected by lumbosacral disease rarely show significant ataxia, and fre-
quently only have mild to moderate paraparesis. Similar to the disc‐associated
wobbler syndrome described above, degenerative lumbosacral stenosis is a
complex condition that results in compression of the cauda equina at the
level of L7–S1 by a combination of intervertebral disc and/or associated bony
and soft tissue structures. It may result in lateralising signs, such as pelvic
limb lameness associated with compression of the L7 nerve roots as they exit
the vertebral canal at this level. It can also present as bilateral lameness, para-
paresis, lower back pain, tail, bladder, or even anal sphincter weakness. A
common presenting sign of lumbosacral stenosis is a dog that has become
reluctant to jump into the car or onto the sofa or is reluctant to go up steps
and stairs. Diagnosis requires confirmation of cauda equina compression
using MRI or CT and exclusion of other causes for the presenting clinical
signs. Treatment may be medical or surgical and, as for wobbler syndrome,
many different surgical techniques have been described. Medical treatment is
successful in a number of dogs, and epidural injection of methylprednisolone
acetate has also been reported to be effective in a high percentage of dogs.

b. Progression of clinical signs

i. Improving signs
• FCE, acute non‐compressive nucleus pulposus extrusion

These two conditions may both show quite rapid improvement, sometimes
within 48 hours. However, more severely affected dogs will take several weeks to
improve, and some cases fail to improve at all, particularly if there is an absence
of nociception (deep pain perception) in the affected limbs or if the lesion involves
the spinal cord grey matter in the C6–T2 or L4–S3 spinal cord regions.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 281

ii. Static signs

• Trauma, Hansen type 1 intervertebral disc extrusion

iii. Deteriorating signs

• Meningomyelitis of unknown origin, infectious disease, syringomyelia, arach-
noid space disorder, cervical spondylomyelopathy, neoplasia, Hansen types 1
and 2 intervertebral disc herniation, degenerative myelopathy

The speed of deterioration for these conditions can be very variable; some
conditions, such as syringomyelia, arachnoid space disorders, and degenerative
myelopathy, take a slow, chronic, progressive course over months. In contrast,
neoplastic conditions affecting the spinal cord can have a very rapid progression
but may also progress more slowly as would be perhaps more expected for neo-
plasia. Hansen type 2 intervertebral disc protrusions usually progress slowly over
weeks to months but can also show an acute deterioration. Hansen type 1
intervertebral disc extrusions normally progress more quickly, and this disease
may take a very variable course; some cases improve following an acute onset,
others progress over hours to days, and yet others have a static or even appar-
ently waxing and waning time course (see below).

c. The presence/absence of pain

i. Non‐painful pain conditions

FCE, acute non‐compressive nucleus pulposus extrusion (after initial 24 hours),
many anomalous diseases (such as arachnoid space disorders), most intramedul-
lary neoplasia, neurodegenerative disorders (e.g. degenerative myelopathy).

ii. Painful conditions

Inflammatory/infectious disorders are frequently painful, including meningomy-
elitis of unknown origin. Some protozoal or viral infections, such as toxoplasmosis
and FIP, may present without apparent pain but most bacterial disease is very
painful. Discospondylitis and epidural empyema may be two of the most painful
conditions seen in small animal practice. Traumatic vertebral fractures are usually
very painful due to compression and inflammation of associated nerve roots and
meninges. Anomalous disorders such as Chiari‐like malformation and syringomy-
elia, as well as AAI, may be significantly painful (see Section 6.9 ‘Neck and/or
Spinal Pain’). Neoplastic disease affecting the vertebral column and spinal cord is
often painful, especially vertebral body osteosarcoma. Most cases of Hansen type
1 and type 2 intervertebral disc herniation are associated with a degree of apparent
pain on examination, with this being particularly true for type 1 disc extrusions.
282 A Practical Approach to Neurology for the Small Animal Practitioner

d. Symmetry of neurological deficits

i. Asymmetrical conditions
FCE, acute non‐compressive nucleus pulposus extrusion, (Hansen type 1
intervertebral disc disease, neoplasia, degenerative myelopathy).

ii. Symmetrical conditions

Most intervertebral disc herniations (especially Hansen type 2 disc protrusions),
inflammatory/infectious disease, anomalous disorders, degenerative myelopathy.

2. Signalment
There may be clues to the most likely differential diagnoses through a knowl-
edge of breed predispositions (see Chapter 2), and although these can rarely, if
ever, be taken as absolutes, they can help the clinician to make informed choices
and provide reasonable advice in situations where specialist referral for diagno-
sis is not an option. A few of the known breed predispositions include the
following.

• Fibrocartilaginous embolism and acute non‐compressive nucleus pulposus extrusion

One study found that Staffordshire Bull Terriers and Border Collies were
over‐represented (Fenn et al. 2016), and this is also the author’s experience.
Furthermore, 70–80% of all cases of FCE occur in middle‐aged and older,
large and giant breed dogs.
• Hansen type 1 intervertebral disc extrusion
At least 75% of cases occur in chondrodystrophic breeds of dog, with the
Dachshund, French Bulldog, and Cocker Spaniel being over‐represented.
• Degenerative myelopathy
The German Shepherd Dog and Pembroke Welsh Corgi are predisposed, but
this disease also occurs in many other breeds of dog (see above).
• Cervical spondylomyelopathy
Young Great Danes are predisposed to the osseous form, where the onset of
clinical signs is usually in juvenile growing dogs. The Dobermann is the breed
most commonly affected by the disc‐associated form, but the disease may also
be seen in other breeds, including the Dalmatian and the Labrador Retriever.
Affected dogs are usually middle‐aged or older.
• Atlantoaxial instability
Chihuahuas, Yorkshire Terriers, and other toy breeds are predisposed to this
condition, with signs usually becoming apparent in young dogs.
• Arachnoid space disorders
Thoracolumbar arachnoid diverticuli are seen mainly in Pugs and French
Bulldogs, often associated with vertebral abnormalities. A recent study found
male dogs are significantly over‐represented (Mauler et al. 2014). Pugs also
 Chapter 6 A Practical Approach to Common Presentations in General Practice 283

suffer from a fibrotic constrictive myelopathy in this region. Larger breeds,

especially the Rottweiler, are affected by cervical arachnoid diverticulum.
There is no significant age predisposition, with the study mentioned above
finding a median affected age of 3 years.

3. Neurological examination
Mentation: Expected to be normal unless affected by severe pain or shock in
trauma cases.
Gait and posture: Tetra‐, hemi‐, or paraparesis with concurrent proprioceptive
ataxia. A low head carriage may be seen in painful cervical lesions and kyphosis
in painful thoracolumbar lesions. Kyphosis and/or scoliosis may also be associ-
ated with vertebral malformations and severe cases of syringomyelia. Schiff–
Sherrington posture may be present in cases of acute, severe thoracolumbar
spinal cord injury, with rigidly extended thoracic limbs and paralysed pelvic
limbs (see Figure 6.10.1, Video 23, and Chapters 3 and 4).
Postural reactions: Abnormalities of either one, two, three, or four limbs,
depending on the lesion location. In cervical lesions, all limbs may be expected
to be abnormal, but if the lesion is markedly lateralised then there may be a
hemiparesis and postural reaction deficits on only the affected side. With thora-
columbar lesions, just the pelvic limbs should be affected, and in a very lateral-
ised lesion just a single pelvic limb may have postural reaction deficits.
Spinal reflexes: May be normal in all limbs for lesions affecting the C1–C5
spinal cord segments. If the lesion affects the C6–T2 spinal cord segments, spinal
reflexes may be reduced in the thoracic limbs, and if the lesion affects the L4–S3
spinal cord segments, the spinal reflexes in the pelvic limbs may be reduced (see
Chapter 4). However, the relative strength of the withdrawal reflexes can be

Figure 6.10.1 Schiff–Sherrington posture in a dog with an acute, severe thoracolumbar spinal
cord injury. The rigid extension of the thoracic limbs is caused by a loss of ascending inhibitory
influence on the thoracic limb extensor muscles from interneurons in the lumbar spinal cord
known as Border cells. Voluntary limb function and postural reactions in the thoracic limbs are
normal in such cases, and this presentation does not affect the prognosis for recovery.
284 A Practical Approach to Neurology for the Small Animal Practitioner

difficult to determine, even for a specialist neurologist, and is open to a degree of

subjectivity which can make neuroanatomic localisation difficult.
In acute, severe thoracolumbar spinal cord lesions, the spinal reflexes may be
reduced in one or both pelvic limbs for a variable period of time by a phenom-
enon known as spinal shock (see Chapters 4 and 7.3). The correct neuroana-
tomic localisation in these cases is usually possible by using the cutaneous trunci
reflex, which is frequently interrupted close to the level of the lesion.
Cranial nerve examination: Expected to be normal. Horner syndrome may be
seen in some cases of cervical spinal disease, especially with lesions affecting the
brachial plexus outflow.
Palpation: Careful palpation for pain may help with the neuroanatomic locali-
sation as well as the list of differential diagnoses (see above).

4. Neuroanatomic localisation
Following the neurological examination, it should be possible to localise the
spinal cord lesion in an animal presenting with paresis and ataxia to one of four
regions within the spinal cord: C1–C5, C6–T2, T3–L3, L4–S3 (see Chapter 4).
The neuroanatomic localisation does not necessarily aid construction of a dif-
ferential diagnosis list, except in cases of certain anatomically restricted diseases,
but may focus diagnostic evaluation. There are, however, certain causes of pare-
sis and proprioceptive ataxia for which a specific localisation would be expected,
such as AAI (C1–C5), disc‐associated wobbler syndrome (C6–T2), and degenera-
tive myelopathy (T3–L3). An alternative neuroanatomic localisation would
make these particular diseases unlikely.

6.10.3 Formulating a Plan

Once a reasonable differential diagnosis list has been produced by adopting the
approach outlined above, the clinician must decide how best to approach the
case (i.e. whether to initiate further investigations or seek specialist assistance
via referral). As before, the purpose of this text is to provide maximum assis-
tance when referral is not an option, but also to give guidance as to when refer-
ral is likely to be most urgent.
Cases can be differentiated in a number of ways, with onset, progression, and
the presence/absence of pain perhaps being most useful when it comes to estab-
lishing potential differential diagnoses and considering an appropriate course of
action.

1. Peracute onset of clinical signs

a. Painful conditions
Trauma is the most likely cause, so consider immediate referral if possible, espe-
cially if neurological deficits are severe. In cases of spinal cord trauma with an
absence of deep pain perception, the prognosis is likely to be grave and recovery
very unlikely, so euthanasia should always be discussed with owners. Cervical
 Chapter 6 A Practical Approach to Common Presentations in General Practice 285

lesions that are severe enough to cause loss of deep pain perception usually
result in death through respiratory failure. Be aware of the possibility for spinal
instability, provide support if possible, and take great care with anaesthesia and
sedation. If referral is not an option and deep pain perception is preserved, con-
sider survey radiographs of the affected region. Cage confinement may lead to
eventual recovery if the spinal cord damage is not too severe and the injury is
stable or can be supported by an external splint or cast, especially in the case of
cervical or low lumbar injuries.

b. Non‐painful conditions
FCE and ANNPE are most likely, especially if the neurological deficits show some
asymmetry and the signs are static or improving. Supportive care should be
instigated as appropriate for acute spinal cord injury, including intravenous fluid
therapy, maintenance of normal systemic mean arterial pressure, nursing care,
and bladder management if required (see Chapter 7). Cases carry a favourable
prognosis and the majority of dogs with intact nociception will recover the abil-
ity to walk with nursing care alone. Referral for advanced imaging is always
appropriate but is not necessary to distinguish between these two conditions
since their basic management is the same (see below). Although some cases of
traumatic, non‐degenerate disc extrusion may lead to a compressive spinal cord
lesion (so‐called compressive HNPE), a recent study showed that outcomes with
surgical and medical management may be very similar (Nessler et al. 2018).

2. Acute or subacute onset of clinical signs

a. Painful conditions
Inflammatory disease, either infectious or non‐infectious, and intervertebral disc
extrusion are the most likely differential diagnoses in this category. The decision
whether to investigate, treat, or refer (if possible) should be governed by the
neurological status at presentation and the speed of progression. Any animal
that is showing a rapid deterioration or is unable to walk at the time of presenta-
tion is a candidate for referral for specialist assessment. Inflammatory and infec-
tious diseases can progress rapidly if appropriate treatment is not initiated, and
some cases of intervertebral disc extrusion may progress to loss of deep pain
perception, in which case the prognosis for recovery is greatly reduced. If the
animal is able to walk, it is reasonable in most cases to consider investigations
in‐house, which may include haematology and serum biochemistry, infectious
disease testing +/− survey radiography of the affected area. Analgesic therapy
should be given, but corticosteroids should be avoided due to their ability to
mask clinical signs, exacerbate infections, and make potential future diagnosis
more difficult. If referral is not an option, then the clinician must make decisions
based on the most likely suspected diagnosis. A more detailed description of the
approach to intervertebral disc disease is given in Section 6.10.4 ‘Intervertebral
Disc Disease’.
286 A Practical Approach to Neurology for the Small Animal Practitioner

b. Non‐painful conditions
There are few non‐painful conditions that will show a genuinely acute onset of
signs, with the exception of acute non‐compressive nucleus pulposus extrusion
and FCE, as already discussed. Some intramedullary neoplasms may be non‐
painful and occasionally present in an acute or subacute manner. Some cases of
arachnoid space disorder may also present relatively acutely and with little pain,
but this is unusual.
Tetanus is a condition that is caused by infection with spores of the bacterium
C. tetani, which release a neurotoxin that affects inhibitory interneurons to the
extensor muscles of the limbs. This leads to a generalised spastic paresis/paralysis
which may initially present as an acutely tetraparetic animal. Other signs may
include facial muscle contraction (‘risus sardonicus’ – Figure 6.10.2) and an ele-
vated or semi‐elevated tail. Occasionally tetanus may be focal, with the clinical
signs restricted to a single limb. It is a rare condition in dogs and cats, with a
potentially guarded prognosis in generalised cases due to the degree of nursing
care required until spontaneous recovery can occur. Referral for specialist advice
and intensive care is recommended in suspected cases, as intensive nursing will
improve the prognosis and may be required for a prolonged period of time. For
further information the reader is referred to the many other texts on specific
neurological diseases.

3. Chronic onset of clinical signs

a. Painful conditions
This group consists mainly of Hansen type 2 intervertebral disc protrusion (and
occasional cases of Hansen type 1 disc extrusion), spinal cord neoplasia, and

Figure 6.10.2 Risus sardonicus in a dog. This facial expression is typically seen in cases with
tetanus due to spasticity of the muscles of facial expression.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 287

certain anomalous diseases, such as syringomyelia (see Section 6.9 ‘Neck and/or
Spinal Pain’). Cervical spondylomyelopathy and degenerative lumbosacral ste-
nosis are often associated with apparent pain on examination, although with
many of these more chronic conditions the degree of pain is variable. Chronic
conditions, by their nature, tend to present in a less severely affected way and
because they are generally slowly progressive, the clinician usually has more
time to consider options and even perform investigations or trial treatment
options. Indications for referral include rapidly deteriorating animals (which
may well have a neoplastic disease), and animals where the pain cannot be con-
trolled or is recurrent. Such animals may be suffering with intervertebral disc
disease, and chronic recurrent pain may justify surgical management.

b. Non‐painful conditions
The most likely presentations in this category would be neurodegenerative dis-
eases (such as degenerative myelopathy), certain intramedullary neoplasms,
and some anomalous conditions (such as arachnoid diverticulum and arachnoid
fibrosis). The signalment should help with deciding which condition is more or
less likely, and again the clinician usually has time to consider further investiga-
tion or referral. Submitting blood for genetic testing for the SOD‐1 mutation
known to predispose to degenerative myelopathy may be worthwhile if signal-
ment and neuroanatomical localisation and signs are consistent. Radiographs
may reveal vertebral column abnormalities, particularly in Pugs, which may be
associated with arachnoid space disorders, or may even suggest severe kyphosis,
which can be the cause of the paresis and ataxia.
One condition that may present as chronic paraparesis, often with a waxing
and waning course, is aortic thromboembolic disease in dogs. Unlike in cats, where
the classical presentation is acute, painful, severe, and easily recognised, the
thromboembolic disease of dogs is commonly partial, leading to a presentation
of exercise intolerance and pelvic limb weakness (see Chapter 3 and Videos 24
and 40). This presentation may therefore be confused for a thoracolumbar mye-
lopathy or myasthenia gravis. Diagnosis is suggested by the presence of poor
femoral pulses on general physical examination but requires imaging confirma-
tion of a thromboembolism in the distal aorta. Treatment is aimed at preventing
further enlargement of the thrombus and reversing, if possible, any underlying
predisposing medical conditions, such as protein‐losing nephropathy and loss of
anti‐thrombotic factors through damaged renal tubules.

6.10.4 Intervertebral Disc Disease

Intervertebral disc disease in one form or another is probably the most common
neurological condition that the general practitioner will face, with one epide-
miological study reporting that around 2% of dogs, and as many as 20% of
Dachshunds, are affected by intervertebral disc disease during their lifetime
(Bergknut et al. 2012).
288 A Practical Approach to Neurology for the Small Animal Practitioner

The intervertebral disc consists of an outer, fibrous annulus fibrosus and an

inner, initially gelatinous nucleus pulposus. The disc undergoes a process of
degeneration in all dogs, with the chondrodystrophic breeds tending to show a
more rapid degeneration, whilst in the larger, non‐chondrodystrophic breeds
degeneration is usually a slower process. There are also differences in the nature
of the degenerative process between breeds of dog, as described initially by
Hansen. These differences are proposed as the reason why chondrodystrophic
breeds tend to suffer more disc extrusion (Hansen type 1 disc disease), where the
nucleus pulposus escapes through a tear in the annulus fibrosus. Non‐chondro-
dystrophic breeds are more likely to suffer a disc protrusion (Hansen type 2 disc
disease), where the annulus remains intact but thickens and bulges in various
ways (Figure 6.10.3).
The differences in degeneration between chondrodystrophic and non‐chon-
drodystrophic breeds are now known to overlap far more than was originally
believed, and this probably explains why a significant number of Hansen type 1
extrusions may also occur in non‐chondrodystrophic breeds, such as Labrador
Retrievers and German Shepherd Dogs. Recent work has also led to the identifi-
cation of a genetic mutation thought to be responsible for the chondrodystrophic
degenerative process, as well as intervertebral disc disease itself (Brown et al.
2017), and this may lead to more effective treatments and breeding strategies in
the future.
Some authors favour the term intervertebral disc herniation to encompass all
the different types of intervertebral disc disease in which displacement of the
disc occurs in some way. The term intervertebral disc disease may include also the
degenerative process itself rather than true herniation. It is well known that a
degenerate, but non‐herniated, disc, is capable of causing pain in human
patients. This should potentially be considered as a possibility in animals,

Protrusion Extrusion

Annulus fibrosus
Nucleus pulposus

Figure 6.10.3 The two main types of intervertebral disc herniation. Hansen type 1 disc
extrusion occurs when degenerate nucleus pulposus material herniates through a ruptured
annulus fibrosus; Hansen type 2 disc protrusion occurs when the degenerate annulus bulges
into the vertebral canal without being ruptured.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 289

although it would be much more difficult to prove. For the purposes of this dis-
cussion, the term intervertebral disc herniation will be used, being defined as
localised displacement of the intervertebral disc beyond the boundaries of the
intervertebral disc space. This displacement may be contiguous with the remain-
der of the disc or may also include material which is separated from the disc and
lying some distance away from the affected intervertebral disc space. Where
discussion is confined to the Hansen type 1 extrusion of degenerate (and often
calcified) nucleus pulposus through a ruptured annulus fibrosus, the term
intervertebral disc extrusion will be used. Likewise, when discussing the Hansen
type 2 protrusion of a degenerate but intact annulus fibrosus, with no escape of
nucleus pulposus, the term intervertebral disc protrusion will be used. When the
term, intervertebral disc herniation is used it refers to the generic displacement of
disc material, and this may encompass both extrusion and protrusion, as well as
escape of non‐degenerate nuclear material as in the acute non‐degenerate
nucleus pulposus extrusion.

1. Hansen type 1 intervertebral disc extrusion

History: Usually acute or subacute, painful, frequently progressive, and often
more or less symmetrical.
Signalment: Mainly chondrodystrophic breeds, especially the Dachshund,
French Bulldog, Beagle, Cocker Spaniel, Pekingese, but can occur in any breed.
Mean age at presentation 5 years but can occur in any dog over 1 year old.
Presenting signs: Can be very variable, ranging from back pain alone through
to complete tetra‐ or paraplegia with absent deep pain perception. Tetraplegia
with loss of deep pain perception is uncommon, as already stated, due to the
vital cardiorespiratory functions that can be affected by such a severe lesion in
the cervical spinal cord. A very common presentation is for an animal to show a
few days of apparent pain or lethargy, which may easily be mistaken for abdomi-
nal pain, followed by a rapid progression to paraparesis or even paraplegia.
The location of Hansen type 1 intervertebral disc extrusions may be cervical
or thoracolumbar, with the most common disc spaces affected in the cervical
region being C2–C3 in small breeds and C6–C7 in large breeds, whilst in the
thoracolumbar region around 90% of extrusions occur between T11 and L3.
Cervical intervertebral disc extrusions commonly present with severe pain (e.g.
vocalisation) and minimal neurological deficits, whereas thoracolumbar extru-
sions more often present with varying degrees of neurological deficit and appar-
ently less severe pain.
Diagnosis: May be presumptive based on the appropriate history and signal-
ment and neurological examination findings pointing to a focal myelopathy in
an appropriate location. Survey radiography may provide further evidence if a
narrowed intervertebral disc space is noted in the suspected region, or calcified
material is seen within the vertebral canal or intervertebral foramen. Survey
radiographs must be of sufficient quality for these findings to be reliable, with
290 A Practical Approach to Neurology for the Small Animal Practitioner

centering over the suspected disc space and good collimation; a disc space nar-
rowing is unreliable if it is seen on the edge of the field of view, and it should be
possible to identify wider spaces on each side of the affected space if the narrow-
ing is genuine. It should also be remembered that T10–T11 frequently appears
narrowed in cats and dogs, and is uncommonly the location of an extrusion.
Confirmation of diagnosis requires advanced imaging; myelography is a rela-
tively reliable technique but has largely been superseded by three‐dimensional
imaging such as CT and MRI. These modalities are increasingly available and,
although still relatively expensive in veterinary medicine, they provide essential
diagnostic information when surgical treatment is being considered or there is
significant doubt surrounding the diagnosis. CT is more rapid and usually relia-
ble in cases of intervertebral disc extrusion, but MRI is superior at eliminating
the possibility of other less common differential diagnoses such as neoplasia and
inflammatory disease.
Treatment options: Conservative or surgical for both cervical and thoracolum-
bar extrusions. Conservative management entails a period of strict rest and con-
finement, together with analgesia. It may be necessary, especially with cervical
disease, to use multimodal analgesic drugs and the author commonly prescribes
a combination of a NSAID, paracetamol (10 mg/kg per os twice daily), and
gabapentin (10 mg/kg per os twice or three times daily). Controlling the pain is
very important for the owner and for successful resolution of signs. Corticosteroids
are best avoided, except in situations where referral is definitely not an option
and the pain has been prolonged, unremitting, and poorly controlled with other
medications. Cage confinement is considered essential to prevent further nucleus
pulposus from extruding and to potentially allow healing of the ruptured annu-
lus fibrosus. The length of time that cage rest should be recommended is not
known, with 2–4 weeks being commonly proposed. However, one study found
no association between the length of cage rest and a successful outcome (Levine
et al. 2007). The author usually recommends an initial week of very strict cage
confinement, followed by a further 3 weeks of gradual relaxation of the
confinement.
The decision as to whether and when to refer for possible surgical treatment
is probably one of the biggest concerns for a general practitioner, therefore a set
of broad guidelines is given below.

a. Suspected cervical intervertebral disc extrusion

Neck pain only: Medical management. Consider referral if pain is not con-
trolled within 48 hours or there are signs of progression to paresis and ataxia.
Pain and ambulatory tetraparesis: Medical management is reasonable initially. If
neurological deterioration occurs then consider referral, but if the clinical signs
are stable and/or improving then medical management may be successful.
Pain and non‐ambulatory tetraparesis: Refer for potential surgical management
if this is an option. If not, medical management may still be successful.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 291

Animal presents with Painful not

Ambulatory
tetraparesis progressive

Painful and/or Medical management of

Non-ambulatory Non-painful
progressive suspected IVDD (see text)

Peracute, non-
progressive, non Progression or failure to
painful and control pain
lateralising

Referral for
Likely ANNPE or specialist advice
FCE (see text)
TETRAPARESIS

Medical management No improvement

Approach to cases of tetraparesis in practice.

b. Suspected thoracolumbar intervertebral disc extrusion

Back pain only: Medical management. Owners should be instructed to pay
careful attention to cage confinement, and to report immediately any signs of
neurological deterioration. They should be warned that after appropriate anal-
gesia their pet may appear recovered, but that the cage confinement is still
essential for prevention of deterioration or recurrence.
In all cases where a suspected thoracolumbar intervertebral disc extrusion is
managed conservatively, it is important for the veterinarian to discuss with the
pet owner that acute deterioration to paraplegia with absent deep pain percep-
tion can occasionally occur, and that this would reduce the prognosis for recov-
ery (see below). The veterinarian must necessarily protect him or herself from
any possible accusation that a future deterioration may have occurred due to
incorrect or false advice or information being provided. Any owner who is
uncomfortable with this should be offered early referral for specialist advice.
Pain and ambulatory paresis: Medical management is appropriate, with the
provisos stated above. Many dogs will recover (recovery rates of 80% are
commonly reported), although recurrence rates may be higher with surgical
treatment. However, the risks and costs of surgical treatment should also be
discussed, since many owners will be unable to afford a second surgical
treatment if there is recurrence after an initial surgery, and recurrence rates
after surgical treatment if multiple site fenestration is not employed may be as
high as 15–20%. For this reason, it may be in the owner’s best interest to
employ medical management in such situations, ‘saving’ any available funds/
insurance for a situation where there is better evidence for the superiority of
surgical treatment.
Non‐ambulatory paresis or paraplegia: Refer for specialist advice and potential
surgical management if possible. If this is not an option, then medical
292 A Practical Approach to Neurology for the Small Animal Practitioner

management may still be successful in as many as 80% of cases where deep

pain perception is retained, although recovery may be prolonged and
incomplete.
Paraplegia with loss of deep pain perception. The loss of the ability to feel a painful
stimulus applied to the deep structures of the foot/toes of the pelvic limb is a sign
of severe spinal cord injury (see Chapter 3). It is the only factor which has been
consistently shown to be linked to prognosis in cases of thoracolumbar interverte-
bral disc extrusion. For dogs that lose deep pain perception, recovery rates are
reduced from around 90% to just over 50% in dogs that are treated surgically. The
recovery rate for dogs treated medically is thought to be considerably lower than
this, although the true rate may be higher since there is very little information
regarding the medical management of dogs with absent deep pain perception. In
any event, recovery is likely to be prolonged and potentially expensive due to the
nursing requirements and associated urinary incontinence which is usually seen.
Referral of dogs that lose pelvic limb deep pain perception should be arranged as
quickly as possible, although a recent study concluded that speed of surgical treat-
ment is not associated with outcome (Jeffery et al. 2016), and most neurosurgeons
are now happy to delay surgery until such time as an animal is stable. The chances
of successful outcome, potential costs involved, and length of time expected for
recovery (recovery to ambulation and regaining ability to urinate may be pro-
longed and usually between 2 and 8 weeks) should be discussed prior to referral,
since some owners may unfortunately elect to euthanise their pet at this point.

Medical management in paraplegic dogs

As already stated, rest is important, although in dogs which are plegic this is not usu-
ally a problem! It is important to ensure that care is taken when handling affected
dogs so as to minimise the risks of causing extrusion of further nucleus pulposus
material into the vertebral canal, although the real risks of this are unknown.

i. Bladder management
Most dogs rendered paraplegic by a thoracolumbar intervertebral disc extrusion
will suffer a period of urinary incontinence associated with loss of the upper
motor neuron control of micturition (see Chapter 3). This presents as a dog that
is unable to empty the bladder, but with a spastic external urethral sphincter so
that the bladder becomes over‐full with urine until the pressure inside is great
enough to force open the sphincter. This is known as urinary retention and
overflow. It is common for veterinarians and nurses who are inexperienced at
dealing with such dogs to mistakenly assume that such urine overflow repre-
sents conscious urination by the dog. This may be a dangerous mistake, since if
the bladder is allowed to remain in an over‐full state with the detrusor muscle
stretched for more than just a couple of days, permanent detrusor damage can
result. This can lead to the very unfortunate situation where a dog recovers the
ability to walk but remains permanently urinary incontinent.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 293

Any dog that is paraplegic or non‐ambulatory paraparetic should have regular

(at least three times a day) bladder checks. Palpation of the caudal abdomen may
be sufficient to determine the level of filling of the bladder, but this also requires a
level of experience in order to be reliable. Where there is any doubt, ultrasound
scanning of the abdomen may give a more reliable picture of the true state of blad-
der filling. When a dog has potentially passed some urine, and either the passing
was unobserved (e.g. found on the dog’s bed) or there is some doubt as to whether
the urination was conscious and voluntary or unconscious overflow, then the
bladder must be checked in some way as soon as possible afterwards. If the urina-
tion was involuntary overflow, then the bladder is likely to be full or overfull
when checked. If, on the other hand, it was a genuine conscious act of bladder
emptying, then the bladder should be small or close to empty when checked.
If there is a concern that the patient is not able to pass urine voluntarily, then
a plan must be put in place to manage bladder emptying. There are three options
which are available to ensure that the bladder is prevented from becoming over-
full, and each has different pros and cons. The clinician may need to be able to
adapt and switch between options depending on how the case is progressing.

Bladder management options in spinal cord disease

Manual expression: Regular manual bladder expression via caudal abdominal
palpation is possible in many cases. The technique is not easy, and it can be dif-
ficult even for an experienced clinician to ensure that the bladder is properly
emptied. As mentioned above, the use of an ultrasound scanner to check blad-
der filling after manual expression is a reliable way of monitoring the effective-
ness of emptying. Where this is not possible, passing a rigid urinary catheter after
manual expression allows the clinician to check their technique. Advantages of
manual expression include reduced cost and level of nursing care, and the pos-
sibility for owners to be trained to express their own animal’s bladder.
Disadvantages revolve around the potential for inadequate emptying, and the
fact that the technique may cause discomfort to the patient, making other nurs-
ing procedures and physiotherapy more difficult.
Intermittent rigid catheterisation: Passing of a rigid catheter at regular intervals is
possible, especially in male dogs. This needs to be performed three times daily in
order to ensure the bladder does not become over‐full, and therefore can become
expensive if it needs to be continued for a prolonged period. It can also lead to
inflammation of the urethra, as well as being technically challenging in females.
Indwelling urinary catheter: Placement of a permanent indwelling soft urinary
catheter allows continuous bladder drainage with minimal handling of the
patient. It also allows for close monitoring of urine output, and is the only way
of ensuring the bladder is kept properly emptied, which can be important, espe-
cially in cases where it may have been over‐full for 24 hours or more. Catheter
management is important, and aseptic precautions should be taken when plac-
ing and handling catheters. The use of closed collection systems is preferred for
294 A Practical Approach to Neurology for the Small Animal Practitioner

both hygiene reasons and to allow proper monitoring of urine production. If

urine output appears to fall, the catheter should always be checked to ensure it
has not become kinked or blocked. A Buster collar or similar needs to be worn
to prevent the patient licking, chewing, or pulling the catheter out. Disadvantages
include added cost and the increased difficulty of moving affected patients with
attached urinary collection bag. However, the author’s preference is to place an
indwelling catheter in most cases that present paraplegic, at least to allow easy
bladder management in the first few days.

With all of the above techniques, urinary tract infection (UTI) is common.
Several studies have shown that UTI is a common complication in dogs suffering
with severe paraparesis and paraplegia associated with spinal cord injury, and so
careful aseptic technique and ensuring that bladders are properly emptied is
important. The use of prophylactic antibiotics has not been shown to be effective
and is not advised during a period of indwelling catheterisation due to the risk of
development of antimicrobial‐resistant bacteria. However, a short period of pro-
phylactic antibiosis following catheter removal may reduce the incidence of clini-
cal UTI (Marschall et al. 2013) and may be considered. Specific antibacterial
treatment should generally be reserved for patients with clinical signs of UTI,
preferably following urine bacterial culture and antibiotic sensitivity testing from
a cystocentesis sample. If a clinical UTI occurs, it is advisable to remove an indwell-
ing catheter and use an alternative method of bladder management. However, it
is important to be aware that the risk of UTI is not significantly different with any
of the above methods, since there is a risk from leaving residual urine in the blad-
der as is likely with manual expression, as well as through the use of catheters.

ii. Physiotherapy and rehabilitation

Active rehabilitation employing physiotherapy techniques and potentially hydro-
therapy is considered an important part of recovery from acute spinal cord injury
whether from intervertebral disc disease or other causes of myelopathy such as
FCE. Care must be taken when dealing with patients suffering with acute Hansen
type 1 intervertebral disc extrusion, since there is always a possibility of further
nucleus pulposus material extruding into the vertebral canal during recovery,
especially in patients managed medically rather than surgically. Furthermore, the
evidence for the effectiveness of physical therapy in neurologic patients is some-
what limited, with one recent study finding no benefit (Olby et al. 2019). In the
author’s experience, passive range of motion exercises and limited physiotherapy
may be beneficial in avoiding joint stiffness especially in long‐term paraplegic
patients, and should be performed in a careful way on acutely paraplegic and
non‐ambulatory paraparetic patients when possible. Once such animals recover
ambulation, the emphasis should be more on exercises aimed at improving coor-
dination and proprioception, and the assistance or involvement of a properly
trained animal physiotherapist or rehabilitation practitioner is advisable. For spi-
nal cord conditions other than intervertebral disc disease, again the evidence for
 Chapter 6 A Practical Approach to Common Presentations in General Practice 295

the effectiveness of physical therapy is varied, but one study showed an increased
life expectancy for dogs suffering from degenerative myelopathy (Kathmann
et al. 2006). The other benefits of employing rehabilitation techniques include
improved well‐being for the patient and greater owner participation in their ani-
mal’s recovery, which for some owners can be a significant factor.
Alternative therapies, such as the use of laser therapy, have so far not been
shown to be of benefit in the recovery of dogs with intervertebral disc disease
(Bennaim et al. 2017). Acupuncture has, however, apparently improved recov-
ery rates in severely affected dogs and reduced the degree of pain associated with
intervertebral disc disease. This therapy is therefore worth considering, espe-
cially in situations when the traditional approach of MRI and decompressive
surgery is not an option (Joaquim et al. 2010).

2. Hansen type 2 intervertebral disc protrusion

History: Chronic, progressive, sometimes painful, usually symmetrical.
Signalment: Large breed, non‐chondrodystrophic dogs, especially German
Shepherd Dogs, Labrador Retrievers, Dalmatians, Dobermanns. Usually older
(>5 years).
Presenting signs: Progressive tetra‐ or paraparesis with proprioceptive ataxia
and variable neck or back pain.
Diagnosis: As for type 1 disc extrusions above.
Treatment: Medical or surgical management may be employed. In a recent
study, surgical treatment was found to be more effective than medical manage-
ment for thoracolumbar disc protrusions (Crawford and De Decker 2017), and
referral should therefore always be discussed with the owner. However, many
affected dogs are older at the time of diagnosis and owners may be reluctant to
pursue surgical treatments which can, in the case of chronic thoracolumbar disc
protrusions, have significant morbidity. Medical management is therefore com-
mon in these cases. In this situation, controlled exercise and the judicious use of
anti‐inflammatory doses of corticosteroids may give superior results to NSAIDs,
at least in the short‐term.
A tapering dose of prednisolone has also been recommended for the medical
management of disc‐associated cervical spondylomyelopathy (0.5 mg/kg twice
daily for 7 days, 0.5 mg/kg once daily for 7 days, 0.5 mg/kg on alternate days).
This condition is seen especially in the Dobermann, where chronic intervertebral
disc protrusion in the caudal cervical region leads to progressive signs of tetrapa-
resis +/− neck pain. This is a specific variant of Hansen type 2 intervertebral disc
protrusion that may also involve other sources of spinal cord compression, both
bony and soft tissue, as well as instability at the intervertebral joint. Corticosteroids
are likely to be efficacious through reduction of vasogenic spinal cord oedema
associated with chronic spinal cord compression in these cases, and it is the
author’s experience that this is often also the case for thoracolumbar disc
­protrusions. This is in contrast to acute intervertebral disc extrusions, in which
296 A Practical Approach to Neurology for the Small Animal Practitioner

the nature of the spinal cord injury differs, and corticosteroids play little role in
the management. For disc‐associated cervical spondylomyelopathy, controversy
remains as to which treatment modality is superior, and many different surgical
approaches have been described.
Prognosis in all cases of Hansen type 2 intervertebral disc protrusion remains
guarded, with most cases showing progression when managed medically, and
outcomes with surgical management are less predictable than for type 1 disc
extrusions.

3. Acute non‐compressive (or moderately compressive) nucleus pulposus

extrusion (ANNPE)
History: Peracute, non‐progressive, initially painful but rapidly becoming
non‐painful, usually asymmetrical.
Signalment: Any age and breed may be affected. Border Collies over‐represented.
Presentation: Peracute onset of moderate to severe neurological deficits, often
asymmetrical, non‐painful within 24 hours of onset, and frequently improving
at a variable rate.
Diagnosis: May be presumptive based on the factors above, with FCE being
the primary differential diagnosis. Confirmation requires MRI.
Treatment: Medical management carries a favourable prognosis, with most
animals that retain deep pain perception recovering ambulation, usually within
2–4 weeks. Analgesia is not usually required, and cage confinement is not neces-
sary. Physiotherapy and rehabilitation techniques from an early stage will poten-
tially assist in the recovery. Initial management of suspected spinal cord contusion
by maintaining adequate mean arterial pressure and oxygenation may be ben-
eficial. Management of FCE is similar and therefore differentiation of these two
conditions is not essential to ensure a favourable prognosis.

Animal presents with Painful not

Ambulatory
paraparesis progressive

Painful and/or Medical management of

Non-ambulatory Non-painful
progressive suspected IVDD (see text)

Peracute, non-
Chronic and/or Progression or failure to
progressive, non
progressive control pain
painful and
lateralising

Referral for
Likely ANNPE or specialist advice
FCE (see text)
PARAPARESIS

Medical management No improvement

Approach to cases of paraparesis in practice.

 Chapter 6 A Practical Approach to Common Presentations in General Practice 297

6.11 ­Monoparesis and Lameness

Paul M. Freeman

Many of the conditions that are discussed in Section 6.10 ‘Paresis, Paralysis, and
Proprioceptive Ataxia’ as possible causes of paresis and ataxia can also present as
a monoparesis or apparent lameness, and these conditions can be difficult to
distinguish from orthopaedic disease (e.g. elbow dysplasia, cranial cruciate liga-
ment disease, hip osteoarthritis, septic arthritis, osteosarcoma). The following
section is a guide to the recognition, differential diagnosis, and approach to
monoparesis in cats and dogs.

6.11.1 Recognition of Potential Neurogenic Lameness

There are a number of potential clues to assist with the recognition of neuro-
genic lameness as opposed to orthopaedic lameness.
Muscle atrophy: Neurogenic muscle atrophy is usually much more rapid and
severe than the atrophy of disuse which is commonly associated with orthopae-
dic disease. However, if an animal presents with a chronic history of gait abnor-
mality the distinction can be more difficult, because significant disuse muscle
atrophy may have already occurred (e.g. secondary to chronic cranial cruciate
ligament insufficiency). In general, whenever an animal is presented with a
lameness that is accompanied by severe muscle atrophy affecting all or part of
the limb, a neurogenic cause should be considered.
Paresis and postural reactions: A reduction in the ability to weight‐bear (lower
motor neuron paresis) or a reduced ability to initiate movement (upper motor
neuron paresis) are features of neurogenic lameness, termed ‘monoparesis’
when they affect a single limb. An animal may drag the toes of the affected
limb leading to abnormal wearing of the nails. Postural reaction deficits (paw
replacement and/or hopping) may also be present, particularly in cases of
upper motor neuron monoparesis. In contrast, orthopaedic lameness results
from a reluctance to weight‐bear on the affected limb and the postural reac-
tions should be normal. However, caution should be exercised when diagnos-
ing a neurogenic lameness based on reduced postural reactions alone, since
painful orthopaedic conditions (such as osteosarcoma) may lead to apparent
deficits of weight‐bearing, paw replacement, and hopping, and may cause toe
dragging during ambulation secondary to pain and reluctance to move the
limb.
Reduced spinal reflexes: The flexor withdrawal reflex, as well as other spinal
reflexes such as the patellar reflex and extensor carpi radialis reflex, may be
significantly reduced in cases with neurogenic lameness and lower motor
neuron monoparesis. Again, the clinician should be careful not to over‐
interpret such signs since an animal with a painful orthopaedic problem may
298 A Practical Approach to Neurology for the Small Animal Practitioner

be reluctant to withdraw the affected limb, and the patella reflex is com-
monly absent in some older dogs and dogs which have significant stifle
pathology (see Chapter 3).
Reduced sensation: Significant nerve damage may lead to loss of sensation in
the skin supplied by the affected nerve (e.g. following traumatic avulsion of the
roots of the brachial plexus). A knowledge of the so‐called autonomous zones
(the areas of skin supplied by an individual nerve, see Figure 1.3) may allow
accurate localisation of a specific nerve injury but is not generally required for
diagnosis and management of the majority of cases in general practice.
Pain: Many cases of neurogenic lameness may be accompanied by significant
pain; a neurogenic cause should be considered in any animal presenting with a
severely painful lameness that is resulting in spontaneous vocalisation.

6.11.2 Differential Diagnosis for Monoparesis

1. Vascular conditions
Fibrocartilaginous embolism (FCE) may cause an acute mono‐ or hemiparesis
dependent on the site and extent of the lesion. In this condition, small frag-
ments of fibrocartilaginous material from an intervertebral disc embolise into
small spinal arterioles leading to a peracute ischaemic myelopathy. If the area
of spinal cord ischaemia is sufficiently lateralised then a monoparesis may
result, which can be severe enough to result in monoplegia. It is rare for a sin-
gle thoracic limb to be involved without a corresponding upper motor neuron
paresis of the ipsilateral pelvic limb, but if lesions occur caudal to the C6–T2
spinal cord segments then monoparesis of a pelvic limb may be seen (see
Video 41). This will be an upper motor neuron monoparesis if the lesion is
cranial to the L3 spinal cord segment, or a lower motor neuron paresis if the
lesion occurs within the L4–S3 spinal cord segments. As discussed in Chapters
3 and 4, upper motor neuron paresis will be accompanied by intact spinal
reflexes, whilst lower motor neuron paresis typically leads to reduced or absent
local spinal reflexes. Dependent on the location of the lesion, there may also
be an interrupted cutaneous trunci reflex just caudal to the site of the lesion.
Diagnosis requires referral for MRI, but a presumptive diagnosis may often be
made based on the clinical history, neurological examination, and signalment.
The prognosis is generally good in cases of monoparesis, although may be
guarded for recovery of limb function if there is severe lower motor neuron
monoparesis/monoplegia. Management of these cases is medical and involves
physiotherapy and rehabilitation (see Section 6.10 ‘Paresis, Paralysis, and
Proprioceptive Ataxia’).
Aortic thromboembolism, as discussed in Section 6.10 ‘Paresis, Paralysis, and
Proprioceptive Ataxia’, may present as a monoparesis or unilateral ‘lameness’. In
cats, a single thoracic limb may be involved, and the prognosis is generally
guarded. In dogs, rare cases may involve just one pelvic limb.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 299

2. Inflammatory conditions
Meningomyelitis of unknown origin (MUO) (see Section 6.10 ‘Paresis, Paralysis,
and Proprioceptive Ataxia’) may rarely present as a monoparesis secondary to
the presence of a focal, asymmetric lesion within the spinal cord; however, this
is very uncommon.
Idiopathic or immune‐mediated neuritis: Occasionally, an autoimmune inflam-
matory response is triggered in an individual peripheral nerve or nerve root,
usually at the level of the spinal cord, that results in lameness and/or monopa-
resis if the affected nerve is responsible for innervating the muscles of a single
limb (e.g. C6–T2 or L4–S2 nerve roots). Reports and information regarding this
condition are limited, but significant nerve root enlargement can occur, mimick-
ing neoplastic disease.

3. Trauma
Trauma is a relatively common cause of peripheral nerve injury and may also
accompany orthopaedic injury (e.g. pelvic fractures following road traffic acci-
dents). The clinical history should facilitate diagnosis, and radiographic evidence
of a fracture in a region of bone that lies close to a peripheral nerve or nerve root
(e.g. the iliac shaft or distal humerus) along with accompanying neurological
deficits should always raise suspicion for concurrent neurological injury.
Traumatic nerve injury may range from neuropraxia, which includes nerve inju-
ries such as stretching, compression, or blunt trauma where the axons remain
intact, through to axonotmesis, which is defined as complete physical disruption
of the axons in a nerve. When nerve injury is suspected, the loss of deep pain
perception in regions of the limb supplied by the nerve carries a guarded prog-
nosis for recovery of function and implies likely axonotmesis. However, care
must be taken in interpreting loss of deep pain perception in animals suffering
from shock, and it is sensible to delay such testing until systemic stabilisation is
complete. Significant pain may be present if there is entrapment of a peripheral
nerve or nerve root within a fracture site, and in animals that present with pelvic
injuries where the pain is difficult or impossible to control, consideration should
always be given to the possibility of nerve entrapment; referral for specialist
assessment should be considered at an early stage in these cases.
Brachial plexus avulsion is a specific condition in which the nerve roots of the
brachial plexus are avulsed from the cervicothoracic spinal cord by significant
trauma, often involving excessive abduction of a thoracic limb. The limb is typi-
cally flaccid and paralysed, with an absent flexor withdrawal reflex, absent pos-
tural reactions, and rapid denervation muscle atrophy. Loss of the ipsilateral
cutaneous trunci reflex and/or the presence of Horner syndrome may also be
seen. In severe cases, with complete loss of motor and sensory function, the
prognosis is guarded. If some degree of function is retained (particularly radial
nerve function and the ability to extend the elbow to bear weight), then many
300 A Practical Approach to Neurology for the Small Animal Practitioner

animals will recover to at least some extent. However, this recovery may be very
protracted and limb amputation should still be considered, particularly if there is
self‐trauma or recurrent damage to the affected distal limb.
Radial nerve paralysis (or paresis) is a specific nerve injury affecting the radial
nerve that is thought to be caused by blunt trauma where this nerve is closely
associated with the distal portion of the humerus. It is therefore also occasionally
associated with humeral fractures. Again, prognosis is related to extent of nerve
damage, and complete loss of motor and sensory function implies a guarded
prognosis.

4. Neoplastic conditions
Peripheral nerve neoplasia is a relatively common cause of monoparesis or neu-
rogenic lameness.
Peripheral nerve tumours may affect a single peripheral nerve (usually proxi-
mally) and commonly cause a chronic, progressive lameness that may be poorly
responsive to analgesics and anti‐inflammatory drugs. These cases are frequently
accompanied by significant muscle atrophy in the affected limb. Hemiparesis
(lower motor neuron paresis of a thoracic limb and upper motor neuron paresis
of the ipsilateral pelvic limb) may be seen secondary to spinal cord compression
if a tumour of the C6–T2 nerve roots invades into the vertebral canal via the
intervertebral foramen. Diagnosis requires MRI in most cases, and treatment
may be palliative or surgical. The prognosis is generally guarded, with most stud-
ies showing median survival times of less than 1 year following surgical excision
and limb amputation. However, a recent study where compartmental excision
and limb‐sparing was performed reported a median survival time of 1303 days
(Stee et al. 2017).
Lymphoma should always be considered as a differential diagnosis in cases
with peripheral nerve or nerve root enlargement, and evaluation for signs of
systemic involvement or other locations of lymphoma may prevent inappropri-
ate treatments or unnecessary referral.

5. Degenerative conditions
Intervertebral disc disease (see Section 6.10 ‘Paresis, Paralysis, and Proprioceptive
Ataxia’). Hansen type 1 intervertebral disc extrusions may occasionally present
as a monoparesis/lameness if the extruded disc material herniates laterally into
the intervertebral foramen in the region of the brachial plexus or lumbosacral
plexus nerve roots. Lameness may be moderate to severe and painful, with per-
manent or intermittent episodes of non‐weight‐bearing (‘nerve root signature’).
Even with advanced imaging, diagnosis can be difficult and surgical treatment
may be technically demanding, dependent upon the location of the extruded
material. Medical management may be successful and is generally reasonable in
the first instance, although persistent pain is an indication for surgical treatment.
However, resolution of lameness can be protracted over weeks or months
 Chapter 6 A Practical Approach to Common Presentations in General Practice 301

whichever treatment method is employed. Hansen type 2 intervertebral disc

protrusions may also present as monoparesis/lameness if an annular protrusion
is lateralised and compresses a peripheral nerve root at the level of the interver-
tebral foramen.
Degenerative lumbosacral stenosis is a syndrome where the vertebral canal at
the level of the lumbosacral junction is narrowed by various bony and/or soft
tissue structures, commonly including the L7–S1 intervertebral disc. It occurs
in middle‐aged and older large breed dogs, notably the German Shepherd
Dog, but many breeds may be affected. Clinical signs commonly include
lower back pain and reluctance to climb stairs or jump up (see Section 6.9
‘Neck and/or Spinal Pain’) but may also involve some degree of tail paresis or
even urinary or faecal incontinence. If the L7–S1 intervertebral foramen is
narrowed on one side, leading to compression of the L7 nerve root, then this
condition may involve a pelvic limb lameness or monoparesis. Definitive
diagnosis requires advanced imaging and treatment may be medical or
surgical. Epidural injection of methylprednisolone acetate can provide pain
relief and reduction of inflammation, with one study reporting good results
with this treatment (Janssens et al. 2009). Diagnosis should preferably be
confirmed prior to using corticosteroid treatment since a possible differential
diagnosis may be bacterial discospondylitis, in which the use of corticosteroids
would be contraindicated.

6.11.3 Approach to Monoparesis

When faced with a case of monoparesis, a knowledge of the conditions that may
present with this clinical sign, and their differences in expected clinical history
and signalment, should allow the clinician to limit the possible differential diag-
noses to a small number. Unfortunately, advanced imaging +/− specialist electro-
diagnostic evaluation is usually required for confirmation of the diagnosis.
Therefore, referral for specialist advice and investigation should always be con-
sidered if an orthopaedic cause of lameness has been ruled out. Referral is sel-
dom an emergency in these situations, except in cases of potential nerve injury
following trauma where surgical intervention to stabilise fractures may be
urgently required to prevent permanent nerve damage. In other peracute pres-
entations, such as FCE and brachial plexus avulsion, referral may help to con-
firm the diagnosis and offer guidance in terms of prognosis but will rarely affect
the outcome.
In subacute and chronic cases, referral should be considered whenever the
diagnosis remains unclear. Survey radiographs to look for evidence of orthopae-
dic disease may be considered, as well as spinal radiographs looking for evidence
of neoplasia, degenerative lumbosacral stenosis, or intervertebral disc disease
when appropriate. Screening for metastatic and primary disease should be con-
sidered if neoplasia appears likely (e.g. lymphoma), although peripheral nerve
tumours are rarely metastatic.
302 A Practical Approach to Neurology for the Small Animal Practitioner

Animal presents with

monoparesis or Acute Likely ANNPE or
Non-painful
lameness history FCE (see text)

Chronic history Painful

No improvement
within 1 week

Trauma

Fracture Refer for specialist

Rule out
orthopaedic advice
disease Nerve root
avulsion

MONOPARESIS / LAMENESS
Suspect
neoplasia

Approach to monoparesis/lameness in practice.

6.12 ­Neuromuscular Weakness

Edward Ives

Neuromuscular disease is the broad term used to describe disorders affecting one
(or more) of the following neuroanatomic structures:

• the peripheral motor and/or sensory nerves residing outside the central nerv-
ous system (CNS)
• the neuromuscular junction (NMJ) that provides the connection between the
peripheral motor nerves and the skeletal muscles they innervate
• the skeletal muscles themselves.

Neuromuscular disorders can therefore be divided into the following

categories:

• peripheral neuropathies
• junctionopathies
• myopathies.

Before considering these individual categories, the most important step is

recognising that the neuromuscular system is affected in the first place. This may
sound obvious; however, disorders affecting other body systems can mimic neu-
romuscular weakness, and neuromuscular disorders can appear clinically similar
to disorders affecting the CNS. The neurological examination should therefore
 Chapter 6 A Practical Approach to Common Presentations in General Practice 303

be repeated and reconsidered until you are as confident as you can be that a
neuromuscular disorder is responsible for the presenting complaint and clinical
signs (Glass and Kent 2002). This will allow you to formulate a list of the most
likely causes, from which a logical and efficient set of diagnostic investigations
can be planned.
Tips for recognising neuromuscular disease and differentiating these disor-
ders from lesions affecting the brain or spinal cord are listed below. The typical
clinical signs associated with neuromuscular disease and the clinical distinction
between peripheral neuropathies, myopathies, and junctionopathies is further
discussed in Chapter 4.

1. Stride length, joint posture, and muscle tone

The peripheral motor nerves, NMJ, and skeletal muscles form the final com-
mon pathway for motor function. Disorders affecting these structures result in
an inability to maintain normal muscle strength and tone. A reduction in
extensor muscle tone will influence the ability to support body weight against
the force of gravity. This will be clinically‐apparent as reduced joint extension
and a short‐strided gait as the animal rapidly shifts its weight from limb to limb
to avoid collapse. The limbs may appear flaccid when the animal is in lateral
recumbency and the flexor withdrawal reflexes may be reduced in all limbs
(see Videos 31 and 42). This generalised reduction in muscle tone and the
recognition of weak withdrawal reflexes in all limbs can be used to differenti-
ate neuromuscular weakness as the cause for non‐ambulatory tetraparesis
from a cervical spinal cord lesion, in which the trunk tone, pelvic limb muscle
tone, and pelvic limb withdrawal reflexes would be expected to be normal.
2. Is the animal ataxic or just weak? Is the proprioception normal?
The NMJ and skeletal muscles are only involved in motor function and play
no role in sensory modalities, such as proprioception or the coordination of
movement. The clinical signs of the most common peripheral neuropathies
primarily reflect peripheral motor nerve involvement, with relative sparing of
sensory function. Therefore, as long as there is sufficient muscle strength to
perform some degree of voluntary movement, animals with neuromuscular
disease will frequently have normal proprioception and will not be ataxic,
even if they are too weak to support their weight (see Video 31). In contrast,
lesions affecting the spinal cord will equally affect the ascending sensory
(proprioceptive) tracts and descending motor fibres, resulting in a combina-
tion of ataxia, paresis, and proprioceptive deficits in the affected limbs. This
relative sparing of sensory function and proprioception in neuromuscular
disease can be very useful to differentiate it from spinal disorders as a cause
for an abnormal gait in all limbs (tetraparesis).
3. Are the neurological deficits symmetric or asymmetric?
The majority of neuromuscular disorders, particularly myopathies and junc-
tionopathies, present with generalised and symmetric clinical signs involving
304 A Practical Approach to Neurology for the Small Animal Practitioner

all limbs (i.e. tetraparesis). These clinical signs may be initially most apparent
in the pelvic limbs, or less commonly in the thoracic limbs, but will usually
progress to involve all limbs over a relatively short period of time. In contrast,
spinal cord and brain lesions can result in markedly asymmetric/lateralised
clinical signs dependent on the lesion location and extent (i.e. hemiparesis).
An exception to this rule is monoparesis secondary to involvement of a one
or more peripheral nerves innervating a single limb (see Section 6.11
‘Monoparesis and Lameness’). Neurological deficits involving individual cra-
nial nerves and the condition of isolated masticatory myositis are discussed in
Section 6.6 ‘Cranial Nerve Dysfunction’. This section will focus on the pres-
entation and clinical approach to generalised neuromuscular weakness.
4. Are the clinical signs exacerbated by exercise?
The reduction in muscle strength and tone resulting from neuromuscular
disease may be more apparent in the face of increased demand during exer-
cise, particularly for junctionopathies and myopathies. Therefore, the clinical
signs may be exacerbated by exercise and some animals will have a clinical
history of exercise intolerance. In contrast, the severity of the neurological
deficits associated with spinal cord lesions is usually independent of exercise
unless there is significant discomfort or vertebral instability.
5. Are there any cranial nerve deficits?
The function of skeletal muscles throughout the body, including those inner-
vated by the cranial nerves, may be affected by neuromuscular disease.
Therefore, a condition affecting the neuromuscular system should always be
considered in animals that present with appendicular muscle weakness and
concurrent cranial nerve deficits (e.g. facial paresis, dropped jaw, pharyngeal
dysphagia, or megaoesophagus). These cranial nerve deficits will usually be
bilateral and, in contrast to brainstem lesions resulting in cranial nerve dys-
function, the level of mentation will be normal.

6.12.1 Differential Diagnoses for Generalised Neuromuscular

Weakness
If neuromuscular weakness is suspected on the basis of the neurological exami-
nation, then the next step is to decide whether this represents a clinical sign of
systemic disease or a primary neuromuscular disorder.

1. A systemic disease that is affecting delivery of oxygen and nutrients to the periph-
eral nerves and muscles resulting in ‘secondary’ neuromuscular weakness
Examples of conditions that can present with clinical signs of generalised
weakness, and thus mimic primary neuromuscular disease, include:
• cardiorespiratory disease (reduced cardiac output or blood oxygenation)
• anaemia or polycythaemia
• thromboembolic disease obstructing delivery of blood to nerves/muscles
• hypoglycaemia
 Chapter 6 A Practical Approach to Common Presentations in General Practice 305

• sepsis
• shock
• hyperthermia
• pheochromocytoma
• diabetic ketoacidosis
• electrolyte abnormalities.
These disorders can often be excluded on the basis of a thorough general phys-
ical examination, blood pressure testing, haematology, serum biochemistry,
and urinalysis. Mimics of neuromuscular weakness should also be excluded at
this time, such as abdominal pain or generalised orthopaedic conditions that
are resulting in a reluctance to walk rather than an inability to support weight.
2. A primary neuromuscular disorder affecting the peripheral nerves, NMJ, or
skeletal muscles
A list of differential diagnoses for primary neuromuscular disease is given
below, separated into those for generalised peripheral neuropathies,
junctionopathies, and myopathies. An asterisk (*) has been used to highlight
the most common conditions that may be observed in general practice. The
reader is referred to the Bibliography for further information regarding
the diagnosis and treatment of these individual conditions.

a. Generalised peripheral neuropathies:

• Inflammatory – chronic inflammatory demyelinating polyneuropathy
• Infectious – N. caninum, T. gondii
• Toxic – vincristine, cisplatin, organophosphates (cats)
• Metabolic – hypothyroidism, diabetes mellitus*, hypoglycaemia,
hyperlipidaemia
• Idiopathic – acute canine polyradiculoneuritis* (Box 6.12.1), motor poly-
neuropathy in young cats* (Box 6.12.2), distal denervating disease
• Neoplastic – insulinoma, paraneoplastic polyneuropathy, lymphoma
• Degenerative – motor neuron diseases, laryngeal‐paralysis polyneuropa-
thy*, sensory neuropathy, other inherited breed‐specific neuropathies.

b. Myopathies:
• Inflammatory – idiopathic polymyositis* (Box 6.12.3)
• Infectious – N. caninum*, T. gondii, Ehrlichia canis, Leptospirosis spp., Leishmania
infantum
• Toxic – adverse drug reaction, snake bite envenomation
• Metabolic – hypothyroidism (dogs)*, hyperthyroidism (cats), hypoadreno-
corticism*, hyperadrenocorticism*, chronic corticosteroid therapy*,
hypokalaemic myopathy*
• Neoplastic – paraneoplastic polymyopathy, lymphoma
• Degenerative – muscular dystrophies, centronuclear myopathy, congenital
myotonia, other inherited breed‐specific myopathies
306 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.12.1 Acute Canine Polyradiculoneuritis

Pathogenesis: Uncertain but suspected to represent an immune‐mediated disorder tar-

geted against peripheral myelin and/or axons (Rupp et al. 2013).
Typical presentation: Acute onset, rapidly‐progressive, flaccid tetraparesis, frequently
starting in the pelvic limbs and progressing to involve the thoracic limbs (see Video 42).
Typically progresses over 5–10 days to non‐ambulatory tetraparesis or tetraplegia.
Proprioception remains normal in those animals with sufficient strength to correct for
changes in limb position. Weak withdrawal reflexes and reduced muscle tone in all
limbs. The cranial nerves and tail function are usually spared, but an altered pitch and
strength of bark (dysphonia) is common in affected dogs. Oesophageal function, uri-
nary and faecal continence are normal. Jack Russell Terriers and West Highland White
Terriers had greater odds of developing acute canine polyradiculoneuritis compared to
a baseline group of dogs in one study (Laws et al. 2017).
Diagnosis: Typical clinical presentation (likely to represent the most common cause of
non‐ambulatory, flaccid tetraparesis in the UK), exclusion of other causes of polyneu-
ropathy (e.g. endocrine disease, neoplasia, N. caninum, T. gondii), electrodiagnostics,
muscle/nerve biopsy.
Treatment: Spontaneous resolution with supportive care – frequent turning, assisted
feeding, intensive physiotherapy. Corticosteroids do not appear effective, can exacerbate
muscle weakness, and predispose to complications (e.g. urinary tract infections). Human
intravenous immunoglobulin may reduce the time to recovery (Hirschvogel et al. 2012).
Prognosis: Usually good. Variable length of recovery from 2 weeks to over 6 months.
Relapses may occur if exposed to same trigger, which is usually unknown (Laws et al.
2017).

Box 6.12.2 Motor Polyneuropathy in Young Cats

Pathogenesis: Currently unknown and likely to be heterogeneous dependent on the

breed and individual.
Typical presentation: Acute onset, relapsing or progressive tetraparesis characterised by
reduced muscle tone in the affected limbs, weak withdrawal reflexes, and wide scapula
excursions if able to walk (see Video 43). The cranial nerves are frequently spared but
facial paresis and dysphonia can be observed. A waxing/waning or relapsing clinical
course is common. Affected cats are typically less than 1 year of age at the onset of the first
clinical manifestations (Aleman et al. 2014). Any breed can be affected but a specific form
of recurrent polyneuropathy has been reported in Bengal cats (Bensfield et al. 2011).
Diagnosis: Typical clinical presentation, exclusion of other causes of polyneuropathy,
electrodiagnostics, muscle/nerve biopsy.
Treatment: The optimal treatment is currently unknown and is likely to vary between cases.
Some cats show a spontaneous resolution of clinical signs without treatment, whilst others
appear to respond to prednisolone (tapering from 1 mg/kg per os twice daily).
Prognosis: Generally good but relapses appear common and some cats may show pro-
gressive clinical signs in spite of attempted treatment.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 307

Box 6.12.3 Idiopathic Polymyositis

Pathogenesis: Unknown but suspected to represent an autoimmune disorder targeted

against certain sarcolemmal antigens (Evans et al. 2004; Podell 2002).
Typical presentation: Most common in middle‐aged, large breed dogs (e.g. Boxers,
Newfoundlands, Labrador Retrievers). Generalised weakness, stiff/stilted gait in all
limbs, lethargy, exercise intolerance, muscle atrophy, weight loss +/− discomfort on
muscle palpation, dysphagia, and regurgitation. Proprioception is normal in all limbs
and withdrawal reflexes are usually adequate. A specific disorder in the Hungarian
Vizsla breed is characterised by dysphagia and masticatory muscle atrophy (Tauro et al.
2015).
Diagnosis: Clinical presentation, elevated serum muscle enzymes, exclusion of other
causes of polymyopathy (e.g. endocrine disease, neoplasia, N. caninum, T. gondii),
electrodiagnostics, muscle biopsy.
Treatment: Immunosuppressive doses of prednisolone (1 mg/kg per os twice daily for
2–4 weeks, tapering to the lowest effective dose). Adjunctive immunosuppressive
agents, such as cyclosporine or azathioprine, can be used in dogs that do not ade-
quately respond to prednisolone alone. These can also be useful as steroid‐sparing
agents, particularly in large dogs that may not tolerate high oral doses of
prednisolone.
Prognosis: Generally good but relapses can occur as treatment is withdrawn.

c. Junctionopathies:
• Inflammatory – acquired myasthenia gravis* (Box 6.12.4)
• Toxic – botulism, tick paralysis, organophosphates, snake bite, Black Widow
spider envenomation
• Anomalous – congenital myasthenia gravis.

6.12.2 Clinical Approach to Generalised Neuromuscular

Weakness
1. Confirm the presence of a neuromuscular disorder
• Clinical history and presenting complaint
• General physical examination
• Neurological examination

As discussed in Chapter 4, the clinical history and neurological examina-

tion findings should first be used to localise the lesion to the neuromuscular
system. Important information to gather from the clinical history should
include concurrent clinical signs (e.g. weight loss, regurgitation), current and
previous medical conditions, medications that the animal is receiving, travel
history, and exposure to toxins. Differentiating between a peripheral neuropa-
308 A Practical Approach to Neurology for the Small Animal Practitioner

Box 6.12.4 Acquired Myasthenia Gravis

Pathogenesis: Autoimmune disease resulting from the production of autoantibodies

against the nicotinic acetylcholine receptor. Blockade and accelerated degradation of
these bound receptors affects normal neuromuscular transmission, resulting in skele-
tal muscle weakness, particularly at times of increased demand (e.g. exercise). A con-
current thymoma has been reported in around 3% of affected dogs and 15–52% of
affected cats (Hague et al. 2015; Shelton 2002; Shelton et al. 1997).
Typical presentation: Reported bimodal age at onset (e.g. 3–4 years old and 10–12 years
old). Rare in cats compared to dogs but Abyssinian and Somali cats are over‐repre-
sented (Hague et al. 2015). Neurological examination may be normal at rest. The focal
form frequently affects the oesophagus, larynx, pharynx, and/or facial muscles result-
ing in clinical signs of regurgitation, dysphagia, dysphonia, and weak palpebral
reflexes. The generalised form results in exercise‐induced/exacerbated muscle weak-
ness presenting as exercise‐intolerance, progressive stiffness when walking (particu-
larly affecting the pelvic limbs), and frequent sitting/lying down at exercise (see Video
44). These signs are commonly accompanied by excessive drooling, megaoesophagus,
and regurgitation in dogs. A less common, acute, and severe fulminant form results in
recumbency, regurgitation +/− respiratory difficulty in affected animals (Dewey et al.
1997; King and Vite 1998).
Diagnosis: Clinical presentation, rule out other causes of neuromuscular weakness,
conscious thoracic radiography (to assess for the presence of a thymoma, megaoe-
sophagus, and aspiration pneumonia), nicotinic acetylcholine receptor antibody test-
ing, edrophonium‐response test, repetitive nerve stimulation.
Treatment: Supportive care and nutrition for an animal with megaoesophagus +/−
omeprazole to manage oesophagitis and to increase the pH of gastric content that may
be aspirated (see Section 6.6.3 ‘Vagus Nerve’) (Khorzad et al. 2011). Anticholinesterase
therapy to increase the amount of acetylcholine available at the NMJ to bind to the
remaining receptors (pyridostigmine bromide 0.5–3.0 mg/kg (dogs) or 0.25 mg/kg
(cats) per os every 8–12 hours). Immunosuppressive medications can be used in ani-
mals that do not respond to supportive care and pyridostigmine therapy, but this
should be carefully monitored. This is because of the high incidence of aspiration
pneumonia in affected animals and the fact that prednisolone administration can
exacerbate muscle weakness. The use of cyclosporine and azathioprine have also been
reported in the management of myasthenia gravis in dogs (Bexfield et al. 2006; Dewey
et al. 1999).
Prognosis: Generally guarded, with a 1‐year mortality rate of 40–60% in dogs. This is
primarily because of the high incidence of megaoesophagus and recurrent aspiration
pneumonia in affected animals. Prognosis can be good in cases without pharyngeal/
oesophageal involvement. Prognosis is poor in fulminant cases (Dewey et al. 1997).

thy, junctionopathy, and myopathy can be difficult on the basis of clinical

examination alone. Therefore, referral for specialist neurological assessment
and advanced investigations, such as electrodiagnostics, is advised in all cases
with suspected neuromuscular disease. If referral is not an option, then the
 Chapter 6 A Practical Approach to Common Presentations in General Practice 309

focus of investigations in general practice should be to exclude systemic dis-

ease and to further investigate metabolic, infectious, or neoplastic causes for
primary neuromuscular weakness.

2. Exclude systemic disease as a cause of ‘secondary’ neuromuscular

weakness
• General physical examination, including cardiac auscultation, heart rate and
rhythm, respiratory rate and rhythm, mucous membrane colour, capillary
refill time, peripheral pulse assessment
• Blood pressure
• Haematology
• Serum biochemistry
• Urinalysis

3. Further investigate causes of primary neuromuscular disease

• Refer for further investigations: this may include electrodiagnostic testing
(electromyography, electroneurography, repetitive nerve stimulation) +/−
CSF analysis, muscle and nerve biopsy for histopathology.
• Perform further investigations in general practice.
• Haematology, serum biochemistry, and urinalysis to further investigate met-
abolic/endocrine disorders.
• Serum muscle enzymes – creatine kinase (CK), AST, and ALT. Whilst ALT
is frequently included on in‐house biochemistry tests, many of these pan-
els do not include CK or AST. As ALT can also be released from damaged
muscle, hepatic disease should not be considered to be the only cause for
ALT elevation. Therefore, if the ALT is elevated on a basic biochemistry
panel, particularly in the absence of changes to other hepatic parameters,
CK and AST should be measured to further investigate the possibility of an
underlying myopathy. However, a myopathy cannot be excluded on the
basis of normal serum muscle enzymes as certain conditions may not
result in significant muscle enzyme elevation. Mild to moderate CK eleva-
tions should also be interpreted with caution, as animals that are recum-
bent for reasons other than a primary myopathy may have elevated levels,
particularly in large breed dogs (CK up to 5000–10 000 IU/l). Necrotising
myopathies and dystrophin‐deficient muscular dystrophy frequently
result in very high serum muscle enzyme levels (e.g. CK >50 000–
100 000 IU/l) (Shelton 2010).
• Total thyroid hormone (T4) and TSH levels can be run if there is a clinical
suspicion for hypothyroidism in dogs. Total T4 +/− free T4 can be used to
diagnose hyperthyroidism in cats.
• Cortisol levels before and after administration of ACTH can be used to
investigate hypo‐ and hyperadrenocorticism.
310 A Practical Approach to Neurology for the Small Animal Practitioner

• Infectious disease testing (e.g. serological testing for N. caninum and T. gondii).
• Body cavity screening for neoplasia (e.g. thoracic radiography, abdominal
ultrasonography, CT of thorax and abdomen).
• Serum nAchR antibody testing for acquired myasthenia gravis. This test will
confirm a diagnosis of acquired myasthenia gravis if positive. However, a
small number of affected animals may have an antibody level within the
normal range (seronegative myasthenia gravis). This can be for several dif-
ferent reasons, including previous corticosteroid administration, the pres-
ence of antibodies targeted to a different muscle membrane protein, or if the
majority of antibodies are bound to their target and unavailable for detec-
tion by the test (Shelton 2010; Shelton et al. 2001). Repeating the assay in
1–2 weeks is recommended for seronegative cases in which there is a high
clinical suspicion of acquired myasthenia gravis. Carefully monitored trial
treatment can be performed if the result remains negative and other possible
causes for the clinical signs have been excluded.
• Muscle biopsy if a primary myopathy is highly suspected.
• Monitoring the clinical course of the disease may help to guide the most
likely diagnosis, particularly in cases with a typical clinical presentation and
for which further investigations are not possible (see Box 6.12.1). This is
important before considering euthanasia, as some disorders may present
with severe clinical signs but can show spontaneous resolution without
treatment (e.g. acute canine polyradiculoneuritis). If the disease is progres-
sive and referral or further investigations are not possible, then trial treat-
ment for the most likely differential diagnosis may be the only option. This
could include pyridostigmine for suspected acquired myasthenia gravis, or
corticosteroids for suspected chronic inflammatory demyelinating polyneu-
ropathy, idiopathic polymyositis, and some forms of motor polyneuropathy
in young cats. It is vital that the owner is always made aware of the potential
risks and limitations associated with this approach. Many veterinary neu-
rologists are happy to discuss such cases over the telephone before proceed-
ing with treatment trials.

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Schwartz, M., Muñana, K.R., and Nettifee‐Osborne, J. (2013). Assessment of the prevalence
and clinical features of cryptogenic epilepsy in dogs: 45 cases (2003–2011). J. Am. Vet. Med.
Assoc. 242: 651–657.
Shaw, N., Trepanier, L.A., Center, S.A., and Garland, S. (1996). High dietary chloride content
associated with loss of therapeutic serum bromide concentrations in an epileptic dog. J. Am.
Vet. Med. Assoc. 208: 234–236.
Shell, L., Scariano, R., and Rishniw, M. (2017). Features of stimulus‐specific seizures in dogs
with reflex epilepsy: 43 cases (2000–2014). J. Am. Vet. Med. Assoc. 250: 75–78.
Shihab, N., Bowen, J., and Volk, H.A. (2011). Behavioral changes in dogs associated with the
development of idiopathic epilepsy. Epilepsy Behav. 21: 160–167.
Smith, P.M., Talbot, C.E., and Jeffery, N.D. (2008). Findings on low‐field cranial MR images in
epileptic dogs that lack interictal neurological deficits. Vet. J. 176: 320–325.
Stabile, F., Barnett, C.R., and De Risio, L. (2017). Phenobarbital administration every eight
hours: improvement of seizure management in idiopathic epileptic dogs with decreased phe-
nobarbital elimination half‐life. Vet. Rec. 180: 178.
Stanciu, G.D., Packer, R.M.A., Pakozdy, A. et al. (2017). Clinical reasoning in feline epilepsy:
which combination of clinical information is useful? Vet. J. 225: 9–12.
Stee, K., Martlé, V., Broeckx, B.J.G. et al. (2017). Imepitoin withdrawal in dogs with idiopathic
epilepsy well‐controlled with imepitoin and phenobarbital and/or potassium bromide does
not increase seizure frequency. Vet. J. 230: 1–5.
Szelecsenyi, A.C., Giger, U., Golini, L. et al. (2017). Survival in 76 cats with epilepsy of unknown
cause: a retrospective study. Vet. Rec. 181: 479.
Tipold, A., Keefe, T.J., Löscher, W. et al. (2015). Clinical efficacy and safety of imepitoin in com-
parison with phenobarbital for the control of idiopathic epilepsy in dogs. J. Vet. Pharmacol.
Ther. 38: 160–168.
Volk, H.A., Matiasek, L.A., Luján Feliu‐Pascual, A. et al. (2008). The efficacy and tolerability of
levetiracetam in pharmacoresistant epileptic dogs. Vet. J. 176: 310–319.
314 A Practical Approach to Neurology for the Small Animal Practitioner

Wahle, A.M., Brühschwein, A., Matiasek, K. et al. (2014). Clinical characterization of epilepsy
of unknown cause in cats. J. Vet. Intern. Med. 28: 182–188.
Watson, F., Rusbridge, C., Packer, R.M.A. et al. (2018). A review of treatment options for behav-
ioural manifestations of clinical anxiety as a comorbidity in dogs with idiopathic epilepsy.
Vet. J. 238: 1–9.
Wielaender, F., James, F.M.K., Cortez, M.A. et al. (2018). Absence seizures as a feature of juve-
nile myoclonic epilepsy in Rhodesian Ridgeback dogs. J. Vet. Intern. Med. 32: 428–432.
Winter, J., Packer, R.M.A., and Volk, H.A. (2018). Preliminary assessment of cognitive impair-
ments in canine idiopathic epilepsy. Vet. Rec. 182: 633.

6.2. Movement Disorders

Bhatti, S.F., Vanhaesebrouck, A.E., Van Soens, I. et al. (2011). Myokymia and neuromyotonia
in 37 Jack Russell terriers. Vet. J. 189: 284–288.
Black, V., Garosi, L., Lowrie, M. et al. (2014). Phenotypic characterisation of canine epileptoid
cramping syndrome in the border terrier. J. Small Anim. Pract. 55: 102–107.
De Risio, L., Bhatti, S., Muñana, K. et al. (2015). International Veterinary Epilepsy Task Force
consensus proposal: diagnostic approach to epilepsy in dogs. BMC Vet. Res. 11: 182.
Galano, H.R., Olby, N.J., Howard, J.F. Jr., and Shelton, G.D. (2005). Myokymia and neuromyo-
tonia in a cat. J. Am. Vet. Med. Assoc. 227: 1608–1612.
Garosi, L.S., Rossmeisl, J.H., de Lahunta, A. et al. (2005). Primary orthostatic tremor in Great
Danes. J. Vet. Intern. Med. 19: 606–609.
Geiger, K.M. and Klopp, L.S. (2009). Use of a selective serotonin reuptake inhibitor for treat-
ment of episodes of hypertonia and kyphosis in a young adult Scottish Terrier. J. Am. Vet. Med.
Assoc. 235: 168–171.
Gill, J.L., Tsai, K.L., Krey, C. et al. (2012). A canine BCAN microdeletion associated with epi-
sodic falling syndrome. Neurobiol. Dis. 45: 130–136.
Gilliam, D., O’Brien, D.P., Coates, J.R. et al. (2014). A homozygous KCNJ10 mutation in Jack
Russell Terriers and related breeds with spinocerebellar ataxia with myokymia, seizures, or
both. J. Vet. Intern. Med. 28: 871–877.
Guevar, J., De Decker, S., Van Ham, L.M. et al. (2014). Idiopathic head tremor in English bull-
dogs. Mov. Disord. 29: 191–194.
Herrtage, M.E. and Palmer, A.C. (1983). Episodic falling in the cavalier King Charles spaniel.
Vet. Rec. 112: 458–459.
Holland, C.T., Holland, J.T., and Rozmanec, M. (2010). Unilateral facial myokymia in a dog with
an intracranial meningioma. Aust. Vet. J. 88: 357–361.
Lowrie, M. and Garosi, L. (2016a). Classification of involuntary movements in dogs: tremors
and twitches. Vet. J. 214: 109–116.
Lowrie, M. and Garosi, L. (2016b). Natural history of canine paroxysmal movement disorders
in Labrador retrievers and Jack Russell terriers. Vet. J. 213: 33–37.
Lowrie, M. and Garosi, L. (2017a). Classification of involuntary movements in dogs: myoclonus
and myotonia. J. Vet. Intern. Med. 31: 979–987.
Lowrie, M. and Garosi, L. (2017b). Classification of involuntary movements in dogs: paroxys-
mal dyskinesias. Vet. J. 220: 65–71.
Lowrie, M., Garden, O.A., Hadjivassiliou, M. et al. (2015). The clinical and serological effect of
a gluten‐free diet in Border Terriers with epileptoid cramping syndrome. J. Vet. Intern. Med. 29:
1564–1568.
Lowrie, M., Bessant, C., Harvey, R.J. et al. (2016a). Audiogenic reflex seizures in cats. J. Feline
Med. Surg. 18: 328–336.
Lowrie, M., Hadjivassiliou, M., Sanders, D.S., and Garden, O.A. (2016b). A presumptive case of
gluten sensitivity in a Border terrier: a multisystem disorder? Vet. Rec. 179: 573.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 315

Lowrie, M., Thomson, S., Bessant, C. et al. (2017). Levetiracetam in the management of feline
audiogenic reflex seizures: a randomised, controlled, open‐label study. J. Feline Med. Surg.
19: 200–206.
Lowrie, M., Garden, O.A., Hadjivassiliou, M. et al. (2018). Characterization of paroxysmal glu-
ten‐sensitive dyskinesia in Border terriers using serological markers. J. Vet. Intern. Med.
32: 775–781.
Mauler, D.A., Van Soens, I., Bhatti, S.F. et al. (2014). Idiopathic generalised tremor syndrome
in two cats. J. Feline Med. Surg. 16: 378–380.
Packer, R.A., Patterson, E.E., Taylor, J.F. et al. (2010). Characterization and mode of inheritance
of a paroxysmal dyskinesia in Chinook dogs. J. Vet. Intern. Med. 24: 1305–1313.
Rogatko, C.P., Glass, E.N., Kent, M. et al. (2016). Use of botulinum toxin type A for the treat-
ment of radiation therapy‐induced myokymia and neuromyotonia in a dog. J. Am. Vet. Med.
Assoc. 248: 532–537.
Schubert, T., Clemmons, R., Miles, S., and Draper, W. (2013). The use of botulinum toxin for
the treatment of generalized myoclonus in a dog. J. Am. Anim. Hosp. Assoc. 49: 122–127.
Swain, L., Key, G., Tauro, A. et al. (2017). Lafora disease in miniature Wirehaired Dachshunds.
PLoS One 12 (8): e0182024.
Urkasemsin, G. and Olby, N.J. (2014). Canine paroxysmal movement disorders. Vet. Clin. North
Am. Small Anim. Pract. 44: 1091–1102.
Urkasemsin, G. and Olby, N.J. (2015). Clinical characteristics of Scottie cramp in 31 cases.
J. Small Anim. Pract. 56: 276–280.
Vanhaesebrouck, A.E., Van Soens, I., Poncelet, L. et al. (2010). Clinical and electrophysiological
characterization of myokymia and neuromyotonia in Jack Russell Terriers. J. Vet. Intern. Med.
24: 882–889.
Vanhaesebrouck, A.E., Shelton, G.D., Garosi, L. et al. (2011). A novel movement disorder in
related male Labrador retrievers characterized by extreme generalized muscle stiffness. J. Vet.
Intern. Med. 25: 1089–1096.
Vanhaesebrouck, A.E., Bhatti, S.F., Franklin, R.J., and Van Ham, L. (2013). Myokymia and
neuromyotonia in veterinary medicine: a comparison with peripheral nerve hyperexcitability
syndrome in humans. Vet. J. 197: 153–162.
Wagner, S.O., Podell, M., and Fenner, W.R. (1997). Generalized tremors in dogs: 24 cases
(1984–1995). J. Am. Vet. Med. Assoc. 211: 731–735.
Walmsley, G.L., Smith, P.M., Herrtage, M.E., and Jeffery, N.D. (2006). Facial myokymia in a
puppy. Vet. Rec. 158: 411–412.

6.3. Altered Mentation

Brutlag, A. and Hommerding, H. (2018). Toxicology of marijuana, synthetic cannabinoids, and
cannabidiol in dogs and cats. Vet. Clin. North Am. Small Anim. Pract. 48: 1087–1102.
Gillespie, S., Gilbert, Z., and De Decker, S. (2019). Results of oral prednisolone administration
or ventriculoperitoneal shunt placement in dogs with congenital hydrocephalus: 40 cases
(2005–2016). J. Am. Vet. Med. Assoc. 254: 835–842.
Hu, H., Barker, A., Harcourt‐Brown, T. et al. (2015). Systematic review of brain tumor treat-
ment in dogs. J. Vet. Intern. Med. 29: 1456–1463.
Mangat, H.S., Wu, X., Gerber et al. (2019. pii: nyz046. doi: https://doi.org/10.1093/neuros/
nyz046). Hypertonic saline is superior to mannitol for the combined effect on intracranial
pressure and cerebral perfusion pressure burdens in patients with severe traumatic brain
injury. Neurosurgery. [Epub ahead of print].
Meola, S.D., Tearney, C.C., Haas, S.A. et al. (2012). Evaluation of trends in marijuana toxicosis
in dogs living in a state with legalized medical marijuana: 125 dogs (2005–2010). J. Vet. Emerg.
Crit. Care (San Antonio) 22: 690–696.
316 A Practical Approach to Neurology for the Small Animal Practitioner

O’Neill, J., Kent, M., Glass, E.N. et al. (2013). Clinicopathologic and MRI characteristics of pre-
sumptive hypertensive encephalopathy in two cats and two dogs. J. Am. Anim. Hosp. Assoc.
49: 412–420.
Parratt, C.A., Firth, A.M., Boag, A.K. et al. (2018). Retrospective characterization of coma and
stupor in dogs and cats presenting to a multicenter out‐of‐hours service (2012–2015): 386
animals. J. Vet. Emerg. Crit. Care (San Antonio) 28: 559–565.
Platt, S.R., Radaelli, S.T., and McDonnell, J.J. (2001). The prognostic value of the modified
Glasgow Coma Scale in head trauma in dogs. J. Vet. Intern. Med. 15: 581–584.
Qureshi, A.I., Wilson, D.A., and Traystman, R.J. (1999). Treatment of elevated intracranial
pressure in experimental intracerebral hemorrhage: comparison between mannitol and
hypertonic saline. Neurosurgery 44: 1055–1063.
Schubert, T.A., Chidester, R.M., and Chrisman, C.L. (2011). Clinical characteristics, manage-
ment and long‐term outcome of suspected rapid eye movement sleep behaviour disorder in
14 dogs. J. Small Anim. Pract. 52: 93–100.
Shea, A., Hatch, A., De Risio, L. et al. (2018). Association between clinically probable REM sleep
behavior disorder and tetanus in dogs. J. Vet. Intern. Med. 32: 2029–2036.
Sokhal, N., Rath, G.P., Chaturvedi, A. et al. (2017). Comparison of 20% mannitol and 3%
hypertonic saline on intracranial pressure and systemic hemodynamics. J. Clin. Neurosci.
42: 148–154.

6.4. Blindness
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Grozdanic, S.D., Matic, M., Sakaguchi, D.S., and Kardon, R.H. (2007). Evaluation of retinal
status using chromatic pupil light reflex activity in healthy and diseased canine eyes. Invest.
Ophthalmol. Vis. Sci. 48: 5178–5183.
Heller, A.R., van der Woerdt, A., Gaarder, J.E. et al. (2017). Sudden acquired retinal degenera-
tion in dogs: breed distribution of 495 canines. Vet. Ophthalmol. 20: 103–106.
Komáromy, A.M., Abrams, K.L., Heckenlively, J.R. et al. (2016). Sudden acquired retinal
degeneration syndrome (SARDS) – a review and proposed strategies toward a better under-
standing of pathogenesis, early diagnosis, and therapy. Vet. Ophthalmol. 19: 319–331.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Mari, L., Stavinohova, R., Dominguez, E. et al. (2018). Ischemic optic neuropathy in a dog with
acute bilateral blindness and primary systemic hypertension. J. Vet. Intern. Med. 32: 423–427.
Martin‐Flores, M., Scrivani, P.V., Loew, E. et al. (2014). Maximal and submaximal mouth open-
ing with mouth gags in cats: implications for maxillary artery blood flow. Vet. J. 200: 60–64.
Meekins, J.M. (2015). Acute blindness. Top. Companion Anim. Med. 30: 118–125.
Meekins, J.M., Guess, S.C., and Rankin, A.J. (2015). Retinopathy associated with ivermectin
toxicosis in five cats. J. Am. Vet. Med. Assoc. 246: 1238–1241.
Montgomery, K.W., van der Woerdt, A., and Cottrill, N.B. (2008). Acute blindness in dogs: sud-
den acquired retinal degeneration syndrome versus neurological disease (140 cases,
2000–2006). Vet. Ophthalmol. 11: 314–320.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
Quitt, P.R., Reese, S., Fischer, A. et al. (2019). Assessment of menace response in neurologically
and ophthalmologically healthy cats. J. Feline Med. Surg. 21: 537–543.
Seruca, C., Ródenas, S., Leiva, M. et al. (2010). Acute postretinal blindness: ophthalmologic,
neurologic, and magnetic resonance imaging findings in dogs and cats (seven cases). Vet.
Ophthalmol. 13: 307–314.
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Stiles, J., Weil, A.B., Packer, R.A., and Lantz, G.C. (2012). Post‐anesthetic cortical blindness in
cats: twenty cases. Vet. J. 193: 367–373.
Stuckey, J.A., Pearce, J.W., Giuliano, E.A. et al. (2013). Long‐term outcome of sudden acquired
retinal degeneration syndrome in dogs. J. Am. Vet. Med. Assoc. 243: 1425–1431.

6.5. Abnormalities of Pupil Size

Boydell, P. (2000a). Idiopathic Horner syndrome in the golden retriever. J. Neuroophthalmol.
20: 288–290.
Boydell, P. (2000b). Iatrogenic pupillary dilation resembling Pourfour du petit syndrome in
three cats. J. Small Anim. Pract. 41: 202–203.
Boydell, P., Pike, R., Crossley, D., and Torrington, A. (1997). Horner’s syndrome following
intrathoracic tube placement. J. Small Anim. Pract. 38: 466–467.
Carpenter, J.L., King, N.W. Jr., and Abrams, K.L. (1987). Bilateral trigeminal nerve paralysis
and Horner’s syndrome associated with myelomonocytic neoplasia in a dog. J. Am. Vet. Med.
Assoc. 191: 1594–1596.
Foote, B.C., Michau, T.M., Welihozkiy, A., and Stine, J.M. (2019). Retrospective analysis of
ocular neuropathies in diabetic dogs following cataract surgery. Vet. Ophthalmol. 22:
284–293.
Grahn, B.H. and Cullen, C.L. (2004). Diagnostic ophthalmology. Iris atrophy. Can. Vet. J. 45:
77–78.
Guevar, J., Gutierrez‐Quintana, R., Peplinski, G. et al. (2014). Cavernous sinus syndrome sec-
ondary to intracranial lymphoma in a cat. J. Feline Med. Surg. 16: 513–516.
Hamzianpour, N., Lam, R., Tetas, R., and Beltran, E. (2018). Clinical signs, imaging findings,
and outcome in twelve cats with internal ophthalmoparesis/ophthalmoplegia. Vet. Ophthalmol.
21: 382–390.
Holland, C.T. (2007). Bilateral Horner’s syndrome in a dog with diabetes mellitus. Vet. Rec. 160:
662–664.
Jones, A.M., Bentley, E., and Rylander, H. (2018). Cavernous sinus syndrome in dogs and cats:
case series (2002–2015). Open Vet. J. 8: 186–192.
Kern, T.J., Aromando, M.C., and Erb, H.N. (1989). Horner’s syndrome in dogs and cats: 100
cases (1975–1985). J. Am. Vet. Med. Assoc. 195: 369–373.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Larocca, R.D. (2000). Unilateral external and internal ophthalmoplegia caused by intracranial
meningioma in a dog. Vet. Ophthalmol. 3: 3–9.
Melián, C., Morales, M., de los Espinosa, Monteros, A., and Peterson, M.E. (1996). Horner’s
syndrome associated with a functional thyroid carcinoma in a dog. J. Small Anim. Pract. 37:
591–593.
Morgan, R.V. and Zanotti, S.W. (1989). Horner’s syndrome in dogs and cats: 49 cases (1980–
1986). J. Am. Vet. Med. Assoc. 194: 1096–1099.
O’Neill, J.J., Kent, M., Glass, E.N. et al. (2013). Insertion of the dorsal oblique muscle in the
dog: an anatomic basis for ventral strabismus associated with oculomotor nerve dysfunction.
Vet. Ophthalmol. 16: 467–471.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
Simpson, K.M., Williams, D.L., and Cherubini, G.B. (2015). Neuropharmacological lesion local-
ization in idiopathic Horner’s syndrome in Golden Retrievers and dogs of other breeds. Vet.
Ophthalmol. 18: 1–5.
Spivack, R.E., Elkins, A.D., Moore, G.E., and Lantz, G.C. (2013). Postoperative complications
following TECA‐LBO in the dog and cat. J. Am. Anim. Hosp. Assoc. 49: 160–168.
318 A Practical Approach to Neurology for the Small Animal Practitioner

Stephan, D.D., Vestre, W.A., Stiles, J., and Krohne, S. (2003). Changes in intraocular pressure
and pupil size following intramuscular administration of hydromorphone hydrochloride and
acepromazine in clinically normal dogs. Vet. Ophthalmol. 6: 73–76.
Tetas Pont, R., Freeman, C., Dennis, R. et al. (2017). Clinical and magnetic resonance imaging
features of idiopathic oculomotor neuropathy in 14 dogs. Vet. Radiol. Ultrasound 58:
334–343.
Viscasillas, J., Sanchis‐Mora, S., Hoy, C., and Alibhai, H. (2013). Transient Horner’s syndrome
after paravertebral brachial plexus blockade in a dog. Vet. Anaesth. Analg. 40: 104–106.
Webb, A.A., Cullen, C.L., Rose, P. et al. (2005). Intracranial meningioma causing internal oph-
thalmoparesis in a dog. Vet. Ophthalmol. 8: 421–425.

6.6. Cranial Nerve Dysfunction

Bagley, R.S., Wheeler, S.J., Klopp, L. et al. (1998). Clinical features of trigeminal nerve‐sheath
tumor in 10 dogs. J. Am. Anim. Hosp. Assoc. 34: 19–25.
Bartges, J.W. and Nielson, D.L. (1992). Reversible megaesophagus associated with atypical pri-
mary hypoadrenocorticism in a dog. J. Am. Vet. Med. Assoc. 201: 889–891.
Bexfield, N.H., Watson, P.J., and Herrtage, M.E. (2006). Esophageal dysmotility in young dogs.
J. Vet. Intern. Med. 20: 1314–1318.
Blazejewski, S.W. and Shelton, G.D. (2018). Trismus, masticatory myositis and antibodies
against type 2M fibers in a mixed breed cat. JFMS Open Rep. 4:2055116918764993.
Bookbinder, L.C., Flanders, J., Bookbinder, P.F. et al. (2016). Idiopathic canine laryngeal paraly-
sis as one sign of a diffuse polyneuropathy: an observational study of 90 cases (2007–2013).
Vet. Surg. 45: 254–260.
Boudrieau, R.J. and Rogers, W.A. (1985). Megaesophagus in the dog: a review of 50 cases.
J. Am. Anim. Hosp. Assoc. 21: 33–40.
Bovens, C., Tennant, K., Reeve, J., and Murphy, K.F. (2014). Basal serum cortisol concentration
as a screening test for hypoadrenocorticism in dogs. J. Vet. Intern. Med. 28: 1541–1545.
Braund, K.G., Steinberg, H.S., Shores, A. et al. (1989). Laryngeal paralysis in immature and
mature dogs as one sign of a more diffuse polyneuropathy. J. Am. Vet. Med. Assoc. 194:
1735–1740.
Braund, K.G., Shores, A., Cochrane, S. et al. (1994). Laryngeal paralysis‐polyneuropathy com-
plex in young Dalmatians. Am. J. Vet. Res. 55: 534–542.
Cauduro, A., Paolo, F., Asperio, R.M. et al. (2013). Use of MRI for the early diagnosis of mastica-
tory muscle myositis. J. Am. Anim. Hosp. Assoc. 49: 347–352.
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Dolera, M., Malfassi, L., Marcarini, S. et al. (2018). High dose hypofractionated frameless volu-
metric modulated arc radiotherapy is a feasible method for treating canine trigeminal nerve
sheath tumors. Vet. Radiol. Ultrasound 59: 624–631.
Evans, J., Levesque, D., and Shelton, G.D. (2004). Canine inflammatory myopathies: a clinico-
pathologic review of 200 cases. J. Vet. Intern. Med. 18: 679–691.
Fracassi, F. and Tamborini, A. (2011). Reversible megaoesophagus associated with primary
hypothyroidism in a dog. Vet. Rec. 329b: 168.
Gabriel, A., Poncelet, L., Van Ham, L. et al. (2006). Laryngeal paralysis‐polyneuropathy com-
plex in young related Pyrenean mountain dogs. J. Small Anim. Pract. 47: 144–149.
Gaynor, A.R., Shofer, F.S., and Washabau, R.J. (1997). Risk factors for acquired megaesophagus
in dogs. J. Am. Vet. Med. Assoc. 211: 1406–1412.
Granger, N. (2011). Canine inherited motor and sensory neuropathies: an updated classification
in 22 breeds and comparison to Charcot‐Marie‐Tooth disease. Vet. J. 188: 274–285.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 319

Haines, J.M. (2019). Survey of owners on population characteristics, diagnosis, and environ-
mental, health, and disease associations in dogs with megaesophagus. Res. Vet. Sci. 123:
1–6.
Hansen, K.S., Zwingenberger, A.L., Théon, A.P. et al. (2016). Treatment of MRI‐diagnosed
trigeminal peripheral nerve sheath tumors by stereotactic radiotherapy in dogs. J. Vet. Intern.
Med. 30: 1112–1120.
Ito, D., Okada, M., Jeffery, N.D. et al. (2009). Symptomatic tongue atrophy due to atypical poly-
myositis in a Pembroke Welsh Corgi. J. Vet. Med. Sci. 71: 1063–1067.
Jaggy, A. and Oliver, J.E. (1994). Neurologic manifestations of thyroid disease. Vet. Clin. North
Am. Small Anim. Pract. 24: 487–494.
Jeandel, A., Thibaud, J.L., and Blot, S. (2016). Facial and vestibular neuropathy of unknown
origin in 16 dogs. J. Small Anim. Pract. 57: 74–78.
Jeffery, N.D., Talbot, C.E., Smith, P.M., and Bacon, N.J. (2006). Acquired idiopathic laryngeal
paralysis as a prominent feature of generalised neuromuscular disease in 39 dogs. Vet. Rec.
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Kent, M., Glass, E.N., de Lahunta, A. et al. (2013). Prevalence of effusion in the tympanic cavity
in dogs with dysfunction of the trigeminal nerve: 18 cases (2004–2013). J. Vet. Intern. Med. 27:
1153–1158.
Kent, M., Talarico, L.R., Glass, E.N. et al. (2015). Denervation of the tensor veli palatini muscle
and effusion in the tympanic cavity. J. Am. Anim. Hosp. Assoc. 51: 424–428.
Kern, T.J. and Erb, H.N. (1987). Facial neuropathy in dogs and cats: 95 cases (1975–1985).
J. Am. Vet. Med. Assoc. 191: 1604–1609.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Mace, S., Shelton, G.D., and Eddlestone, S. (2012). Megaesophagus. Compend. Contin. Educ. Vet.
34: E1.
Macphail, C. (2014). Laryngeal disease in dogs and cats. Vet. Clin. North Am. Small Anim. Pract.
44: 19–31.
Mahony, O.M., Knowles, K.E., Braund, K.G. et al. (1998). Laryngeal paralysis‐polyneuropathy
complex in young Rottweilers. J. Vet. Intern. Med. 12: 330–337.
Manning, K., Birkenheuer, A.J., Briley, J. et al. (2016). Intermittent at‐home suctioning of
esophageal content for prevention of recurrent aspiration pneumonia in 4 dogs with megae-
sophagus. J. Vet. Intern. Med. 30: 1715–1719.
Matheis, F.L., Walser‐Reinhardt, L., and Spiess, B.M. (2012). Canine neurogenic
Keratoconjunctivitis sicca: 11 cases (2006–2010). Vet. Ophthalmol. 15: 288–290.
Mayhew, P.D., Bush, W.W., and Glass, E.N. (2002). Trigeminal neuropathy in dogs: a retrospec-
tive study of 29 cases (1991–2000). J. Am. Anim. Hosp. Assoc. 38: 262–270.
McBrearty, A.R., Ramsey, I.K., Courcier, E.A. et al. (2011). Clinical factors associated with death
before discharge and overall survival time in dogs with generalized megaesophagus. J. Am.
Vet. Med. Assoc. 238: 1622–1628.
Milodowski, E.J., Amengual‐Batle, P., Beltran, E. et al. (2018). Clinical findings and outcome of
dogs with unilateral masticatory muscle atrophy. J. Vet. Intern. Med. https://doi.org/10.1111/
jvim.15373.
Monnet, E. (2016). Surgical treatment of laryngeal paralysis. Vet. Clin. North Am. Small Anim.
Pract. 46: 709–717.
Nakagawa, T., Doi, A., Ohno, K. et al. (2019). Clinical features and prognosis of canine megae-
sophagus in Japan. J. Vet. Med. Sci. https://doi.org/10.1292/jvms.18‐0493.
Paciello, O., Shelton, G.D., and Papparella, S. (2007). Expression of major histocompatibility
complex class I and class II antigens in canine masticatory muscle myositis. Neuromuscul.
Disord. 17: 313–320.
320 A Practical Approach to Neurology for the Small Animal Practitioner

Pagano, T.B., Wojcik, S., Costagliola, A. et al. (2015). Age related skeletal muscle atrophy and
upregulation of autophagy in dogs. Vet. J. 206: 54–60.
Panciera, R.J., Ritchey, J.W., Baker, J.E., and DiGregorio, M. (2002). Trigeminal and polyradicu-
loneuritis in a dog presenting with masticatory muscle atrophy and Horner’s syndrome. Vet.
Pathol. 39: 146–149.
Parzefall, B., Fischer, A., Blutke, A. et al. (2011). Naturally‐occurring canine herpesvirus‐1
infection of the vestibular labyrinth and ganglion of dogs. Vet. J. 189: 100–102.
Pfaff, A.M., March, P.A., and Fishman, C. (2000). Acute bilateral trigeminal neuropathy associ-
ated with nervous system lymphosarcoma in a dog. J. Am. Anim. Hosp. Assoc. 36: 57–61.
von Pfeil, D.J.F., Zellner, E., Fritz, M.C. et al. (2018). Congenital laryngeal paralysis in Alaskan
huskies: 25 cases (2009–2014). J. Am. Vet. Med. Assoc. 253: 1057–1065.
Pitcher, G.D. and Hahn, C.N. (2007). Atypical masticatory muscle myositis in three cavalier
King Charles spaniel littermates. J. Small Anim. Pract. 48: 226–228.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
Quintavalla, F., Menozzi, A., Pozzoli, C. et al. (2017). Sildenafil improves clinical signs and
radiographic features in dogs with congenital idiopathic megaoesophagus: a randomised con-
trolled trial. Vet. Rec. 180: 404.
Reiter, A.M. and Schwarz, T. (2007). Computed tomographic appearance of masticatory myosi-
tis in dogs: 7 cases (1999–2006). J. Am. Vet. Med. Assoc. 231: 924–930.
Roynard, P., Behr, S., Barone, G. et al. (2012). Idiopathic hypertrophic pachymeningitis in six
dogs: MRI, CSF and histological findings, treatment and outcome. J. Small Anim. Pract. 53:
543–548.
Schmidt, R.F., Yick, F., Boghani, Z. et al. (2013). Malignant peripheral nerve sheath tumors of
the trigeminal nerve: a systematic review of 36 cases. Neurosurg. Focus. 34: E5.
Schultz, R.M., Tucker, R.L., Gavin, P.R. et al. (2007). Magnetic resonance imaging of acquired
trigeminal nerve disorders in six dogs. Vet. Radiol. Ultrasound 48: 101–104.
Shelton, G.D., Cardinet, G.H. 3rd, and Bandman, E. (1987). Canine masticatory muscle disor-
ders: a study of 29 cases. Muscle Nerve 10: 753–766.
Shelton, G.D., Podell, M., Poncelet, L. et al. (2003). Inherited polyneuropathy in Leonberger
dogs: a mixed or intermediate form of Charcot‐Marie‐Tooth disease? Muscle Nerve 27:
471–477.
Smith, P.M., Gonçalves, R., and McConnell, J.F. (2012). Sensitivity and specificity of MRI for
detecting facial nerve abnormalities in dogs with facial neuropathy. Vet. Rec. 171: 349.
Strøm, P.C., Marks, S.L., Rivera, J.A., and Shelton, G.D. (2018). Dysphagia secondary to focal
inflammatory myopathy and consequent dorsiflexion of the tongue in a dog. J. Small Anim.
Pract. 59: 714–718.
Swift, K.E., McGrath, S., Nolan, M.W. et al. (2017). Clinical and imaging findings, treatments,
and outcomes in 27 dogs with imaging diagnosed trigeminal nerve sheath tumors: a multi‐
center study. Vet. Radiol. Ultrasound 58: 679–689.
Tauro, A., Addicott, D., Foale, R.D. et al. (2015). Clinical features of idiopathic inflammatory
polymyopathy in the Hungarian Vizsla. BMC Vet. Res. 11: 97.
Thieman, K.M., Krahwinkel, D.J., Sims, M.H., and Shelton, G.D. (2010). Histopathological con-
firmation of polyneuropathy in 11 dogs with laryngeal paralysis. J. Am. Anim. Hosp. Assoc. 46:
161–167.
Toyoda, K., Uchida, K., Matsuki, N. et al. (2010). Inflammatory myopathy with severe tongue
atrophy in Pembroke Welsh Corgi dogs. J. Vet. Diagn. Investig. 22: 876–885.
Vamvakidis, C.D., Koutinas, A.F., Kanakoudis, G. et al. (2000). Masticatory and skeletal muscle
myositis in canine leishmaniasis (Leishmania infantum). Vet. Rec. 146: 698–703.
Varejão, A.S., Muñoz, A., and Lorenzo, V. (2006). Magnetic resonance imaging of the intratem-
poral facial nerve in idiopathic facial paralysis in the dog. Vet. Radiol. Ultrasound 47: 328–333.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 321

Wessmann, A., Hennessey, A., Goncalves, R. et al. (2013). The association of middle ear effu-
sion with trigeminal nerve mass lesions in dogs. Vet. Rec. 173: 449.
Whitley, N.T. (1995). Megaoesophagus and glucocorticoid‐deficient hypoadrenocorticism in a
dog. J. Small Anim. Pract. 36: 132–135.
Wilson, D. and Monnet, E. (2016). Risk factors for the development of aspiration pneumonia
after unilateral arytenoid lateralization in dogs with laryngeal paralysis: 232 cases (1987–
2012). J. Am. Vet. Med. Assoc. 248: 188–194.
Wray, J.D. and Sparkes, A.H. (2006). Use of radiographic measurements in distinguishing
myasthenia gravis from other causes of canine megaoesophagus. J. Small Anim. Pract. 47:
256–263.
Yam, P.S., Shelton, G.D., and Simpson, J.W. (1996). Megaoesophagus secondary to acquired
myasthenia gravis. J. Small Anim. Pract. 37: 179–183.

6.7. Vestibular Syndrome

Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Garosi, L.S., Dennis, R., and Penderis, J. (2001). Results of magnetic resonance imaging in dogs
with vestibular disorders: 85 cases (1996–1999). J. Am. Vet. Med. Assoc. 218: 385–391.
Garosi, L.S., Lowrie, M.L., and Swinbourne, N.F. (2012). Neurological manifestations of ear
disease in dogs and cats. Vet. Clin. North Am. Small Anim. Pract. 42: 1143–1160.
Jeandel, A., Thibaud, J.L., and Blot, S. (2016). Facial and vestibular neuropathy of unknown
origin in 16 dogs. J. Small Anim. Pract. 57: 74–78.
Kent, M., Platt, S.R., and Schatzberg, S.J. (2010). The neurology of balance: function and dys-
function of the vestibular system in dogs and cats. Vet. J. 185: 247–258.
Lowrie, M. (2012a). Vestibular disease: anatomy, physiology, and clinical signs. Compend. Contin.
Educ. Vet. 34: E1.
Lowrie, M. (2012b). Vestibular disease: diseases causing vestibular signs. Compend. Contin. Educ.
Vet. 34: E2.
Marks, S.L., Lipsitz, D., Vernau, K.M. et al. (2011). Reversible encephalopathy secondary to
thiamine deficiency in 3 cats ingesting commercial diets. J. Vet. Intern. Med. 25: 949–953.
Skelly, B.J. and Franklin, R.J. (2002). Recognition and diagnosis of lysosomal storage diseases
in the cat and dog. J. Vet. Intern. Med. 16: 133–141.

6.8. Cerebellar Dysfunction

Altay, U.M., Skerritt, G.C., Hilbe, M. et al. (2011). Feline cerebrovascular disease: clinical and
histopathologic findings in 16 cats. J. Am. Anim. Hosp. Assoc. 47: 89–97.
Bertalan, A., Glass, E.N., Kent, M. et al. (2014). Late‐onset cerebellar abiotrophy in a Labrador
retriever. Aust. Vet. J. 92: 339–342.
Boudreau, C.E. (2018). An update on cerebrovascular disease in dogs and cats. Vet. Clin. North
Am. Small Anim. Pract. 48: 45–62.
Brown, C.A., Munday, J.S., Mathur, S., and Brown, S.A. (2005). Hypertensive encephalopathy
in cats with reduced renal function. Vet. Pathol. 42: 642–649.
Cardy, T.J., Lam, R., Peters, L.M. et al. (2017). Successful medical management of a domestic
longhair cat with subdural intracranial empyema and multifocal pneumonia. J. Vet. Emerg.
Crit. Care (San Antonio) 27: 238–242.
Cherubini, G.B., Rusbridge, C., Singh, B.P. et al. (2007). Rostral cerebellar arterial infarct in two
cats. J. Feline Med. Surg. 9: 246–253.
Chrisman, C.L., Cork, L.C., and Gamble, D.A. (1984). Neuroaxonal dystrophy of Rottweiler
dogs. J. Am. Vet. Med. Assoc. 184: 464–467.
Cornelis, I., Van Ham, L., Gielen, I. et al. (2019). Clinical presentation, diagnostic findings, prog-
322 A Practical Approach to Neurology for the Small Animal Practitioner

nostic factors, treatment and outcome in dogs with meningoencephalomyelitis of unknown

origin: a review. Vet. J. 244: 37–44.
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Evans, J., Levesque, D., Knowles, K. et al. (2003). Diazepam as a treatment for metronidazole
toxicosis in dogs: a retrospective study of 21 cases. J. Vet. Intern. Med. 17: 304–310.
Garosi, L., McConnell, J.E., Platt, S.R. et al. (2005). Results of diagnostic investigations and long‐
term outcome of 33 dogs with brain infarction (2000–2004). J. Vet. Intern. Med. 19: 725–731.
Garosi, L., McConnell, J.F., Platt, S.R. et al. (2006). Clinical and topographic magnetic resonance
characteristics of suspected brain infarction in 40 dogs. J. Vet. Intern. Med. 20: 311–321.
Garosi, L., Dawson, A., Couturier, J. et al. (2010). Necrotizing cerebellitis and cerebellar atrophy
caused by Neospora caninum infection: magnetic resonance imaging and clinicopathologic
findings in seven dogs. J. Vet. Intern. Med. 24: 571–578.
Hahn, K., Rohdin, C., Jagannathan, V. et al. (2015). TECPR2 associated neuroaxonal dystrophy
in Spanish water dogs. PLoS One 10: e0141824.
Henke, D., Böttcher, P., Doherr, M.G. et al. (2008). Computer‐assisted magnetic resonance
imaging brain morphometry in American Staffordshire Terriers with cerebellar cortical
degeneration. J. Vet. Intern. Med. 22: 969–975.
Hoon‐Hanks, L.L., McGrath, S., Tyler, K.L. et al. (2018). Metagenomic investigation of idio-
pathic meningoencephalomyelitis in dogs. J. Vet. Intern. Med. 32: 324–330.
Inada, S., Mochizuki, M., Izumo, S. et al. (1996). Study of hereditary cerebellar degeneration in
cats. Am. J. Vet. Res. 57: 296–301.
Ives, E.J., MacKillop, E., and Olby, N.J. (2018). Saccadic oscillations in 4 dogs and 1 cat. J. Vet.
Intern. Med. 32: 1392–1396.
Kent, M., Glass, E.N., Haley, A.C. et al. (2014). Ischemic stroke in greyhounds: 21 cases (2007–
2013). J. Am. Vet. Med. Assoc. 245: 113–117.
Kwiatkowska, M., Pomianowski, A., Adamiak, Z., and Bocheńska, A. (2013). Magnetic reso-
nance imaging and brainstem auditory evoked responses in the diagnosis of cerebellar corti-
cal degeneration in american staffordshire terriers. Acta Vet. Hung. 61: 9–18.
de Lahunta, A. (1980). Diseases of the cerebellum. Vet. Clin. North Am. Small Anim. Pract. 10:
91–101.
de Lahunta, A. and Averill, D.R. Jr. (1976). Hereditary cerebellar cortical and extrapyramidal
nuclear abiotrophy in Kerry Blue Terriers. J. Am. Vet. Med. Assoc. 168: 1119–1124.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Lowrie, M. and Garosi, L. (2016). Classification of involuntary movements in dogs: tremors and
twitches. Vet. J. 214: 109–116.
Lowrie, M., De Risio, L., Dennis, R. et al. (2012). Concurrent medical conditions and long‐term
outcome in dogs with nontraumatic intracranial hemorrhage. Vet. Radiol. Ultrasound 53:
381–388.
Lucot, K.L., Dickinson, P.J., Finno, C.J. et al. (2018). A missense mutation in the vacuolar pro-
tein sorting 11 (VPS11) gene is associated with neuroaxonal dystrophy in Rottweiler dogs.
G3 (Bethesda) 8: 2773–2780.
Martin‐Vaquero, P., da Costa, R.C., and Daniels, J.B. (2011). Presumptive meningoencephalitis
secondary to extension of otitis media/interna caused by Streptococcus equi subspecies
zooepidemicus in a cat. J. Feline Med. Surg. 13: 606–609.
Mauler, D.A., Van Soens, I., Bhatti, S.F. et al. (2014). Idiopathic generalised tremor syndrome
in two cats. J. Feline Med. Surg. 16: 378–380.
McConnell, J.F., Garosi, L., and Platt, S.R. (2005). Magnetic resonance imaging findings of pre-
sumed cerebellar cerebrovascular accident in twelve dogs. Vet. Radiol. Ultrasound 46: 1–10.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 323

Negrin, A., Gaitero, L., and Añor, S. (2009). Presumptive caudal cerebellar artery infarct in a
dog: clinical and MRI findings. J. Small Anim. Pract. 50: 615–618.
Negrin, A., Taeymans, O.N.J., Spencer, S.E., and Cherubini, G.B. (2018). Presumed caudal cer-
ebellar artery infarction in three cats: neurological signs, MRI findings, and outcome. Front.
Vet. Sci. 5: 155.
Nibe, K., Kita, C., Morozumi, M. et al. (2007). Clinicopathological features of canine neuroax-
onal dystrophy and cerebellar cortical abiotrophy in Papillon and Papillon‐related dogs. J. Vet.
Med. Sci. 69: 1047–1052.
Nibe, K., Nakayama, H., and Uchida, K. (2010). Comparative study of cerebellar degeneration
in canine neuroaxonal dystrophy, cerebellar cortical abiotrophy, and neuronal ceroid‐
lipofuscinosis. J. Vet. Med. Sci. 72: 1495–1499.
Olby, N., Blot, S., Thibaud, J.L. et al. (2004). Cerebellar cortical degeneration in adult American
Staffordshire Terriers. J. Vet. Intern. Med. 18: 201–208.
O’Neill, J., Kent, M., Glass, E.N., and Platt, S.R. (2013). Clinicopathologic and MRI characteris-
tics of presumptive hypertensive encephalopathy in two cats and two dogs. J. Am. Anim. Hosp.
Assoc. 49: 412–420.
Parzefall, B., Driver, C.J., Benigni, L., and Davies, E. (2014). Magnetic resonance imaging char-
acteristics in four dogs with central nervous system neosporosis. Vet. Radiol. Ultrasound 55:
539–546.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
Platt, S., Hicks, J., and Matiasek, L. (2016). Intracranial intra‐arachnoid diverticula and cyst‐like
abnormalities of the brain. Vet. Clin. North Am. Small Anim. Pract. 46: 253–263.
Poncelet, L., Héraud, C., Springinsfeld, M. et al. (2013). Identification of feline panleukopenia
virus proteins expressed in Purkinje cell nuclei of cats with cerebellar hypoplasia. Vet. J. 196:
381–387.
Sewell, A.C., Haskins, M.E., and Giger, U. (2012). Dried blood spots for the enzymatic diagnosis
of lysosomal storage diseases in dogs and cats. Vet. Clin. Pathol. 41: 548–557.
Sisó, S., Ferrer, I., and Pumarola, M. (2001). Juvenile neuroaxonal dystrophy in a Rottweiler:
accumulation of synaptic proteins in dystrophic axons. Acta Neuropathol. 102: 501–504.
Skelly, B.J. and Franklin, R.J. (2002). Recognition and diagnosis of lysosomal storage diseases
in the cat and dog. J. Vet. Intern. Med. 16: 133–141.
Steinberg, T., Matiasek, K., Brühschwein, A., and Fischer, A. (2007). Imaging diagnosis–
intracranial epidermoid cyst in a Doberman Pinscher. Vet. Radiol. Ultrasound 48: 250–253.
Stuetzer, B. and Hartmann, K. (2014). Feline parvovirus infection and associated diseases. Vet. J.
201: 150–155.
Sturges, B.K., Dickinson, P.J., Kortz, G.D. et al. (2006). Clinical signs, magnetic resonance imag-
ing features, and outcome after surgical and medical treatment of otogenic intracranial infec-
tion in 11 cats and 4 dogs. J. Vet. Intern. Med. 20: 648–656.
Tauro, A., Beltran, E., Cherubini, G.B. et al. (2018). Metronidazole‐induced neurotoxicity in
26 dogs. Aust. Vet. J. 96: 495–501.
Thomsen, B., Garosi, L., Skerritt, G. et al. (2016). Neurological signs in 23 dogs with suspected
rostral cerebellar ischaemic stroke. Acta Vet. Scand. 58: 40.
Urkasemsin, G., Linder, K.E., Bell, J.S. et al. (2010). Hereditary cerebellar degeneration in
Scottish terriers. J. Vet. Intern. Med. 24: 565–570.
Wagner, S.O., Podell, M., and Fenner, W.R. (1997). Generalized tremors in dogs: 24 cases
(1984–1995). J. Am. Vet. Med. Assoc. 211: 731–735.
Whittaker, D.E., Drees, R., and Beltran, E.M.R.I. (2018). Clinical characteristics of suspected
cerebrovascular accident in nine cats. J. Feline Med. Surg. 20: 674–684.
324 A Practical Approach to Neurology for the Small Animal Practitioner

6.9. Neck and/or Spinal Pain

Bathen‐Noethen, A., Carlson, R., Menzel, D. et al. (2008). Concentrations of acute‐phase pro-
teins in dogs with steroid responsive meningitis‐arteritis. J. Vet. Intern. Med. 22: 1149–1156.
Brisson, B.A. (2010). Intervertebral disc disease in dogs. Vet. Clin. North Am. Small Anim. Pract.
40: 829–858.
Coelho, A.M., Cherubini, G., De Stefani, A. et al. (2019). Serological prevalence of toxoplasmo-
sis and neosporosis in dogs diagnosed with suspected meningoencephalitis in the UK. J. Small
Anim. Pract. 60: 44–50.
Cummings, K.R., Vilaplana Grosso, F., Moore, G.E. et al. (2018). Objective measurements of the
atlantoaxial joint on radiographs performed without flexion can increase the confidence of
diagnosis of atlantoaxial instability in toy breed dogs. Vet. Radiol. Ultrasound 59: 667–676.
De Strobel, F., Paluš, V., Vettorato, E. et al. (2019). Cervical hyperaesthesia in dogs: an epide-
miological retrospective study of 185 cases. J. Small Anim. Pract. 60: 404–410.
Girod, M., Allerton, F., Gommeren, K. et al. (2016). Evaluation of the effect of oral omeprazole
on canine cerebrospinal fluid production: a pilot study. Vet. J. 209: 119–124.
Graham, G.G., Davies, M.J., Day, R.O. et al. (2013). The modern pharmacology of paracetamol:
therapeutic actions, mechanism of action, metabolism, toxicity and recent pharmacological
findings. Inflammopharmacology 21: 201–232.
Hechler, A.C. and Moore, S.A. (2018). Understanding and treating Chiari‐like malformation
and syringomyelia in dogs. Top. Companion Anim. Med. 33: 1–11.
Kiviranta, A.M., Rusbridge, C., Laitinen‐Vapaavuori, O. et al. (2017). Syringomyelia and crani-
ocervical junction abnormalities in Chihuahuas. J. Vet. Intern. Med. 31: 1771–1781.
Lowrie, M., Penderis, J., McLaughlin, M. et al. (2009). Steroid responsive meningitis‐arteritis: a
prospective study of potential disease markers, prednisolone treatment, and long‐term out-
come in 20 dogs (2006–2008). J. Vet. Intern. Med. 23: 862–870.
Plessas, I.N., Rusbridge, C., Driver, C.J. et al. (2012). Long‐term outcome of Cavalier King
Charles spaniel dogs with clinical signs associated with Chiari‐like malformation and syringo-
myelia. Vet. Rec. 171: 501.
Rusbridge, C., McFadyen, A.K., and Knower, S.P. (2019). Behavioral and clinical signs of
Chiari‐like malformation‐associated pain and syringomyelia in Cavalier King Charles span-
iels. J. Vet. Intern. Med. 33: 2138–2150.
Schueler, R.O., White, G., Schueler, R.L. et al. (2018). Canine pancreatic lipase immunoreactiv-
ity concentrations associated with intervertebral disc disease in 84 dogs. J. Small Anim. Pract.
59: 305–310.
Schulze, S., Refai, M., Deutschland, M. et al. (2018). Prevalence of syringomyelia in clinically
unaffected Cavalier King Charles spaniels in Germany (2006–2016). Tierarztl. Prax. Ausg.
K Kleintiere Heimtiere 46: 157–162.
Slanina, M.C. (2016). Atlantoaxial instability. Vet. Clin. North Am. Small Anim. Pract. 46:
265–275.
Tipold, A. and Schatzberg, S.J. (2010). An update on steroid responsive meningitis‐arteritis.
J. Small Anim. Pract. 51: 150–154.
Tipold, A. and Stein, V.M. (2010). Inflammatory diseases of the spine in small animals. Vet. Clin.
North Am. Small Anim. Pract. 40: 871–879.
Webb, A.A., Taylor, S.M., and Muir, G.D. (2002). Steroid‐responsive meningitis‐arteritis in dogs
with noninfectious, nonerosive, idiopathic, immune‐mediated polyarthritis. J. Vet. Intern.
Med. 16: 269–273.
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6.10. Paresis, Paralysis, and Proprioceptive Ataxia

Bennaim, M., Porato, M., Jarleton, A. et al. (2017). Preliminary evaluation of the effects of
photobiomodulation therapy and physical rehabilitation on early postoperative recovery of
dogs undergoing hemilaminectomy for treatment of thoracolumbar intervertebral disk dis-
ease. Am. J. Vet. Res. 78 (2): 195–206.
Bergknut, N., Egenvall, A., Hagman, R. et al. (2012). Incidence of intervertebral disk degenera-
tion–related diseases and associated mortality rates in dogs. J. Am. Vet. Med. Assoc. 240 (11):
1300–1309.
Brown, E.A., Dickinson, P.J., Mansour, T. et al. (2017). FGF4 retrogene on CFA12 is responsible
for chondrodystrophy and intervertebral disc disease in dogs. Proc. Natl. Acad. Sci. U. S. A. 114
(43): 11476–11481.
Bubenik, L. and Hosgood, G. (2008). Urinary tract infection in dogs with thoracolumbar
intervertebral disc herniation and urinary tract dysfunction managed by manual expression,
indwelling catheterization or intermittent catheterization. Vet. Surg. 37 (8): 791–800.
Bubenik, L.J., Hosgood, G.L., Waldron, D.R. et al. (2007). Frequency of urinary tract infection
in catheterized dogs and comparison of bacterial culture and susceptibility testing results for
catheterized and noncatheterized dogs with urinary tract infections. J. Am. Vet. Med. Assoc. 231
(6): 893–899.
Cardy, T.J., De Decker, S., Kenny, P.J., and Volk, H.A. (2015). Clinical reasoning in canine spinal
disease: what combination of clinical information is useful? Vet. Rec. 177 (7): 171.
Crawford, A.H. and De Decker, S. (2017). Clinical presentation and outcome of dogs treated
medically or surgically for thoracolumbar intervertebral disc protrusion. Vet. Rec. 180
(23): 569.
Da Costa, R.C. and Parent, J.M. (2007). One‐year clinical and magnetic resonance imaging fol-
low‐up of Doberman Pinschers with cervical spondylomyelopathy treated medically or surgi-
cally. J. Am. Vet. Med. Assoc. 231 (2): 243–250.
De Decker, S., Bhatti, S.F., Duchateau, L. et al. (2009). Clinical evaluation of 51 dogs treated
conservatively for disc‐associated wobbler syndrome. J. Small Anim. Pract. 50 (3): 136–142.
De Risio, L.A. (2015). Review of fibrocartilaginous embolic myelopathy and different types of
peracute non‐compressive intervertebral disk extrusions in dogs and cats. Front. Vet. Sci. 2: 24.
De Risio, L., Adams, V., Dennis, R. et al. (2008). Association of clinical and magnetic resonance
imaging findings with outcome in dogs suspected to have ischemic myelopathy: 50 cases
(2000–2006). J. Am. Vet. Med. Assoc. 233: 129–135.
Doran, C., Platt, S.R., and Garosi, L.S. (2019). Long‐term imaging follow‐up of a conservatively
managed presumptive osseous cervical stenotic myelopathy in a puppy. J. Small Anim. Pract.
60: 198.
Drum, M.G. (2010). Physical rehabilitation of the canine neurologic patient. Vet. Clin. North Am.
Small Anim. Pract. 40 (1): 181–193.
Fenn, J., Drees, R., Volk, H.A., and De Decker, S. (2016). Comparison of clinical signs and out-
comes between dogs with presumptive ischemic myelopathy and dogs with acute noncom-
pressive nucleus pulposus extrusion. J. Am. Vet. Med. Assoc. 249 (7): 767–775.
Forterre, F., Konar, M., Tomek, A. et al. (2008). Accuracy of the withdrawal reflex for localiza-
tion of the site of cervical disk herniation in dogs: 35 cases (2004–2007). J. Am. Vet. Med. Assoc.
232: 559–563.
Freeman, P. and Jeffery, N.D. (2017). Re‐opening the window on fenestration as a treatment for
acute thoracolumbar intervertebral disc herniation in dogs. J. Small Anim. Pract. 58 (4):
199–204.
326 A Practical Approach to Neurology for the Small Animal Practitioner

Full, A.M., Heller, H.L., and Mercier, M. (2016). Prevalence, clinical presentation, prognosis,
and outcome of 17 dogs with spinal shock and acute thoracolumbar spinal cord disease. J. Vet.
Emerg. Crit. Care (San Antonio) 26 (3): 412–418.
Gonçalves, R., Penderis, J., Chang, Y.P. et al. (2008). Clinical and neurological characteristics of
aortic thromboembolism in dogs. J. Small Anim. Pract. 49 (4): 178–184.
Hansen, T., Smolders, L.A., Tryfonidou, M.A. et al. (2017). The myth of fibroid degeneration in
the canine intervertebral disc: a histopathological comparison of intervertebral disc degenera-
tion in chondrodystrophic and nonchondrodystrophic dogs. Vet. Pathol. 54 (6): 945–952.
Hayashi, A.M., Matera, J.M., and Fonseca Pinto, A.C. (2007). Evaluation of electroacupuncture
treatment for thoracolumbar intervertebral disk disease in dogs. J. Am. Vet. Med. Assoc. 231 (6):
913–918.
Janssens, L., Beosier, Y., and Daems, R. (2009). Lumbosacral degenerative stenosis in the dog.
The results of epidural infiltration with methylprednisolone acetate: a retrospective study. Vet.
Comp. Orthop. Traumatol. 22 (6): 486–491.
Jeffery, N.D. and Freeman, P.M. (2018). The role of fenestration in management of Type I thora-
columbar disk degeneration. Vet. Clin. North Am. Small Anim. Pract. 48 (1): 187–200.
Jeffery, N.D., Barker, A.K., Hu, H.Z. et al. (2016). Factors associated with recovery from para-
plegia in dogs with loss of pain perception in the pelvic limbs following intervertebral disk
herniation. J. Am. Vet. Med. Assoc. 248 (4): 386–394.
Jeffery, N.D., Harcourt‐Brown, T.R., Barker, A.K. et al. (2018). Choices and decisions in decom-
pressive surgery for thoracolumbar intervertebral disk herniation. Vet. Clin. North Am. Small
Anim. Pract. 48 (1): 169–186.
Joaquim, J.G., Luna, S.P., Brondani, J.T. et al. (2010). Comparison of decompressive surgery,
electroacupuncture, and decompressive surgery followed by electroacupuncture for the
treatment of dogs with intervertebral disk disease with long‐standing severe neurologic defi-
cits. J. Am. Vet. Med. Assoc. 236 (11): 1225–1229.
Kathmann, I., Cizinauskas, S., Doherr, M.G. et al. (2006). Daily controlled physiotherapy
increases survival time in dogs with suspected degenerative myelopathy. J. Vet. Intern. Med.
20: 927–932.
Levine, J.M., Levine, G.J., Johnson, S.I. et al. (2007). Evaluation of the success of medical man-
agement for presumptive thoracolumbar intervertebral disk herniation in dogs. Vet. Surg. 36
(5): 482–491.
Mari, L., Behr, S., Shea, A. et al. (2017). Outcome comparison in dogs with a presumptive diag-
nosis of thoracolumbar fibrocartilaginous embolic myelopathy and acute non‐compressive
nucleus pulposus extrusion. Vet. Rec. 181 (11): 293.
Marschall, J., Carpenter, C.R., Fowler, S. et al. (2013). Antibiotic prophylaxis for urinary tract
infections after removal of urinary catheter: meta‐analysis. BMJ f3147: 346.
Mauler, D.A., De Decker, S., De Risio, L. et al. (2014). Signalment, clinical presentation, and diag-
nostic findings in 122 dogs with spinal arachnoid diverticula. J. Vet. Intern. Med. 28 (1): 175–181.
Nessler, J., Flieshardt, C., Tünsmeyer, J. et al. (2018). Comparison of surgical and conservative
treatment of hydrated nucleus pulposus extrusion in dogs. J. Vet. Intern. Med. 32 (6):
1989–1995.
Olby, N.J., MacKillop, E., Cerda‐Gonzalez, S. et al. (2010). Prevalence of urinary tract infection
in dogs after surgery for thoracolumbar intervertebral disc extrusion. J. Vet. Intern. Med. 24 (5):
1106–1111.
Olby, N.J., Lim, J.H., Wagner, N. et al. (2019). Time course and prognostic value of serum GFAP,
pNFH, and S100β concentrations in dogs with complete spinal cord injury because of interver-
tebral disc extrusion. J. Vet. Intern. Med. 33 (2): 726–734.
Palamara, J.D., Bonczynski, J.J., Berg, J.M. et al. (2016). Perioperative cefovecin to reduce the
incidence of urinary tract infection in dogs undergoing hemilaminectomy. J. Am. Anim. Hosp.
Assoc. 52 (5): 297–304.
 Chapter 6 A Practical Approach to Common Presentations in General Practice 327

Skytte, D. and Schmökel, H. (2018). Relationship of preoperative neurologic score with inter-
vals to regaining micturition and ambulation following surgical treatment of thoracolumbar
disk herniation in dogs. J. Am. Vet. Med. Assoc. 253: 196–200.
Sullivan, L.A., Campbell, V.L., and Onuma, S.C. (2010). Evaluation of open versus closed urine
collection systems and development of nosocomial bacteriuria in dogs. J. Am. Vet. Med. Assoc.
237 (2): 187–190.
Zidan, N., Sims, C., Fenn, J. et al. (2018). A randomized, blinded, prospective clinical trial of
postoperative rehabilitation in dogs after surgical decompression of acute thoracolumbar
intervertebral disc herniation. J. Vet. Intern. Med. 32 (3) : 1133–1144.

6.11. Monoparesis and Lameness

Griffiths, I.R., Duncan, I.D., and Lawson, D.D. (1974). Avulsion of the brachial plexus–2.
Clinical aspects. J. Small Anim. Pract. 15: 177–183.
Janssens, L., Beosier, Y., and Daems, R. (2009). Lumbosacral degenerative stenosis in the dog.
The results of epidural infiltration with methylprednisolone acetate: a retrospective study. Vet.
Comp. Orthop. Traumatol. 22: 486–491.
Lacassagne, K., Hearon, K., Berg, J. et al. (2018). Canine spinal meningiomas and nerve sheath
tumours in 34 dogs (2008–2016): distribution and long‐term outcome based upon histopa-
thology and treatment modality. Vet. Comp. Oncol. 16: 344–351.
Ródenas, S., Summers, B.A., Saveraid, T. et al. (2013). Chronic hypertrophic ganglioneuritis
mimicking spinal nerve neoplasia: clinical, imaging, pathologic findings, and outcome after
surgical treatment. Vet. Surg. 42: 91–98.
Van Stee, L., Boston, S., Teske, E. et al. (2017). Compartmental resection of peripheral nerve
tumours with limb preservation in 16 dogs (1995–2011). Vet. J. 226: 40–45.

6.12. Neuromuscular Weakness

Aleman, M., Dickinson, P.J., Williams, D.C. et al. (2014). Electrophysiologic confirmation of
heterogenous motor polyneuropathy in young cats. J. Vet. Intern. Med. 28: 1789–1798.
Añor, S. (2014). Acute lower motor neuron tetraparesis. Vet. Clin. North Am. Small Anim. Pract.
44: 1201–1222.
Bensfield, A.C., Evans, J., Pesayco, J.P. et al. (2011). Recurrent demyelination and remyelina-
tion in 37 young Bengal cats with polyneuropathy. J. Vet. Intern. Med. 25: 882–889.
Bexfield, N.H., Watson, P.J., and Herrtage, M.E. (2006). Management of myasthenia gravis
using cyclosporine in 2 dogs. J. Vet. Intern. Med. 20: 1487–1490.
Dewey, C.W. and da Costa, R.C. (2015). Practical Guide to Canine and Feline Neurology, 3e.
Hoboken, NJ: Wiley Blackwell.
Dewey, C.W., Bailey, C.S., Shelton, G.D. et al. (1997). Clinical forms of acquired myasthenia
gravis in dogs: 25 cases (1988–1995). J. Vet. Intern. Med. 11: 50–57.
Dewey, C.W., Coates, J.R., Ducoté, J.M. et al. (1999). Azathioprine therapy for acquired myas-
thenia gravis in five dogs. J. Am. Anim. Hosp. Assoc. 35: 396–402.
Evans, J., Levesque, D., and Shelton, G.D. (2004). Canine inflammatory myopathies: a clinico-
pathologic review of 200 cases. J. Vet. Intern. Med. 18: 679–691.
Farrow, B.R., Murrell, W.G., Revington, M.L. et al. (1983). Type C botulism in young dogs. Aust.
Vet. J. 60: 374–377.
Giannuzzi, A.P., Ricciardi, M., De Simone, A., and Gernone, F. (2017). Neurological manifesta-
tions in dogs naturally infected by Leishmania infantum: descriptions of 10 cases and a review
of the literature. J. Small Anim. Pract. 58: 125–138.
Glass, E.N. and Kent, M. (2002). The clinical examination for neuromuscular disease. Vet. Clin.
North Am. Small Anim. Pract. 32: 1–29.
328 A Practical Approach to Neurology for the Small Animal Practitioner

Hague, D.W., Humphries, H.D., Mitchell, M.A., and S.G.D. (2015). Risk factors and outcomes in
cats with acquired myasthenia gravis (2001–2012). J. Vet. Intern. Med. 29: 1307–1312.
Hirschvogel, K., Jurina, K., Steinberg, T.A. et al. (2012). Clinical course of acute canine polyra-
diculoneuritis following treatment with human IV immunoglobulin. J. Am. Anim. Hosp. Assoc.
48: 299–309.
Holt, N., Murray, M., Cuddon, P.A., and Lappin, M.R. (2011). Seroprevalence of various infec-
tious agents in dogs with suspected acute canine polyradiculoneuritis. J. Vet. Intern. Med. 25:
261–266.
Khorzad, R., Whelan, M., Sisson, A., and Shelton, G.D. (2011). Myasthenia gravis in dogs with
an emphasis on treatment and critical care management. J. Vet. Emerg. Crit. Care (San Antonio)
21: 193–208.
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Med. Assoc. 212: 830–834.
de Lahunta, A., Glass, E., and Kent, M. (2015). Veterinary Neuroanatomy and Clinical Neurology,
4e. St Louis, MO: Elsevier Saunders.
Laws, E.J., Harcourt‐Brown, T.R., Granger, N., and Rose, J.H. (2017). An exploratory study into
factors influencing development of acute canine polyradiculoneuritis in the UK. J. Small
Anim. Pract. 58: 437–443.
Platt, S. and Olby, N. (2013). BSAVA Manual of Canine and Feline Neurology, 4e. Gloucester, UK:
British Small Animal Veterinary Association.
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come in dogs with thymoma: 116 cases (1999–2010). J. Am. Vet. Med. Assoc. 243: 1448–1454.
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polymyopathy in the Hungarian Vizsla. BMC Vet. Res. 11: 97.
Chapter 7  eurological
N
Emergencies
Edward Ives and Paul M. Freeman

This chapter will summarise a logical approach to the following emergency pres-
entations, with a focus on management in general practice:

• head trauma and traumatic brain injury (TBI)

• status epilepticus and acute repetitive seizures
• acute spinal cord injury.

Having confidence in how to approach these cases is vital, as many animals

may be unfit to travel to a referral centre at the time of presentation and the
initial management is often most important to optimise the prognosis. However,
this also means that such cases can be incredibly rewarding for vets and nurses
to manage in general practice. As for many aspects of veterinary medicine, a
‘back‐to‐basics’ approach is recommended, and the focus should be on life‐
threatening injuries and systemic stabilisation before considering further
investigations or complex treatments. This is to ensure that the injured brain
or spinal cord is provided with adequate perfusion of oxygenated blood at all
times.

7.1 ­Head Trauma in Dogs and Cats

Edward Ives

Head trauma is a relatively common presentation in general practice, with the most
frequently reported causes including road traffic accidents, bites, kicks, and falls.
Fortunately, many animals will only require basic supportive care together with

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

329
330 A Practical Approach to Neurology for the Small Animal Practitioner

management of superficial wounds, and ocular, jaw, or dental injuries. However,

head trauma may also result in potentially fatal, structural or physiological disrup-
tion of the brain, termed traumatic brain injury (TBI). Early recognition and man-
agement of TBI is vital to give the best chance of a successful outcome. Affected
animals may appear severely affected at the time of initial presentation and it is
easy to assume that the prognosis will be poor. However, with appropriate stabilisa-
tion and supportive care many animals will show a remarkable ability to compen-
sate for even severe TBI and can recover to have a good quality of life.
Head trauma can result in two forms of brain injury.

1. Primary injury
This is the direct physical disruption of the brain and its associated tissues that
occurs at the time of trauma. Examples of primary injury include:
• Contusion or laceration of the brain parenchyma.
• Skull fractures – skull fractures are commonly observed following head
trauma but are not always associated with TBI. This is dependent on the
region of the skull affected and the extent of skull fragment displacement.
• Rupture of intracranial blood vessels resulting in haemorrhage and haema-
toma formation.
Expanding haematomas or depressed skull fractures that are compressing the
brain parenchyma may benefit from surgical management. However, in the
majority of cases the primary brain injury cannot be prevented or directly
treated. If this injury has not resulted in death at the time of trauma, then its
main significance in terms of clinical management is in the initiation of a
complex cascade of biochemical processes, termed ‘secondary injury’.
2. Secondary injury
Secondary injury occurs over minutes to days following primary injury and
has the potential to result in a catastrophic, expanding focus of tissue damage
and cell death. Therefore, the prevention and treatment of secondary injury
forms a vital part of TBI management.

The main drivers of secondary injury include:

• Release of excitatory neurotransmitters (e.g. glutamate) from damaged regions

of the brain, resulting in an increased cerebral metabolic activity, energy
depletion, and failure of ion homeostasis via ATP‐dependent cell membrane
ion pumps. The subsequent influx of positively charged ions, such as sodium
and calcium, results in a vicious cycle of further depolarisation, cellular swell-
ing (cytotoxic oedema), activation of destructive intracellular enzymes, and
programmed cell death (apoptosis).
• Local production of reactive oxygen species (ROS) secondary to reduced tissue
perfusion, increased iron levels following haemorrhage, and local tissue acidosis all
contribute towards further damage to the lipid‐rich neuronal cell membranes.
 Chapter 7 Neurological Emergencies 331

• Release of inflammatory cytokines from injured tissues results in disruption

to the blood–brain barrier, local nitric oxide production, chemotaxis, and
accumulation of inflammatory cells. Nitric oxide is a potent vasodilator and
the subsequent increase in intracranial blood volume can perpetuate any
elevation of intracranial pressure (ICP).

Head trauma is frequently accompanied by systemic changes such as hypo-

tension, hypoxaemia, hypercapnia, and derangements in electrolyte and glucose
levels. These changes will exacerbate secondary injury by compromising cere-
bral perfusion and oxygen delivery, thus further driving ischaemia, excitotoxic-
ity, energy depletion, and cell death. It is for this reason that systemic stabilisation
forms such an important part of TBI management in humans and animals.

7.1.1 Intracranial Pressure and Cerebral Perfusion

The cranial vault can be thought of as a closed box constrained by a rigid skull.
The contents of this box include three basic compartments:

• brain parenchyma – c.80% of intracranial volume

• blood – c.10% of intracranial volume, with venous blood being the majority
• cerebrospinal fluid (CSF) – c.10% of intracranial volume.

There is a constant low pressure of 5–12 mmHg within this box that is exerted
by the tissues and fluids contained within it. This is the intracranial pressure
(ICP), against which the mean arterial blood pressure (MABP) must pump to
provide the brain with an adequate supply of oxygen and nutrients. Thus, the
cerebral perfusion pressure (CPP) can be defined as the MABP minus the ICP.
It is important that the ICP is kept tightly regulated at all times to ensure that
there is an optimal environment for the brain to function. According to the
principles of intracranial compliance and the Monrie–Kellie doctrine, an
increase in the volume of one compartment (e.g. brain, blood, or CSF), or the
appearance of a new substance within this closed box (e.g. tumour, haema-
toma, skull fragment), must be met by an equal and opposite decrease in the
volume of another compartment. This is to ensure that the ICP remains con-
stant and usually involves compensatory shunting of venous blood or CSF out
of the intracranial vault. If this compensatory capacity is overwhelmed, then
even a small additional increase in volume will result in an exponentially large
increase in ICP. The oedema, haemorrhage, and other changes that accompany
primary and secondary brain injury can rapidly overwhelm this compensatory
mechanism. If the ICP rises to over 20 mmHg then this can result in death sec-
ondary to reduced cerebral perfusion, brain herniation, brainstem compression,
and cardiorespiratory failure.
Regulatory mechanisms also exist to ensure adequate cerebral blood flow (CBF)
in the face of fluctuations in MABP and cerebral oxygen and carbon dioxide levels.
332 A Practical Approach to Neurology for the Small Animal Practitioner

1. Pressure autoregulation
In the normal animal, the CBF is kept constant over a wide range of MABPs
(50–150 mmHg) by altering the cerebral vascular resistance; vasoconstriction
in response to increased CPP and vasodilation in response to reduced CPP.
This regulatory mechanism can fail following TBI, meaning that CBF changes
in a more linear relationship with MABP. This can result in cerebral ischaemia
if the CBF becomes inadequate to maintain cerebral oxygen demand in the
face of systemic hypotension.
2. Chemical autoregulation
The processes of chemical autoregulation alter the cerebral vascular resist-
ance to optimise CBF in response to changes in cerebral oxygen and carbon
dioxide levels.
• Cerebral arterial vasodilation to increase CBF in response to hypercapnia,
hypoxaemia, increases in cerebral metabolic rate, or the release of vasoac-
tive substances (e.g. nitric oxide). CBF increases in a linear relationship
with pa(CO2) levels between 20 and 80 mmHg.
• Cerebral arterial vasoconstriction in response to hypocapnia.

As previously discussed, systemic derangements are commonly observed in

trauma cases, including hypoxaemia and hypercapnia secondary to thoracic
injuries and hypoventilation. In contrast to pressure autoregulation, chemical
autoregulation may be maintained following TBI and this can be counterproduc-
tive as the systemic derangements will stimulate cerebral arterial vasodilation.
This will result in an increased intracranial blood volume which has the poten-
tial to exacerbate ICP elevation.
Whilst these processes may appear complex, their primary significance is to
reinforce the vital importance of systemic stabilisation and the maintenance of
appropriate blood pressure and oxygen and carbon dioxide levels in animals fol-
lowing TBI.

7.1.2 Management of Head Trauma in Dogs and Cats

A logical approach to any case presenting with a history of head trauma, or a
clinical examination compatible with it, can be divided into the following
considerations:

1. Triage and general assessment

2. Systemic stabilisation, including seizure management if applicable
3. Neurological assessment
4. Management of increased ICP
5. Analgesia and sedation
6. Supportive care and nutrition
 Chapter 7 Neurological Emergencies 333

Successful management of a trauma case often requires multiple tasks being

performed at the same time. Recruiting help from veterinary nurses and other
practitioners as soon as possible after presentation means that a stressful situa-
tion can appear more manageable and ensures optimal care of the animal.

1. Triage and general assessment

The initial assessment of any trauma patient should focus on the ‘ABC’ of emer-
gency care and identification of any life‐threatening injuries before a neurologi-
cal examination is performed.
Airway: Endotracheal intubation or tracheostomy may be required if the air-
way is not patent.
Breathing: Endotracheal intubation and manual or mechanical ventilation is
required if the animal presents with apnoea. Assessment and monitoring of res-
piratory function should include:

• thoracic auscultation
• respiratory rate and effort
• saturation of peripheral oxygen [Sp(O2)] by pulse oximetry
• end‐tidal carbon dioxide [Et(CO2)] by capnography.

Thoracic focused assessment with sonography for trauma (TFAST) can be per-
formed to assess for pneumothorax, pleural effusion (e.g. haemothorax), or pul-
monary contusion. Systemic stabilisation should be prioritised over diagnostic
imaging unless there is a clinical suspicion of pneumothorax or significant pleural
effusion that may require emergency drainage to ensure adequate ventilation.
Circulation: Animals will often present in hypovolaemic shock following
trauma. It is essential that this is recognised and addressed as soon as possible to
establish normovolaemia, restore cerebral perfusion, and minimise the extent of
secondary brain injury. Basic assessment should include:

• pulse rate and peripheral pulse quality

• mucous membrane colour and capillary refill time
• blood pressure
• electrocardiography (ECG) – thoracic trauma concurrent with head trauma
may result in traumatic myocarditis and subsequent cardiac arrhythmia.

Readers are referred to the many excellent texts on veterinary emergency

and critical care for a more in‐depth discussion on triage of a trauma patient and
methods of cardiopulmonary resuscitation.
Head trauma may be accompanied by injury to other body regions and the
initial assessment should include identification of both life‐threatening injuries
334 A Practical Approach to Neurology for the Small Animal Practitioner

and those that are likely to require further treatment (e.g. long bone fractures).
This is very important so that the owner can be informed regarding the potential
long‐term prognosis, including anticipated surgeries that may be required and
their associated costs.

• Assessment for sites of external haemorrhage or wounds requiring cleaning

and dressing.
• Limb palpation to assess for fractures – open fractures may require emergency
management to minimise the risk of infection and fixation failure. Closed frac-
tures do not usually require urgent fixation and can be initially managed using
support dressings.
• Abdominal palpation for body wall rupture and bladder integrity.

Thoracic radiography, abdominal radiography, abdominal focused assess-

ment with sonography for trauma (AFAST), TFAST, and/or whole body com-
puted tomography (CT) can be performed following systemic stabilisation to
further assess for concurrent injuries to other body regions.

2. Systemic stabilisation and seizure management

a. Seizure management
If an animal presents in a state of generalised seizure activity, then this should be
managed as a priority in order to minimise the potential for exacerbating ICP
elevation (Box 7.1). The approach to seizure management following head
trauma is the same as for any animal presenting in status epilepticus and is sum-
marised in Section 7.2 ‘Status Epilepticus and Acute Repetitive Seizures’. It is
important to note that systemic stabilisation should always be continued between
drug doses whilst attempts are made to control the seizure activity.

Box 7.1 Post‐traumatic Epilepsy

Seizures following head injury can be classified as either early (<7 days) or late
(>7 days). If an animal presents in a state of generalised seizure activity or suffers a
seizure at any point during management of TBI, then stopping the seizure is a priority
to avoid the detrimental effects on the brain and other organs. The prophylactic use of
antiepileptic medications before potential seizure development remains controversial
in human medicine and has not been shown to reduce the incidence of seizures occur-
ring more than 7 days after injury. It is currently not recommended to start antiepilep-
tic medications in every animal with known head trauma, and consideration should
also be made to the potential cardiorespiratory effects associated with their use.
However, owners should be warned that an estimated 6–10% of dogs suffering head
trauma may develop seizures in later life, a condition termed post‐traumatic epilepsy
(Friedenburg et al. 2012; Steinmetz et al. 2013).
 Chapter 7 Neurological Emergencies 335

b. Systemic stabilisation
Systemic stabilisation is the most important factor determining the outcome fol-
lowing TBI in humans and animals, with both hypoxaemia and hypovolaemia
strongly correlated with elevated ICP and increased mortality in human patients.
The focus of stabilisation is to establish adequate oxygenation, ventilation, and
normovolaemia.

i. Oxygenation
Oxygen delivery to the brain is vital to prevent cerebral ischaemia and to miti-
gate secondary brain injury. The mortality rate in humans with documented
hypoxia after TBI is twice that of patients without hypoxia. Oxygen should be
delivered by flow‐by, with or without a mask. Nasal oxygen prongs or cannulas
should be used with care as they may stimulate sneezing, which can further
increase ICP. The use of an oxygen cage is not advised as their use would pre-
clude the frequent monitoring required in these cases. As previously mentioned,
intubation may be required in apnoeic or comatose animals.
Goals for oxygenation are:

• normal mucous membrane colour, respiratory rate, and pattern

• Sp(O2) of >95% (reflecting a pa(O2) of >80 mmHg)
• pa(O2) of >80–90 mmHg.

ii. Ventilation
Adequate ventilation is required for both oxygenation of the blood and carbon
dioxide exchange. The pa(CO2) is a potent regulator of CBF, with hypercapnia
resulting in cerebral arterial vasodilation, increased cerebral blood volume, and
possible exacerbation of ICP elevation. Conversely, hypocapnia results in cere-
bral arterial vasoconstriction, reduced CBF, and the potential for cerebral ischae-
mia. Airway obstruction, thoracic injury or pain, damage to the brainstem
respiratory centres, or the cardiorespiratory depressive effects of sedative and
antiepileptic medications may all contribute towards hypoventilation in trauma
cases. The goal of ventilation in these cases (whether spontaneous, manual, or
mechanical) is to maintain a normal pa(CO2) level of 35–40 mmHg. If arterial
blood gas analysis is not available, then venous CO2 levels or Et(CO2) levels can
be monitored; venous CO2 is usually around 5 mmHg higher than pa(CO2), and
Et(CO2) tends to underestimate the actual pa(CO2) level.
Deliberate hyperventilation in an attempt to reduce the ICP by lowering the
pa(CO2) and inducing cerebral arterial vasoconstriction has been suggested in
both humans and animals following TBI. However, this is not currently recom-
mended due to the risk of exacerbating cellular ischaemia and it is advised that
the pa(CO2) level is maintained above 35 mmHg in these cases.
336 A Practical Approach to Neurology for the Small Animal Practitioner

iii. Achieve intravenous access

Intravenous access by placement of one or more wide‐bore intravenous cannu-
las is essential to allow fluid resuscitation and administration of medications.

iv. Establish a minimum database

A reasonable minimum database would comprise a packed cell volume (PCV),
total protein (TP), blood glucose, urea, electrolyte levels, and urine specific grav-
ity. Blood can be collected at the time of intravenous catheter placement.
Sampling from the jugular veins should be avoided if possible, as jugular occlu-
sion could reduce venous drainage from the head and elevate ICP.

v. Fluid therapy
The goal of fluid therapy is the rapid restoration of circulating fluid volume to
ensure an adequate CBF and oxygen delivery to vital organs. The benefits
obtained by restoration of cerebral perfusion are widely regarded to outweigh
the potential risks of exacerbating cerebral oedema by fluid administration; a
150% increase in mortality has been reported for human TBI patients with a
systolic blood pressure <90 mmHg (Chestnut et al. 1993).
The choice of fluid to use following head trauma remains controversial and
will also depend upon availability in general practice. However, regardless of the
fluid used, vital parameters should be assessed regularly and the fluids titrated to
avoid volume overload. The goal should be to achieve a systolic blood pressure
of 100–120 mmHg.

• Isotonic crystalloids – Boluses of 15–20 ml/kg (dog) or 10–15 ml/kg (cat) of 0.9%
sodium chloride until there is normalisation of the heart rate, pulse quality,
capillary refill time, mucous membrane colour, and blood pressure (MABP
80–100 mmHg).
• Hypertonic saline (7.5% sodium chloride) – Smaller volumes of this hypertonic
solution may be used to produce a rapid rise in blood osmolarity, drawing fluid
into the circulation from the interstitial and intracellular compartments. This
volume‐expanding effect occurs within minutes and lasts for 15–75 minutes
before redistribution to other fluid compartments occurs. The recommended
dose is 4 ml/kg of 7.5% sodium chloride administered over 3–5 minutes. The
administration of isotonic crystalloids following the use of hypertonic saline is
essential to prevent tissue dehydration, provide maintenance fluid require-
ments, and correct for on‐going losses.
• Colloids – It has been suggested that colloids may act synergistically with hyper-
tonic solutions for restoring blood volume, and that co‐administration pro-
longs the volume‐expanding effects. However, a Cochrane database systematic
review failed to show a benefit of colloids over crystalloids for fluid resuscita-
tion in critically ill humans, including those with TBI (Lewis et al. 2018). The
availability of colloids in veterinary general practice may also limit their use in
 Chapter 7 Neurological Emergencies 337

animals and hypertonic saline has other potential benefits in the management
of ICP elevation following head trauma, as discussed below.

vi. Positioning
To aid venous drainage from the head and avoid increases in cerebral blood vol-
ume that could exacerbate raised ICP, the animal’s head should be midline and
elevated by 10–30°. A tilted, rigid board can be useful as it avoids neck kinking
and potential jugular compression. Jugular blood sampling, jugular catheter
placement, and constrictive collars or neck dressings should also be avoided in
these cases.

3. Neurological assessment
Neurological assessment should ideally be performed once normotension,
appropriate oxygenation, and ventilation are achieved. Many animals may
appear severely affected when they present in hypotensive shock, but the level
of mentation and neurological function will be significantly improved following
systemic stabilisation and fluid resuscitation. The potential influence of analgesic
or sedative medications on the interpretation of the neurological examination
should also be considered, but never at the expense of leaving an animal in dis-
comfort. Frequent reassessment and recording of trends are vital to guide the
response to treatment and potential prognosis. Repeat assessment is recom-
mended every 30–60 minutes until the animal appears stable to ensure prompt
recognition of animals that are deteriorating in spite of treatment.
The use of a scoring system allows for a more objective assessment of neuro-
logic dysfunction, aids in the consistency of monitoring clinical progression, and
assists in case handover between the staff responsible for animal care. The use of
two different scoring systems has been reported for head trauma in veterinary
medicine:

a. Modified Glasgow Coma Scale (MGCS)

b. Animal trauma triage (ATT) score.

a. Modified Glasgow Coma Scale (MGCS)

The MGCS focuses on assessment of three broad categories of neurologic func-
tion: level of consciousness, voluntary motor activity, and brainstem reflexes
(Figure 7.1). Each category is graded from 1 to 6 to give a total score from 3 (most
severely affected) to 18 (normal). From a neuroanatomical perspective, changes
in this score broadly reflect alterations in brainstem and diffuse cerebrocortical
function. As the ICP rises, herniation of the forebrain underneath the tentorium
cerebelli and/or herniation of the cerebellum through the foramen magnum can
result in progressive compression of the brainstem. Direct trauma to the brain-
stem, bilateral or global cerebral abnormalities, and intraparenchymal haemor-
rhage can also result in loss of neurologic functions and a lower MGCS.
338 A Practical Approach to Neurology for the Small Animal Practitioner

Score

Motor activity
Normal gait and spinal reflexes 6
Hemiparesis, tetraparesis, or decerebrate activity 5
Recumbent, intermittent extensor rigidity 4
Recumbent, constant extensor rigidity 3
Recumbent, constant extensor rigidity with opisthotonus 2
Recumbent, hypotonia, depressed or absent spinal reflexes 1
Brainstem reflexes
Normal PLR and oculocephalic (vestibulo‐ocular) reflexes 6
Slow PLR and normal to reduced oculocephalic (vestibulo‐ocular) reflexes 5
Bilateral unresponsive miosis with normal to reduced oculocephalic (vestibulo‐ocular) 4
reflexes
Pinpoint pupils with reduced to absent oculocephalic (vestibulo‐ocular) reflexes 3
Unilateral, unresponsive mydriasis with reduced/absent oculocephalic (vestibulo‐ocular) 2
reflexes
Bilateral unresponsive mydriasis with reduced/absent oculocephalic (vestibulo‐ocular) 1
reflexes
Level of consciousness
Occasional periods of alertness and responsive to environment 6
Depression or delirium, capable of responding but response may be inappropriate 5
Semi‐comatose, responsive to visual stimuli 4
Semi‐comatose, responsive to auditory stimuli 3
Semi‐comatose, responsive only to repeated noxious stimuli 2
Comatose, unresponsive to repeated noxious stimuli 1

Figure 7.1 The modified Glasgow Coma Scale (MGCS).

A recent study examined the MGCS as a predictor of mortality outcome

(death or euthanasia) in over 3500 injured dogs (Ash et al. 2018). The MGCS
showed a good performance for trauma cases as a whole, and particularly for
head trauma cases. A previous study also demonstrated that survival to
48 hours from head trauma was correlated with MGCS on admission, with a
score of 8 approximating a 50% chance of survival (Platt et al. 2001). This
study did not look at survival beyond 48 hours or the quality of life/functional
outcome of animals that did survive. Until further studies are performed, the
MGCS may be better used to monitor clinical progression rather than to accu-
rately guide prognosis; however, animals presenting in a coma with unre-
sponsive pupils have a guarded prognosis. Limitations of the MGCS that need
to be considered are that it remains a subjective scoring system that is ordinal
and not linear. This means that a change in score from one point to another
should not be interpreted as an equal change in underlying pathology. It is
also important to consider the influence of injuries to other body systems.
Limb or spinal injuries may greatly influence the motor score, and ocular
injuries may result in a ‘falsely’ decreased score for brainstem reflexes as they
 Chapter 7 Neurological Emergencies 339

can interfere with accurate assessment of pupil size (e.g. miosis as a result of
traumatic uveitis).

b. Animal trauma triage (ATT) score

In contrast to the MGCS, this scoring system focuses on a broader, systemic
assessment, with six categories being scored from 0 (normal or slight injury) to
3 (severe injury): perfusion, cardiac, respiratory, eye/muscle/skin, skeletal, neu-
rological. In the same multi‐centre study that looked at the MGCS in over 3500
dogs following trauma, the ATT score showed a linear relationship with mortal-
ity risk (Ash et al. 2018). When assessment was restricted to the 341 dogs with
head injury, the ATT score out‐performed the MGCS as a predictor of mortality
(death or euthanasia). This may be related to the fact that it provides a more
global assessment of the animal, which will reflect the systemic abnormalities
that both exacerbate secondary brain injury and could influence the decision for
euthanasia in the veterinary setting. A refined ATT score focusing only on perfu-
sion, respiratory, and neurological categories still provided a good objective pre-
dictor of mortality risk in this study.

4. Management of increased intracranial pressure

If there is a concern from the neurological assessment regarding persistently
increased ICP in spite of systemic stabilisation, then further management is
required to reduce the ICP. This most commonly involves the administration of
hyperosmolar agents, such as mannitol or hypertonic saline. The theory behind

Box 7.2 The Cushing Reflex

If the ICP rises to the point at which cerebral perfusion is compromised, then elevated
pa(CO2) levels will trigger a reflex increase in arterial blood pressure in an attempt to
maintain cerebral perfusion. This increase in MABP (often in the region of
>160–180 mmHg) triggers a baroreceptor reflex, with resultant marked bradycardia
(e.g. 40–60 beats per minute). This combination of systemic hypertension and brady-
cardia is known as the cerebral ischaemic response or ‘Cushing reflex’. This reflex will
only be seen in animals with significant ICP elevation and will therefore always be
accompanied by other indicators of elevated ICP (e.g. reduced level of mentation,
recumbency, pupil abnormalities, loss of gag reflex). A dog that is bright and alert,
walking normally, and has a normal cranial nerve examination should not immediately
be assumed to have a Cushing reflex if the blood pressure is elevated and the heart rate
is lower than expected. Other possible causes for this combination of parameters, such
as the effects of previously administered medications (e.g. opiates, dexmedetomidine),
should be considered in these cases. Management of animals with a high suspicion of a
true Cushing reflex should focus on aggressive management of elevated ICP. The use of
agents to increase the heart rate (e.g. atropine or glycopyrrolate) is not recommended
as the bradycardia is protective and should normalise once the ICP is reduced by other
means.
340 A Practical Approach to Neurology for the Small Animal Practitioner

the use of these fluids is to increase the osmotic gradient across the blood–brain
barrier and shift water from the interstitial space into the intravascular space,
thus reducing cerebral oedema and the ICP. An increase in the circulating fluid
volume will also decrease the blood viscosity, which improves cerebral perfusion
and oxygen delivery. This decrease in viscosity also triggers cerebral vasocon-
striction, resulting in a reduced intracranial blood volume and ICP. In euvolae-
mic animals that fail to respond to one of mannitol or hypertonic saline, the use
of the other agent should be considered.

• Mannitol: 0.5–1 g/kg given IV over 15–20 minutes

Mannitol is an osmotic diuretic that can be used to reduce ICP by a combina-
tion of reduced blood viscosity and by drawing extracellular fluid from nor-
mal and damaged brain tissue into the peripheral circulation. The reduction
in blood viscosity persists for approximately 75 minutes, and the altered
osmotic gradient across the blood–brain barrier lasts approximately 5–8 hours.
The diuretic effect of mannitol is a concern in hypotensive animals and its use
should be reserved for animals that are clinically deteriorating in spite of vol-
ume resuscitation. In animals that are in hypovolaemic shock, such as at the
time of initial presentation, hypertonic saline is a more appropriate fluid
choice. The concurrent administration of furosemide and mannitol is not
currently recommended given the risk of further worsening hypovolaemia.
Previous concerns regarding the use of mannitol in animals with suspected
cerebral haemorrhage have not been supported by good clinical evidence and
should not influence the decision to use this agent. The benefits of mannitol
often outweigh the potential risks in animals with elevated ICP; however,
these risks include exacerbation of hypovolaemia, electrolyte abnormalities
(hyponatraemia, hypochloraemia, hyperkalaemia), acidosis, renal compro-
mise, volume overload, and pulmonary oedema. It is essential that mannitol
administration is followed by appropriate rates of isotonic crystalloids to
avoid dehydration.
• Hypertonic saline: 4 ml/kg of 7.5% solution given IV over 3–5 minutes
As previously discussed, hypertonic saline is a useful first‐line fluid for the
restoration of circulating fluid volume following trauma. This expansion of
plasma volume increases the MABP, decreases blood viscosity, and improves
cerebral perfusion and oxygen delivery. The intact blood–brain barrier is rela-
tively impermeable to sodium and chloride, and water will follow the higher
intravascular concentrations of these ions down an osmotic gradient away
from the interstitial and intracellular spaces. This results in a decreased brain
water content and a reduced ICP. Other suggested benefits of hypertonic
saline include reduction in cerebrovascular endothelial oedema that improves
CBF, and immunomodulatory effects that decrease brain excitotoxicity by
promoting glutamate re‐uptake. The use of hypertonic saline should be
avoided in cases with systemic dehydration, hypernatraemia, or chronic
 Chapter 7 Neurological Emergencies 341

hyponatraemia. It is also essential that administration is followed by appro-

priate rates of isotonic crystalloids to avoid dehydration.

5. Analgesia and sedation

The provision of analgesia is vital for any animal following trauma, and this is
particularly relevant in head trauma as pain and anxiety may increase the ICP.
Opiates are the most commonly used analgesics in critically ill cases (e.g. metha-
done 0.1–0.3 mg/kg every 4–6 hours, butorphanol 0.1–0.3 mg/kg every 1–2 hours).
The dose should be carefully titrated to achieve adequate analgesia whilst avoid-
ing hypotension and respiratory depression. If available, short‐acting agents such
as fentanyl can be very effective when given as constant rate infusions (fentanyl
2–6 μg/kg/hour). The use of non‐steroidal anti‐inflammatory drugs (NSAIDs)
should ideally be delayed until euvolaemia is established and renal perfusion is
not compromised.
Sedatives, such as midazolam, are widely used in human medicine following
severe head trauma, with the aim of maintaining a normal ICP by reducing the
cerebral metabolic rate. They can also be useful adjuncts to opiates by providing
anxiolysis with minimal cardiovascular and respiratory effects. However, neuro-
logical status becomes more difficult to interpret as the level of sedation increases.
This complicates the monitoring of clinical progression and response to treat-
ment in heavily sedated patients. Clinical decision‐making in human medicine
relies heavily upon direct ICP monitoring. The high cost of this equipment cur-
rently limits its widespread use in veterinary medicine, thus complicating the
routine use of many sedative protocols; however, direct ICP monitoring in ani-
mals may become more common in the future.
The role of ketamine and alpha‐2 agonists to provide sedation, anxiolysis,
and/or analgesia in dogs and cats with head trauma remains uncertain, with
mixed evidence for their potential benefit in human medicine. Until further
studies are performed, the use of these agents should be avoided unless other
sedatives or analgesics with fewer potential adverse effects are not available.

6. Supportive care and nutrition

Dogs and cats may be recumbent following head trauma and require intensive
nursing to avoid further complications such as aspiration pneumonia, decubital
ulcers, and corneal ulcers. Nursing considerations should include:

• Frequent turning and the provision of soft, clean, dry bedding.

• Physiotherapy to maintain joint mobility and avoid contractures.
• Placement of a urinary catheter to allow monitoring of fluid ‘ins‐and‐outs’
and to relieve anxiety or discomfort that could be associated with a need to
urinate. Intermittent catheterisation or manual bladder expression can also be
performed to reduce the risk of urinary tract infections associated with the
prolonged use of indwelling catheters.
342 A Practical Approach to Neurology for the Small Animal Practitioner

• Gastric ulcer prophylaxis to reduce the incidence of stress ulceration and gas-
tric bleeding that has been associated with TBI in humans (e.g. omeprazole,
famotidine, sucralfate).
• Maintenance of a normal body temperature (37–38.5 °C) to avoid increases in
cerebral metabolic rate and ICP associated with hyperthermia.
• Nutrition and maintenance of normoglycaemia – early nutritional support is
essential to maintain gastrointestinal health and to manage the trauma‐
induced hypermetabolic state. If an animal cannot protect their airway to
allow enteral feeding, then a feeding tube can be placed to allow early feeding.
Nasogastric tube placement has the advantage of not requiring anaesthesia
but should be placed carefully to avoid sneezing, coughing, or gagging that
may increase ICP. Animals should be systemically stable before being anaes-
thetised for the surgical placement of oesophagostomy feeding tubes. This is to
avoid exacerbation of secondary injury associated with the influence of anaes-
thetic agents on blood pressure and ICP, with inhalational agents contraindi-
cated in animals with increased ICP. Total intravenous anaesthesia, using
agents such as propofol, can be performed in these cases; however, careful
dosing and monitoring is still required to avoid hypotension and hypoventila-
tion. Medications that promote gastric motility, such as metoclopramide, may
be useful to manage the delayed gastric emptying that can be seen in trauma
cases, thereby improving tolerance of enteral feeding and reducing the risk of
aspiration pneumonia.

7.1.3 The Role of Corticosteroids in Head Trauma

A large randomised, placebo‐controlled trial of intravenous corticosteroid
administration to humans with TBI demonstrated an increased mortality in the
corticosteroid group (Edwards et al. 2005). It is now widely accepted that the use
of corticosteroids, particularly high intravenous doses of methylprednisolone
sodium succinate (MPSS), is contraindicated in the management of head trauma
in humans and animals.

7.1.4 Diagnostic Imaging

Diagnostic imaging in head trauma cases should initially focus on the identifica-
tion of polytrauma and any injuries that may require urgent attention. As previ-
ously discussed, thoracic and abdominal radiography, TFAST and AFAST, or
whole‐body CT can be performed in the conscious animal, or under the influ-
ence of light sedation once normovolaemia and adequate oxygenation/ventila-
tion have been established. Spinal radiographs can be taken to assess for injuries
that may influence both the safe handling of the patient and interpretation of
the neurological examination. It is not uncommon for patients with head trauma
to have concurrent spinal injuries (e.g. cervical fractures), therefore all patients
with known trauma should be handled with care and ideally not sedated until
the presence of an unstable spinal injury is excluded. Radiography of the skull
 Chapter 7 Neurological Emergencies 343

can be useful to assess for mandibular fractures that may require further treat-
ment but is of limited value in the recognition of fractures involving other bones
of the skull or in the assessment of intracranial structures.
Advanced imaging of the head can be performed to identify skull fractures
and regions of haemorrhage and to assess the brain parenchyma itself. Computed
tomography (CT) is the initial modality of choice as it is faster and lower in cost
compared to magnetic resonance imaging (MRI), and does not usually require
general anaesthesia (Figure 7.2). A study evaluating the CT findings in 27 dogs
with head trauma identified cranial vault fractures and/or parenchymal abnor-
malities in 89% of these dogs (Chai et al. 2017). The presence of haemorrhage
and ventricular asymmetry were negatively associated with short‐term (10 days)
and long‐term (>6 months) survival. A study of 50 dogs that had an MRI scan
within 14 days of head trauma (median 1 day) reported a significant association
between the MRI findings (midline shift, parenchymal lesions, brain herniation,
skull fractures) and both the clinical status at presentation (MGCS) and progno-
sis (Beltran et al. 2014). The results of recent studies appear to indicate a poten-
tial role of advanced imaging in guiding the prognosis for dogs and cats with TBI.
However, in light of the fact that surgical management may not be an option for
many owners, and that some animals with significant injury can still go on to
have a good functional outcome, whether the findings of advanced imaging sig-
nificantly influence the management choices in the majority of cases remains
uncertain.

Figure 7.2 Left and right lateral views of a three‐dimensional CT reconstruction of the skull
of a 1‐year‐old terrier dog that was bitten on the head by another dog. There are multiple
skull fractures involving parietal and frontal bones, with impingement of some of the skull
fragments into the cranial vault. These fragments were compressing the olfactory lobes, with
associated parenchymal oedema, intracranial haemorrhage, and secondary frontal lobe shift.
Other injuries observed on the CT scan included fracture of the cribriform plate, traumatic
pneumocephalus, bilateral frontal sinus fractures with associated sinusitis/haemorrhage,
bilateral comminuted nasal fractures with associated bleeding within the nasal cavities, and
complete, transverse, mildly displaced fractures of the rami of both mandibles.
344 A Practical Approach to Neurology for the Small Animal Practitioner

7.1.5 Prognosis
The reported mortality rate in dogs following head trauma is around 20%. Poor
prognostic indicators reported in the literature include a higher ATT score,
decreased MGCS (<11), poor perfusion, and the need for intubation or hyper-
tonic saline administration (Sharma and Holowaychuk 2015). As previously dis-
cussed, the findings of both CT and MRI have also been suggested to guide
prognosis in dogs with TBI (Beltran et al. 2014; Chai et al. 2017; Yanai et al.
2015).
In summary, the management of animals presenting with head trauma
should focus on initial triage for life‐threatening injuries, systemic stabilisation,
and frequent monitoring of neurological status. Rapid recognition of those ani-
mals that are not responding to normalisation of vital parameters allows for the
instigation of further treatments in an attempt to reduce the ICP. A treatment
algorithm for head trauma cases can be found in Figure 7.3.

Box 7.3 Hormonal Abnormalities Following Head Trauma

Together with the possibility of acquiring post‐traumatic epilepsy, hypothalamic–ante-

rior pituitary hormone deficiencies have also been reported in dogs following TBI
(Murtagh et al. 2015). This can include decreased IGF‐1, total thyroid hormone, and
basal cortisol concentrations. Therefore, animals should be monitored for clinical signs
that could indicate a hormonal abnormality following head trauma and their owners
warned of these possible sequelae.

Head trauma Start CPR if cardiorespiratory arrest

Intubate if non-responsive, apnoeic or no gag-reflex

ABC of emergency care

Yes 1) Benzodiazepine IV +/– Levetiracetam IV

Treat the seizures 2) Phenobarbitone IV
Is the animal seizuring?
(see section 7.2) 3) Propofol IV
No

Triage for life-threatening

injuries or haemorrhage PaO2 >80 mmHg
Oxygenation (flow-by, face mask)
SpO2 >95%

Systemic stabilisation Ventilation PaCO2 35–40 mmHg

Crystalloid boluses HR, pulse quality

Perfusion – establish IV access
Hypertonic saline Systolic BP >90 mmHg
Serial neurologic
assessments (e.g. MGCS)
Elevate head 30 degrees

Analgesia, nutrition and Suspected elevated intracranial pressure Hypertonic saline

supportive nursing care or deteriorating neurologic status (MGCS <8)
Mannitol

Figure 7.3 A summary of the clinical approach to an animal following head trauma.
 Chapter 7 Neurological Emergencies 345

7.2 ­Status Epilepticus and Acute Repetitive Seizures

Edward Ives

An epileptic seizure is a stressful event for the owner of a dog or cat, particularly
if their animal has no previous history of seizures. They are therefore a common
reason for out‐of‐hours telephone advice calls and emergency appointments.
The majority of epileptic seizures are fortunately self‐limiting and do not require
emergency treatment (further discussion on the approach to seizures can be
found in Chapter 6). In a minority of cases, the seizure activity is not self‐limit-
ing or may recur a short time after the last event. This can have deleterious
effects on the central nervous system (CNS) and other organs, therefore prompt
recognition and treatment of prolonged or recurrent seizure activity is
essential.

7.2.1 What Is Status Epilepticus?

Status epilepticus is the term used to describe a state of continuous seizure activ-
ity that is not self‐limiting. Irreversible neuronal damage may occur after
20–30 minutes and previous definitions of status epilepticus were based upon
this finding. However, this definition has been modified to account for the fact
that emergency management should be instituted as soon as possible, before
irreversible neuronal damage occurs. Status epilepticus is now widely defined as
either:

• continuous seizure activity for longer than 5 minutes

• or two or more seizures over a 30 minute period without recovery of con-
sciousness between.

Acute repetitive seizures (cluster seizures) also represent a neurological

emergency and are defined as the occurrence of two or more isolated seizures
within a 24‐hour period, with a recovery of consciousness between events.

7.2.2 Why Does Status Epilepticus Occur?

An epileptic seizure results from excessive and hypersynchronous neuronal
activity in the cerebral cortex. The pathophysiology underlying why the exces-
sive neuronal activity fails to stop in cases of status epilepticus is incompletely
understood but is likely to depend upon genetic factors and the cause of the
seizure itself. Possible mechanisms may include:

• Failure of inhibition of neuronal excitation resulting from alterations in the

expression, location, or number of receptors for the inhibitory neurotransmit-
ter gamma‐aminobutyric acid (GABA).
346 A Practical Approach to Neurology for the Small Animal Practitioner

• Excessive neuronal excitation mediated by excitatory neurotransmitters such

as glutamate, aspartate, and acetylcholine.

7.2.3 How Common Is Status Epilepticus in Veterinary

Medicine?
Status epilepticus may be the first manifestation of seizure activity in dogs and
cats, particularly following toxin exposure. It is more commonly reported sec-
ondary to structural brain disease and metabolic‐toxic disorders; however, one
study reported that 59% of dogs with idiopathic epilepsy had one or more epi-
sodes of status epilepticus in their lifetime (Saito et al. 2001). This may occur
even if the animal’s epilepsy has been well‐controlled on antiepileptic medica-
tions prior to this event.
Acute repetitive seizures have been reported to affect 38–77% of dogs with
idiopathic epilepsy, with certain breeds (e.g. German Shepherd Dog) and dogs of
a younger age at seizure onset more likely to be affected (Monteiro et al. 2012;
Packer et al. 2016). These dogs may have a reduced likelihood of achieving sei-
zure freedom and a decreased survival time from diagnosis.

7.2.4 Why Is Emergency Treatment of Status Epilepticus

Required?
Similar to the management of TBI, the emergency treatment of status epilep-
ticus is essential to reduce the risk of irreversible neuronal injury and to
manage the severe systemic effects associated with prolonged seizure activ-
ity. In the early stages, increased skeletal muscle activity and autonomic
stimulation leads to a combination of hypertension, tachycardia, hypergly-
caemia, and hyperthermia. As compensatory processes start to fail, and the
body is unable to meet the increased cerebral metabolic demand, death may
result from cardiac arrhythmias, rhabdomyolysis, acute renal tubular necro-
sis, hypoglycaemia, acidosis, hyperkalaemia, hypoxaemia, and hypotension.
Early, aggressive treatment is therefore important and studies in human
medicine have demonstrated that whilst mortality rates are primarily depend-
ent on the underlying cause, they are also influenced by seizure duration
prior to treatment. A mortality rate of 25% was reported in a retrospective
study of 156 dogs with status epilepticus or cluster seizures, with a worse
prognosis if seizure control was lost after 6 hours of hospitalisation (Bateman
and Parent 1999).

7.2.5 Clinical Approach to Status Epilepticus/Acute Repetitive

Seizures
The clinical approach to the management of a dog or cat presenting for status
epilepticus, or with a history of multiple seizures in the preceding 24 hours,
can be divided into the following considerations and is summarised in
Figure 7.4.
 Status epilepticus

100% oxygen by Take a concise clinical history

Seek assistance from other staff members
mask or flow-by (e.g. toxin exposure, trauma)

Intravenous fluid therapy Basic blood profile Correct metabolic

Systemic stabilisation Stop the seizure
(0.9% NaCl 2–10 ml/kg/hr) (e.g. glucose, Ca) cause for seizures

Maintain temperature Anticonvulsant medications

37.5–38.5°C
If seizure
Diazepam 0.5–1 mg/kg IV, 1–2 mg/kg PR persists 2nd bolus of diazepam or midazolam
or Midazolam 0.1–0.3 mg/kg IV, IM or IN >5 mins +/– load levetiracetam (60 mg/kg IV)
When seizure control is achieved:
• Investigate underlying cause If seizure persists >5 mins
• Continue AED maintenance dose
• Supportive care 3rd bolus of diazepam or midazolam +
phenobarbitone bolus (5–10 mg/kg slow IV)

If seizure persists >20 mins

If seizure If seizure
persists persists Repeated phenobarbitone boluses (4–5 mg/kg)
Propofol infusion Propofol bolus to effect
every 20 mins until cessation of seizures or
(0.1–0.6 mg/kg/min IV) (1–4 mg/kg IV)
total dose of 20-24 mg/kg

Figure 7.4 The clinical approach to an animal presenting in status epilepticus.

348 A Practical Approach to Neurology for the Small Animal Practitioner

1. Is this an epileptic seizure?

2. Seek assistance from other staff members
3. Take a concise clinical history
4. Systemic stabilisation
5. Stop the seizure activity
6. Nursing care of a hospitalised animal
7. Identify the underlying cause for the seizure activity
8. Introduce or continue maintenance antiepileptic drug therapy

1. Is this an epileptic seizure?

Owners may report that their pet is having an epileptic seizure when in reality
the event represents an alternative cause for collapse or involuntary motor
activity. Differentiating these ‘seizure mimics’ from a true epileptic seizure is
important to ensure appropriate case management. Potential seizure mimics
include syncope, vestibular disorders, paroxysmal dyskinesias (‘movement dis-
orders’, see Video 10), neuromuscular disease, or neck pain with associated
muscle spasms (see Video 8). Further discussion regarding mimics of epileptic
seizures can be found in Chapters 1 and 6.

2. Seek assistance from other staff members

It is extremely difficult to provide the care required for an animal in status epi-
lepticus without assistance. The placement of intravenous catheters, blood sam-
pling, and provision of oxygen ideally requires at least two trained members of
staff and is further complicated by the continuous muscle activity and limb
movements associated with on‐going seizure activity. The exact time at either
the onset of seizure activity (if observed) or when treatment was started should
be recorded to assist in the planning and timing of interventions.

3. Take a concise clinical history

During the initial assessment and stabilisation, another veterinarian or nurse
should take a concise clinical history from the owner. This is important as it may
guide possible differential diagnoses and the choice of appropriate medications
and drug doses. Questions should focus on:

• known or suspected toxin exposure (e.g. metaldehyde in slug pellets, myco-

toxins in mouldy food, topical application of permethrin in cats)
• the current seizure history – onset, duration, and appearance
• previous diagnoses of a seizure disorder (e.g. idiopathic epilepsy, meningoen-
cephalitis, intracranial neoplasia)
• concurrent medical conditions (e.g. diabetes mellitus, hepatic disease)
• current medications and doses, including both antiepileptic medications and
other medications (e.g. insulin, antibiotics, parasiticides)
• any medications administered in the last 24 hours (e.g. rectal Diazepam prior
to presentation).
 Chapter 7 Neurological Emergencies 349

4. Systemic stabilisation
The approach to systemic stabilisation of animals in status epilepticus is very
similar to that described for head trauma and should start with assessment of the
airway, breathing, and circulation. A face mask can be used to administer 100%
oxygen and intravenous access should be acquired as soon as possible to allow
for drug administration and fluid therapy. The following parameters should be
recorded and monitored, with the aim of maintaining parameters within the
normal range (e.g. Sp(O2) > 95%, pa(O2) > 80 mmHg, MABP 80–100 mmHg):

• heart rate, pulse quality, mucous membrane colour, capillary refill time
• respiratory rate and effort
• Sp(O2) by pulse oximetry
• systolic blood pressure
• cardiac rhythm by electrocardiography.

Hyperthermia is a common consequence of prolonged seizure activity. The

temperature should therefore be monitored, and passive cooling started if the
temperature exceeds 39.5 °C (aiming for 37.5–38.5 °C).
Intravenous fluid therapy is essential to manage the systemic effects of sei-
zure activity and to optimise cerebral blood flow (CBF). Isotonic crystalloids,
such as 0.9% sodium chloride, can be started at 2–10 ml/kg/hour or be given as
intravenous boluses of 10–15 ml/kg, with the aim of restoring and maintaining
an adequate arterial blood pressure (MABP 80–100 mmHg).

5. Stop the seizure activity

At the same time as systemic stabilisation, the priority of treatment should be to
stop any on‐going seizure activity. This may be achieved by:

a. either correcting an underlying metabolic cause for the seizure activity

b. or administration of anticonvulsant medications.

a. Correcting a metabolic cause for seizure activity

Rectifying a metabolic derangement, if present, will often be the most rapid and
effective way of stopping any associated seizure activity. A baseline blood sample
should always be taken at the time of presentation and can usually be achieved
when the intravenous catheter is placed. A minimum database should comprise
a PCV, total solids, urea, calcium, glucose, and electrolytes (sodium, chloride,
and potassium). Serum ammonia can also be useful in cases with suspected
hepatic dysfunction (e.g. congenital portosystemic shunt). Surplus blood can be
collected for additional testing after emergency management, such as serum bile
acids or antiepileptic drug serum levels if the dog is already receiving treatment
(e.g. phenobarbitone or potassium bromide).
The two most common metabolic abnormalities that can result in acute sei-
zure activity are hypocalcaemia (e.g. post‐partum eclampsia, hypoparathy-
350 A Practical Approach to Neurology for the Small Animal Practitioner

roidism) and hypoglycaemia (e.g. insulin overdose, insulinoma, xylitol toxicity).

The clinical history may raise the index of suspicion for these conditions and
confirming normoglycaemia, at a minimum, is vital before focusing on anticon-
vulsant therapy.

i. Hypoglycaemia
Seizure activity may occur at serum levels <2–2.5 mmol/l.
Correction: A bolus of 0.5–1 ml/kg 50% glucose solution should be adminis-
tered by intravenous injection. Dilution with an equal volume of saline is rec-
ommended to reduce the risk of phlebitis associated with this hyperosmolar
solution. This can be followed by a 5% dextrose solution to meet the mainte-
nance fluid and glucose requirements.

ii. Hypocalcaemia
Dependent on ionised calcium levels, neurological signs such as muscle tremors/
fasciculations, cramping, pain, facial pruritus, and seizures may be observed at
serum total calcium levels <1.9 mmol/l.
Correction: A bolus of 1 ml/kg 10% calcium gluconate solution should be
administered by intravenous injection over 20 minutes. Care should be taken
regarding perivascular injection as tissue necrosis and skin sloughing can occur.
It is important to monitor the heart rate and rhythm during administration
for possible bradycardia.

b. Administration of anticonvulsant medications

i. Acute repetitive seizures
If an animal presents with a history of two or more generalised seizures over the
last 24 hours but has recovered by the time of presentation, then the emergency
administration of anticonvulsant medications may not be required. It remains
important to take a detailed clinical history, determine whether the previous
events are likely to have represented epileptic seizures, and ensure that systemic
parameters are stable. An intravenous catheter should be placed as soon as pos-
sible to allow for the prompt administration of medications in the event of fur-
ther seizures. A blood sample should also be taken to investigate possible
extra‐cranial causes for the previous events. If there is a recurrence of seizure
activity during the hospitalisation period, then the approach described below for
status epilepticus should be followed.
If no apparent cause for the acute repetitive seizures is identified from the
clinical history and blood tests, then the option of referring the animal for fur-
ther investigations should be discussed with the owner. Toxin exposure is a com-
mon cause for status epilepticus but would be less likely to result in multiple
isolated seizures with full recovery between, unless there is repeat exposure
over a short period of time. In animals receiving treatment for previously diag-
nosed idiopathic epilepsy, blood should also be taken to determine the current
 Chapter 7 Neurological Emergencies 351

serum drug levels. Consideration can then be given as to whether the dose(s)
need to be increased, or whether an additional maintenance drug should be
started.
Some dogs with idiopathic epilepsy may show a tendency for recurrent clus-
ters of acute repetitive seizures, separated by a normal inter‐ictal period. The use
of levetiracetam as a pulse therapy, in addition to other maintenance drugs, has
been suggested in these cases, with the aim of reducing the total number of sei-
zures in each cluster:
• 60 mg/kg single oral loading dose of levetiracetam after recovery from the first
observed seizure, followed by 20–30 mg/kg every 8 hours for 2–3 days.

ii. Status epilepticus

There is a lack consensus regarding the optimal protocol for the medical man-
agement of status epilepticus in both humans and veterinary medicine. It is
unlikely that a single protocol would be appropriate for all patients, given differ-
ences in underlying seizure aetiology, the potential influence of concurrent
medical conditions (e.g. hepatic or renal dysfunction), and the variability in
whether a patient is already receiving antiepileptic medications. The use of elec-
troencephalography (EEG) to record cerebrocortical neuronal activity is com-
mon for therapeutic decision‐making in human medicine, such as when weaning
or introducing agents used for seizure control. The use of EEG in veterinary
medicine is currently limited to specialist centres and defined therapeutic end
points remain controversial in human medicine, particularly in relation to
patient outcome.

First‐line drugs:

• Diazepam
• Midazolam

Most protocols involve the first‐line administration of a lipophilic anticon-

vulsant medication to rapidly cross the blood–brain barrier and stop seizure
activity. The most frequently used drugs in veterinary medicine are the benzodi-
azepines diazepam and midazolam. If intravenous access is not available, then
they may be administered by intramuscular injection, intranasal, or per rectum
dependent on the medication.
Diazepam can be administered by intravenous injection (0.5–1 mg/kg) or by
the per rectum or intranasal routes (1–2 mg/kg). Intramuscular injection results
in local tissue irritation and should be avoided.
Midazolam can be administered by the intravenous, intramuscular, or intra-
nasal routes (0.1–0.3 mg/kg). Midazolam results in less CNS and respiratory
depression compared to diazepam, and a recent study demonstrated superior
efficacy of intranasal midazolam (administered using a mucosal atomisation
352 A Practical Approach to Neurology for the Small Animal Practitioner

device) when compared to rectal diazepam for the management of status epilep-
ticus in dogs (Charalambous et al. 2017).
Repeated bolus administration of benzodiazepines may result in drug accu-
mulation within the CNS and the potential for detrimental cardiorespiratory
depression. An interval of 3–5 minutes is recommended between boluses to give
time for the medication to achieve adequate CNS concentrations. This avoids the
potential for unnecessary repeated administration. If there is continuous seizure
activity (or rapid seizure recurrence) following the use of two or three benzodi-
azepine boluses, then it is important that further seizures are not managed with
repeated boluses of benzodiazepines alone. Administration of an antiepileptic
medication with a longer half‐life, that can also be used as daily maintenance
therapy, should always be introduced at this time to improve seizure control.

Second‐line drugs:

• Levetiracetam
• Phenobarbitone

Levetiracetam is a novel anticonvulsant medication that is not currently

licensed for use in dogs or cats. The primary anticonvulsant effect is thought to
result from binding to the synaptic vesicle protein 2A (SVP2A), resulting in
decreased release of glutamate from the pre‐synaptic membrane. Multiple other
mechanisms of action have also been suggested, and the fact that these differ to
those of benzodiazepines and barbiturates make it an attractive choice in the
emergency management of prolonged or recurrent seizures. Levetiracetam may
also have both neuroprotective properties and influence the complex process of
seizure generation (epileptogenesis), reducing the likelihood of further seizures
developing.
Levetiracetam can be administered by the intravenous, subcutaneous, intra-
muscular, oral, or rectal routes. It has minimal hepatic metabolism, few reported
adverse effects, and shows minimal interaction with other medications. The
minimal hepatic metabolism means that its use should be considered in animals
with known or suspected hepatic dysfunction. The availability and high cost of
the intravenous formulation may limit its use in general practice; however, it
appears to be a safe and potentially effective second‐line agent for status epilep-
ticus. A randomised, double‐masked, placebo‐controlled prospective study of 19
dogs with status epilepticus or acute repetitive seizures demonstrated that dogs
receiving intravenous levetiracetam after a single dose of diazepam required sig-
nificantly fewer further boluses of diazepam compared to those receiving pla-
cebo (Hardy et al. 2012). A greater proportion of dogs receiving levetiracetam
(56%) compared to placebo (10%) showed no further seizure activity but this
did not reach statistical significance. A recent case report described a fatal adverse
event following the rapid intravenous administration of undiluted levetiracetam
 Chapter 7 Neurological Emergencies 353

(60 mg/kg) to a dog (Biddick et al. 2018). It is therefore advised to dilute the
solution 1 : 10 with saline and to administer by slow intravenous injection.
A suggested protocol for the use of levetiracetam in the emergency manage-
ment of status epilepticus is as follows:

• 60 mg/kg single intravenous dose if seizure activity persists for >5 minutes
after a single bolus of diazepam or midazolam
• followed by 20–30 mg/kg IV or per os every 8 hours.

Phenobarbitone is a barbiturate that acts at a different binding site on the

GABA‐A receptor to benzodiazepines. It is widely used in veterinary medicine
for the emergency management of seizures that are not responding to benzodi-
azepines alone. It can be administered by the intravenous or intramuscular
routes, with higher ‘loading’ doses used to more rapidly achieve therapeutic
serum concentrations. The majority of intravenous formulations require dilut-
ing 1 : 10 with saline and should be administered by slow intravenous injection.
Phenobarbitone takes 20–30 minutes to distribute to the brain following admin-
istration and animals should be monitored closely for hypotension and cardi-
orespiratory depression following intravenous injection, particularly after
concurrent benzodiazepine administration. Intravenous fluid therapy and the
provision of intubation and ventilation should therefore be available.
The following protocol can be used for animals that have not responded to
the administration of benzodiazepines +/− levetiracetam:

• 5–10 mg/kg intravenous bolus if seizure activity persists for >5 minutes after a
single bolus of benzodiazepine
• repeated 4–5 mg/kg intravenous boluses every 20 minutes until cessation of
seizure activity is observed, or a total dose of 20–24 mg/kg is reached
• continue as a maintenance therapy at 2–3 mg/kg IV or per os every 12 hours.

The total loading dose may also be calculated in dogs not currently receiving
phenobarbitone according to the following formula, with a target serum concen-
tration of 25 μg/ml being a reasonable goal:

loading dose(mg) body weight (kg) 0.8 target serum concentration ( g / ml)

Third‐line drugs:

• Propofol
• Other agents with a potential role in the control of persistent seizure activity

If seizures persist following two or three boluses of diazepam/mida-

zolam, levetiracetam administration (if available), and intravenous loading of
354 A Practical Approach to Neurology for the Small Animal Practitioner

phenobarbitone, then it can be assumed that the animal has been in a state of
continuous seizure activity for at least 25–30 minutes. Treatment options at this
stage include use of a benzodiazepine constant rate infusion (e.g. midazolam at
0.2 mg/kg/hour) or introduction of a new agent, with propofol being the most
widely used in veterinary medicine.
Propofol is an alkylphenol that has multiple potential anticonvulsant mecha-
nisms, including acting as a GABA‐A agonist, modulation of calcium channels,
and inhibition of excitatory glutamate receptors. In animals that are not respond-
ing to the protocols described above, or for which phenobarbitone use is con-
traindicated, then the following dosing schedule can be considered:

• 1–4 mg/kg intravenous bolus to effect

• followed by a constant rate infusion of 0.1–0.6 mg/kg/minute for a minimum
of 6–24 hours.
• If seizures are subsequently controlled, then the dose should be tapered by
25% every 6 hours, unless EEG is available to monitor for epileptiform
activity.

Propofol formulations that do not contain the preservative benzoyl alcohol

should be used for constant rate infusions, and Heinz body formation can com-
plicate the use of propofol infusions in cats. Vital parameters should be con-
stantly monitored, with provision for intubation and ventilation available at all
times. All animals should receive oxygen by flow‐by or face mask if not intu-
bated, together with regular monitoring of heart rate, pulse quality, respiratory
rate and effort, pulse oximetry, temperature, and blood pressure. Corneal lubri-
cation should be provided regularly, and animals should be turned every
1–2 hours if unable to do so themselves.
During recovery from a seizure, and particularly following propofol adminis-
tration, tonicity or movements such as paddling can be observed that are diffi-
cult to distinguish from a recurrence of seizure activity. This may result in the
inappropriate administration of medications to an animal that would have oth-
erwise continued to recover. These movements will often lack the sustained
tonicity and involuntary, rhythmic nature of a true seizure recurrence.
If status epilepticus is refractory to benzodiazepines, phenobarbitone, leveti-
racetam, and propofol, then the prognosis is unfortunately likely to be poor. The
evidence to support the use of other agents is currently lacking in veterinary
medicine but further options could include the following.

• Inhalational anaesthetic agents (e.g. isoflurane, sevoflurane)

The use of inhalational anaesthetic agents is reserved for refractory status
epilepticus in humans and, until further evidence is available, the same
should apply for veterinary medicine. Exacerbation of ICP elevation and the
hypotensive effects of these agents are significant concerns. Isoflurane may
 Chapter 7 Neurological Emergencies 355

be preferred over sevoflurane, as the latter undergoes greater metabolism,

increasing the risk of organ damage and resulting in the production of epilep-
togenic metabolites. The prolonged use of inhalational anaesthesia in human
patients with refractory status epilepticus (e.g. over 7 days) is unlikely to be
feasible in veterinary medicine.
• Ketamine
Ketamine is a glutamate receptor antagonist with conflicting evidence regard-
ing its use for refractory status epilepticus in humans. It has been shown to
have neuroprotective effects in rodent models of status epilepticus and may
assist in suppression of epileptiform activity on EEG. However, concerns
regarding its use include exacerbation of elevated ICP and the potential to
cause neuronal damage and cerebral atrophy in humans. A single case report
in veterinary medicine described the use of two intravenous boluses of keta-
mine (5 mg/kg), followed by a constant rate infusion (5 mg/kg/hour) in a dog
with inflammatory brain disease and seizures that were inadequately con-
trolled with diazepam, phenobarbitone, and propofol (Serrano et al. 2006).
The dog survived to discharge but was subsequently euthanised due to persis-
tent neurological deficits. No evidence of NMDA‐antagonist neurotoxicity
was observed at post‐mortem in this case.
• Dexmedetomidine
The use of dexmedetomidine as a possible anticonvulsant medication is
mainly limited to experimental models and a single conference presentation
describing its use as an adjunctive medication in the management of status
epilepticus in dogs. The evidence to support its use is currently weak and the
potential anticonvulsant effects are likely to be dependent on the species and
dose used. Epileptic seizures have also been described in a neonatal child fol-
lowing the administration of dexmedetomidine, suspected to be related to
reduction in the anticonvulsant activity of neurons located in the locus coer-
uleus (Kubota et al. 2013). The routine use of dexmedetomidine in the man-
agement of status epilepticus in dogs and cats is currently not recommended;
however, intramuscular administration could be considered to assist with
intravenous catheter placement in animals with severe involuntary motor
activity, or for the management of severe tremors without loss of conscious-
ness (e.g. tremorgenic mycotoxicosis).
• Imepitoin
The use of imepitoin is not currently recommended in the management of
acute repetitive seizures or status epilepticus. Animals that are already receiv-
ing the medication as maintenance therapy should be continued on the cur-
rent dosing regime, if oral administration is possible.
• Potassium bromide
The limited availability of intravenous formulations of potassium bromide
restricts its use for the emergency management of seizures. Potassium
356 A Practical Approach to Neurology for the Small Animal Practitioner

­ romide undergoes renal excretion and can therefore be a useful drug in

b
dogs with hepatic dysfunction. It should be used with caution in dogs with
renal disease and should not be used in cats due to the potential to cause
severe bronchial inflammation. The long half‐life of potassium bromide
means that loading is required to more rapidly achieve therapeutic serum
concentrations. This can be performed per rectum (100 mg/kg every 6 hours
for 24 hours) if oral loading is not possible.

6. Nursing care of a hospitalised animal

The nursing care and monitoring required during and after the emergency man-
agement of seizures will depend upon the degree of neurological compromise,
the systemic stability of the animal, and the requirement for continued use of
sedative or anaesthetic medications to control seizure activity. Intensive care
may be required in many cases and this can be costly for the owner, involving
24‐hour nursing of an animal that is not fit for transport to a dedicated referral
centre or out‐of‐hours provider.
The following factors should be considered in all cases:

• Provision of clean, soft, dry bedding and turning every 2–4 hours.
• Ocular lubrication to avoid corneal ulceration, particularly in deeply sedated
or anaesthetised animals.
• Intermittent bladder expression or placement of an in‐dwelling urinary
catheter.
• Frequent monitoring of heart rate, pulse quality, mucous membrane colour,
capillary refill time, respiratory rate and pattern, body temperature, pulse oxi-
metry, blood pressure +/− end‐tidal CO2 for intubated animals.
• Monitoring of blood glucose and electrolytes, with supplementation of intra-
venous fluid therapy as required.
• Nutritional support for anorexic patients, with consideration regarding the
increased risk of aspiration pneumonia in recumbent or sedated animals that
cannot protect their airway.
• Provision of analgesia if there is a concurrent painful condition, or if the ani-
mal appears in discomfort.
• Frequent neurological assessment, particularly in animals with an unidenti-
fied cause for seizure activity. An objective scoring system such as the MGCS
can be used to assist in monitoring of trends and allow prompt recognition of
a deterioration in clinical status.

7. Identify the underlying cause for the seizure activity

The decision to perform further investigations should be made once an animal is
stable and the seizure activity is well‐controlled. This will depend on the clinical
history and owner factors. The underlying cause will already be known, or
highly suspected, in animals with a history of head trauma, observed toxin
 Chapter 7 Neurological Emergencies 357

exposure, or a consistent metabolic abnormality on blood testing. An underlying

structural cause for status epilepticus or acute repetitive seizures should always
be considered if there are persistent neurological deficits beyond the post‐ictal
period, even in animals with a prior history of idiopathic epilepsy. Further diag-
nostic investigations should be recommended in these cases, which will usually
involve referral to a specialist centre for MRI of the brain and cerebrospinal fluid
analysis (see Chapter 6).
If referral is not an option following careful discussion with the owner, then
maintenance antiepileptic drug therapy should be started or continued. The
most appropriate diagnostic investigations to perform in general practice will be
dependent on the clinical history and signalment of the animal:

• A portosystemic shunt may be suspected in a 6‐month‐old Yorkshire Terrier

with a history of seizures, lethargy after eating, stunted growth, and gastroin-
testinal signs. Bile acid stimulation testing, serum ammonia, and abdominal
ultrasound would be most appropriate in this case.
• Inflammatory brain disease (e.g. meningoencephalitis of unknown origin)
may be suspected in a young or middle aged, small breed dog (e.g. Chihuahua
or Pug) with persistent inter‐ictal neurological deficits that are consistent with
a multifocal intracranial, or forebrain, neuroanatomic localisation. If referral is
not an option and the animal is deteriorating clinically, then a trial of immu-
nosuppressive prednisolone (1 mg/kg twice daily) could be considered. This
should only follow discussion with the owner regarding the clinical suspicion,
and the risks and limitations of this approach if there is a different underlying
cause.
• Intracranial neoplasia would be highly suspected in an older large breed dog (e.g.
Boxer) that presents in status epilepticus or shows an acute onset of frequent
generalised seizures, particularly if asymmetric inter‐ictal neurological deficits are
identified. If referral is not an option, then palliative medical management using
a maintenance antiepileptic medication and an anti‐inflammatory dose of predni-
solone (0.5 mg/kg once daily) could be considered in this case.
• Idiopathic epilepsy would be the most likely diagnosis in a 2‐year‐old Labrador
Retriever or Border Collie that has no history of toxin exposure, has a normal
inter‐ictal neurological examination, and normal haematology and serum bio-
chemistry. Close monitoring of clinical progression and use of a maintenance
antiepileptic drug alone would not be inappropriate in this instance. An alter-
native diagnosis should always be investigated if the subsequent clinical course
is inconsistent with a diagnosis of idiopathic epilepsy, particularly the appear-
ance of inter‐ictal neurological deficits.

8. Introduce or continue maintenance antiepileptic drug therapy

Oral maintenance antiepileptic drug therapy should be started/continued in all
animals presenting for acute repetitive seizures or status epilepticus until a
358 A Practical Approach to Neurology for the Small Animal Practitioner

definitive cause for the seizure activity is identified. The decision can then be
made as to whether long‐term medical management is required. This may not
be required in animals for which an identified metabolic abnormality has been
corrected (e.g. hypoglycaemia), or if there was a known history of toxin expo-
sure. A retrospective study on 20 dogs with prolonged status epilepticus second-
ary to intoxication (13/20 dogs having a seizure duration longer than 12 hours),
reported that no dogs had further seizures and suggested that long‐term treat-
ment might not be needed after short‐term control of status epilepticus (Jull
et al. 2011).

7.3 ­Acute Spinal Cord Injury

Paul M. Freeman

7.3.1 Causes of Spinal Cord Injury

There are many potential causes of significant spinal cord injury, including vas-
cular disorders (e.g. fibrocartilaginous embolism), sterile inflammatory disorders
(e.g. meningomyelitis of unknown origin), infectious disease (e.g. spinal empy-
ema), injury associated with congenital anomalies (e.g. atlantoaxial instability),
acute intervertebral disc extrusion, or even acute deterioration of chronic
intervertebral disc protrusion. The diagnostic approach and management of
these conditions has already been discussed in Chapter 6, and this chapter there-
fore focuses primarily on acute spinal cord injury that may result from vertebral
fracture and/or luxation. However, it should be remembered that any animal
presenting with an acute onset of severe paraparesis/paraplegia, or severe tetra-
paresis/tetraplegia, should be considered as a potential neurological emergency.
Although this section is concerned largely with traumatic spinal cord injury,
mention will be made of other conditions when appropriate, and the guidelines
for patient evaluation and management are applicable whatever the cause of
spinal cord injury.

7.3.2 Pathophysiology of Acute Spinal Cord Injury

The spinal cord may be injured in a variety of ways, and several different mecha-
nisms may be involved in the same case.
Contusion: Contusion or bruising of the spinal cord is caused by direct impact
leading to rupture of the microvasculature. This can be through intrinsic trauma,
such as from the explosive extrusion of an intervertebral disc, through to external
impact such as in a road traffic accident. Contusion causes release of local inflam-
matory mediators, cytotoxic substances, and excitatory neurotransmitters that
induce a chain of secondary events leading to ischaemia and energy depletion
 Chapter 7 Neurological Emergencies 359

within cells. This in turn can lead to the development of cytotoxic oedema due to
a failure of the energy‐dependent sodium channels in the neuronal cell walls,
accumulation of intracellular sodium ions, and subsequent swelling of cells. This
is a pre‐morbid process, ultimately ending in cell necrosis and apoptosis which
may continue for several days.
Compression: Acute spinal cord compression may be caused by herniated
intervertebral disc material, haemorrhage, or by an unstable vertebral fracture/
luxation. The spinal cord is able to tolerate a high degree of compression, espe-
cially if it occurs slowly, but acute compression is less well tolerated and may be
a further cause of contusion through crushing of microvasculature. In addition,
compression may impede blood flow to the spinal cord parenchyma and further
increase the ischaemia which results from severe contusion. Compression can
mechanically disrupt and distort axons, myelin sheaths, and neuronal cell bod-
ies; if severe enough, this too may lead to irreversible cellular changes and cell
death. Chronic compression leads to demyelination and axonal loss, and this
should also be considered when planning treatment following vertebral fracture
or luxation.
Laceration: Physical disruption of spinal cord tissue is most commonly caused by
vertebral fracture/luxation, or external factors such as gunshot. The axons may be
torn, myelin sheaths disrupted, and cell bodies may be crushed. Complete physical
disruption of the spinal cord may be caused by a severe, traumatic vertebral frac-
ture/luxation, and this is likely to be irreversible even after months or years.

7.3.3 Patient Assessment

Most vertebral fractures and luxations are associated with road traffic accidents,
especially in the dog. Cats may present more commonly with either an unknown
history or a history of falling from a height. Therefore, it is common to find con-
comitant injuries to many other body systems, some of which may be immedi-
ately life‐threatening. As for head trauma, patient assessment should always
begin with the ‘ABC’ of airway, breathing, and circulation. The initial assess-
ment should focus on the vital physiological and cardiovascular parameters,
since many patients presenting with spinal cord injury following external trauma
will also be suffering from hypovolaemic shock or blood loss. Although these
issues should be considered first, extreme care should be taken when moving an
animal that has been involved in a road traffic accident as vertebral instability
may be present. If it is necessary to move the patient, then attempts should be
made to provide some kind of external support, and the use of a firm stretcher is
advisable. The need to support the circulatory system and to ensure that there is
a good airway and breathing are of paramount importance in all cases. Therefore,
if the animal has to be moved in order to provide essential life support, then of
course this takes priority over any suspected spinal cord injury. Furthermore,
physiological stabilisation is very important in protecting the spinal cord from
further damage in acute severe spinal cord injury.
360 A Practical Approach to Neurology for the Small Animal Practitioner

Baseline heart rate and rhythm, breathing rate and quality, and rectal tem-
perature should be recorded. In cervical spinal cord injury, the breathing may be
affected by damage to the upper motor neurons from the respiratory centres in
the brainstem. Various other mechanisms may also influence the breathing,
such as diaphragmatic rupture, rib fractures, and pneumothorax. Thoracic radi-
ography may therefore need to be performed rapidly and pneumothorax
addressed if present. If there is airway compromise or persistent breathing diffi-
culty, then intubation and ventilation may be required.
The mean arterial blood pressure (MABP) and, if possible, blood gas meas-
urement should be performed. Pulse oximetry should be used to monitor the
Sp(O2). Maintenance of adequate systemic blood pressure and blood oxygen
saturation are the mainstays of neuroprotection in cases of acute CNS injury (see
below and Section 7.1 ‘Head Trauma in Dogs and Cats’).

Neurological examination
A neurological assessment should be performed as soon as the patient is stable.
An attempt should be made to anatomically localise the region of suspected
injury, since this will guide imaging and therapy. In some instances of severe
trauma, it may not be possible to effectively evaluate the level of mentation, and
the possibility of brain trauma rather than spinal cord injury may exist (see
Section 7.1 ‘Head Trauma in Dogs and Cats’). However, in most cases it will be
clear that one is dealing with spinal cord injury alone.
Important tests to perform include evaluation of the spinal reflexes (e.g.
flexor withdrawal reflex) in all limbs and the cutaneous trunci reflex. In cases
of tetraparesis or tetraplegia, then a distinction needs to be made between a
lesion affecting the C1–C5 spinal cord segments and a lesion affecting C6–T2
segments. This may be best evaluated using the flexor withdrawal reflexes in
the thoracic limbs, although interpretation may be difficult and unreliable.
Other possible indicators of a C6–T2 lesion would include Horner syndrome
and absence of the cutaneous trunci reflex at any level of stimulation.
Ultimately, it may not be possible or overly important to differentiate between
a C1–C5 and C6–T2 lesion, since this is unlikely to make a significant differ-
ence to imaging requirements in most dogs and cats. However, a more cranial
cervical injury can be more immediately life‐threatening than a caudal cervi-
cal injury due to potential disruption of phrenic nerve and diaphragmatic
function, and the need to provide external support may be more critical in
this region due to the inherent instability compared to the caudal cervical
spine.
Several studies have found that the thoracolumbar region is the most com-
mon location for vertebral fractures and luxations, followed by the lumbar and
lumbosacral regions. The cervical vertebral column is the least common region
to be affected, and in one study no cats were found with fracture or luxation in
the cervical vertebral column (Bali et al. 2009).
 Chapter 7 Neurological Emergencies 361

Care should be taken not to misinterpret the Schiff–Sherrington posture as an

indicator of tetraparesis (see Chapters 3 and 4). This rigid extension of the t­ horacic
limbs in conjunction with paraplegia can be seen in acute severe thoracolumbar
spinal cord injuries. It is caused by disruption of inhibitory ascending interneurons
(Border cells) which normally serve to inhibit extensor muscle tone in the
­thoracic limbs as part of the mechanism of thoracic and pelvic limb coordination
(see Figure 6.10.1 in Section 6.10 ‘Paresis, Paralysis, and Proprioceptive Ataxia’
and Video 23).
An animal presenting with suspected Schiff–Sherrington posture must also
be distinguished from an animal that has suffered a brain injury and is present-
ing in a decerebrate or decerebellate posture; more detail of these presentations
and how to distinguish them may be found in Chapter 3. For this reason, it is
important to perform a full neurological examination whenever possible, in
order that potentially confusing signs may be correctly interpreted. A patient
with severe tetraparesis or tetraplegia may have normal or reduced spinal
reflexes depending on the precise location of the injury, but the postural reac-
tions and voluntary motor function will always be affected in both the thoracic
and pelvic limbs. In contrast, an animal with paraplegia and Schiff–Sherrington
posture will have normal spinal reflexes, normal postural reactions, and good
voluntary movement in the thoracic limbs. However, assessing this may not be
easy if there is doubt about spinal stability. Therefore, the clinician must perform
the neurological examination carefully and systematically in order to arrive at
the correct conclusion and neuroanatomic localisation.
In cases of paraplegia, it should be apparent that the thoracic limbs are nor-
mal (except in the cases of Schiff–Sherrington posture described above). The
pelvic limb flexor withdrawal reflexes and the patellar reflexes may assist in dif-
ferentiating between a lesion affecting the T3–L3 spinal cord segments (normal
reflexes) from one affecting the L4–S3 spinal cord segments (reduced reflexes).
Again, this may be difficult and can be complicated by the phenomenon known
as spinal shock, which results in a counterintuitive weakness of the pelvic limb
withdrawal reflexes secondary to an acute upper motor neuron lesion (see
Chapter 4). Therefore, when presented with an animal that is paraplegic and
appears to have reduced pelvic limb spinal reflexes, a careful examination of the
cutaneous trunci reflex should always be performed in order to ensure that the
lesion is not mistakenly localised to the L4–S3 segments rather than the T3–L3
segments. In genuine lower motor neuron lesions (L4–S3 segments), the cuta-
neous trunci reflex should be intact and there may also be loss of tail tone and
perineal reflex.
The most important prognostic indicator in acute spinal cord injury is the
presence or absence of deep pain perception in the distal limbs (see Chapter 3
and Video 15). As previously stated, it is unusual for an animal to be presented
with absent deep pain perception in all four limbs since most such animals will
have died as a result of such a severe cervical spinal cord injury. If absent deep
362 A Practical Approach to Neurology for the Small Animal Practitioner

pain perception in all four limbs is suspected, the clinician must be certain that
the test is being performed correctly and that the animal’s responses are not
being affected by shock or analgesic medication.
In acute thoracolumbar spinal cord injuries, the absence of pelvic limb deep
pain perception is the only factor that has been shown to have prognostic
value. In cases of Hansen type 1 intervertebral disc extrusion, the prognosis for
recovery in dogs with absent pelvic limb deep pain perception is around 55%
with surgical treatment. In cases of vertebral fracture/luxation and traumatic
spinal cord injury, the prognosis is believed to be much worse and therefore
euthanasia should be considered. However, caution should be exercised in the
interpretation of deep pain perception testing at the time of presentation, and
dogs or cats that present with absent deep pain perception should always be
considered candidates for potential referral as soon as they are stable.
Furthermore, it may be prudent to delay any decision to perform euthanasia
for at least 24 hours following an acute injury, since the effects of initial shock
may lead to confusing neurological signs including, on occasion, the apparent
absence of deep pain perception which subsequently returns once the animal
has been stabilised.
Recently, a study has shown the potential prognostic value of a serum glial
fibrillary acidic protein (GFAP) test in predicting recovery in deep pain‐negative
dogs caused by acute intervertebral disc extrusion (Olby et al. 2019). Should
this test become commercially available, it may prove a useful addition to
patient assessment and prediction of potential recovery. So far, no work has
been published regarding the utility of this test in cases of vertebral fracture and
luxation.

7.3.4 Management of Acute Spinal Cord Injury

Aside from the general management factors discussed above, there are some
specific considerations for limiting the effects of spinal cord injury. At present,
there is little that can be done to prevent the effects of contusion. The primary
goal of treatment is to maintain blood flow to the injured spinal cord and there
is convincing evidence in the human literature that hypotension plays a role in
secondary spinal cord injury. Therefore, ensuring that the mean arterial pressure
is maintained within normal limits is vital. Monitoring the blood pressure and
the appropriate use of fluid therapy, including volume expanders such as hyper-
tonic saline where necessary, is one of the few ways to tackle the effects of
ischaemia and secondary spinal cord damage.
Maintaining oxygenation is the other significant factor which can be influ-
enced by good patient management. This ensures that the spinal cord is supplied
with adequate energy to minimise the effects of ischaemia. Blood gas monitoring
is ideal, but when not available, pulse oximetry is valuable. The use of flow‐by
oxygen therapy or, in some situations, intubation and ventilation may be
appropriate.
 Chapter 7 Neurological Emergencies 363

1. Pharmacological agents
High dose corticosteroid therapy was once favoured in the treatment of human
spinal cord injury but has fallen out of use due to more recent work showing a pos-
sible detrimental effect. Currently, there is no evidence to support the use of corti-
costeroids in acute severe spinal cord injury in cats and dogs. Their use is associated
with significant morbidity, and they are of limited or no value in reducing the
cytotoxic oedema which predominates in such injury, as opposed to the vasogenic
oedema associated with neoplasia and chronic compressive spinal cord lesions.
Other potentially beneficial agents, such as polyethylene glycol (PEG), are
undergoing clinical trials but as yet there is no evidence for the efficacy of any
such compounds. Therefore, the focus should be on ensuring appropriate analge-
sia in cases of spinal cord trauma, since the pain associated with such injuries may
be significant. Opioids such as methadone may be used, providing care is taken
over any possible respiratory depressive effects. Intravenous paracetamol may
also be considered. NSAIDs, such as meloxicam or carprofen, may also be appro-
priate, although their use should be avoided in hypovolaemic animals as they
may have significant gastrointestinal and renal side‐effects in such situations.

2. Diagnostic investigations
Survey radiographs of the entire spine should be taken as soon as the patient is
stable. If possible, general anaesthesia should be avoided due to the potential loss
of the spinal stabilising effect of muscular spasm. Sedation with a combination of
an α2 agonist such as medetomidine in combination with an opioid analgesic is
preferred. Radiographs should be taken by centring on the region of suspected
injury based on the neurological examination, and orthogonal views are manda-
tory for identifying vertebral fracture/luxation (see Figure 7.5). Identification of

Figure 7.5 Radiographs of a comminuted fracture of the L6 vertebra; it can be seen that the
fracture is much more obvious on the lateral view than on the ventrodorsal view; care should
always be taken when reviewing radiographs of animals suffering with suspected vertebral
trauma and it is important, if possible, to ensure that orthogonal views are available in such
cases.
364 A Practical Approach to Neurology for the Small Animal Practitioner

a potentially unstable fracture or luxation is an indication for surgical referral if

possible.
Assessment of spinal radiographs requires an understanding of normal verte-
bral column anatomy, as well as the ligamentous structures and mechanisms
involved in vertebral column stability. The vertebral column is made up of func-
tional units consisting of an adjacent pair of vertebrae, the intervertebral disc
lying between them, the articular facet joints on each side, and the joint capsule
and ligaments which connect the vertebrae. Three‐dimensional imaging using
computed tomography (CT) can provide additional information regarding verte-
bral fracture/luxation and is particularly beneficial in cases where there is doubt
about the presence of a fracture(s), or when assessment of stability is difficult. It
is also very beneficial for surgical planning if surgical stabilisation is considered.
Furthermore, one study found that the sensitivity of survey radiography for iden-
tifying vertebral fractures/luxations was only around 75% compared to CT as the
gold standard (Kinns et al. 2006). Therefore, practitioners should always be aware
of the potential to miss a fracture or luxation on plain radiography alone.

3. Management of vertebral fracture/luxation

If a vertebral fracture and/or luxation is present, referral for surgical decompres-
sion and stabilisation may be necessary for recovery. A three‐compartment
model has been proposed for vertebral trauma, with the dorsal spine, dorsal
arch, and articular facet joints forming the dorsal compartment, the ventral
pedicle, dorsal annulus fibrosus, and dorsal part of the vertebral body forming
the middle compartment, and the ventral part of the vertebral body and remain-
der of the intervertebral disc forming the ventral compartment (see Figure 7.6).
It is proposed that if damage is limited to a single compartment, then the fracture
should be stable and may be managed conservatively. Damage to two or more
compartments, however, will be unstable and require surgical stabilisation.
For most cases of vertebral fracture/luxation, surgical stabilisation and/or
decompression is likely to give the best prognosis for recovery. Surgical treat-

dorsal

middle

ventral

Figure 7.6 Illustration to show the proposed three‐compartment model used in the
assessment of vertebral column stability associated with spinal fractures.
 Chapter 7 Neurological Emergencies 365

ment methods are beyond the scope of this text but for the practitioner faced
with a case of vertebral fracture/luxation, there are some situations where non‐
surgical management may be appropriate, or for cases when referral for surgical
management is not an option. If only a single compartment is affected, deep pain
perception is preserved, and referral is not an option, then either external splint-
ing or strict cage rest may allow fracture healing to occur. This applies to frac-
tures of any region of the vertebral column, including the thoracic and lumbar
regions. However, any suggestion of instability or significant vertebral displace-
ment that is causing disruption of the vertebral canal would be contraindications
for a conservative approach. As already stated, thoracic and lumbar vertebral
fractures/luxations that are accompanied by a loss of pelvic limb deep pain per-
ception carry an extremely poor prognosis. If this neurological finding is con-
firmed by repeated assessment following systemic stabilisation, then serious
consideration should be given to euthanasia of such severely affected animals.
Furthermore, if external splinting or cage confinement is initially applied but the
animal shows further neurological deterioration, then this implies potential
instability and referral for surgical treatment should again be considered.
In terms of conservative management techniques, mid‐cervical fracture/lux-
ations are probably best suited to external splinting since it may be possible to
simply wrap the neck in a well‐padded bandage in order to provide some sup-
port to these injuries. Even in the case of a fracture of the dens of C2, conserva-
tive management may be successful with this approach. However, persistent
pain may make this very difficult even in small and toy breeds. More caudal
cervical injuries are more difficult to stabilise in this way, and great care must be
taken to avoid compromise to the airway. If a padded bandage or splint is applied
to the neck whilst an animal is anaesthetised or heavily sedated, then the animal
must be very carefully observed during recovery to ensure that there is no air-
way compromise.
External splinting of thoracic and lumbar vertebral fracture/luxations is more
difficult to achieve effectively and attempts often end in disappointment. Further
problems associated with soft tissue necrosis and pressure sores can also be com-
mon. Strict cage confinement may be a better option with injuries in this loca-
tion. For caudal lumbar and lumbosacral injuries, it must be remembered that
the spinal cord ends at approximately the L5–L6 level in dogs and L6–L7 in cats,
so injuries caudal to this will cause damage to the cauda equina rather than the
spinal cord itself. This has implications for prognosis, given that recovery after
nerve root or peripheral nerve injury is usually better than after spinal cord
injury. Therefore, the prognosis is generally better with injuries at the caudal
lumbar and lumbosacral level than in the more cranial lumbar and thoracolum-
bar regions. Conservative management of vertebral fracture/luxations at this
level is also likely to have a better prognosis, although the pain associated with
spinal nerve compression may be significant and a reason to consider surgical
treatment.
366 A Practical Approach to Neurology for the Small Animal Practitioner

4. Care of animals recovering from spinal cord trauma

The major considerations for the management of animals recovering from spinal
cord injury are providing adequate analgesia, minimising the risks of recum-
bency (e.g. pressure sores and pneumonia), and management of the urinary
bladder. As discussed above, opioids such as methadone and morphine are likely
to be required in the early stages, alongside a NSAID +/− paracetamol. Gabapentin
may be a useful additional analgesic, although is only available as an oral formu-
lation. Regular assessment for pain and adaptation of the analgesic protocol in
order to most appropriately manage the individual is also important to reduce
the potentially detrimental effects associated particularly with opioids.
Avoiding the risks of prolonged recumbency requires regular moving and
turning, with the use of slings and lifting aids where necessary. Regular turning
of recumbent patients (every 2–4 hours) can help to avoid pressure sores, as well
as reduce the risk of lung congestion and potential pneumonia. The use of well‐
padded beds for recumbent animals can further reduce the risk of decubitus
ulcers, and some form of plastic padded mattress covered by a soft stay‐dry bed-
ding such as ‘Vet‐Bed’ can be very effective. Care with nutrition is also impor-
tant. Animals should be fed in sternal recumbency, or preferably helped into a
sitting or standing position if possible, and great care taken to avoid any poten-
tial aspiration of food or water. If anorexia is prolonged, or face/jaw injuries
make eating impossible, consideration should be given to the placement of a
feeding tube.
Management of bladder emptying problems may be achieved in a number of
ways. Manual expression may be possible in some situations, particularly in the
case of the so‐called ‘lower motor neuron’ bladder which is seen following dam-
age to the S1–S3 spinal cord segments or nerve roots. In such cases, there is loss
of sphincter and detrusor muscle tone and manual expression may be relatively
easy. However, there is often significant urine leakage which can lead to urine
scalding and exacerbate problems of soft‐tissue management associated with
recumbency.
Placement of an indwelling urinary catheter is likely to be the best way to
manage many cases with an ‘upper motor neuron’ bladder, as observed in spinal
cord lesions cranial to the L4 spinal segments (i.e. the majority of cervical, thora-
columbar, and lumbar spinal injuries). In such cases, there is often strong ure-
thral sphincter tone which makes manual bladder expression difficult, and many
animals become very resistant to attempts to express their bladder. For the rea-
sons stated above, the author may also use an indwelling urinary catheter in
cases with a lower motor neuron bladder, especially in the early stages of reha-
bilitation; this can simplify case management and reduce animal distress associ-
ated with frequent bladder expression. It is always important to monitor the
urine output, as urinary catheters can become kinked or blocked. Inevitably
with time there is a significant risk of developing a urinary tract infection if an
 Chapter 7 Neurological Emergencies 367

indwelling urinary catheter is placed, although one study found that this risk
was no greater than with either manual expression or repetitive rigid catheteri-
sation (Bubenik and Hosgood 2008).

7.3.5 Summary
In summary, acute severe spinal cord injury will usually present as either para-
plegia or tetraplegia, depending on the location of the injury, and a focused
neurological examination should be performed in order to establish the most
likely location of the lesion. The spine should be supported whilst the patient is
assessed, and careful consideration should be given to the rest of the body as
animals with spinal cord trauma commonly will have traumatic injuries
elsewhere.
The presence or absence of deep pain perception in the paralysed limbs
remains the most important prognostic indicator, but care should be taken when
interpreting this test in a shocked animal at the time of presentation. Once the
animal is stable, survey radiographs should be taken of the region of suspected
trauma in order to identify any potential instability of the vertebral column.
Referral should always be offered if vertebral fracture/luxation is diagnosed or
suspected, but an animal that has truly lost deep pain perception in the pelvic
limbs as a result of external spinal cord trauma unfortunately has a very guarded
prognosis for recovery even with surgical treatment.

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7.3. Acute Spinal Cord Injury

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Olby, N.J., Lim, J.H., Wagner, N. et al. (2019). Time course and prognostic value of serum GFAP,
pNFH, and S100β concentrations in dogs with complete spinal cord injury because of interver-
tebral disc extrusion. J. Vet. Intern. Med. 33: 726–734.
Rouanet, C., Reges, D., Rocha, E. et al. (2017). Traumatic spinal cord injury: current concepts
and treatment update. Arq. Neuropsiquiatr. 75: 387–393.
Smith, P.M. and Jeffery, N.D. (2005). Spinal shock‐‐comparative aspects and clinical relevance.
J. Vet. Intern. Med. 19: 788–793.
Index

Page locators in bold indicate tables. Page locators in italics indicate figures.

AAI see atlantoaxial instability age‐related conditions

ABC see airway, breathing, circulation cerebellar dysfunction, 256–257
abdominal focused assessment with clinical history and signalment, 38–39
sonography for trauma (AFAST), 334, differential diagnosis, 122
342–343 mentation, 172–173
abdominal pain, 271–272 movement disorders, 164
abducent nerve dysfunction, 64 vestibular syndrome, 237
acquired myasthenia gravis, 305, 308 airway, breathing, circulation (ABC),
activated charcoal, 179 333, 349, 359–360
acute canine polyradiculoneuritis, alanine aminotransferase (ALT), 150
305, 306 alertness, 50–51
acute non‐compressive nucleus pulposus alkaline phosphatase (ALP), 150
extrusion (ANNPE), 32, 276–277, alpha‐2‐agonists, 262, 341
280–282, 285, 296 ALT see alanine aminotransferase
acute repetitive seizures see status altered mentation see mentation
epilepticus and acute repetitive seizures amantadine, 262, 274
acute spinal cord injury, 358–367 amaurosis see post‐retinal blindness
care of recovering animals, 366–367 anaesthesia, 354–355
causes, 358 analgesia
diagnostic investigations, 363–364, 363 acute spinal cord injury, 363, 366
management, 362–367 clinical history and signalment, 35
neurological examination, 360–362 head trauma in dogs and cats, 341
pathophysiology, 358–359 mentation, 179–180
patient assessment, 359–362 neck and/or spinal pain, 262–263
pharmacological management, 363 paresis/plegia and proprioceptive
vertebral fracture/luxation, 363–365, ataxia, 285, 290
363–364 status epilepticus and acute repetitive
AED see antiepileptic drugs seizures, 356
AFAST see abdominal focused assessment anal tone, 89, 111
with sonography for trauma Angiostrongylus vasorum, 26–27

A Practical Approach to Neurology for the Small Animal Practitioner, First Edition. Paul M. Freeman and Edward Ives.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion Website: www.wiley.com/go/freeman/neurology

371
372 Index

animal trauma triage (ATT) score, 339 cerebellar ataxia, 16, 60–61, 242, 250
anisocoria clinical history and signalment, 36,
clinical approach to unilateral 276–283
miosis, 205–207 diagnostic approach, 275–284
clinical approach to unilateral formulating a plan, 284–287, 286
mydriasis, 200–202 lesion localisation, 104–106, 107, 284
neurological examination, 69–70, 74 neck and/or spinal pain, 264–265
presentations in general neuroanatomic basis, 275
practice, 196–207 neurological evaluation, 3, 15–16
unilateral miosis, 202–207, 202–205 neurological examination, 59–61,
unilateral mydriasis, 197–202, 283–284, 283
199–200 neuromuscular disorders, 303
ANNPE see acute non‐compressive nucleus onset of clinical signs, 276–280,
pulposus extrusion 284–287
anomalous disorders physiotherapy and rehabilitation, 295
cerebellar dysfunction, 253–254 presence/absence of pain, 281, 284–287
differential diagnosis, 128–129 presentations in general
epileptic seizures, 138 practice, 275–287, 290, 295
neck and/or spinal pain, 266–268, progression of clinical signs, 280–281
267–268, 273–274 spinal/proprioceptive ataxia, 15–16,
vestibular syndrome, 236, 238 60, 107, 275–287, 290, 295
antiepileptic drugs (AED), 6, 140, symmetry/asymmetry of neurological
148–156, 149, 350–358 deficits, 282
anti‐parasite treatment, 26–27 vestibular ataxia, 15–16, 60,
anxiety/stress, 88, 169, 174 232–233, 234
aortic thromboembolic (ATE) disease ATE see aortic thromboembolic disease
clinical history and signalment, 30, 33 atlantoaxial instability (AAI)
in cats, 58 diagnosis, 266
in dogs, 60 management, 273
monoparesis and lameness, 298 neck and/or spinal pain, 261,
neurological examination, 58, 60 266–267, 267, 273
paresis/plegia and proprioceptive paresis/plegia and proprioceptive
ataxia, 287 ataxia, 282
appetite, 259 atropine, 194, 195, 200
arachnoid space disease, 279, 282–283 ATT see animal trauma triage score
ascending reticular activating system audiogenic reflex seizures, 136, 140, 164
(ARAS) axonotmesis, 299
lesion localisation, 104
mentation, 170–171 bacterial infections
neurological examination, 50–51, 67 clinical history and signalment, 34, 35
vestibular syndrome, 235 neck and/or spinal pain, 264–265, 265
aspartate aminotransferase (AST), 150 paresis/plegia and proprioceptive
asymmetry see symmetry/asymmetry ataxia, 277–278, 286
ataxia BAER see brainstem auditory evoked
blindness, 183 response
 Index 373

behavioural abnormalities neurological examination, 62,

blindness, 183, 188 65–69, 68
clinical history and signalment, 33 spontaneous blinking, 217
lesion localisation, 103 Borrelia burgdorferi, 27
mentation, 169–170, 182 brachial plexus avulsion, 299–300
neurological evaluation, 7, 9–10 brainstem
neurological examination, 51 cerebellar dysfunction, 241–243
belladonna, 195 cranial nerve deficits, 208, 210–211,
Bell’s palsy, 221 218–219, 225–231
benign, idiopathic postural tremor, 160 lesion localisation, 103–105
biceps brachii, 88–89 mentation, 170–171, 174
bilateral miosis, 195–196 neurological evaluation, 2–3
bilateral mydriasis, 194–195 neurological examination, 72–73
bilateral ventrolateral strabismus, 18 vestibular syndrome, 231
biopsy, 215 brainstem auditory evoked response
bladder (BAER), 12
acute spinal cord injury, 366–367 brainstem reflexes, 337–339, 338
management in spinal cord breed‐specific disorders
disease, 292–294 cerebellar dysfunction, 254–256
neurological evaluation, 22–23 clinical history and signalment, 37,
neurological examination, 90–92, 91 40–43
see also micturition differential diagnosis, 122
blindness epileptic seizures, 139
clinical approach, 188–191 mentation, 172
differential diagnosis, 190–191 movement disorders, 162–164,
forebrain lesions, 188 166–168
intracranial lesions, 190–191 neck and/or spinal pain, 264,
lesion localisation, 184–188 268–270
neurological evaluation, 10–12, 183 paresis/plegia and proprioceptive
neurological examination, 183–184, ataxia, 278–280, 282–283, 288
189–191
ophthalmic and retinal cachexia, 77
examination, 189 cage rest, 290–292
ophthalmic disease, 184–185 canine distemper virus (CDV), 26, 251
pathway tested by PLR, 187–188, 187 canine idiopathic head tremor
post‐retinal blindness, 185, 186–188, syndrome, 160–161
186–187 cannabis intoxication, 171, 179
presentations in general carbamate toxicity, 196
practice, 183–191 cardiopulmonary resuscitation, 333
pupil size, 195, 197 carpal hyperextension, 54, 55
unilateral versus bilateral vision cataplexy, 7, 141
loss, 187, 189 catheterisation, 293–294, 366–367
blinking cavernous sinus syndrome, 198
cerebellar dysfunction, 241 CBF see cerebral blood flow
facial paralysis, 217 CCP see cerebral perfusion pressure
374 Index

CDRM see chronic degenerative cervical spondylomyelopathy, 279–280,

radiculomyelopathy 282, 287
CDV see canine distemper virus Chiari‐like malformation, 267–268, 268,
central cord syndrome, 113 273–274
central nervous system (CNS) chromatic pupillary light reflex (cPLR),
blindness, 185 185
clinical history and signalment, 26–29, chronic degenerative radiculomyelopathy
31–36, 39 (CDRM), 54, 278–279, 282
lesion localisation, 100, 101 chronic renal disease, 28
mentation, 170–171 circling, 51, 103, 188
neurological evaluation, 2–3, 13–14 clinical history and signalment, 25–44
neuromuscular disorders, 302 age, 38–39
cerebellar dysfunction anti‐parasite treatment, 26–27
anomalous disorders, 253–254 cerebellar dysfunction, 241–243,
cerebellar ataxia, 16, 60–61, 242, 250 243–245, 256–257
clinical approach, 256–257 cranial nerve deficits, 208, 212–213,
clinical history and signalment, 241–243, 217–218, 217, 219, 222–226
243–245, 256–257 differential diagnosis, 30, 122
degenerative disease, 254–256 epileptic seizures, 143
differential diagnosis, 246–256 general medical history, 25–29
infectious disease, 249–251, 250, 252 general questions regarding
inflammatory (sterile) disease, 248–249 household, 29
lesion localisation, 105 history of asymmetry, 35–36
movement disorders, 159 lesion localisation, 100
neoplastic disease, 254 mentation, 171–173
neurological evaluation, 3, 16 movement disorders, 27, 161–163
onset and progression, 256–257 neck and/or spinal pain, 257–260,
presentations in general 258–259
practice, 241–257 onset, 29–31, 122–123, 123
pupil size, 199, 200 ownership history, 26
toxin exposure, 252–253 paresis/plegia and proprioceptive
trauma, 252 ataxia, 276–283
vascular disease, 246–248, 247 presence or absence of pain, 33–34
vestibular syndrome, 231 previous and concurrent illness, 28
cerebral blood flow (CBF), 331–332, progression, 31–32, 122–123, 123
335 response to medication, 35
cerebral cortex, 170–171 sex‐linked conditions, 38
cerebral perfusion pressure (CPP), signalment, 37–39
331–332 specific history of the neurological
cerebrospinal fluid (CSF) problem, 29–36, 37
cerebellar dysfunction, 248–249 status epilepticus and acute repetitive
head trauma in dogs and cats, 331 seizures, 348
mentation, 178–179 toxin exposure, 27–28
neck and/or spinal pain, 268, 270 trauma, 28–29
cervical intervertebral disc extrusion, travel history, 27
290–291 vaccination status, 26
 Index 375

vestibular syndrome, 232–234, paresis/plegia and proprioceptive

233–235 ataxia, 285, 290, 295–296
see also breed‐specific disorders cotton‐ball test, 11
Clostridium tetani, 161–162, 286 cough, 222
cluster seizures see status epilepticus and cPLR see chromatic pupillary light reflex
acute repetitive seizures cranial nerve deficits
CNS see central nervous system bilateral masticatory muscle atrophy/
coagulopathy, 178 masticatory myositis, 214–216, 216
collapse, 7–8 bilateral trigeminal nerve
colloids, 336–337 dysfunction, 212–216, 216
coma central lesions, 207–208, 218–219
neurological evaluation, 9 clinical approach, 207–209, 214
neurological examination, 51 clinical history and signalment, 208,
presentations in general practice, 169, 212–213, 217–218, 217, 219,
180–182 222–226
compartment syndrome, 90 differential diagnosis, 208, 212,
compression of the spinal cord, 359 223–225, 227–228
computed tomography (CT) facial nerve, 217–222, 217, 219–220
acute spinal cord injury, 364 hypoglossal nerve, 229–231, 230
blindness, 190 idiopathic trigeminal neuropathy, 213
epileptic seizures, 145, 146 laryngeal paralysis, 222–225
head trauma in dogs and cats, 334, lesion localisation, 102, 104, 118,
342–343, 343 207–208, 226–227
neck and/or spinal pain, 266 megaoesophagus, 225–229, 227
paresis/plegia and proprioceptive mentation, 174–175
ataxia, 290 neuromuscular disorders, 304
pupil size, 201 peripheral lesions, 207–208, 219–222
congenital anomalies, 128–129 presentations in general practice,
congenital idiopathic megaoesophagus, 207–231
225, 229 pupil size, 201
congenital laryngeal paralysis, 222–223 trigeminal nerve, 209–216,
consciousness 210–211, 216
head trauma in dogs and cats, 337–339 unilateral trigeminal nerve
mentation, 168–169 dysfunction, 210–212, 210–211
neurological evaluation, 5–6 vagus nerve, 222–229, 227
neurological examination, 51 vestibular syndrome, 235–236
conservative management in spinal cord cranial nerve examination
injury, 365 basic cranial nerve functions, 62–65,
contusion of the spinal cord, 358–359 63–64
convergence–retraction pulses, 72 eyes, 66–75, 68, 73–74
corneal reflex, 65–66 mouth and jaws, 75, 76
corticosteroids neurological examination, 66–76, 68,
acute spinal cord injury, 363 73–74, 76
clinical history and signalment, 35 nose, 76
cranial nerve deficits, 214 paresis/plegia and proprioceptive
head trauma in dogs and cats, 342 ataxia, 284
376 Index

CSF see cerebrospinal fluid epileptic seizures, 156–157

Cushing reflex, 339 megaoesophagus, 229
cutaneous trunci reflex, 92–94, 93 vestibular syndrome, 238
see also nutritional support
dazzle reflex dietary salt, 151
blindness, 184 differential diagnosis, 121–132
neurological examination, 73–75 anomalous disorders, 128–129
pupil size, 195 blindness, 190–191
deafness, 12 categories of disease, 124–131
decerebellate rigidity, 55, 56, 242, cerebellar dysfunction, 246–256
243, 361 clinical history and signalment, 30, 122
decerebrate rigidity, 55, 361 constructing the list of differential
deep brain electrodes, 157 diagnoses, 121–124, 123
deep pain perception (DPP) cranial nerve deficits, 208, 212,
acute spinal cord injury, 361–362, 365 223–225, 227–228
neurological evaluation, 14 degenerative disorders, 130–131
neurological examination, 95–96 epileptic seizures, 142–144, 144,
paresis/plegia and proprioceptive 158, 165
ataxia, 292 idiopathic disorders, 129
degenerative disease inflammatory/infectious disease, 127
blindness, 184–185 lateralisation of neurological
cerebellar dysfunction, 254–256 defects, 123
clinical history and signalment, 32, lesion localisation, 123
34, 39 mentation, 171–172, 175, 180
differential diagnosis, 130–131 metabolic disorders, 129
epileptic seizures, 138 monoparesis and lameness, 298–301
intervertebral disc disease, 278–282, movement disorders, 158, 165
287–296 neck and/or spinal pain, 263–270
monoparesis and lameness, 300–301 neoplastic disease, 130
neck and/or spinal pain, 269–270 neurological examination, 46
paresis/plegia and proprioceptive neuromuscular disorders, 208,
ataxia, 278–280, 282, 286–296 304–307
vestibular syndrome, 238 nutritional disorders, 130
degenerative lumbosacral stenosis (DLSS) physical examination, 122
monoparesis and lameness, 301 presence or absence of
neurological evaluation, 19–20, 21 discomfort, 123–124
paresis/plegia and proprioceptive pupil size, 198–199, 203
ataxia, 280, 286 reported onset and progression of
degenerative myelopathy, 278–279, 282 clinical signs, 122–123, 123
denervation atrophy, 209–210, 211–212 signalment of the particular
depression, 33, 50–51 animal, 122
developmental anomalies, 128–129 toxin exposure, 128
dexmedetomidine, 355 trauma, 128
diabetes, 172 vascular disease, 125–127
diazepam, 158, 351–352 vestibular syndrome, 231, 236–239
dietary modification VITAMIN D mnemonic, 124–125, 126
 Index 377

digital rectal examination, 94 correcting the underlying disease, 148

disc‐associated wobbler syndrome, definition and
279–280, 282 pathophysiology, 134–135
discospondylitis, 30, 264–265, 265, 273 diagnostic approach, 141–146
DLSS see degenerative lumbosacral differential diagnosis, 142–144, 144,
stenosis 158, 165
DPP see deep pain perception epileptic myoclonus, 163–164
drooling, 212, 217 extracranial disorders, 137
drooping ears, 217, 217 focal seizures, 135
drooping lips, 217 further investigations in general
dropped jaw, 212–213 practice, 144–145
dry eye, 218 generalized seizures, 135–136
dyskinesia, 6, 8–9, 164–168 goals of seizure management, 147
see also movement disorders head trauma in dogs and cats, 334
dysmetria, 82 ictus, 136
dysmyelination, 159–160 idiopathic epilepsy, 139–141, 357
dysphonia, 222 intracranial disorders, 137–141, 138
lesion localisation, 103, 104–105, 142
electrocardiography (ECG), 333 management, 146–157
electroencephalography (EEG) mentation, 170
epileptic seizures, 5, 7, 140, 141–142 neurological evaluation, 5–7,
status epilepticus and acute repetitive 141–142
seizures, 351 neurological examination, 45, 61–62,
electromyography (EMG), 216, 221 143–144
electroretinography (ERG), 184, 189 non‐pharmacological
elevated tail posture, 57, 57 treatment, 156–157
emergency presentations, 329–370 owner communication, 146–147
acute spinal cord injury, 358–367 pharmacological treatment, 140,
clinical approach, 329 148–156, 149
head trauma in dogs and cats, 329–344 post‐ictal phase, 136
status epilepticus and acute repetitive presentations in general
seizures, 345–358 practice, 134–158
empyema, 277–278 prodrome, 135
encephalomyelitis, 164 pupil size, 197
endocrine disorders, 172, 178 referral, 146
endotracheal intubation, 333 refractory epilepsy, 157
eosinophilic bronchitis, 151 seizure management in the home
epileptic seizures environment, 158
aura, 136 status epilepticus and acute repetitive
blindness, 136, 188 seizures, 136, 140, 158, 334,
classification by clinical 345–358
presentation, 135–136 structural epilepsy, 138, 138
classification by underlying when to start treatment, 147–148
aetiology, 137–141, 137–138 episodic collapse, 7, 158
clinical history and signalment, 29–30, episodic hypertonicity
32, 143 syndrome, 166–167
378 Index

episodic pain, 7 monoparesis and lameness, 298

ERG see electroretinography neurological examination, 55
euthanasia, 310 paresis/plegia and proprioceptive
excitatory neurotransmitters, 330 ataxia, 276, 280–282, 285
exercise intolerance FIP see feline infectious peritonitis
cranial nerve deficits, 222 FIV see feline immunodeficiency virus
lesion localisation, 118 flexor withdrawal reflex see withdrawal
neurological examination, 48–49, 59 reflex
neuromuscular disorders, 304 fluid therapy/resuscitation
exposure keratitis, 217 head trauma in dogs and
extensor carpi radialis, 88–89, 297–298 cats, 336–337, 340–341
extensor postural thrust, 82–83 status epilepticus and acute repetitive
extracranial disorders, 137 seizures, 349–350
eyes/visual response fly‐catching, 7, 170
abnormalities of pupil size, 191–207 focal muscular atrophy, 76–77, 78
blindness, 183–191 focal seizures, 5, 135
cerebellar dysfunction, 243–244 focused stereotactic radiation
lesion localisation, 103, 105–106 therapy, 212
neurological examination, 66–75, 68, forebrain
73–74 blindness, 188
vestibular syndrome, 233–236, lesion localisation, 103
234–235 mentation, 174
neurological evaluation, 2
facial asymmetry, 62, 63, 217 neurological examination, 51
facial nerve fungal infections, 27
central lesions, 218–219
clinical history and gabapentin, 262, 274
signalment, 217–218, 217, 219 gagging, 226
peripheral lesions, 219–222 gag reflex, 49, 75
presentations in general gait
practice, 217–222 cerebellar dysfunction, 241–242
vestibular syndrome, 236–237 lesion localisation, 105–106, 107–111,
facial paralysis, 217–222 109, 114, 118–119
fasciculations, 161 mentation, 174
FCE see fibrocartilaginous embolism neurological evaluation, 15–16
feline audiogenic reflex seizures, 136, neurological examination, 48–49,
140, 164 58–61, 82
feline coronavirus, 249–251 paresis/plegia and proprioceptive
feline immunodeficiency virus (FIV), 26 ataxia, 283
feline infectious peritonitis (FIP), 38, vestibular syndrome, 235
249–251 gamma glutamyltransferase (GGT), 150
feline leukaemia virus (FeLV), 26 gastrocnemius, 88–89
feline panleukopaenia virus, 26, 251 generalised muscular atrophy, 76–77,
FeLV see feline leukaemia virus 302, 307
fibrocartilaginous embolism (FCE) generalised neuromuscular disorders see
clinical history and signalment, 30, 36 neuromuscular disorders
 Index 379

generalised polyneuropathy, 120, 302, traumatic brain injury, 330–332,

305, 306 334–335, 343
general medical history, 25–29 triage and general
genetic testing, 37, 40–43 assessment, 333–334
GFAP see glial fibrillary acidic protein head tremor, 12–13, 105–106,
GGT see gamma glutamyltransferase 160–161, 242
glaucoma, 194, 197, 200 head turn, 17, 52–53
glial fibrillary acidic protein (GFAP) hemi‐facial spasm, 164
test, 362 hemi‐walking, 82
gluten sensitivity, 166 hepatic encephalopathy, 32
granulomatous meningoencephalitis hepatotoxicity, 150
(GME), 248–249 hip dysplasia, 112
histiocytic sarcoma, 130
haemorrhage HNPE see hydrated nucleus pulposus
acute spinal cord injury, 359 extrusion
differential diagnosis, 125 hopping, 80–82
head trauma in dogs and cats, 334 hormonal abnormalities, 344
mentation, 173 Horner syndrome
haemorrhagic stroke acute spinal cord injury, 360
cerebellar dysfunction, 246, 248 cranial nerve deficits, 213
mentation, 178 diagnostic approach, 202–207
vestibular syndrome, 238–239, 240 idiopathic Horner syndrome, 205
head down posture, 257–258, 258 paresis/plegia and proprioceptive
head tilt ataxia, 284
cerebellar dysfunction, 242–243, presentations in general practice, 196,
244–245 199, 202–207, 202–205
neurological evaluation, 16–17, 17 vestibular syndrome, 236
neurological examination, 52–53, 52 hydrated nucleus pulposus extrusion
vestibular syndrome, 232, 233 (HNPE), 276–277, 285
head trauma in dogs and cats, 329–344 hydrocephalus
analgesia and sedation, 341 clinical history and signalment, 30, 32,
clinical approach, 344 38–39
diagnostic imaging, 333–334, 342–343 epileptic seizures, 138, 143
intracranial pressure and cerebral management, 178–179
perfusion, 331–332, 339–341 hypaesthesia see reduced sensation
management, 332–343 hyperadrenocorticism, 28, 214
neurological examination, 337–339, hyperexcitability of peripheral
338 nerves, 161–163
presentations in general practice, hyperkeratosis of nasal planum, 218, 219
329–330 hypermetric gait
prognosis, 344 cerebellar dysfunction, 241–242
role of corticosteroids, 342 lesion localisation, 105–106
supportive care and neurological evaluation, 16
nutrition, 341–342 neurological examination, 60, 82
systemic stabilisation and seizure hypersensitivity, 261
management, 334–337 hypertension, 178, 246, 248
380 Index

hyperthermia, 349 clinical history and signalment, 35

hypertonic saline, 336, 340–341 cranial nerve deficits, 216
hypoadrenocorticism neck and/or spinal pain, 272–274
clinical history and signalment, 28 neuromuscular disorders, 307–308
cranial nerve deficits IMPA see immune‐mediated polyarthritis
(megaoesophagus), 228–229 incontinence, 22–23, 90–92, 259
mentation, 172, 178 indwelling urinary catheter, 293–294
hypocalcaemia, 349–350 inflammatory cytokines, 331
hypoglossal nerve, 229–231, 230 inflammatory/infectious disease
hypoglycaemia, 137, 148, 350 cerebellar dysfunction, 248–251, 250,
hypomyelination, 159–160 252
hypovolaemic shock, 333, 359 clinical history and signalment, 31,
33–35, 38–39
ICP see intracranial pressure cranial nerve deficits, 211, 214–216,
idiopathic acquired megaoesophagus, 216, 219, 223
225–226 differential diagnosis, 127
idiopathic cranial polyneuropathy, 237 epileptic seizures, 138
idiopathic disease monoparesis and lameness, 299
clinical history and signalment, 31 neck and/or spinal pain, 264–265, 265,
differential diagnosis, 129 272–273
movement disorders, 160–161 paresis/plegia and proprioceptive
idiopathic epilepsy (IE), 139–141, 357 ataxia, 277–278, 281, 285, 294
idiopathic facial neuropathy, 220–222 status epilepticus and acute repetitive
idiopathic generalised tremor seizures, 357
syndrome, 7, 160, 249 vestibular syndrome, 236, 238
idiopathic head bobbing/tremors, 12–13, infraspinatus muscle, 77, 78
160–161 inhalational anaesthetic agents,
idiopathic Horner syndrome, 205–207 354–355
idiopathic neuritis, 299 inspiratory stridor, 222, 224
idiopathic oculomotor neuropathy, intention tremors, 105–106, 159, 242
198–199, 201 interaction with the environment, 50–51
idiopathic polymyositis, 270–271, intermittent rigid catheterisation, 293
305, 307 intervertebral disc disease
idiopathic postural tremor, 160 acute spinal cord injury, 362
idiopathic trigeminal neuropathy, 213 bladder management, 292–294
idiopathic vestibular syndrome, 237 clinical history and signalment, 32,
IE see idiopathic epilepsy 34–36, 39
imepitoin, 148, 152–153, 355 Hansen type 1 intervertebral disc
immune‐mediated neuritis, 299 extrusion, 289–292
immune‐mediated polyarthritis Hansen type 2 intervertebral disc
(IMPA), 270 protrusion, 295–296
immune‐mediated monoparesis and lameness, 300–301
polymyositis, 270–271 neck and/or spinal pain, 269–270, 272
immunosuppression neuroanatomic basis, 287–289, 288
cerebellar dysfunction, 248, 251 neurological examination, 55
 Index 381

physiotherapy and neurological examination, 70–71

rehabilitation, 294–296 vestibular syndrome, 233
presentations in general joint extension, 53–54, 54
practice, 278–282, 287–296 junctionopathies
suspected cervical intervertebral disc cranial nerve deficits, 218, 227
extrusion, 290–291 lesion localisation, 119–120
suspected thoracolumbar intervertebral neuromuscular disorders, 302–305,
disc extrusion, 291–292 308
intoxication
cannabis, 171, 179 keratoconjunctivitis sicca (KCS), 218
metronidazole, 252–253 ketamine, 262, 341, 355
intracranial lesions kinetic tremors, 159–160
blindness, 190–191 kyphosis
brainstem, 103–105 neck and/or spinal pain, 259, 259
cerebellum, 105, 241 neurological examination, 56–57
cranial nerve dysfunction, 207 paresis/plegia and proprioceptive
epileptic seizures, 137–141, 138 ataxia, 283
forebrain, 103
lesion localisation, 102–106, 107 laboratory tests
vestibular syndrome, 231 blindness, 189–190
intracranial neoplasia, 240, 357 cranial nerve deficits, 215, 219, 228
intracranial pressure (ICP) epileptic seizures, 145
head trauma in dogs and head trauma in dogs and cats, 336
cats, 331–332, 335, 339–341 mentation, 176
mentation, 169, 173, 176–177, neuromuscular disorders, 309–310
181–182 status epilepticus and acute repetitive
neurological evaluation, 9 seizures, 349
intravenous access, 336, 349 vestibular syndrome, 239–240
involuntary movements, 61–62, laceration of the spinal cord, 359
134–136, 158–168 Lafora disease, 163
iris atrophy, 195, 197 laryngeal paralysis, 222–225
ischaemic stroke laryngeal paralysis‐polyneuropathy
cerebellar dysfunction, 246–248, 247 syndrome (LPP), 224, 227
clinical history and signalment, 30 lateralisation of neurological
clinical presentation, 125 defects, 123
mentation, 177–178 lesion localisation, 99–120
vestibular syndrome, 238, 240 all limbs affected, 109–110, 109
isoflurane, 354–355 blindness, 184–188
isotonic crystalloids, 336 both thoracic limbs only, 113
brainstem, 103–105
jaw tone and position, 64, 75, 210, cerebellum, 105, 241–257
212–214 clinical history and signalment, 100
jerk nystagmus concepts and definitions, 99–100
cerebellar dysfunction, 243 cranial nerve deficits, 102, 207–208,
neurological evaluation, 18 226–227
382 Index

lesion localisation (contd.) LPP see laryngeal paralysis‐polyneuropathy

differential diagnosis, 123 syndrome
epileptic seizures, 142 lumbosacral pain, 259–260, 261
forebrain, 103 lymphadenopathy, 173
hemiparesis, 110–111 lymphoma, 130, 300
intracranial lesions, 102–106 lymphosarcoma, 213
mentation, 170–171, 175 lysosomal storage diseases, 39
monoparesis, 112–113
movement disorders, 105–106, 161 MABP see mean arterial blood pressure
multifocal or diffuse localisation, 100 magnetic resonance imaging (MRI)
neuromuscular disorders, 101–102, blindness, 190
101, 111–112, 117–120, 117, 302–304 cerebellar dysfunction, 245, 247,
paraparesis, 111–112, 111 248–249, 250, 252
paresis/plegia and proprioceptive cranial nerve deficits, 211–212, 211,
ataxia, 284 215–216, 216, 220–221, 220, 230
potential pitfalls in spinal cord lesion epileptic seizures, 138, 141, 143–144,
localisation, 114–116 144, 146
principles of lesion head trauma in dogs and cats, 343
localisation, 100–102, 101 monoparesis and lameness, 298, 300
Schiff–Sherrington posture, 115–116 movement disorders, 160
spinal cord lesions, 84–87, 106–116 neck and/or spinal pain, 268
spinal shock phenomenon, 116 neurological examination, 46–47, 73
vestibular syndrome, 234–236 paresis/plegia and proprioceptive
why to perform a neurological ataxia, 290
examination, 46–47, 47 pupil size, 198–199, 199–200, 201
lethargy, 259, 260 mannitol, 340
levetiracetam, 140, 154–156, 158, 351, masticatory muscles
352–353 cranial nerve deficits, 209–216, 216
limb palpation, 76–77, 78 lesion localisation, 118
limb placement, 59 neck and/or spinal pain, 271
limb withdrawal reflex see withdrawal neurological examination, 75, 76
reflex masticatory myositis, 214–216, 216, 271
little white shaker disease, 7, 160, 249 MCT see medium‐chain triglyceride
liver enzymes, 150–151 mean arterial blood pressure (MABP)
lordosis, 57, 94 acute spinal cord injury, 360
loss of consciousness see consciousness head trauma in dogs and
loss of sensation see reduced sensation/ cats, 331–332, 339
hypoaesthesia status epilepticus and acute repetitive
lower motor neurons (LMN) seizures, 349
acute spinal cord injury, 366–367 medial longitudinal fasciculus (MLF), 231
lesion localisation, 106, 113, 117 medium‐chain triglyceride (MCT)
monoparesis and lameness, 297–298 diet, 157
neurological evaluation, 3, 13–15, medulla, 3
22–23 megaoesophagus
neurological examination, 82–83, 91 classification, 225–226
low head carriage, 257–258, 258 clinical history and signalment, 226
 Index 383

diagnosis and neuroanatomic head trauma in dogs and cats, 337

localisation, 226–227, 227 intracranial pressure, 169, 173,
diagnostic approach, 228 176–177, 181–182
management, 229 lesion localisation, 103–104, 170–171,
presentations in general 175
practice, 225–229 movement disorders, 158
menace response neurological evaluation, 9–10,
blindness, 183–184 169–170
cranial nerve deficits, 217 neurological examination, 67,
lesion localisation, 103, 105–106 168–169, 173–175
movement disorders, 162 obtundation, 169, 173–180
neurological evaluation, 11 paresis/plegia and proprioceptive
neurological examination, 67–69, 68 ataxia, 283
pupil size, 195, 197, 201 physical examination, 168–169, 173
meningoencephalomyelitis of unknown presentations in general
origin (MUO) practice, 168–182
blindness, 190–191 referral, 175–176
cerebellar dysfunction, 248–249 stupor, 169, 180–182
clinical history and signalment, 30, 38 treatment of specific suspected
mentation, 173 causes, 177–180
monoparesis and lameness, 299 vestibular syndrome, 234–235
neck and/or spinal pain, 264, metabolic disease
272–273 clinical history and signalment, 30–31,
neurological evaluation, 11 32, 39
paresis/plegia and proprioceptive cranial nerve deficits, 220
ataxia, 277–278 differential diagnosis, 129
status epilepticus and acute repetitive epileptic seizures, 137
seizures, 357 mentation, 172
vestibular syndrome, 238–239 movement disorders, 166
mentation status epilepticus and acute repetitive
behaviour/quality of seizures, 349–350
mentation, 169–170, 182 vestibular syndrome, 236–237, 238
blindness, 183, 188 metastatic disease, 130
cerebellar dysfunction, 242 metronidazole, 28, 252–253
clinical history and MGCS see modified Glasgow Coma Scale
signalment, 171–173 micturition
coma, 169, 180–182 acute spinal cord injury, 366–367
consciousness/level of head trauma in dogs and cats, 341
mentation, 168–169 neurological evaluation, 21–23, 22
definitions and terminology, 168 neurological examination, 90–92, 91
diagnostic approach, 171–175 paresis/plegia and proprioceptive
differential diagnosis, 171–172, ataxia, 292–294
175, 180 status epilepticus and acute repetitive
epileptic seizures, 170 seizures, 356
formulating a plan, 175–176, midazolam, 341, 351–352
180–182 minimum database, 336, 349
384 Index

miosis tremors, 12–13, 27, 105–106,

neurological examination, 69, 75 159–161, 242
presentations in general MUO see meningoencephalomyelitis of
practice, 195–196, 202–207, unknown origin
202–205 muscle tone
MLF see medial longitudinal fasciculus cerebellar dysfunction, 242
modified Glasgow Coma Scale lesion localisation, 110–113, 117
(MGCS), 180–182, 337–339, 338 movement disorders, 161–162
monoparesis and lameness neurological examination, 76–77
approach to monoparesis/lameness in neuromuscular disorders, 303
practice, 301–302 paresis/plegia and proprioceptive
degenerative disease, 300–301 ataxia, 286, 286
differential diagnosis, 298–301 vestibular syndrome, 232–233
inflammatory/infectious disease, 299 muscular atrophy
lesion localisation, 113 cranial nerve deficits, 209–216, 216
neck and/or spinal pain, 258–260, lesion localisation, 110, 117–118
258 monoparesis and lameness, 297
neoplastic disease, 300 neurological examination, 75–77,
neurological evaluation, 19–20, 76, 78
297–298 myasthenia gravis
neurological examination, 48–49 cranial nerve deficits, 225–229, 227
presentations in general neuromuscular disorders, 305, 308
practice, 297–302 mydriasis
trauma, 299–300 neurological examination, 69, 75
vascular disease, 298 presentations in general practice,
motor activity, 337–339, 338 194–195, 197–202, 199–200
motor polyneuropathy, 305, 306 myoclonic epilepsy of unknown
mouth and jaw examination, 75, 76 origin, 164
movement disorders myoclonic seizures, 5
cerebellar dysfunction, 241–244 myoclonus, 163–164
clinical history and signalment, 27, myokymia, 161–163
161–163 myopathies
definitions and cranial nerve deficits, 218, 223–224,
pathophysiology, 158–159 227–231
differential diagnosis, 158, 165 lesion localisation, 119–120
lesion localisation, 105–106, 161 neuromuscular disorders, 302–305, 307
myoclonus, 163–164
neurological evaluation, 6, 8–9 narcolepsy, 7
neurological examination, 45 narrow‐based stance, 53
paroxysmal dyskinesias, 164–168 nasal septum nociception, 76
peripheral nerve NCL see neuronal ceroid lipofuscinosis
hyperexcitability, 161–163 neck and/or spinal pain
presentations in general abdominal pain, 271–272
practice, 158–168 anomalous disorders, 266–268,
pupil size, 197 267–268, 273–274
 Index 385

cats in pain, 260, 261 pupil size, 198, 200, 203–204

clinical history and status epilepticus and acute repetitive
signalment, 257–260, 258–259 seizures, 357
confounders of spinal pain, 270–272 vestibular syndrome, 237, 238, 240
degenerative disease, 269–270 Neospora caninum, 214–216, 251, 252
differential diagnosis for pain‐only nerve root signature, 258–259, 258
conditions, 263–270 neuroaxonal dystrophy, 255
immune‐mediated arthritis/ neurogenic keratitis, 209
polymyositis, 270–271 neurogenic keratoconjunctivitis sicca, 218
inflammatory/infectious neurological evaluation, 1–24
disease, 264–265, 265, 272–273 acute spinal cord injury, 359–360
lumbosacral pain, 259–260, 261 ataxia, 15–16
management of pain‐only blindness, 10–12, 183
conditions, 272–274 collapse, 7–8
neck pain, 257–259, 258–259, 260–261 concepts and definitions, 1
neoplastic disease, 269, 271 deafness, 12
neuropharmacology and epileptic seizures, 141–142
targets, 262–263 establishing the problem, 1–2
orthopaedic disease, 260, 261, 271 head position and eyeball position/
pathophysiology of pain, 262–263 movement, 16–18, 17
physical examination, 260–261 lameness, 19–20
presentations in general manifestations of diseases of the
practice, 257–274 nervous system, 4–23
referral of pain‐only spinal mentation, 169–170
disease, 274 mentation and behaviour, 7, 9–10
thoracolumbar pain, 259, 259, 261 micturition, 21–23, 22
trauma, 265–266, 266 monoparesis and lameness, 297–298
vascular disease, 264 movement disorders, 6, 8–9
neck manipulation, 94–95 neuroanatomy, 2–4, 4
neck tremor, 105–106 neurological examination, 46
neoplastic disease neuromuscular disorders, 303–304,
blindness, 189, 191 307–308
cerebellar dysfunction, 254 pain/hyperaesthesia, 20–21
clinical history and signalment, 31, 32, paresis/plegia, 13–15, 19
34–35, 38–39 recognising problem as neurological, 2
cranial nerve deficits, 210–2W13, reduced sensation/hypaesthesia, 19, 20
210–211, 220, 223 seizures, 5–7
differential diagnosis, 130 status epilepticus and acute repetitive
epileptic seizures, 138, 138 seizures, 348, 356
mentation, 172–173, 179–180 tremor, 12–13
monoparesis and lameness, 300 neurological examination, 45–98
neck and/or spinal pain, 269, 271 abnormal posture, 52–58
neurological evaluation, 11 acute spinal cord injury, 360–362
paresis/plegia and proprioceptive basic cranial nerve functions, 62–65,
ataxia, 278–280, 286 63–64
386 Index

neurological examination (contd.) tongue symmetry and tone, 65, 75

blindness, 183–184, 189–191 vestibular syndrome, 234–236
body and spinal postures, 55–57, 56 wheelbarrow testing, 82
concepts and definitions, 45 when to perform a neurological
cranial nerve examination, 66–76, 68, examination, 47–48
73–74, 76 where to perform a neurological
cutaneous trunci reflex, 92–94, 93 examination, 48–49
differential diagnosis, 46 why to perform a neurological
epileptic seizures, 143–144 examination, 45–47, 47
extensor postural thrust, 82–83 withdrawal reflex, 85–87
eyes, 66–75, 68, 73–74 see also lesion localisation
gait, 48–49, 58–61 neuromuscular disorders
hands‐on assessment, 65–97 acquired myasthenia gravis, 305, 308
head position, 52–53, 52 acute canine polyradiculoneuritis, 305,
head trauma in dogs and 306
cats, 337–339, 338 clinical approach, 307–310
hemi‐walking, 82 differential diagnosis, 208, 220,
hopping, 80–82 223–224, 304–307
how to perform a neurological lesion localisation, 101–102, 101,
examination, 49–96 111–112, 117–120, 117
involuntary movements, 61–62 motor polyneuropathy, 305, 306
jaw tone and position, 64, 75 neuroanatomic basis, 302–303
level of alertness and interaction with neurological evaluation, 303–304,
the environment, 50–51 307–308
limb and joint position, 53–54, 54–55 neurological examination, 77
limb palpation, 76–77, 78 presentations in general
mentation, 168–169, 173–175 practice, 302–310
mouth and jaws, 64–65, 75, 76 neuromuscular junction (NMJ), 208,
neurological evaluation, 46 302, 305
nose, 76 neuromyotonia, 161–163
observation, 50–65, 96 neuronal ceroid lipofuscinosis (NCL), 164
other limb reflexes, 88–89 neuropraxia, 299
other tests of proprioception, 83–84 NMJ see neuromuscular junction
pain reception, 95–96 nociception see pain/hyperaesthesia
paresis/plegia and proprioceptive non‐epileptic myoclonus, 164
ataxia, 283–284, 283 non‐steroidal anti‐inflammatory drugs
patellar reflex, 87–88 (NSAID)
paw replacement, 79–80, 80 clinical history and signalment, 35
perineal reflex, anal tone, tail tone, and head trauma in dogs and cats, 341
bladder function, 89–92, 91 neck and/or spinal pain, 262, 274
proprioception, 77–84, 80 nose examination, 76
pupil size, 201, 206 NSAID see non‐steroidal anti‐
spinal palpation and neck inflammatory drugs
manipulation, 94–95 nucleus pulposus extrusion, 276–277,
spinal reflex testing, 84–94 280–282, 285, 296
summary, 96–97 nutritional disorders, 130
tail postures, 57–58, 57 nutritional support
 Index 387

acute spinal cord injury, 366 cranial nerve deficits, 219

head trauma in dogs and cats, 341–342 posture, 52
status epilepticus and acute repetitive vestibular syndrome, 236
seizures, 356 owner communication, 146–147
nystagmus ownership history, 26
cerebellar dysfunction, 243 oxygenation
neurological evaluation, 18 acute spinal cord injury, 362
neurological examination, 70–71 head trauma in dogs and cats, 335
vestibular syndrome, 233–236, 234 status epilepticus and acute repetitive
seizures, 349
obsessive/compulsive behaviour
blindness, 188 pain/hyperaesthesia
mentation, 170 blindness, 188
neurological examination, 51 clinical history and signalment, 33–35
obtundation mentation, 172, 173
differential diagnosis, 175 monoparesis and lameness, 298–300
formulating a plan, 175–176 neck and/or spinal pain, 257–274
intracranial pressure, 176–177 neurological evaluation, 7, 20–21
lesion localisation, 175 neurological examination, 95–96
neurological evaluation, 9 neuropharmacology and
neurological examination, 50–51, targets, 262–263
173–174 paresis/plegia and proprioceptive
presentations in general practice, 169, ataxia, 281, 284–287, 290–292
173–180 pathophysiology of pain, 262–263
treatment of specific suspected vestibular syndrome, 236
causes, 177–180 palliative care, 212
oculomotor nerve dysfunction, 63 palpation
oesophageal muscles, 118 head trauma in dogs and cats, 334
open fractures, 334 lesion localisation, 107
ophthalmic disease, 184–185 mentation, 175
ophthalmic examination, 189, 200, 206 neck and/or spinal pain, 260–261
ophthalmoparesis/ophthalmoplegia, 198 neurological examination, 75, 76–77,
opioids 90–92, 94–95
head trauma in dogs and cats, 341 paresis/plegia and proprioceptive
neck and/or spinal pain, 262 ataxia, 284, 293
pupil size, 196 pupil size, 204, 206
opsoclonus, 72, 243–244 vestibular syndrome, 236
optic nerve disease, 11 palpebral reflex, 66–67, 209, 217
organophosphate toxicity, 196 paper slide test, 83
orthopaedic disease paradoxical vestibular syndrome, 16,
clinical history and signalment, 33 235, 243, 244
neck and/or spinal pain, 260, 261, 271 paraneoplastic syndrome, 28
orthostatic tremor, 13, 160 parasitic infections
osseous‐associated wobbler cerebellar dysfunction, 249–251, 250,
syndrome, 279–280, 282 252
otitis media/externa, 250 clinical history and signalment, 26–27
otitis media/interna cranial nerve deficits, 214–216, 216
388 Index

parasympathetic oculomotor nuclei, nonkinesigenic dyskinesia in Labrador

195–198, 201 Retriever/Jack Russell
paresis/plegia Terrier, 167–168
acute spinal cord injury, 358, 361 presentations in general
all limbs affected, 109–110, 109 practice, 164–168
approach to paraparesis in Scottie cramp in Scottish Terriers, 167
practice, 296 patellar reflex
approach to tetraparesis in lesion localisation, 108, 110–116
practice, 291 monoparesis and lameness, 297–298
clinical history and neurological examination, 87–88
signalment, 276–283 pathological nystagmus, 18
diagnostic approach, 275–284 patient positioning, 337
formulating a plan, 284–287, 286 paw replacement test, 79–80, 80, 174
hemiparesis, 110–111 pedal withdrawal reflex see withdrawal
intervertebral disc disease, 278–282, reflex
287–296 PEG see polyethylene glycol
lesion localisation, 104, 106, 107–116, pelvic limbs
284 acute spinal cord injury, 361
monoparesis, 112–113 lesion localisation, 109–111, 112–113,
neck and/or spinal pain, 264 115
neuroanatomic basis, 275 neurological examination, 81–83,
neurological evaluation, 13–15, 19 86–87
neurological examination, 61, 62, 63, pendular nystagmus, 18
69, 283–284, 283 perineal reflex, 89, 111–112
neuromuscular disorders, 303–304 peripheral nerve
onset of clinical signs, 276–280, hyperexcitability, 161–163
284–287 peripheral nerve sheath tumour
paraparesis, 111–112, 111, 296 (PNST), 210–212, 210–211
physiotherapy and peripheral nerve tumours, 300
rehabilitation, 294–296 peripheral nervous system (PNS)
presence/absence of pain, 281, 284–287 clinical history and signalment, 31–32
presentations in general lesion localisation, 100, 101, 113, 117,
practice, 275–296 117
progression of clinical signs, 280–281 neurological evaluation, 2, 3, 14
pupil size, 198 neurological examination, 84–85
spinal shock phenomenon, 116 peripheral neuropathies, 119–120,
symmetry/asymmetry of neurological 302–306
deficits, 282 permethrin toxicity, 26
vestibular syndrome, 236 phantom scratching, 268
see also monoparesis and lameness phenobarbitone, 140, 148–151, 352–353
paroxysmal dyskinesias phenylephrine response test, 207
episodic hypertonicity syndrome in physical examination
Cavalier King Charles differential diagnosis, 122
Spaniel, 166–167 epileptic seizures, 143
gluten‐sensitive dyskinesia in Border head trauma in dogs and
Terriers, 166 cats, 333–334
 Index 389

mentation, 168–169, 173 vestibular syndrome, 235

neck and/or spinal pain, 260–261 potassium bromide, 140, 148, 151–152,
physiological nystagmus, 18 170, 355–356
physiotherapy and Pourfour du Petit syndrome, 199
rehabilitation, 294–296 prednisolone, 178–179, 191, 216,
pilocarpine response test, 195, 196, 201 273–274, 295, 307–308
plegia see paresis/plegia pre‐ganglionic neurons, 194, 204, 204
PLR see pupillary light reflex primary cerebellar cortical
pneumothorax, 333, 359 degeneration, 255–256
PNS see peripheral nervous system propofol, 353–354
PNST see peripheral nerve sheath tumour proprioception
poisonings see toxin exposure blindness, 188
polyethylene glycol (PEG), 363 extensor postural thrust, 82–83
portosystemic shunt, 357 hemi‐walking, 82
positional nystagmus, 71 hopping, 80–82
positional strabismus, 18 lesion localisation, 103–105, 107
post‐anaesthetic cortical blindness, 191 mentation, 174
post‐ganglionic neurons, 194, 204–205, neurological examination, 77–84, 80
205 neuromuscular disorders, 303
post‐retinal blindness, 185, 186–188, other tests of proprioception, 83–84
186–187 paw replacement, 79–80, 80
postural reactions spinal/proprioceptive ataxia, 15–16,
acute spinal cord injury, 361 60, 107, 275–287, 290, 295
cerebellar dysfunction, 241–242 wheelbarrow testing, 82
monoparesis and lameness, 297 prosencephalon, 2
neck and/or spinal pain, 259–260 protozoal infections, 30, 34
paresis/plegia and proprioceptive ptosis, 198
ataxia, 283 pupillary light reflex (PLR)
vestibular syndrome, 235 abnormalities of pupil size, 192–195,
postural tremors, 160–161 192, 197
posture blindness, 184–188, 187
acute spinal cord injury, 361 neurological evaluation, 11
assessment of proprioception, 77–84, 80 neurological examination, 49, 69,
body and spinal postures, 55–57, 56 73–75, 74
cerebellar dysfunction, 241–242, 243 pupil size and symmetry
head position, 52–53, 52 active constriction in response to
lesion localisation, 115–116 light, 192–193, 192
limb and joint position, 53–54, 54–55 active dilation in response to sympathetic
mentation, 174 stimulation, 193–194, 193
neck and/or spinal pain, 257–260, anisocoria, 196–207
258–259 bilateral miosis, 195–196
neurological examination, 52–58 bilateral mydriasis, 194–195
neuromuscular disorders, 303 clinical approach to unilateral
paresis/plegia and proprioceptive miosis, 205–207
ataxia, 283, 283 clinical approach to unilateral
tail postures, 57–58, 57 mydriasis, 200–202
390 Index

pupil size and symmetry (contd.) reflex dyssynergia, 23

definitions and terminology, 191–192 reflex seizures, 136
differential diagnosis, 198–199, 203 refractory epilepsy, 157
neurological examination, 69–70, 201, REM see rapid eye movement
206 renal insufficiency, 151
presentations in general response to medication, 35, 172
practice, 191–207 retinal examination, 189
unilateral miosis, 202–207, 202–205 retrobulbar disease, 205–206
unilateral mydriasis, 197–202, 199–200 risus sardonicus, 286, 286
pyrexia, 127 ROS see reactive oxygen species

radial nerve paresis/plegia, 300 saccadic eye movements, 71, 243–244

radiation therapy, 212 SARDS see sudden acquired retinal
radiography degeneration syndrome
acute spinal cord injury, 363–364, 363 SCA see spinocerebellar ataxia
blindness, 190 Schiff–Sherrington posture
cranial nerve deficits, 226, 227, acute spinal cord injury, 361
230–231 lesion localisation, 115–116
head trauma in dogs and cats, 334, neurological examination, 55–56
342–343 paresis/plegia and proprioceptive
neck and/or spinal pain, 265–267, ataxia, 283, 283
265–267 sciatic nerve, 88, 113
neurological examination, 46–47, 47 scoliosis, 57
rapid eye movement (REM) sleep Scottie cramp, 167
disorder, 7, 170 sedation, 341
reactive oxygen species (ROS), 330–331 seizures see epileptic seizures
reactive seizures, 137 sevoflurane, 354–355
rectal diazepam, 158 sex‐linked conditions, 38, 122
recumbency, 366 SOD see superoxide dismutase
reduced sensation/hypoaesthesia spinal cord lesions
acute spinal cord injury, 361–362, 365 acute spinal cord injury, 358–367
cranial nerve deficits, 209, 210, 213 all limbs affected, 109–110, 109
lesion localisation, 107 anatomy and physiology, 106–107, 106
monoparesis and lameness, 298 both thoracic limbs only, 113
neurological evaluation, 19, 20 hemiparesis, 110–111
paresis/plegia and proprioceptive lesion localisation, 106–116
ataxia, 292 monoparesis, 112–113
referral neck and/or spinal pain, 257–274
blindness, 189 neurological evaluation, 3, 14–16, 21
epileptic seizures, 146 neuromuscular disorders, 303
mentation, 175–176 paraparesis, 111–112, 111
neck and/or spinal pain, 274 paresis/plegia and proprioceptive
paresis/plegia and proprioceptive ataxia, 283–284, 293–294
ataxia, 286, 290–292 potential pitfalls in lesion
presentations in general localisation, 114–116
practice, 133–134 pupil size, 203–204, 203–204
 Index 391

regional/segmental incidence and prevalence, 346

localisation, 108–109, 108 maintenance antiepileptic drug
Schiff–Sherrington posture, 115–116 therapy, 357–358
spinal shock phenomenon, 116 neuroanatomical basis, 345–346
vestibular syndrome, 231 neurological evaluation, 348, 356
spinal empyema, 265 nursing care of hospitalised
spinal nephroblastoma, 38 animals, 356
spinal palpation, 94–95 pharmacological treatment, 140
spinal/proprioceptive ataxia, 15–16, 60, seizure management in the home
107, 275–287, 290, 295 environment, 158
spinal reflexes stopping the seizure activity, 349–356
acute spinal cord injury, 360 systemic stabilisation, 349
cerebellar dysfunction, 242 why emergency treatment is
cutaneous trunci reflex, 92–94, 93 required, 346
mentation, 175 steroid‐responsive meningitis arteritis
monoparesis and lameness, 297–298 (SRMA)
neurological evaluation, 14 clinical history and signalment, 31, 34,
neurological examination, 84–94 35, 38
other limb reflexes, 88–89 management, 272–273
paresis/plegia and proprioceptive neck and/or spinal pain, 264
ataxia, 283–284 neurological evaluation, 21
patellar reflex, 87–88 steroid therapy, 214
perineal reflex, anal tone, tail tone, and stifle joint extension, 53–54, 54
bladder function, 89–92, 91 strabismus
vestibular syndrome, 236 neurological evaluation, 18
withdrawal reflex, 85–87 neurological examination, 62–64, 64
spinal shock, 116, 361 pupil size, 198
spinocerebellar ataxia (SCA), 162–163 vestibular syndrome, 234–236, 235
spontaneous blinking, 217 stress/anxiety, 88, 169, 174
spontaneous eye movements, 70–72 stride length
SRMA see steroid‐responsive meningitis lesion localisation, 114
arteritis neurological examination, 59
static strabismus, 18 neuromuscular disorders, 303
status epilepticus and acute repetitive stridor, 222, 224
seizures, 345–358 stroke
anticonvulsant medications, 350–356 cerebellar dysfunction, 246–248, 247
assistance from other staff members, 348 mentation, 177–178
classification by clinical vestibular syndrome, 238–239, 240
presentation, 136, 345 structural epilepsy, 138, 138
clinical approach, 346–358, 347 stupor
clinical history and signalment, 348 neurological evaluation, 9
correction of any metabolic neurological examination, 51
cause, 349–350 presentations in general practice, 169,
head trauma in dogs and cats, 334 180–182
identifying the underlying sudden acquired retinal degeneration
cause, 356–357 syndrome (SARDS), 11, 184–185
392 Index

superoxide dismutase (SOD), 278–280 TFAST see thoracic focused assessment

supportive care with sonography for trauma
acute spinal cord injury, 366–367 thalamus, 170–171
head trauma in dogs and thiamine deficiency, 238
cats, 341–342 third eyelid protrusion, 202, 203, 217
palliative care, 212 thoracic focused assessment with
status epilepticus and acute repetitive sonography for trauma (TFAST), 333–
seizures, 356 334, 342–343
supraspinatus muscle, 77, 78 thoracic limbs
surgical resection, 212 acute spinal cord injury, 361
symmetry/asymmetry lesion localisation, 109–115
cerebellar dysfunction, 242–243, neurological examination, 81–83, 86
244–245 thoracic segments, 3
clinical history and signalment, 35–36 thoracolumbar intervertebral disc
cranial nerve deficits, 210, 220–221 extrusion, 291–292
neurological examination, 62, 63, 65, thoracolumbar pain, 259, 259, 261
69–70 tibialis cranialis, 88–89
neuromuscular disorders, 303–304 tongue
paresis/plegia and proprioceptive cranial nerve deficits, 229–231, 230
ataxia, 282 symmetry and tone, 65, 75
syncope, 6 toxin exposure
syringo(hydro)myelia, 30, 32, 267–268, cerebellar dysfunction, 252–253
268, 273–274, 278–280 clinical history and signalment,
systemic disease, 304–305 27–28, 34
systemic stabilisation cranial nerve deficits, 225
acute spinal cord injury, 362 differential diagnosis, 128
fluid therapy/resuscitation, 336–337, epileptic seizures, 137
349–350 pupil size, 195–196
head trauma in dogs and vestibular syndrome, 236, 238
cats, 335–337 Toxoplasma gondii, 249–251
intravenous access, 336, 349 transient vestibular events, 7
minimum database, 336, 349 trauma
oxygenation, 335, 349, 362 acute spinal cord injury, 358–367
patient positioning, 337 cerebellar dysfunction, 252
status epilepticus and acute repetitive clinical history and signalment, 28–29,
seizures, 349 30–32, 34
ventilation, 335 cranial nerve deficits, 211, 220, 223
differential diagnosis, 128
tactile placing, 83–84 epileptic seizures, 138
tail‐pull injury, 23 head trauma in dogs and cats,
tail tone/carriage 329–344
lesion localisation, 111–112 mentation, 171, 173, 180
neurological examination, 57–58, 57, monoparesis and lameness, 299–300
89–90 neck and/or spinal pain, 265–266,
TBI see traumatic brain injury 266
tetanus/tetany, 161–162, 286 neurological examination, 90
 Index 393

paresis/plegia and proprioceptive neurological examination, 90–92, 91

ataxia, 276–277, 280–282, 285, 296 urinary tract infection (UTI), 294
vestibular syndrome, 236, 238
traumatic brain injury (TBI), 330–332, vaccination, 26, 251
334–335, 343 vagus nerve
traumatic disc extrusion, 276–277, laryngeal paralysis, 222–225
280–282, 285, 296 megaoesophagus, 225–229, 227
travel history, 27 presentations in general practice, 157,
tremors 222–229
clinical history and signalment, 27 stimulation, 157
lesion localisation, 105–106 vascular disease
neurological evaluation, 12–13 cerebellar dysfunction, 246–248, 247
presentations in general clinical history and signalment,
practice, 159–161, 242 30–31, 38
triage, 333–334 differential diagnosis, 125–127
triceps, 88–89 epileptic seizures, 138
trigeminal nerve mentation, 176–178
bilateral masticatory muscle atrophy/ monoparesis and lameness, 298
masticatory myositis, 214–216, 216 neck and/or spinal pain, 264
bilateral trigeminal nerve vasculitis, 28
dysfunction, 212–216, 216 ventilation, 333, 335
idiopathic trigeminal neuropathy, 213 vertebral fracture/luxation, 55, 90, 277,
presentations in general 363–365, 363–364
practice, 209–216 vestibular syndrome
pupil size, 204–205 anatomy of the vestibular system,
unilateral trigeminal nerve 231, 232
dysfunction, 210–212, 210–211 central lesions, 238–239
trochlear nerve dysfunction, 63–64 cerebellar dysfunction, 242–243, 244
tropicamide, 194, 200 clinical history and
two‐engine gait, 110, 114 signalment, 232–234, 233–235
diagnostic approach, 234–239
ultrasonography, 190, 333–334, 342–343 differential diagnosis, 231, 236–239
UMN see upper motor neurons head tilt, 232, 233
unilateral miosis, 202–207, 202–205 idiopathic/geriatric vestibular syndrome,
unilateral mydriasis, 197–202, 199–200 237
upper motor neurons (UMN) investigation, 239–240
acute spinal cord injury, 361, 366–367 lesion localisation, 104, 106, 234–236
lesion localisation, 106, 106, 114–116 management, 240–241
monoparesis and lameness, 298 neurological evaluation, 18
neurological evaluation, 3, 13–15, neurological examination, 234–236
22–23 nystagmus, 233–236, 234
neurological examination, 59, 61, 84, peripheral lesions, 236–237
88, 91–92 presentations in general practice,
pupil size, 194, 203, 203 231–241
urinary tract strabismus, 234–236, 235
neurological evaluation, 21–23, 22 vestibular ataxia, 15–16, 60, 232–233, 234
394 Index

vestibulo‐ocular reflex testing, 72–73, 73 wheelbarrow testing, 82

VIBE‐MRI see Volumetric interpolated whole‐body tremor, 12–13
breath‐hold examination magnetic wide‐based stance, 53, 54
resonance imaging withdrawal from medication, 153–154
viral infections, 26, 249–251 withdrawal reflex
visual response see eyes/visual response lesion localisation, 108, 109–116, 117,
visual tracking, 183 119–120
VITAMIN D mnemonic, 124–125, 126 monoparesis and lameness,
vocalisation 297–298
clinical history and signalment, 33–34 neurological examination, 85–87
mentation, 172 neuromuscular disorders, 303
neck and/or spinal pain, 260 paresis/plegia and proprioceptive
neurological evaluation, 20 ataxia, 283–284
Volumetric interpolated breath‐hold wobbler syndrome, 279–280, 282
examination magnetic resonance
imaging (VIBE‐MRI), 221 xeromycteria, 218, 219
voluntary blinking see blinking
vomiting, 226 zonisamide, 156