Nervous System : 560

DAMAGE TO A LOBE RESULTS IN THE IMPAIRMENT OF THE SPECIFIC FUNCTION DIRECTED OF THAT
LOBE

CRANIAL NERVES: TWELVE PAIRS OF CN

EVOLVE FROM THE BRAIN OR BRAIN STEM
AND TRANSMIT MOTOR AND SENSORY
MESSAGES

CRANIAL NERVE TYPE OF IMPULSE FUNCTION

OLFACTORY NERVE SENSORY CARRIES SMELL IMPULSES
FROM NASAL MUCOUS
MEMBRANE TO THE BRAIN
OPTIC NERVE SENSORY CARRIES VISUAL IMPULSES
FROM EYE TO BRAIN
OCULOMOTOR NERVE MOTOR CONTRACTS EYE MUSCLES TO
CONTROL EYE MOVEMENT
(INFERIOR LATERAL, MEDIAL,
SUPERIOR), CONSTRICTS
PUPILS, AND ELEVATES EYELIDS
(ACCOMMODATION)
TROCHLEAR NERVE MOTOR CONTRACTS ONE EYE MUSCLE
TO CONTROL INFEROMEDIAL
EYE MOVEMENT
TRIGEMINAL NERVE SENSORY MOTOR CARRIES SENSORY IMPULSES OF
PAIN, TOUCH, AND
TEMPERATURE FROM THE FACE
TO THE BRAIN, INFLUENCE
CLENCHING AND LATERAL JAW
MOVEMENTS (BITING AND
CHEWING)
ABDUCEN NERVE MOTOR CONTROLS LATERAL
MOVEMENTS
FACIAL NERVE SENSORY MOTOR SENSORY FIBERS FOR TASTE
(2/3RD ANTERIOR), STIMULATES
SALIVARY GLANDS EXCEPT
PAROTID GLANDS AND TEARS
FROM LACRIMAL GLANDS
FACIAL MUSCLES AND AFFECTS
FACIAL EXPRESSIONS
VESTIBULOCOCHLEAR NERVE SENSORY HEARING AND BALANCE
GLOSSOPHARYNGEAL NERVE SENSORY MOTOR TASTE (1/3 POSTERIOR),
SENSORY FIBERS OF THE
PHARAYNX THAT RESULTS IN
THE GAG REFLEX WHEN
STIMULATES
SECRETORY FIBERS TO THE
PAROTID SALIVARY GLANDS;
PROMOTES SWALLOWING
MOVEMENTS
VAGUS NERVE SENSORY MOTOR SENSATION FROM THE THROAT,
LARYNX, HEART, LUNGS,
BRONCHI, GASTROINTESTINAL
TRACT, AND ABDOMINAL
VISCERA
PROMOTES SWALLOWING
TALKING AND PRODCUTION OF
THE DIGESTIVE JUICES
SPINAL ACCESSORY NERVE MOTOE NECK MUSCLES
(STERNOCLEIDOMASTOID AND
TRAPEZIUS) PROMOTE
MOVEMENT OF THE
SHOULDERS AND HEAD
ROTATION
MOVEMENT OF THE LARYNX
HYPOGLOSSAL NERVE MOTOR MOVEMENT OF THE TONGUE
TO PROMOTE MOVEMENT OF
FOOD AND TALKING

SPINAL NERVES

: THE SENSORY (AFFERENT) FIBER ENTERS THE DORSAL ROOTS OF THE CORD; THE MOTOR
(EFFERENT) FIBER ENTERS THE VENTRAL ROOTS OF THE CORD

: THE SENSORY ROOT OF EACH SPINAL NERVE INNERVATES AN AREA OF THE SKIN CALLED A
DERMATOME
HOW TO USE A REFLEX HAMMER:
GLASGOW COMA SCALE
CRANIAL NERVES ASSESSMENT: DOCUMENT THE FINDINGS

CRANIAL NERVES NORMAL ABNORMAL

OLFACTORY NERVE: Do not INTACT CN I Impairment can be due to
use noxious odors, since they  LEFT SOAP/ nasal obstruction,
may stimulate pain fibers HESITANT damage to the olfactory
from CN V. CN I is often not  RIGHTCOFFEE nerves in the nasal
tested unless specific mucosa, damage to the
pathology such as a sub nerves as they cross the
frontal brain tumor is cribriform plate, or
suspected. intracranial lesions
affecting the olfactory
bulbs.
OPTIC NERVE: This exam allows direct
 Check the internal visualization of damage to the
structures of the eye retina or retinal vessels, optic
nerve atrophic changes,
 Visual acuity papilledema
(Test visual acuity for
each eye separately  Visual Extinction In
(by covering one eye visual extinction, a
at a time) using an eye form of hemineglect,
chart) and Color Vision patients do not report
(Test each eye seeing the fingers on
separately for ability the affected (usually
to distinguish colors. left) side of the visual
Test for red field, although they
desaturation, a can see fingers when
sign of subtle they are presented to
asymmetry in optic that side alone.
nerve function seen,  Visual Fields: In
for example, in optic comatose or
neuritis uncooperative
(see Neuroanatomy patients, visual fields
through Clinical can be tested roughly
Cases, Key Clinical using blink-to-threat,
Concepts 11.4), by in which the
asking the patient to examiner's fingers are
cover each eye moved rapidly
alternately while towards the patient's
looking at a red object eyes from each
and report any quadrant to see if a
relative dullness of blink occurs.
the color in one eye)
 Visual Fields Blink to threat Damage
(Test visual fields for anywhere in the visual
each eye by asking the pathway from the eye to
patient to fixate the visual cortex can cause
straight ahead and to specific deficits in the
report when a finger visual fields of one or both
can be seen moving in eyes (see Neuroanatomy
each quadrant.
through Clinical Cases,
Alternatively, ask the
patient to report how Figure 11.15). Importantly,
many fingers are some visual information
being shown in each from each eye crosses to
quadrant. More the opposite side at
precise mapping of the optic chiasm.
visual fields can be Therefore, lesions in front
done in the laboratory of the optic chiasm (eye,
for patients who will optic nerve) cause visual
be followed over time deficits in one eye, while
(see Neuroanatomy lesions behind the optic
Through Clinical
chiasm (optic tract,
Cases, Key Clinical
Concepts 11.2) thalamus, white matter,
 Visual Extinction visual cortex) cause visual
(Test visual fields for field deficits that are
 each eye by asking the
patient to fixate similar for both eyes.
straight ahead and to
report when a finger Visual hemineglect or
can be seen moving in
extinction is usually
each quadrant.
Alternatively, ask the caused by contralateral
patient to report how parietal lesions, and less
many fingers are often by frontal or
being shown in each thalamic lesions. Neglect
quadrant. More is usually more robust
precise mapping of in lesions of the right
visual fields can be hemisphere
done in the laboratory
for patients who will
be followed over time
(see Neuroanatomy
Through Clinical
Cases, Key Clinical
Concepts 11.2)
PUPILLARY RESPONSES (CN II, AFFERENT PUPILLARY DEFECT:
III)  First, record the pupil AFFERENT PUPILLARY DEFECT:
size and shape at rest. Next, NOTE SWINGING FLASHLIGHT In an afferent pupillary
note the direct response, defect there is a decreased direct response caused by
meaning constriction of decreased visual function in one eye. This can be
the illuminated pupil, as demonstrated with the swinging flashlight test, in which
well as the consensual the light is moved back and forth between the eyes
response, meaning every two to three seconds. The afferent pupillary
constriction of the defect becomes obvious when the flashlight is moved from
opposite pupil. the normal to the affected eye, and the affected
 Pupil Light Reflex pupil dilates in response to light. Under normal
 Swinging Flashlight conditions, the pupil constricts in response to light.
 Accommodation Brief oscillations of pupillary size called hippus occur
normally in response to light which should not be confused
with an afferent pupillary defect.

ACCOMODATION:
  test the pupillary response to accommodation.
Normally, the pupils constrict while fixating on
an object being moved from far away to near
the eyes.

Direct response (pupil illuminated). The direct

response is impaired in lesions of the ipsilateral
optic nerve, the pretectal area, the ipsilateral
parasympathetics traveling in CN III, or the
pupillary constrictor muscle of the iris.

Consensual response (contralateral pupil

illuminated). The consensual response is impaired
 in lesions of the contralateral optic nerve, the
pretectal area, the ipsilateral parasympathetics
traveling in CN III, or the pupillary constrictor
muscle.

Accommodation (response to looking at

something moving toward the eye).
Accommodation is impaired in lesions of the
ipsilateral optic nerve, the ipsilateral
parasympathetics traveling in CN III, or the
pupillary constrictor muscle, or in bilateral
lesions of the pathways from the optic tracts to
the visual cortex. Accommodation is spared in
lesions of the pretectal area.

EXTRAOCULAR MOVEMENTS Check extraocular movements (eye movements) by

(CN III, IV, VI) having the patient look in all directions without moving their
head and ask them if they experience any double vision. 

SMOOTH PURSUIT having the patient follow an object

moved across their full range of horizontal and vertical eye
movements

CONVERGENCE movements by having the patient fixate

on an object as it is moved slowly towards a point right
between the patient's eyes.; Also, observe the eyes at rest to
see if there are any abnormalities such as spontaneous
nystagmus (see below) or dysconjugate gaze (eyes not
both fixated on the same point) resulting in diplopia (double
vision)

SACCADES eye movements used to rapidly refixate from

one object to another. The examiner can test saccades by
holding two widely spaced targets in front of the patient (such
as the examiner's thumb on one hand and index finger on the
other) and asking the patient to look back and forth between
the targets.

OPTOKINETIC NYSTAGMUS (OKN)  Test optokinetic

nystagmus (OKN) by moving a strip with parallel stripes on
it in front of the patient's eyes and asking them to watch the
stripes go by. Normally, rhythmic eye movements
called nystagmus occur consisting of an alternating slow
phase with slow pursuit movements in the direction of strip
movement, and a rapid phase with quick refixations back to
midline
 OCULOCEPHALIC TESTING/ MANEUVERS In comatose or
severely lethargic patients, the vestibulo-ocular reflex can
be used to test whether brainstem eye movement pathways
are intact. The oculocephalic reflex, a form of the
vestibulo-ocular reflex, is tested by holding the eyes open and
rotating the head from side to side or up and down. These
maneuvers obviously should not be performed in cases of
head injury or other cases of suspected cervical spine trauma
unless complete cervical spine films are normal. The reflex is
present if the eyes move in the opposite direction of the head
movements, and it is therefore sometimes called doll's eyes.
Note that in awake patients, doll's eyes are usually not
present because voluntary eye movements mask the reflex.
Thus, the absence of doll's eyes suggests brainstem
dysfunction in the comatose patient but can be normal in the
awake patient. Another, more potent stimulus of the
vestibulo-ocular reflex used to evaluate comatose patients
is caloric stimulation

Careful testing can often identify abnormalities in individual

muscles or in particular cranial nerves (oculomotor,
trochlear, or abducens) in their course from the brainstem to
the orbit, in the brainstem nuclei, or finally, in the higher-
order centers and pathways in the cortex and brainstem that
control eye movements (for more details, see Neuroanatomy
Through Clinical Cases, Chapter 14). Spontaneous
nystagmus can indicate toxic or metabolic conditions
such as drug overdose or alcohol intoxication, or
peripheral or central vestibular dysfunction.
FACIAL SENSATION AND FACIAL SENSATION
MUSCLES OF MASTICATION (CN  Test facial sensation using a cotton wisp and a
V) sharp object. Also test for tactile extinction using
double simultaneous stimulation.
CORNEAL REFLEX
 which involves both CN V and CN VII, is tested by
touching each cornea gently with a cotton wisp
and observing any asymmetries in the blink
response.

MASSETER
 Feel the masseter muscles during jaw clench. Test for
a jaw jerk reflex by gently tapping on the jaw with the
mouth slightly open.

 JERK JAW REFLEX

Facial sensation can be impaired by lesions of

the trigeminal nerve (CN V), the trigeminal sensory
nuclei in the brainstem, or ascending sensory
 pathways to the thalamus and somatosensory
cortex in the postcentral gyrus (see Neuroanatomy
through Clinical Cases, Chapters 7 and 12). The
corneal blink reflex is mediated by polysynaptic
connections in the brainstem between the
trigeminal (CN V) and facial (CN VII) nerves and
can be impaired by lesions anywhere in this
circuit.

Tactile Extinction in the presence of intact primary

sensation is usually caused by right parietal lesions.

Weakness of the muscles of mastication can be

due to lesions in the upper motor neuron (UMN)
pathways synapsing onto the trigeminal (CN V)
motor nucleus, in the lower motor neurons
(LMNs) of the trigeminal motor nucleus in the
pons or as they exit the brainstem to reach the
muscles of mastication, in the neuromuscular
junction, or in the muscles themselves.

Presence of a jaw jerk reflex is abnormal,

especially if it is prominent. It is a sign of
hyperreflexia associated with lesions of UMN
pathways projecting to the trigeminal motor
nucleus. Both the afferent and the efferent limbs
of the jaw jerk reflex are mediated by CN V.

MUSCLES OF FACIAL FACIAL MUSCLES:

EXPRESSION AND TASTE ( CN  Look for asymmetry in facial shape or in depth
VII) of furrows such as the nasolabial fold. Also look
for asymmetries in spontaneous facial
expressions and blinking. Ask patient to smile,
puff out their cheeks, clench their eyes tight, wrinkle
their brow, and so on. Old photographs of the
patient can often aid your recognition of
subtle changes.
TASTE:
 Check taste with sugar, salt, or lemon juice on cotton
swabs applied to the lateral aspect of each side of the
tongue. Like olfaction, taste is often tested only when
specific pathology is suspected, such as in lesions of
the facial nerve, or in lesions of the gustatory nucleus
(nucleus solitarius).
 Facial weakness can be caused by lesions of
 upper motor neurons in the contralateral
motor cortex or descending central nervous
system pathways, lower motor neurons in the
ipsilateral facial nerve nucleus (CN VII) or
exiting nerve fibers, the neuromuscular
junction, or the face muscles. Note that the
upper motor neurons for the upper face (the
upper portions of the orbicularis oculi and the
frontalis muscles of the forehead) project to
the facial nuclei bilaterally (see Neuroanatomy
Through Clinical Cases, Figure 12.12).
Therefore, upper motor neuron lesions, such as a
stroke, cause contralateral face weakness
sparing the forehead, while lower motor
neuron lesions, such as a facial nerve injury,
typically cause weakness involving the whole
ipsilateral face.
HEARING AND VESTIBULAR  HEARING: Can the patient hear fingers rubbed together
SENSE (CN VIII) or words whispered just outside of the auditory canal
and identify which ear hears the sound? A tuning fork
can be used to distinguish neural from mechanical
conductive hearing problems
 RINNE TEST: Rinne test the sound heard when
holding a vibrating tuning fork just outside each ear
(air conduction); is compared to the sound heard
when placing the tuning fork handle on each mastoid
process (bone conduction)
 CONDUCTIVE HEARING LOSS In conductive hearing
loss, bone conduction is greater than air
conduction, because bone conduction bypasses
problems in the external or middle ear.
 SENSORINEURAL HEARING LOSS air conduction is
greater than bone conduction in both ears (as
in normal hearing), however, hearing is
decreased in the affected ear.
 WEBER’S TEST  the tuning fork is placed on the
vertex of the skull in the midline, and the
patient is asked to report the side where the
tone sounds louder
 C0NDUCTIVE HEARING LOSS tone is louder on the
affected side; You can verify that the tone is louder on
the side of conductive hearing loss on yourself by
closing each ear alternately while humming
 VESTIBULAR SENSE Vestibular sense is generally not
specifically tested, except for in the following
important situations:
 PATIENTS WITH VERTIGO  Barany or Hall-Pike
Positional Testing: can help distinguish peripheral
from central causes of vertigo. The patient sits on
the bed or examining table, and the examiner
 supports the patient's head as the patient lays back
with one ear down, and with the head extending over
the edge of the table. This maneuver does not need to
be done especially briskly. The patient is asked to keep
their eyes open and report any sensations of vertigo,
while the examiner looks for nystagmus. This change
of position causes maximal stimulation of the
posterior semicircular canal of the ear that is down,
and of the anterior semicircular canal of the ear that is
up. The maneuver is also done with the other ear
down.
 With peripheral lesions: there is usually a delay
of a few seconds before the onset of nystagmus
and vertigo. The nystagmus is horizontal or
rotatory and does not change directions.
Nystagmus and vertigo then fade away within
about a minute. If the same maneuver is repeated,
there is often adaptation, so that the nystagmus
and vertigo are briefer and less intense each
time.
 In contrast, with central lesions: the nystagmus
and vertigo may begin immediately, and there
tends to be no adaptation. Horizontal or
rotatory nystagmus can also be seen with
central lesions. However, vertical nystagmus,
nystagmus that changes directions, or
prominent nystagmus in the absence of vertigo
are seen only in central, and not in peripheral
lesions.
 Patients with limitations of horizontal or
vertical gaze. Testing the vestibulo-ocular
reflex can help localize the lesion
(see Neuroanatomy through Clinical Cases, Chapter
13). As we mentioned when discussing Extraocular
Muscles the vestibulo-ocular reflex can be tested in
two ways.
 The first is using the oculocephalic maneuver, in
which the eyes are held open and the head is turned
rapidly either from side to side or up and down.
 The second is using caloric testing, in which cold or
warm water is instilled into one ear, producing
asymmetric stimulation of the semicircular canals.
 Patients in coma The vestibulo-ocular reflex is
often the only way to test eye movements in these
patients. Further details of these tests and their
significance are provided in Neuroanatomy Through
Clinical Cases Chapters 3, 12 and 13.)
 Hearing loss can be caused by lesions in the
acoustic and mechanical elements of the ear,
the neural elements of the cochlea, or the
acoustic nerve (CN VIII). After the hearing
 pathways enter the brainstem, they cross over at
multiple levels and ascend bilaterally to the thalamus
and auditory cortex. Therefore, clinically significant
unilateral hearing loss is invariably caused by
peripheral neural or mechanical lesions.
Abnormalities in vestibular testing can be associated
with lesions in the vestibular apparatus of the inner
ear, the vestibular portion of CN VIII, the vestibular
nuclei in the brainstem, the cerebellum, or pathways
in the brainstem (such as the medial longitudinal
fasciculus) that connect the vestibular and oculomotor
systems. See Neuroanatomy through Clinical Cases,
Chapters 12 and 14 for greater details)
PALATE ELEVATION AND GAG  Does the palate elevate symmetrically when the
REFLEX (CN IX AND X) patient says, "Aah"? Does the patient gag when the
posterior pharynx is brushed? The gag reflex needs to
be tested only in patients with suspected brainstem
pathology, impaired consciousness, or impaired
swallowing.
 Palate elevation and the gag reflex are impaired in
lesions involving CN IX, CN X, the
neuromuscular junction, or the pharyngeal
muscles.
MUSCLES OF ARTICULATION  Is the patient's speech hoarse, slurred, quiet,
(CN V, VII, IX, X, XII) breathy, nasal, low or high pitched, and so on?
It is often important to ask if the patient's
speech has changed from baseline. Note
that dysarthria (see Neuroanatomy through
Clinical Cases, Key Clinical Concept 12.8), or
abnormal pronunciation of speech, is not the
same as aphasia, which is an abnormality in
language production or comprehension.
 Abnormal articulation of speech can occur in
lesions involving the muscles of articulation,
the neuromuscular junction, or the peripheral
or central portions of CN V, VII, IX, X, or XII.
Furthermore, speech production can be
abnormal as a result of lesions in the motor
cortex, cerebellum, basal ganglia, or
descending pathways to the brainstem
STERNOCLEIDOMASTOID AND  Ask the patient to shrug their shoulders, turn their
TRAPEZIUS MUSCLES (CN XI) head in both directions, and raise their head from the
bed, flexing forward against the force of your hands.
 Weakness in the sternocleidomastoid or trapezius
muscles can be caused by lesions in the muscles,
neuromuscular junction, or lower motor neurons
of the accessory spinal nerve (CN XI).
Unilateral upper motor neuron lesions in the
cortex or descending pathways cause
contralateral weakness of the trapezius, with
relative sparing of sternocleidomastoid
 strength. This may be explained by bilateral upper
motor neuron projections controlling the
sternocleidomastoid, in analogy to the bilateral
projections controlling the upper face.
TONGUE MUSCLES (CN XII)  Note any atrophy
or fasciculations (spontaneous quivering
movements caused by firing of muscle motor
units) of the tongue while it is resting on the
floor of the mouth. Ask the patient to stick their
tongue straight out and note whether it curves to one
side or the other. Ask the patient to move their tongue
from side to side and push it forcefully against the
inside of each cheek.
 Fasciculations and atrophy are signs of lower
motor neuron lesions. Unilateral tongue
weakness causes the tongue to deviate
toward the weak side. Tongue weakness can
result from lesions of the tongue muscles, the
neuromuscular junction, the lower motor
neurons of the hypoglossal nerve (CN XII), or
the upper motor neurons originating in the
motor cortex. Lesions of the motor cortex cause
MOTOR EXAM contralateral tongue weakness.

 MOTOR EXAM
 OBSERVATION, INSPECTION, PALPATION,
MUSCLE TONE TESTING, FUNCTIONAL TESTING,
STRENGTH TESTING OF INDIVIDUAL MUSCLE
GROUPS

First, carefully observe the patient to detect any

twitches, tremors, or other involuntary
movements, as well as any unusual paucity of
movement suggestive of a movement disorder
(see Neuroanatomy Through Clinical Cases, Key
Clinical Concepts 15.2, and 16.1). Note also the
patient's posture. Next inspect several individual
muscles to see if muscle wasting, hypertrophy, or
fasciculations (spontaneous quivering
movements caused by firing of muscle motor
units) are present. The best muscles to look at for
fasciculations in generalized LMN disorders
are the intrinsic hand muscles, shoulder
girdle, and thigh. In cases of suspected
myositis, palpate the muscles to see if there is
tenderness.

 ATROPHY? FASCICULATIONS
 UPPER EXTREMITY TONE (MUSCLE TONE)
 :  Ask the patient to relax, and then passively move
each limb at several joints to get a feeling for any
resistance or rigidity that may be present.
 LOWER EXTREMITY TONE (MUSCLE TONE)
 DRIFT Before formally testing strength in
each muscle, it is useful to do a few
general functional tests that help detect subtle
abnormalities.
 DRIFT Check for drift by having the patient hold
up both arms or both legs and close their eyes.
 RAPID HAND MOVEMENTS: Check fine
movements by testing rapid finger tapping,
rapid hand pronation—supination (as in
screwing in a light bulb), rapid hand tapping,
and rapid foot tapping against the floor or
other
 RAPID FOOT TAPPING

Involuntary movements and tremors are

commonly associated with lesions of the basal
ganglia or cerebellum (see Neuroanatomy Through
Clinical Cases, Key Clinical Concepts 15.2, and 16.1).
Tremors can also occasionally be seen with
peripheral nerve lesions.

Many parts of the motor exam can help distinguish

between upper motor neuron and lower motor
neuron lesions (see Neuroanatomy through Clinical
Cases Chapters 2 and 6). Recall that upper motor
neurons project via the corticospinal tract to
lower motor neurons located in the anterior
horn of the spinal cord. Signs of lower motor neuron
lesions include weakness, atrophy, fasciculations,
and hyporeflexia (reduced reflexes). Signs of
upper motor neuron lesions include weakness,
hyperreflexia (increased reflexes), and
increased tone. The hyperreflexia and increased
tone seen with corticospinal lesions is
apparently caused by damage to pathways that
travel in close association with the corticospinal
tract rather than directly by damage to the
corticospinal tract itself. Note that
with acute upper motor neuron lesions there is
often flaccid paralysis with decreased tone and
decreased reflexes. With time (hours to weeks),
increased tone and hyperreflexia usually
 develop.

Signs of Upper Motor Neuron (UMN) and

Lower Motor Neuron (LMN) Lesions
SIGN UMN LMN LESIONS
LESIONS
WEAKNESS YES YES
ATROPHY NO YES
FASCICULATION NO YES
S
REFLEXES INCREASED DECREASED
TONE INCREASED DECREASED
*Mild atrophy may develop due to disuse.
Increased tone can occur in upper motor neuron lesions,
but can also occur in basal ganglia dysfunction
(see Neuroanatomy Through Clinical Cases, Key
Clinical Concept 16.1). In addition, slow or awkward fine
finger movements or toe tapping in the absence of
weakness can signify a subtle abnormality of the
corticospinal pathways, but can also occur in lesions of
the cerebellum or basal ganglia

STRENGTH OF INDIVIDUAL  Patterns of weakness can help localize a

MUSCLE GROUPS lesion to a particular cortical or white
matter region, spinal cord level, nerve
root, peripheral nerve, or muscle. Test the
strength of each muscle group and record
it in a systematic fashion. It is wise to pair
the testing of each muscle group
immediately with testing of its
contralateral counterpart to enhance
detection of any asymmetries. Muscle
strength is often rated on a scale of 0/5 to 5/5
as follows:

 0/5: no contraction
 1/5: muscle flicker, but no movement
 2/5: movement possible, but not against gravity
(test the joint in its horizontal plane)
 3/5: movement possible against gravity, but not
against resistance by the examiner
 4/5: movement possible against some resistance
by the examiner (sometimes this category is
 subdivided further into 4–/5, 4/5, and 4+/5)
 5/5: normal strength

While testing muscle strength, it is important to keep in

mind anatomic information such as which
nerves, nerve roots, and brain areas control
each muscle and to allow this information to
guide the exam. Also compare proximal versus
distal weakness because these features can
sometimes suggest muscle versus nerve disease,
respectively. A detailed discussion of patterns of
muscle weakness and localization is provided
in Neuroanatomy through Clinical Cases Key Clinical
Concepts 6.3, and in Chapters 8 and 9. In the tables
below we briefly summarize some of the main actions,
muscle groups, peripheral nerves, and nerve roots tested
during the motor exam.

 UPPER EXTREMITY STRENGTH

 DETAILED HAND TEST
 LOWER EXTREMITY TEST
 FOOT EVERSION, INVERSION

Upper Extremity Strength Testing

Nerve
Action Muscles Nerves
Roots
Extensor
digitorum,
Radial nerve
Extensor
Finger (posterior
indicis, C7, C8
extension interosseous
Extensor
nerve)
digiti
minimi
Radial nerve
Thumb Abductor
(posterior
abduction in pollicis C7, C8
interosseous
plane of palm longus
nerve)
Dorsal
interossei,
Finger
Abductor Ulnar nerve C8, T1
abduction
digiti
minimi
Finger and Adductor Ulnar nerve C8, T1
thumb pollicis,
adduction in Palmar
plane of palm interossei
Thumb Opponens
Median nerve C8, T1
opposition pollicis
Thumb
Abductor
abduction
pollicis Median nerve C8, T1
perpendicular to
brevis
plane of palm
Flexor
Flexion at distal digitorum
interphalangeal profundus Median nerve C7, C8
joints digits 2, 3 to digits 2,
3
Flexor
Flexion at distal digitorum
interphalangeal profundus Ulnar nerve C7, C8
joints digits 4, 5 to digits 4,
5
Wrist flexion Flexor
and hand carpi Median nerve C6, C7
abduction radialis
Wrist flexion Flexor
C7, C8,
and hand carpi Ulnar nerve
T1
adduction ulnaris
Wrist extension Extensor
and hand carpi Radial nerve C5, C6
abduction radialis
Elbow flexion
Biceps, Musculocutaneous
(with forearm C5, C6
Brachialis nerve
supinated)
C6, C7,
Elbow extension Triceps Radial nerve
C8
Arm abduction
Deltoid Axillary nerve C5, C6
at shoulder
Lower Extremity Strength Testing

Nerve
Action Muscles Nerves
Roots
Femoral
L1,
nerve, and
Hip flexion Iliopsoas L2, L3,
L1-L3 nerve
L4
roots
Knee Femoral L2, L3,
Quadriceps
extension nerve L4
Knee flexion Hamstrings Sciatic L5, S1,
 (semitendinosus,
semimembranosus, nerve S2
biceps femoris)
Gluteus medius, Superior
Leg L4, L5,
Gluteus minimus, gluteal
abduction S1
Tensor fasciae latae nerve
Obturator externus,
Leg Adductor longus, Obturator L2, L3,
adduction magnus, and brevis, nerve L4
Gracilis
Extensor hallucis Deep
Toe
longus, Extensor peroneal L5, S1
dorsiflexion
digitorum longus nerve
Deep
Foot
Tibialis anterior peroneal L4, L5
dorsiflexion
nerve
Triceps surae
Foot plantar
(gastrocnemius, Tibial nerve S1, S2
flexion
soleus)
Superficial
Foot Peroneus longus,
peroneal L5, S1
eversion Peroneus brevis
nerve
Foot
Tibalis posterior Tibal nerve L4, L5
inversion
When more than one nerve root participates in an
action, emphasis indicates the most important nerve
roots.
DEEP TENDON REFLEXES  BICEPS C5, C6
 BRACHIORADIALIS C6
 TRICEPS C7
 PATELLAR L4
 ACHILLES S1

Check the deep tendon reflexes using impulses from

a reflex hammer to stretch the muscle and tendon.
The limbs should be in a relaxed
and symmetric position, since these factors can
influence reflex amplitude. As in muscle strength
testing, it is important to compare each reflex
immediately with its contralateral counterpart
so that any asymmetries can be detected. If you
cannot elicit a reflex, you can sometimes bring it out
by certain reinforcement procedures. For example,
have the patient gently contract the muscle being
tested by raising the limb very slightly, or have
them concentrate on forcefully contracting a
different muscle group just at the moment when
the reflex is tested. When reflexes are very
brisk, clonus is sometimes seen. This is a
repetitive vibratory contraction of the muscle
that occurs in response to muscle and tendon
stretch. Deep tendon reflexes are often rated according
to the following scale:

 0: absent reflex
 1+: trace, or seen only with reinforcement
 2+: normal
 3+: brisk
 4+: nonsustained clonus (i.e., repetitive vibratory
movements)
 5+: sustained clonus

Deep tendon reflexes are normal if they are 1+, 2+, or

3+ unless they are asymmetric or there is a
dramatic difference between the arms and the
legs. Reflexes rated as 0, 4+, or 5+ are usually considered
abnormal. In addition to clonus, other signs
of hyperreflexia include spreading of reflexes to
other muscles not directly being tested
and crossed adduction of the opposite leg when
the medial aspect of the knee is tapped.

Deep tendon reflexes (see Neuroanatomy Through

Clinical Cases, Figure 2.21) may be diminished by
abnormalities in muscles, sensory neurons, lower
motor neurons, and the neuromuscular
junction; acute upper motor neuron lesions; and
mechanical factors such as joint disease.
Abnormally increased reflexes are associated
with upper motor neuron lesions. Note that deep
tendon reflexes can be influenced by age, metabolic
factors such as thyroid dysfunction or electrolyte
abnormalities, and anxiety level of the patient.
The main spinal nerve roots involved in testing
the deep tendon reflexes are summarized in the
following table:

Deep Tendon Reflexes

Reflex Main Spinal Nerve Roots Involved

Biceps C5, C6
Brachioradialis C6
 Triceps C7
Patellar L4
Achilles Tendon S1
PLANTAR RESPONSE  Test the plantar response by scraping an object
across the sole of the foot beginning from the
heel, moving forward toward the small toe, and
then arcing medially toward the big toe. The
normal response is downward contraction of the
toes. The abnormal response, called Babinski's
sign, is characterized by an upgoing big toe and
fanning outward of the other toes. In some
patients the toes are "silent," moving neither up nor
down. If the toes are down going on one side and
silent on the other, the silent side is considered
abnormal. The presence of Babinski's sign is always
abnormal in adults, but it is often present in
infants, up to the age of about 1 year.

FINGER FLEXIORS  There is no precise hand equivalent for the plantar

response, however, finger flexor reflexes can help
demonstrate hyperreflexia in the upper
extremities. Test finger flexors by tapping
gently on the palm with the reflex hammer.
Alternatively, heightened reflexes can be
demonstrated by the presence of Hoffmann's sign.
You can elicit this sign by holding the patient's
middle finger loosely and flicking the
fingernail downward, causing the finger to
rebound slightly into extension. If the thumb
flexes and adducts in response, Hoffmann's
sign is present.
 Babinski's sign is associated with upper motor
neuron lesions anywhere along the
corticospinal tract. Note that it may not be
possible to elicit Babinski's sign if there is
severe weakness of the toe extensors.
Hoffmann's sign, or heightened finger flexor
reflexes suggest an upper motor neuron lesion
affecting the hands.

REFLEXES TESTED IN SPECIAL  Additional reflexes are tested in special situations

SITUATIONS such as coma, spinal cord injury, frontal lobe
dysfunction, and neurodegenerative disorders. These
reflexes and their interpretation are discussed in the
section "Reflexes in Special Situations"
in Neuroanatomy Through Clinical Cases, Chapter 3

COORDINATION AND GAIT  Coordination and gait are usually described

under a separate section because cerebellar
disorders can disrupt coordination or gait
 while leaving other motor functions
relatively intact. There is much overlap,
however, between the systems being examined in
this section and those examined in the earlier
general motor exam section. Keep in mind that
disturbances of coordination and gait can be
caused by lesions in many systems other
than the cerebellum.
 The term ataxia  is often used to describe the
abnormal movements seen in
coordination disorders. In ataxia there are
medium- to large-amplitude involuntary
movements with an irregular oscillatory
quality superimposed on and interfering
with the normal smooth trajectory of
movement. Overshoot is also commonly seen
as part of ataxic movements and is sometimes
referred to as past pointing when target-
oriented movements are being discussed. Another
feature of coordination disorder
is dysdiadochokinesia—that is, abnormal
alternating movements.
 Cerebellar lesions can cause different kinds of
coordination problems depending on their
location. One important distinction is between
truncal ataxia and appendicular
ataxia. Appendicular ataxia affects
movements of the extremities and is
usually caused by lesions of the cerebellar
hemispheres and associated
pathways. Truncal ataxia affects the
proximal musculature, especially that
involved in gait stability, and is caused by
midline damage to the cerebellar vermis
and associated pathways (see Neuroanatomy
through Clinical Cases, Figure 15-3, and Key
Clinical Concepts 15-2)

ROMBERG TEST  Ask the patient to stand with their feet together
(touching each other). Then ask the patient to close
their eyes. Remain close at hand in case the patient
begins to sway or fall.
 With the eyes open, three sensory systems provide
input to the cerebellum to maintain truncal
stability. These are vision, proprioception, and
vestibular sense. If there is a mild lesion in the
vestibular or proprioception systems, the
patient is usually able to compensate with the
 eyes open. When the patient closes their eyes,
however, visual input is removed and
instability can be brought out. If there is a more
severe proprioceptive or vestibular lesion, or
if there is a midline cerebellar lesion causing
truncal instability, the patient will be unable to
maintain this position even with their eyes
open. Note that instability can also be seen with
lesions in other parts of the nervous system
such as the upper or lower motor neurons or
the basal ganglia, so these should be tested for
separately in other parts of the exam.

GAIT  A patient's gait can be difficult to describe in a

reproducible fashion. Observe the patient
walking toward you and away from you in an
open area with plenty of room.
 Note stance (how far apart the feet are), posture,
stability, how high the feet are raised off the floor,
trajectory of leg swing and whether there
is circumduction (an arced trajectory in the medial
to lateral direction), leg stiffness and degree of knee
bending, arm swing, tendency to fall or swerve in any
particular direction, rate and speed, difficulty
initiating or stopping gait, and any involuntary
movements that are brought out by walking. Turns
should also be observed closely. When following a
patient over several visits, it may be useful to time him
walking a fixed distance, and to count the number of
steps he took and the number of steps he required to
turn around. The patient's ability to rise from a chair
with or without assistance should also be recorded.
 To bring out abnormalities in gait and balance, ask the
patient to do more difficult maneuvers.
 Test tandem gait by asking the patient to walk a
straight line while touching the heel of one
foot to the toe of the other with each step.
 Patients with truncal ataxia caused by damage to
the cerebellar vermis or associated pathways will have
particular difficulty with this task, since they tend to
have a wide-based, unsteady gait, and become
more unsteady when attempting to keep their
feet close together. To bring out subtle gait
abnormalities or asymmetries, it may be
appropriate in some cases to ask the patient to
walk on their heels, their toes, or the insides
or outsides of their feet, to stand or hop on one
leg, or to walk up stairs
 Gait apraxia is a perplexing (and somewhat
controversial) abnormality in which the
patient is able to carry out all of the
 movements required for gait normally when
lying down, but is unable to walk in the
standing position, thought to be associated
with frontal disorders or normal pressure
hydrocephalus (KCC 5.7).

As with tests of appendicular coordination, gait

involves multiple sensory and motor systems. These
include vision, proprioception, lower motor neurons,
upper motor neurons, basal ganglia, the cerebellum,
and higher-order motor planning systems in the
association cortex. Once again, it is important to test
each of these systems for normal function before
concluding that a gait disturbance is caused by a
cerebellar lesion. Localization and diagnosis of gait
disorders is described further in Neuroanatomy Through
Clinical Cases, Key Clinical Concept 6.5, and Table 6.6.)
PRIMARY SENSATION-  Light touch is best tested with a cotton-tipped swab,
ASYMMETRY, SENSORY LEVEL but a light finger touch will often suffice, as long as
care is taken to make the stimulus fairly reproducible.
You can test the relative sharpness of pain by
randomly alternating stimuli with the sharp or dull
end of a safety pin (always use a new pin for each
patient).
 Temperature sensation tested with a cool
piece of metal such as tuning fork

 Vibration sense placing a vibrating

tuning fork on the ball of the patient's
right or left large toe or fingers and asking
him to report when the vibration stops.
Take care not to place the tuning fork on a bone,
since bones conduct the vibration to much more
proximal sites, where they can be detected by
nerves far from the location being tested.

 Joint Position Tense moving one of the

patient's fingers or toes up and down and asking
the patient to report which way it moves. Hold
the digit lightly by the sides while doing this so
that tactile inputs don't provide significant clues
to the direction of movement. The digit should be
moved very slightly because normal individuals
can detect movements that are barely perceptible
by eye.

Two-point discrimination can be tested with a

special pair of calipers, or a bent paper clip, alternating
randomly between touching the patient with one or both
 points. The minimal separation (in millimeters) at which
the patient can distinguish these stimuli should be
recorded in each extremity As in other parts of the
exam, the patient's deficits, as well as the anatomy of the
nerves, nerve roots, and central pathways, should be
used to guide the exam (see Neuroanatomy through
Clinical Cases Chapters 7, 8, and 9). Comparisons
should be made from one side of the body to the other
and from proximal to distal on each extremity. Note
especially if there is a sensory level corresponding to a
particular spinal segment below which sensation
abruptly changes, since such a change may indicate a
spinal cord lesion requiring emergency intervention.
Whenever there are uncertainties in the sensory exam,
or other parts of the exam, a good strategy is to repeat
the relevant portions of the exam several times.
Cortical Sensation, Including  Higher-order aspects of sensation, or cortical
Extinction sensation, should be tested as well. To
test graphesthesia, ask the patient to close their
eyes and identify letters or numbers that are being
traced onto their palm or the tip of their finger. To
test stereognosis, ask the patient to close their eyes
and identify various objects by touch using one hand
at a time. Test also for tactile extinction on double
simultaneous tactile stimulation. Note that
graphesthesia, stereognosis, and extinction cannot
reliably be tested for unless primary sensation
is intact bilaterally.

 Somatosensory deficits can be caused by

lesions in peripheral nerves, nerve roots, the
posterior columns or anterolateral sensory
systems in the spinal cord or brainstem, the
thalamus, or sensory cortex. Recall that
position and vibration sense ascend in the
posterior column pathway and cross over
in the medulla, while pain and
temperature sense cross over shortly after
entering the spinal cord and then ascend
in the anterolateral pathway
(see Neuroanatomy through Clinical Cases,
Figures 2.13, 2.18 and 2.19). Intact primary
sensation with deficits in cortical sensation such
as agraphesthesia or astereognosis suggests a
lesion in the contralateral sensory cortex. Note,
however, that severe cortical lesions can cause
deficits in primary sensation as well. Extinction
 with intact primary sensation is a form of
hemineglect that is most commonly associated
with lesions of the right parietal lobe.
Extinction can also be seen in right frontal or
subcortical lesions, or sometimes in left
hemisphere lesions causing mild right
hemineglect.

 The pattern of sensory loss can provide important

information that helps localize lesions to
particular nerves, nerve roots, and regions
of the spinal cord, brainstem, thalamus, or
cortex (see Neuroanatomy Through Clinical
Cases, Key Clinical Concept 7.3).

REFLEXES

REFLEXES NORMAL FINDINGS

BICEPS CONTRACTION OF THE BICEPS MUSCLE AND
FLEXION OF THE FOREARM
TRICEPS CONTRACTION OF THE TRICEPS MUSCLE AND
EXTENSION OF THE FOREARM
BRACIRADIALIS SUPINATION OF THE HAND AND FLEXION OF
THE FOREARM AT THE ELBOW
PATELLAR CONTRACTION OF THE QUADRICEPS MUSCLE IN
THE THIGH WITH EXTENSION OF THE LEG
ACHILLES PLANTARFLEXION
PLANTAR RESPONSE PLANTAR FLEXION OF THE BIG TOE; FLEXION
AND ADDUCTION OF OTHER TOES  FLEXOR
PLANTAR REFLEX
ABDOMINAL REFLEX MOVEMENT OF THE UMBILICUS TOWARD THE
STIMULUS

PRIMITIVE REFLEX ON ADULTS

REFLEX ABNORMAL FINDINGS

GRASP REFLEX INDEX FINGER AND THUMB CORTICAL OR
PREMOTOR CORTEX DAMAGE
SNOUT REFLEX PURSING OF THE LIP INDICATES FRONTAL LOBE
DAMAGE
SUCKING REFLEX CORTICAL DAMAGE ADVANCED DEMENTIA
 GLABELLA RESPONSE TAPPING OF THE BRIDGE OF THE PATIENT’S
NOSE DIFFUSE CORTICAL DYSFUNCTION

Video: NOTES

Neurological Examination

- Comprehensive Neurological Nursing -> to ensure that important physical signs are not missed

 Hand Hygiene

 WIPER- Wash hands, introduce yourself, permission and pain, expose patient, reposition
patient
 Observe the patient’s gait weakness, swinging of arm, coordination= heel to toe (Tandem
Gait), Romberg’s test (eyes open, eyes closed)
 Handedness Cerebral Hemisphere Dominance hand dominance is clinically significant
 Testing Receptive Aphasia
 Mental Test: Simple General Knowledge Test and Memory Test
 Cranial Nerve Examination
o Olfactory Nerve
o Optic Nerve: Visual Acuity, Pupil Reflex, Examine the Fundi (Right to Right; Left to
Left), Visual Fields (Aligned the visual field’ confrontation test_
o CN III, IV, VIEye Movement 6th= Lateral Rectus (outward), 4th= Inferomedial
gaze Superior Oblique, 3rd= Inferior Oblique (Superolateral gaze), Superior Rectus
(Superior gaze), Medial Rectus (Medial gaze), Inferior rectus (Inferior gaze)
 Testing for Nystagmus
 Testing for Accommodation
 Trigeminal Nerve Sensory Motor0 Ophthalmic, Maxillary, Mandibular
 Testing Motor Function Testing Jaw Jerk  Testing Corneal Reflex
 Testing Facial Nerve
 Auditory Nerve) Vestibulocochlear Nerve
o Rinne’s Test Air Conduction and Bone Conduction
o Unilateral Conductive and Perceptive Deafness
o Differentiating Nerve Perception and Air Conduction Deafness
o Weber’s Test
 Test CN IX and X
o Positioning of the UVULA
o Gag Reflex
 CN XI
o Sternocleidomastoid and Trapezius
 CN XII
o Motor function of the tongue (note atrophy, fasciculations, and tremor
 Testing Motor Function
 o Musculature
o Muscle Atrophy  reduction in bulk and a flabby appearance
o Tremor involuntary spontaneous movements of the limbs or fingers
o Examine of Tone Flaccidity, Rigidity, Spasticity
o Examine the Muscle. Strength normal power for the patient (Resistance) Shoulders
and working down  Against Resistance
 Assessing Reflexes
o Reflex arc and the supraspinal influences which operate on it
 Biceps Reflex
 Triceps Reflex
 Patellar Reflex
 Ankle Reflex
 Reinforcement by Gritting Teeth or Clenching Hands
 Testing for Clonus bristly dorsiflexing the footif present the foot will
continue to jerk backwards and forwards
 Testing the Plantar Reflex Babinski Response applying a firm pressure
usually with your fingernail or a neurotypical border of the dorsum of the foot
and observing the MTP joint of the great toe
 Normal the toe goes down (flexes)
 In UML, the great to extends (extensor response)  with associated
fanning (abducting) of the toes
 Test for Coordination and Sensation
 Coordination (upper and lower limb) touch the finger and the nose
 Test for Dysdiadochokinesia: an inability to perform rapidly
repeated movements  Lower limb run their heel down their shin
(Heel to Shin test=not if there is significant weakness on their limbs)
 Simple Memory Test Recall
 Testing Light Touch wisp of cotton ball applied to a single point with the
patient’s eyes closed  do not drag the wool across skin as this sensation may
be transmitted via pain fibers
 Testing Pain Receptors
 Testing for Sensory Loss in a Glove Distribution  if the sensory lost looks as if
it is a glove or stocking distribution start at the tips of the fingers or toes and
work up until you find the sensory level
 Vibration Sense tested using a c128 tuning fork for testing both the lower
and upper limbs and the trunk
 Test for Proprioception Joint Position Sense eyes closed fingers and
toes should be separated for any adjacent digits and the joint being tested
moved up and/ or down  asked the patient which way is being moved
 Testing Temperature Sense
 Assessing Related Structures
 Skeletal Structures Skull, Spine,
 Extra-cranial Blood Vessels, and the Skin
 Look for Bony Defects or Swellings
  Spinal Curvature and Palpate for Spinal Tenderness
 Test Spinal Movements
 Auscultate the Carotid Arteries for Bruits
 Inspect the Skin for Vascular Malformations, Neuromas, Café au Lait
Spots  Can be seen in associated with certain neurological diseases
 Completion help the patient dress and wash hands