1. Sensation: definition. Analyzer: structure, kinds, function.

Sensitivity
classification. Subjective and objective sorts of sensory disturbance. Sorts of
pain. Reactive pain examination.
Sensation is an ability of an organism to accept stimuli from external and internal
environment.
Analyzer is a sole functional system that consists of three parts:
 Receiving apparatus (receptors) - receptor part
 Sensory explorers - conductive part
 Part of cortex, which receives information, analyzes and synthesizes it.
The main function of Analyzer is to accept and analyze stimuli. Types: Visual,
Acoustical, Sensual, Testate
 Classification, which is based on the place of originating of stimuli.
Exteroceptive, Interoceptive, Proprioceptive
 Classification, which is based on biological principle of originating of
sensation. Protopatical (vital, nociceptive, thalamic). Epicritical sensation
is connected with cortex and it is based on the differentiation of stimuli
according to their modality, intensity, localization etc.
 In clinical practice usually we use classification, which is based on the kind
of stimuli.
 Superficial: light touch, superficial pain, temperature, Trihoesthesia(touch of
hair), hydroesthesia(humidity), tickling, electric current
 Deep: Bathyesthesia(joint sense), Seismesthesia (vibration sense),
Baroesthesia (weight sense), pressure, kinaesthetic sense
 Complicated: Stereognosis (identify objects by palpation), Graphism
(determine number or letters on body, localization sense, discrimination sense
(2 point discrimination), Baragnosis
Objective sorts of sensory disorders:
 Anesthesia - complete loss of any sorts of sensation. For example:
Analgesia - loss of pain sense.
Thermoanesthesia - loss of a temperature sense
Bathyanesthesia - loss of deep joint sense
Astereognosia - loss of stereognostic sense
Topanesthesia - loss of localization sense
Pallanesthesia – loss of vibratory sense
 Hypoesthesia - lowering of sensation.
 Hyperesthesia - sensitization as result of lowering a threshold of
energization in cortex of brain.
 Dysesthesia - distortion of sensitivity, when instead of one stimulus the
patient feels absolutely other. For example, warm touch one feels as cold.
  Hyperpathia - results from rise of a threshold of energization, when there are
strong, unpleasant, badly localized sensations of stimuli. Thus the mild stimuli
are not received absolutely. In basis of hyperpathia the disturbance of the
analytical function of cortex lays.
 Synesthesia - sensation of stimuli not only in a place of its plotting, but also
in the other place.
 Polyesthesia - means sensation of one stimulus as several ones.
 Alloheyria - sensation of stimuli in symmetrical sites on an opposite body
part.
 Alloesthesia - sensation of stimuli in the other place.
 Dissociation of sense - phenomenon of fallout of some kind of sensitivity
while saving others in the area of segment innervation.
Subjective sorts of sensory disturbances:
 Paresthesia is a creeping sensation, cold, burning sensation, fever,
numbness, itch, the pricking etc. Frequently paresthesia is the first sign of
nervous system lesion.
 Pain. The pain sensations can arise at stimuli by the pathological process of
sensitive analyzers at any level (from receptors up to cortex).
Determine the following sorts of pain:
 Local pain - is pain, for example, at palpation of the nervous trunk. That is
pain, which coincides with the place of lesion.
 Projectional pain - is a pain in zone of innervation not only in place of
stimuli, but also distally on a course of nerves or roots
 Irradiating pains - are pains, which are distributed from one nerve branch
to another, not struck.
 Displayed pains - are pains in zones Zacharyin-Hed’s at diseases of inner
organs, when irradiation arises to certain zone on skin through cells of dorsal
horns of spinal cord
 Causalgia (Greek causes - burning sensation, algos - pain). It is intensive
thermalgia originating, for example, at traumas. It is pain without stimulation.
 Reactive pains - are pains that originate at expansion of nerves. The pains
can arise at palpation of pain points and at band spread of nervous trunks.

2. Anatomy of superficial and deep sensory explorers.

Superficial sensation has three neurons.
 The first neuron is situated in unipolar cell bodies. The last are located in
dorsal root ganglia of the spinal cord and homologous ganglia of the
cranial nerves (ganglion intervertebral or ganglion spinals). Their
dendrites are routed on peripherals within plexuses, peripheral nerves. There
 they are finished in various sensory skin receptors. The axons of these
unipolar cells enter the spinal cord through the dorsal roots in a basis of dorsal
horns.
 The second neuron - the cells of the second neuron are situated in dorsal
horns of the spinal cord. The axons create tractus spinothalamicus. The
axons of these neurons cross the midline through the ventral commissura
and go to the opposite lateral funiculus and then run in the lateral
spinothalamic tracts. These tracts run upwards to the brain stem, where they
pass through the oblong brain, the Varoliy’s pons, and peduncles of brain and
are finished in nuclei of thalamus. In case of extramedular pathological
process the ascending type of sensitive disturbance. In case of
intramedular pathologic process (when first lesion of medial fibers is in
lateral funiculus of spinal cord) sensitive disturbance will be distributed from
above downwards, that is descending type of sensitive disturbance.
 The third neuron is located in the nucleus of thalamus. The axons form
thalamocortical tract and pass through internal capsule, then within radiate
crown, and are ended in post central gyrus and parietal lobes of brain
hemisphere, and in upper parts of a gyrus – the sensation from lower
extremities, on the average – from upper extremities, in lower – from the
face and tongue are ended.
Anatomy of Deep sensation explorers: This pathway has also 3 neurons.
 The first neuron The unipolar cell bodies are located in the dorsal root
ganglia of the spinal cord and homologous ganglia of the cranial nerves
(ganglion intervertebral or ganglion spinals). The dendrites are routed on
peripherals within plexuses, peripheral nerves, where they are ended in
various sensory receptors in muscles, tendons and joints. The axons of these
unipolar cells enter the spinal cord through the dorsal root and run in
dorsal funiculus on one side of the spinal cord, where it divides into two
paths – medial thin Holl’s pathway and lateral Burdach’s pathway. In
Holl’s pathways fibers pass from segment Th4 and below, and in
Burdach’s pathway, from segment Th4 and higher. That means the Holl’s
path carries out deep sense from lower extremities and bottom of a trunk, and
Burdach’s path - from upper extremities and top of a trunk. At extramedular
processes (for example, in cervical part of spinal cord) the disturbance of
deep sense accrue for the descending type, and, on the contrary, at
intramedular processes of spinal cord disturbance of deep sense occurs
for the ascending type.
 The second neuron is in Holl’s and Burdach’s nuclear of oblong brain.
The axons of the second neuron create bulbothalamic tract. The fibers of
this path are crossed on olives level of oblong brain, on the pons of brain stem
 they join fibers of spinothalamic tract lateral and create a medial closed
loop. The medial closed loop (lemniscus medialis) consists of fibers of
spinothalamic tract and bulbothalamic tract. The axons of the second
neurons carry all sorts of sensation from opposite side of the body. The
medial closed loop is ended in ventral nucleus of thalamus.
 The third neuron - is in thalamus, from which cells thalamocortical tract
starts. The axons of this path go through internal capsule, radiation crown and
are ended in a postcentral gyrus, partially in the right central gyrus and in
parietal lobes of a share. It is necessary to tell, that a part of fibers from the
second neurons of deep sense are routed not to a thalamus, but to a cerebellum
through lower legs of a cerebellum.

3. Examination of superficial, deep and complex types of sensitivity.

Examination of superficial sensation
 Light touch: Symmetrically touch face, extremities and trunk with
something soft such as brush or cotton wool and ask patient if they feel it
equally on both sides or if touch is increased or decreased.
 Pain: Use neurological pin symmetrically on face, extremities, trunk and
compare the pain. Conclude whether Normoalgesia, hyperalgesia or
hypoalgesia.
 Temperature: Patient closes eyes and you put something hot then cold, or
metal and rubber part of reflex hammer and ask them to distinguish which
one is which. Conclude whether Thermoanesthesia or Thermoesthesia.
Examination of deep sensation
 Joint sense: Patient closes eyes and you Move patient’s joints up and down
and ask the patient to tell you when you move joint up or down. Loss of joint
sense is Bathyanesthesia
 Vibration: Use tuning fork on bony prominence of arm or shins and ask
patient to tell you when he can’t feel the vibration. In Norm patient should
feel vibration for 15-20 seconds on arm and 10-15 seconds on legs. Loss of
vibration sense is Seismanesthesia
Examination of complicated sensation
 Stereognosis: with eyes closed, give patient an object and ask them to
identify what it is by palpation. Loss of this sense is astereognosis
 Graphism: draw number on different areas on patient’s body and ask them
to identify which number you wrote. Loss of this sense is Graphanesthesia
 Localization: patient closes eyes and you touch them with neurological pin
on different location and ask them to point place where they felt the pin.
They can be 2cm off in norm. Loss of this sense is Topanesthesia
  Discrimination: Use 2 pins and prick the patient, bringing the pins towards
each other till patient feels a single pin.

4. Types and subtypes of sensory disturbances.

Types of sensory disturbances:
1. Peripheral
2. Segmental (sectional)
3. Conductive
The peripheral type occurs at lesion of dendrites of the first neuron of all sorts of
sensation. The peripheral type is divided on:
 Mononeuritic (or neural) pattern - is observed at lesion of one peripheral
nerve and consists of disturbance of all sorts of sensation in innervative
zone of this nerve. There is a pain in the field of nerve, sometimes
hyperpathia, hyperalgesia, causalgia, tension signs of nerve, pain at palpation.
 Polyneuritic pattern - is observed at multiple, frequently symmetric lesion
of all peripheral nerves. Appears by sensory disturbance in distal parts of
extremities as "socks" on legs and "gloves" on arms. The “stocking-glove”
pattern of sensory loss is typical for peripheral neuropathy. But sometimes
cerebral or spinal lesion may cause distal sensory loss, usually of a single
extremity in the case of cerebral disease, and often in association with
hyperreflexia and the Babinski sign in cases of either cerebral or spinal
lesions.
 Plexal pattern - occurs at lesion of dorsal root ganglia and appears by
sensation disturbance in innervative zone of a plexus. In this case there are
pains, tension signs of nerves going from a plexus, movement disturbance -
peripheral paresis of muscles group, which innervated from this plexus.
 “Saddle-area” pattern of sensory loss. This area is the “tail-end” of the body
and is innervated by the sacral segments of the spinal cord and the sacral
roots. A lesion producing saddle-area sensory loss will be found in the upper
lumbar spinal level if it is due to a lesion of the cord (conus medullaris). The
lesion will be at the middle of lower lumbar or upper sacral spinal level if it
involved the cauda equina. Defective control of the urinary bladder and
anal sphincter are regularly associated with this type of sensory deficit.
The segmental (sectional) type disturbance of sensation is observed at lesion of
sensitive fibers at segment level of spinal cord, and, means, at lesion of dorsal
root ganglion, dorsal roots, dorsal horns of spinal cord, front white soldering.
 Segmental - radicular pattern occurs at a lesion of dorsal root or
simultaneous lesion of root and dorsal root sensitive ganglion. At lesion of
dorsal root there is a loss of all sorts of sensation in its zone innervation
according to the segmental type. The sensitive disturbance is appeared as
 transversal strip on a trunk and longitudinal strip on extremities (in
human being there are 36 sensitive segments (31 spinal segments are on trunk
and extremities and 5 segments at the expense of trigeminal nerve on the face).
This type of disturbance of sensation arises at radiculopathies, at extramedular
tumors. At lesion of dorsal root ganglion occurs herpes exanthema in a zone
innervation of the struck segment (at a ganglionitis or ganglioneuritis) as
bubbles (so-called herpes zoster), sharp pains and anesthesia in a segment.
 Segmental - dissociated pattern. It is observed at lesion of dorsal horns of
spinal cord and front grey soldering. Thus the disturbance of sensation
appear as loss or lowering pain and thermoanesthesia and saving tactile
and joint sense in given segment. Such disturbance are called dissociated
and result from that in dorsal horns and front grey soldering pass explorers of
superficial sensation, and from the explorers of deep feeling that do not go to
a dorsal horn of spinal cord (recollect anatomy).The dissociated type of
disturbance of sensitivity more often arises at a myelosyringosis, when the
sensitive disturbance are observed in certain dermatomes as "jacket" or
"half jacket" at lesion of dorsal horns of spinal cord in thoracic segments,
or "trousers" - at lesion of dorsal horns of spinal cord in lumbar
segments.
Conductive type. The lesion of sensory explorers in spinothalamic tract, Holl’s
and Burdach’s pathways, bulbothalamic tract, medial closed loop and
thalamocortical tract in limits spinal cord or brain cause conductive type of sensory
loss. This type is divided on:
 Spinal pattern can be:
 Complete transversal (is observed at a lesion that involves a diameter
of a spinal cord, at which all sorts of sensation below that level of a
lesion drop out, pain and temperature sense drop out on 1-2
segments below than level of a lesion, and deep - from the same
level. Usually, the deficits are in the lower trunk and legs, are bilateral
and almost symmetric.
 Half transversal or Brown-Sequard pattern - arises at a lesion of
a lateral half diameter of a spinal cord, thus the deep feeling drops
out on the side of a lesion, and pain and temperature sense- on
the opposite side, since a level on 1-2 segments is lower.
 Descending or Ascending, depending on extra- or intramedular
lesion
 Monotype
 Hemitype
 Cerebral pattern is divided on:
  Brain stem pattern (alternating). At lesion of sensory fibbers in
brain stem there is fallout of sensation on the face according to
the segmental type on the side of lesion both fallout pain and
thermoanaesthesia on trunk and extremities on opposite sides.
Lesions in the pons and below in medulla and cord may result in
dissociated sensory loss on one or both sides of the body because of
different levels of crossing of the sensory pathways. A lesion of the
lateral medulla (lateral medullar syndrome, called Wallenberg’s
syndrome) will cause loss of pain sensation on the same side of the
face and the opposite side of the body. In this situation, touch is
preserved in areas where there is loss of pain perception.
 The thalamic pattern (at a lesion of thalamus) is observed:
Hemihypoesthesia of all sorts of sensation on opposite side from
the pathological focus. Hyperpathia - the disturbance of deep
feeling prevail. There are thalamic pains (burning, intolerable).
Hemiataxia - as result of lowering deep joint feeling.
 Capsular pattern - in case of a lesion of sensory fibers in back leg
of internal capsule arises hemi anesthesia of all sorts of sensation
on opposite sides and hemiataxia owing to fallout of deep feeling.
 Cortical pattern - arises at a lesion of a postcentral gyrus and upper
parietal gyrus. Thus the sensation drops out on monotype in an
arm either in a leg, or on the face depending on localization of a
lesion in a postcentral gyrus.

5. Reflexes (definition, classification and characteristic). Reflex arches (nerves,

muscles, segments) of tendon, periosteal and dermal reflexes.
Reflex – is a reaction of our organism to various outside and inside effects. It is
provided by nervous system. All the reflexes can be divided into different groups -
simple and complex, inborn and trained, conditioned and unconditioned.
Unconditioned reflexes: They are inborn ones. They are phylogenetically old, that
means they were formed in course of phylogenesis. They are based on certain
anatomic structures (segments of spinal cord or brain stem). They exist even
without brain cortex influence. They are inherited. They can be regulated by brain
cortex. They are basis for the conditioned reflexes.
Conditioned reflexes: They are the result of the individual experience and are
formed during ontogenesis. They are unstable, that means they need constant
support. They aren’t based on certain anatomic structures. They are fixed in brain
cortex.
Unconditioned reflexes are divided into such groups:
  Superficial and deep
 Simple and complex
 Proprioceptive (stretch, periosteal, articular)
 Exteroceptive (dermal, from mucose membrane)
 Interoceptive (from mucose membrane of internal organs – for example
urination in case of internal sphincter irritation)
Reflex The group Muscles Nerves Segments
of reflex
Subeyesbrow Deep, M. orbicularis N. trigeminus ( Medulla
periostal oculi V ) – N.facialis oblongata
reflex (VII) and pons
Corneal (lid) Superficial, M. orbicularis N. trigeminus ( Medulla
from oculi V ) – N.facialis oblongata
mucose (VII) and pons
membrane
Jaw Jerk Deep, M.masseter N. trigeminus ( Medulla
(mandibular, chin, periostal V ) – oblongata
masseter) reflex reflex N.mandibularis and pons
(Bechterev’s) (sensory and
motor )
Pharyngeal Superficial, Mm. N.glosso- Medulla
from constrictores pharyngeus, oblongata
mucose pharyngis and n.vagus
membrane others (sensory and
motor), 9th and
10th pair of
CCN
Palatal (palatine) Superficial, Mm. levatores N.glosso- Medulla
from velli palatini pharyngeus, oblongata
mucose n.vagus
membrane (sensory and
motor)
Biceps Deep, M.biceps N.musculo- C5-C6
stretch brachii cutaneus
reflex
Triceps Deep, M.triceps N.radialis C7-C8
stretch brachii
reflex
Radial Deep, Mm.pronatores N.medianus, C5-C8
(carporadial, periostal flexores, N. radialis, N.
brachioradial) reflex digitorum, musculo-
brachioradialis, cutaneus
biceps
Scapulo- humeral Deep, Mm. teres N. C5-C6
(scapuloperiosteal) periostal major, subscapularis
reflex reflex subscapularis
(Bechterev’s)
Upper superficial Superficial, Mm. N.intercostales T7-T8
abdominal dermal transversus,
obliquus,
rectus
abdominis
Middle superficial Superficial, Mm. N.intercostales T9-T10
abdominal dermal transversus,
obliquus,
rectus
abdominis
Lower superficial Superficial, Mm. N.intercostales T11-T12
abdominal dermal transversus,
obliquus,
rectus
abdominis
Cremasteric Superficial, M.cremaster N.genito- L1-L2
dermal femoralis
Knee jerk, or Deep, M.quadriceps N.femoralis L3-L4
patellar reflex stretch femoris
(quadriceps stretch reflex
reflex)
Achilles (ankle Deep, M.triceps surae N.tibialis S1-S2
jerk) stretch (n.ischiadicus )
reflex
Plantar (sole) Superficial, Mm. flexores N.ischiadicus L5-S1
dermal digitorum
pedis and
others
Anal Superficial, M.sphinter ani Nn. S4-S5
dermal externus anococcygei
6. Anatomy and symptoms of lesion of cortical-spinal tract and cortical-
nuclear tract.
The fibers of tr.corticospinalis are of Betz cells origin. Most of its fibers originate
from anterior central gyrus, posterior parts of upper and middle frontal gyri and
paracentral lobe (area 2,4,6). The Betz cells in central anterior gyrus are presented
vice versa to the parts of the body:
 in upper part the muscles of lower extremities are presented;
 in middle part - the muscles of upper extremities are presented;
 in lower part – the face muscles are presented.
The axons of Betz cells that create tr. corticospinalis go through corona
radiata to internal capsula via its anterior 2/3 of posterior crus. Then the axons
of motor way go through the peduncles, pons to medulla oblongata to form
pyramides.
 80 % of all fibers make decussationon the border between medulla
oblongata and spinal cord. The crossed fibers go to the lateral foniculus of
spinal cord on the opposite side and create tr. corticospinalis lateralis. The
last provides lower and upper extremities muscles innervation.
 The rest – 20 % of all fibers aren’t crossed. They go to foniculus anterior
and create tr. corticospinalis anterior ( fasciculus Turka ). This one
provides neck, trunk, perineum muscles innervation.
The fibers of tr. corticospinalis are finished in motorneurons of spinal cord
anterior horns.

The first central neuron Of face innervation is called tractus corticonuclearis.

The first neuron cells are situated in the lower part of anterior central gyrus.
The axons go through corona radiata, the knee of internal capsula to brain
stem (that means peduncles, pons and medulla oblongata). There are nuclei of
Cranial Nerves in brain stem.
And one more peculiarity – the fibers of tractus corticonuclearis make decussation
above all the nuclei. This decussation is incomplete. The only exception is lower
nucleus of VII CN and nuclei of XII CN. In this case decussation is complete.
The second neuron is situated in motor nucleus of CNs. This way to face muscles
is called tractus nucleomuscularis.
Thus we can make the following conclusions:
 The face muscles have bilateral cortex innervation except the mimic muscles
and tongue muscles that have unilateral innervation from the opposite
hemisphere.
  The muscles of upper and lower extremities, lower mimic muscles and tongue
muscles have unilateral cortical innervation.
 All the other muscles (the muscles of neck, trunk, perineum, m.
oculomotorial, m. masseter, pharyngeal and palatal muscles) have bilateral
cortical innervation.
 Lesion of these tracts causes central paralysis or paresis

7. Anatomy and symptoms of lesion of cortical-muscular tract.

This system provides conduction of nervous impulse from brain cortex to muscles.
The way of this impulse is known as motor way or tractus corticomuscularis. It
consists of two neurons:
 first (central) neuron is called tractus corticospinali
 The second (peripheral) neuron is called tractus spinomuscularis.
The fibers of tr.corticospinalis are of Betz cells origin. Most of its fibers originate
from anterior central gyrus, posterior parts of upper and middle frontal gyri and
paracentral lobe (area 2,4,6). The Betz cells in central anterior gyrus are presented
vice versa to the parts of the body:
 in upper part the muscles of lower extremities are presented;
 in middle part - the muscles of upper extremities are presented;
 in lower part – the face muscles are presented.
The axons of Betz cells that create tr. corticospinalis go through corona radiata to
internal capsula via its anterior 2/3 of posterior crus. Then the axons of motor way
go through the peduncles, pons to medulla oblongata to form pyramides.
 80 % of all fibers make decussationon the border between medulla
oblongata and spinal cord. The crossed fibers go to the lateral foniculus of
spinal cord on the opposite side and create tr. corticospinalis lateralis. The
last provides lower and upper extremities muscles innervation.
 The rest – 20 % of all fibers aren’t crossed. They go to foniculus anterior
and create tr. corticospinalis anterior ( fasciculus Turka ). This one provides
neck, trunk, perineum muscles innervation.
The fibers of tr. corticospinalis are finished in motorneurons of spinal cord
anterior horns.
The second neuron – peripheral - tractus spinomuscularis.
Neurons of C1-C4 anterior horns innervate neck muscles, C5-Th1-2 – muscles
of upper extremities, Th2-Th12 – trunk muscles, L1-S2 – muscles of lower
extremities, S3-S5 – muscles of pelvic organs.
The second neuron originates from anterior horns alpha-motor-neurons of
spinal cord. Axons of these neurons go within anterior roots and then join with
posterior ones to form the spinal nerve. Each spinal nerve gives 4 branches:
  ramus anterior ( together they form plexus – cervical, brachial, lumbar and
sacral)
 ramus posterior (it is spinal nerve, which innervates posterior trunk
muscles)
 ramus meningeus
 ramus comunicante albi.
thus, the motor impulse goes from anterior horns through anterior roots, spinal
nerve, plexus and peripheral nerves to muscles.
That’s the reason to make following conclusions:
 The muscles of upper and lower extremities have unilateral cortical
innervation from contralateral hemisphere
 The muscles of neck, trunk and pelvic organs have bilateral innervation
from both hemispheres. In case of unilateral pathologic focus these
structures do not suffer.
Symptom of lesion: In case of complete lesion of motor way (tractus
corticomuscularis) paralysis (plegia) occurs. That means the absence of active
movements In case of incomplete lesion of motor way paresis occurs. That means
active movements disorders – hemi-, tetra-, mono-, tri- and paraparesis.
Central or spastic paralysis is caused by the lesion of central neuron and its
fibers (tr. corticospinalis or tr. corticonuclearis).
Peripheral or flaccid paralysis is caused by the lesion of peripheral neuron
(tractus spinomuscularis or tractus nucleomuscularis).

8. Clinical signs of a central (spastic) paralysis (paresis). Differential signs

between spastic and plastic muscular hypertony.
Central or spastic paralysis is caused by the lesion of central neuron and its
fibers (tr. corticospinalis or tr. corticonuclearis).
Main features of central or spastic paralysis are:
 It is a diffuse paralysis.
 There is spastic hypertonus of muscles
 Tonus is increased in the group of flexors in upper extremities and in
the group of extensors in lower extremities
 “ clasp – knife “ symptom
 in course of evaluation tonus decreases
 Hyperreflexion of stretch and periostal reflexes.
 There are pathologic reflexes.They are considered to be reliable signs of
central paralysis
 Oral pathological reflexes: Bechterev, nasolabial, sucking, distance-
oral, palm mental.
  Pathological reflexes of lower extremities extensor: Babinski,
Oppenheim, Chaddock, Gordon, Schaffer’s
 Pathological reflexes of lower extremities flexing: Rossolimo,
bechterev, jukovski
 Upper extremities pathological reflexes: Bechterev, Jukovski,
rossolimo, tremner, Jakobson-laske reflex, klippel veil
 Protective reflexes: Reflex of spinal automatism: Squeeze foot by
tendon causes flexion of paralyzed extremity
 Pathological synkinesis: voluntary movements accompanied by
involuntary movements. Can be Global or generalized. Co-
ordinatory: spread of response from one muscle or group of muscle to
others. Immitating: involuntary movement in paralysed extremity while
moving healthy extremity.

Rigidity (plastic hypertonus) Spastic hypertonus

Cogged-wheel symptom Clasp-knife symptom
Tonus increased during Tonus decreased during evaluation of muscle
evaluation of muscle tone tone
Tonus is expressed in same Tonus increased in flexors of upper
manner in flexors and extensors extremities and extensors of lower extremities

9. Examination of motor dysfunction - paralysis (paresis) and its signs.

Clinical signs of a peripheral (flaccid) paralysis (paresis).
Peripheral or flaccid paralysis is caused by the lesion of peripheral neuron (tractus
spinomuscularis or tractus nucleomuscularis).
The main features of peripheral paralysis are :
 Areflexion or hyporeflexion
 Atonia or hypotonia
 Muscular atrophy
 Fasciculation of muscles
 It is limited paralysis
 There is reaction of degeneration.
Examination of Motor system:
 Active movement: ask patient to abduct, adduct, flex, extend, pronate and
supinate different joints in the body: fingers, wrist, elbow, shoulder, hip, knee,
ankle and toes etc.
 Passive movements: Doctor Make movement in patients joints abduct,
adduct, flex, extend, pronate and supinate different joints in the body: fingers,
wrist, elbow, shoulder, hip, knee, ankle and toes etc.
  Muscle strength: Ask patient to resist the pressure of force you exert on
different joints and rate according to scale. 0-plegia or paralysis, 1-minimal
active movement, 2-severe, 3-moderate strength, 4-mild strength, 5-normal
strength
 Muscle tone: flex and extend elbow and knee 7-10 times while you feel biceps
and triceps muscle and feel if tone is present, normal or increased

10. Symptoms of lesion of motor and sensory explorers of the brain in

different levels.
 The lesion of anterior central gyrus usually cause monoplegia ( or
monoparesis ) on the opposite side . If the focus is situated in upper part of
anterior central gyrus , paralysis of lower extremity occurs.If it is in middle
part of anterior central gyrus, we can observe paralysis of upper extremity. If
it is in lower one, face suffers. In case of anterior central gyrus irritation
Motor Jackson takes place. Motor Jackson is a set of local seizures that
can cause generalized seizures.
 Lesion of a medial closed loop – hemianesthesia, sensitive hemiataxia
 Lesion of thalamus – hemianestesia, sensitive hemiataxia, hemianopsia,
hemialgia. Since the thalamus is concerned with sensory impulses from the
opposite side of the body, the pain resulting from lesions within it is confined
to the opposite side of the body. In large lesions the entire opposite half of the
body, including the head, may exhibit hyperpathia discomfort. In less
extensive lesions the pain may be limited to large contiguous portions of the
body, such as the whole lower extremity and lower part of the trunk or the
side of the head, upper extremity, and chest. thalamic pains are persistent
and are greatly aggravated by emotional stress and fatigue. They are
usually described as burning, drawing, and feeling of pulling, swelling, and
tenseness, above all they have a peculiar, highly distressing quality.
 The lesion of corona radiate usually cause central hemiplegia on the
opposite side ( that means that arm, leg, lower mimic muscles and tongue
muscles are involved ). By the way, if the process is much more expressed in
upper part of corona radiata, paralysis in lower extremity dominates. If the
process is much more expressed in middle part of corona radiata , paralysis
in upper extremity prevales. If the process is much more expressed in lower
part of corona radiata, paralysis in face muscles dominates. Besides
hemianesthesia can join hemiplegia.
 The lesion of internal capsula part of motor way can cause hemiplegia on
the opposite side, central paresis of tongue muscles and lower mimic
muscles . Hemihypesthesia often joins all the other symptoms. Vernike –
Mann posture is typical for this lesion.
  The lesion of brain stem cause central paralysis on the opposite side and
peripheral paralysis of face muscles on the side of lesion. It is known as
alternating syndrome. The last are divided into peduncle, pontine and
bulbar ones.
 The lesion of pyramidal decussation part of motor way usually cause
central paralysis of upper extremity on the side of lesion and paralysis
of lower extremity on the opposite side . Sometimes tetraplegia or triplegia
is observed.

11. Symptoms of lesion of motor and sensory explorers of the spinal cord.
Lesion of Sensory of spinal cord: As a rule, the pain extends to regions that
approximate the dermatome distribution of the nerve root supplying the irritated
viscous or deep somatic structures. root pain is frequently produced or, when
present, is aggravated by coughing, sneezing, straining, as in defecation, or any
other measures that suddenly increase intra-thoracic and intra-abdominal pressure.
root pain may be awaken in the patient at night after several hours of sleep
and may be relieved approximately 15 to 30 minutes after the upright position
is assumed. root pain often results from, or is intensified by, other maneuvers that
stretch the involved roots.
 Lesion of a sensory (dorsal) root and ganglion - same manifestations +
herpes zoster.
 The lesion of a sensory (dorsal) horn of a spinal cord cause the same
manifestations, as well as at lesions of sensory (dorsal) root, dissociated
disorders of sensation only are observed.
 The lesion of front grey soldering cause sectional type - dissociated
disorders of sensation symmetric on both sides as "butterfly".
 The lesion of dorsal funiculus of spinal cord - deep feeling drops out on
one side according to the conductive type
 The lesions of lateral funiculus of spinal cord - pain and temperature sense
drops out on the opposite side according to the conductive type.
 The lesion of half of diameter of a spinal cord, Brown-Sequard sign - on the
side of the focus deep sense drops out according to the conductive type
from level of lesion. Paresis of an extremity, the zone of an anesthesia at level
of lesion and radicular pain, is observed on opposite side - drops out pain
and temperature sense 2 segments lower than level of focus.
 Lesion of diameter of a spinal cord – there is anesthesia of all sorts of
sensation according to the conductive type is lower than a level of focus:
deep sense from a level of focus, superficial sense – 2-3 segments lower.
Central paralysis. Defective control of the urinary bladder and anal sphincter
according to the central type. Trophic disorders.
Motor System lesion of spinal cord
 The lesion of motor way in lateral foniculus of spinal cord cause central
paralysis below the level C1-C4, C5-Th1, Th1- Th12, L1-S2.
 The lesion of anterior horns or motor nucleus of CCNs cause peripheral
paralysis of certain muscles . At chronic process we can observe
fasciculation of muscles. Also there are early atrophy and degenerative
reaction.
 Anterior roots lesion cause also peripheral paralysis . In most of cases it
is observed only when several roots are damaged

12. Symptoms of lesion of the grey matter of spinal cord.

Regions the gray matter is subdivided into: anterior horns, lateral horns,
posterior horns and gray commissure.
 Anterior horns: contains the somatic motor nucleus. The lesion of anterior
horns or motor nucleus of CCNs cause peripheral paralysis of certain
muscles . At chronic process we can observe fasciculation of muscles. Also
there are early atrophy and degenerative reaction.
 lateral horns: contains the autonomic motor nucleus
 posterior horns: contains the sensory nucleus. The lesion of a sensory
(dorsal) horn of a spinal cord cause the pain along the distribution of nerve
root, as well as at lesions of sensory (dorsal) root, dissociated disorders of
sensation only are observed.
 gray commissure: connection in gray matter. The lesion of front grey
soldering cause sectional type - dissociated disorders of sensation
symmetric on both sides as "butterfly".

13. Symptoms of lesion of the spinal cord half transversal diameter on the
level С1-С4.
• Central hemi- or quadriparesis (quadraparesis, tetraplegia) ipsilateral.
Paresis of neck muscles.
• Sensory loss: loss of deep sensation on neck ipsilateral. Loss of pain and
temperature sensation 1-2segments below lesion contralaterally.
• Radicular irritation – neck pain
• Paresis of the diaphragm (n. frenicus - C4)
C1-C2: Inability to breathe without assistance from a ventilator. Inability or
reduced ability to speak. Loss of feeling or sensation below the level of injury.
Paralysis in the arms, hands, trunk, and legs .Limited neck and/or head movement
C3: No flexion and extension on side of lesion. Loss of diaphragm function.
Requirement of a ventilator for breathing. Paralysis in arms, hands, torso, and legs.
Trouble controlling bladder and bowel function
C4: Loss of diaphragm function. Potential requirement of a ventilator for
breathing. Limited range of motion. Paralysis in arms, hands, torso, and legs.
Trouble controlling bladder and bowel function

14. Symptoms of lesion of the spinal cord half transversal diameter on the
level С5 - T1.
 Peripheral paralysis at site of lesion ipsilaterally and central
paralysis below lesion
 radicular irritation – shoulder girdle pain
 sensory loss: loss of deep sensation ipsilaterally. Loss of pain and
temperature sensation contralaterally
C5: C5 vertebra affects the vocal cords, biceps, and deltoid muscles in the upper
arms. Will cause peripheral paralysis or paresis in these muscles ipsilatterally. And
central paralysis of legs, wrists, torso.
C6: false case of carpal tunnel syndrome. numbness and / or tingling in the
fingers, hands, and arms. Paralysis in the legs, torso, and/or hands. Inability to
control nerves that impact wrist extension. Inability to control bladder and bowel
function. Ability to speak, but breathing may be taxed
C7: communicates with the tricep muscles. Burning pain in the shoulder blade
and/or back of the arms (triceps). Some ability to extend shoulders, arms, and
fingers but dexterity may be compromised in the hands and/or fingers. Lack of
control of their bowels and bladder. Breathing may be taxed though the patient
should not need ventilation
C8 injury will lead to paralysis of the legs, trunk, and hands, with patients
maintaining shoulder and arm movement.
T1 vertebrae: the medial side of the forearm, and flexes the wrist . Causes
paralysis of these muscles ipsilaterally
T2 vertebrae: the posterior aspect of the upper arms. Paralysis of these muscles
ipsilaterally

15. Symptoms of lesion of the spinal cord half transversal diameter on the
level T-T12
• mono- or paraparesis of the legs…central
• arms: normal
• sensory loss: loss of deep sensation on side of lesion. Loss of pain and
temperature sensation contralaterally 1-2segments below lesion.
• urinary retention
T1 - T8 levels may experience: Lack of function in the legs and/or torso, resulting
in paraplegia. Lack of dexterity in the fingers and/or hands. Reduced ability or
inability to control the abdominal muscles or trunk of the body. Lack of bowel
and/or bladder function
T9 - T12 levels may experience: Good upper body control depending on the level
of cord damage. Lack of function in the legs and/or torso, resulting in paraplegia.
Lack of bowel and/or bladder control. Possible reduced ability to control the trunk
of the body or abdominal muscles. Good balance while in a sitting position. Ability
to stand in a specialized frame, or walk with braces

16. Symptoms of lesion of spinal cord transversal diameter on the level L1-L2.
 mono- or paraparesis of the legs…peripheral at the level of segmental
cord damage (and upper motor neuron lesion below the lesion, detecting
level of cord damage)
 paresis of the thigh muscles weakness of flexors and adductors of the
thigh and of extensors of the shin (crus)
 deep tendon reflexes L2-4 are absent:Knee jerk reflex absent
 sensory loss in areae radiculares
 urinary incontinence (sympathetic lesion)
 cremasteric reflex is absent in L1-2 segmental lesion
Patients with lumbar spinal cord injuries may experience: Paraplegia with
functional independence. The need for a manual wheelchair for part-time or full-
time use. Ability to ambulate using braces or other walking devices. Lack of
control of bowels or bladder

17. Symptoms of lesion of horse tail (cauda equina) and conus of spinal cord.
“Saddle-area” pattern of sensory loss. This area is the “tail-end” of the body and is
innervated by the sacral segments of the spinal cord and the sacral roots. A lesion
producing saddle-area sensory loss will be found in the upper lumbar spinal level if
it is due to a lesion of the cord (conus medullaris). The lesion will be at the middle
of lower lumbar or upper sacral spinal level if it involved the cauda equina.
Defective control of the urinary bladder and anal sphincter are regularly
associated with this type of sensory deficit.
Conus lesion – segments S3 – S5
 paraparesis…is not present!
 sensory disturbance – saddle anesthesia over the “saddle area”
 pain over the “saddle area”
 sphincteric paralysis:
o disturbance of urination (denervated autonomous bladder – retention)
o faecal incontinence
o sexual dysfunction – impotence
Cauda equina lesion – roots L3 – S5. Loss of sensation not movement
 paresis – peripheral, asymmetrical (with reflex loss, usually foot drop…)
 sensory loss
 radicular areas – hypesthesia over the sacral area (perianal, perigenital, may be
hemi-)
 radicular leg pain
 sphincter disorders
o acute retention of urine
o constipation

18. Anatomy and function of cerebellar hemispheres and worm. Tracts of the
cerebellar peduncles. Anatomy of the cortical-cerebellar-muscular tract.
Cerebellum is located in the posterior cranial fossa. It contains two large lateral
hemispheres, flocculo-nodular lobe and three pairs of peduncles. Equilibrium and
regulation of muscle tone are the functions of flocculo-nodular lobe. Coordination
of the movement and synergy are the functions of the cerebellum hemispheres.
 The lower peduncles (corpora restiformia) provide connection with oblong
brain and spinal cord:
· Tr. spinocerebellaris dorsalis (Flexig’s)
· Tr. vestibulocohlearis (from nuclei vestibularis to nucleus fastigii)
· Tr. olivocerebelaris (from lower olives to nucleus dentatus)
· Fibre arcuate externe (from nuclei Holl and Burdach to hemispheres and vermis).
 The middle peduncles (pedunculum cerebellaris medii) provide connection
with pons. They are presented by fibers of tr. pontocerebellaris. They
connect nuclei of pons with the opposite hemisphere of cerebellum.
 The upper peduncles of cerebellum (pedunculi cerebellaris superior)
connect cerebellum with middle brain. They include two systems:
· Afferent one – from spinal cord to cerebellum – tr. spinocerebellaris ventralis
(Hover’s)
· Efferent one – from cerebellum to the structures of extrapyramidal nervous
system – tr. cerebellotegmentalis et tr. dentorubralis.
Way of cerebellum correction are provided by 6 neurons
The first neuron – tr. fronto-temporo – occipito- pontinus
The second neuron – tr. pontocerebellaris (pontino- cerebellaris decussation)
The third neuron – tr. cerebello – dentatus
The forth neuron – tr. dentorubralis (Vernekink’s decussation)
The fifth neuron – tr. rubrospinalis (Forel’s decussation)
The sixth neuron – tr. spinomuscularis
Thus brain cortex and nuclei rubri are connected with opposite hemispheres of
cerebellum. And the segments of spinal cord have homolateral connection.

19. Examination of the cerebellar pathology.

Static ataxia lesion of vermix. Loss if equilibrium and muscle tone: Romberg test:
patient stand with eyes closed and arms forward. Test is positive when
unsteadiness increases with closed eyes.
Dynamic ataxia loss of co-ordination of movement and synergy examination
 Asynergy: Babinski test: cross arms while laying down and ask patient to sit
up. Positive result will be bending knees to sit
 Stockholm test: while checking muscle strength, pull arm with resistant and
let go abruptly, Positive result, patient will hit himself.
 Nystagmus: horizontal, vertical rotary or mixed
 Scant speech
 Intention tremor: tremor worsens with movement: finger to nose test, finger
to finger test, heel to knee test.
 Muscle hypotonia, macrography, dysmetria
 Adiadokinesis: inability to perform rapid alternating movement. Examined
by petruska test: twist hand in air like changing light bulb. Pronatus
supinatus test.

20. Sorts of ataxias and their differential signs.

-Cerebellar (cerebellum lesion): drunken sailor gait. Lesion of vermix causes
static ataxia characterized by Romberg test. Lesion of hemisphere causes dynamic
ataxia characterized by nystagmus, scanning speech, intention tremor,
macrographia, dysmetria, adiadochokinesia, asynergy, muscle hypotonia
-Sensitive (loss of deep joint sense): loss of vibration or deep joint sense.
Stomping gait, ataxic hand.
-Frontal (cortical) (lesion of Frontal lobe)
-Vestibular (lesion of vestibular apparatus): vertigo, nausea, vomiting, nystagmus
-Hysterical (in case of Hysteria)
-Mixed

21. Anatomy, physiology and function of extrapyramidal system.

Extrapyramidal system consists of:
-cortical areas 4, 6, 8
-the basal ganglia: n. caudatus, n.lenticularis (putamen, globus palidus)
-the nuclei of brain stem (black substance, red nucleus, vestibular nuclei, reticular
nuclei, nucleus of Darkshevych, Lues’ body, lower olives)
-spinal cord: gamma-motor neurons and alpha-small motor neurons, which are
located in anterior horns of the spinal cord
There are two parts of Extrapyramidal system:
 pallidum (globus palidus, black substance, red nuclei, vestibular nuclei,
nucleus of Darkshevych, lower olives, Lues body)
 striatum (cortical areas 4,6,8, n. caudatus, putamen)
Pallidum is phylogenetically older then striatum. That’s why in newborn babies
pallidum dominates. And only at the age of 4 – 5 months old striatum starts to
influence on motor functions.
The main functions of Extrapyramidal system are:
 It prepares muscles to smooth economical movements
 It determines the posture
 It makes automatical involuntary regulation of conscious movements
 It provides automatical stereotyped movements and reflector protective
movements
 It provides motor manifestation of emotions.
Physiology: Normal function in the basal ganglia appears to depend on a
homeostatic relationship between various neurotransmitter agents - DA and
GABA. Neurophysiologically this balance may be viewed as existing between
those action is inhibitory in nature (DA and GABA) versus those with excitatory
properties (ACH).

22. Clinical features of pallidum lesion. Differential diagnosis of Parkinson

syndrome.
Lesion of pallidum causes Parkinson syndrome. Features
There are three basic symptoms of Parkinson’s syndrome:
- Hypokinesia (Akinesia)
- Rigidity
- Tremor
-Autonomic signs
Hypokinesia (Akinesia).
 the head and the shoulders are stooped forward, the arms are slightly
abducted, the forearms are party flexed, and the phalangeal joints are
extended at the interphalangeal joints.
 Poverty of movement which result from the bradykinetic and akinetic
state.
 The gait is shuffling and the steps are slight.
 Parallel footprints.
  The loss of associated swinging of the arm or arms when walking -
(acheirokynesis).
 A lack of mobility of facial expression (Bechterev’s symptome)
 Infrequent blinking of the eyelids (Mary’ s symptome)
 Fixed look.
 Inertia of rest (that means it is very difficult for patient to start moving).
 Inertia of movement
 Micrography – handwriting is too small.
 Speach is quite and inexpressive (bradylalia).
 Pardoxical kynesia is possible after strong impression or great emotions.
Rigidity (plastic type of increased muscle tone):
 Cogged-wheel symptom
 Tonus increases in course of evaluation of nervous system state
 Tonus is expressed in the same manner in the group of flexors and
extensors.
Tremor:
 Are much more expressed in distal parts of extremities, sometimes tremor
of lips or lower jaw can occur
 It looks like coins counting
 It is much more expressed while resting. It disappears or decreases while
moving
 Its frequency is 3 – 6 times per second.
Besides these basic features of Parkinson’s disease sometimes can occur:
 Bradyphrenia (thoughts are too slow)
 Bradymnenia (recollection is slow too)
 While speaking such patients are boring (akairia - Astwatsaturov
symptome)
 Usually they are in a bad mood. Depression is very typical for the patients
with Parkinson disease.
 Sometimes they have autonomic disorders. Parasympathetic nervous system
dominates in such patients – they have running saliva (aeriel symptome),
hyperhydrosis, fatty skin and type of hair, bradicardia and arterial
hypotension.

23. Clinical features of striatum lesion. Name kinds of hyperkinesis.

at striatum lesion, is hyperkynetic–hypotonic
The main clinical signs of this syndrome are:
 Muscular hypotonia
  Involuntary movements – hyperkynesis.
Symptoms and disorders of striatum lesion
 Chorea spontaneous, irregular, purposeless and asymmetric
movements. they are present at rest and subside during sleep. eyes and
tongue symptom ( or Hersonsky’s symptom ) - the patients are unable to
maintain tongue protrusion for more than a few seconds; Hordon’s II
symptom – while checking knee – reflex crus stays in the position of
extension for a while and then slowly goes down; Cherni symptom -
pathologic sudden abdomen at breath. The most common diseases with
chorea syndrome are Huntington’s chorea (inherited disease), Sydenhams
(juvenile disease).
 Athetosis: Movements are slower and more sustained than choreiform
movements. they affect primarily the distal portion of extremities.
snakelike movement of any combination of flexion, extension, adduction
and abduction in varying degrees. They are regularly associated with
increased muscular tone. It is supposed that athetosis is the result of
nucleus caudated lesion.
 Ballism and hemiballism: Its the more or less continues gross abrupt
contractions of axial and proximal muscles of the extremities; In the
most cases this movement disorder is confined to one side of the body
(hemiballism) . It may be associated with hypotonia.
 Myoclonus is a jerking movement of one or more muscle groups (for
example palatine, tongue, pharynx, larynx, diaphragm and skeletal muscles).
usually only one muscle group is involved .They are synchronous in most of
cases and sometimes they are asynchronous. Their frequency is about 15 –
18 per minute. They may be induced by visual, tactile, or auditory
stimuli (stimulus-sensitive myoclonus) or by the initiation of the
voluntary movement (intention myoclonus). Myoclonus – epilepsy is
typical for chronic form of forest spring form encephalitis
 Torsion spasm: Twisting or turning movements. The muscles of trunk
and neck are involved. Sometimes torticollis can occur. Usually it is the
result of putamen lesion.
 Tics are an involuntary compulsive stereotyped movements . they may be
simple or complex. tics may involve any portion of the body ( they are most
common about the face where they are manifest as blinking, grinning,
smirking, lip licking, nose wrinkling).
 Facial cramp is tonic seizure in facial muscles
 Tremor Is rhythmical jerking of arms, legs or head. Its frequency is
about 4 – 6 per second
24. Signs of lesion of the Olfactory analyzer on different levels.
Olfactory nerve bundles (CN-I) serving the SENSE OF SMELL have their cells
of origins in the olfactory mucosa in the nasal cavity; this olfactory region
comprises the mucosa of the superior nasal concha and the opposite part of the
nasal septum.
In severe head injuries involving the anterior cranial fossa, the olfactory bulb may
be separated from olfactory nerves or the nerves may be torn, producing
ANOSMIA.
Signs of lesion:
- patient can’t identify the smell
- he may be unable to name the test substance
- hyposmia
- anosmia
- olfactory hallucination
- unilateral anosmia suggests compression of the olfactory bulb or olfactory
tract by a frontal lobe abscess or glioma, olfactory groove meningioma,
sphenoid ridge meningioma, and pituitary and parasellar tumors. Tumors
may extend pos-terolaterally to involve the ipsilateral optic nerve causing
optic atrophy. The same tumor mass may also cause increased intracranial
pressure with papilledema of the opposite optic nerve. The combination of
unilateral anosmia with ipsilateral optic atrophy and contralateral
papilledema is known as the Foster-Kennedy syndrome.
- Central lesions in the hemispheres do not produce anosmia because of the
decussation of olfactory fibers in the anterior commissure.

25. Symptoms of lesion of the Optic analyzer on different levels.

-Complete lesion of the optic nerve of one side leads to complete blindness in
the corresponding eye.
-Compression of optic chiasma causes bitemporal hemianopia because the nasal
fibers from both sides are interrupted.
-Lesion of the optic tract of one side leads to corresponding nasal &
contralateral temporal hemianopia.
-Lesion of the optic radiation of one side leads to corresponding nasal &
contralateral temporal hemianopia.
Signs of lesion:
- amblyopia (decreased vision in eye) scotoma(central blindness)
- bitemporal hemianopsia: lesion of optic chiasm
- binasal hemianopsia
- homonymous hemianopsia: lesion after optic tract
- quadrantic hemianopsia: lesion of optic tract
 - retinal lesions («choked disk»; «retrobulbar neuritis», primary optic atrophy,
secondary optic atrophy, retinal emboli)
- optic hallucination
-Blindness: lesion of optic nerve

26. The cortex and pons centers of voluntary conjugate movements of head
and eyes. Name the symptoms of lesion.
Abnormalities of voluntary conjugate eye movements may be due to:
 Disease of one frontal lobe. This causes paralysis of voluntary conjugate
gaze to one side. There is an inability to direct the gaze away from the
side of the lesion on command.
 Diffuse disease involving both hemispheres. This results in impairment
of smooth pursuit conjugate eye movements. These are replaced by coarse,
interrupted, conjugate saccadic movements and occur when the patient
attempts to follow a moving object in a horizontal plane.
 Diffuse degenerative processes involving both hemispheres. This may
result in ocular impersistence. The patient cannot sustain gaze on an
object once movement of it ceases.
 Bilateral involvement of corticobulbar tracts, which enter the brainstem
at the level of the midbrain. This can produce loss of gaze in any direction
on command or in following a moving object. Initial impairment is
usually in upward gaze.

27. Sympathetic and parasympathetic innervation of the eyes. Reflex arch of

pupils photoreaction.
Sympathetic innervation of eye
 mydriasis- contract pupillary dilator muscle ( receptor)
1
 contract superior tarsal muscle to hold eyelid open ( receptor)
1
 Relax ciliary muscle for distant vision (ß receptors)
2
 Enhance aqueous humor formation (ß receptors)
2
 Inhibit aqueous humor formation ( receptors)
2
Parasympathetic innervation of eye
• focus eye for near vision (ciliary muscle contraction)
• constrict pupil (miosis)-(pupillary sphincter contraction)
• Enhance drainage of aqueous humor (trabecular meshwork & canal of
Schlemm)
• All of these effects mediated by muscarinic receptors
LIGHT REFLEX The afferent pathway for the pupillary light reflex is activated
by light, which stimulates the rods and cones in the retina. The afferent pathway
passes via the optic nerve with partial decussation in the optic chiasm and then
continues bilaterally through both optic tracts and the brachium of the superior
colliculi to the pretectal region of the midbrain. From the pretectal region the fibers
pass forward close to the aqueduct to enter the Edinger-Westphal nucleus on the
same side or pass through the posterior commissure to enter the nucleus on the op-
posite side. The efferent side of the reflex is completed by fibers that pass from the
neurons in the Edinger-Westphal nucleus through the oculomotor nerve to the
ciliary ganglion, and thereafter by short ciliary nerves to the constrictor muscles
of the iris.

28. Topical diagnostic of Trigeminal nerve lesions.

A lesion of the whole trigeminal nerve causes anaesthesia of the anterior half of
the scalp, of the face (except a small area near the angle of mandible), of the cornea
& conjunctiva, the mucosae of the nose, mouth and presulcal part of the tongue.
Paralysis and atrophy occur in the muscles supplied by the nerve also.
TRIGEMINAL NEURALGIA
characterized by pain in the distribution of branches of the trigeminal nerve, is
the most common condition affecting the sensory part of the nerve.
 With the maxillary nerve affected, the pain is usually felt deeply in the face
& nose between the mouth and orbit. The cause of maxillary neuralgia is often
neoplasms & empyema of the maxillary sinus.
 With the mandibular nerve affected, the pain is usually felt from mouth
upto the ear and the temporal region. The most common cause is carious
mandibular tooth or an ulcer & carcinoma of tongue.
 With the ophthalmic nerve affected, the pain is usually felt in supraorbital
region and is often associated with glaucoma or with frontal or ethmoidal
sinusitis.
Signs of lesion V nerve (trigeminal)
- facial pain
- sensory disturbance in the face
- corneal reflex is decreased or absent
- temporal and masseter muscles are atrophic or hypotrophic, atonic or
hypotonic
- jaw is seen to deviated toward the side of the weakened muscle

29. Symptoms of Facial nerve lesions on different levels.

Supranuclear facial paralysis, involving upper motor neurons pathway is
usually a part of hemiplegia. It involves paralysis of the lower part of the face
but not the upper (forehead and orbicularis oculi) because the facial nerve
nucleus innervating the upper part of face receives fibers from cerebral cortex of
both sides whereas the lower part innervating the lower part of the face receives
contralateral fibers. However emotional movements of the lower face, as in
smiling and laughing, are still possible (presumably there is an alternative pathway
from the cerebrum).
Infranuclear lesions vary in its effects depending on the site of lesion. Due to
the anatomical location of facial nerve, neighbouring structures are inevitably
involved.
 If the facial nucleus or facial pontine fibers are involved, there may be
damage to the abducent nucleus (paralysis of lateral rectus), motor
trigeminal nucleus may be involved (paralysis of masticatory muscles),
principal sensory nucleus and spinal trigeminal nucleus may also be
involved (sensory loss of face).
 Lesions in the posterior cranial fossa or internal acoustic meatus may
involve vestibulocochlear nerve, resulting in loss of taste from anterior
part of tongue with ipsilateral deafness & facial paralysis.
 Lesions of facial nerve in the facial canal may involve nerve to stapedius
causing excessive sensitivity to sound in one ear.
 When damage is in the petrous temporal bone, chorda tympani is usually
involved resulting in loss of taste from anterior two thirds of the tongue.
Signs of lesion of the VII nerve (Facial)
 Facial asymmetry
 patient can’t wrinkle the forehead, close eyes, purse the lips, retract the
buccal angles in a smile
 impairment of taste on the anterior two third of the tongue
 corneal reflex is decreased or absent
Bell’s palsy: It is caused due to inflammation of facial nerve near the stylomastoid
foramen or compression of its fibers near facial canal or stylomastoid foramen. If
the lesion is complete, the facial muscles are all equally affected, with the
following complications:
-There is facial asymmetry and the affected side is immobile.
-The eyebrows are drooped, wrinkles are smoothed out, and the palpebral
fissure is widened by the unopposed action of levator palpebrae.
-The lips remain in contact and cannot be pursued; in attempting to smile the
angle of the mouth is not drawn up on the affected side, the lips remaining
nearly closed.
-Food accumulates in the cheek, from paralysis of buccinator, and dribbles, or is
pushed out between the paralysed lips.
-Platysma and the auricular muscles are paralysed.
-Tears will flow over the lower eyelid and saliva will dribble from the corner of
the mouth.

30. Symptoms of Acoustical and Vestibular analyzer lesions on different

levels.
VESTIBULAR NERVE: Disturbances of vestibular nerve function include
giddiness (VERTIGO) and NYSTAGMUS. Vestibular nystagmus is an
uncontrollable rhythmic oscillation of the eyes. This form of nystagmus is an
essentially a disturbance in the reflex control of the extraocular muscles, which is
one of the functions of the semicircular canals. The causes of the vertigo include
diseases of labyrinth, lesions of the vestibular nerve & the cerebrellum,
multiple sclerosis, tumours and vascular lesions of the brainstem.
COCHLEAR NERVE: Disturbances of the cochlear nerve function produce
DEAFNESS and TINNITUS. Loss of hearing may be due to a defect of the
auditory conducting mechanism in the middle ear, damage to the receptor cells in
the spiral organ of Corti in the cochlea, lesions of the cochlear nerve due to
acoustic neuroma and trauma, or lesion of the cerebral cortex of temporal lobe due
to multiple sclerosis.

31. Common and differential signs of bulbar and pseudobulbar syndromes’.

Bulbar syndrome - produces the lesion of nucleus or radix of the n.
Glossopharingeal, n. Vagus and n. Hypoglossal.
-dysarthria
- dysphagia
- dysphonia
- gag reflex is absent or decreased
- the tongue is atrophic
- paralysis is unilateral or bilateral
- may be (dyspnea, apnea, periodic respiration - Cheyne-Stokes breathing)
Pseudobulbar syndrome - produces the bilateral lesion of the tr. Cortical-nuclear.
- dysarthria
- dysphagia
- dysphonia
- the pathologic oral reflexes are present
- Involuntary crying, smiling
- paralysis is only bilateral
Bulbar syndrome Pseudobulbar syndrome
 gag reflex is absent or decreased gag reflex is present
the tongue is atrophic the tongue is not atrophic
the pathologic oral reflexes is absent the pathologic oral reflexes are present
paralysis is unilateral or bilateral paralysis is only bilateral
may be (dyspnea, apnea, periodic ---
respiration - Cheyne-Stokes breathing)

32. Alternating syndromes of the brain stem.

The lesion of brain stem cause central paralysis on the opposite side and
peripheral paralysis of face muscles on the side of lesion. It is known as alternating
syndrome. The last are divided into peduncle, pontine and bulbar ones..
Alternate intramedular syndromes:
 Jackson’s syndrome - Hypoglossal nerve palsy on the site of the lesion and
opposite hemiplegia.
 Aweli’s syndrome - peripheral palsy of the palatal and laryngeal muscles on
the site of the lesion and a contralateral hemiplegia.
 Schmidt’s syndrome - peripheral palsy of the muscles (palatal, laryngeal,
tongue and m. sternoclaidomastoideus, m. trapezius) on the site of the lesion
and a contralateral hemiplegia.
 Valenberg - Zakcharchenko’ syndrome - on the site of the lesion
(nystagmus, Horner’s syndrome, peripheral palsy of the palatal and laryngeal
muscles, a fallout of sensation on the face for the segmental type, cerebellar
ataxia) and a contralateral hemiplegia, hemianestesia.

33. Alternating syndromes of midbrain.

 Weber’s syndrome - a lesion in the base of the cerebral peduncle affects
the root of the third cranial nerve and the corticospinal pathway,
producing Oculomotor nerve palsy (ptosis and mydriasis) and a
contralateral hemiplegia.
 Benedict’s syndrome - Oculomotor nerve palsy and a contralateral
choreoatetosis and intention tremor.
 Clod’s syndrome - Oculomotor nerve palsy and a contralateral
cerebellar ataxia. Contralateral hemiparesis

34. Alternating syndromes of pons.

 Raymond syndrome - a fallout of sensation on the face according to the
segmental type on the side of the lesion both fallout pain and thermoesthesia
on a trunk and extremities on opposite side.
  Miyar-Gubler syndrome - peripheral palsy of the facial muscles on the site
of the lesion and a contralateral hemiplegia.
 Fovill syndrome - peripheral palsy of the facial muscles and the external
rectus eyes’ muscle on the site of the lesion and a contralateral hemiplegia.

35. Anatomy and symptoms of Oculomotor nerve lesion on different levels

(nucleus, radix and nerve).
Oculomotor nerve may undergo complete or incomplete lesions.
Complete lesions of oculomotor nerve leads to
 Ptosis - drooping of the eyelid due to paralysis of levator palpabrae.
 External strabismus due to unopposed action of lateral rectus & superior
oblique.
 Pupillo- dilatation due to paralysis of sphincter pupillae.
 Loss of accommodation & of light reflex due to paralysis of sphincter
pupillae & ciliaris.
 Diplopia –the false image being the higher.
Incomplete lesions of oculomotor nerve are common and may spare the
extraocular or intraocular muscles.
 The condition in which the innervation of extraocular muscles is spared with
selective loss of autonomic innervation is called INTERNAL
OPHTHALMOPLEGIA.
 The condition in which the intraocular muscles are spared with paralysis of
extraocular muscles is called EXTERNAL OPHTHALMOPLEGIA
Signs of lesion of the III nerve (Oculomotor)
-ptosis
-diplopia
-outside cross eye, rotation of the eye outward and slightly downward
-paralysis of convergation
-inability to move the eye upward, inward, or downward
-exophthalmus
- midriasis (dilatation of the pupil) with iridoplegia and cycloplegia
-paralysis of accommodation

36. Frontal lobe: functions and symptoms of lesion.

Frontal lobe Localization of functions
Frontal lobe provides motor activity, motor mechanisms of speech, behaviour,
mental activity and memory of human being.
1. Precentral gyrus provides motor activity of the opposite side of the body.
 The projection of certain muscle groups is represented vice verse to its location
on the body:
· The upper part of precentral gyrus – is responsible for the lower extremity;
· The middle part of precentral gyrus - is responsible for the upper extremity;
· The lower part of precentral gyrus - is responsible for the muscles of face,
tongue, pharynx, and larynx.
2. Posterior part of upper frontal gyrus is the center of straight walking and
straight standing. It provides movements of the body and is connected with
opposite hemisphere of cerebellum.
3. Posterior part of middle frontal gyrus is the center of eyes movements in the
opposite direction. It is connected with the fasciculus longitudinalis posterior in
the brain stem.
4. The center of writing is located not far from the center of head and eyes
movements in the opposite direction.
5. The center of Broca or the center of motor expressive speech is situated in the
posterior part of left lower frontal gyrus.
The main symptoms of lesion and irritation
1. The lesion of precentral gyrus causes central paralysis and paresis. Usually it
manifests as monoparesis or monoplegia on the opposite side.
2. The irritation of precentral gyrus causes Jackson’s epilepsy in the certain
muscular groups (according to the involved part of the brain cortex). It occurs on
the opposite side and isn’t associated with the loss of consciousness.
3. The irritation of posterior part of upper lobe gyrus causes sudden seizures of
the opposite muscles with the loss of consciousness.
4. The irritation of posterior parts of middle frontal gyrus causes movements of
head and eyes in the opposite direction.
5. The irritation of opercular part of lower frontal gyrus causes rhythmical
chewing, licking and smacking of one’s lips.
6. The lesion of anterior parts of upper and middle frontal gyri causes frontal
ataxia. The last one manifests as astasia (inability to standing) and abasia
(inability to walking without paresis). There is fox-like gait.
7. The lesion of posterior parts of middle frontal gyrus causes gaze into the side
of lesion. It is called cortical gaze paralysis.
8. The lesion of posterior part of lower frontal lobe (the center of Broca) causes
Broca’s aphasia occurs in case of motor encoding area involved and means the
impairment of spontaneous speech, repetition, reading aloud, naming (but
recognizes object) and writing, retained the comprehension of both spoken and
 Afferent motor aphasia is associated with the lesion of lower parts of
postcentral gyrus which provide innervation of oral muscles. In this case
 articulation of sounds suffers. That means the loss of automatically speech,
repetition, naming. This kind of aphasia is connected with oral apraxia.
 Efferent motor aphasia is Broca’s aphasia. It means it occurs at lesion of the
center of Broca. At partial aphasia he uses only nouns.
 Dynamic motor aphasia is usually caused by lesion of cortical zone in front
of Broca’s center. For this type of aphasia aspontanic speech is typical. The
patient refuses to speech in active manner. But he is able to repeat certain
sentences, words, answer the questions.
9. Agraphia – the loss of ability to write. The patient with agraphia will be unable
to take dictation, to copy letters he sees, or to imitate letters or words that are written
for him. Milder degrees of agraphia will show up as poorly formed letters, reversals
of letters, and substitutions.
10. Subcortical reflexes can be observed at frontal lobe lesion.
11. Grasp phenomena. The patient grasps everything that touches his palm.
12. Counteraction phenomena. The patient counteracts the doctor in his attemp to
change the patient’s extremities position.
13. Mental disorders are developed at diffuse lesion of frontal lobe or the lesion
of polus of frontal lobe. It is known as frontal mental disorders. Apathy, torpid
mental reactions, slackening of memory and attention, the absence of
criticism, inadequate appreciation of disease severity, euphoria, gross
humor, the patients are childish, untidiness
14. Sometimes general hypokinesia can be observed, because of extrapyramidal
system lesion.
15. Frontal apraxia. It is a disturbance of purposeful movement. written language
function. Loss of expressive speech.

37. Parietal lobe: functions and symptoms of lesion.

The main function of Parietal lobe is associated with space, time orientation
and analysis of information from sensory stimuli.
Localization of functions
1. There is nucleus of general sensitivity analyser in the postcentral gyrus.
Sensitivity from lower extremities is represented in upper parts of postcentral
gyrus, sensitivity from upper extremities is represented in middle parts of
postcentral gyrus, and sensitivity from face is represented in lower parts of
postcentral gyrus.
2. Complicated kinds of sensitivity are located in upper parietal lobe. They are
stereognosis, sense of localization, discrimination, sense of weight, pressure,
position of different parts of the body in space.
3. The center of praxis is situated in gyrus supramarginalis. The center of
reading and calculation are located in the gyrus angularis.
The main symptoms of parietal lobe lesion
1. The lesion of postcentral gyrus causes conductive sensory disorders on the
opposite side of the body. They are called monoanesthesia.
2. The irritation of postcentral gyrus causes the attacks of sensory Jackson’s
epilepsy. That means parasthesia in certain extremities of the opposite side.
3. The lesion of upper parietal lobe causes bathyanesthesia, the loss of light
touch sense, the sense of localization and discrimination, asthereognosis.
4. The lesion of upper parietal lobe can cause in non dominant hemisphere
· Autotopagnosia (somatotopagnosia) includes disturbances in recognition of
the patient's own body or body parts.
· Pseudomelia - the patient has a sensation of presence (pseudopolymelia) or
the absence (pseudoamelia) of additional extremities.
· Anosognosia is lack of awareness or denial of the existence of disease. An
obvious example is a denial by the hemiplegic patient that he is paralyzed.
5.Apraxia occurs at lesion of gyrus supramarginalis lesion of the dominant
hemisphere. Apraxia – is a disturbance of purposeful movements which is not due
to elementary motor or sensory impairments. Apraxia is divided on:
 Motor or Kinetic Apraxia The patient has lost the ability to make fine skilled
movements such as finger wiggling, opposition, writing, or piano playing.
 Ideational Apraxia In ideational apraxia there is inability or failure to
comprehend, develop, or retain the concept of what is desired (step 1). Such a
patient will have difficulty in understanding what is desired and will fail to
complete the desired act. Ideokinetic Apraxia. Another common form of
apraxia is known as "ideokinetic" or "ideomotor" apraxia. This occurs when
there is a break in transmitting or converting the idea into the appropriate
motor act (as in step 2). Despite knowing what is desired, the patient is unable
to carry out a desired complex performance.
 Constructional and Dressing Apraxia Constructional apraxia may be
demonstrated by having the patient try to copy geometric forms or draw the
face of a clock. Further testing includes having the patient try to arrange sticks
in a specific pattern or to arrange Kohs blocks in a desired design. Dressing
apraxia is tested simply by asking the patient to put on a shirt or bathrobe
6. Alexia and acalculia occurs at lesion of gyrus angularis of the dominant
hemisphere. That means the patient is not able to read, write (optical agraphy).
Acalculia means one is not able to count.

38. Temporal lobe: functions and symptoms of lesion.

Temporal lobe Localization of functions
This lobe receives information from auditory, smell, taste stimuli and speech
sounds.
1. Auditory zone is located in upper temporal gyrus.
2. Smell zone is located in gyrus parahippocampalis.
3. Taste zone is located not far from the smell one.
These zones of each hemisphere have connections with both – right and left
receptors.
4. Wernicke center (the center of sensory speech) is located in the left upper
temporal lobe.
5. The center of mnestic speech (the center of naming) is situated in posterior
parts of temporal and lower parts of parietal lobes.
The main symptoms of lesion
1. Wernicke’s aphasia occurs in case of auditory association area involved and
means the impairment of comprehension of spoken language, repetition of
spoken language, naming comprehension of written language, spontaneous
speech, the spoken language is fluent but impaired (jargon). Loss of impressive
speech.
2. Anomic (nominal) aphasia is impairment of naming objects and spontaneous
speech. Spoken language fluent but rambling and vague. Retained the repetition,
comprehension of both spoken and written language. This type of aphasia may be
seen at small lesions in the angular gyrus, toxic or metabolic encephalopathy, or
with focal space-occupying lesions far from the speech area, but which exert
pressure effects.
3. Semantic aphasia occurs at lesion of temporal-parietal-occipital border of left
hemisphere. The patients cannot realize the difference between “The brother
of the father“and “the father of the brother “.
4. Lesion of the temporal lobe tends to produce quadrantic defects which extend to
the point of fixation without macular sparing. Lesion of the temporal lobe around
the inferior horn of the lateral ventricle give rise to defects in upper quadrants of
the homonymous half-fields on the side opposite the lesion.
5. Lesion of the temporal lobe may produce temporal ataxia.
6. The attacks of vestibular-cortical dizziness, associated with auditory
hallucinations.
7. Auditory verbal agnosia. Such patients can read, speak, and write appropriately
but are unable to understand or respond to what is said to them.
8. Smell and taste agnosia.
9. Irritative lesions of the temporal lobes produce the auditory, smell, and taste
hallucinations. Usually it is the first symptom of epileptic attack.
10. Petit mal is a typical symptom of temporal lobe lesion. Usually it manifests as
short lasting loss of consciousness.
11. Development of sleep like state is very typical for temporal lobe lesion. In this
case it seems to the patient that everything around him is unreal, unnatural, but at
the same time it seems to him that he has seen it before.

39. Occipital lobe: functions and symptoms of lesion.

Occipital lobe Localization of functions
Visual zone is located in the internal surface of occipital lobes in the depth of
fissura calcarine. The region above the sulcus calcarinus is called cuneus and it
represents the lower quadrants of visual fields. The region below the sulcus
calcarinus is called gyrus lingualis and it represents upper quadrants of visual
fields.
The symptoms of lesion
1. Quadrant hemianopsia. At cuneus lesion the lower quadrant visual fields are
lost. At gyrus lingualis lesion the upper visual fields are lost.
2. Homonymous hemianopsia of opposite visual fields occurs at lesion in fissura
calcarina on the internal surface of occipital lobe.
3. Scotoma is a defect within the visual fields.
4. Hemiambliopia – decreased vision.
5. An early symptom of visual analyzer lesion is the loss of color sense in the
opposite visual fields.
6. At lesion of sulcus calcarinus seldom cause total blindness. Usually central or
macular vision of both eyes is preserved.
The lesion of convex surface of occipital lobe causes next symptoms:
7. Visual agnosia: Visual object recognition is simply the ability to recognize
objects that are seen. Formal testing may not be necessary if it is apparent that the
patient can name and use various objects. If there is any doubt, his ability can be
tested by presenting him with one object and having him pick out the matching
object from a group; or, for convenience, pictures may be used instead of objects.
8. Metamorphopsia means disability to recognize objects’ contours. It seems to
the patient that they are destroyed, damaged.
9. Irritation of the occipital lobe can cause visual hallucinations. Thus simple
hallucination (fotoma) occurs at irritation of sulci calcarini. They manifest as
light or coloured phenomena, for example flash, fire, shadow.
10. Complex hallucinations occur at external surface of occipital lobe irritation.
They manifest as figures, moving subjects. As a rule they are aura of epileptic
attack.

40. Name aphasias. The lesions of what lobes can cause aphasias?
-Impressive speech: ability to understand and follow instructions
-Expressive: Articulation (ask patient to repeat complicated words),
automatic speech, conversation.
-Language is in dominant hemisphere, left side of brain for right handed and
vice versa.
Type of aphasia:
 Motor aphasia: Broca’s aphasia occurs due to lesion in frontal lobe. Loss of
expressive speech can be classified as
 Afferent motor aphasia is associated with the lesion of lower parts
of postcentral gyrus which provide innervation of oral muscles. In this
case articulation of sounds suffers. That means the loss of
automatically speech, repetition, naming. This kind of aphasia is
connected with oral apraxia.
 Efferent motor aphasia is Broca’s aphasia. It means it occurs at lesion
of the center of Broca. At partial aphasia he uses only nouns.
 Dynamic motor aphasia is usually caused by lesion of cortical zone
in front of Broca’s center. For this type of aphasia aspontanic speech
is typical. The patient refuses to speech in active manner. But he is able
to repeat certain sentences, words, answer the questions.
 Sensory aphasia: Wernicke aphasia: Loss of impressive speeh. Lesion on
wernickes area on temporal lobe
 Anomic (nominal) aphasia is impairment of naming objects and
spontaneous speech. Spoken language fluent but rambling and vague.
Retained the repetition, comprehension of both spoken and written language.
This type of aphasia may be seen at small lesions in the angular gyrus, toxic
or metabolic encephalopathy, or with focal space-occupying lesions far from
the speech area, but which exert pressure effects.
 Semantic aphasia occurs at lesion of temporal-parietal-occipital border
of left hemisphere. Loss of recognition of phases, logical connectionThe
patients cannot realize the difference between “The brother of the
father“and “the father of the brother “.

41. Name agnosias. The lesions of what lobes can cause agnosias?
Agnosia is inability to process sensory information
The lesion of upper parietal lobe can cause
· Autotopagnosia (somatotopagnosia) includes disturbances in recognition of
the patient's own body or body parts.
· Pseudomelia - the patient has a sensation of presence (pseudopolymelia) or
the absence (pseudoamelia) of additional extremities.
· Anosognosia is lack of awareness or denial of the existence of disease. An
obvious example is a denial by the hemiplegic patient that he is paralyzed.
Lesion of Temporal lobe
 Auditory verbal agnosia. Such patients can read, speak, and write
appropriately but are unable to understand or respond to what is said to them.
 Acoustic agnosia: patient can hear but not recognize what he hears
 Smell agnosia: patient can smell but can’t recognize what they smell
 Gustatory agnosia: patient can taste but can’t recognize what they are tasting
Lesion of Occipital lobe
 Visual agnosia: Patient can see but can’t recognize what they see

42. Symptoms of vegetative system lesions on different levels (peripheral

nerves, radix, Ciliry ganglion, sympathetic nodes, lateral horn, vegetative
nuclei of brain stem).
The lesion signs:
Sympathy adrenal attack Vagoinsular attacks
a) periarthritis a) incontinence of urine and feces
b) epicondilitis b) ischuria /retention of urine
c) miositis c) eye accommodation paralysis
d) hyperkeratosis d) midriasis
e) fissures of skin e) breath
f) arthropatias f) dyspnea
g) trophic ulcer g) apnea
h) alopecia h) cardiac arrhythmia
i) hyperpigmentation i) asystolia
j) Horner’s sign j) collapse
(ptosis, miosis, enophthalmia):
Miosis, mydriasis: lesion of ciliary ganglia
Dyspnea, apnea, cardiac arrhythmia, asystole: lesion of brain stem
Dry skin, hyperhidrosis, edema, paleness, cyanosis, arthropathy: lesion of lateral
horn
43. Name the hypothalamic realizing and inhibition factors. Function and
symptoms of lesion of the limbic-reticular complex.
The very important role belongs to the releasing factors. In hypophysis there are 7
tropic hormones that activate the production of certain hypophysis hormone:
 Corticoliberinum
 Tirioliberinum
 Luliberinum
 Foliliberinum
  Somatoliberinum
 Prolactoliberinum
 Melanocytoliberinum
There are 3 inhibiting hormones:
 Prolactostatinum
 Melanocytostatinum
 Somatostatinum
Function of limbic system
 Emotional reactions
 The reception of afferent impulses from internal organs
 It is a memory substratum; it preserves information about previous
genetically inherited experience
 It provides motivation to thirstiness, hunger, sexual desire
 It regulates the state of sleepiness and liveliness
 It indirectly regulates the function of internal organs
Function of Reticular formation
 The control of sleepiness and liveliness.
 To accept the information from the environment.
 To keep in tonus all the forms of behaviour, those have long – lasting
character.
Lesion of limbic-reticular complex;
 Emotional disturbances
 Anorexia, bulimia
 Sexual disturbances
 Loss of memory (Korsakov’s sign)
 Endocrinal disturbances
 Illusions, hallucinations
 Consciousness pathology
 Temporal epilepsy

44. Hypothalamus: anatomy, function. Hypothalamic syndromes.

Hypothalamic region has 32 pairs of nuclei of cranial nerves. They can be
divided into three groups.
 Anterior – it is associated with parasympathetic function
 Middle – endocrine – trophic
 Posterior – has mainly sympathetic influence.
The function of hypothalamus
 Regulation of heart – vascular activity
 Regulation of lipid, water, mineral metabolism
  Thermoregulation
 Regulation of vessels’ and tissue membranes penetrance
 Regulation of endocrine glands’ function
 Constant internal surroundings support
 Adaptation, Biorhythm
 Emotional behaviour
Hypothalamic syndromes are those that are associated with the lesion or
deficiency of hypothalamus. They include:
1. Autonomic – vascular – visceral – is associated with crisis of paroxysmal
character.
 Sympathetic – adrenal a pale and dry skin, shortness of breath, dizziness or
faintness, high blood pressure, tachycardia, feeling of internal tremor, fear of
dying
 Vago – insular hyperemia of the face, sweating, bradycardia, decreasing
blood pressure.
 Mixed begin as the sympathy-adrenal and finish as the vagoinsular crisis or
vice versa
2. Neuro – endocrine – metabolic – is associated with increasing or decreasing
of hypophysis function (Itsenko – Kushing, acromegaly, early climax, impotence,
non sugar diabetes, tyreotoxicosis).
3. Neuro – trophic is associated with trophic disturbances (dryness,
neurodermitis, ulcers, bed sores, acute perforates of stomach and esophagus).
4. Neuro – muscular – hypothalamus provides chemical and biochemical
activity of extrapyramidal nervous system and cerebellum. Myasthenia.
Myotonia. Paroxysmal myoplegia
5. Thermoregulation disturbances – the temperature is 37,1 – 37,5, there is
asymmetry under the arms, in the mouth and in rectum. Sometimes this
symptom has paroxysmal character and is associated with trembling.
6. Sleeping disorders
 Insomnia
 Lethargy (a special form – narcolepsy) – sudden attack of sleepiness that can
happen in any place and position of the patient. Sometimes they are associated
with catalepsy (the loss of muscle tonus)
 Sleeping inversion

45. Clinical feature of sympathy-adrenal attack. Emergency treatment in this

cause.
Sympathy-adrenal attacks:
a) skin is pale
b) xerostomia
c) dryness of hair and skin
d) tachycardia
e) high blood pressure
f) midriasis and widing of eye-slit
g) exophthalmia
h) tremor
i) gooseflesh
In sympathetic-adrenal crisis treatment is:
 series: Euphyllin (2.4% solution) — 10 mL, Glucose (20% soluton) — 40
mL I/V in flow, Pentamine (15% solution) 1 mL I/V drip-feed; Clofellin
(0.01% solution) — 1 mL, Lasix 80 mg (4 mL) I/M.
 In tachyarrhythmia the Propranololum (Obzidan or Inderal per 5 mg I/V in
salt solution) and Anaprilin (60– 80 mg per os daily) are indicated.
 Sometimes the α-adrenolytic Clofellin is prescribed (I/M per 0.1 mg every
1–2 hours up to maximum daily dose 0.4–0.6 mg).
 In face, larynx, tongue and extremities swelling the calcium preparations,
ephedrinum and diuretics are to be applied.
 Supportingcourse management includes Suprastin 0.025 in noon and
Seduxen (0.01) with Pyrroxan (0.015) before night for 4–6 months, medical
glycerin per 50 mL for glass of fruit juice once a day after meals for month,
following diet restricted for salt, weekly bowels wash.

46. Clinical feature of vago-insular attack. Emergency treatment in this cause.

Vagoinsular attacks:
a) hyperemia
b) hyperhidrosis
c) oily skin and hair
d) bradycardia
e) low blood pressure
f) miosis
g) angina pectoris
h) salivation
i) breathlessness
j) abdominal spastic pain
k) diarrhea,
l) frequent and abundant urination
vago-insular crises Treatment includes:
  the pain neuro-vascular (Analgin 50% solution — 2 mL, Cyanocobalamin
0.5–1 mg, No-spanum 2 mL
 selectively — Baralgin, Trigan, Maxigan 5–10 mL, Lasix 40 mg (2 mL)
I/M)
 vestibular-vegetative syndromes (Atropine sulphate 0.1% — 1 mL,
Dimedrolum 1% — 1 mL or Seduxen 0.5% — 1 mL).
 Crisis can be relieved through the drip-feed of ex tempore prepared Sodium
bicarbonate 5% solution per 100–150 mL every other day, 0.25% Novocaine
solution — 100 mL

47. Normal cerebral-spinal fluid (CSF) indices. Pathological CSF syndromes.

Characteristics of Normal Cerebrospinal Fluid
Appearance clear and colorless
Pressure Less than 180 mm of CSF.
Cells 0 to 5, usually lymphocytes (more than 8 cells is
abnormal)
Total protein 0,15 to 0,33 mmol/ liter
Glucose 2,2 to 3,3 mmol/ liter
Chlorides 120-130 mEq. Per liter
Meningeal syndrome Cerebrospinal fluid’s hypertension
syndrome
Headache Headache (in the morning)
vomiting vomiting
common hyperesthesia dizziness
Nuchal rigidity, Kernig’s sign, convulsive seizure
Brudzinski’s signs, Bechterev’s
symptom
hallucination lesion of cranial nerves
the pulse is rapid prostration
cell-protein dissociation protein- cell dissociation
the patient is irritable Optic fundus edema
hemorrhages in the cerebrospinal fluid increased pressure of the cerebrospinal
fluid
meningeal posture
48. Symptoms of Meningeal syndrome. Lumbar puncture indications.
Meningeal syndrome (meningitis, encephalitis, vascular disorders): symptoms
are headache, vomiting, hallucination, rapid pulse, cell-protein dissociation, patient
is irritable, hemorrhages in CSF, meningeal posture and they manifests as neck
stiffness, Kernig sign, Brudzinski signs (upper, middle and lower ones), Lessage
symptom (in children), Bechterev’s cheek bone phenomena. Increased intracranial
pressure causes bulging of an unclosed anterior fontanelle in children.

The nuchal rigidity - the patient can’t to flex the head and place the chin on the
chest.
The Kernig’s sign. With the patient in the supine position the examiner flexes the
hip and then extends the knee as far as possible without producing significant pain.
Normally the knee can be extended so that the angle between the posterior surface
of the thigh and leg is approximately 135 degrees. Results of the test are considered
positive if extension of the knee is limited decidedly by involuntary spasm of the
hamstring muscles and, as a rule, if pain evoked.
Brudzinski’s signs:
upper: when the head is flexed on the chest - the knees are flexion too;
middle: when the examiner to do the Kernig’s test - the contralateral leg is flex.
Lower: Pres pubic bone, if patient bends leg, sign is positive
Lumbar puncture indications
 Spinal and epidural anaesthesia
 Infection: meningitis, encephalitis, myelitis
 Inflammatory: Multiple sclerosis, Gullian-Barre
 Oncologic- leukemia
 Metabolic disease

49. Subjective and objective symptoms of intracranial (liquor) hypertension.

General – cerebral (hypertensive) syndromes are the result of increased intra
cranial pressure.
The main reasons of increased intra cranial pressure are:
 The tumor mass
 Brain edema
 Blood and CSF drain disturbances
 CSF absorption disturbances
The main clinical signs of intra cranial hypertension
 1. Headache: in morning, increased during cough or exercise, decreased
after vomiting.
 2. Vomiting: occurs only due to severe headache. Occur due to irritation of
vagus nerve
 3. Choked disks of II CN: Foster kennedy atrophy of optic nerve. Optic
atrophy on ipsilateral eye and disc edema in contralateral eye
 4. Pulse, AP and breathing disturbances. Tachycardia, arrhythmia.
hypertension
  5. Epileptic attacks
 6. Psychiatric disorders: memory disturbance, loss of orientation,
inhibition, spoor and coma
 7. CSF changes: increased CSF pressure. Protein-cellular dissociation
 8. Craniogram changes: osteoporosis of Turkish saddle, unclosed cranial
sutures, osteoporosis of pyramids of temporal bone and edge of occipital
foramen. Increased skull sizes and thin skull bones.

50. Diagnostic abilities of CT-scan and MRI of the brain and spinal cord. CT-
scan picture of strokes, tumours of the brain, brain edema, internal and
external hydrocephaly
They are osteoporosis of Turkish saddle, well expressed digital depressions, well
expressed vessels picture, unclosed cranial sutures, osteoporosis of pyramids of
temporal bone and edge of occipital foramen, increased skull sizes and thin skull
bones.
Ischemic stroke: hypodensive focus
Hemorrhagic stroke: hyperdensive focus

51. Symptoms of the vertebrogenous syndrome.

Vertebrogenous syndrome points that the pathological process is associated with
spinal cord.
 Limitation of movements in lumbar – sacral part of spinal cord (bending
forward, backward) and increasing of pain while movements, coughing
and laughing.
 Protective straining of long back muscles
 Extension of lumbar lordosis, cyphosis in lumbar – sacral division.
 Scoliosis, sometimes with rotation
 Painful paravertebral points
 Painful vertebral processes
 Discharge – postures and symptoms
o Knee – elbow position
o While standing the patient keeps his leg aside in order to make the
load less on his leg
o While lying in the bed he bends his leg in all joints.
 The symptoms of spinal cord instability (it is difficult for the patient to
stand, to wash himself, but it is much more easier to walk).

52. Muscular-tonic syndromes of vertebral ostheochondrosis: clinical features,

treatment.
Muscle – tonic Clinical features are connected with secondary lesion of nerves
according to the compressive – ischemic type, the type of tunnel syndrome as a
result of muscles spasm and straining. Piriformis syndrome, Scalenus syndrome
and pectoralis minor syndrome.
Piriformis syndrome lumbo-sacral Clinical features:
 Painful palpation of Trochanter major
 Painful m.Piriformis
 Symptom of Soobrase (painful cross-legged position)
 Symptom of Bone – Bobrovnikova (painful abduction of leg)
 Popelyansky intermittent claudication (while walking the patient is forced to
sit down because of the pain. That is the result of spasm of the vessels
 Insignificant sphincter disorders (pause before the urination) as a result of n.
pudendus irritation
 Insignificant signs of n. ischiadicus lesion (muscles hypotrophy, low Achille
reflex, hyposthesia, pain)
Scalenus – syndrome It is connected with straining of m. scalenus. The muscle
starts from transversal processes C3 – C4 and it is attached to the first rib. There
are subclavian artery, vein and lower truncus of brachial plexus between the
muscle and the rib.
 There are pains above and under clavicle at the muscle straining
 There are pains at head movements with irradiation in the arm
 Edema in above clavicle region
 Positive Adson test – during the arm adduction there is pain over a.
subclavia and slow pulsation in a. radialis
 Weakness of hand
 Tenar hypotrophy . Hypalgesia of the hand ulnar surface
 Hand edema. Paleness of the hand
M. pectoralis minor syndrome At this muscle straining the distal part of vascular
– nervous trunk is pressed.
 Pain in anterior thoracic part and in ulnar surface of hand
 Hand weakness
 IV – th – V – th fingers paresthesia
Treatment
 orthodopedic
 at edema-euphilinum 2.4% 10.0
 analgesic; Reopirini 2.5% 3.0, tramadol
 spasmolytic: platiphilinum, no-shpa
 myorelaxants; midocalm, baclofen
  vitamins
 physical methods

53. Cervicocranialgia: pathogenesis and main symptoms.

Pathogenesis:
 Irritation of a. vertebralis sympathetic plexus – posterior cervical
sympathetic syndrome.
 Irritation of cervical muscles, fibrous tissues receptors.
Clinical features of posterior cervical sympathetic syndrome:
 Cranialgia – occipital pain with irradiation in temporal, parietal parts
 Vestibulo – cochlear disturbances – dizziness, vomiting
 Eyes symptoms – eyes pain, tears
 Autonomic upper quadrant syndrome – asymmetry of blood pressure,
temperature, pulse, sensation, cardiac pain and so on

54. Classification and pathogenesis of neurological syndromes of vertebral

ostheochondrosis on cervical, lumbar and thoracic levels.
Neurological signs at lumbar-sacral classification
 reflex syndromes;-lumbago, lumbalgia, lumbar ischialgia
 compressive radicular syndromes
 compressive vascular radicular-spinal syndromes( radicular ischemia)-
acute (transient, stroke), chronic ischemic myelopathy
Neurological signs of osteochondrosis at cervical level
 Reflex symptoms: stiff neck, cervicalgia, cervical brachialgia
 Compressive radicular syndrome
 Compressive-spinal syndrome
 Compressive vascular radicular- spinal syndrome: acute(transient,
stroke), chronic ischemic myelopathy
 A.vertebralis syndrome( radiculopathy of c8 radix, disc c7-c8)
Pathogenesis of neurological syndromes
 Compressive syndrome occurs at compression and deformation of radix,
vessels and spinal cord.
 Reflex syndrome occurs at irritation of different receptors (such as
Lushka nerve). That means reflex muscular – tonic disturbances, extension
of muscles, and pain at palpation of muscles. That is usually the reason of
local pain and pain in distance. Such zones of pain are called trigger
zones. Pathogenetical process in these zones is known as neuroosteofibrosis,
 the painful nodes in muscles are called nodes of Kornelius, muscular
hypertonus – hypertonus of Muller.

55. Reflex syndromes of neurological complications of cervical

osteochondrosis. Clinical features, diagnostic procedures, treatment.
-Stiff neck It is sudden acute pain in neck that lasts from several days up to 1 – 2
weeks.
-Cervicalgia It is severe dull pain in cervical part of the spinal cord. Usually it
appears in the morning, while coughing. There are signs of vertebrogenous
syndrome in cervical level - limitation of movements in cervical part of the spinal
cord, painful paravertebral points and vertebral processes. There are positive
symptoms of muscles straining.
-Cervical cranialgia.
 Cranialgia – occipital pain with irradiation in temporal, parietal parts
 Vestibulo – cochlear disturbances – dizziness, vomiting
 Eyes symptoms – eyes pain, tears
 Autonomic upper quadrant syndrome – asymmetry of blood pressure,
temperature, pulse, sensation, cardiac pain and so on
Cervical brachialgia.
 Muscle – tonic form: scalenus syndrome, pectoralis minor syndrome
 Neurodystrophic form: shoulder-scapula periartrosis (pain and limitation
of arm and shoulder), shoulder-hand syndrome(autonomic-trophic changes
of hand+ shoulder-scapula periartosis), Epicondilosis
 Autonomic – vascular form
Diagnosis: Made on irritation of reflex, painful points. CT, MRI, Myelography,
Spinal x-ray exam
Treatment
 orthodopedic
 at edema-euphilinum 2.4% 10.0
 analgesic; Reopirini 2.5% 3.0, tramadol
 spasmolytic: platiphilinum, no-shpa
 myorelaxants; midocalm, baclofen
 vitamins
 physical methods
 Chondroprotectors: Rumalon

56. Reflex syndromes of neurological complications of lumbar

osteochondrosis. Clinical features, diagnostic procedures, treatment.
-Lumbago It is acute, sudden, attack – like low back pain. It usually begins at
lifting something heavy, catching cold or sometimes spontaneously. Pain is very
severe and the patient stays in the same position for a long time. At first the pain
cannot be localized. Later the patient can localize it and refers the pain to the
low back region. It lasts for 1 – 3 up to 6 days.
-Lumbalgia The pain is not so severe. It has subacute or chronic character. It
lasts for weeks or even months. The pain can be increased or decreased
according to different factors.
-Lumbar ischalgia The source of pain impulse is receptor. The pain irradiate
into hips, leg.. Muscle tonic (piriformis syndrome), neurodystrophic (sacroiliac
periartosis, knee joint periartrosis, popliteal syndrome, coccygodynia), autonomic-
vascular
The points of pain:
 Pain along the crista iliaca
 The point of iliosacral joint
 The point of m. gluteus minimus (just under the crista iliaca)
 The point of m. gluteus medius (1 sm lower)
 The point under the backside fold
 Trochanter os iliaca
 Along the ischiadic nerve (the posterior surface of hip and fossa subpoplitea)
The symptoms of strain
 Lasegue’s symptom – in case of straining and lifting the leg the low back
pain appears
 Neri symptom – there is pain in leg at bending head forward
 Matskevych symptom – there is pain in the anterior surface of the leg at
knee bending while lying on abdomen
 Wasserman symptom – there is pain in the anterior surface of the leg at
lifting the leg while lying on abdomen
 Sequar symptom – there is pain on posterior surface of leg at foot flexing
 Turin symptom – the same clinical picture at toe’s flexing
 Bechterev’s symptom – there is pain at knee – flexed leg extension
 Dejerine’s symptom - there is pain in posterior surface of the leg at
coughing, sneezing
Diagnosis: Made on irritation of reflex, painful pounts. CT, MRI, Myelography,
Spinal x-ray exam
Treatment
 orthodopedic
 at edema-euphilinum 2.4% 10.0
 analgesic; Reopirini 2.5% 3.0, tramadol
  spasmolytic: platiphilinum, no-shpa
 myorelaxants; midocalm, baclofen
 vitamins
 physical methods
 Chondroprotectors: Rumalon

57. Radix compresive syndromes of cervical osteochondrosis (signs of lesion

C6,C7,C8).
-Radiculopathy C6 radix (C5 – C6 discs)
 Pain, parasthesia and hypalgesia on anterior external surface of arm
 Weakness, hypotrophy of m. biceps brachii
 Absent or low biceps reflex
-Radiculopathy C7 radix (C6 – C7 discs)
 Pain, parasthesia and hypalgesia
 Weakness, hypotrophy of m. triceps brachii
 Low triceps reflex
-Radiculopathy C8 radix (C7 – C8 discs)
 Pain, parasthesia and hypalgesia
 Low triceps elbow and carpo – radial reflex

58. Radix compresive syndromes of lumbar osteochondrosis (signs of lesion

L4,L5, S1).
-Radix L5 ( Disc L4 – L5)
 Pain in the external edge of hip, on the anterior –external surface of crus
until the internal surface of foot and great toe
 Sensory disorders (hypalgesia, analgesia) in the same zones
 Paresis of great toe extensors and foot extensors
 Hypotonia and hypotrophy on the anterior surface of crus
 The patient cannot stand on heels
-Radix S1 (Disc L5 – S1)
 Pain in external – posterior surface of hip, crus, foot, the IV –th and Vth toes
 Sensory disorders (hypalgesia, analgesia) in the same zones
 Paresis of toes flexors
 Absent or low Achille reflex
-Radix L4 (Disc L3 – L4)
 Pain in anterior – internal surface of hip
 Sensory disorders (hypalgesia, analgesia) in the same zones prevail over
motor ones
  Weakness of m. Quadriceps femoris
 Hypotrophy of m. Quadriceps femoris
 Knee reflex is low or sometimes increased

59. Treatment of neurological syndromes of vertebral osteochondrosis (reflex

and compresive) in acute and residual stage
 Orthopedic
 Medicines:
o At edema: Euphyllinum 2.4% 10.0; Lasix 2.0; Dexamethasonum 4 – 8
mg; NaCl 0.9% 200.0 i/v by drops
o Platiphillinum, No – spa, Baralginum
o Analgesics - Reopirini, Voltareni 2.5% 3.0; Tramadol, Aminasini
o Non steroids medicines– Ketanov, Dicloberl, Movalis, Ranselex,
Celecoxib
o Myorelaxants – Midocalm, Baclofen
o Chondro- protectors – Rumalon
o Vitamins and biostimulators
o Physical methods
 Surgical methods indication
o Horse tail compression
o Long lasting (3 – 6 months) pains
o Huge hernia (over )
o Acute compression of radicular – spinal artery
 Sanatorium
 Prevention
o Hypokinesia prevention
o Moderate physical activity
o Treatment of chronic diseases

60. Acute demyelinating polyradiculoneuropathy of Guillain-Barre. Etiology,

pathogenesis, clinical features, diagnostic procedures, complications, and
treatment.
Guillain – Barre polyneuropathy – it is an acute autoimmune auto-allergic
disease. In most cases it is developed after infections, trauma and surgery.
Etiology and Pathology
The Guillain-Barre syndrome often follows a nonspecific respiratory or
gastrointestinal illness but has also been described after a number of specific
infections such as cytomegalovirus, Epstein-Barr virus, enterovirus,
Campylobacter jejuni or mycoplasma, and after immunization. The disease is
believed to be due to lymphocytic sensitization to peripheral nerve antigen. There
is diffuse, patchy, segmental demyelination of peripheral nerves. Light microscopy
reveals an intense lymphocytic, inflammatory infiltrate at the sites of
demyelination
The peculiarities of clinical picture: ascending type of polyneuropathy
 There is flaccid tetraparesis, much more expressed in proximal parts of
extremities. Begins in feet then trunk then arms then
 IX, X, VII CN’s are often involved (bulbar syndrome with respiratory
disturbances)
 There are respiratory disorders in case of between ribs nerves involvement.
 Sensory disorders are slightly expressed or absent
 It is often associated with meningoradicular syndrome, (+) Kernig,
Lasseg, Neri signs.
 The course of the disease has its own peculiarities: the clinical picture
develops rapidly during 7 – 10 days. By the way, the more rapidly it is
developed, the better it will regress. In case of typical course of the disease
¾ of all patients recover completely.
Diagnostic Procedures
 The CSF cell count may be normal, or there may be a mild lymphocytic
pleocytosis in the early stages of the disease. Protein-cell dissociation
 Nerve conduction studies show conduction velocities less than 60 percent
of normal in most cases. Distal and motor latencies are prolonged, and
proximal stimulation of nerves shows a decrease in amplitude, owing to
dispersion of the action potential or conduction block. F-wave responses
may be absent or show prolonged latency.
 About 10 percent of patients show incomplete recovery. A prolonged period
(more than 3 weeks) from maximal weakness to initial improvement,
associated with reduced motor nerve conduction velocities and evidence of
denervation by electromyography, are indicative of a possible incomplete
recovery.
Treatment:
 desintoxication
 dehydration
 desensibilization
 plasmapheresis (8 – 10 seances)
 Intravenous immunoglobulins: bioven 0.4mg/kg, Sandoven
 bladder cathetirization
 Glucocorticoids
Complications
  Respiratory impairment
 Autonomic instability may present as urinary retention in the early stages
of the disease. Fluctuations in blood pressure, orthostatichypotension, and a
rare complication of persistent hypertension are late events.
 Bulbar palsy should always be considered when bilateral facial weakness is
present.
 Pain presenting as myalgia in the lower limbs is an early symptom in some
cases, but pain may be a prominent symptom throughout the acute phase of
the illness, requiring appropriate and adequate therapy.
 Secondary infection is a risk with pneumonia complicating respiratory
insufficiency and increased risk of urinary tract infection and infected
decubitus ulcers.
 Immobility predisposes to deep venous thrombosis in the lower limbs
and pulmonary embolism.
 Similarly, immobility and failure to change position increase the risk of skin
breakdown and decubitus ulcers.
 Fluid and electrolyte imbalance is not unusual when intake is restricted to
parenteral fluids because of bulbar palsy.

61. Diabetic polyneuropathy. Clinical features, diagnostic procedures,

treatment.
It s the sensory disturbance of the lower and upper exxtremities like paresthesia,
hyperparesthesia, hypaesthesia, associated with diabetes melitus.
The peculiarities of clinical picture.
 Sensory disturbances on lower and upper extremities such as
parasthesia, hyperesthesia, hypesthesia and pain are dominant.
 There are autonomic disorders: dryness of skin, an- or hyperhydrosis,
trophic ulcers and so on.
 Knee and ankle reflexes are lost at the beginning of the disease.
 Severe paresis is very rare in this case.
 There is visceral form of diabetic polyneuropathy with progressive
autonomic insufficiency. Cardiac arrhythmia, extrasystole. Gastroptosis,
diarrhea.
 Proximal amyotrophy polyneuropathy: paresis, atrophy of proximal
muscle of hips
 Distal symmetrical polyneuropathy
 Microangiopathy: lacunar stroke
 Macroangiopathy: atherothrombotic stroke
Diagnosis
  Diabetes in anamnesis, with complaints
 CT or MRI
 Electromyography
 Doppler imaging
Treatment
 Foot care, including regular follow-up, patient education, and referral as
appropriate
 Tight, stable glycemic control (most important for slowing progression of
neuropathy)
 Pain management (eg, with pregabalin, gabapentin, sodium valproate,
dextromethorphan, morphine sulfate, tramadol, oxycodone, duloxetine,
topical capsaicin, transdermal lidocaine)
 Treatment of diabetic gastroparesis (eg, with erythromycin, metoclopramide,
polyethylene glycol 3350, tegaserod
 Experimental therapies include aldose reductase inhibitors, alpha-lipoic acid
(berlithion, dialipon, thiogamma), actovegin, and spinal cord stimulators
 Trental, Reopolyglucin, Vitamin B, ATP, Proserin

62. Diphtheric polyneuropathy. Clinical features, diagnostic procedures,

treatment.
It occurs as a complication of diphtheria. Dyphtheric toxinum is fixed mainly in
peripheral nerves and its nuclei, anterior roots, root nerves.
The clinical picture is developed on the background of upper respiratory ways
diphtheria in 5 – 6 days. Sometimes diphtheria is diagnosed afterwards because of
the peculiarities of polyneuritic syndrome development.
The peculiarities of clinical picture.
 At the beginning of the disease there are accommodation paralysis and
other eye movements disorders with development of diplopia and strabismus
 Bulbar syndrome (IX – X CN’s are involved) with respiratory disorders
and pneumonia.
 Heart – vascular disorders (bradycardia, myocarditis with arythmia,
tachycardia) most dangerous complication toxic myocarditis
 In a 1 month polyneuropathy of lower extremities is developed. Mainly it
is sensory – motor form.
 Polyneuropathy of upper extremities could be developed in a month
afterwards.
 Residual signs: paresis, atrophy of muscles
Diagnosis
1. Shick test; for previously acquired immunity to diphteria.
2. Test for CSF protein or diphtheria in CSF
In treatment anti-diphtheric serum and Glucocorticoids are used

63. Alcohol polyneuropathy. Clinical features, diagnostic procedures,

treatment.
It is a neurological disorder in which multiple peripheral nerves throughout the
body mulfunction simultaneously. It is developed in 32- 97% of people with
chronic alcoholism. Alcohol directly influences on neuronal metabolism.
Classification
 Acute; one paresis develope rapidly
 chronic; one clinical picture manifeat gradually
Clinical picture
 Lower extremities suffer at first then upper
 Well expressed lesion of peroneal nerve, feet extensors, weakness, and
specific gait disorders.
 Increase flex reflex at the beginning.
 Ankle reflexes disappear at the early beginning of the disease
 Sensory disturbances at first are irritating; pain, paresthesia,
hyperesthesia and hyperpathy dominate
 There is sensitive ataxia because of the deep sensation disturbances
 Amnestic Corsakov syndrome
 Chronic hepatitis, cirrhosis
Diagnosis
 Nerve conduction studies
 Electromyography
 Vibrometer
 Assessment of thiamine, vitaminB12 and folic acid
Treatment
 Stop drinking
 NSAIDS for pain
 High dose of vitamin B
 Desintoxication liver protectors : essentiale
 Berlition
 Dialipon

64. Mercury polyneuropathy. Clinical features, diagnostic procedures,

treatment.
Clinical features
  Skin discolouration, swelling and desquamation
 Sensory > Motor: Itching, burning or pain in skim
 Sensory loss: Distal; Legs > Arms; Pan modal; Romberg sign
 Discomfort: Pain & Paresthesias
 Tendon reflexes: Absent at ankles
 Weakness: Distal feet or None
 Prognosis: Improvement after removal of Hg exposure
Diagnosis:
 Urine and serum levels of mercury
 NCV: Small amplitude SNAPs
 EMG: Chronic denervation in feet
Treatment
 Chelation therapy for acute inorganic mercury poisoning can be done with
DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine
(DPCN), or dimercaprol (BAL).
 Alpha lipoic acid
 sprinolactone

65. Arsenic polyneuropathy. Clinical features, diagnostic procedures,

treatment.
It is developed at acute or chronic poisoning. Acute one is characterized by
enteritis associated with polyneuritis.
Clinical Peculiarities.
 Sensory disorders prevail (pain, parasthesia, cramps, feet and hands
hyperesthesia, poliesthesia)
 Atrophy of interostal spaces on hands and feet
 Sensetive ataxia is often developed because of the deep sensation
disturbances
 CN’s lesion (VIII, II, sometimes III, VII)
 Trophic disorders: feet and hands edema, white strips on nails
 Sensory loss: Stocking-glove; Large > Small fiber
 Weakness: Mild
 CSF: Protein mildly increased
 Pathology: Axonal loss; Distal
Diagnosis: Serum and urine arsenic levels
Treatment: Chelation
 BAL (Dimercaprol; IM; 100 mg/ml in peanut oil)
 D-penicillamine: May produce neurological complications
  ? 2,3-dimercaptopropanesulphate (DMPS): 5 mg/kg q 4 hours
 unitiolum and desintoxication

66. Clinical feature of Radial nerve lesion.

 Forearm extensors weakness
 Hand extensors weakness
 Fingers basal phalanx extensors weakness
 Impossible supination
 Impossible adduction of thumb
 Lost sensation on dorsal thumb surface and in space between the I st and II
and small bones

67. Clinical feature of Ulnar nerve lesion.

 Hand flexors weakness
 The IV th and V th fingers distal phalanx extensors weakness
 Thumb abductors weakness
 Hypothenar hypotrophy
 Hand looks like bird paw
 The patient cannot scrawl with the nail of the V th finger, play on the piano
and keep the sheet of paper with the I st and II nd fingers
 Anesthesia in the V th finger and hypothenar

68. Clinical feature of Medial nerve lesion.

 Impossible pronation
 Hand flexors weakness (especially of the I, II and III fingers)
 Thenar hypotrophy
 Hand looks like monkey paw
 Disability to opposite the thumb to the rest fingers
 Disability to make a fit as a result of thumb flexors weakness
 + mill sign
 Anesthesia on hands palm surface except the half of the IV th and V th
finger
 Severe autonomic disorders

69. Clinical feature of Femoral, Peroneal and Sciatic nerve lesion.

The symptoms of lesion Peroneal nerve. Femoral nerve lesion
 Feet and toes extensors weakness
dull aching pain in the genital area, numbness in
any part of the leg, muscle weakness of the lower
extremity, feeling like the knee or leg is going to
buckle, and difficulties in extending the knee as a
result of weakness in the quadriceps.
  Feet adductors weakness
 Typical gait – cock like
 Anesthesia of external edge of shin and dorsal surface of feet
The symptoms of lesion Sciatic nerve
 Complete paralysis of foot and toes
 Impossible flexion in knee joint and shin – foot joint
 Shin and hip atrophy

70. Trigeminal neuralgia: etiology, pathogenesis, clinical feature and

treatment.
Trigeminal neuralgia is a condition characterized by sudden, severe, lancinating
pain occurring in the distribution of the trigeminal nerve.
Etiology and Pathology theories
 Degenerative changes in the trigeminal (gasserian) ganglion, producing
paroxysmal discharge of neurons.
 Pressure on the trigeminal nerve root by an aberrant or arteriosclerotic
vessel, by a tumor,
 Caused by sinusitis, otitis
 Focus in trigeminal nucleus, irritation causes generalization
Clinical feature
 paroxysms of pain occurring in the maxillary or mandibular division of the
trigeminal nerve with later spread from one division to involve the other
division.
 may involve both sides of the face, but paroxysms never occur
simultaneously on the two sides
 pain may be provoked by touching the face, chewing, talking, drinking,
brushing the teeth, shaving, or the movement of air across the affected
side of the face
 depression, suicidal thoughts, and weight loss.
 Pain paroxysms that are caused by the movements of mimic muscles,
talking, eating, face washing. They can continue up to 1 – 2 min.
 Pain tics – facial hyperkinesis
 Trigger points – touching of these points can cause severe pain
Treatment
 anti seizures medications : carbamazepine, Gabapentin
 Analgesics
 Non steroid drugs
 Acupuncture
  Medical treatment using carbamazepine (Tegretol), Phenytoin (Dilantin),
Baclofen, benzodiazepines, gabapentin, or pi-mozide

71. Facial neuropathy: pathogenetic mechanism, clinical feature and

treatment.
Also known as Bells palsy (facial nerve neuropathy)
Pathogenetic Mechanism: The nerve lesion occurs due to ischemic anoxia as a
result of cold catching, inherited narrowing of facial nerve canal, local infectious-
allergic processes. Edema and ischemia
Clinical feature: facial mimic muscles paralysis, facial asymmetry, lagophthalm,
Bells sign, taste disorders and tears or dryness of the eye
Treatment in acute period
 Dehydration (Euphillinum, Lasix, Dexamethasonum i/v)
 Anti-inflammatory therapy (Glucocorticoids)
 Non steroid anti-inflammatory drugs (Diclofenac, Movalis, Naclofen,
Messulid) Fonoforesis with Hydrocortisonum
 Microcirculation improving (Actovegin, Solkoseril, Pentoxiphillin)
At recovery:
 Massage
 Electrophoresis with Proserinum, Nicotin acid
 Warming procedures
 Biostimulants (Plasmol, Aloe)
 Vitamins B, PP
 Acupuncture

72. Classification, causes and risk factors of cerebral circulation disorders.

-Causes: Atherosclerosis of cerebral vessels and general atherosclerosis,
Combination of atherosclerosis and hypertension. Heart diseases such as inborn
and acquired cardiac abnormalities, arrhythmias, IHD, cardiosclerosis, angina
pectoris, myocardial infarction. Infectious and infectious – allergic vasculitis (at
rheumatism, connective tissue diseases, lues). Arterial hypotension. Vasomotor
dystonia. Blood diseases (polycythemia, leucosis, haemophilia). Kidney diseases.
Endocrine diseases (diseases of thyroid gland, pancreas, suprarenal glands).
Diabetes mellitus. Traumatic lesion of vessels (at haemorrhage - subdural,
epidural, ventricular, parenchymatous). Artery and vein compression (especially
in cervical part of spinal cord – for example at osteochondrosis). Inborn and
acquired Willis circle abnormalities - occlusion, stenosis of MAH and neck,
aneurism, constriction of vessels. Brain tumours.
-Risk factors: Age (the elder person is, the highest risk of cerebrovascular disease
is). Sex (at the age of up to 55 – 60 years fatality from cerebrovascular disease is
higher in men, after 55 – 60 years – it is higher in women). Heredity (in particular
to heart and cerebrovascular diseases). Alcohol abuse. Cigarette smoking.
Hyperlipidemia and hyperglycaemia. Arterial hypertension. Hypodynamia.
Meteorological dependence ( especially people with labile autonomic nervous
system ). Personal type (picnotic type), stress, high carbohydrate diet.
Classification
A. Premonitary and initial symptoms of brain blood supply insufficiency
B. Acute cerebral blood circulation disturbances
1. Dynamic cerebral blood circulation disturbances
2. Acute hypertonic encephalopathy
3. Haemorrhage – subdural, epidural
4. Intracerebral hemorrhage
5. Brain infarction
a) cardioembolic,
b) atherothrombotic,
c) hemodynamic,
d) hemorheologic,
e)lacuna
C. Dyscirculative encephalopathy or chronic cerebral blood circulation
insufficiency or slowly progressive insufficiency of cerebral blood circulation.

73. Early signs of cerebral circulation reduce: pathogenesis, clinical picture,

treatment.
-Trouble with speaking and understanding. may experience confusion or slur
words or have difficulty understanding speech.
-Paralysis or numbness of the face, arm or leg. sudden numbness, weakness or
paralysis in your face, arm or leg, especially on one side of your body. Try to raise
both your arms over head at the same time. If one arm begins to fall, you may be
having a stroke. Similarly, one side of your mouth may droop when you try to
smile.
-Trouble with seeing in one or both eyes. suddenly have blurred or blackened
vision in one or both eyes, or you may see double.
-Headache. A sudden, severe headache, which may be accompanied by vomiting,
dizziness or altered consciousness, may indicate you're having a stroke.
-Trouble with walking. You may stumble or experience sudden dizziness, loss of
balance or loss of coordination.
Pathogenesis
-Arteriogenic microembols are small units that originate from clots and are the
result of destroyed atherosclerotic plaques.
-Thrombocytic embols are crumbling. That is the main reason of rapid involution
of neurological deficit.
-Cardiogenic microembols can cause TIA in patients with arrhythmias, heart
abnormalities, after myocardial infarction, in patients with rheumatic endocarditis.
-Hemodynamic
Treatment
-Antiagreggants: Aspirin, Ticlidi
-Improve brain hemodynamic: euphilini
-Antioxidant: Vitamin E
-Headache: tramadol, analgin
-Vomiting: haloperidol, aminasin, validol
Anticoagulant: Heparin, fraxiparini

74. Dyscirculative encephalopathy: clinical feature (according stadium),

treatment. Dyscirculative encephalopathy - Is slowly progressive insufficiently
of blood supplying of the brain, which caused developing of many small focuses of
brain tissue necrosis and manifests gradually grousing defects of cerebral functions
І (initial) stadium DE:
• headache
• dizziness
• loss of memory
• cephalic, optic, vestibular-cochlear, syncope, cardiac paroxysms lasting to
10 min
ІІ stadium (subcompensation) DЕ:
• vestibular
• vestibular - coordinator
• pyramidal
• extrapyramidal
• hypothalamic
• convulsive
• asthenic-depressive
ІІІ stadium (decompensation) DE:
 pseudobulbar
 aphasic
 apractic
 epileptic
  cerebellar ataxia
 pyramidal
 parkinsonian
 dementia

75. Transient disorders of cerebral circulation: definition, classification. The

main etiologic and pathogenetic mechanisms.Treatment
DCBCD – are acute brain dyscirculation events which usually are developed against
the main diseases . They are associated with temporary general and focal brain
symptoms . They have tendency to involution during 24 hours .
Classification
 Transient ischemic attacks ( TIA ) – they take about 1/3 of all DCBCD
 Hypertonic crisis - it takes about 2/3 of all DCBCD
Etiology
 Atherosclerosis
 Stenotic lesions of MAH
 Heart diseases ( abnormalities, myocardial infarction )
 Sometimes vasculitis , systemic vascular diseases
Pathogenesis
The main pathogenic mechanisms are
 Thromboembolic
o Arteriogenic microembols are small units that originate from clots and
are the result of destroyed atherosclerotic plaques .
o Thrombocytic embols are crumbling. That is the main reason of rapid
involution of neurological deficit.
o Cardiogenic microembols can cause TIA in patients with dysrhythmias,
heart abnormalities, after myocardial infarction, in patients with
rheumatic endocarditis
 Haemodynamic
o Atherosclerotic stenosis of cerebral vessels or MAH, especially in
association with hypotension, dysrhythmias and myocardial infarction.
o Thrombosis of neck magistral artery.
o In the subclavian steal syndrome the patient has a narrowed subclavian
artery and the arm “steals” blood from the basilar artery via the
vertebral artery. There may be a cervical bruit and a difference in blood
pressure between the arms. At times of arm exercise the patient may
experience vertebrobasilar insufficiency.
o Spasm of cerebral vessels and as a result perivascular edema and
hypoxia of brain tissue.
 o Inborn stenosis , abnormalities of MAH
o Compression of vertebral artery by osteophytes at cervical
osteochondrosis.
o Vessels insufficiency ( contradiction between real and demandable
blood supply ) . This can occur at heart failure, hypotension, internal
bleeding.

76. Clinical feature of TIAs in Carotid distribution.

Carotid distribution – is a territory of internal carotid arteries and their branches –
ophthalmic artery, anterior cerebral artery, and middle cerebral artery. Via
anterior cerebral artery carotid distribution supplies anterior part of frontal
lobe, internal surface of hemisphere to sulcus parietooccipitalis , via middle
cerebral artery – the cortex of frontal, parietal, temporal lobe, internal
capsula and nucleus.
 subjective sensory disorders, such as numbness, tingling in face and
extremities; and objective sensory disorders such as hyperesthesia of
superficial sensation in face and extremities, sometimes deep sensation in
fingers and toes.
 Very often motor disorders together with sensory ones are observed.
They are central paresis of extremity or fingers with hyperreflexia,
pathologic signs of Babinski (stroke heel to toe medial surface of foot
positive faning of big toe, Rossolimo tap ball of foot cause flexing of toes.
Hemiparesis or hemiplegia is observed only in severe cases.
 Sometimes distorting language (transient aphasia) is observed.
 TIA occurs in the internal carotid artery territory ophthalmic – piramidal
syndrome is developed. It usually manifests as blindness or reduction of
vision on the same side and hemiparesis on the opposite side. It is known
as Lasko – Radowich syndrome.
 Focal Jackson motor or sensory epileptic attacks are observed in patients
with MAH pathology. A set of local seizures that can cause general seizures

77. Clinical feature of TIAs in Vertebra-basilar distribution.

 Vestibular syndrome. systemic dizziness, occipital headache, nystagmus,
equilibrium disorders.
 Brainstem – cerebellum syndrome. It manifests as equilibrium,
coordination and synergy of action disorders.
 Paresis of oculomotor muscles with convergence disorders, diplopia, cross
– eye.
  Bulbar syndrome with swallowing, voice and speech disorders. Dysarthria,
dysphonia, absent gag reflex, atrophic tongue
 Alternation syndromes are quite rare.
 Vision disorders of cortex character such as photopsias, hemianopsia,
quadric hemianopsia and optic phenomena.
 Atonic – adynamic syndrome. acute ischemia of reticular formation and
lower olives in medulla oblongata in case of “drop – attacks “ – the
attacks of sudden loss of muscle tone that cause patient’s falling down
without loss of consciousness .These attacks manifest at cervical spinal
cord disorders in case of sudden turning out or head retroversion. Sometimes
symptom of Sistine chapel can occur when loss of muscle tone is associated
with loss of consciousness.
 At ischemia of mediobasal structures of temporal lobe one can Korsakov
syndrome observe – the attacks of temporary memory disorders on
current events associated with confabulator component and
disorientation.
 Paroxysmal hypersomnic and katalepsic syndromes with autonomic –
vascular crisis are observed at ischemia of hypothalamic structures.
 Syndrome of temporal epilepsy.
 In the subclavian steal syndrome the patient has a narrowed subclavian
artery and the arm “steals” blood from the basilar artery via the vertebral
artery. There may be a cervical bruit and a difference in blood pressure
between the arms. At times of arm exercise the patient may experience
vertebrobasilar insufficiency.

78. Treatment of TIA (the main pathogenetic groups of medicines)

 Blood pressure normalization
o At heart failure and systolic blood pressure less than 120 mm glycosides
are used: Corglyconi, Cordiamini, Sulfocamfocaini, Cofeini, Mesatoni
o At hypertension hypotensive therapy and spasmolytics are used in usual
doses.
 To improve brain hemodynamic vasoactive medications are used:
Euphilini, Cavintoni, Sermioni, Ksantinoli nicotinas
 To improve microcirculation and rheologic properties of blood, to
prevent aggregation of blood cells. (It is especially important in case of
well expressed focal neurological symptoms in order to prevent stroke).
o Direct anticoagulants: Heparini, Fraxiparini
o Indirect anticoagulants: Pelentani, Fenilini, Syncumar
  Antiagregants: Aspirini , Ticlidi, Trentali, Agapurini, Reopoliglucini ,
Solcoserili, Ksantinoli nicotinas , Curantili
 To prevent brain edema, to decrease intracranial hypertension:
Furasemide, Lasix, Manitoli, Dexoni , Albumini, Vit E
 To improve brain metabolism: Nootropil, Instenoni , Solcoserili,
Actovegini, Cerebrolisini
 Antioxydants: Vit E, Tiatriasolini, Emoxipini
 Symptomatic treatment:
o At vomiting and hiccup – cerukal, aminasini, galoperidol, validol
o At headache – tramadol, analgini
o At agitation – sedatives and anxyolytics

79. Acute hypertensive encephalopathy: pathogenesis, clinical feature,

treatment.
Defined as an acute organic brain syndrome or delirium in the setting of severe
hypertension
Pathogenesis: Loss of Cerebral Autoregulation of blood flow resulting in
hyperperfusion of the brain, loss of integrity of the blood brain barrier, and
vascular necrosis. Loss of Autoregulation occurs at a constant cerebral blood flow
of above MAP 150 to 160 mmHg. Acute Onset. Reversible
Symptoms:
 Headache, Nausea/Vomiting, Lethargy,
 Confusion, Lateralizing neurological symptoms
 That are not often in an anatomical distribution.
Signs:
 Papilledema, Retinal Hemorrhages
 Decreased level of consciousness, Coma
 Focal neurological findings
 Clinical manifestation of cerebral edema and microhemorrhages seen with
dysfunction of cerebral autoregulation
Treatment: Nipride, Fenoldopam, Labatalol, Nicardipine
80. Strokes: definition, classification, periods, acute period stadiums.
Stroke is a rapidly developing clinical signs of focal (at times global)
disturbance of cerebral function, lasting more than 24 hours or leading to
death with no apparent cause other than that of vascular origin”.
Classification.
 Haemorrhage: Membrane: subdural, epidural. Intracerebral. Ventricular,
combined
  Brain infarction (atherothrombotic, cardioembolic, hemodynamic,
hemorheologic, lacunar infarction)
Periods.
 Acute up to 1 month
 Renewal: Early (1-6Month) and Late (6Month to 1year).
 Residual. 1yr till the end of life.
Acute period stages.
 Precursor stage: Characterized with Transient Ischemic attack and
Hypertensive crisis.
 Apoplectic stroke.
 Focal Signs.

81. Atherothrombotic stroke: pathogenesis, clinical feature, diagnostic

procedures, treatment.
It is a type of Ischemic stroke that occurs in case of plugging of extra cranial or
intracranial vessel by atherosclerotic plaque.
Pathogenesis.
Occurs at thrombosis in case of atherosclerotic lesions, disturbance of rheologic
blood properties, central hemodynamic disorders.
Clinical Feature.
 TIA present in Anamnesis: transient vertigo, paresis, speech disorder
 Developed at night or in the morning time.
 Pale skin, soft and frequent pulse, fluctuations in blood pressure
hypotension and hypertension. Consciousness present/impaired, easy
stupor
 Single/repeated episode of global amnesia, sudden disorientation in
space, poor memory for past events
 Decreased of internal Carotid artery pulsation on the neck.
 Stenosis and occlusion of MAH at ultrasound examination.
Diagnosis.
 History of TIA in Anamnesis.
 EEG - There is focus of pathologic activity
 USD finds out occlusion, stenosis of carotid and vertebral arteries
 CT reveals hypodensive focus
 MRI helps to find out small focuses and those, located in the brain stem
Treatment.
o Symptomatic treatment: Antipyretic, Entiedema and Antiepileptic
drugs.
 o Antioxidants
o Anticoagulant
o Antiplatelet
o Neuroproctective drugs
o Nootropics.

82. Cardioembolic stroke: pathogenesis, clinical feature, diagnostic

procedures.
It is a type of Ischemic stroke which occurs in case of plugging of extra cranial or
intracranial vessel by thrombus or embolus from the heart.
Clinical Features.
 Precursor signs are absent.
 Acute onset at emotional and physician activity.
 General Cerebral signs like: Loss of consciousness, severe headache,
seizures, psychomotor agitation are very intensive.
 Embolism of different arteries of the brain.
 Embolism of cortical branches of the brain arteries.
 Embolism in inner organs such as heart, lungs, limbs, retina
 Wernicke aphasia/global aphasia with hemiparesis
 Posterior circulation cardioembolism can produce wallenbergs syndrome:
cerebellar infarct, top of basilar syndrome, post cerebral artery infarct.
Diagnosis.
 USD finds out occlusion, stenosis of carotid and vertebral arteries
 CT reveals hypodensive focus
 MRI helps to find out small focuses and those, located in the brain stem
 History of TIA in Anamnesis.
 EEG - There is focus of pathologic activity

83. Hemodynamic stroke: pathogenesis, clinical feature, diagnostic

procedures.
Hemodynamic - one occurs at angiospasm in case of atherosclerosis, vascular
insufficiency, central hemodynamics disorders. Severe decreasing of BP, angina
pectoris, decreased cardiac output and ejection fraction, orthostatic hypotension,
increased BP with vessel spasm. Deep boderzone or watershed infarction,
bilateral infarction of parietal occipital lobe.
Clinical feature.
 Numbness
 Reduced sensation
  Hyperreflexia.
Diagnosis
 History of TIA in Anamnesis.
 EEG - There is focus of pathologic activity
 USD finds out occlusion, stenosis of carotid and vertebral arteries
 CT reveals hypodensive focus
 MRI helps to find out small focuses and those, located in the brain stem

84. Lacunar stroke: pathogenesis, clinical feature, diagnostic procedures.

This condition is associated with small areas of infarction deep in the cerebral
white matter of the cerebral hemispheres or in the pons, resulting from:
1. Small vessel disease with lipohyalinosis and fibrinoid degeneration
2. Decreased perfusion of penetrating arteries from proximal narrowing of
larger vessels
3. Branch artery atheromatous occlusion
4. Embolism
The lacunar stroke may be defined as a unilateral motor or sensory deficit
without visual field deficit or disturbance of consciousness or language. The
CT scan may show a small, sharply marginated hypodense lesion in the subcortical
area, with the diameter smaller than . Multiple lacunes are strongly related to
hypertension and diabetes mellitus. Lacunar infarction is an acute onset of focal
neurological deficits lasting more than 24 h. There are six recognized lacunar
syndromes:
 Pure motor, hemiplegia or hemiparesis
 Dysarthria, clumsy hand syndrome
 Ataxic hemiparesis
 Sensorimotor stroke
 Pure sensory stroke
 Unilateral dystonia and involuntary movements such as choreoathetosis
following lacunar infarction of the putamen or globus pallidus or
hemiballismus owing to subthalamic infarction
Risk factors include hypertension, diabetes mellitus, heart disease, heavy
alcohol consumption, cigarette smoking, and lack of physical exercise. Lacunar
infarcts are the most common finding in cerebral infarction in young adults.
Diagnostic Procedures All patients should receive full evaluation for diseases of
the blood vessels, atheroselerosis, arteriosclerosis heart disease abnormalities of
blood constituents, and reduced cerebral perfusion. These investigations have been
outlined under diagnostic procedures for TIAs.
Future developments of MRI with diffusion and perfusion studies, PET, and
SPECT will define the location and extent of damage to cerebral tissue, and may
permit earlier identification of blood vessel involvement in the lacunar state.

85. Intracerebral hemorrhage (or apoplectic stroke): clinical picture,

diagnostic procedures, emergency treatment.
It is a type of stroke caused by bleeding within the brain tissue itself, caused by
hypertension, arteriovenous malformations or head trauma, causing damage to the
brain.
 General cerebral symptoms: severe headache, nausea, vomiting, seizures,
consciousness disorder: sopor(deep sleep, difficult to arouse, respond to
pain, sound, light. Stupor: patient respond only to pain. Coma and semi
coma)
 Large hemisphere hemorrhage is often complicated by secondary brain
stem syndrome. It manifests as progressive breathing disorders,
disturbance of heart activity, consciousness, eye movements, changes of
muscle tonus (hormetonia), autonomic disorders (sweating, tachycardia,
hyperthermia).
Diagnosis.
 CT angiogram Scan: hyperdensive focus in cerebrum
 USG Angiography
 MRI angiogram
Treatment generally involves surgery to relieve the pressure from the
accumulation of blood and to repair damaged blood vessels. Open craniotomy to
do surgical clipping of vessels by endovascular coiling or coil embolization.
Symptomatic treatment includes
-Anti-hypertensive
-Liquidate brain edema and decrease BP: diuretics, corticosteroids, albumin
-Prevent and treat vessel spasm: Nimodipine
-Normalize vital and autonomic function
-Headaches: Baraltini and analgin
-Vomiting: Haloperidol, droperidol.

86. Ventricular hemorrhage: clinical feature, diagnostic procedures.

Intraventricular hemorrhage (IVH) denotes the presence of blood within the
ventricular system of the brain where the cerebrospinal fluid is produced and
circulates through towards the subarachnoid space , and is responsible for
significant morbidity due to the development of obstructive hydrocephalus in many
patients.
Clinical picture.
o Patients experience sudden onset of severe headache, photophobia,
nausea and vomiting, consciousness disorder
o Meningeal signs are also present: neck stiffness, brudzinski upper,
middle and lower. kernig).
o Larger hemorrhages can result in loss of consciousness, seizures,
and brainstem compression with cardiorespiratory compromise,
hormeotonia, hyperthermia
Diagnosis
o CT scan. Hyperdensity focus around the ventricle.
o MRI
o Lumbar puncture

87. Subarachnoid hemorrhage: etiology, pathogenesis, the main clinical

symptoms, treatment, complications.
Etiology The most common cause of SH is aneurysm rupture. The other causes
include hypertension, atherosclerosis, blood diseases, rheumatism, brain tumors,
and uremia and so on
 The first signs of SH are severe headache or feeling of hot liquid flowing
in the Brain or thunderclap headache. At the beginning this pain is local
(in the region of occipital lobe) than it becomes more diffuse. Later pains in
neck, back appear, sometimes they irradiate in legs. Simultaneously with
headache vomiting and nausea occur.
 Besides these symptoms there are often general cerebral symptoms, such
as short loss of consciousness, psychomotor excitement, seizures.
 In a few hours or the next day meningeal syndrome occur. It manifests as
rigidity of occipital muscles, symptoms of Kernig, Brudzinski, and general
hyperesthesia.
Diagnosis
o USG (Doppler), PET scan
o MRI
o Angiography(for the location and size of aneurysm)
o CT Scan
Treatment.
 NSAIDs, to reduce pain
 Nimodipine to prevent vasospasm
 Antihypertensive drugs, to reduce BP
 Surgery: To stop bleeding. Open craniotomy (surgical clipping),
endovascular coiling or coil embolization
Complications.
 Brain Edema
 Recurrent Subarachnoid Hemorrhage
 Occlusive hydrocephalus due to obstruction of CSF pathways
 Brain infarction.: due to vasospasm, occurs 3 days after SAH

88. Focal symptoms of stoke in the region of anterior cerebral artery.

Anterior cerebral artery blood – supplies the cortex of frontal lobe (superior
frontal gyrus), superior part of anterior central gyrus, superior part of posterior
central gyrus, corpus callosum, a part of superior parietal lobulus, orbital part of
frontal lobe, lobulus paracentralis.
Infarction in the area of the anterior cerebral artery causes:
 spastic hemiparesis with the prevalence in proximal part of upper extremity
and distal part of lower extremity.
 the symptoms of oral automatism,
 psychiatric disorders- frontal mental disorder
 dysphagia, dysphonia,
 astasia: inability to stand upright unassisted
 abasia: lack of motor coordination in walking
 motor aphasia (Broca-loss of expressive speech) ischemia on (dominant
hemisphere in right handed left side of brain, vice versa)
 retention of urine: lesion of paracentral lobe

89. Focal symptoms of stoke in the region of middle cerebral artery.

Middle cerebral artery blood - supplies basal nuclei, internal capsule, a part of
temporal lobe, middle and lower parts or pre – and post central gyruses, opercular
region, a part of parietal lobe, gyrus angularis, posterior parts of upper and middle
frontal gyruses.
If the artery’s main trunk is occluded:
 hemiplegia,
 hemianesthesia,
 gaze paresis,
 visual disorders - Hemianopsia
 speech disorders (such as motor, sensory, total aphasia) occur when the
lesion is in left hemisphere
If the artery’s cortical branches are occluded:
 motor and sensory disorders in upper extremity,
 hemianopsia,
  sensomotor aphasia,
 apraxia,
 alexia,
 acalculia occur when the lesion is in left hemisphere
When the lesion is right hemisphere - Apracto – agnostic syndrome
 Anozognosia: patient denies disease
 Astereognosis: inability to identify things by palpation
 Autotopognosia: cant recognize himself
 Apraxia
If the artery’s posterior branches are occluded:
 hemianesthesia,
 bathianesthesia,
 astereognosis,
 afferent paresis of extremities,
 hemianopsia,
 sensory aphasia,
 agraphia, alexia,
 acalculia
 apraxia.

90. Focal symptoms of stoke in the region of posterior cerebral artery.

Posterior cerebral artery blood supplies occipital lobe, posterior part of lower and
middle temporal gyruses, basal and mediobasal part of temporal lobe, deep
thalamocollicular branches blood supply thalamus, hypothalamus, posterior – lower
parts of cortex of parietal lobe.
Infarction in the region of the posterior cerebral artery causes:
 hemianopsia,
 visual agnosia,
 hemianesthesia,
 hyperpathia,
 desorientation in space and time,
 disorders of space –optical gnosis.
Infarction in the region of deep branches of posterior cerebral artery that
blood supplies thalamus, posterior part of occipital lobe, corpus callosum, radiate
crown, causes Thalamic syndrome of Dejerin – Russi. Than last manifests as:
 hemianesthesia,
 hyperpathia,
 dysesthesia,
  Thalamic pains,
 hemianopsia,
 pseudoathetosis,
 hemiataxia,
 dynamic hemiparesis on the opposite side.

91. Focal symptoms of stoke in vertebro-basilar distribution.

Infarctions in the region of vertebral artery Vertebral artery blood supplies brain
stem; oblongata brain, cerebellum, cortex of occipital lobe, part of cervical part of
the spinal cord. It can be damaged extra – or intracranially.
In case of extracranial lesion:
 systemic dizziness,
 hearing disorders ,
 visual disorders,
 eye movements disorders,
 vestibular disorders,
 equilibrium disorders
 Paresis with sensory disturbances in extremities are observed.
 Some patients have “drop- attacks “
 hypersomnia
 Autonomic disorders
 Disorders of breathiness, heart function
 Mental disorders – Korsakov syndrome
In case of intracranial lesion alternating syndromes of oblongata brain occur.
Alternate intramedular (oblong brain) syndromes:
 Jackson’ syndrome (medial medullar syndrome): Peripheral palsy half of
tongue. Central hemiparesis in opposite extremities
 Awelis’s syndrome (palatine-pharyngeal syndrome): Plegia of palatine.
Plegia of pharyngeal muscles. Central hemiparesis with hemianesthesia in
opposite extremities
 Schmidt’s syndrome: Palsy of palatine, pharynx and voice ligamentum.
Palsy of m. Sternocleidomasthoideus and upper part of m. Trapezius. Central
hemiparesis with hemianesthesia in opposite extremities
 Valenberg - Zakcharchenko’ syndrome: Paresis of palatine and voice
ligamentum. Anesthesia of pharynx. Sensory disorders on the face. Horner’s
syndrome. Hemiataxia on side of lesion cerebellar ways. Breathiness
disorders (in case of large focus in oblong brain). hemiplegia (hemiparesis),
analgesia and thermoanesthesia on opposite side
 Babinski-Najott syndrome: Paresis of palatine. Hemiasynergia. lateropulsion
(lesion of lower cerebelar leg and olivo-cerebellar tract), Miosis or Horner’s
syndrome on pathology side. Central hemiparesis with hemianesthesia in opposite
extremities
Bilateral thrombosis of Vertebral artery: Bulbar syndrome. breathing disorders
and lesion of heart function. Paralysis of extremities. Loss of consciousness and
deep cerebral coma
Infarctions in the region of basilar artery cause the lesion of pons, cerebellum,
hypothalamus, cortex of occipital lobe.
In case of acute occlusion:
 loss of consciousness,
 eye movements disorders,
 pseudobulbar syndrome,
 tetraplegia,
 muscle tone disturbance,
 sometimes even cerebellar symptoms
 cortical blindness occur.
 most of these patients die because of the vital functions disorders.
When the lesion is in pons syndromes of Miyar – Hyubler, Fowil, Brisso – Siquar
and alternating hemianesthesia occur.
Alternate pond’ syndromes:
 Raymond syndrome: a lost of sensation on the face according to the
segmental type on the side of the lesion. lost superficial sensation on a trunk
and extremities on opposite side.
 Miyar-Gubler syndrome: peripheral palsy of the facial muscles on the side
of the lesion. contralateral hemiplegia.
 Fovill syndrome: peripheral palsy of the facial muscles and the external
rectus eyes’ muscle on the side of the lesion. contralateral hemiplegia.
Infarction in the region of mesencephalon causes Parino syndrome, which manifests
as gaze paresis upwards.
Infarction in the region of brain peduncles causes Weber or Benedict alternating
syndrome. Sometimes Clode and Fua – Nikolesku syndrome can be observed.
Alternate midbrain syndrome:
Weber’s syndrome: Oculomotor nerve palsy. contralateral hemiplegia.
Benedict’s syndrome: Oculomotor nerve palsy. contralateral choreoatetosis and
intention tremor.
Clod’s syndrome: Oculomotor nerve palsy. contralateral cerebellar ataxia.
92. Diagnostic procedures and differential treatment of Intracerebral
hemorrhage in acute period.
Based on complaints as in q85
Diagnosis.
- CT angiogram Scan: hyperdensive focus in cerebrum
- USG Angiography
- MRI angiogram
Treatment
 Hemostatic: Tranexamic acid, vikasol
 To lower increased blood pressure: beta blockers(anaprilin), calcium
agonist(nifidipine), ACE inhibitors: (captopril)
 To liquidate brain edema and lower intracranial pressure: diuretics
(furosemide, mannitol),corticosteroid, albumin, mannitol, ganglion blockers
 To increase coagulative properties of blood and decrease penetrance of
vessels wall: Calcium chloride, vitamin C, Diconini, Trasilili
 To prevent and treat cerebral vessels spasm: Nimodipine
 To normalize vital and autonomic functions and prevent complications
 To treat hypoxia and brain metabolism disorders
 Symptomatic
o Headache:baralgin, analgin
o Vomiting: haloperidole, droperidole
o Seizures: Sibazoni, Natrii oxybutyrate
o Renewal period: cerebrolysin, piracetam, actovegin

93. Diagnostic procedures and differential treatment of Ischemic stroke in

acute period.
Diagnostics of Brain Infarction The main peculiarities are:
 Before stroke period in the previous history (TIA in anamnesis)
 The beginning of the stroke is gradual
 Data of somatic and neurological status
 Additional methods of diagnostics
 Liquor is pellucid, without significant changes. There is focus of pathologic
activity on EEG. USG finds out occlusion, stenosis of carotic and vertebral
arteries.
 Angiography
 CT reveals hypodensive focus on the second day. MRI helps to find out
small focuses and those, located in the brain stem.
Differential treatment of brain infarction
  To renew blood circulation in zone of ischemia: Actilase, difenin, Nimotop
 To correct rheologic and coagulative properties of blood, to improve
microcirculation. Anticoagulant (heparin), Antiagregant(pentoxyphylin,
aspirin, Ticlid. Hemodilution (reopolyglucin)
 To prevent disorders of cerebral metabolism.
 To decrease brain edema: Mannitol, Lasix, Albumin
 To treat brain hypoxia: Vitamin E, piracetam

94. Nondifferential emergency therapy of strokes.

=Prevention and treatment of pulmonary insufficiency
 the patient is lying on the bed with his head elevated
 cleaning of patient’s oral cavity
 tracheostomia (at inspiratory muscles paralysis)
 at lung edema patient is given oxygen; narcosis, Bobrov’s apparatus, 2 ml 1
% lazix, 2 ml 1% dimedroli, 2 ml 0.1 % atropini I / m are used.
 Antibiotics are used in order to prevent pneumonia
=Liquidation of heart – vascular disorders
 At increased blood pressure we use:
o Clofelini 1 – 3 ml 0.01 % solution i/m, i/v.
o Dibasoli 3 – 4 ml 1 % solution i/v
o Droperidoli 1 ml 0.25 % solution i/v
o Rasedili 1 – 2 ml 0.1 % i/v, I / m,
o -
adrenoblockers (anaprilini, obzidani, inderal )
o In case of hypokynetic type of blood circulation we use peripheral
vasodilatators (Natrii nytroprussidi , appresini) in combination with
euphyllini
 At low blood pressure we prescribe
o Dexamethazoni 4 – 8 mg i/v by drops in physiological solution
o Prednizoloni 60 – 120 mg i/v by drops in physiological solution
o In order to improve heart activity we use strofantini, corgliconi,
cordiamini
-Brain edema treatment Diuretics, corticosteroids, albumini, ganglioblockers, 20
% mannit, manitoli, glycerini, lazix, diakarbi are used.
=Normalization of water – electrolytes balance and acid – alkali balance
An average water necessity is 35 ml per kg, in patients with loss of consciousness
it is 50 ml per kg. We should correct patient’s hyper- or hyponatriemia, hyper- or
hypokaliemia. 4 % solution of natrium bicarbonates i/v, trisaminum is used at
metabolic acidosis. KCl i/v is used at metabolic alkalosis.
=Osmose correction Normally blood osmose is within 280 – 295, urine osmose is
600 – 900 mosm per liter. At stroke usually we have hyperosmose, which
manifests as increased hematocritis, hyperagrigation.
6. Improving of brain metabolism Vit E, piracetami, aminaloni, cerebrolysini
natrii oxybutiras are used.
7. Liquidation of hyperthermia and other autonomic disorders.
At hyperthermia we use
· reopirini 5ml
· analgini 50 % 2.0
· aspizoli 0.5 g
At autonomic disorders we introduce
· sibazoni 0.5 % 1 ml
· haloperidoli 0.5 % 1 ml
· dimedroli 1 % 2 ml
· natrii oxybutiras 20 % 10 ml
95.Therapy of strokes in chronic stage
 Bobath: focuses to control responses from damaged postural reflex
mechanism. Emphasis is placed on affected inputs facilitation and normal
movement patterns
 Brunnstrom approach is one form of neurological exercise therapy in the
rehabilitation of stroke patients.
 Rood Emphasise the use of activities in developmental sequences, sensation
stimulation and muscle work classification. Cutaneous stimuli such as icing,
tapping and brushing are employed to facilitate activities.
 Proprioceptive neuromuscular facilitation (PNF) the use of peripheral
inputs as stretch and resisted movement to reinforce existing motor response.
Total patterns of movement are used in treatment and are followed in a
developmental sequence.
 Conductive education. The patient is taught how to guide his movements
towards each task-part of the task by using his own speech - rhythmical
intention.
 Functional electrical stimulation (FES) is a modality that applied a short
burst of electrical current to the hemiplegic muscle or nerve. In Stroke
Physical Therapy, FES has been demonstrated to be beneficial to restore
motor control, spasticity, and reduction of hemiplegic shoulder pain and
subluxation.
 Exercise: Active weight bearing exercise can be used as a means of
improving motor control of the affected arm; introducing and grading tactile,
proprioceptive, and kinesthetic stimulation; and preventing edema and pain.
  Speech therapy

96.Symptoms on pathological focus side and contralateral side in apoplectic

phase of hemorrhage stroke.
On the side of lesion there is anizokoria, Bechterev phenomena, painful trigeminal
and occipital points, automatic movements, gaze paralysis, Kerning sign and
parakinesis.
On the opposite side – positive Bare’s sign, mouth angle is located lower than
normally. foot is turned outside, pathological signs (Babinski), arm fall down like
bine, hypotonia of muscles, hyporeflexia
Focal signs depends upon the area of brain involved. If the dominant
hemisphere (usually the left) is involved, a syndrome consisting of the following
may result:
 Right hemiparesis
 Right hemisensory loss
 Left gaze preference
 Right visual field cut
 Aphasia
 Neglect (atypical)
If the nondominant (usually the right) hemisphere is involved, a syndrome
consisting of the following may result:
 Left hemiparesis
 Left hemisensory loss
 Right gaze preference
 Left visual field cut
Nondominant hemisphere syndrome may also result in neglect when the patient has
left-sided hemi-inattention and ignores the left side.

97.Differential diagnosis of ischemic and hemorrhagic strokes

ISCHEMIC STROKE HEMORHAGIC STROKE
ONSET Gradual Acute
AGE Elderly Middle aged
DOMINANT
SYNDROMES Focal syndrome General cerebral
DANGER FOR LIFE Less dangerous, Can lead to acute death
CT SCAN Hyperdensive focus Hypodensive focus
ETIOLOGY Embolism, thrombosis hemorrhage
 PATHOGENESIS necrosis of brain tissue bleeding into brain tissue
PHYSICAL THERAPY Less efective more effevtive
CHANGES IN SYSTEM Moderate to severe mild to moderate

98. Modern theory of Multiple sclerosis etiology and pathogenesis.

 Connection of ALS with Prion Diseases. This can be proved by high
content of Arginaza in the brain of animals in experiment and in the CSF of
patients with ALS. Besides this we can find morphologic changes in the
brain of such patients. They are spongiosis and synapse degeneration. This
can be explained by the deficiency of Argininum.
 Autoimmune theory. There are certain changes in cell – mediated and
humoral immunity.
 Genetic theory. The patients with familial forms of ALS have changes of
gene, located in the 21st chromosome. This gene is responsible for the
production of endogenous antioxidants. The deficiency of such antioxidants
can cause activation of free radical oxidation that leads to the death of
neurons of anterior horn.
 Amino acids, neuromediators, neuropeptides metabolism disorders. And
those chemical substances are responsible for the apoptosis. That’s why the
patients with ALS have low content of Mg, Mn, AL, Se in biologic fluids.
99. Beginning and the typical symptoms of Multiple sclerosis.
The beginning of the disease usually is slow. The first symptom is one of the next
ones:
 Paresthesia. It is the feeling of numbness or tingling in one of the extremity.
It can be spread during the next 3 – 4 days and lasts for about 1 – 2 weeks,
then gradually disappear.
 Motor disorders - weakness in lower extremities. This symptom is much
more common at the age of 25 – 40 years.
 Retrobulbar neuritis is a progressive loss of vision, colour vision
disturbances. It lasts for about several weeks.
 N. Oculomotorius disorders (diplopia and cross eye).
 Pelvis disorders (retention of urine, micturition)
 Acute vestibular syndrome
 Cerebellar disorders – ataxia, disorders of coordination.
The typical clinical features of MS:
 Motor disorders – paralysis or paresis of both upper or lower limbs
(paraparesis). Spastic hypertonus, hypotonus or dystonus
 Ataxia – cerebellar, sensitive and vestibular
  Sensory disorders – pains and sensitive ataxia -
 Brain stem symptoms – vestibular syndrome, dysarthria, CN’s lesion. Bulbar
syndrome: dysarthria, dysphagia
 Visual and eye movements disorders – optic neuritis (sudden vision loss),
pain on eye movements, unilateral headache, total vision loss in affected
eye.
 Autonomic disturbances – pelvic and sexual disorders
 Nonspecific symptoms – cognitive, memory disturbances, loss of attention
 Paroxysmal symptoms: lemitt symptom: flexion of head result in electric
shock passing down spinal cord. Paroxysmal itching, choreoathetosis,
nystagmus, facial hemispasm. Uthoff’s symptoms can be observed – it is the
worsening of patients state after the hot bathroom or hot meal.
100. Treatment of Multiple sclerosis in the stage of exacerbation.
Corticosteroids and ACTH: These medicines have immune suppressive action
and can shorten the period of exacerbation. The main representatives are –
Prednisone, Methylprednisolone, Dexamethasone.
Cytokines, interferons: They are used mainly for exacerbations’ prevention and
selective immune correction. There are 3 types of Interferonum – α, β (beta 1a:
avonex. Cinnovex, rebif, recigen), beta 2b(betaserone), γ.
Symptomatic treatment of MS
 Pelvis disorders: Proserinum, Halantaminum decrease m. Detrussor
hyperreflexion.
 α - Adrenoblockers decrease dysynergy of Sphincter and Detrussor.
 Spasticity: Baclofen 5 mg 3 times per day, Sirdalude 4 mg 3 times per day
 Tremor: β - Adrenoblockers are used at postural tremor , Clonasepam,
Carbamasepam are used at intention
 Hyperkinetic form: Adrenoblockers, Antidepressants
 Asthenia: Psychostimulants, Dopaminergic medicines
 Paroxysmal signs: Carbamasepinum, Filepsin

101. Clinical forms, degrees of severity, stages and forms of course at Multiple
sclerosis.
Clinical forms
 Cerebral foms:
o cortical (epileptic attacks, psychiatric disorders)
o visual
o brain stem
o cerebellar
  Spinal foms:
o Cervical
o Thoracic
o lumbar – sacral
o pseudotabes
 Cerebrospinal
The course of the disease:
 Acute
 Subacute
 Chronic
o PRMS: Progressive Relapsing MS: steady decline since onset with
superimposed attacks, steady worsening of condition at onset
o SPMS: Secondary Progressive MS: Initial RRMS that suddenly
begins to decline without periods of remission and relapses.
Symptoms constant, occasional relapse, no remission
o PPMS: Primary Progressive MS: gradual progression of the disease
from its onset with no relapses or remissions. Slow onset, continuous
worsening condition
o RRMS: Relapsing/Remitting MS: Unpredictable attacks which may or
may not leave permanent deficits followed by periods of remission.
Attacks followed by partial or complete recovery. Symptoms may be
inactive for months.
The periods of the disease:
 Exacerbation
 Remission (complete, incomplete)
 Stable period
102. Preventive treatment of Multiple sclerosis.
Prevention of MS To avoid catching cold, acute respiratory infections, stress,
pregnancy and childbirth, isolation and heating procedures. Take drugs:
 Interferon beta-1a (Avonex, Cinovex, Recifen, Rebif)
 Interferon beta-1b (betaseron)
 Glatiramer acetate (Copaxone)
 Natalizumab
 Mitoxantrone (Tyasabri)
 Fingolimod (gilenya)

103. Clinical forms of acute disseminated encephalomyelitis. Treatment of

acute disseminated encephalomyelitis in acute and residual periods.
It is an infectious – allergic disease that is characterized by acute multiple lesion of
the brain and spinal cord
Clinical forms of the disease
 Encephalomyelopoliradiculoneuritis – it is the most common form of the
disease, which is characterized by the lesion of all parts of nervous system.
 Polioencephalomyelitis – it is characterized by the lesion of CN’s nuclei
and spinal cord gray substance.
 Opticoencephalomyelitis and opticomyelitis – are characterized by optic
nerve neuritis and symptoms of lesion of brain and spinal cord.
 Disseminated myelitis – the spinal cord is damaged on different levels.
Treatment of the disease
 Corticoids are used in order to treat such patients. Among them are
Prednisolone and Methylprednisolone. The last one is used in dose 10 – 15
mg per kg i/v by drops per day. Later we can use it in pills - 1.5 – 2 mg/kg
every other day.
 Together with this medicine we prescribe anabolics , K, Ca, vitamin C.
 In acute stage we prescribe desensibilizating and dehydrating medicines.
In case of severe bulbar disorders we include resuscitation measures.
 Plasmapheresis and vitamin B are also used.
 In residual period we prescribe massage, dibasol, KJ, biostomulants, Lidasa,
Seduxen, sanatorium treatment.

104. Clinical feature of disseminated myelitis (thorax and lumbar levels of

spinal cord), complications.
 Thoracic: A lesion of the thoracic spinal cord (T1–12) will produce upper
motor neuron signs in the lower limbs, presenting as a spastic diplegia. This
is the most common location of the lesion, and therefore most individuals
will have weakness of the lower limbs
 Lumbar: A lesion of the lower part of the spinal cord (L1–S5) often
produces a combination of upper and lower motor neuron signs in the lower
limbs.
Symptoms include weakness and numbness of the limbs, deficits in sensation and
motor skills, dysfunctional sphincter activities, and dysfunction of the autonomic
nervous system. Symptoms typically develop over the course of hours or days and
may progress after weeks. Sensory symptoms of transverse myelitis may include a
sensation of pins and needles traveling up from the feet. Back pain can occur at the
level of the inflamed segment of the spinal cord. The degree and type of sensory
loss will depend upon the extent of the involvement of the various sensory tracts,
but there is often a "sensory level" (at the sensory segmental level of the spinal
cord below which sensation to pain or light touch is impaired). Motor weakness
occurs due to involvement of the pyramidal tracts and mainly affects the muscles
that flex the legs and extend the arms. Involvement of the autonomic nervous
system is common and frequently leads to impaired function of the bladder and
bowel and can also lead to episodes of high blood pressure.
Complications
 Pain, one of the most common debilitating long-term complications of the
disorder.
 Stiffness, tightness or painful spasms in your muscles (muscle spasticity).
This is most common in the buttocks and legs.
 Partial or total paralysis of your arms, legs or both. This may persist after
the first symptoms.
 Sexual dysfunction, a common complication of transverse myelitis. Men
may experience difficulty achieving an erection or reaching orgasm. Women
may have difficulty reaching orgasm.
 Depression or anxiety, which is common in those with long-term
complications because of the significant changes in lifestyle, the stress of
chronic pain or disability, and the impact of sexual dysfunction on
relationships.

105. Treatment of disseminated myelitis in acute and residual periods.

Treatment of the disease
 Corticoids are used in order to treat such patients. Among them are
Prednisolone and Methylprednisolone. The last one is used in dose 10 – 15
mg per kg i/v by drops per day. Later we can use it in pills - 1.5 – 2 mg/kg
every other day.
 Together with this medicine we prescribe anabolics , K, Ca, vitamin C.
 In acute stage we prescribe desensibilizating and dehydrating medicines.
In case of severe bulbar disorders we include resuscitation measures.
 Plasmapheresis and vitamin B are also used.
 In residual period we prescribe massage, dibasol, KJ, biostomulants, Lidasa,
Seduxen, sanatorium treatment.
Additional therapies focus on long-term recovery and care:
 Physical therapy. This helps improve strength and coordination. Your
physical therapist can teach you how to use any needed assistive devices,
such as a wheelchair, canes or braces.
  Occupational therapy. This helps people with transverse myelitis learn new
ways of performing day-to-day activities, such as bathing, preparing a meal
and housecleaning.
 Psychotherapy. A psychotherapist can use talk therapy to treat anxiety,
depression, sexual dysfunction, and other emotional or behavioral issues
from coping with transverse myelitis.

106. Etiology, clinical feature and modern diagnostic procedures for

treatment of brain abscess.
A brain abscess can result from
 Direct extension of cranial infections (eg, osteomyelitis, mastoiditis,
sinusitis, subdural empyema)
 Penetrating head wounds (including neurosurgical procedures)
 Hematogenous spread (eg, in bacterial endocarditis, congenital heart disease
with right-to-left shunt, or IV drug abuse)
 Unknown causes
The triad of fever, headache (often severe and on the side of the abscess), and
focal neurologic deficit occurs in less than half of patients. The frequency of
common symptoms and signs is as follows:
 Headache -
 Mental status changes (may indicate cerebral edema) -
 Focal neurologic deficits -
 Fever -
 Seizures
 Nausea and vomiting
 Nuchal rigidity
 Papilledema
According to location of abscess
 Brainstem abscess - Facial weakness, headache, fever, vomiting, dysphagia,
and hemiparesis
 Frontal abscess - Headache, inattention, drowsiness, mental status
deterioration, motor speech disorder, hemiparesis with unilateral motor
signs, and grand mal seizures
 Temporal lobe abscess - Headache, ipsilateral aphasia (if in the dominant
hemisphere), and visual defects
 Occipital abscess- Neck rigidity
Diagnosis:
 CBC:Moderate leukocytosis is present, and the ESR and CRP level are
generally elevated. Serum sodium levels may be low because of
 inappropriate antidiuretic hormone production. Platelet counts may be high
or low.
 Lumbar puncture: The white blood cell count is generally high. It reaches
100,000/µL or higher when the abscess ruptures into the ventricle. Many red
blood cells are generally observed at that time, and the CSF lactic acid level
is then elevated to more than 500 mg
 CT or MRI with contrast
Treatment: Before the abscess has become encapsulated and localized,
antimicrobial therapy, accompanied by measures to control increasing intracranial
pressure, is essential. Once an abscess has formed, surgical excision or drainage
combined with prolonged antibiotics (usually 4-8 wk) remains the treatment of
choice (penicillin, vancomycin, Chloramphenicol, Metronidazole, Cefotaxime,
Ceftriaxone etc..

107. Clinical feature, diagnostic procedures, and treatment of epidemic

cerebrospinal meningitis. Early and late complications.
Incubation period of meningococcal infection lasts from 2 to 10 days (usually
about 3 – 7 days).The onset of meningococcal meningitis is acute (about several
hours). The temperature is elevated at 39 –
The main peculiarities of clinical picture are:
 General cerebral syndrome is well – expressed and increases rapidly:
headache, vomiting, nausea, hyperesthesia, loss of consciousness, seizures.
 General infectious syndrome: headache, shiver, inflammatory changes of
blood, rash, tachycardia, tachypnea, rhythm disorders. Meningeal
syndrome increases during 2 – 3 days: kernigs sign, brudzinski sign (upper,
middle and lower), lessage sign, bechterev cheek phenomenon.
 Focal neurologic symptoms manifest as lesion of III-rd and IV- th CN’s -
diplopia, ptosis, cross – eye, anizokoria.
 Herpes labialis is often observed on the 2 – nd or 5 –th day. Sometimes
hemorrhagic rash occurs, that is the sign of meningococcemia.
 Sometimes brain tissue is involved. Then there is clinical picture of
meningoencephalitis. That means occurrence of hyperkinesis, ataxia,
nystagmus, paralysis, seizures, sometimes epistatus.
 At severe meningoencephalitis inflammation of ventricles occurs. The last
manifests as hormetonia, edema of optic nerves’ disk, disturbances of
breathing and cardiac activity.
Diagnosis:
Cerebrospinal fluid is cloudy (purulent), cell-protein dissociation. the cell count in
the fluid is usually between hundreds and thousands/mm³. The protein content is
increased to 10 – 15 g/l. The sugar content is decreased. Meningococcus can be
found out in CSF.
Complications
 Early: Endotoxic shock, acute brain edema, pneumonia
 Late: Myocarditis, Pericarditis
Treatment
Currently, a third-generation cephalosporin (ceftriaxone or cefotaxime) is the drug
of choice for the treatment of meningococcal meningitis and septicemia. Penicillin
G, ampicillin, chloramphenicol, fluoroquinolone, and aztreonam are alternatives
therapies

108. Secondary purulent meningitis. Clinical picture, diagnostic procedures,

treatment.
Secondary purulent meningitis are observed in case of pyogenic source in the
body. The disease is developed after direct extension from pyogenic source (for
example pyogenic middle ear infection) or by means of metastasis from faraway
pyogenic focuses (abscess, ulcerous endocarditis).
Usually secondary purulent meningitis is caused by different coccus
(pneumococcus, staphylococcus), Hemophilus influenza
Clinical features
The onset of the disease is accompanied by chills and fever to 40º. Then
meningeal syndrome, seizures, consciousness disorders, focal neurologic
symptoms, autonomic disorders occur. Sometimes the clinical picture is very
similar to sepsis.
Diagnosis
In CSF is cloudy or yellow the cell count is very high. The protein content is
significantly increased. Glucose decreased
Treatment:
 Etiotropic treatment : Penicillin, Nystatin, ampicillin, cephalomycin,
cephazolin, gentamycin, amikacin, sulfamonomethoxine
 Pathogenic treatment : Rheopolyglucin, albumin, panangin, dexamethasone,
mannitol, Lasix, pyracetam, nootropil, actovegin
 Symptomatic treatment: analgin, baralgin, tramadol, sibazon, nootropil.
hemodialysis
109. Tuberculous meningitis. Clinical picture, diagnostic procedures,
treatment.
Tuberculous meningitis is always secondary to tuberculosis elsewhere in the body.
The primary focus of infection is usually in the lungs but may be in the lymph
glands, bones, nasal sinuses or any organ of the body. This disease is observed in
both – children and adults.
CLINICAL Features
 Tuberculous meningitis develops very slowly.
 There are three periods of the disease :
o prodromal stage (with loss of appetite, general weakness, headache,
irritability, increased temperature and sometimes vomiting) lasts for 2
– 3 weeks.
o meningeal stage. Meningeal syndrome not well expressed
o paralytic stage (encephalitic stage)
 Meningeal syndrome is not well – expressed.
 Temperature is increased up to 38º sometimes 39º.
 Focal neurologic signs – paresis and paralysis of Oculomotor n. (III),
Abducens n. (IV), Facial n. (VII), Optic n. (II). Sometimes
Vestibulocochlear n. (VIII) is involved.
 Encephalitic syndrome manifests as paresis, paralysis, aphasia,
hyperkinesis, cerebellar disturbances.
 Subacute course of the disease. Sometimes acute course is observed in
children. Chronic course may be in those persons who had used
antituberculosis treatment previously.
Diagnosis
 Increased pressure
 Slightly cloudy
 Increased protein content to 1 – 5 g per l
 Moderate pleocytosis of 100 – 300 cells/mm³, 70 – 80 % of them are
lymphocytes
 Decreased sugar content with values in the range of 0.15 to 0.3 g/l
 Formation of a clot on standing during 12 – 24 hours, where bacilli of
tuberculosis are usually found out.
 In blood sometimes leucocytosis and increased ESR (sedimentation rate) is
observed.
TREATMENT OF TUBERCULOUS MENINGITIS
 Etiotropic treatment includes: Isoniazid 15 mg/kg 3 times per day,
Rifampicinum 600 mg once a day, Pyrazinamide 30 mg/kg (1.5 – 2.5 g per
day) twice a day. They are used during three months. Then we use only
Isoniazid and Rifampicinum during 7 months. The most recent medications
are combinative ones such as Rifogal, Rifater (Rifampicinum 120 mg,
Isoniazid 50 mg, Pyrazinamide 300 mg). Streptomycinum is used in dose 1
g once a day. Ethambutol – 25 mg/kg per day.
  Pathogenic treatment : Rheopolyglucin, albumin, panangin, dexamethasone,
mannitol, Lasix, pyracetam, nootropil, actovegin
 Symptomatic treatment: analgin, baralgin, tramadol, sibazon, nootropil.
hemodialysis
110. Viral meningitis. Classification, etiology, clinical picture, diagnostic
procedures, treatment, prophylactic program.
CLASSIFICATION OF VIRAL MENINGITIS
Acute lymphocytic choriomeningitis, parotid meningitis, influenza-
meningitis, enteroviral, herpes – adenoviral – meningitis
Etiology
 Acute Lymphocytic choriomeningitis: Armstrong virus from domestic mice
 Parotid meningitis: After parotitis
 Enteroviral meningitis: Coxakie Echo virus
 Influenza meningitis: influenza
 Herpes Virus, adenovirus.
CLINICAL feature
 Incubation period lasts for 1 – 2 weeks
 The onset is with headache, running nose, sore throat. General infectious
syndrome: shiver, inflammatory changes of blood, rash, tachycardia,
tachypnoe, rhythm disorder
 Moderate meningeal syndrome (kernig, brudzinski, lessage, neck rigidity,
bechterev) against high temperature – 39º – 40 º
 On 7- th or 10- th day general – infectious and meningeal signs disappear
 There are some atypical forms of meningitis, such as Flu – like,
Encephalomyelitic , Poliradiculoneuritic ,Visceral
 Alopecia and orhitis can occur at the 7 th week of the disease.
DIAGNOSTIC PROCEDURE OF VIRAL MENINGITIS
 CSF is pellucid, pleocytosis is 300 – 500 cells, most of them are
lymphocytes. The content of protein and sugar is the same. Pressure and
glucose is normal
 Virologic examination of smear
TREATMENT OF VIRAL MENINGITIS
 Etiotropic treatment : Interferonum , Reaferonum, Virolex, Aciclovir,
Virasolom, Prodigiosan, Acidi ascorbinici , vit. B1, B, Antibiotics in order
to prevent pneumonia.
 Pathogenetic treatment: Desintoxication, Dehydratation, Desensibilization,
Hormones, Nootrops
Prophylaxis: liquidate mice in house, wash hands, avoid contact with infected
people, treat virus well

111. Epidemic encephalitis. Clinical forms of acute phase. Clinical signs of

chronic phase. Treatment on acute and chronic periods.
There are three main symptoms in acute stage:
 Fever. It manifests as increased temperature to 38 – 39º against general
cerebral symptoms, such as headache, nausea, vomiting, muscle pain.
Sometimes there are complains on upper respiratory ways disorders. This
period lasts for about 2 weeks.
 Sleep disorders. This syndrome usually manifests as pathologic sleepiness.
Sometimes pathologic insomnia can occur. In some cases the patient sleeps
in day – time and cannot fall asleep at night.
 Eye movement disorders. These symptoms usually occur in case of nuclei
of Oculomotor nerve lesion. It manifests as diplopia, anizokoria, gaze
paresis, converse symptom of Argil – Robertson, ptosis, cross eye,
midriasis, nystagmus, ophthalmoplegia.
Besides these three main syndromes of acute period sometimes we can observe
the others. They are:
 Vestibular disorders
 Lesion of VII, XII, V CN’s
 Hyperkinesis
 Hypothalamic disturbances: disturbances of sweating, salivation, fatty
skin, loss of flesh.
 Against general cerebral symptoms consciousness disorders appear such as
– sopor, psychomotor agitation, fear, hallucinations.
 In blood analysis there are leucocytosis (lymphocytic), increased ESR.
 In CSF there is slight lymphocytic pleocytosis to 20 – 40 cells in 1 mm³,
slightly increased sugar and protein content.
Besides typical form of acute stage sometimes atypical forms are observed.
They are:
 Abortive - when all the symptoms of acute stage are not well expressed.
 Oculocephalgic – when eye movements disorders and severe headache
dominate over the other symptoms.
 Vestibular – when vestibular syndrome dominates ( there are dizziness,
vomiting, ataxia )
 Hyperkinetic - against the symptoms of acute stage hyperkinesis occur.
Sometimes in this case sleep disorders, amyostatic symptoms and thalamic
pains are observed.
  Flu – associated – It looks like flu – infection. General infectious symptoms
prevail.
Chronic stage
It manifests as Parkinson syndrome in 90 % of patients or Hyperkinetic syndrome
in 10 %.
There are three main groups of symptoms at Parkinson syndrome:
 Akinesia or hypokinesia : shuffling gait, loss of swinging of arms when
walking, infrequent blinking of eyelids, inertia of rest and movements.
 Plastic hypertonia : cogged wheel symptom, tonus increases in course of
evaluation. Tonus same in flexors and extensors
 Static tremor: more in distal extremities, looks like coin counting, resting
tremor
Treatment
 Acute stage Etiotropic treatment: Interferonum , Reaferonum, Virolex,
Aciclovir, Virasolom, Prodigiosan, Acidi ascorbinici , vit. B1, B, Antibiotics
in order to prevent pneumonia.
 Chronic stage Etiotropic treatment
o Synthetic holinolytics: Cyclodolum (0.01, 0.005), Romparkin,
Parkopan (0.001, 0.002)
o Stimulators of dophamine secretion
o Amantadine medications increase sensation of dophamine receptors to
dophamine, excite dophamine receptors. Midantan (0.1 3 times per
day), Amantadinum.
o Inhibitors of MAO (Jumex) - 5 mg 1 – 2 times per day.
o Stimulators of dophamine receptors – Bromcriptine, Akineton,
Norakin (0.001 – 0.002).
o Medications that decrease converse catch of dophamine.
Amitriptilinum, Amipraminum, Melipraminum.
o Substitutional therapy. Sinemet 3 – 6 tablets per day. Nacom - 3 – 6
tablets per day.
o In order to decrease tremor we use b – adrenoblockers: Anaprilinum
10 mg 3 times per day, Amitriptilinum 25 mg 3 times per day.
o In order to decrease muscle tonus Midocalm, Baclofen are used.
o Nootrops
o Physiotherapeutic methods.
 Pathogenetic treatment: Desintoxication, Dehydratation, Desensibilization,
Hormones, Nootrops
 Symptomatic treatment
112. Russian tick-bone encephalitis. Infection ways. Clinical forms, features,
diagnostic procedures, complications. Treatment in acute and residual
periods. Prophylactic methods.
Epedemiology: Russia
Resevoir: Birds and mammals
Vector: TICKS
Infection routes: skin and intestine
Clinical manifestation: Incubation period 10-14 days. Onset of disease is an
acute, with high temperatures above 40 degrees. Accompanied by chill, severe,
headache, pains in the loin, region pains in the eye balls. In some case short
prodromal period occurs: Weakness, fatigue, headache, sleeplessness, sometimes
psychic violations. Initial phase with predominance of general toxic syndrome,
phase of neurological disorders with different variants of the lesion of CNS, the
phase of outcomes (recovery or residual manifestations- paresis, paralysis)
Forms of disease
 Feverish form
 Meningeal form
 Meningoencephalitic form
 Meningoencephalomyelitic form
 Polyradiculoneuritic form
The diagnosis of tick encephalitis is based on the epidemiological (Russia) and
laboratory data.
The specific diagnostics is concluded in detachment of the virus from the blood
and CSF in early periods of disease (4-7 days). Culture of chicken embryo,
kidney’s epithelium and other. Biological method of infection by material from
sick infant white mouses. Identification by fluorescence antibodies, serological,
Complement fixation, indirect hemagglutination and neutralization.
Treatment:
With antiencephalitic donors gammaglobuln injected 5-10ml intramuscularly
during 3 days. Pathogenetic treatment: desintoxication, dehydration, sedative and
hyperbaric oxygenation
The prophylaxis of tick encephalitis is performed in the area of the disease. The
living or killed attanuative vaccines are used. The vaccine is injected
subcutaneosly in a dose of 1,0 ml three times with interval 3 – 4 months. The
revaccination is performed one time every year (1,0 ml of vaccine,
subcutaneously).Besides that the measures of the individual prevention are used
special clothes, repellents.
113. Encephalitis and encephalomyelitis in causes of general infections
(measles, chickenpox, epidemic parotitis, after immunization). Clinical
features, treatment.
Secondary encephalitis: This type of encephalitis is very common at early
childhood. Allergic process takes a special place in its pathogenesis. This
encephalitis is usually associated with various infections in children, such as
measles, scarlet fever, rubella, small pox.
 Parainfectious ( at measles, small pox, rubella, scarlet fever, poliomyelitis )
 Postvaccinal ( after antirabies, antipoliomyelitic, antidiphtheric vaccine)
Measles encephalitis and encephalomyelitis Clinical features:
 The disease develops rapidly on the third – fifth day after the rash when the
temperature is usually normal.
 Then temperature increases to 39 – 40º, the child becomes sleepy
 consciousness disorders, psychomotor agitation, seizures, sometimes
meningeal syndrome is associated.
 In some cases focal signs can be observed such as paresis, paralysis,
hyperkinesis, coordination disorders, lesion of II, III, VII CN’s.
 When the spinal cord is involved in the process there is also paralysis of
lower extremities, sensory disorders according to the conductive type,
disturbance of function of pelvic organs.
 There is mild lymphocytic pleocytosis to 200 cells per 1 mm³, increased
content of protein in the CSF.
Small pox encephalitis Clinical features
 The disease is usually developed on the third – seventh day after the rash.
 In 50 % of children there is benign cerebellar ataxia.
 In the rest ones there are pyramidal and extrapyramidal symptoms against
general infectious, general cerebral and meningeal syndromes.
 There is lymphocytic pleocytosis to 100 – 200 cells, increased protein
content in the CSF.
Treatment for smallpox and measles encephalitis
 Desensibilizative medications
 Hormones
 Against edema medications
 Dezintoxication
 Nootrops
 Symptomatic treatment
 Vitamins B1, B6, C
Post vaccinal encephalitis Clinical features
  Usually this disease develops in vaccinated children, especially at late
vaccination and revaccination.
 The disease develops on the 7 th – 12 th day after the vaccination and starts
with increased temperature to 39 – 40 º, severe headache, vomiting,
consciousness disorders, seizures.
 Sometimes meningeal signs appear.
 In some cases paresis, paralysis and coordination disorders are observed.
 There is mild lymphocytic pleocytosis in the CSF.
Treatment
 Desensibilizative medications
 Hormones
 Diuretics \
 Anti seizures medications
 Antipyretics
114. Rheumatic and flu-associated encephalitis. Clinical features. Treatment.
Flu – associated encephalitis– It looks like flu – infection. General infectious
symptoms prevail.
It is caused by A1, A2, A3, B viruses and is usually the result of flu. The virus has
toxic influence on the brain vessels receptors.
The main syndromes are:
 general cerebral, general infectious syndrome
 Cortical syndrome – psychotic disorders, seizures: general weakness,
depression, irritation, emotional instability appear. Psychotic disorders
manifest as hallucinations, paranoids, delirium. Seizures are usually tonic –
clonic with involuntary urination and tongue biting.
 Brain stem disorders - lesion of III, IV, VI CN’s with eye movements
disorders, ptosis, diplopia, cross – eye. Sometimes VII and XII CN’s and
pyramidal path ways are involved ( in this case we can observe paresis of
mimic muscles, tongue deviation, asymmetric stretch reflexes, pathologic
reflexes of Babinski and others. In most severe cases spastic paralysis and
paresis are developed.)
 Hypothalamic: changes of pulse, heart rate, skin colour.
 Cerebellar syndrome: means ataxia, coordination disorders
 Subcortical syndrome usually manifests as hyperkinesis against low
muscle tone.
Treatment
 Desintoxication
 Diuretics
  Gamma globulinum 6 mg per day i/m, Rimantadinum 0.1 3 times per day
 Dexamethazonum, Prednisolonum
 Antibiotics in order to prevent pneumonia
Rheumatic encephalitis also known as sydenham’s chorea clinical features
 abrupt onset (sometimes within a few hours) of neurologic symptoms,
classically chorea, usually affecting all four limbs. O
 ther neurologic symptoms include behavior change, dysarthria, gait
disturbance, loss of fine and gross motor control with resultant
deterioration of handwriting, headache, slowed cognition, facial
grimacing, fidgetiness and hypotonia.
 there may be tongue fasciculations ("bag of worms") and a "milk sign",
which is a relapsing grip demonstrated by alternate increases and decreases
in tension, as if hand milking. Trosseau sign: carpopedal spasm while
checking bp (leaving cuff for 2min). Chvotsek sign: tap cheek causes
fasciculation.
Treatment of Sydenham's Chorea is based on the following three principles:
 eliminate the streptococcus at a primary, secondary and tertiary level.
Strategies involve the adequate treatment of throat and skin infections, with
a course of penicillin when Sydenham's Chorea is newly diagnosed,
followed by long-term penicillin prophylaxis.
 Treatment of movement disorders. Haloperidol, pimozide, clonidine,
valproic acid, carbamazepine and phenobarbitone.
 Immunomodulatory interventions include steroids, intravenous
immunoglobulins

115. Poliomyelitis. Clinical forms, treatment.

Polioencephalitis – when gray substance of the brain is mainly involved
Polioencephalomyelitic (typical form)
 On the third - fourth day of the disease there are:
 Spinal form: Flaccid paresis or paralysis in the shoulders, neck muscles (as a
result of lesion in the anterior horns of the cervical segments). There is
symptom of the “hanging head“.
 Bulbar Form with paresis of the muscles of pharynx, larynx, breathing
disorders.
 Spinobulbar form
Poliomyelitic form: This form is associated with flaccid paralysis and paresis of
extremities.
Non paralytic forms: This form manifest as acute serous meningitis. General
infectious syndrome
Treatment
There is no cure for polio. The focus of modern treatment has been on providing
relief of symptoms, speeding recovery and preventing complications. Supportive
measures include antibiotics to prevent infections in weakened muscles, analgesics
for pain, moderate exercise and a nutritious diet. Treatment of polio often requires
long-term rehabilitation, including occupational therapy, physical therapy, braces,
corrective shoes and, in some cases, orthopedic surgery.

116. Herpetic encephalitis. Clinical features, diagnostic procedures, treatment.

Clinical features The clinical picture is the same as at any other encephalitis
(increased temperature, general cerebral symptoms).
Peculiarities
 General epileptic attacks
 Focal symptoms of temporal and frontal lobe
o Smell and taste hallucinations
o Anosmia
o Memory disorders
o Psychiatric disorders
o Hemiparesis
o Hyperkinesis
Diagnosis
 There is increased pressure, lymphocytic pleocytosis (from 100 to 500 cells
in mm³), slightly increased protein content, sometimes erythrocytes in the
CSF
 There are periodic high amplitude quick waves in temporal lobes on EEG
 There are hypodensive zones as a result of inflammatory changes as well as
edema, small hemorrhages in frontal and temporal lobes on CT and MRI
 Positive serologic reactions
 Immunofluorescentive method
Treatment Herpetic encephalitis has effective specific treatment.
 Acyclovir (Zovirax, Virolex) is used in dose 200 mg 5 times per day orally
or i/v in dose 10 – 30 mg per kg 3 times per day.
 DNA – daza 25 mg i/m every 4 hours
 Interferonum 500 000 U i/m once a day
 Mannit, Manitol, Lasix
 Rheopoliglucinum, Rheoglumanum, Hemodes
 Immunomodulators (Immunoglobulin, T – activin, Timalinum)
 Symptomatic treatment
117. Amyotrophic Lateral Sclerosis. Etiology, pathogenesis, classification,
diagnosis, treatment.
ALS is a chronic progressive disease of nervous system and is defined
pathologically as one which there is degeneration of both upper and lower motor
neurons of brain and spinal cord.
Etiology: unknown
Pathogenesis theories
 ALS with Prion Disease: spongiosis and synapse degeneration due to
deficiency of Argininum.
 Autoimmune theory: cell mediated and humoral immunity
 Genetic theory: changes of genes on chromosome 21 cause activation of free
radical oxidation that leads to the death of neurons of anterior horn
 Amino acid, neuromediators, neuropeptides metabolism disorders
Classification
 Classical or sporadic ALS
 Familial ALS associated with:
o Dementia
o Extrapyramidal disorders
o Extrapyramidal and cerebellar disorders
o Extrapyramidal and sensory disorders
o Peripheral neuropathy
 Complex-ALS- Parkinson disease- Dementia
 According to location: Cerebral, Bulbar, Cervical-thoracic, Lumbar-sacral
Diagnosis
 ENMG: Regular rhythmical fasciculations, decreased speed of impulse
conductance along motor fibres but preserved along sensory fibres.
 MRI: atrophy and bilateral degeneration of corticospinal tract. If high lesion
focus in posterior crus of internal capsule
 PET: Low content of glucose in anterior central gyrus
 CSF exam: Increased protein level, increased activity of arginase
Treatment: There is not effective treatment but for stabilization of the
process:
 Vitamin E, Vitamin B, Biostimulators
 Anabolics: Nerobol, Retabolil
 Pathogenetic treatment: Delargil
 Tireotropinum, Riluzan
  At hypertonus: Myorelaxants
 Dipheninum prescribed at cramps
 Antidepressive medicines
 Electro-therapy

118. Clinical forms and systemic syndromes of Amyotrophic Lateral Sclerosis.

Traditional and modern treatment.
Clinical forms
 Cerebral: Spastic tetraparesis and pseudobulbar syndrome. If
extrapyramidal system: Parkinsons disease, if frontal lobe: signs of dementia
 Bulbar: Lesion of cranial nerves IX,X,XI,XII leading to bulbar syndrome,
joined by anterior horns amyotrophy and pyramidal disorder
 Cervical-thoracic: Weakness and reduced muscles of proximal and later
distal parts of the upper extremities. Well expressed hypotrophy, spastic
hypertonus, hyperreflexia, pathologic signs. Mixed paresis. In course of
disease, reflexes fade away, peripheral palsy dominates
 Lumbar-sacral form: high stretch reflexes, pathologic signs, of peroneal
muscles.
Traditional Treatment: There is not effective treatment but for stabilization of
the process:
 Vitamin E, Vitamin B, Biostimulators
 Anabolics: Nerobol, Retabolil
 Pathogenetic treatment: Delargil
 Tireotropinum, Riluzan
 At hypertonus: Myorelaxants
 Dipheninum prescribed at cramps
 Antidepressive medicines
 Electro-therapy
Modern Treatment: Riluzole (Rilutek) and symptomatic treatment

119. Myopathy classifications. Clinical features of myopathy (Duchene’s

miodystrophy, Erba-Rotta).
Myopathies are conditions in which the symptoms are due to dysfunction of
muscle with progressive weakness, impaired relaxation (myotonia), cramps or
contracture (in McArdle disease), or myoglobinuria. They are inherited, due to
weakness, progressive weakness, no abnormalities in muscles either than
degeneration and regeneration
Classification. They divide the cases into such groups:
 Duschen pseudo-hypertrophic muscle dystrophy
 Late Bekker pseudo-hypertrophic muscle dystrophy
 Shoulder-scapula-facial form of Landouzy Degerina
 Erba dystrophy
Duchenne muscular dystrophy is an X-linked recessive disorder.
Affected children appear normal at birth and may be extremely placid. There is
normal achievement of early milestones, but there is delay in standing and
walking. The child then develops a clumsy, waddling gait and
pseudohypertrophy of the calf muscles, associated with difficulty climbing
stairs and rising from a chair. Older children have a pronounced lumbar
lordosis caused by weakness of the pelvic musculature and the erector spinae. This
results in forward tilting of the pelvis, protrusion of the abdomen, and
compensatory backward arching of the upper thoracic spine and shoulders. The
affected child has difficulty rising to a standing position. He must first roll to a
prone position, pull himself to his hands and knees, push with his arms until only
his hands and feet are on the floor, and finally, "walk" up his lower extremities
until he can extend his trunk and stand. This method of assuming a standing posi-
tion in the presence of severe proximal weakness has been termed Gower's sign.
Eventually the child can no longer ambulate and becomes confined to a wheel-
chair by the age of 10.
Limb-Girdle Muscle Dystrophy (erbs dystrophy)
The earliest symptoms consist of weakness of the pelvic girdle or proximal
lower limb muscles, which presents at any age from childhood to adulthood, with
a mean age of onset of 21 years. The autosomal dominant form of the disease
presents in adults and exhibits a slower progression of weakness. The initial
symptoms are followed by involvement of upper limb-girdle muscles, then by
progressive weakness of truncal or more distal limb muscles, with loss of
walking ability 10 to 20 years after onset. Cardiomyopathy is rare and usually
asymptomatic, but cardiac failure has been reported.

120. Differential-diagnostic criteria of primary and neurogenic amyotrophy.

Primary amyotrophy Neurogenic amytrophy
Signs and Proximal weakness and Distal weakness and wasting
symptoms wasting plus
 sensory signs and symptoms,
hypertonus,
Fasciculations
Serum muscle
enzymes Increased Normal
Nerve condition
velocities Normal Slowed
Low amplitude, polyphasic Increased insertion activity
Electromyography motor fibrillations,
unit. Potentials of brief Fasciculations, positive sharp
duration waves
Angular fibers, target fibres,
Muscle biopsy Variation in fiber diameters. pyknotic
Internal nuclei degeneration of clumping. Type grouping type I
fibers fibres,
increased endimysial Small type 2 fibres,
connective tissue hypertrophied

121. Neurogenic miodystrophy Scharcot-Mary: clinical feature, diagnostic

procedures, treatment.
Clinical features. The pathologic changes are of three types. There are:
 Demyelination of the peripheral nerve with axonal loss and some
hypertrophy of the Schwann cells, producing hypertrophic neuropathic
changes. In Type I Charcot-Marie-Tooth syndrome, symptoms begin in
the first or second decade of life with foot-drop and a stoppage gait. Distal
muscle atrophy produces a "stork leg" deformity; intrinsic hand muscle
atrophy develops later. Distal tendon reflexes are diminished or absent and
a stocking-and-glove sensory defect is present. Scoliosis and high pedal
arches or club feet are common. Peripheral nerves are often palpably
enlarged. Tremor is prominent in some patients; the clinical constellation of
Charcot-Marie-Tooth syndrome with tremor is termed the Roussy-Levy
syndrome.
 Neuronal loss of anterior horn cells and posterior nerve root ganglion
neurons in the lumbar and sacral segments (hereditary motor and sensory
neuropathy, Type II). The first symptoms of peroneal muscular atrophy
often appear in adult life, but foot deformities may be evident much earlier.
The progression is slow with muscle weakness and wasting confined to
the feet and sometimes involving the leg muscles. The involvement may
 be asymmetric. Atrophy and weakness of distal muscles, stocking-and-
glove sensory impairment is minimal or absent, and depression of tendon
reflexes in the lower limbs but normal in the arms. Deficits are usually less
severe and nerves are not palpably enlarged.
 Anterior horn cell involvement with secondary axonal loss and
demyelination of motor fibers.
Diagnosis
 Lumbar puncture. CSF protein content is frequently elevated in Type I
Charcot-Marie-Tooth syndrome, but is normal in Type II. The CSF is
otherwise normal, as are blood and urine.
 Nerve conduction velocities. Motor and sensory nerve velocities are very
slow in the peripheral nerve demyelinating type but are normal or only
slightly delayed in the other two types.
 Nerve biopsy. Nerve biopsy is normal and should differentiate the three
types of the disease.
Treatment: There is no specific treatment. Braces for correction of the foot-drop
and hand deformities can be helped ambulatory by splinting and orthopedic
procedures.
122. Myasthenia gravis. Clinical forms. Myasthenic crisis. Clinical feature.
Emergency treatment.
Myasthenia gravis (MG) is caused by a defect of neuromuscular transmission due
to an antibody-mediated attack on nicotinic acetylcholine receptors (AchR) at
neuromuscular junctions
Clinical features The typical sign of myasthenia is muscles weakness. One of the
most specific features of this weakness is its increasing with movements.
According to the course of the disease there are such forms: Progressive,
Stationary, Mysthenic episodes
Clinical forms:
 Ophthalmic: ptosis, diplopia and eyes movement disturbances,
opthalmoplegia
 Bulbar: Weakness of mimic muscles – especially oral muscles. Weakness of
chewing muscles. Weakness of pharyngeal, laryngeal muscles and muscles
of tongue. Tongue muscles function disorders. Breathing disturbance.
 Skeletal: Extremities function disturbances (especially proximal parts).
Neck muscles weakness – hanging of the head. Body muscles weakness that
leads to duck – like gait
 General
Myasthenia crisis: There fasciculations, seizures, bradycardia, salivation,
hyperhydrosis and abdominal pain.
At myasthenic crisis:
 Plasmapheresis
 Ig i/v (2 g per kg 2 – 5 days)
 Corticoids (100 mg prednisonum)
 Proserinum 1 – 2 ml i/v
 SLV, oxygen
 Halloperidolum at excitation
Emergency Treatment – Atropinum 1 ml 0.1 % s/c or i/v.
123. Clinical forms and treatment of hepatic-cerebral dystrophy.
Hepatocerebral dystrophy (HCD)( Wilson – Konovalov disease)
This disease is connected with disorders of ceruloplasminum metabolism.
Ceruloplasminum is a blood protein responsible for Cu transport. It is produced in
liver. Pathologically there is accommodation of Cu in subcortical ganglions
(especially n. Lenticularis), brain cortex, cerebellum, liver, spleen, iris.
The disease is genetically autosomal – recessive. And it is observed in male and
female with the same frequency.
Clinical signs of the disease
The first signs of the disease are observed in early childhood. There are neck
stiffness, different hyperkinesis and psychiatric changes. Sometimes seizures
can be observed. There is also liver enlargement. One of the most specific
changes is Kaizer – Fleishner ring in the iris.
According to the Konovalov classification there are 4 main neurological types
of the disease:
 Rigid – arythmokinetic
 Trembling – rigid
 Trembling
 Extrapyramidal – cortical
Sometimes the disease manifests only as liver insufficiency and neurological signs
are joined later.
Diagnosis
 Family history
 The typical signs of the disease – Kaizer – Fleishner ring, lesion of liver, low
quantity of ceruloplasminum in the blood, increased quantity of Cu in urine.

124. Clinical forms and treatment of Parkinson disease.

Parkinsonism – is a chronic progressive neurodegenerative syndrome that is
characterized by motor disorders as a result of extrapyramidal system involvement.
Parkinson disease (PD) – is a chronic progressive degenerative disease of CNS
that manifest as voluntary movements disorders
The main clinical forms
 Trembling: More expressed in distal part of extremities. Looks like coins
counting. More expressed at rest, disappears or decreases while moving
 Rigidity: cogged wheel symptom. Tonus increased in course of evaluation
of nervous state. Tonus in same manner in flexors and extensors
 Mixed
At present, treatment is aimed at controlling symptoms because no drug or
surgical approach unequivocally prevents progression of the disease
 Synthetic cholinolytics : Cyclodolum , Romparkin, Parkopan
 Stimulators of dophamine secretion ; carbidopa, levodopa
 Amantadine medications increase sensation of dophamine receptors to
dophamine, excite dophamine receptors. Midantan ( 0.1 3 times per day ),
Amantadinum.
 Inhibitors of MAO ( Jumex ) - 5 mg 1 – 2 times per day.
 Stimulators of dophamine receptors – Bromcriptine, Akineton, Norakin.
 Medications that decrease converse catch of dophamine. Amitriptilinum,
Amipraminum, Melipraminum.
 Substitutional therapy . Sinemet 3 – 6 tablets per day. Nacom - 3 – 6 tablets
per day.
 In order to decrease tremor we use b – adrenoblockers : Anaprilinum ,
Amitriptilinum
 In order to decrease muscle tonus Midocalm, Baclofen are used.
 Nootrops
 Physiotherapeutic methods.

125. Clinical feature of Huntington’s chorea and treatment.

It is a progressive hereditary disorder that usually appears in adult life. It is the
result of systemic degeneration of extrapyramidal structures and brain cortex.
It has autosomal – dominant type of inheritance.
Clinical features of the disease The disease usually appears in adult life and it is
very rare in children. Male and female can suffer from this disease.
The main clinical symptoms of classic form are:
 Choreic movements
 Extrapyramidal rigidity
 Slowly progressive dementia
Diagnosis
  Clinical and genetic analysis
 CT and MRI of brain (atrophic changes of brain hemispheres)
 EEG
 DNA – analysis
There is no treatment to stop or reverse Huntington's disease, however there are
some medications that can help keep symptoms under control. Treatment for HD
includes the drug tetrabenazine, antipsychotic drugs, antidepressants, and
tranquilizers.

126. Heredity-degenerate diseases with pyramidal tract and cerebellum

lesions (Shtrupel, ataxia of Pier-Mary and Friedreikh ataxia).
Spastic paraplegia of Shtrumpel
This disease is the result of pyramidal tracts and cerebellar connections
degeneration. The disease is genetically recessive in most cases but in some
families it show dominant inheritance.
Clinical features. The first signs of the disease are observed at the age of 10–15.
The typical signs of the disease are lower spastic paraplegia with increased
muscle tonus, high stretch reflexes, pathological reflexes. Usually the lesion of
lower extremities is symmetrical. Sometimes motor disorders can be developed in
upper extremities. In some cases pseudobulbar symptoms are joined.
The typical signs of the disease:
 The dominance of spastic tonus over motor disorders
 Well preserved abdominal reflexes
 The absence of pelvic disorders
 The typical clinical picture of spastic paraplegia is often associated with
cerebellar symptoms and symptoms of posterior spinal columns.
Hereditary cerebellar ataxia of Pier – Mary
The main signs of the disease are:
 The beginning at the age of 30 – 50
 Cereballar ataxia
 Dysarthria
 Hyperreflexia
 Spastic muscle hypertonia
 The inheritance of the disease is autosomal – dominant.
 Clinical feature of the disease The disease begins gradually with gait
disorders, disorders of coordination, nystagmus, dysarthria. There are
high reflexes, increased muscle tonus according to spastic type (mainly
in lower extremities), pathologic reflexes. Eye movements disorders are
 often observed in such patients. There are mental, memory and emotional
disorders.
Spinal Fridreich ataxia: The disease is characterized by spinal cord degeneration
and degenerative – dystrophic changes in posterior and lateral columns.
The disease is characterized by autosomal – recessive type of inheritance.
Clinical features of the disease The disease begins at the age of 10 – 12 and then
slowly progresses. The main clinical signs are sensitive – cerebellar ataxia,
nystagmus, muscle hypotonia and areflexia, gait disorders. At the beginning of
the disease there is deep sensation disorders according to the conductive type on
lower extremities. In the course of the disease coordination disorders, scan
speech, body and upper extremities ataxia appear. The disease is characterized
by some bone abnormalities, cardiomyopathy, mental disorders and the symptoms
of lesion of pyramidal tracts.
127. Clinical feature of supratentorial brain tumors.
Supratentorial tumours are located in the base of anterior and middle cranial fossa
i.e. Cerebral hemispheres and diencephalon (thalamus and hypothalamus).
Frontal lobe tumors
 Frontal psychiatric disorders – decreased attention, critics, behavioral
changes, speech and motor depression, the loss of social and professional
skills, untidiness, excitement, aggression, low mental activity, rude humor.
 In case of anterior central gyrus lesion – there are central hemiparesis with
domination in one extremity and facial paresis on the opposite side.
 In case of irritation of anterior central gyrus there are epileptic attacks like
“Motor Jackson “.
 In case of irritation of anterior adversive region there are adversive attacks.
They start with gaze and head turning into the opposite direction.
 Frontal ataxia – which can later cause astasia – abasia. It is characterized by
standing and walking disturbances with tendency to falling down into the
opposite direction.
 Catching phenomena of Yanishevskyy.
 Hypoosmia and anosmia (at olfactory meningiomas)
 Motor aphasia – when the process is localized in posterior part of lower
frontal gyrus. Agraphy and gaze paresis is observed at tumor in posterior part
of middle frontal gyrus.
 Foster – Kennedy symptom – is the result of direct influence of tumor on
optic nerve or increased intra cranial pressure.
 If the tumor is localized in paracentral lobe there is lower paraparesis,
urination central disorders.
Parietal lobe tumors
  In case of irritation of posterior central gyrus there are sensory Jackson
attacks with parasthesia sensation in one of the extremity.
 In case of posterior central gyrus lesion there is loss of sensation according
to the cortical monotype.
 The loss of deep sensation in the extremities or afferent paresis of the
opposite side extremity.
 Autotopognosia, anosognosia, pseudomelia, astereognosia. (At right – side
localization)
 Alexia, acalculia, agraphia. (At left – side localization)
 Apraxia (at tumors of gyrus supramarginalis )
Temporal lobe tumors
 Epileptic attacks with auditory, olfactory, gustatory, visual and visceral
hallucinations. The patients complain often on unpleasant internal sensations,
depressions with time and space loss of orientation (especially when the tumor
is localized between the temporal and parietal lobe)
 Olfactory, auditory, gustatory agnosia
 Homonimic hemianopsy (when the tumor is deep in the posterior part)
 Sensory aphasia
 Amnestic aphasia
 Pseudocerebellar ataxia
 Vestibulo – cochlear dizziness.
 Memory disorders on current events at mediobasal parts lesion
 Psycho – motor automatisms.
Occipital lobe tumors (They are very rare)
 Simple visual hallucinations or photopsy (light, flash)
 Homonimic hemianopsy (this symptoms appears at destruction of cortical
neurons).
 Colour vision disturbances (dyschromatopsy)
 Visual agnosia
 Optic metamorphopsy
 Central gaze paralysis
 Quadrant hemianopsy
Subcortical structures tumors
They are located very close to the CSF pathways. Hypertension and dislocation
develop very early
 Hyperkinesis
 Amyostatic syndrome with plastic hypertonus
 Hemiplegia, hemianesthesia, hemianopsy – capsule syndrome
Thalamus tumors: There are hemianesthesia on the opposite side with burning
- like unpleasant pains.
Corpus Callosum tumors
 Psychiatric disorders with memory disturbances on current and past events
 Dementia
 Apraxia
 One or two – side paralysis
Third ventricle tumors
 Hormonal disorders (Non sugar diabetes, obesity)
 The attacks of general weakness with muscle tone disorders
 Headaches with autonomic reactions
 Occlusive – hypertensive syndrome with memory disorders and psychiatric
disturbances
Chiasma and saddle tumors Usually there are basal meningiomas, hypophysis
adenomas, chiasmatic gliomas, optic nerve gliomas.
 Endocrine disorders
 Primary atrophy of optic nerve disk
 Bitemporal hemianopsy
 III, IV, VI, V CN’s lesion
 Foster – Kennedy syndrome
 Local hyperostosis or osteolysis in case of tumor’s expansion into the base
of the skull

128. Clinical picture of subtentorial brain tumors.

Subtentorial brain tumours are tumours that are located in the cerebellum, fourth
ventricle and brain stem.
Posterior fossa tumors (tumors of cerebellum and IV – th ventricle and brain
stem tumors).
In this case hypertension increases very quickly. There are radicular and nuclei
lesions of CN’s and alternating brain stem syndromes, bulbar syndrome and
brain stem nystagmus. At cerebellar tumors there are muscular hypotonia,
coordination disorders, ataxia (intention tremor, adiadokinesis, loss of
equilibrium and balance), enforced head position (the patient is lying on the
tumor), occipital headache, asynergy, adiadochokinesis. There are early
symptoms of increased intracranial pressure.
Fourth ventricle tumors (ependimomas): Hydeocephalus, progressive cerebellar
ataxia. Progressive spastic hemiparesis or quadriparesis.
 All these symptoms are united into the Bruns attacks (severe headache,
vomiting, skin autonomic reaction, breathing disorders, arrhythmic
 pulse, enforced head position). The main reason is– acute occlusion of IV –
th ventricle exit.
Brain stem tumors. They are gliomas (benign tumors) and sarcomas (malignant
tumors) or metastasis in brain stem. Heart – vascular and breathing disorders are
often joined.
 At midbrain tumors there are peduncle alternating syndromes
o Weber’s syndrome - a lesion in the base of the cerebral peduncle
affects the root of the third cranial nerve and the corticospinal
pathway, producing Oculomotor nerve palsy (ptosis and mydriasis)
and a contralateral hemiplegia.
o Benedict’s syndrome - Oculomotor nerve palsy and a
contralateral choreoatetosis and intention tremor.
 At pons tumors there are alternating syndromes of Fovil, Miyar – Hubler.
o Miyar-Gubler syndrome - peripheral palsy of the facial muscles on
the site of the lesion and a contralateral hemiplegia.
o Fovill syndrome - peripheral palsy of the facial muscles and the
external rectus eyes’ muscle on the site of the lesion and a contralateral
hemiplegia.
 At medulla oblongate there are syndromes of Jackson, Avelis, Shmidt,
Valenberg – Zaharchenko.
o Jackson’s syndrome - Hypoglossal nerve palsy on the site of the lesion
and opposite hemiplegia.
o Aweli’s syndrome - peripheral palsy of the palatal and laryngeal
muscles on the site of the lesion and a contralateral hemiplegia.
o Schmidt’s syndrome - peripheral palsy of the muscles (palatal,
laryngeal, tongue and m. sternoclaidomastoideus, m. trapezius) on the
site of the lesion and a contralateral hemiplegia.
o Valenberg - Zakcharchenko’ syndrome - on the site of the lesion
(nystagmus, Horner’s syndrome, peripheral palsy of the palatal and
laryngeal muscles, a fallout of sensation on the face for the segmental
type, cerebellar ataxia) and a contralateral hemiplegia, hemianestesia.

129. Clinical picture of intra- and extramedullar spinal cord tumors.

Extra – medullar tumors stages:
1. Radix – associated – not well expressed: loss of all sorts of sensation in its zone
innervation according to the segmental type. The sensitive disturbance is
appeared as transversal strip on a trunk and longitudinal strip on extremities
2. Stage of Brown – Sequard syndrome: deep feeling drops out on the side of a
lesion, and pain and temperature sense- on the opposite side, since a level on 1-2
segments is lower.
3. Stage of complete spinal cord diameter lesion: all sorts of sensation below
that level of a lesion drop out, pain and temperature sense drop out on 1-2 segments
below than level of a lesion, and deep - from the same level. Usually, the deficits are
in the lower trunk and legs, are bilateral and almost symmetric.
Intra – medullar tumors stages:
1. Segmental (segmental – dissociative disorders): loss or lowering pain and
thermoanesthesia and saving tactile and joint sense in given segment.
2. Stage of complete spinal cord diameter lesion: all sorts of sensation below that
level of a lesion drop out, pain and temperature sense drop out on 1-2 segments
below than level of a lesion, and deep - from the same level. Usually, the deficits are
in the lower trunk and legs, are bilateral and almost symmetric.
3. Radix – associated: not well expressed: loss of all sorts of sensation in its zone
innervation according to the segmental type. The sensitive disturbance is
appeared as transversal strip on a trunk and longitudinal strip on extremities
At extra – medullar tumors superficial sensory disorders are slowly moving
upwards, while at intra – medullar tumors these disorders are slowly moving
downwards.

130. Clinical feature of hypophysis tumours.

Adenoma of hypophysis can be hormonally active or non active. There are
adenomas with increased production of Prolactinum, Somatotropinum, ACTH,
Tyriotropic hormone with typical clinical picture. Hormonally active tumors can
expand into the neighbouring regions. Microadenomas in the Turkish saddle do not
show clinical picture.
Other signs may include:
 Endocrine disorders
 Primary atrophy of optic nerve disk
 Bitemporal hemianopsy
 III, IV, VI, V CN’s lesion
 Foster – Kennedy syndrome: unilateral anosmia with ipsilateral optic atrophy
and contralateral papilledema
 Local hyperostosis or osteolysis in case of tumor’s expansion into the base of
the skull

131. Etiology, pathomorphology, pathogenesis and treatment of Epilepsy.

Epilepsy is a brain disease that is characterized by persistent tendency to the
development of epileptic seizures and neurobiological, cognitive, psychological
and social sequences of the state.
Etiology:
  Cryptogenic seizures: is a seizure that occurs from unknown cause
 Symptomatic seizure: occurs from known or suspected insult
 Idiopathic epilepsy syndromes: syndromes with specific age of seizure
onset, clinical features, EEG features, prognosis and presumed general
mechanism.
Pathomorphology: Each epileptic attack causes hypoxic changes in brain and
leads to the development of encephalopathy.
Pathologic physiology
 There is a group of neurons with pathologic activity, which is called epileptic
focus
 There is the ability to enforce and spread the activity
 Weakness of anti - epileptic protection. (It is provided by caudal parts of
the brain)
Neurochemistry of epilepsy: Disorders of balance between glutamate (exciting
neurotransmitter), GABA (inhibitory neurotransmitter
Treatment: The main principals of epilepsy treatment should be – emergency,
accordance to stages, following.
On the way to hospital:
1. To release breathing air ways
2. Digitalis drugs
3. Sibazonum 0.01g
In ambulance:
1. Sibazonum 30 ml in 150 ml of physiological solution, in 10 min we add the
medication up to 100 – 120 mg
2. Magnesiii sulfas 25% 10.0 in glucose 40 %
3. Anesthesia with nitrous oxide
4. Dosed anesthesia
5. Aminazinum 25% 1-2 ml
6. Atropinum 0.1% 1.0 s/c
7. Cardiac, antihistamine, diuretics
8. Natrii tiopentali 1g in 10 ml of physiological solution
New anti-epileptic medications: Lamotrigine, Levetiracetam, Topiramate,
Oxcarbazepine, Lacosamide, Zonisamide

132. Kinds of partial seizures.

There are three groups of focal attacks:
1. Simple
 Simple motor
o Focal motor without march
 o Focal motor with march
o Adversive
o Postural
o Phonatory simple
 Simple sensory
o Somatosensory (with and without march)
o Visual, acoustical, gustatory, smell
 Simple autonomic – visceral
 Simple with psychiatric disorders
o Aphatic
o Dysmnestic
o With thinking disturbances (ideatory)
o Emotional
o Hallucinatory
2. Complex
 Temporal pseudoabsance
 Automatisims
3. Simple with generalization(secondary general)
Focal attacks are characterized by different symptoms – motor, sensory, autonomic
or psychiatric that depends on focus localization and the peculiarities of morpho–
functional organization of epileptic system. Motor attacks are caused by discharges
in certain part of motor cortex. Somato–motor or motor Jackson attacks are
seizures in certain muscle group according to the focus localization. They can
be local or involve other group of muscles according to the topical localization in
the brain cortex.
In case of epileptic discharges in motor speech center speech disorders or
involuntary vocalization – involuntary repetition of words are observed.
Sensory attacks manifest as simple or complex sensory disorders, such as
somatosensory, visual, acoustical, olphactory, taste attacks and epileptic
attacks of dizziness.
Somatosensory Jackson attacks are associated with numbness, tingling in some
part of the body. They can be localized or involve other parts of the body. They are
caused by epileptic discharges in Post – Rollandic region. Very often the attack
begins as somatosensory and then converts into somatomotor.
As for visual, acoustical, olphactory, taste attacks and epileptic attacks of
dizziness they can manifest as simple disorders or complex illusion or
hallucinations.

133. Kinds of general convulsive and without seizers attack.

Epileptic general tonic – clonic attack (grandmal) usually begins with short
initial stage that lasts several seconds. The last can manifest as:
 Bilateral general muscle jerks
 Loss of consciousness
 Autonomic changes
 Enlargement of pupils
The tonic stage lasts about 10 – 20 seconds. During this stage seizures involve all
the muscles. Usually seizures dominate in the extensors but at the beginning
flexors are even more involved. The eyes are opened and are looking upwards.
Mouth is opened too. Seizures start from axial muscles and then involve
extremities. Shoulders are lifted and adducted. Muscles of lower extremities are
seldom involved.
Then tonic stage is converted in clonic one. This stage is often associated with
tongue biting, clonic vocalization. This phase lasts 30–40 seconds. During the
tonic–clonic attack there are severe autonomic disorders – apnoe, cyanosis, small
skin hemorrhages, pulsation of carotic arteries. Pulsation is frequent, AP is
increased. There is also midriasis with pupils areflexia, hypersalivation that
usually manifest as bloody foam. After attack the next stage can be divided into
early and late ones.
Early stage lasts 1 – 5 min and is characterized by: after the last clonic attack a
new phase of tonic contraction appears. The last is very similar to the one at the
beginning. But the seizure dominates in the face, especially in chewing muscles
and causes trismus. Deep reflexes are increased. There is loss of consciousness.
And that means that the patient is in coma.
Late after attack (recovery) stage is characterized by decreasing of midriasis,
normal superficial reflexes, decreased deep reflexes and Babinski sign. The
behavior of the patient is often automatic. When the patients are conscious they
can complain on headache, muscles pain and complete amnesia. This period
lasts 5 – 15 min.
Without seizure attacks
Absentia epileptica are characterized by sudden and short – lasting (2–30 sec)
loss of consciousness and EEG – peculiarities. They are associated with absent
gaze, interruption of patient’s activity, autonomic disorders (paleness or
hyperemia of face, midriasis). The attack is finished suddenly. The patient
doesn’t remember anything about it. This picture is typical for simple attack,
when motor activity, seizures or loss of muscles tonus are absent.
If absentia is associated with any motor component it is called complex absentia.
Complex absentia can be divided into myoclonic, atonic, tonic and with
automatisms.
Myoclonic absentia is characterized by loss of consciousness, rhythmic bilateral
myoclonus in face and upper extremities. There are jerks of eyelids,
periorbital muscles, mouth edges, eye bulbs. The patient can loose some objects
he is holding in his arms.
Atonic absentia is characterized by decreasing of postural tonus, hanging head
and sudden drops.
Tonic absentia is associated with looking of eyes upwards. There is domination
of either extensor or flexor component, symmetric or asymmetric.
Absentia with automatism can be the sign of focal attack and absentia. The main
condition for automatism is incomplete loss of consciousness. Differential
diagnosis in this case is very complicated. That’s why EEG should be made for
such patients.
Typical absentia are associated with bilateral symmetric complexes “top – waves”
with frequency 3 per sec in frontal – central lobe.
Typical absentia are much more common in children and can be caused by
hyperventilation or light. They are very refractory to the antiepileptic drugs.
Atypical absentia are associated with such EEG changes:
 Bilateral symmetric complex of “top – wave” which are rhythmically
repeated with frequency 2 per sec.
 Epileptic rhythm of gathering with frequency 10 per sec.
 Epileptic rhythm of gathering with frequency 20 per sec.
 Complex of multiple spikes – waves with frequency 4 – 6 per sec.
 Atypical absentia are resistant to hyperventilation and paroxysmal light.

134. Epileptic status. Clinical feature and emergency treatment.

Status epilepticus (SE) is a single epileptic seizure lasting more than five minutes
or two or more seizures within a five-minute period without the person returning to
normal consciousness between them.
Clinical features: convulsive, non convulsive. Features in previous question
TREATMENT ;
 To provide permeability of respiratory airways
 To evaluate the function of the heart – vascular system and respiratory
system
 To provide free ways to veins
 Lorazepam 4mg i/v or diazepam 10mg every 5minutes for 20minutes then
general anesthesia if patient does not recover

135. Differential diagnostic of seizers and hysteric attack.

 Hysteria Epilepsy

1) Patient does not get hysteria attack 1) Attack of epilepsy can occur any
while sleeping but gets the attack when time. Even if patient is sleeping.
he is being observed by someone. Associated with short loss of
Patient usually conscious. consciousness.

2) Hysteria attack occurs slowly and is 2) epilepsy attack occurs suddenly and
related to mental state. is not related to mental state.

3) Duration of hysteria attack lasts for a 3) duration of epilepsy attack lasts for
longer time. few time.

4) Patient speaks and mumbles during

4) patient does not speak or mumbles.
attack.

5) Sound of ghrrr..ghrrrr comes in 5) sounds of ghrrr..ghrrr comes in

breathing. breathing.

6) Patient tries to control himself and

6) patient falls down suddenly and hurts
tries to hold something while falling
himself.
down in this attack.

7) Pressure of urine and stool does not 7) ) pressure of urine and stool can
release during the attack. release during the attack.

8) Patient keeps his eyes closed and

8) ) eyes are closed and eyelids are
eyelids do not stay stable. Gets
stable.
sensitive to light.

9) Hysteria disease mostly affects 9) Epilepsy equally affects men and

women. women.

10) Light reflexes of pupila maintained

10)light reflexes of pupils usually lost
during attack
136. Principles and methods of epilepsy treatment.
First line drugs: Carbamezapine, sodium valproate, lamotrigine
Second line: Levetiracetam, Topiramate, Pegabaline
New drugs: Zonisamide, Esclicarbazepine, Retigabine
On the way to hospital:
 To release breathing air ways
 Digitalis drugs
 Sibazonum 0.01g
In ambulance:
 Sibazonum 30 ml in 150 ml of physiological solution, in 10 min we add the
medication up to 100 – 120 mg
 Magnesiii sulfas 25% 10.0 in glucose 40 %
 Anesthesia with nitrous oxide
 Aminazinum 25% 1-2 ml
 Atropinum 0.1% 1.0 s/c
 Cardiac, antihistamine, diuretics
 Natrii tiopentali 1g in 10 ml of physiological solution
Epileptic status
 To provide permeability of respiratory airways
 To evaluate the function of heart – vascular and respiratory systems
 Lorazepam 4mg i/v or Diazepam 10 mg every 5minutes until 20minutes then
general anesthesia if patient does not recover
 If patient recovers: 50% glucose, Thiamine IV
Next half an hour:
 to introduce the medication through the naso – gastral probe
 Fenitoin 18 mg per kg or Phenobarbitalum 15 mg per kg i/v by drop 100 mg
per kg
Surgical methods of treatment:
 Resections : Anterior temporal lobectomy. Selective
amygdalohypocampoectomia. Calosotomia. Hemisphereectomia
 Stereotaxic : Destruction of deep temporal structures. This procedure on
lateral part normally decreases seizures, on medial ones – aggression.
 Radio – surgical with γ – knife. γ – waves from 201 sources are focused on
certain aims. The effectiveness of this procedure is 70 – 80 %.
 Electrostimulative – stimulation of certain structures: Nucleus dentatus,
the caput of nucleus caudatus. Stimulation of n. vagus – this method is one
of the newest one. It is indicated at partial seizures with secondary
generalization.
137. Hydrocephalus. Clinical feature, diagnostic procedures, treatment.
Hydrocephalus is the buildup of too much cerebrospinal fluid in the brain.
Normally, this fluid cushions your brain. When you have too much, though, it puts
harmful pressure on your brain.
Clinical feature,
 Headache, Nausea and vomiting
 Loss of bladder control (urinary incontinence);
 Loss of coordination and trouble walking;
 Blurry vision or double vision
 Irritability; Seizures;
 Separated sutures;
 Changes in personality, memory, or the ability to reason or think;
 Changes in facial appearance and eye spacing;
 Crossed eyes or uncontrolled eye movements;
 Irritability, poor temper control;
 Muscle spasticity (spasm);
 Slow growth (child 0–5 years);
 Slow or restricted movement;
Diagnostic procedures
 CT
 MRI
 pressure-monitoring techniques
 Ultrasound of fontanelle in children
Treatment. : Conservative: acetazolamide and furosemide. Hydrocephalus is
most often treated by surgically inserting a shunt system. This system diverts
the flow of CSF from the CNS to another area of the body where it can be
absorbed as part of the normal circulatory process.
 Ventriculoperitoneal (VP) shunt (most common)
 Ventriculoatrial (VA) shunt (or "vascular shunt")
 Lumboperitoneal shunt: Only used for communicating hydrocephalus,
CSF fistula, or pseudotumor cerebri)
 Torkildsen shunt (rarely): Effective only in acquired obstructive
hydrocephalus
 Ventriculopleural shunt (second-line therapy): Used if other shunt types
contraindicated