МИНИСТЕРСТВО ЗДРАВООХРАНЕНИЯ УКРАИНЫ

Харьковский национальный медицинский университет

Григорова И.А., Лещенко К.А., Григорова А.А.

NEUROLOGY
(in tables and pictures)

Textbook for students

11th edition, revised

НЕВРОЛОГИЯ
(в таблицах и рисунках)

Учебное пособие для студентов

11 издание, дополненное

Харьков
ХНМУ
2018
УДК 616.8(075.8)
N50
Авторы:
И.А.Григорова, К.А.Лещенко, А.А. Григорова, Е.К.Резниченко, О.А.Тесленко, А.Р.Ескин,
Л.В.Тихонова, Е.Л.Ибрагимова.

Утверждено Ученым Советом ХНМУ. Протокол № 5 от 17.05.21.2018.

Рецензенты:

Мищенко Т.С.– д.мед.наук., проф. (Харьковский национальный университет им. Каразина)

Морозова О.Г. – д.мед. наук, проф. (Харьковская академия последипомного образования)

Contributors:
Iryna Grygorova, Konstantin Leschenko, Alina Grygorova, Elena Resnichenko, Olga Teslenko,
Alexander Eskin, Ludmila Tikhonova, Elena Ibragimova

N50 I.A.Grygorova, K.A.Leschenko, A.A.Grygorova, E.K.Reznichenko, O.A.Teslenko, A.R.Es-

kin, L.V.Tikhonova, E.L.Ibragimova. Neurology in tables and pictures (11-th edition, re-
vised). Gudelines for students – Kharkov, KhNMU, 2018. – 118 p.

Н50 И.А.Григорова, К.А.Лещенко, Е.К.Резниченко, А.А.Григорова, О.А.Тесленко,

А.Р.Ескин, Л.В.Тихонова, Е.Л.Ибрагимова. Неврология в таблицях, рисунках на англ.
языке. (издание 11, дополненное). Уч. пособие – Харьков: ХНМУ, 2018. – 118 с.

Annotation
The main goal of this manual is a laconic coverage of the main features of topical diagnosis and clinical fea-
tures of diseases of the nervous system, which enables students of different specialties to systematize the
knowledge they have acquired in neurology and to qualitatively prepare for the delivery of final lessons and
examinations.

Аннотация
Основной целью данного пособия является лаконичное освещение основных особеностей топической
диагностики и клинических особенностей заболеваний нервной системы, что дает возможность
студентам разных специальностей систематизировать полученные знания по неврологии и более
качественно подготовиться к сдаче итоговых занятий и экзаменов.

УДК 64 (091) (477.54) (075)

Н50

© Харьковский национальный
медициниский университет,
2018
Григорова И.А., Лещенко К.А.,
Григорова А.А., Резниченко
Е.К., Тесленко О.А., Ескин А.Р.,
Тихонова Л.В , Ибрагимова
Е.Л. 2018.

2
 CONTENT
Anatomy of cortico-muscular tract 6
Disturbances of voluntary movements (paralisis and paresis) 7
Topical diagnosis of disturbances of voluntary movements 9
Extrapyramidal system and its pathology 10
Cerebellum and its pathology 12
Types of ataxia 14
Anatomy of sensory tracts 15
Topical diagnosis of sensory disturbances 17
Olfactory nerve 18
Optic nerve 20
Oculomotor nerve 22
Trochlear and abducent nerves 24
Trigeminal nerve 25
Signs of trigeminal nerve lesion 27
Trigeminal neuralgia 28
Facial nerve 29
Signs of the facial nerve lesion 31
Vestibulochlear nerve 32
Bulbar group of cranial nerves (glossopharyngeal, vagus, accessory, hy-
poglossal) 34
Signs of damage in bulbar group of cranial nerves (bulbar and pseudob-
ulbar syndromes) 36
Anatomy of autonomic nervous system 37
Pathology of autonomic nervous system 39
The brain cortex and disturbances of higher cerebral functions 40
Main topical neurological syndromes 41
Scheme of patient examination 42
Headache 43
Migraine 45
Syndrome of intracranial hypotension 47
Syndrome of intracranial hypertension 48
Transient disorders of cerebral blood circulation 49
Acute disturbances of cerebral blood circulation 52
Acute disturbances of spinal blood circulation 53
Somatoneurological syndromes 56
Classification of vertebrogenic neurological syndromes 59
Syndromes of cerebrospinal fluid and its pathology (liquor) 61
Meningeal syndrome 62
Meningitis 62
Myelitis 64
Acute poliomyelitis and poliomyelitis-like diseases 65
Encephalitis 67

3
Arachnoiditis 71
Multiple sclerosis 72
Amyotrophic lateral sclerosis 73
Epilepsy 74
Nonepileptic paroxysmal states 75
Children's palsy 75
Hereditary ataxias 76
Hereditary degenerative diseases with lesion of the extrapyramidal sys- 77
tem
Hereditary degenerative neuromuscular diseases 78
Muscular dystonia 80
Myasthenia gravis 81
Hereditary neuromuscular diseases 82
Neuroses 83
Parkinson’s disease 85
Glossalgia 86
HIV-assotiated nervous system disorders 87
Polyneuropathies 89
Neurosyphilis 90
Syringomyelia 91
Tumors of the brain and spinal cord 92
Craniocerebral and spinal traumas 93
Signs of peripheral nerves affection 94
Tunnel neuropathies 97
Dysfunctions of pelvic organs 99
Disturbances of consciousness 102
Main clinical signs of tentorial impaction and impaction to the great 106
foramen
Main neurological terms 107
Drugs frequently used in neurology 115

4
 Foreword

Today clinical neurology occupies a leading place in medicine. Its development,

integration with other clinical sciences, differentiation into a number of individ-
ual branches made this science a basic one in training doctors of various spe-
cialties and broadened its limits. A large volume of neurology requires a skill to
be able to define the most important ideas. The selection and explanation of such
principal ideas was implemented in this manual. The purpose of this manual is
not to substitute the textbooks and scientific literatute but to help the doctor to
orient in a large group of neurological diseases, to emphasize the most essential
information. The book consists of charts, which generalize all areas of general
neurology as well as commonest diseases of the nervous system.
The book was prepared by prof. I.A.Grygorova, ass. prof. K.A.Leschenko, ass.
prof A.A.Grygorova, ass. prof. E.K.Reznichenko, ass. prof. O.A.Teslenko, ass.
prof. A.R.Eskin, ass. prof. L.V.Tikhonova, ass. E.L.Ibragimova.

Acknowledgement

The authors are thankful to the colleagues from Foreign Languages Department
for their help with the preparation of the manuscript.

5
 ANATOMY OF CORTICO-MUSCULAR TRACT

The impulses of voluntary movements go through a two-neuron cortico-muscu-

lar tracts, consisting of central and peripheral motor neurons.

Central (1st) neuron

Cortico-spinal tracts Cortico-nuclear tracts

Begins in upper and middle portions of the Begins in lower portions of the pre-
anterior central gyrus (Bets cells) central gyrus (Bets cells)
Forms anterior 2/3 of posterior thigh of the
Forms a knee of the inner capsule
inner capsule
In the brain trunk axons of the 1st neu-
Passing along the trunk, in the oblong brain ron approach to the motor nuclei of
cranial nerves on the both sides (ex-
80-85% of the fiber of the pyramid tracts go cept for the lower portion of the nu-
to the opposite side (crossing of the pyra- cleus of the VII and the nucleus of the
XII pair of the cranial nerves, which
mids) are supplied only from the opposite
side)
Further axons of the 1st neuron go through the
lateral trunks of the spinal cord (tractus cortico-
muscularis lateralis), each segment terminates
on the cells of the anterior horn. The rest of the
fibers which do not cross (15-20%) go along
their side in the anterior column of the spine
(tractus corticomuscularis anterior) and termi-
nate on the motor cells of the anterior horn
Peripheral(2nd) neuron
Motor nuclei of the cranial nerves
The peripheral neuron begins in the anterior
(III, IV, V, VI, VII, IX, X, XI, XII
horns of the spine (motor cells)
pairs of the cranial nerves)
Oculomotor, mastication, mimic
Anterior roots  common root  nervous
muscles, muscles of the pharynx, lar-
plexi  peripheral nerves  muscles
ynx and the tongue

6
 Pic.1. Pyramidal tract

Pic.2. Primary motor cortex

Disturbances of voluntary movements
(in affections of cortico-muscular pathway

7
 DISTURBANCES OF VOLUNTARY MOVEMENTS
(Paralysis and paresis)
Type of
Central (spastic) Peripheral (atrophic)
paralysis
In affections of the 1st (central) neu- In disturbances of 2nd (periph-
When occurs eral) neuron (anterior horn,
ron (corticospinal pathway)
root, plexuses, nerves)
Switching off deceleration influence Disturbances of integrity of
of upper portions on the spine, man- spinal reflex arches and ex-
Pathogenesis ifestation of spinal automatism clusion of trophic influence
of the anterior horns on the
muscles
- Spastic hypertonia of the muscles -Hypo (а-)trophy of the mus-
in the flexors of the arm and ex- cles
tensors of the leg with clasp- -Hypotonia of the muscles
knife sign -Hypo (а)reflexia
- Hyperreflexia of tendon (deep) re- -Degeneration reaction
flexes (changes in electrical excita-
Signs and - Reduction or disappearing of cuta- tion of the muscles)
symptoms of neous abdominal and plantar (su- -Electromyogra-phy:
paralysis perficial) reflexes Marked reduction of ampli-
- Pathological reflexes (Babinski’s, tude and velocity of impulse
Rossolimo, Oppenheim, Gordon, in the involved nerve
Schaeffer)
- Protective reflexes
- Clonuses
- Pathological synkinesias

8
 TOPICAL DIAGNOSIS OF VOLUNTARY MOVEMENT
(Syndromes of cortico-muscular tract disorders at various levels)

Levels of the disorder Syndromes of movement disorders:

1. Syndrome of loss of function: central
Anterior central gyrus of the brain monoparesis on the side opposite the focus
cortex 2. Irritation syndrome: Jacksonian motor
epilepsy
Central hemiparesis(plegia) with central
paresis of the facial and sublingual nerves
Internal capsule
on the side opposite the focus

Alternating paralysis: involvement of the cra-

Brain trunk nial nerve on the side of the focus and central
hemiparesis on the opposite side
Above the cervical en-
Central tetraparesis with sphincter disorders
largement (С1-С4)
Spinal Mixed tetraparesis: in the upper limbs - pe-
cord Cervical enlargement
ripheral, in the lower limbs – central with
(the (С5-Th1)
whole
sphincter disorders
trans- Lower central paraparesis with sphincter disor-
Thoracic spine
verse ders
section) Lumbar enlargement Lower peripheral paraparesis with sphincter
( L2-S1) disorders
Cone Sphincter disorders
Segment peripheral paralysis with fascicular
Anterior horn of the spinal cord. twitching on the side of the focus without
sensitivity disorders
Segment peripheral paralysis on the side of
the focus without sensitivity disorders, may
Anterior root
be fascicular twitching, fibrillations at elec-
tromyelography
Peripheral paralysis with sensitivity disor-
Peripheral nerve
ders in the zone supplied by the nerve

9
 EXTRAPYRAMIDAL SYSTEM AND ITS PATHOLOGY
(DISTURBANCES OF INVOLUNTARY MOVEMENT)

Evolution Neostriatum Paleostriatum

structures (younger) (older)
1. Pale globe
2. Black substance
3. Red nucleus
As well а) Luis body (epithalamus)
1. Caudate nucleus
as: б) upper portions of reticular
Struc- 2. Shell
formation
tures 3. Amygdaloid nucleus
в) Lamina tecti
4. Claustrum
г) Darshkevich's nucleus
д) blue spot
е) vestibular nuclei
ж) lower olive
Dysfunction of dopamin- Reduction of dopamine amount in the nigrostri-
Patho- ergic serotonin and other ate neurons, reduction of dopamine receptor sen-
genesis neurotransmission sys- sitivity, increase of caudate nucleus activity
tems
Synd- 1.Hyperkinetic syn- Hypokinetic-hypertonic syndrome
romes drome: (parkinsonism syndrome):
- athetosis 1. Hypokinesia («mask-like face», «flexion
- chorea position», acheirokinesis, shafting gait)
- hemiballism 2. Plastic rigidity of the muscles – even in-
- tics crease of the tone in all groups of the mus-
2. Hypo- or dystonic cles with cogwheel sign
syndrome: 3. Static tremor (head – “yes-yes” and “no-
- muscular dystonia syn- no” type, hands – coin counting, pill rolling)
drome 4. Posture instability (pulsions)
(see special chapter)

10
 Pic. 3. Extrapyramidal system.

Pic.4. Extrapyramidal system disorders

11
 CEREBELLUM AND ITS PATHOLOGY
Cerebellum is the organ of balance, coordination and muscular tone

Struc- Vermis Hemispheres Nuclei (located in the white matter of

ture (phylogenet- (phylogenetically the hemispheres)
ically older younger portion) - dentate nucleus
portion) - spherical nucleus
- emboliform nucleus
Regu- Mainly stat- Mainly coordination - nucleus of the fastigium
lates ics

Relations of the cerebellum and various divisions of the nervous system

Lower limbs connect Medial limbs connect het- Upper limbs connect the
homolaterally the erolaterally the brain cortex cerebellum homolaterally
spinal cord with the and the cerebellum through with the spinal cord through
cerebellum through the the pons the red nuclei and with ex-
oblong brain trapyramidal system and
reticular formation through
the visual
Include:
-posterior spino-cere- - Anterior spino-cerebellar
- Fronto-ponto-cerebellar
bellar (Flexig’s)
tract (Gowers’)
-fibers of thin and
tract
wedge-shaped nuclei, - Rubrocerebellar tract
olives, nuclei of
- Parieto-temporo-cerebellar (Monakov’s)
vestibulocochlear,
trigeminal and vagal - Vestibulospinal tract
tract
nerves, reticular forma-
- Reticulospinal tract
tion
- Static ataxia (deviation to the affection focus at Romberg’s test )
- Dynamic ataxia (disturbances of gait, intention tremor and failure at
finger-nose and knee-heel test)
Affection - Staccato speech (slow, by syllables, clipped)
- Nystagmus
syndromes - Changes in the handwriting (macrography)
- Muscular hypotonia
- Adiadochokinesis
- Asynergism, dysmetria

12
 Pic. 5. Cerebellar tracts

Pic. 6. Cerebellum anatomy

13
 TYPES OF ATAXIA

Sensitive Cerebellar
At affections of the posterior At affection of the cerebellum and its tracts (static
columns of the spinal cord, and dynamic):
multiple affection of the pe- - Romberg’s test shows deviations or falling to the
ripheral nerves (polyneu- side of affection
rotic), visual tuber (thalamic): -"cerebellar gait" – staggering gait with widely put
- "stamping gait" due to dis- legs
turbances of neuromuscular - nystagmus
feeling - staccato speech
- increase of symptoms when - intention tremor
visual control is absent - muscular hypotonia
- dysmetria, Babinski’s asynergism
- relatively low influence of the vision control on
the signs
Vestibular Cortical
On affection of the vestibular
apparatus and nuclei of the
VIII pair of the cranial
nerves: At affection of the cortex and corticocerebellar
- systemic dizziness tracts:
- nystagmus Deviation to the side opposite to the affection in
- parasympathetic reactions Romberg’s test, unsteady gait, especially on turn-
(nausea, vomiting, changes ing
in the heart rate, arterial Accompanied
pressure, color of the skin) - mental changes, grasp reflex (frontal lobe)
- increasing signs at sharp - olfactory disturbances (temporal lobe)
head movements - homonymous hemianopsia (occipital lobe)
- increased excitability of the - auditory and olfactory hallucinations (temporal-
vestibular apparatus (accord- occipital region)
ing to caloric tests)
- hearing disturbances on the
site of affection

14
 ANATOMY OF SENSORY TRACTS
Sensory impulses go from extero- and proprioceptors along three-neuron ways
of superficial and deep sensation

Tracts of superficial sensitivity Tracts of deep sensitivity

1st neuron – spinal ganglia (bipolar 1st neuron - spinal ganglia (bipolar
cells). The dendrites form peripheral cells). The dendrites form the periph-
nerves, go to exteroceptors; axons – pos- eral nerves, go to proprioceptors. The
terior roots go to posterior horns axons forming the posterior roots go to
the posterior columns of their side form-
ing Goll and Burdach tracts. Impulses
collected from the lower part of the body
are conducted by Goll tract. Starting from
the level of Th6 impulses are conducted
by Burdach tract
2nd neuron - posterior horns of the spine. 2nd neuron – Goll and Burdach nuclei in
Further through the white commissure 2-3 the oblong brain.. Further the axons go
segments higher the axons transit obliquely to the opposite side and join the medial
to the opposite side and go as a part of lat- loop.
eral columns (spinothalamic tract: anterior
– pain and temperature sensitivity, lateral -
tactile). They pass the brain stem and join
the medial loop.
3rd neuron – ventro-lateral nucleus of the 3rd neuron – ventrolateral nucleus of
thalamus. Further the axons pass the poste- the thalamus. Further the axons pass the
rior third of the posterior femur of the inner posterior third of the posterior femur of
capsule as a part of thalamocortical bundle the inner capsule and terminate in the up-
and as a radiation go to the parietal lobe per and median portions of the posterior
and terminate in the upper and median por- central gyrus
tions of the posterior central gyrus

15
Pic. 7. Sensory impulse pathways

Pic. 8. Somatosensory Map

16
 TOPICAL DIAGNOSIS OF SENSORY DISTURBANCES

Affection syn- Clinical signs

dromes:
Peripheral nerve Disturbances of all types of sensitivity in the zone of innervation,
pain, paresthesias
Intervertebral ganglia Segment anesthesia, pain, herpetic rash on the side of affection along the
peripheral nerve
Posterior root Segment anesthesia, pain, and signs of strain on the side of affection
(Wasserman, Lassag)
Posterior horn Segment-dissociated sensitivity disturbances (disturbance of pain and
temperature sensitivity at preserved deep types of sensitivity)
Lateral column of the Anesthesia of the superficial types of sensitivity on the opposite side
spinal cord 2-3 segment lower the focus of affection
Posterior cord Conductor disturbances of deep sensitivity from the level of affection,
sensitive ataxia on the side of the focus
Medial loop of the Hemianesthesia, hemiataxia on the opposite side
brain stem
Spinal cord (half of Brown-Sekhar syndrome: motor disturbances and disturbances of
transverse section) deep sensitivity on the side of affection, disturbances of superficial
sensitivity on the opposite side (conductor type)
Visual tuber Hemianesthesia, hemianopsia, hemiataxia, thalamic pains on the op-
posite side
Inner capsule Hemianesthesia, hemianopsia, hemiataxia and hemiplegia (paresis) on
the opposite side
Radiate crown Depending on the location of the focus, monoanesthesia on the op-
posite side is more common
Posterior central Monoanesthesia, on irritation – attacks of sensory Jacksonian epilep-
gyrus (brain cortex) sia on the opposite side

TYPES OF SENSITIVITY:

1. Superficial 2. Deep 3. Complex

1.1 pain 2.1 musculoarticular 3.1 discriminant

1.2 tactile 2.2 vibration 3.2 stereognostic
1.3 temperature (cold, hot) 2.3 sensation of pressure 3.3 two-dimensional-spa-
2.4 sensation of mass tial
2.5 kinesthesia 3.4. sense of localization
Types of sensitivity disorders:
Types of sensitivity disorders:
1. Anesthesia
1. Mononeuritic 2.Hyper-, hypesthesia
3. Hyperpathia
2. Polyneuritic 4. Paresthesia
3. Root 5. Polyesthesia
4. Segment-dissociated 6. Synesthesia
7. Disesthesia
5. Conductive

17
 1ST PAIR – OLFACTORY NERVE
n. olfactorius (sensory)

Main components of olfactory

Structures Affection signs
tracts
st
1. Olfactory receptors 1 neuron (in the nasal mucosa) - Hyposmia
2. Bipolar cells - Anosmia
3. Olfactory tracts - Hyperosmia
1. Olfactory bulb 2nd neuron (on the base of the - Dysosmia
frontal lobes)
2. Olfactory tract
Should be differenti-
1. Olfactory triangle rd
3 neuron At a unilateral affec- ated with olfactory
(primary disturbances of non-
2. transparent partition tion, olfactory disor-
subcorti- neurologic origin:
3. Anterior perforated cal olfac- ders are not obvious
tory cen- Respiratory
substance as their function is
ters) In pregnancy
4. Tracts over and un- compensated by the In poisoning with
chemical substances
der the corpus callo- center on the oppo-
In psychosis
sum, partially going to site side
the opposite
1. Hippocampus 1. Olfactory halluci-
2. Uncus Cortical olfactory center nations (irritation
3. Dentate gyrus (temporal lobe of the brain) syndrome)
4. cornu Ammonis 2. Olfactory agnosia

18
Pic. 9. Cranial Nerves.

Pic. 10. Olfactory nerve

19
 2ND PAIR OPTIC NERVE
n. opticus (sensory)
DEPARTMENTS:
1. Peripheral: rods and cones  bipolar cells  ganglia cells  proper nerve  chi-
asma  optic tract
2. Central: lateral geniculate bodies, upper tubers of the lamina quadrigemina,
cushion of the visual tuber (subcortical centers)
Grasolier fascicle (visual radiation)  calcarine fissure of the occipital lobe (corti-
cal analyzer)

Levels of affec- Signs of affection

tion
Nerve Amaurosis, amblyopia
Direct pupillary areflexia with unchanged consensual reaction
Atrophy of the optic nerve papilla
Chiasm Bitemporal or binasal hemianopsia
Loss of hemianoptic pupil reaction
Atrophy of the optic nerve papilla
Tract Contralateral homonymous hemianopsia
Loss of hemianoptic pupil reaction
Atrophy of the optic nerve papilla
Visual tuber Contralateral homonymous hemianopsia
Hemiataxia
Hemianesthesia
Internal capsule Homonymous hemianopsia
Central hemiplegia (Wernicke-Mann position)
Hemianesthesia
Hemiataxia
Central affection of VII and XII cranial nerves
Grasiolier Quadrantic hemianopsia
Fascicle Negative scotoma
Cortex of the Quadrantic hemianopsia
occipital lobe Complex visual hallucinations – macro-micropsia,
Metamorphopsia (irritation of occipiti-parieto-temporal re-
gion)
Simple visual hallucinations – photopsia (irritation of the area
of the calcarine fissure)
Visual agnosia

20
Pic. 11. Optic nerve pathway

21
 III PAIR – OCULOMOTOR NERVE
n. oculomotorius (mixed)

Located at the level of the upper tubercles of the lamina tecti

on the bed of aqueduct of Sylvius (upper stem – brain pedi-
cles)
Nuclei Parasympathetic (small-cell)
Motor
(paired large-cell) Yakubovich-Edinger
Perlia (un-
-
paired)
Westphal (paired)
Place of exit in
the base of the At an anterior border of the pons between the brain pedicles
brain
Musculus levator
palpebrae superioris
Supplying mus- Upper straight Musculus
Sphincter pupillae
cles Lower straight ciliaris
Median straight
Lower oblique
-Ptosis
-Absence of voluntary
upward, downward and -Mydriasis
- Accomoda-
Signs of affection inward movements of -Absence of reaction
tion paralysis
the eyeball to light
-Convergent squint
-Diplopia
Affection of the Signs of affection of the oculomotor nerve on the side of the
nerve nuclei (of focus
the brain stem) Central hemiparesis on the opposite side (alternating Webers
syndrome)

22
Pic. 12. Oculomotor group of nerves

Pic. 13. Oculomotor nerve’s disorders

23
 TROCHLEARIS AND ABDUCENS NERVES

IV pair – trochlear nerve VI pair – abducting nerve

n. trochlearis n.abducens
(motor) (motor)
Located on the bed of the rhom-
Located at the level of
Nuclei lower tubercles of the lam- boid fossa in the dorsal portion of
ina tecti (brain pedicles) the pons
Aside of the frenulum of
Place of exit on the superior medullary Between the pons and pyramid of
the brain base velum, then surrounds the the oblong brain
brain pedicle laterally
Supplied mus-
Upper oblique Lateral straight
cles
Convergent squint
Syndromes of Absence of voluntary movements
Convergent squint
the nerve affec- when looking outside
Doubling at looking down
tion Doubling at looking into the dis-
tance
Signs of affection on the side of
Affection of
the focus accompanied by central
the nerve nu-
hemiparesis on the opposite side
clei (of the
and peripheral neuropathy of the
brain stem)
facial nerve (Foville’s syndrome)

24
 V PAIR- TRIGEMINAL NERVE
n. trigeminalis (mixed nerve)

Nerve I – ophthalmic II – maxillary III – mandibular nerve, n.

branches nerve; nerve; n. Maxil- mandibularis, mixed branch; the
and zones n. ophtalmicus laris sensitive fibers supply the skin
of supply supplies the skin Supplies the re- of the lower jaw, lower lip, an-
of the forehead, gion of the up- terior portion of the auricle,
upper eyelid, an- per jaw, includ- acoustic meatus, mucous mem-
terior hair portion ing the teeth, brane, of the cheek, lower jaw,
of the head, inner wing of nostril, including the teeth, mucous
angle of the eye, upper eyelid, membrane of the tongue, dura
ridge of the nose, upper lip, nasal mater. Motor fibers supply
conjunctiva and mucosa, soft and mastication muscles (temporal,
cornea, dura hard palate, ton- mastication, lateral and medial
mater sils, dura mater lateral and medial pterigoideus),
musculus mylohyoideus and an-
terior belly of the digastric mus-
cle, m.tensor tympani.
Place of Upper orbit – Round foramen
entrance to supraorbital – infraorbital
Oval foramen – mental foramen
- exit from notch canal
the skull
Trigeminal bundle is located in the trigeminal cavity (splitting of the
I neuron dura mater in the area of the trigeminal impression on the anterior sur-
face of the temporal pyramid)
Sensitive nuclei: nucleus of the spinal tract – from the level of the su-
perior colliculi of the plate of the roof of through the whole stem to С II
(superficial sensitivity), nuclei of the midbrain tract (deep sensitivity),
nucleus of the trigeminal nerve pons – on the border of the upper and
middle thirds of the pons (tactile sensitivity)
II neuron
Motor nucleus of the trigeminal nerve – located in the posterior por-
tion of the pons (operculum)
The fibers of the II neuron cross the median line (lemniscus trigemi-
nalis), joining the median loop (lemniscus medialis), and as a part of
the latter reach the visual tuber
Ventrolateral nuclei of the thalamus. The fibers if the III neuron go
through the posterior part of the posterior femur of the inner capsule
III neuron
and terminate in the lower portions of the posterior central gyrus (pari-
etal lobe)

25
Pic. 14. Trigeminal nerve anatomy

Pic. 15. Trigeminal nerve pathology

26
 SIGNS OF TRIGEMINAL NERVE LESION

Disturbance of all types of sensitivity in the zone of inner-

vation of the respective branches
Usually severe fit-like pains in the back in the zone supplied
by the affected branch, pain in the place of exit of the af-
Affection of trigem- fected branch
inal nerve branches Reduction of corneal, supraorbital and mandibular reflexes
At affection of the motor portion – paresis of the mastica-
tion muscles on the side of the focus (deviation of the jaw,
disturbances of mastication, hypotrophy of mastication mus-
cles)
Spasmodic pain in the whole half of the face on the side of
affection
Disturbances of all types of sensitivity in the whole half of the
Affection of the face on the side of affection
trigeminal bundle Pain in the place of exit of the trigeminal nerve branches on
the affected side
Reduction of corneal, supraorbital and mandibular reflexes
Herpetic eruption in the zone supplied by the affected node
Nuclei of the spinal tract – causes dissociated type of distur-
bance in superficial sensitivity on the side of affection
Affection of the
Nuclei of the midbrain tract – ab- Sensitivity in the whole
sensitive nuclei of
sence of deep half of the face on the
the trigeminal nerve
Pons nuclei – reduction of tac- side of affection
tile
Hemihypesthesia of all types of sensitivity on the side of the
Affection of the face and trunk opposite to the affected focus
visual tuber Thalamic pains of a half of the face and trunk opposite to the
affected focus
Affection or irrita- Sensor Jacksonian epilepsy on the side opposite the focus
tion of the cortex Local zones: an- or hypesthesia on the side opposite the fo-
(lower portion of the cus
posterior central
gyrus)

27
 TRIGEMINAL NEURALGIA (neuropathy)

Atherosclerosis of the brain vessels, hypertension, narrow-

ing of the bone canals along which the nerve passes, den-
Etiology
tal diseases, diseases of the sinuses, demyelinating infec-
tious diseases, metabolic disorders, internal diseases
The disease develops like a multineuronal reflex due to
prolonged pathological pulsation from the periphery of
Pathogenesis
both specific and unspecific structures of the brain stem,
subcortical formations
- primary (essential)
Clinical forms
- secondary
Is accompanied by degenerative-dystrophic processes of
the respective branches of the trigeminal nerve, various
Pathomorphology
fibers are subjected to this, but in the majority of cases
these are small fibers
Glaucoma, reflected pains in the diseases of the internal
Differential diagnosis
organs, prosopalgias
Anticonvulsants (finlepsin, tegretol), analgesics, tranquil-
izers, desensibilizing (peritol, dimedrol, suprastin), meta-
Treatment
bolic drugs, reflexotherapy, acupuncture, laser therapy,
UHF-therapy, physiotherapy, surgery

28
 VII PAIR – FACIAL NERVE
n. facialis (mixed)
(discussed with the XIII pair – intermediate nerve, n.Wrisbergi)

I neuron Betz’ cells of the lower part of the central gyrus

Tracts Corticonuclear
II neuron Nuclei on the bed of the rhomboid fossa — tegmentum
of pons:
The upper potion of the motor nucleus receives cortical
innervation from the both sides, the lower portion of the
motor nucleus only from the opposite side.
Secretory parasympathetic nuclei
Common for the IX and X pairs
(n.tractus solitarii, n. salivatorius superior)
nuclei of the intermediate nerve
Cluster of parasympathetic cells
(innervation of the lacrimal gland)
The greater petrosal nerve – the lacrimal gland
The The nerve to stapedius muscle — the muscle of the
branches of stapedius
the nerve Tympanichord — the bulbs of the anterior 2/3 of the
and the sup- tongue; parasympathetic salvation fibers of the submaxil-
plied struc- lary and sublingual glands
tures Proper facial nerve — mimic muscles of the face, except
for the elevator muscle of the upper eyelid

29
Pic. 16. Facial nerve anatomy

Pic. 17. Facial nerve disorders

30
 SIGNS OF THE FACIAL NERVE LESION

Type of
Peripheral Central
paresis
The af- Anterior
central
fected Cerebral trunk gyrus
The facial nerve in Pontocere- Inner (lower
(nucleus of the
struc- the canal bellar angle capsule portion)
facial nerve)
tures

1. To the level of Paresis of 1.Millard- Paresis Paresis

the origin of the the whole Gubler syn- of the of the
greater petrosal half of the drome: lower lower
nerve: dryness of the mimic mus- paresis of the mimic portion
eye, hyperacusia, cles on the mimic mus- muscles of
taste disorders, pare- side of the cles on the and mimic
sis of the mimic mus- focus side of the fo- hemi- muscles
cles of the whole half Hearing cus, central paresis on the
of the face disorders on hemiparesis on the oppo-
2. To the level of the side of on the oppo- opposite site side
origin of the nerve of the focus site side side
Signs of stapedius muscle: Sensitivity 2.Foville’s
lacrimation, hypera- disturbances syndrome:
affec- cusia, taste disorders, in the half of paresis of the
paresis of the mimic the face on whole half of
tion muscles of the whole the side of the mimic
part of the face the focus muscles and
3. To the level of  Cerebellar convergent
origin of the tympani- ataxia on the strabismus on
chord: taste disorders, side of the the side of the
paresis of the mimic focus focus, central
muscles of the whole hemiparesis on
half of the face the opposite
4. In the place of side
exit from the canal:
paresis of the mimic
muscles of the whole
half of the face

31
 VIII PAIR OF THE CRANIAL NERVES
VESTIBULOCOCHLEAR NERVE
n. vestibulocochlearis (sensory)

Cochlear Vestibular
1. Auditory receptors – 1. Vestibular receptors of
Corti’s hair cells labyrinth (in ampullas semi-
1st neu- 2. Spiral node (in the st
1 neu- circular canals and two utri-
ron cochlea of the labyrinth) ron cles)
2. Vestibular ganglion (inter-
nal auditory canal
Proper cochlear nerve in the Proper vestibular nerve (in
inner auditory canal and the the internal auditory canal)
Tracts root of the cochlear nerve in Tracts The root of the vestibular
the pontocerebellar angle nerve (pontocerebbellar an-
gle)
2nd neu- Cochlear nuclei of the 2nd neu- Nuclei of the pons: lateral,
ron ppons – ventral and dorsal ron medial, upper, lower
Lower tubers of the With the spine
quadrigeminal plate With cerebellum
Medial geniculate body With the nuclei of the oculo-
3rd neuron
Cortical auditory centers Connec- moter nerves
(primary
(medial portion of the upper tions of With the dorsal nucleus of the
subcorti-
temporal gyrus of the both the vagal nerve
cal audi-
hemispheres – bilateral corti- vestibular With reticular formation
tory cen-
cal connection) nuclei With the structures of the ex-
ters)
trapyramid system
With the cortex of the greater
hemispheres
Anacusion Vestibular syndrome (dizzi-
Hypoacusion ness, nistagmus, disturbance of
Hyperacusion balance and coordination, veg-
Signs of Auditory hallucinations at Signs of etative disorders, nausea, vom-
affection irritation of the cortical cen- affection iting, etc. )
ters
Auditory agnosia at cortical
auditory nerves affectionв

32
Pic. 18. Vestibulocochlear nerve anatomy

Pic. 19. Vagus nerve anatomy

33
 BULBAR GROUP OF CRANIAL NERVES
(GLOSSOFARINGEAL, VAGUS, ACCESSORY, HYPOGLOSSAL)

IХ pair – ХI pair – ac-

ХII pair –
Glossopharyngeal Х pair – cessory nerve
sublingual
nerve Vagus nerve n. n. Accesorius
nerve n. Hy-
n. glossopharyn- Vagus (motor)
poglossus
geus (mixed)
(motor)
(mixed)
Is located in the tentorium of the oblong brain
Long motor nu- Motor double nu- Motor nucleus Motor nu-
cleus (common cleus (common of the accessory cleus
with Х) with IХ) nerve
Nucleus of general Sensory (common
nuclei sensitivity (com- with IХ)
mon with ) Visceral
Taste nucleus of (parasympathetic)
the solitary tract Nucleus of the
Lower salivation solitary tract
nucleus
5-6 roots outside 12-16 roots behind Cranial roots – 10-15 roots
and behind the the olives (under behind the between the
Place
olives the glossopharyn- olives, spinal – pyramid and
of ori-
geal nerve ) from the lateral oliva
gin on
funicle of the
the
spine between
base
the anterior and
posterior roots
Muscles of the Muscles of the Sternocleido- Genioglossal,
pharynx pharynx, larynx, mastoid, upper hyoido-
Taste on the poste- vocal cords. portion of glossal, trans-
Sup- rior third of the Sensitivity of the trapezius mus- verse sty-
plied tongue dura mater, poste- cle loglossus,
struc- Secretion of the rior fossa, external transverse
tures salivary gland auditory meatus muscle of the
and posterior sur- tongue
face of the auricle.
Inner organs

34
Fig. 20. Accessory nerve anatomy

Pic. 21. Hypoglossal nerve anatomy

35
 SIGNS OF DAMAGE OF BULBAR GROUP OF CRANIAL NERVES
(BULBAR AND PSEUDOBULBAR SYNDROMES)

IХ pair – Х pair– ХI pair – ХII pair –

glos- Vagus nerve accessory Sublingual nerve
sopharyn- nerve
geal
Anesthe- 1. At unilat- Atrophy of 1. Central paresis: deviation of
sia of the eral affection the sup- the tongue to the side op-
mucous : plied mus- posite to the focus
membrane - the soft palate cles, caus- 2. Peripheral paresis:
of the up- hangs down ing asym- a. in unilateral affection:
per phar- on the side of metry of - Atrophy of the muscles of
ynx affection the shoul- the half of the tongue
Dyspha- - pharyngeal der girdle ("geographic tongue)
gia, taste reflex is re- and diffi- - Fibrillar twitching
distur- duced cult turning - deviation of the tongue to
bance - dysphonia of the head the side of affection (the
Signs of Dryness 2. At bilateral to the unaf- tongue “points” to the focus)
affection in the affection: fected side б. In bilateral affection:
mouth - paralysis of - glossoplegia
the soft - dysarthria, dysphagia
palate (as- - atrophy and fibrillar twitch-
phyxia) ing of all muscles of the
- aphonia tongue
- aphagia 3. Alternating Jackson’s syn-
3. At irritation drome: homolateral central
of the nerve: paresis of the XII pair with
bradycardia, contralateral central hemi-
increased paresis
peristalsis.
Signs of
affection Bulbar syndrome:
of the nu- Dysarthria, dysphagia, dysphonia, paresis of the soft palate, liquid
clei of the food poors out of the nose, atrophy and fibrillar twitching of the
oblong tongue muscles
brain
Signs of
bilateral Pseudobulbar syndrome:
affection Dysarthria, dysphagia, paresis of the soft palate, absence of atrophia
of corti- and fibrillar twitching of the tongue muscles, but pathological re-
conuclear flexes of oral automatism, forced laugh and cry are present
tract

36
 ANATOMY OFAUTONOMIC NERVOUS SYSTEM
Suprasegmental Segment VNS
VNS sympathetic parasympathetic
Nuclei of the cranial
Anato- Hypothalamus, cin- Neurons of lateral
nerves (III, VII, IХ, Х)
my gulate gyrus,, hip- horns of С8 – L2
Neurons of lateral horns
pocampus, amyg- Paravertebral or pre-
of sacral segments
daloid complex, vertebral nodes and
Prevertebral and intramu-
reticular formation plexuses
ral ganglia or plexuses
Func- Vegetative dystonia
tion dis- syndrome: Peripheral nerve affection:
tur- Types of the course: a. Vegetative trophic disturbances in the inner-
bance 1. Permanent vation zone (dryness of skin, fragile nails)
а. Vegetovascular b. Vegetative vasomotor dysidrias (edemas,
dystonia cyanosis, marble skin in the zone of innervation)
b. Neurogastric dys- c. sympathalgia in the zone of innervation
tonia polyneuropathy:
c. hyperventilation d. Vegetative trophic disturbances in distal por-
syndrome tions of the extremities
d. Thermoregulation e. Vegetative vasomotor disturbances in distal
disturbances portions of the extremities
e. Combined affec- f. sympathalgia in the distal portions
tions vegetative ganglia and plexuses: - sympathalgia
2. Paroxysmal affection of the lateral horn: Vegetative trophic
a. Sympathoadrenal disturbances in the respective segments
crises loss of function of cervical sympathetic innerva-
b. Vagoinsular tion of the eye (C8 - Th1):
crises Horner’s syndrome (ptosis, myosis, enopthal-
c. mixed crises mus),
3. Hypothalamus Affection of parasympathetic nuclei of the III pair
syndrome of cranial nerves.:
а. Neuroendocrine Mydriasis, accomodation disturbances
syndrome Affection of lacrimation nuclei of the fibers of the
b. Motivation dis- VII pair.:
turbances lacrimation disturbances
c. sleep and vigi- Affection of salivation nuclei and fibers of the
lance disturbance VII, IX, X pairs:
d. permanent vege- salivation disturbances
tative dystonia

37
Pic. 22. Autonomic nervous system

38
 PATHOLOGY OF AUTONOMIC NERVOUS SYSTEM

Etiology : -constitution
-against a background of endocrine changes in the organism
-in primary affection of visceral organs
-in primary diseases of peripheral endocrine glands
-allergy
-pathology of segment peripheral nervous system
-organic diseases of the brain
-neurosis
Syndromes : 1)cardiovascular 5)sexual dysfunction
2)hyperventilation 6)thermoregulation distur -
bances
3)neurogastric asternia 7)sleep disorders
4)perspiration disturbances
Types of Permanent Paroxysmal mixed
course
Vegetative Sympathoadrenal Vagoinsular mixed
crises
(“panic at-
tacks”)
Clinical pic- Unpleasant sensations dizziness, nausea, de- Signs of sympa-
ture in the chest and head, creased AP, brady- thetic and
tachycardia, increased cardia, extrasystole, parasympathetic
AP, mydriasis, chill- difficult breathing, activation which
like hyperkinesis, sen- gastrointestinal dysk- develop simulta-
sation of fear, anxiety, inesia neously or alter-
the attack end with nate
polyuria with light
urine
Treatment Tranquilizers (sibason, Tranquilizers, tranquilizers, bel-
relanium), valocardin, Cholinolytics (atron- loid,
corvalol, ine sulphate, platifill- bellaspon, bel-
- blockers (pyrroxan, ine hydrotartrate, lataminal,
fentolaxin), -blockers amizid, cyclodol, bu- antidepressants
(anaprilin, trasicor), tiroxane), antidepres- (Zoloft, Paxil,
antidepressants sants Prozac).

39
 THE BRAIN CORTEX AND DISTURBANCES OF
HIGER COTICAL FUNCTIONS

Irritation syndromes LOBES Deficiency syndromes

Motor aphasia, monoparesis,
monoparalysis (anterior central
gyrus); frontal ataxia, agraphia,
Motor Jacksonian epilepsy
Frontal lobes behavior disturbances, catching
(anterior central gyrus)
phenomenon (Yanishevky’s re-
flex), visual paralysis, anosog-
nosia
Auditory and olfactory hal-
Sensor aphasia,, alexia, amnestic
lucinations, combines visual
Temporal lobes aphasia, agnosia (olfactory, audi-
hallucinations (metamor-
tory, taste)
phopsia)
Sensor Jacksonian epilepsy Hypo- or anesthesia of mono-
(posterior central gyrus) Temporal lobes type, astereognosis, alexia,
apraxia, acalculia
Simple visual hallucinations Visual agnosia, homonymous
(photopsia) Occipital lobes quadrant hemianopsia, color ag-
nosia
Peculiarities of signs of interhemispheric asymmetry
Disturbances of logical and verbal thinking, apha-
Left hemisphere
sia, agraphia
Disturbances of emotional artistic activity and cre-
Right hemisphere
ative thinking

40
 MAIN TOPICAL NEUROLOGICAL SYNDROMES

Mononeuritic
Polyneuritic
In peripheral nervous system diseases
Plexitis
Radicular
Posterior horn, segment-dissociated
Anterior horn
Lateral horns
Anterior gray adhesion
In spine diseases Conductive posterior trunk
Conductive of the lateral trunk
Half of the cross-section (Brown-Se-
quard syndrome)
Complete cross-section
1. Truncal
- bulbar
- alternating
2. Pseudobulbar
3. Thalamic
4. Hypothalamic
5. Extrapyramidal
6. Internal capsule
In diseases of the brain and meninges
7. Cortical :
- frontal
- parietal
- temporal
- occipital
- combined
8. Meningeal

41
 SCHEME OF PATIENT EXAMINATION

Demographic data
History tak-
Complaints
ing
History
Objective General condition Neurologic examination:
examination 1. appearance of the patient 1. consciousness examina-
2. stature tion
3. skin 2. cranial nerve examination
4. skeletal system 3. sensory testing
5. muscular system 4. system of involuntary
6. respiratory system movements
7. cardiovascular system 5. system of voluntary
8. digestive system movements
9. genitourinary system 6. coordination and posture
10. endocrine system 7. vegetative system
8. higher nervous activity
9. mental state
Additional Laboratory: general clinical, biochemical, immunological, muscle
examinations biopsy.
Instrumental: electroencephalography, rheovasography, echo-en-
cephalography; electromyography, transcranial doppler study; ra-
diography of the skull and spinal column, computed tomography
and magnetic resonance imaging, positron emission tomography,
angiography, myelography, ophthalmoscopy
Topical diagnosis
Presumptive clinical diagnosis
Summary of the neurological condition
Differential diagnosis
Final clinical diagnosis
Methods of prevention and follow-up
Assessment of ability to work
Filling-in the case history

42
 HEADACHE
Etiology  acute and chronic diseases of the brain vessels
 diseases of vegetative nervous system (vegetative dystonias)
 neurosis
 diseases of peripheral vegetative structures
 general infectious diseases and infections of the brain and meninges, as
well as eye, ENT
 head injuries
 brain tumors
 dysmetabolic disorders and brain hypoxia due to somatic diseases
 drugs (nitrates, calcium agonists, antibiotics, oral contraceptives,
etc.),prolonged administration of analgesics
Mechanisms of
headache: Main clinical signs Treatment principles
1. Vascular Feeling of heavy head in the morning or after Venotonic drugs
long lying. The pain reduces after active move-
ments of the muscles in the shoulder girdle.
- venous
Swelling of the eyelids, sometimes in the morn-
ing

Calcium antagonists, er-

- vasomotor Pulsing headache
gotamine drugs

Antiaggregants (aspirin,
curantil, Ticlid)
- ischemic hy-
Pressing dull headache Drugs influencing micro-
poxic
circulation (Trental, nico-
tinic acid)
2. Liquor dy- Распирающий headache accompanied by nau-
namic sea, vomiting, syncope
Pain at movement of the eyeballs
At marked hypertension the volume of eyeball
-intracranial hy- movement is reduced, diplopia, strabismus,
Dehydration therapy
pertension (hyper- congestion in the fundus
production of Signs of intracranial hypertension on the
liquor, distur- EchoEG, CT, MRI
bances of liquor Improvement of general condition after dehy-
outflow) dration
-intracranial hy- The pain increases at standing up, walking, and
Hydration of the organ-
potension decreases when the patient lies ism
Reflective actions
Squeezing headache with sensation of “tight
3. Strain cephal- Sedatives
hat” which develops after emotional, mental
gia (neurotic) Tranquilizers
overstrain, long stay in the same position
Myorelaxants
Carbamazepine drugs
Paroxysmal short unbearable pain in the zone
Analgesics
4. Neuralgic of innervation of the respective nerve with
Reflex treatment
presence of “trigger” zones.
(acupuncture)
5. Psychalgia
Pain of “hysteric type” or constant slight pain
(pain as equivalent Antidepressants
which does not limit ability to work
of depression)

43
 Pic. 22. Types of headache.

Pic. 23. Migraine pathophysiology

44
 MIGRAINE

Migraine (hemicrania) – paroxysmal pain in one half of the head (in the area
of the temple or back of the head), is accompanied by vomiting,
photo- and phonophobia
Etiology 1. Hereditary constitutional factors (characteristics of autonomic
humoral regulation and reaction to environmental factors are inher-
ited)
2. factors which provoke the onset of the disease: emotional, en-
docrine, toxic, allergic, food rich in tyramine
Pathoge- 1. Neurogenic mechanisms (generalized disturbance of central vaso-
nesis motor regulation due to adrenergic insufficiency)
2. Humoral mechanisms (due to changes in the amount of vasoactive
substances: serotonin, tyramine, histamine, bradykinin,
prostaglandins, estrogens, etc.).
3. Trigeminal-vascular theory
Clinical 1. Migraine without aura – unilateral throbbing pain in the orbital-
picture frontal-temporal region , accompanied by nausea, vomiting, photo-
and/or phonophobia, lasting for 1 or several hours and days.
2. Migraine with aura (associated) – headache with focal neurologi-
cal signs depending on the form:
- ophthalmic (classical) - ophthalmoplegic
- hemiplegic - basilar

Diagnosis
The diagnosis is made clinically:
Paroxysmal course
Unilateral cephalgia
Throbbing pain
Complete regression of the focal signs (in associated form)
Satisfactory condition between the attacks
Absence of CT and MRI foci
History of at least two attacks for migraine with aura and five at-
tacks for migraine without aura
presence of at least one of the accompanying conditions: nausea,
vomiting, photo- and phonophobia

45
 Continuation

 with acute disturbances brain circulation, including

aneurysm rupture
 with mass
Differential
 with inflammatory ENT diseases
diagnosis
 with temporal arteritis
 with trigeminal neuralgia
 with glaucoma

1. During the attack

 Acetylsalicylic acid with coffeine
 Ergotamine drugs
 Antihistamine drugs
 Tranquilizers and antidepressants
 Serotonin receptor agonists (sumatriptan)
 Dehydration
 Corticosteroids
 Anticonvulsants
Treatment
2. Between the attacks (at frequent attacks at least 2-3 per month)
 Serotonin antagonists
 Calcium antagonists
 Antihistamine drugs
 Β-adrenoreceptor blockers
 antidepressants
 diet with limited amount of tyramine-containing foods (choco-
late, citrus, smoked food, cheese)
 reflex-therapy

46
 SYNDROMES OF INTRACRANIAL HYPOTENSION

Therapeutic and diagnostic interventions of the

liquor system
Lliquor fistula with liquorrhea
Disturbances in the water-salt metabolism (fre-
Etiopathogenetic fac- quent vomiting, diarrhea, forced diuresis)
tors Rreduced liquor production (following brain
injury, due to sclerosis of vessels in the plexus
of the chorioid artery, as a result of autonomic
dysregulation)
Arterial hypotension
Headache, often gripping in character
Desire to hang the head
Subjective data Nausea or vomiting
General malaise
Meningeal signs
Sparing position of the head
Tachycardia
Clinical and instru-
Reduced pressure at lumbar puncture
mental data
Augmentation of all the symptoms in the verti-
cal position and their alleviation in the recum-
bent one or when hanging the head

47
 SYNDROME OF INTRACRANIAL HYPERTENSION

Increased Increased Troubled out-

Reactive Troubled
intracranial liquor flow of liquor
Etiopatho-
space (ede- cerebral venous out- from the ven-
genetic fac- produc-
mas, tricular cerebral
tors edema flow
hematomas, tion system (oc-
abscesses clusal hydro-
etc.) cephaly)
Headache of obturating Nausea, vomiting
nature, feeling of eye- Dizziness (optional
Subjective (increased when
ball pressure, feeling of symptom)
data
"sand in the eyes", changing body po-
painful sensations at
sition)
eye movement
Changed pulse and Mental disorders
Lesion of the cranial with expressed hy-
Clinical breath, other vis-
nerves (mainly pair VI) pertension (progress-
findings
cerovegetative dis- ing functioning, dor-
mancy, stupor,
orders
coma)
Modified cranial Stagnant
Enlarged ven- X-ray photo-
graphs: discs of
Findings of tricular com-
Increased pressure increased digital optical
instrumen- plex in impressions
in lumbar puncture osteoporosis of nerves
tal studies EchoEG and
ephippicum (in oph-
CT increased vascu-
lar picture thal-
spread of sutures moscopy
in children

48
 TRANSIENT DISORDERS OF CEREBRAL BLOOD CIRCULATION
disorders of cerebral blood supply in which cerebral dysfunctions regress in 24 hours

Hypertension, atherosclerosis of cerebral vessels, vasculitis of vari-

Etiology ous etiology, blood diseases, anomalies of cerebral vessels (malfor-
mations) cardial pathology, cervical osteochondrosis etc.
Spasm or paresis of cerebral vessels (local or general); ischemia and
Pathoge- hypoxia of cerebral tissue; changes of physical and chemical prop-
nesis erties of blood.

1. Transient ischemic attacks

Symptoms depend on the vascular basin involved:
- carotid system (contralateral mono- hemiparesis, mono- hemihy-
pesthesia, aphasia, cross optical pyramidal syndrome, syndromes of
cortical affection)
- system of spinal and basilar arteries (vestibular-atactic, cerebellar
syndrome, visual disorders, bulbar disorders, alternating syndrome)
Basic clini- 2. Transient disorders of cerebral circulation of hypertonic crisis
cal symp- type.
toms a) general cerebral symptoms (headache, noise, tinnitus, asystemic
dizziness, obnubilation, weakness, vasomotor reactions, psychomo-
tor excitement), cervical sympathalogical syndrome (hot feeling in
the back of the head, neck, scalp, paresthesia in extremities)
b) combination of general cerebral with local symptoms, connected
with disorder of circulation in systems of carotic, spinal and basilar
arteries

Somatic, neurologic and ophthalmologic investigations, x-ray, REG,

Diagnosis EEG, EchoEG; blood count etc.

With vegetative-vascular crises

With suprarenal crises
Differential With solar crises
diagnosis With epileptic and non-epileptic paroxysmal conditions
With hypertension-hydrocephalic crises
Principles of Normalization of arterial pressure, heart activity, improvement of
treatment blood flow and metabolism of brain, anticoagulants, neuro and an-
gioprotectors, symptomatic means after indications

49
 ACUTE HYPERTENSIVE ENCEPHALOPATHY

Etiology Hypertensive disease

Spasm of peripheral cerebral arteries and veins, brain edema,
Pathogenesis ischemia and hypoxia of the brain tissue; changes in the physic-
ochemical properties of the blood

Increased blood pressure ( 200/120 mm Hg), local and general-

ized convulsions, disturbances of consciousness (torpor, sopor,
Main clinical
coma, psychomotor excitation, twilight states of consciousness),
manifestations
meningism (meningeal symptoms owing to an irritation of the
meninges)

Somatic, neurological and ophthalmological studies, radiogra-

Diagnosis phy, REG, EEG, EchoEG, transcranial doppler ultrasound, CT,
coagulogram and other investigations

With autonomic vascular crises

With adrenal crises
Differential diag- With solar crises
With epileptic and nonepileptic paroxysmal states
nosis With hypertensive-hydrocephalic crises
With a subarachnoid hemorrhage
With a brain tumour
These include antihypertensive drugs (normalization of the
blood pressure), anticonvulsive therapy, antiedemic therapy,
Principles of normalization of the activity of the heart, improvement of the
treatment blood flow and metabolism in the brain, anticoagulants, neuro-
and angioprotectors, symptomatic remedies according to indica-
tions

50
 Pic. 24. Ischemic stroke pathogenesis

Pic. 25. Hemorrhagic stroke pathogenesis

51
 ACUTE DISTURBANCES OF CEREBRAL BLOOD CIRCULATION
(strokes)

Essential hypertension, cerebral atherosclerosis, vasculitis, cardiac pathology (cil-

iary arrhythmia, atrial fibrillation, etc.), diseases of the blood, abnormalities of the
Etiology
cerebral vessels, injuries of the cerebral vessels and meninges, cervical osteochon-
drosis, vegetative vascular dystonia
In hemorrhages: In ischemia (infarct):
Pathoge- - rupture of vascular wall or aneurysm - occlusion of a vessel as a result of
nesis - increased permeability of the vascu- thrombosis, embolism
lar wall: diapedesis - vasospasm or vasoparesis
Parenchymatous – hemorrhage into Thrombotic – as a result of thrombosis
the brain substance Embolic – as a result of embolism with
Subarachnoid – hemorrhage into the atheromatous plaques or thrombotic
Classifica-
submeningeal space masses
tion
Subarachnoid-parenchymatous Nonthrombotic – as a result of vasospasm
(mixed) or vasoparesis
young and middle age, increased old age, normal or elevated blood pressure,
blood pressure, the somatic status has the somatic status has symptoms of
signs of arterial hypertension, the de- atherosclerotic lesion, cardiac arrhythmia;
velopment is apoplectiform; the con- the symptoms appear gradually or
Leading sciousness may be changed both by abruptly, the consciousness is not dis-
clinical the suppressive and productive type; turbed, rarer its disturbance is short-term;
manifesta- there is manifestation of general cere- focal signs prevail over the general cere-
tions bral and focal signs, hormetonias; bral ones, meningeal signs are absent;
meningeal signs, compression and dis- signs of dislocation are absent or appear
location of the brain are observed; the slowly, the liquor is unchanged
liquor may be xanthochromic or hem-
orrhagic
Somatic, neurological and ophthalmological studies, CSF diagnosis, radiography,
magnetic resonance imaging and CT, positron emission tomography, angiography,
Diagnosis
REG, EEG, EchoEG, coagulogram, other investigations according to indications

Differen- To differentiate the character of the stroke, to exclude coma of somatic genesis,
tial diag- brain tumour, acute neuroinfections and infectious diseases with severe course
nosis
Undifferentiated treatment (irrespective of the character of the stroke) envisages
normalization of the blood pressure, cardiac activity, respiration, measures against
brain edema, hyperthermia, disturbances in fluid-electrolyte balance, neuroprotec-
tors, diet and care.
Differentiated treatment. The most effective one is within the first 1-3 hours
Principles
after stroke development, at the stage of penumbra, before some irreversible
of treat-
changes in neurons take place (“therapeutic window”).
ment
In hemorrhages, the treatment includes coagulants and angioprotectors, in subarach-
noid hemorrhages – calcium antagonists (Nimotop), in infarcts – thrombolytics (at
the conditions of PET under a strong control over hemostasis within the first
hours), anticoagulants, antiaggregants, calcium antagonists. Surgical treatment of
hemorrhagic stroke according to strict indications.

52
 ACUTE DISTURBANCES OF SPINAL BLOOD CIRCULATION
HEMORRHAGIC DIS-
ISCHEMIC DISTURBANCES OF SPINAL CIRCU-
TURBANCES OF SPINAL
LATION
CIRCULATION
1) Cardiovascular diseases (congenital– Spinal injury, essential hy-
etiology arteriovenous malformations, aneurysms, pertension,
aorta coarctations, hypoplasia of spinal ves- Anomalies of the spinal
sels. Acquired –essential hypertension, aor- vascular system(arteriove-
tic branches atherosclerosis, arteritis, nous malformations)
phlebitis, insufficiency of blood in myocar- Hemorrhagic diathesis,
dial infarction, ciliary arrhythmia.) Infectious vasculitis, etc.
2) Compression factors (compression of
the aorta and its branches with tumors,
metastases, lymph nodes, uterus in preg-
nancy. Compression of radiculospinal arter-
ies and radicular veins with disk hernia, epi-
and subdural tumor, inflammatory infiltrate,
etc.)
3)iatrogenic factors (myeloischemia as a
complication of surgery, prolonged com-
pression or plastic surgery of the aorta with
exclusion of intercostal and lumbar arteries,
operations in the paravertebral area, injec-
tions – epidural blockades, spinal anesthesia)

pathogen- Rupture of the wall of the

esis Thrombosis, embolism, compression. vessel or aneurysm, in-
Vasospasm, vasoparesis creased permeability of the
vascular wall (diapedesis)
classifica- Hemorrhagic spinal stroke
tion Transient distur- Ischemic spinal (hematomyelia, spinal sub-
bances of spinal stroke. arachnoid hemorrhage, hem-
circulation. orrhagic infarction

53
 Continued
Focal signs depending on localization of the focus
along the certain spinal structures and across transverse section of the
spinal cord.
1. motor disorders in the form of spastic, atrophic or mixed para- or
tetraparesis, paralysis
2. Segment and conductive sensitivity disorders
3. Sphincter disorders
Vegetative-trophic disorders
Transient distur- Ischemic spinal Hemorrhagic disturbances of
bances of spinal stroke. spinal circulation 1) the de-
circulation. 1) Stroke develop- velopment is frequently pre-
Focal spinal signs ment may be pre- ceded by sudden physical or
subside within 24 ceded by a period of mental overstrain, injury
Main clini- hours pre-cursors (myelo- 2) acute development (suba-
cal manifes- 1) drop syndrome genic intermittent cute is possible if the source
tations 2)Unterharn- claudication, transient of hematoma is microan-
sheidt’s syndrome paresis, sensitivity gioma)
3)myelogenic in- disturbances, tran- 3) characterized by intensive
termittent claudi- sient sphincter disor- pain of segment character (in
cation ders, radiculalgia etc. subarachnoid hemorrhage
4 caudogenic in- 2)development – knife-like pain)
termittent claudi- from sudden (in em- 4) fever is possible
cation bolism or acute com- 5) in subarachnoid hemor-
pression of the ves- rhage – meningeal signs,
sels) to several hours general cerebral signs are
and days possible
3)characterized by 6) blood in the CSF
subsiding the pain
(after myeloischemia
development
Neurologic examination, CSF analysis, selective spinal angiography,
Diagnosis CT, MRI, spondylography, myelography,
Differential Differentiate the character of the stroke, exclude acute meningitis, mul-
diagnosis tiple sclerosis, tumors, medullar metastases, poliomyelitis

54
 Continued
Principles Undifferentiated treatment – normalization of respiratory function and
of treat- heart activity, BP correction, prevention of spinal cord edema (mannitol,
ment Lasix), neuroprotectors (pirazetam, vitamin E, antiglutamate prepara-
tions), antibacterial drugs for secondary complications prevention (pneu-
monia, cystitis, urosepsis). Bedsores prevention.
Treatment of ischemic spinal circulatory disturbances. Thrombolytic
drugs (first 4 – 6 hours), anticoagulants (heparin, fractiparin), drugs im-
proving collateral blood circulation, spasmolytics (papaverine, eu-
phylline, cavinton), drugs improving microcirculation (rheopolyglukin,
nicotinic acid, antiaggregating agents (Ticlid, acetylsalicylic acid com-
bined with dipyridamole, pentoxifylline), calcium antagonists
(stugerone, cinnarizine, Nimotop, nemotane).
Tanakan (drug of complex effect), actovegin, cerebrolyzin (improving
brain tissue metabolism).
In cases of spinal vascular compression disturbances the treatment is di-
rected to constriction elimination.
In discogenic process orthopedic and physiotherapeutic measures are ad-
ministered (close bed, spine stretching, orthopedic corset, massage). In
case of failure of drug and orthopedic treatment they determine indica-
tions for surgical treatment.
Neurosurgery in patients with intra- and extravertebral tumors.
Surgery in case of aorta damage (coarctation, atherosclerotic aneurysm).
Treatment of hemorrhagic spinal circulatory disturbances. Complete
rest in an acute state, coagulants (mostly with angioprotective effect –
dycinon, ethamsylate), angioprotective drugs – acetylsalicylic acid, as-
corutine, calcium antagonists (Nimotop, nemotane).
Spinal punctures – in subarachnoid hemorrhage.
In spine trauma with extensive hematoma – surgical treatment.
In all kinds of spinal circulatory disturbances – symptomatic therapy, in
a recovery period – physiotherapeutic procedures, therapeutic physical
training , massage.

55
 SOMATONEUROLOGICAL SYNDROMES
 Toxic action of somatic pathology and metabolic disturbances in
Main nerve tissue associated with it.
mecha-  Hypoxia caused by insufficient oxygen supply and cerebral metabo-
nisms of lism disturbances.
develop-  Pathologic reflex effects from damaged organs and tissues, which
ment result in fermentative and mediator nervous system activity distur-
bances.
 Distal
 Hyperglycemic
polyneuropa-
encephalopathy
thy and  Hypoglycemic
(asthenia syn-
polyneuropa- encephalopathy
drome, thirst,
Diabetes thy of cere- (syncope, anxiety,
polyneuropathy,
mellitus brospinal delirium, epileptic
vestibulopathy,
nerves fits, agitation, hal-
In en- acetone odor
 Angiopathy lucinations)
docrine from mouth,
of brain ves-
diseases polyuria, coma)
sels
 Myopathy  Paroxysmal my-
Hypothy- syndrome  Polyneuropathy oplegia
roidism with pseudo- syndrome  Pseudomyotonic
hypertrophy syndrome
Thyroto-  Myasthenia  Neurostenoid syn-  Myopathy syn-
xicosis syndrome drome drome
Pernicious
 Funicular myelosis (central pareses, pareses
anemia
nervous system disorders causes formation of infiltrates
of different localization with compression causing
In hema- Leukemia myelitic and meningeal syndromes, epileptic fits and pos-
tologic sible development of hemorrhagic cerebral stroke
diseases
Against a background of neurological disorders there are
Hodgkin’s infiltrates affecting as compression and causing spinal
disease cord damages resembling spinal tumors

56
 Table continued
In respi- lung diseases betalepsia venous hemo- polyneuropa-
ratory (pneumonia, brain abscess dynamic impair- thy hypoxia
diseases bronchiectatic metastases to ment psy- meningeal
disease, lung the brain and chomotor excite- syndrome
abscess, lung spinal cord ment
cancer)
chronic bron- hypoxic venous encephalopathy (headache, vertigo,
chitis syncope etc.)
In gas- gastritis, duo- polyneuropa- asthenic syn- encephalopa-
troin- denitis, ulcera- thy drome thy  vegeta-
testinal tive diseases, tive vascular
diseases gastroentero- dystonia
colitis
liver diseases encephalopa- impairment of radicular syn-
thy,asthenic syn- the nd pair cra- drom hyperki-
drom nial nerves netic syndrom
Pathol- encephalopathy secondary renal acute impair-
ogy of  neurasthe- hypertension ment of cerebral
liver nia-like syn- paroxismal circulationure
drome myoplegy mic coma
Heart Coronary artery  encephalopa- syncope (in- transient is-
and aorta disease, ar- thy with asthenic cluding Mor- chemic attacks
diseases rhythmia, my- state, au- gagni-Adams- acute impair-
ocarditis, car- tonomovascular Stokes syndrom) ment of cerebral
diac anomaly, dystonia, discirculative circulation
aortic vestibular- and encephalopathy
aneurysm, aor- little brain-atac-
tic coarctation tic disorders
oncologi- - paraneoplastic polyneuropathy, myopathy; - Myasthenic syndroms
cal dis- (Lambert-Eaton syndrom) –Compression syndroms
eases of
inner or-
gans

57
 Radiation sickness

ACUTE RADIATION SICK- CHRONIC radiation sickness

NESS
ethology single exposure dose over 100 – continued radiation exposure
1000 R
Clinical polyneuritic (including cranial asthenic  vegetative vascular
syn- nerves impairment - bulbar syn- dystonia (vegetative paroxysm,
dromes drome) expressed asthenicof including syncopal states) myas-
vegetal dysfunction en- thenoform vestibular and little
cephalomyeloradiculoneuropathy brain impairments sensory-veg-
etative polyneuropathy ex-
trapyramidal impairments

PNEUMATIC HAMMER DISEASE

CLINICAL STAGE CARDINAL SYMPTOMS

primary manifestation (I) peripheral angiodystonic syndrome sen-
sory-vegetative polyneuropathy
moderately expressed manifesta- peripheral angiodystonic syndrom (Ray-
tions (II) naud's type) cerebral angiodystonic syn-
drome sensory-vegetative polyneuropathy
with dystrophic impairments(myofibrosis,
arthrosis, periarthrosis)

expressed manifestations (III) sensory, vegetative, motor polyneuropathy

myelopathy encephalopathy

58
 CLASSIFICATION OF VERTEBROGENIC
NEUROLOGICAL SYNDROMES

А. cervical level
I. Reflex syndromes:
1. cervicalgia
2. cervicocranialgia (back cervical sympathetic syndrome etc.)
3. cervicobrachialgia and cervicoplexalgia with myotonic, vegetative vascular or neu-
rodystrophic manifestations (syndromes: scalenus anterior syndrome, frozen shoul-
der, painful shoulder, epicondylitis, styloiditis, noncoronarogenic cardialgia etc.)
II. radicular syndromes: discogenic (vertebrogenic) radices impairment(«radiculitis»)
III. spinal syndromes (spine compression by herniated disk, osteophyte etc.)
IV. vascular radiculospinal syndromes (radiculoischemia, radiculomyeloischemia,
myeloischemia).
V. spinal artery syndrome

B. thoracic level
I. I. Reflex syndromes: thoracalgia with myotonic, vegetative visceral or neurodys-
trophic manifestations (syndromes- scapulocostal syndrome, anterior chest wall,
cardialgia etc.)
II. radicular syndromes: discogenic (vertebrogenic) radices impairment(«radiculitis»)
III. spinal syndromes : 1) vascular, 2)compression

C. Lumbar level

I. Reflex syndromes:
1) lumbago
2) lumbalgia
3) lumboischalgia with myotonic, vegetative vascular or neurodystrophic manifesta-
tions (syndromes: piriform muscle, hip and knee periarthrosis, coccyalgia, achillo-
dynia etc.)
II. radicular syndromes: discogenic (vertebrogenic) radices impairment(«radiculi-
tis»),including cauda equina syndrome
III. vascular radiculospinal syndromes :
1. radiculoischemia,
2. radiculomyeloischemia,
3. myeloischemia (transient or persistent)

59
NEUROLOGICAL SYNDROMES OF VERTEBRAL OSTEOCHONDROSIS

COMPRESSION SYNDROMES Reflex syndromes

Path Radix radicu- Spine Syndromes- lumbalgia
o- compres- lospinal compres- cervico- and lum-
genet sion arteries sion brachial boischialgia
ic com- small pec-
me- pression toral mus-
cha- cle, pear-
nism shaped and
other mus-
cles
Clin- - paresthe- - pains, - growing - tenderness - pain in - dull pains -heada-
ical sia or dart- often locomo- and local gleno- in lumbus ches of oc-
man- ing pains without tor im- myotonia of humeral area worse cipital lo-
ifes- along sensi- pairments correspond- joint re- when bend- calization
ta- radix-loss tivity (paresis, ing muscles gion and ing and in (throbbing,
tions of sensitiv- loss general – secondary limitation standing gnawing) -
ity accord- symp- paresis ) - vegetative, of motor and sitting cochleovest
ing to "rad- toms - sensitiv- sensitive activity in position - ibular im-
ical" type - weak- ity im- and motor it, more in pains in pairments -
antalgic ness of pairments impairments epicondy- lumbus area visile im-
scoliosis - certain of the caused by lar region, radiating to pairments
local mus- groups conductor transient worse by the leg (by
cular de- of mus- type - costoclavic- pronator lumbois-
fense -ten- cles and sphinc- ular com- and chialgia) -
derness of reduc- teral im- pression supinator local mus-
paraverte- tion of pairments motions in cular de-
bral points reflexes such as elbow fense, - pos-
by palpa- (charac- rectal and joint -ten- itive trac-
tion-reduc- teristic) urinary derness in tion symp-
tion or loss inconti- styloid tom without
of corre- nence or process re- disorders in
sponding delay gion sensory and
reflexes reflex
sphere
positive traction signs (Lassag , Wassermann, Neri etc)
Trea rest, analgesics and antihydropic preparations, Novocain blockade (paravertebral and и
tment muscular in scalenus, piriform, small pectoral muscle), physiotherapy, underwater or dry
traction, manual therapy

60
 SYNDROMES OF CEREBROSPINAL FLUID AND ITS PATHOLOGY
(LIQUOR)

Investi-
External as-
gation pa- Pressure Cells Protein Glucose
pect
rameters
Normal 0,15-0,33 2,2-3,3
70-120 mm
cerebro- Transparent 0-5 lympho- g/l ммol/l
in side pos-
spinal liq- and colorless cytes (0,15-0,33 (40-60 mg
ture
uid mg%) %)
Usually
Inclined to normal,
Usually Norm or in- Norm or
Intracranial considera- there is de-
transparent significant moderate
tumor ble increas- creasing in
and colorless increasing increasing
ing meningeal
carcinosis
Normal or
Usually Norm or Norm or
Ischemic insignifi-
transparent slight in- slight in- Norm
stroke cant in-
and colorless creasing creasing
creasing
Erythro-
cytes num-
Rose to
Sponta- ber is con- Increasing
bloody
neous sub- siderably is in propor-
Rarely trans- Norm or in-
arachnoidal Increased increasing, tion to the
parent dur- creasing
hemor- the number number of
ing the first
rhage of leuko- erythrocytes
puncture
cytes in-
creases
Consider-
ably in-
Moderately Different: creased (to Moderate
Acute bac- Moderate or
or consid- Opaque, tur- 10000- or consid-
terial considerable
erably in- bid to puru- 50000). Ma- erable de-
meningitis increasing
creased lent jority - creasing
polynucle-
ars
Increasing
Tubercu- Slightly or From trans- Moderate
sometimes
lous moderately parent to lymphocytic Decreasing
to 5 g/l (5
meningitis increased opaque pleocytosis
mg%)

61
 MENINGEAL SYNDROME

General cerebral Headache, general hyperesthesia, vomiting

symptoms

 Kerning’s sign, Brudzinski’s sign (upper,

Meningeal middle, low)
Meningeal posture
symptoms:  Neck muscles rigidity
 Lessage's sign in children

Additional research data: liquor changing in visual, biochemical, serological and microscopic
investigations

Purulent meningitis

Epidemiological cerebrospinal Secondary purulent meningitis

Forms
meningitis (primary)
V. Meningococcus Pneumococcus, staphylococci, strepto-
Etiology
cocci
Is transmitted by direct contact or by Sources of infection – otogenous,
air through mucous membrane of rhinogenous, sepsis, lung abscess etc.,
fauces and rhinopharynx, then in- ways of infection penetration into sub-
Pathogenesis
volves the meninges by hematogenic arachnoidal area are as following – by
route contact, perineural, hematogenous,
lymphogenous
Purulent inflammation of arachnoid membrane, pus accumulation, plethoric
Pathomorphology brain; in brain cortex – toxic degenerative, vascular – inflammatory processes,
and topica pneumomalacia foci, microabscesses; in acute course of disease pyramidal
tract and spinal nerves are affected
 Meningeal syndrome
Clinic  General infection syndrome
 Intracranial hypertension syndrome
Lumbar puncture, in liquor – albuminocytologic dissociation, turbid puru-
lent liquor, in liquor – neutrophiles (to 10000 in 1 microl, protein increas-
Diagnosis
ing to 1 – 16 g/l, in liqor smears – meningococcus or pneumococcus,
staphylococcus, streptococcus
Differential diagno- Between all forms of meningitis
sis Subarachnoidal stroke
1. Antibacterial preparations (including intralobarly)
2. Deintoxication infusion therapy
Treatment 3. Dehydration therapy
4. Neurometabolics
5. Symptomatic therapy

62
 SEROUS MENINGITIS

Tuberculous meningitis acute lymphocyte choriomeningi-

Forms
tis
Filterable virus. The reservoir is do-
Etiol- Tuberculosis bacilli from the pri-
mestic mice, infection through con-
ogy mary focus
taminated foodstuff
Hematogenic dissemination in chil- Hematogenic dissemination.
Patho-
dren and teen-agers, affection of Meninges affection. Serous inflam-
gene-
meninges with serous inflammatory matory changes. Edema and in-
sis
changes flammatory foci in the brain
Meninges of the bran base,
Patho- ependyma of the III and IV ventri- Diffuse affection of the meninges.
mor- cles, vascular plexuses are affected. In severe course, brain, spine and
phol- peripheral nervous system are in-
ogy Exudate and proliferative changes
volved
are present.
Clini- Acute beginning with rapid devel-
cal The onset is gradual with aggrava- opment of meningeal syndrome, af-
mani- tion of meningeal syndrome and fection of cranial nerves, some-
festa- signs of cranial nerves affection times with encephalomyelitis,
tions polyradiculopathy
Presence of tuberculosis of the inner Lumbar puncture: considerable in-
organs. Lumbar puncture: CSF pres- crease of CSF pressure, lympho-
sure is increased, CSF is opalescent,
lymphocyte pleocytosis up to 600- cyte pleocytosis, protein, sugar and
Diag-
800х10/l, increased protein amount chloride amount is normal; etiolog-
nosis
up to 2-3 g/l, decreased sugar up to ical diagnosis isolation of the virus,
0.15-0.5 g/l and chloride amount up neutralization reaction and reaction
to 5 g/l, fibrin precipitation, my-
cobacteria in 2/3 cases of complement conjugation.
Differ-
With tuberculous meningitis
ential
With serous forms of meningitis
diag- With secondary encephalitis
nosis
Nucleases (ribonuclease, desoxyri-
Antituberculosis drugs
bonuclease)
corticosteroids
Treat- Desensibilizing treatment
dehydration
ment Dehydration
neurometabolics
neurometabolics
symptomatic treatment
symptomatic treatment

63
 MYELITIS

Infection, intoxication. Primary myelitis is can be caused by

viruses, tuberculosis, syphilis. Secondary myelitis is a com-
Etiology plication of common infections (measles, scarlet fever, ty-
phus, pneumonia, flu) or a purulent focus in the organism
and sepsis. Postvaccination myelitis is possible

In a primary disease the infection is hematogenic, involving

the spine; in secondary – allergic factor and hematogenic in-
Pathogenesis
fection of the spinal cord play a role.

The pathological process can develop in 1) the lumbar spine;

2) thoracic spine; 3) at the level of the cervical intumes-
cence; 4) upper cervical spine. The area of the foci is charac-
Pathomorphology
terized by hyperemia, edema, small hemorrhages, myelin de-
composition

Neurological symptom-complex of transverse spine affec-

Clinical signs tion according to the level of the affection against a back-
ground of intoxication

Acute onset with rapid development of transverse spine af-

fection against a background of intoxication, inflammatory
changes in the CSF, blockade is absent. It is important to
Diagnosis and dif- differentiate with epiduritis, which is treated neurosurgically.
ferential diagnosis Differential diagnosis with Guien-Barre polyneuropathy,
spinal tumors, hematomyelia, hemothorax, disseminated en-
cephalomyelitis

Antibiotics, glycocorticoids, deintoxication, neurometabol-

Treatment ics, symptomatic treatment, care for the patient, prevention
of bedsores

64
 ACUTE POLIOMYELITIS

Etiology Three strains od a filterable virus ( types 1, 2, 3)

The source of the disease are healthy carriers and reconvales-

Epidemiology cents with abortive forms. Main rout of the infection is personal
contacts and feco-oral.

Incubation 17 days – 5 weeks. The virus multiplies in the mucous

Pathogenesis membrane of the intestine, then invades the blood. Enters the ner-
vous system through the blood-brain barrier.
The spine is swollen, soft, with small hemorrhages in the gray mat-
ter. Histological changes are prominent in the gray matter of the
Pathomor-
spine (cells of anterior horns) and oblong brain, the changes range
phology
from light chromatolysis to complete destruction with neuronopha-
gia.
1. Non-paralytic form – signs of serous meningitis or radicular syn-
drome
2. Paralytic forms:
Clinical pic-  Encephalitic (affection of cortex and subcortex)
ture  pontobulbar (affection of the pons and oblong brain)
 spinal (affection of the anterior horns – peripheral paralysis)
 polyneuritis(multiple affection of peripheral nerves)
 incubation
 prodromal
 pre-paralytic
Stages  paralytic
 recovery
 residual stage

 with meningitis of other etiology

Differential  with infection meningitis
diagnosis  with Guien-Barre polyneuropathy
 with stem encephalitis

Specific treatment is not available. Symptomatic treatment - rest.

Treatment In respiratory and bulbar disorders – artificial ventilation, suction
of secretion, tubal feeding. Antibiotics to prevent pneumonia
The patient should be isolated for 6 weeks; the children who
Prevention have been in contact are administered gamma globulin, 3-6 ml.
General prevention - vaccination

65
 POLIOMYELITIS-LIKE DISEASES CAUSED BY
KOKSAKI AND ECHO VIRUSES

etiology Infection with enteroviruses KOKSAKI and ECHO

With food or air droplets, which is followed by virusemia. Virus
pathogenesis fixation in different organs and systems (muscles, nerves, mu-
cous and serous membranes, etc.)
Pathomorphol- Hyperemia and swelling of meninges, increased amount of the
ogy CSF in the subarachnoid space and brain ventricles
 Serous enterovirus meningitis
 Spinal poliomyelitis-like form
Clinical forms
 Polyradiculoneuritis form
 Epidemic myalgia
 General infection
Main clinical
 Meningeal
syndromes
 Transitory atrophic paresis
Virological studies
Feces studies
Diagnosis
Epidemiological studies
Lumbar puncture
 with acute poliomyelitis
Differential di-  with flue meningoencephalitis
agnosis  with all types of meningitis
 with food poisoning
 antiviral gamma-globulin, ribonuclease
 corticosteroids
 dehydration
Treatment
 analgesics
 desensibilization
 vitamins

66
 PRIMARY ENCEPHALITIS

Tick encephalitis Herpetic en- Epidemic encephalitis

Forms (spring-summer) cephalitis

Neurotropic virus, type 1 herpes

Pathogenic organism has
Etiology carried by ticks simplex virus
not been discovered.
Natural-focus zones, General toxic The disease is low-conta-
the source is small ro- gious; for acute stage
dents, birds, domestic and focus- symptoms of inflamma-
animals; penetrates tory nature, for chronic
the human organism necrotic lesion of stage symptoms of pro-
Epidemi- via tick bite or with gressive-degenerative na-
ology food, into CNS via the cortical sub- ture are characteristic; the
dissemination and interval between the
viremia stance stages lasts from several
months up to 5-10 years.

Inflammatory-de- Necrotic herpetic

Inflammatory-degenera-
encephalitis.
Pathologi- generative changes tive changes in the cere-
Spinal cord may
cal mor- in the cerebral cortex bral peduncle, reticular
be involved (en-
phology and trunk, cervical formation, trunk, hypo-
cephalomyelitis)
spine thalamus, black matter.
In acute stage:
Disorders of sleep and at-
Necrotic en- tention
Polioen-
cephalitis with Oculomotor disorders
cephalomyelitis
In acute stage:
Main clin- Meningeal acute focal neu- Parkinsonism syndrome
ical forms Kozhevnik's
rologic signs Contemporary forms:
epilepsy
Vestibular
Hyperkinetic
Hypothalamic

67
 Continued
Stay in the epidemic
focus, a tick bite,
disease acquired in
spring or summer,
isolation of the virus  General infectious
1. Serologic in-
inthe blood and cere- phenomena
Diagnosis vestigation
 Hypersomnia
brospinal fluid, posi- 2. Specific viro-
 Oculomotor dys-
tive complement logic typing
functions
clotting reaction, neu-
tralization reaction,
hemagglutination de-
celeration reaction
In serous meningi-
In acute stage – with
tis, meningoen-
cephalitis serous meningitis
Differential In all types of en- In encephalitis of In chronic stage - with
diagnosis cephalitis different etiology
pathology of subcorti-
In acute dysfunc-
tion of cerebral cal formations (parkin-
circulation (hem- sonism syndrome)
orrhagic form)
In acute stage: In acute stage
o Blood serum of Specific antiviral
the persons reveverd treatment (Zovi- o corticosteroids
of the disease rax, Valtrex) o desensibilizing
o γ-globulin, ri- γ-globulin medicines
Treatment
bonuclease o dehydration therapy
Dehydration
o dehydration In chronic stage
In chronic stage: preparations o treatment of parkin-
o symptomatic ther- Symptomatic ther- sonism syndrome
apy apy
o neurometabolics

68
 SECONDARY ENCEPHALITIS

Forms Rheumatic encephalitis Flu encephalitis

Etiology Rheumatism A1, A2, A3, B virus
Vascular changes (endarteritis, pan- Thrombovasculitis, small
Pathomor-
vasculitis, periarteritis, perivascular
hemorrhages, perivascular in-
phology
inflammation and infiltration, glia filtration, focal lesions of the
changes brain
 Hemorrhagic flue en-
cephalitis
Main clini- - Rheumatic vasculitis
 Flu diencephalopathy with
cal forms - Chorea minor (Sydenham’s)
asthenic, vegetative vascular
dystonia, intracranial hyper-
tension syndromes
Clinical findings Clinical findings
Lymphopleocytosis increased Serology study Virology
Diagnosis
liquor pressure in the liquor. Posi- study
tive acute-phase parameters and Lymphopleocytosis, increased
specific rheumatic tests liquor pressure.
With serous meningitis,
meningoencephalitis
Differential With other forms of encephali-
With all forms of encephalitis
diagnosis tis
With acute disturbances of
brain circulation
Treatment of rheumatism Corticosteroids
Neurometabolics Gamma-globulin
Dehydration Dehydration
Treatment
Antispasmodics Hemostatics
Symptomatic treatment Symptomatic treatment
In hyperkinesis – haloperidol,
fenibut, Aminosyn, phenobarbital

69
 SECONDARY ENCEPHALITIS

Forms Vaccinal encephalitis Measles encephalitis

Anti-smallpox, anti-diphtheria- Severe measles complications
Etiology tetanus, anti-diphtheria-tetanus-
measles vaccines

Pathogene- Allergic reaction with cerebral le- Infectious-allergic reaction

sis sion with cerebral lesion

Inflammatory lesion of cerebral Fibrinogenous swelling of

vessels, perivascular infiltrations, vascular walls, formation of
Patho- diapedetic hemorrhage, cerebral perivenous foci of demyelin-
morphology edema; the changes are localized in ization mainly of the white
the white smatter of the brain and substance of the brain
spinal cord being sources of de-
myelinization

Main clini- Encephalomyelitic

Encephalomyelitic
cal forms Polyneuritic
Measles encephalopathy

Lymphopleocytosis, increased The amount of CSF protein

liquor pressure in the liquor, in- and sugar is elevated, moder-
Diagnosis
creased amount of protein and ate lymphocytosis, high CSF
sugar pressure

Differential Carried out with all forms of

With all forms of encephalitis
diagnosis encephalitis
Desensibilizing preparations, im- Treatment of measles: neu-
Principles munodepressants (corticosteroids), rometabolis, immunodepres-
of treatment dehydration, neurometabolics, sants; desensibilizing therapy;
and preven- symptomatic therapy in hyperkinesia - haloperidol,
tion phenibut, aninasin

70
 CEREBRAL ARACHNOIDITIS

neuroinfections, general infections (measles, scarlet fever), in-

etiology toxication, brain injury
Nonspecific autoimmune and autoallergic reactions of the
pathogenesis arachnoid and pia matter, vascular plexuses and ependyma of
the ventricles with proliferative changes in them

Clouding and thickening of the arachnoid, cysts, filled with tur-

pathomorphol- bid or transparent fluid; disseminated, limited, adhesive, cystic,
ogy and cystic-adhesive forms are distinguished

 Convex (of the convex surface of the hemispheres )

localization  Opticochiasmic
 Basal :  cerebellopontine angle
 posterior fossa
Clinical mani- Neurological signs are formed according to the localization
festations
diagnosis focal signs, CT

Differential di-
With brain tumors
agnosis
Etiotropic treatment
Resorptive drugs
Dehydration
Treatment Neurometabolics
Symptomatic treatment
Neurosurgery

71
 MULTIPLE SCLEROSIS

Autoimmune disease, viruses or other etiological factors causing the

Etiology disease have not been revealed. Genetic predisposition to the disease
is known.
Oligidendrogliocytes of the myelin membranes are affected due to forma-
tion of autoantibodies to myelin with development of inflammatory reac-
tion with participation of cytokines (mediators secreted by immune cells,
Pathogen- lymphocytes and macrophages) which opens the access to the CNS to
esis greater number of immune cells with deintegration of myelin, changes syn-
thesis of proper glial cells. Increased lipid peroxidation in the nervous sys-
tem plays a role.

Multiple demyelinization foci in the brain and spine; gliofibrosis replaces

Pathomor- the dead cells (sclerotic plaques) but axial cylinders are preserved, the
phology most frequent localization of the patches – lateral funiculi, cerebellar
tracts, optic nerves.
Clinical 1. cerebral: -stem - cerebellar -optic -hyperkinetic
forms 3. cerebrospinal 2. spinal
Chariot’s triad (nystagmus, intention tremor, scanning speech)
Clinical Marburg’s pentalogy (lower spastic paraparesis, nystagmus, intention
signs tremor, absence of abdominal reflexes, partial atrophy of the optic nerve
papillae – pale temporal halves)
 multiple foci
Diagnosis  unstable signs even within a day
 periodic course with remissions and exacerbations

With trembling form of hepatocerebral dystrophy (Konovalov-Wilson

Differen-
disease)
tial diag-
With acute infectious encephalomyelitis
nosis
With hereditary cerebellar ataxias
During exacerbations: corticosteroids, : cytostatics, nonsteroid immunode-
pressants, plasmaphereses, desensibilizing treatment, antihistamine drugs,
antioxidants
Treatment During remissions: immunomodulators (T-activin, thymalin), which
improve trophism of the nervous system (phosphaden, vitamin B,
nootropil), vascular drugs (Trental), ACTH and glucocorticoids, im-
munodepressants

72
 AMYOTROPHIC LATERAL SCLEROSIS
(Charcot-Kozhevnikov disease)

Affection of peripheral neurons and central mononeurons

Etiology, pathogene- and central mononeurons due to increased function of
sis glutamate receptors
Degenerative changes of cells of anterior horns of the
spine in the area of cervical and lumbosacral segments,
Pathomorphology in the stem (nuclei of the 7, 9, 10, 11, 12 the pairs of the
cranial nerves and supranuclear tracts) as well as pyra-
mid tracts localized in the lateral columns of the spine
 bulbar
Main clinical forms  cervicothoracic
 lumbosacral

simultaneous combination of the signs of central and pe-

ripheral with localization depending on the clinical
Diagnosis form, fibrillar twitching of the muscles, prevailing pare-
sis over atrophy of the muscles

 with vertebrogenic cervical encephalopathy

 with brain tumors
Differential diagnosis  with multiple sclerosis
 with syringomyelia
Antiglutamate drugs (riluzole)
Vitamins E and B
Drug which influence tissue metabolism (pyracetam, en-
cephabol, cerebrolysin, cocarboxylase, glutamic acid,
berlition)
Treatment
Increased doses of anabolic hormones in repeated cour-
ses (1-2 months) (retabolil, nerabol, nerabolil)
Biostimulators (Acephen)
In increased salivation – atropine drugs, in respiratory
and bulbar disorders (proserin reanimation

73
 EPILEPSY

1. endogenic: hereditary predisposition of the brain to paroxysmal

states
Etiology
2. exogenic: diseases causing organic lesions of the brain and its meninges
(injuries, infections, intoxications, tumors, aneurysms of brain vessels)
Formation of epileptic focus from a group of neurons with depolarized
Patho- membranes resulting in generalization of hypersynchronic discharge of
genesis excitation

1. generalized 2. partial (focal): 3. secondary

-grand mal (tonic- а) motor  Jacksonian epilepsy
generalized:
 aversion
clonic);
 speech -Begin with a
-tonic;  Kozhevnikov’s partial attack
Classifi- -clonic epilepsy
б) sensor and become
cation of -absence:  Jacksonian epilepsy
generalized.
 Visual, auditory, olfactory, gus-
attacks  simple
tatory hallucinations
 akinetic  sensitive
Focal compo-
 psychosensory
 myoclonic
в) vegetative-visceral nent known as
г) epileptic automatisms (twi- aura
light states)
Diagno- Clinical manifestations, EEG, craniography, MRI, brain CT
sis
Treat- differential
ment constant
complex Anti-convulsant therapy
individual

Control:
The attacks fol- IV administration of benzodiazepine drugs (rela-
Epileptic low each other nium?, Sibson), fengidan?, rectal administration of
state diazepam. When ineffective, inhalation narcosis. Pre-
without break vention of brain edema. Lumbar puncture is indi-
cated.

74
 NONEPILEPTIC PAROXYSMAL STATES
(Absence of epilepsy activity focus)

Convulsive Non-convulsive
1. Vegetative and vascular paroxysms:

 sympathoadrenal
- febrile convulsions in children
 vagoinsular
 mixed
- spasmophilia (develops as a result of a high
2. Syncopal states (fainting fits):
peripheral nervous and muscular excitability)
 neurogenous (reflex, vagovasal)
 cardiogenic
- toxic cramps (exogenous, endogenous)
 in blood homeostasis and cerebral me-
tabolism disturbances
- hysterical convulsions
3. Migraine

CHILDREN’S PALSY

Pathology of intrauterine development (in pregnancy pathology, in preg-

Etiology nant women diseases, intoxications, immunologic blood incompatibility
of mother and fetus) and mechanical causes (birth trauma)
Fetus brain hypoxia; presence of embryonal cells in cerebral cortex,
Pathogenesis and
meningomalacia zones (areas), cavities with glial walls, necrosis in sub-
Pathomorphology
cortical ganglions, various developmental anomalies of the brain
Pyramidal (pareses, paralyses)
Extrapyramidal (various kinds of hyperkineses)
Basic clinical
Muscular-dystonic
syndromes
Cerebellar
Intellect impairment
hemiplegic, tetraplegic
Little’s
Clinical forms spastic
cerebellar
hyperkinetic
Diagnosis Clinical data, history, brain MRI and CT
physiotherapeutic exercises
balneo- and therapeutic mud-baths
nootropes?
Treatment Cholinolytics
dopamine agonists and antagonists
muscular relaxants
vascular therapy

75
 HEREDITARY ATAXIAS

Forms Friedreich's ataxia Marie's ataxia

Type of autosomal recessive autosomal dominant
heredity
Pathogenesis is not fully studied reduction of carbonate metabo-
lism enzymes and increase of
hydrolytic enzyme activity

Patho- thinning of the spinal cord's back reduction of the cerebellum

morphology funiculi, of spinocerebellar size, degenerative changes in
tracts of back radices, thinning of Purkinje's cells of the cerebellar
upper cerebellar pedicles, degen- nuclei cortex, in lower olivae,
eration of pyramid tracts in the spinocerebellar paths
spinal cord
cardinal clin- begins in people under 20 begins in people under 20-30
ical symp- years of age cerebellar ataxia in years of age cerebelloataxic
toms legs impairment of deep sensi- syndrome pyramidal sympto-
tivitydystal paresis with an matic syndromeoculomotor
early loss of tendon reflexes impairments synod absence
muscular hypotony extraneu- of skeletal anomalies syndrome
ral symptoms (skeletal anomalies mental disorders
– Friedreich's foot, chest defor-
mation)

diagnosis Clinical data. to differentiate with various types of degeneration

and differen- (olivocerebellar, olivopontocerebellar, late corticocerebellar etc)
tial diagno-
sis
treatment symptomatic preparations, improving brain metabolism
restorative

76
 HEREDITARY DEGENERATIVE DISEASES WITH LESION OF THE
EXTRAPYRAMIDAL SYSTEM

Forms: Hepatocerebral dystrophy (Wilson's chronic progressive

disease) chorea

Type of autosomal recessive autosomal dominant

heredity:
Pathogenesis: genetically stipulated impairment - changing of neurotrans-
of synthesis of ceruloplasmin which mitters and neuromodula-
conveys copper impairment of tors metabolism (GABA,
copper exchange with its sedimenta- dopamine, cholinergic)
tion in liver, brain, kidneys, cornea

Pathomor- Degenerative dystrophic changes - degeneration and atrophy

phology with center softening, growth of of globus pallidum, black
neuroglia matter, brain cortex neu-
rons.

cardinal clini- Clinical forms 1. Rigid arrhythmo- - choreal hyperkinesis – de-

cal syn- hyperkinetic 2. Rigid tremulous 3. mentia
dromes: Tremulous 4. Extrapyramidal corti-
cal 5. Abdominal

diagnosis: Clinical data, Kayser-Fleischer ring, clinical data

hypercupremia, hypercupruria, and electroencephalography
reduction of ceruloplasmin level in
blood.
differential di- with rheumatic chorea with - with hepatocerebral dys-
agnosis: chronic progressive choreawith trophia - with rheumatic
multiple sclerosis chorea

treatment: preparations with cupruric action nootropic preparations

(cuprinil, D-penicillamine) im- neurolepticstranquiliz-
provement of liver functions diet ersdopamine antagonists
with limitation of copper-contain-
ing products

77
 HEREDITARY DEGENERATIVE NEUROMUSCULAR DISEASES
PROGRESSIVE MUSCULAR DYSTROPHIAS MYOPATHY

Forms Pseudohypertrophic Erb-Rot juvenile Facioscapulo-

(Duchen’s) humeral dystrophy
(Landouzy-Dejer-
ine)

Type of Linked with X-chro- Autosomal reces- autosomal dominant

heredity mosome sive

etiology, Genetically determined muscular defect, by which albumin

pathoge- catabolism prevails its anabolism
nesis:
cardinal Myopathy syndrome Myopathy syn- Weakness and atro-
clinical pseudohypertrophy of drome. phy of facial and
manifesta- calves, acromio- Weakness and atro- brachial muscles.
tions: humeral, strap mus- phy of proximal «Myopathic» face.
cles. Cardiomyopathy. parts of limbs (wad- Polished forehead
Endocrine disorders. dling gait) . " lad- sign Ophthalmople-
Intellectual disorders. der"sign". Hyperlor- gia. Lagophthalmus.
dosis. Transverse smile
" winging of the pout lips, winging
scapulae ". of the scapulae "

diagnosis - clinical manifestations

and differ- - biochemical studies (increased blood creatinphosphokinase, cre-
ential diag- atinuria)
nosis - electromyography
- biopsy of muscles

principles of Amino-acid complexes.

therapy Protein diet.
Anabolic steroids (retabolil, phenobolil etc) drugs imprroving mus-
cular trophism (ATP, cocarboxylase, vitamin Е etc.),
massage. in juvenile and facioscapulohumeral forms - -
adrenoblockers

78
 HEREDITARY DEGENERATIVE NEUROMUSCULAR DISEASES
PROGRESSIVE MUSCULAR DYSTROPHIAS AMYOTROPHY

Forms: Spinal Verdnig- Spinal Kugelberg- Neural Charcot-Mari-

Hoffmann Welander Tut
Type of autosomal recessive Autosomal recessive autosomal dominant
hered-
ity:
patho- impairment of muscular trophism due to de- muscular defect in distal
genesis: generation of anterior spinal horns parts due to degenera-
tion of peripheral nerves

Patho- bundle character of muscular atrophy degenerative changes in

mor- axis cylinders and
phology myelin membrane of pe-
ripheral nerves

cardinal Malignant growth be- Weakness of trunk Distal peripheral tetra-

clinical gins from birth or muscles and proxi- paresis
manifes- early childhood. Pe- mal parts of limbs. Polyneuritic disorders of
tations: ripheral tetraparesis Fascicular tic. distal sensitivity
and paresis of trunk peripheral tetrapare- Friedreich's foot. Distal
muscles. fascicular sis. polyneuritic vegetative vasomotor
tic. Bulbar syndrome. type of sensitivity and trophic disorders.
Slow course. begins impairment
in adulthood

diagno- Clinical manifestations, electromyography, Clinical manifestations,

sis biopsy of muscles EMG

differen- With acute poliomyelitis with myopathy. with various types of

tial di- polyneuropathy
agnosis
princi- Symptomatic treatment.
ples of Anticholinesterase drugs.
therapy Vascular therapy (Trental, preparations of nicotinic acid)
physiotherapy, balneation and curative mud bath.
Orthopedic shoes.
Massage.
Drugs improving myelinization: vitamins of group B, -lipoic acid.
Drugs improving muscular trophism

79
 MUSCULAR DYSTONIA
Large group of pathological syndromes manifesting as constant or periodical muscles
spasms and typical dystonic positions

Primary heredi- Secondary dystonias arise as a result of or-

Classifi- tary or sporadic ganic brain diseases (degenerative – dys-
cation trophic, traumatic, vascular etc.)

I Focal-blepharospasm, facial hemispasm, spasmodic torticollis,

oromandibular dystonia, hand dystonia, foot dystonia, dystonia
“musculorum deformans”
II Segmental-dystonic manifestations occur in two adjacent seg-
ments (spasmodic torticollis, writer's cramp)
According III Multifocal-dystonic manifestations occur in two or more non-ad-
to localiza- jacent segments (blepharospasm and foot dystonia)
tion IV Hemidystonia-dystonic manifestations occur in one side of the
body (foot and hand dystonia at the same side)
V Generalized dystonias begin as focal. Spasmodic torticollis and
then generalization process develops accompanied by other vari-
ants of deforming muscular dystonia

genetic Dysfunction of neurotransmitted Different drugs

dopamine systems-mostly serotoninenergetic taking-neurolep-
defect (in and noradrenergic (in primary dys- tics, psychostim-
Etiology primary tonias without evident hereditary ulantrs etc.
hereditary factors), infections aftereffects,
dystonias) traumas, emotional overstrains

Normalization of neurotransmitters disturbances

- in hereditary dystonias, connected with dopamine deficiency
- dopamine agonists
Methods of - blockers of dopamine receptors-haloperidol
treatment - sedatives
- injection into spasmic muscles of botulinus toxin “Botox”

80
 MYASTHENIA GRAVIS

Etiology Autoimmune disease, in which the thymus plays a significant role

 Antibodies produced by thymocytes have a competitive attitude

toward acetylcholine for postsynaptically plate and thus blocking

nerves and muscles transmission.
Pathogenesis  Antibodies produce accelerated degradation of cholinoreceptors
and decrease receptive area of acetylcholine.
 Fermentative defect of acetylcholine synthesis.

 Optic
 Bulbar
Main clinical
 Generalized
forms
All forms are characterized by increased manifestations at loading
of the corresponding muscles

Complica- Myasthenic crisis (acute muscular weakness which may result in

tions asphyxia)
Clinical manifestations of pathological muscular weakness
Proserine test
Diagnosis
Thymus examination
EMG
Differential
In intoxications, infections, neoplasms with myasthenic syndrome
diagnosis
1. Surgical (in thymus pathology) – thymectomy
2. Conservative
 Immunodepressants (corticosteroids)
Treatment
 Anticholine esterase preparations
3. In myasthenic crisis – prednisolone, artificial ventilation, pros-
erin IV

81
 HEREDITARY NEUROMUSCULAR DISEASES

Myotonias paroxysmal myoplegia

Congenital Dystrophic hypokalemic hyper- Normokali
(Tameness’ (Curschman kaliemic emic
Forms disease) n-Steinert)

Type of
autosomal dominant Autosomal dominant
here-dity
disturbances of cellular mem- Disturbances of metabolite exchange and carbohy-
brane permeability drate metabolism with redistribution of extra- and
pathogene-
changes in ion and mediator intracellular potassium and sodium
sis
metabolism Disturbances of membrane potential with forma-
tion of hyperpolarization and depolarization block
Myotonic Myotonic con- Myoplegia of the Develops at Prolonged
contracture tracture limbs developing daytime. develop-
developing af- Myopathic during sleep or Caused by cold. ment of
ter a consider- syndrome after it. Involves the paralysis
able contrac- Endocrine and Cardiac arrhyth- muscles of the and slow
tion dystrophic dis- mia. body and head. exit from
Athletic orders Caused by carbo- Cardiac arrhyth- the attack
Main clini-
stature hydrate intake. mia. (up to 2
cal manifes-
Increased ex- Duration: several The attacks are weeks)
tations
citability of days. short. Potassium
the muscles, Reduction of Increase of amount is
"muscular potassium level potassium level normal.
cylinder" or a in the blood in the blood
depression at a serum  3.3 serum during
stroke with a mmol/l the attack >5.5
hammer mmol/l
Diphenin Diphenin Potassium Potassium ex- Diet rich
Chinin Chinin preparations. creting diuret- in salt.
Diacarb Diacarb Potassium-pre- ics.
Treatment of serving diuret- Glycose and
myopathic ics. physiological
syndrome Diet with potas- saline solution
Treatment
(see Myopa- sium. IV.
thy) Diet with in-
creased
amount of car-
bohydrates and
salt.

82
 NEUROSES
(Psychogenic diseases characterized by formation of psychological conflict
And manifesting by transient disorders in emotional, somatic, vegetative spheres)

Classification
of the types of
the nervous Intellectual Intermediate type
Artistic type of mental activ-
system accord- type of mental (balance of sig-
ity
ing to signal activity nals systems)
systems of ac-
tivity
Hysteria: Obsessive Neurasthenia:
- Hysterical characters states neuro- -cephalgia
- Emotional affective disor- sis: (headache)
ders  Obsessive -sleep disorders
- Pseudoorganic syndromes: fears (pho- (dyssomnias)
Predisposition  Hysteric pareses bias) -neuropsychic
to neuroses  Hysteric convulsions  Obsessive disorders
 Hysteric disturbances of thoughts, -vegetative vis-
sensitivity doubts, ceral disorders
 Hysteric blindness move-
 Hysteric deafness ments, ac-
tions

To reveal and eliminate the cause of neurosis. Psychotherapy.

Symptomatic treatment: sedatives, antidepressants, tranquilizers,
Treatment
nootropic drugs, vitamins. Regimen, massage, exercises, health
resort.

83
 CLASSIFICATION OF NEUROTIC DISORDERS
IN COMPLIANCE WITH ICD OF THE 10TH REVISION

SOMATOFORM DISORDERS
- somatoform autonomic dysfunction
of
- the heart and cardiovascular system - somatized disorder
- the upper portion of the gastroin- - somatoform undifferentiated disorder
testinal tract - somatoform disorder with a persis-
- the lower portion of the gastroin- tent pain syndrome
testinal tract - other somatoform disorders
- the respiratory system - unspecified somatoform disorder
- the urogenital system
- other organs and systems
NEUROTIC DISORDERS, ASSOCIATED WITH STRESS, AND ANXIOUS-
PHOBIC SOMATOFORM DISORDERS
- agoraphobia - specific isolated phobias
- without panic disorder - other anxious-phobic disorders
- with panic disorder - unspecified phobic anxious disorders
- social phobias
OTHER NEUROTIC DISORDERS
- neurasthenia - other specific neurotic disorders
- syndrome of depersonalization and - unspecified neurotic disorders
derealization
SYNDROMES OF BEHAVIORAL DISTURBANCES, ASSOCIATED WITH
PHYSIOLOGICAL DISTURBANCES, AND PHYSIOLOGICAL FACTORS,
ASSOCIATED WITH TAKING OF FOOD
- nervous anorexia, including atypical - vomiting owing to other mental disor-
one ders
- nervous bulimia - other disorders associated with taking
- overeating owing to other mental dis- of food
orders - unspecified disorders associated with
taking of food

84
 DEGENERATIVE DISEASES OF THE EXTRAPYRAMIDAL SYSTEM
Parkinson’s disease

Age-related degeneration of nigrostriatal

Medicinal parkin-
neurons
sonism (neurolep-
Epidemic encephalitis (postencephalitic
Etiology tics, rauwolfia)
parkinsonism)
Brain injuries
Toxic effects (Mn, Co, narcotic drugs, etc.)
vascular factor (ischemia of nigrostriatal neurons)
genetically based inferiority of the enzyme systems controlling
catecholamine exchange in the brain, reduced dopamine con-
Pathogenesis
centration in nigrostriatal neurons. Pathology of dopamine re-
ceptors
Pathological
anatomy and
Degenerative changes in neurons of the black substance
localization of
lesion
Leading clini- 1. Hypokinesia 3. Tremor at rest
cal manifesta- 2. Rigidity of muscles 4. Postural disturbances
tions (plastic)
Diagnosis and
To differentiate vascular, toxic and postencephalitic parkinson-
differential di-
ism
agnosis
1 increase of dopamine synthesis in the black substance by ad-
ministration of L-DOPA, a metabolic precursor of dopamine, as
well as drug preparations which contain L-DOPA and inhibitor
of DOPA-decarboxylase: nacom, madopar, Sinemet
2. Influence on postsynaptic dopamine receptors in the caudate
nucleus: bromocriptine, pergolide, lazurid
3. decreased reverse capture of dopamine by the presynaptic
membrane: antidepressants (amitriptyline)
Principles of 4. Dopamine release from dopamine depots: amantadine, midan-
therapy tan
5. reduced dopamine catabolism: MAO-B inhibitors (jumex)
6. Inhibition of cholinergic mechanisms in the caudate nucleus:
benzhexol (hydrochloride), Practipan
7. decrease of tremor: beta-adrenoblockers in small doses
(anaprylline, obzidan, coreole)
8. Use of neuroprotectors: remasemid, lubeluzole, vitamin E
9. Surgical treatment: transplantation of the nigrostriatal struc-
tures in the embryo

85
 GLOSSALGIA

Etiopatho- Dysfunction of oral and digestive systems. Occurs under

genesis condition of neurotization of obsession syndrome

Clinical Unpleasant sensation in the tongue (paresthesia of burning

signs type, prickly sensation, numness, pain in the tongue)

Elimination of the cause of the disease. Symptomatic therapy,

Treatment
sedatives

86
 HIV-ASSOTIATED NERVOUS SYSTEM DISORDERS

AIDS is a terminal stage of the course of the infection caused by human immunodeficiency
virus (HIV) and developing with lesion of practically all the organs and systems of the human; even
at early stages disorders of CNS and peripheral nervous system (PNS) play the leading role.

Etiology Virus of AIDS belongs to non-oncogenic retroviruses of the human, disturbing im-
munity, capable for persistence in the organism, having durable incubation period,
possessing tropism to macrophages, lymphocytes and cells of nervous tissue

Pathoge- Clinical and pathomorphological data of neuro-AIDS demonstrate direct (primary) lesion
nesis of the nervous system and numerous neurological complications, caused by infections
and neoplasms, appearing as a result of deep depression of immunity in patients

Bradykinesia and postural dysfunctions parkinsonism-like, but without specific

tremor. At final stages, mutism, paraplegia and dysfunction of pelvic organs are ob-
served. CT, MRI, PET demonstrate diffuse atrophy of cortex with enlarged ventri-
cles of the brain, the degree of which increases with deterioration of clinical signs.
There can be no changes of EEG at early stage, and diffuse changes of inhibited
EEG activity at later stages. Nidus or paroxysmal changes are not typical.
Acute meningoencephalitis and atypical aseptic meningitis are regarded as rarely
appearing primary forms of lesion of the central nervous system in AIDS. Clinical
sings characteristic for the disease can utterly disappear in several weeks. Further
development of chronic encephalopathy is possible.
Lesion of the spinal cord may occur alone or combined with chronic AIDS-en-
cephalopathy. In this form of myelopathy lateral and posterior spinal columns are
mainly affected, especially on the level of sternal segments. Clinically the disease
manifests itself with spastic paraparesis and sensor ataxy.
Lesion of the peripheral nevous system is a frequent neurologic manifestation. The
Leading
most frequent form of peripheral neuropathy, connected with HIV-infection is sen-
clinical
sor neuropathy, referred to distal axonopathy at the level of neurons of sensitive
signs
ganglions. Inflammatory-demyelinating polyneuropathy have been described, simi-
lar to Guienne-Barre syndrome or chronic progressive polyneuropathy.
Lesion of nervous system connected with infections developing on the base of immunod-
eficiency.
An important role in the structure of neurologic complications of AIDS belongs to le-
sions of the nervous system, caused by toxoplasmosis. Cerebral toxoplasmosis can be
manifested as clinical meningitis, meningoencephalitis and spatial cerebral lesion. Diag-
nosis can be made by means of stereotaxic biopsy under CT control based on absent his-
tological and immunohistological investigations.
Among viral infections complicating AIDS course the following have been described:
cytomegaloviral infection, lesions caused by virus of plain hepatitis and papovavirus.
Clinical picture caused by cytomegalovirus is similar to that of encephalitis, polyradicu-
loneuropathy and manifests by lesion of frontal roots of spinal nerve and motor cranial
nerves. Herpes simplex virus may cause encephalitis and radiculitis.

87
Leading Accompanied by herpetic eruptions. In AIDS, papovavirus leads to the develop-
clinical ment of progressing multifocal leukoencephalopathy. The patients suffer from men-
manifest- tal disturbances, aphasias, pareses, ataxia. CT reveals multiple foci of decreased
tations density of the white matter.
Fungal complications in AIDS (cryptococcosis, candidiasis) may manifest by
meningoencephalitis, meningitis and brain abscess. The multifocal character of the
impairment causes neurological signs.
Bacterial infections are relatively rare; they result in development of meningitis and
brain abscess.
Tumors of the CNS
The most frequent of them is primary lymphoma of the CNS. Its clinical picture is
variable: mental disturbances, headache, and fits of convulsions, hemipareses, and
aphasias. In AIDS, impairment of the CNS may be caused by systemic lymphoma.
It involves meninges with the development of carcinomatous meningitis and neu-
ropathy of the cranial nerves, or there is an affection of the substance in the brain
and spinal cord, clinically corresponding to neurological syndromes of disruption
of the brain functions and the signs of compression of the spinal cord. Initially,
Kaposi’s sarcoma develops in the lungs, while brain impairment is most frequently
of a metastatic character, the neurological symptoms depend upon the localization.
Impairment of the cerebral circulation in patients with AIDS
There is development of cerebrovascular complications of the type of ischemic and
hemorrhagic strokes, transitory ischemic attacks

Diagno- Investigation of the neurological and neuropsychological status.

sis EEG.
CT, MRI, PET
CSF diagnosis, immunological examination

There is no etiotropic therapy for AIDS; azidothymidine is used by 5 mg/kg for IV

administration and 10 mg/kg orally.
If the nervous system is involved, acyclovir 20-30 mg/kg for 10 days and rimanta-
dine are used.
Treat- For toxoplasmosis: pyrimethamine by 50 mg/day and sulfamethoxydiazine by 500
ment mg/day during several weeks. If the nervous system is affected with fungi (crypto-
cocci), amphotericin (0.3 mg/kg per day, IV) for 6 weeks is used.
Therapeutic measures consist of immunomodulators, immunostimulants (including
interleukins) and transplantation of the bone marrow.

88
 POLYNEUROPATHIES
(multiple impairments of peripheral nerves)

- infectious (primary, secondary)

- toxic (exogenous, endogenous)
- avitaminous
Etiology - medicinal
- hereditary
- radiation

- demyelinating polyneuropathies
Pathogenesis - axonal polyneuropathies

- distal-symmetrical segmentary demyelinization of nerve fib-

Pathological
bers
morphology
- degenerative-dystrophic processes in the axial cylinders of pe-
and the place
ripheral nerves
of lesion
- polyneuropathic syndrome
a) peripheral distal tetraparesis;
Leading clini- b) disturbances of sensation in the hands and feet;
cal manifesta- c) pains and autonomotrophic disturbances
tions - isolated forms with preferential affection of the motor, sensory
or autonomic fibbers

- electromyography, determination of antibodies to the

Diagnosis and myelin of peripheral nerves in the blood serum
differential di- - with all the forms of polyneuropathies, with Raynaud’s dis-
agnosis ease, with diseases of the connective tissue, liver, blood

Exchange plasmapheresis; hemosorption; antiviral agents; corti-

Principles of costeroids; anticholinesterase, desensibilizing and disintoxica-
therapy tion drugs; dehydration; vitamins; physiotherapy

89
 NEUROSYPHILIS

Etiology: Infection (causative agent – spirochaeta pallidum)

Early forms – primary affection of membranes and vessels (mesenchymal reaction); Late
Pathomor- forms – affection of nervous cells, fibers and glia (inflamed dystrophic and proliferative
phology: character of changes)

1. Optic oculomotor impairments (reduction of visual activity, concentric narrowing

of visual fields, s.Argail Robertson, non-uniformity of pupils, ptosis)
General 2. Acoustic vestibular dissociation and symptoms of affection of other craniocere-
signs bral nerves
3. Radicular syndrome ( in the form of reduction or loss of tendon and knee re-
flexes, paresthesia, radicular pains)

Early (mesenchymal) neurosyphilis Late (parenchymatous) ) neurosyphilis

Sub acute
Vascular Gumma- Progressive
(basal menin- Spinal sclerosis
syphilis tous form paralysis
gitis)
The most
-meningeal stroke -hyperten- -shooting pains -expressed
wide-
syndrome course sive syn- -paresthesia mental dis-
spread
-affection of drome -sensitive ataxia turbances
clinical
craniocerebral me -tabetic crises on the
forms:
nerves -nidus -s. Argail Robertson background
symptoms -grey atrophy of optic of neuro-
nerves logical
-arthropathy and osteopa- symptoma-
thy tology
-disturbances of pelvic or-
gans

Additional  positive Wasserman reaction in blood and CSF (not always);

methods  positive serologic reactions, immobilization of treponema pallidum and immunofluo-
of rescence ;
investi-  positive Lange’s test with liquor;
gation  lymphocyte pleocytosis and albumin in liquor (at meningeal forms)

- with meningitides of non-syphilitic etiology;

Differen- - stroke (vascular syphilis);
tial - volumetric processes in brain (gummous form);
diagnosis: - myelitis and the spinal form of lateral amyotrophic sclerosis (amyotrophic syphilis)

1) penicillin
Treatment 2) preparations of iodine and salt of heavy metals
3) preparations improving hemodynamics
4) biogenic stimulators, vitamins

90
 SYRINGOMYELIA

1. In the basis there is the defect of embryonic development, unheal-

Etiology ing of posterior suture of the cerebral tube.
Pathogene- 2. Provoking factors – trauma, infections.
sis 3. In grey matter of the spinal cord it is marked: а) growth of glia with
Pathomor- formation of cavities – gliomatous form; б) expansion of the central
phology channel of the spinal cord -
Hydromyelia
Clinical
Syringomyelia Syringobulbia
forms
Localiza-
Spinal cord Medulla oblongata
tion of foci
1. Posterior horn syndrome – segmen- 1. Bulbar syndrome (le-
tal dissociated disturbances of pain sions of nucleus of IX, X,
and temperature sensitivity XII pairs of craniocerebral
2. Anterior horn syndrome – periph- nerves)
eral paresis and paralyses 2. Stapler dissociated
3. Affection syndrome of lateral horn – disturbances of pain and tem-
vegetotrophic abnormalities (osteolysis, perature sensitivity ( lesion of
Main clini- Charcot`s joint) spinal nucleus of V cranio-
cal syn- cerebral nerve)
dromes
4. Affection syndromes of conducting ways of white substance of lateral
and posterior columns of the spinal
cord, central inferior paresis, sphincter disturbances, conductive distur-
bances of sensitivity
5. Dysraphic status – anomalies of development, dysplasia of the os-
seous articulate apparatus

presence of syndromes of affection of posterior, anterior, lateral
horns, stapler dissociated disturbances of sensitivity on the face, bul-
Diagnostic
bar syndrome, dysraphic status
criteria
 Chronic-progressive course

amy-
Lateral amy- Lep-
Differential Hemomyel Intramedullary Humeral otrophic
otrophic rosy
diagnosis ia tumor plexitis
sclerosis
spinal
syphilis
Therapeu- 1. X-ray therapy, treatment with radioactive isotopes
tic princi- 2. drugs, improving the trophic functions, anti-cholinesterase drugs
ples 3. Massage, exercise therapy.

91
 TUMORS OF THE BRAIN AND SPINAL CORD

Cerebral Spinal
1. Neuroectodermal
Classifica- 2. Membrane-vascular
tion 3. Tuberohypophysial
4. Osseous
5. Metastatic

1. Supratentorial 1. Extra medullar

Localization
2. Infratentorial 2. Intramedullary

1. Radicular syndrome
2. Segmental
1. Hypertensive syndrome
Clinical syn- 3. Brown-Sequard`s syn-
2. Nidus syndrome
dromes drome (cross-section affec-
3. Dislocated syndrome
tion)
4. Conductive syndrome
Craniography, echocardiogram, MRI, CT, x-ray study of the
angiography, rheoencephalogra- spine, myelography, pneu-
phy, MRI, EEG, ventriculogra- momyelography, radioisotope
phy, computed tomography, scanning, electric magnetic
positron emission tomography, field, venospondylography
Diagnosis ophthalmoscopy, CSF study, ra-
dioisotope scanning, neurologi-
cal and psychiatric investigation

1. Operative
2. Radiation therapy
Treatment 3. Chemotherapy
4. Symptomatic

92
 CRANIOCEREBRAL AND SPINAL TRAUMAS

Brain Spinal cord

1. Contusion 1.Contusion
2. Bruise 2. Bruise
Clinical 3. Compression 3. Compression
forms 4. Diffuse axonal affection
5. Fracture of the basis of skull

 General  Vegetative dysfunc-  Symptoms of brain

cerebral tion compression (introduc-
Clinical  Nidus  Intracranial hyperten- tion of fragments, contu-
syn-  Dislocated sion sion foci, pneumo-
dromes  Loss of consciousness cephalus, intracerebral
hematomas)

 Craniography, angiography  CT, МRI, PET

 rheoencephalography, EEG, echocardio-  Radiography of spine
gram  myelography
Methods  CT, MRI, PET  pneumomyelography
of inves-  Ophthalmoscopy  venospondylography
tigation  CSF study

1. Orthopedic
Treat- 1. Operative 2. Operative
ment 2. Conservative 3. Conservative
-dehydration -pathogenetic
-antioxidant therapy -symptomatic
-nootropic -reanimation
-venotonics -rehabilitation
-hyposensitizers

93
 SIGNS OF PERIPHERAL NERVES AFFECTION

The
name of Segments Innervation Clinical picture of affection
nerve
all muscles of an-
terior bending
group of the "Monkey hand" Pain paresthesiae, hy-
hand and fingers peresthesia in the zone of innervations,
Median (except elbow weakness of flexors of the hand and
С6 -Тh1
nerve flexor of the hand muscles, contrasting and abduction the
and fingers), mus- thumb. Hypotrophy of thenar muscles.
cles of raising of Dyshidrosis of the palm.
the thumb

"Drop hand" or "Wristdrop"

Basically – the Hypoesthesia in the zone of innerva-
muscles, unbend- tions. Weakness of extensors of fore-
ing a forearm, arms, weakness of extension and ab-
hand, fingers, tri- duction of thumb (it is resulted to in-
Ventral
Radial ceps and an- dex), hypotrophy of dorsal surface of
branches
nerve coneus muscles of shoulder and forearm. Downturn or ab-
С5 – С8
a shoulder. Also sence of a reflex with triceps muscle of
periosteum of ra- a shoulder. "Crutch paralysis", syn-
dial and ulnar drome of "Saturday night".
bone

Anconeus flexor "Clawhand " Deduction of subjects be-

of wrists, medial tween the 1st and 2nd fingers is com-
part of deep plicated. Cyanosis, a cold snap of inter-
flexor of fingers, nal edge of a hand, thinness and dry-
Ulnar short muscle of ness of a skin. Hypoesthesia in the
С7- Th1
nerve palm, all hy- zone of innervations. Hypotrophy of
pothenar muscles the muscles of the 1 dorsal interval, in-
terosseous and hypothenar muscles.

94
 Continued
Pain in the inguinal area with irradia-
Iliac, greater and tion to lumbar area and to the thigh.
smaller psoas muscles, Sometimes at hemorrhage at the level
quadriceps muscle of of iliac muscle – paresis of innervations
Femoral thigh, pectineal and tai- muscles
L2 - L4
nerve lor’s muscles. Skin of (+) Wasserman symptom.
inferior 2/3 anterointer-
nal surface of thigh,
shin, medial anklebone.
Paresthetic meralgia (Roth-Bernhardt
Lateral cu- disease): numbness and paresthesia on
taneous Skin of an external the anteroexternal surfaces of thigh, in
L2 - L 3
nerve of surface of a thigh 68% - hypoesthesia, sometimes –
thigh
causalgic pains.

Pain in groin with irradiation on the in-

ternal part of thigh, paresthesia and
numbness, hypoesthesia of medial and
inferior third of an internal surface of
Longer and shorter ad-
Obturator thigh, hypotrophy of muscles of an in-
L2 - L4 ductor muscles, gracilis
nerve ternal surface of thigh. Because of loss
and pectineal muscles.
of function of adductor muscles of thigh
stability is broken at standing and walk-
ing, difficulty at laying a sick leg on
healthy one. Anhidrosis.

The feeling of weight in a leg, blunt

Obturator internus and
pain, hypoesthesia on the skin of shin
quadrate muscles of
and foot, bending of the leg in knee is
thigh, semimembra-
broken, active movements in foot and
Sciatic nosus and semitendi-
nerve
L4 – S3 fingers are absent, at walking the
nous, long head of bi-
straightened leg is carried out forward,
ceps muscles, posterior
like stilts.
part of greater adductor
(+) Lasegue`s test, morbidity in Valle`s
muscle
points

95
 Continued
Pains, paresthesia, numbness, hypoes-
thesia on the external edge of foot and
Talocrural and tarsal the 5 finger. Paralysis of innervation
joints. The skin of muscles – impossibility of bending the leg
external edge of foot in ankle joint, distal phalanxes of foot: the
Tibial
L4 - S3 and the 5 finger up foot in position of a dorsal inflection with
nerve
to a final interpha- claw position of fingers - "Calcaneal
langeal joint. Mus- foot", a rise on tiptoe is not possible, at
cles of a shin. waking the support is on the heel. Atro-
phy of muscles.

The skin of lateral

Impossibility of extension of foot, ab-
side of the shin , tib-
Per- duction and pronation: "Drop foot" or
ial, anterior peroneal
oneal L 4 - S2 "Tip foot". Gate – “steppage”. Atrophy
muscles, long exten-
nerve of muscles of anteroexternal surface of the
sor of fingers, exten-
shin.
sor of thumb

Diagnosis: electroneuromyography
Pathogenesis:
1. Compressive-ischemic factor ( tunnel syndrome)
2. Trauma
3. Toxic influence
General principles of treatment:
1. Elimination of etiological factor (medicamentous or operative)
2. Antiedematous therapy
3. Anticholinesterase
4. Improvement of microcirculation
5. Improvement of metabolism
6. Restorative balneotherapy, mud treatment, electrotherapy
7. Massage. Exercise therapy.

96
TUNNEL NEUROPATHY – (often compressive-ischemic) – clinical complexes of
symptoms, caused by compression of nerves and vessels in anatomic canals or tun-
nels and also in other narrow intervals.

Congenital narrowness of the canal, osteochondrosis, endocrine

pathology with ossification of muscles, traumatic deformation of the
Etiology tunnel, tumoral formations, overstrain of muscles because of their
edema

-muscular(femoral nerve in hunter -osseous-fibrous (cubital)

canal)
Types -fibrous-muscular (rib and clavicular) -osseous (Fallopian canal)
-osseous- muscular (obturator);

General mani-
Local pains, symptoms of neuropathy on conductive type, an-
festations of
giospastic symptoms, Tinel`s symptom – the reflected pains, de-
tunnel syn-
compensated tests.
dromes
Stages of de- I. Irritative;
velopment of II. Irritative-deficient;
tunnel syn- III. Deficient.
dromes
-sighs of main or provoking disease;
General clini- -Local symptoms and symptoms of a compression of nerves and
cal manifesta- vessels found out in distal places of compression
tions -Often proximal irritation of pains (false representations about
their radicular genesis).

CLINICAL SIGNS OF TUNNEL SYNDROMES

I group Strain, morbidity, hypo- and hypertrophy of some muscles, revealed
Local by special palpation and electromyographic researches; morbidity of
changes ligatures of projections of some nerves: median, ulnar, tibial, etc.
The change of sensitivity in distal projections of the painful tunnel is
II group rarely more proximal, it is often observed a hypalgesia, not often - hy-
Neurologi- peralgesia. Deep sensitivity as rule does not suffer. Motor abnormal-
cal affec- ities: paresis of hands, feet, separate fingers, muscular atrophy.
tions

III group The change of skin temperature; trophic changes of skin, hair, nails;
Vegetovas- acrocyanosis, changes of arterial pressure, PS, amplitudes of oscil-
cular affec- lations at muscular-tonic neuropathy; regional vascular affections in
tions a zone of nerves innervation.

97
 Continued
Clinical variants of tunnel neuropathy depending on the localization of the tunnel
process
 Neuropathy of the neck  Neuropathy of the  Neuropathy of the cra-
and shoulder girdle pelvic girdle and legs nial nerves
 Neuropathy of the arm

Clinical findings
X-ray study of the zone of interest
Diagnosis
Electromyography

I. Surgical (decompression of the nerves).

II. Drugs.
-substances with biological activity of the connective tissue ;
-drugs improving conductivity in the neuromuscular synapse (anti-
choline estherase etc.);
-drugs which control pain syndrome;
-analgesics, including combined;
-nonsteroid anti-inflammatory drugs (injections, tablets, ointments);
-drugs with intensify nerve tissue regeneration;
-metabolic therapy;
Principles of -myorelaxants with anti-inflammatory action;
- antidepressants, neuroleptics, antispasmodics;
treatment -antioxidants, compexone;
-drugs which improve blood rheology and microcirculation;
-dehydration drugs;
-local blockers.
III. Physiotherapy.
IV. Manual therapy, postisometric relaxation, massage, stretching
the vertebral column, stimulation electromyography, phobnophore-
sis, sinusoid current, magnetotherapy with alternating and pulsed
magnetic field , amplipulse, barotherapy, ultrasound, percutaneous
electroanalgesia, laser therapy, balneotherapy, paraffin, muds,
acupuncture.

98
 DYSFUNCTION OF PELVIC ORGANS

Urination
Influence on the
Stages of the Levels of Clinical manifesta-
supplied struc- Physiology
act affection tions
tures
Spinal
True incontinence
Involuntary- conus
reflex Sacral seg-
Urine retention
-
Weakening ments
- spinal cen- of the outer
ter of sphincter Act of uri- Paradoxical is-
parasympa- - Detrusor con- nation Sacral seg- churia: the bladder
thetic inner- traction ments (irri- is overfilled, the
vation of the tation) urine is discharged
bladder in drops
( S2 – S4)
Vegetative True incontinence
- spinal cen-
pre-gan- Urine discharge
ter of sym-
glia neu-
pathetic in- - contraction of
rons
nervation of the inner
the bladder sphincter Urine re- Bilateral Absence of desire to
tention affection urinate, urine reten-
(Jacobson’s - detrusor re-
of the cer- tion, periodic reflex
cells in the laxation
vical and emptying of the blad-
lateral horns
thoracic der
(D12 - L2 )
segments
Voluptuary Motor cortical Voluntary hypothala- Short-term urine re-
- paracentral lobe zone of urina- control of mus tention
tion and defeca- urination
tion (inhibited
or in-
creased de-
sire to uri-
nate)

99
 Continued
Act stages Influence on Physio- Levels of Clinical manifestations
the supplied logical affection
structures function
-precentral Sensor cor- Sensa- Bilateral Loss of desire to urinate, passage
gyrus tical area of tion of distur- of urine through the urethra, ab-
urination filled bance of sence of voluntary control of the
bladder connec- act. Retention of urine in the begin-
tion be- ning followed by periodic inconti-
tween nence due to increased reflex exci-
the corti- tation of the segment apparatus of
cal cen- the spine. At complete loss of vol-
ters untary control – intermittent incon-
tinence (phenomenon of autonomic
bladder, reflex voiding).
Defecation
Involuntary- - increased Spinal
peristalsis Fecal incontinence
reflex conus
- relaxation Sacral
- spinal center of the Fecal and gas incontinence,
segments
of parasympa- outer defeca- constipation in solid stool
(affection)
thetic innerva- sphincter tion
tion of the Sacral
rectum segments Fecal and gas incontinence
( S2 – S4) (irritation)
- - spinal cen-
ter of sympa- -contrac- Bilateral
thetic innerva- tion of affection
tion of the the inner Feces Absence of desire to defecate,
of the cer-
rectum sphincter reten- retention of stools, periodic re-
vical and
(D12 - L2 ) -decreased tion flex emptying of the rectum
thoracic
peristal-
segments
sis

100
 Continued
Influence
Physio-
on the Levels of
Act stages logical Clinical manifestations
supplied affection
function
structures
Voluntary Volun-
- paracentral Motor tary con-
Loss of desire to defecate, pas-
lobe cortical trol of Bilateral
sage of feces through the rectum,
area of defeca- distur-
absence of voluntary control of
defeca- tion (in- bance of
the act. Retention of feces in the
tion and hibited or connec-
beginning followed by periodic
urination increased tion be-
incontinence due to increased re-
desire) tween
flex excitation of the segment ap-
-precentral the corti-
Sensor paratus of the spine. At complete
gyrus Feeling cal cen-
cortical loss of voluntary control – inter-
of filled ters
area of mittent incontinence.
bladder
urination

101
 DISTURBANCES OF CONSCIOUSNESS
I. Syndrome of inhibited consciousness

Type Clinical signs

 Delayed answers, necessity of repeated questions
Torpor -
 Sleepiness, weakness, poor mimics, low mobility
Partial
 the instructions are performed with delay sometimes
switching
Moderate after they are repeated,
off of the
 preserved complete spatiotemporal orientation
with pre-
 possible focal, cerebral, meningeal signs
serves
verbal
contact  partial spatiotemporal disorientation
against a  inhibition of thinking, sleepy state
back-  rapid fatigue at long contact, transition from productive
ground of contact to formal (yes-no answers)
increased  difficulties with performing complex instructions, per-
perception forming elementary instructions
threshold Deep  possible focal, cerebral, meningeal signs
of all ex-
ternal
stimuli
and de-
creased
activity
 absence of verbal and mimic-manual contact
Sopor –  instructions are not performed
switching off of the  pupil reactions, superficial and deep reflexes are
consciousness without preserved,
verbal contact, coordi-  reaction to the pain is localized (oriented)
nated defensive reac-  possible focal, cerebral, meningeal signs
tions to pain stimulus is
preserved

102
  complete loss of consciousness and any
contact
 the reaction to pain is not localized, the pa-
Coma –
tient responds by a general motor reaction
Com-
Moderate  pupil reaction is decreased
plete
 superficial and deep reflexes are preserved
switch- (stage I)
 disturbances of swallowing and sphincter
ing off
control
the con-
 possible focal, cerebral, meningeal signs
scious-
ness with
total loss  respiratory disturbances of truncal type with
of per- paradoxical breathing (Cheyne-Stokes,
ception Biota, Kussmaul)
and  instability of general hemodynamics de-
marked creased AP, bradyarrhythmia
neuro-  muscular hypotonia
logical Deep  considerably reduced reflexes
and veg- (stage II)  absence of pupil reaction and corneal reflex
etative  absence of reaction to any stimulus (includ-
distur- ing pain)
bances  difficult (impossible) to reveal focal and
meningeal signs

103
 Table continued
 parasympathicotonia (bradycardia, arterial hypotension,
hypothermia, generalized hyperhidrosis, bilateral termi-
nal mydriasis)
 adequate hemodynamics only at drug support
 adequate respiration at instrumental support (artificial
ventilation)
Terminal  diffuse muscular agonia (gutta-percha by syndrome)
(stage III)  the eyes are open due to eyelid hypotonia
 mydriasis
 dullness of the cornea (last tear sign)
 areflexia
 signs of focal affection of the nervous system are diffi-
cult to reveal

I. changed consciousness syndromes

Type Clinical signs

Psychomotor excita- "automatic gestures" – stroking, rubbing, pinching of some
tion areas of the body, grasp reflex.

Acute confusion of consciousness with deorientation in

the environment and personality. Anxiety, fear, marked
motor excitation sometimes with aggression, visual (audi-
Delirium tory) hallucinations, bright delirium emotions followed by
amnesia.
It is necessary to exclude all possible causes before the di-
agnosis of delirium tremens is maid!

104
 Table continued
Sudden deorientation, frequent hallucinations, anger, fear,
anxiety with aggression sometimes purposeful (understand-
Twilight state ing of the environment is absent) followed by amnesia.
Prone to destructive actions.
Combination of the real environment and abundant bright
Oneiroid state emotional experience, the patient is unable to differentiate
dreams and real events.

Acute deorganization with delayed cognitive processes. The

Amentia patients cannot evaluate the environment as a whole. Fussi-
ness is accompanied by apathy.

Speech, active movement, pain reaction are absent, the eyes

Akinetic mutism are open, which gives a false idea about preserved con-
sciousness.

Absence of movement, speech, emotional reaction, memory.

The muscular tone is increased. The patients do not swal-
low. The patients open the eyes when addresses but the eye
Apallic syndrome
movements are not coordinated. They respond to pain by
chaotic motor reaction.

Locked in syn-
drome (absence Clear consciousness with loss of motor functions and
of motor func- speech, oculomotor muscle function is preserved
tions)
Vegetative state State after a long coma

105
 Main clinical signs of tentorial impaction and impaction to great foramen
Tentorial impaction
impaction to great
Clinical signs Midbrain syndrome
foramen
Diencephalic stage Metencephalic stage
Clear conscious-
Consciousness ness or slight tor- Steadily progressing inhibition of consciousness to
state por. somno- deep coma
lescense
Pupils: - size Medium diameter, Widened pupils on the Maximum widening
slightly dimin- side of the pathological fo- of the both pupils
ished, even cus, diminished on the op-
posite side.
-light reac- Preserved but Absent
tion slightly slow inhibited, especially on the
side of the pathological fo-
cus, can be absent,
The position is Active moments are ab- Active movements
Eyeballs normal sent, paresis of looking up, are absent. Dall’s eyes
divergent strabismus phenomenon
Disordered movements,
psychomotor oxidation.
Motor function unchanged Paresis of the extremities absent
on the opposite side, later
on the side of the widened
pupil.
Position of the Usual or with ten-
body and extrem- dency to extension Extensor
lower
position of the
extremities, flexor – Extremities atonia
ities in the lower ex- of the lower
tremities
Tendon reflexes present Sharply increased Absent
Focal signs increased Unchanged Not observed
Table continued
Pyramid patho- Absent or present Bilateral, marked bilateral
logical signs contralaterally
Sphincter func- unchanged Involuntary urination and defecation
tion
Respiratory dis- Absent or are slight Hyperventilation, Chain- Increasing
turbances Stokes or Bitot type bradypnea , respira-
tory arrest
Tonic phenom- Absent or poorly Pain stimuli augment the absent
ena marked described position
Normal or with Acute, increasing tachy- Increasing bradycar-
pulse tendency to tachy- cardia dia
cardia
Arterial pressure Fluctuates or in- Increased Increasing reduction
creased
Body tempera- Normal or sub- Gradual reduction
ture febrile Marked hyperemia

Perspiration Periodic Constant marked hyper- Gradual reduction

hidrosis

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 MAIN NEUROLOGICAL TERMS

Abasia, abasia, - inability to walk due to marked disorder of coordination when

paralyses and pareses are absent.
Absence, absentia, - short absence of consciousness, in patients with epilepsy
Abulia, abulia, - pathologic absence of willpower, absence of will.
Automatism, automatismus – development of feelings, thoughts, movements
without the will and desire of the patient (automatism ambulatory, mental, motor, af-
fective, cenesthopathic).
Ageusia, ageusia, - absence of taste sensation.
Agnosia, agnosia, - disturbance of the processes of recognition of objects by their
features (appearance, color, smell) when mental disorder is absent. The following
types are distinguished: visual, auditory, tactile, olfactory, and gustatory.
Aggravation, aggravatio – voluntary overestimation of the state by the patient
Agrypnia, agrypnia– sleeplessness
Agraphia agraphia, - loss of ability to write at preserved motor function of the
hand and arm without cognitive disturbances
Adiadochokinesis, adiadochokinesis, - loss of ability to perform opposite actions
by the extremities (quickly one after another – flexion – extension, pronation –
supination).
Adynamia, adynamia, - extreme weakness.
Agitation, agitatio – motor excitation with anxiety and fear.
Acalculia, acalculia, - disturbance of ability to operate figures.
Acrocyanosis, acrocyanosis, - cyanosis of the distal parts of the body due to ve-
nous congestion, insufficient function of the right half of the heart, spasm of small ar-
teries.
Amnesia, amnesia, - partial or complete loss of memory.
Asthenia, asthenia, - adaptation reaction which develops after somatic diseases,
surgery, neuroinfections, injuries, intoxication, and other pathological processes re-
sulting in restoration of the function.
Alalia, alalia, - absence of restriction of speech in children due to impairment in
pre-speech period of the speech zones, can be sensory, motor, total.
Alexia, alexia, - loss of ability to read as well as to differentiate separate letters
and words; word blindness (a sign of aphasia).
Amaurosis, amaurosis, - blindness caused by complete loss of conductivity be-
tween the fibers of visual tracts; complete blindness of central origin without objec-
tive changes in the eye.

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 Amblyopia, amblyopia, - weakening of vision without evident objective changes
in the eye.
Amimia, amimia, - loss of mimic expressiveness of the face. Mask-like face.
Amyotrophia, amyotrophia, - muscular atrophia caused by a disease.
Amnesia, amnesia, – partial or complete loss of memory, gap in memories.
Analgesia, analgesia, - loss of ability to feel pain; insensitivity to pain stimuli.
Anarthria, anarthria, - absence of speech due to the loss of function of the muscles
of the tongue. Lower jaw, lips, loss of distinct speech.
Anesthesia, aneasthesia, - loss of all or several types of sensitivity.
Anisocoria, anisocoria, - different sizes of the pupils.
Anisoreflexia, anisoreflexia, - difference in reflexes of the left and right side of the
body.
Anosmia, anosmia, - lack of sense of smell.
Apraxia, apraxia, - disturbance of complicated movements.
Areflexia, areflexia, – lack of reflexes.
Astasia, astasia, - inability to stand, lack of equilibrium (without paralysis and
paresis).
Ataxia, ataxia, - disturbance of coordination, coordinated action of the muscles
Athetosis, athetosis – repetitive involuntary slow movements of fingers and toes.
Atony, atonia – lack of normal tone (usually muscular), flexibility and elasticity;
weakness.
Atrophy, atrophia – literally lack of tissue nutrition, decrease in size of a normally de-
veloped organs and tissues.
Aura aura – sensations experienced before the onset of a disease or convulsion (usually
in epilepsy).
Autotopagnosia, autotopagnosia – lack of ability to recognize parts of the body,
right and left side.
Aphagia, aphagia – inability to swallow.
Aphasia, aphasia – inability to speak due to disorders of cortical centres of the
dominant hemisphere.
Aphonia, aphonia – loss of voice sound.
Afferent, afferens – conducting towards a center, conducting impulses from the
periphery to the nerve centers.
Ballism, ballismus – forced movement, hyperkinesis - sudden, frequent involun-
tary movements, resembling chorea.
Blepharospasm, blepharospasmus – spasm of muscles of the eyes and eyelids.
Brachialgia, brachialgia – pain in the arm along the brachial plexus.

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 Bulimia, bulimia – an insatiable appetite, pathological increase of the appetite.
Bulbar, bulbarus – pertaining to the oblong brain.
Vertigo, vertigo – dizziness.
Vestibular, vestibularis – pertaining to vestibular system, coordination; pertaining
to the labyrinthine vestibule.
Hematomyelia, heamatomyelia – hemorrhage to the spine (its substance).
Hepatorrhexis, heamatorrhachis – hemorrhage to the spinal canal, originating form
the spine meninges.
Hemianesthesia, hemianeasthesis – loss of sensitivity in the left or right side of the
body.
Hemianopsia, hemianopsia – loss of the field of vision in each eye.
Hemiatrophy, hemiatrophia – reduction in nutrition of the tissues in a half of the body
or its portion.
Hemiballism, hemiballismus - involuntary forced frequent motions in the extrem-
ities in a half of the body or its portion.
Hemihypertrophy, hemihypertrophia – hypertrophy of a half of the body or its portion.
Hemicrania, hemicrania – headache in one side of the head, migraine.
Hemiplegia, hemiplegia – paralysis of extremities on one side of the body.
Hemispasm, hemispasmus – contraction of the muscles of one side of the face,
one or several muscles on one side of the body.
Hydrocephaly, hydrocephalia – abundant accumulation of fluid in the skull, hy-
drops of the brain.
Hypacusia, hypacusis – lack of hearing due to reduction in excitability of the
acoustic nerve.
Hyperacusia, hyperacusis – abnormally increased hearing acuity; increased per-
ception of moderate sounds due to increased excitability of the acoustic nerve.
Hypalgesia, hypalgesia – reduction of pain perception.
Hyperhidrosis, hyperhidrosis, - increased perspiratio of different origin.
Hyperesthesia, hyperasthesia – increased sensitivity to various stimuli.
Hyperkinesis, hyperkinesis – abundant, involuntary movements.
Hyperosmia hyperosmia – pathological increase of olfaction.
Hyperreflexia, hyperreflexia – sharp increase in reflexes.
Hypesthesia, hypaesthesia – decreased sensitivity, touch in particular.
Hypomnesia, hypomnesia – weakening of memory.
Hyposmia, hyposmia – lack of olfaction.
Hypotrophy hypotrophia – functional insufficiency of the tissues due to lack in
nutrition.

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 Glossalgia, glossalgia – cramping excruciating burning pain in the tongue, some-
times irradiating to the adjacent tissues.
Glossodynia, glossodynia – feeling of burning prickling in the tongue.
Dementia, dementia – reduction of cognitive abilities due to organic disease of the
brain.
Dermographism, dermographismus – vasomotor reaction of the skin, white and
red lines after
irritation of the skin.
Dysarthria, dysarthria – lack of distinctive speech due to disorders of the speech
apparatus.
Dysesthesia, dysaesthesia – perverted perception of some sensations.
Dyssomnia, dyssomnia, - disturbance of sleep of various origin.
Dysphagia, dysphagia, - disturbance of swallowing.
Dysosmia, dysosmia – lack of olfaction, disturbance of olfaction.
Diplopia, diplopia, - vision disorder, double vision.
Dysphonia, dysphonia - hoarse o voice.
Insomnia, insomnia – sleeplessness.
Ischemia, ischemia – local deficiency of blood in some part of the body; reduction
or arrest of blood supply.
Ischialgia, ischalgia – pain along the sciatic nerve.
Causalgia, causalgia – burning sharp unbearable pain, observed in disorders of
peripheral vegetative fibers.
Coccygodynia, coccygodynia – pain in the coccyx; neuralgic pain in the area of the
tailbone more frequent in women after injury or inflammation of the coccyx.
Collapse, collapsus, - acute vascular insufficiency accompanied by reduction in the
vascular tone, reduction of the volume of circulating blood, AP, brain hypoxia and inhibi-
tion of vital functions of the organism.
Coma, koma, - Loss of consciousness due to inhibition of the CNS, disturbances of
stem function.
Contracture, contractum, - stable limitation of movement in the joints due to distur-
bances of the nerve supply of the muscles.
Cramps, crampi – painful tonic spasms (more frequent in gastrocnemius muscles at
night), manifestation of neurological complications of osteochondrosis.
Leukodystrophy, leucodystrophia – hereditary disease of the nervous system
caused by enzyme defects and disturbances of myelin metabolism involving primar-
ily the conductive tracts.

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 Leptomeningitis, leptomeningitis – inflammation of pia mater and arachnoid
meninges; manifests by development of meningeal signs, inflammatory changes in
the cerebrospinal fluid.
Lumbago, lumbago – cramp-like intensive pain in the lumbar area, limiting the move-
ment of the spinal column in the lumbosacral portion.
Meningism, meningismus – syndrome of meninges involvement in the pathologi-
cal process without inflammatory changes in the latter.
Meningitis meningitis – inflammation of the meninges; manifests by meningeal
syndrome.
Myalgia, myalgia – pain in the muscles.
Myasthenia, myasthenia – neuromuscular disease characterized primarily by in-
creased muscular fatigue.
Migraine, migraine, - cramp-like headaches.
Mydriasis, midrias, - pathologic widening of the pupil in various diseases.
Myelopathy, myelopathia, - noninflammatory affection of the spine.
Myatonia, myatonia – disease accompanied by reduction of the muscular tone and
its loss; lack of muscular tone.
Myelitis, myelitis – inflammation of the spinal cord.
Myoclonia, myoclonia – quick irregular involuntary movements due to contraction of
some muscles or groups of muscles, chiefly in the extremities.
Myopathy, myopathia – a group of hereditary diseases of the muscles resulting
form disturbances in contractile ability of the muscular fibers and manifesting by
weakness, reduced volume of active movements, decreased tone, atrophy.
Myoplegia, myoplegia – neuromuscular disease characterized by attacks of mus-
cular weakness and paralyses of the extremities.
Myotonia, myotonia – pathological state of the muscles manifested by difficult re-
laxation after considerable contraction.
Neuralgia, neuralgia – intensive pain along the trunk or branches of a sensitive
nerve.
Neuropathy, neurophathia – disease due to disjunction of the vegetative nervous
system.
Nystagmus nistagmus, - involuntary rhythmic movement, repeated trembling, os-
cillations of the eyes with slow and rapid phases.
Ophthalmoplegia, ophthalmoplegia – disturbance of eyeball movement due to af-
fection of the nerves, neuromuscular synapses or oculomotor nuclei, simultaneous
paralysis of all or several cranial nerves supplying the muscles of the eye.

111
 Paralysis, paralitis, - complete loss of ability to perform voluntary (active) move-
ments caused by deinnervation of the respective muscles.
Paraspasm, paraspasmus – spastic hypertension of extremities, bilateral, mainly in
the lower extremities, a part of pyramid symptom-complex (associated with paralytic
phenomena).
Paraphasia, paraphasia – distorted speech, in which the patient misses, repeats or
changes some words or sounds. Formation of new words.
Paresis, paresis – partial paralysis, incomplete loss of ability to perform volun-
tary movements.
Paraesthesia, paraesthesia - spontaneous unpleasant sensation of creeps due to af-
fection of sensitive fibers of the peripheral nerve, conducting tracts or sensitive area
of the cortex.
Paresthetic meralgia, meralgia paraesthetica – Rot-Bernhardt disease, painful
panesthesia of the external
Side of the thigh in the area of the lateral cutaneous nerve of the thigh.
Parkinsonism, parkinsonismus – a group of clinical manifestations with the signs
resembling shaking palsy (Parkinson’s disease).
Paroxysm, paroxysmos - sudden short intensification of the signs of the disease.
Pachymeningitis, pachymeningitis – inflammation of the dura mater.
Perineurium, perineurium – connective-tissue membrane of the nerve or a bundle
of nervous fibers.
Plexitis, plexitis – disease of the nervous plexus.
Graphospasm, spasmus scriptorius - disturbance of synergism of the hand mus-
cles causing disturbances of writing, the while ability to make tine movements is pre-
served.
Poliomyelitis, poliomyelitis – acute inflammation of the CNS with affection of an-
terior horns of the spine, the course is characterized by atrophic muscular paralyses.
Polyradiculoneuritis, polyradyculoneuritis – disease with multiple affection of the
radices of the spine and nervous trunks (peripheral nerves), characterized by pains, pares-
thesias, muscular weakness in the extremities, flaccid paralyses.
Prosopalgia, prosopalgia – pain in the face not associated with neuralgia.
Propulsion, propulsio – falling forward, uncontrollable movement forward at a
slight push.
Ptosis, ptosis – drooping of the upper eyelid due to paralysis of the muscles erect-
ing it.

112
 Radiculitis, radiculitis – affection of the roots of the spine, intradural portion of
the spine, its entrance to the intervertebral foramen or its potion between the foramen
and the nervous plexus.
Rigidity, rigiditas – difficult movement, stiffness.
Sacralization, sacralisatio – partial or complete fusion of the fifth lumbar vertebra
with the sacrum
Sacrodynia, sarcodynia – pain in the sacrum and sacral area.
Sympathalgia, sympathalgia – fit-like pain arising at affection of the vegetative sympa-
thetic nodes or sympathetic nervous fibers.
Sympathoganglionitis, sympathoganglionitis – disease due to affection of the sym-
pathetic nervous node.
Synkinesia, synkinesis – involuntary simultaneous movements on the side of
paralysis of paresis during active movements with healthy extremities.
Syncope, syncope – paroxysmal short-time loss of consciousness due to transient
hemodynamic disturbances caused by brain ischemia.
Syringobulbia, syringobulbia – syringomyelitis process involving the oblong brain or
going in cranial direction from the spine.
Syringomyelia, syringomyelia – disease characterized by formation of cavities and
cysts chiefly in the spinal cord.
Somnolence, somnolentia – pathological sleepiness; the patient can be waked up
only for a short time with words or touch.
Sopor, sopor – deep pathological sleep, a form of deep disturbance of conscious-
ness; the state of being indifferent to the surrounding.
Stupor, stupor – state of mental and physical lethargy, manifesting by absence of
movements, mutism, weak reaction to the stimuli.
Spasm, spasmus – sudden short involuntary contraction of the muscles with or
without loss of consciousness.
Thermanesthesia thermanaesthesia – loss of thermal sensitivity, ability to recog-
nize temperature differences.
Tetany, tetanоs – painful severe long contraction of muscles of groups of mus-
cles.
Tremor, tremor – rhythmic trembling, quick involuntary contractions and relax-
ations of groups of muscles, causing rhythmic low-amplitude motions of various
parts of the body.
Trismus, trimos – spasm of jaw muscles at tonic contraction of mastication mus-
cles

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 Spastic torticollis – spastic wryneck caused by tonicoclonic spasms of the stern-
ocleidomastoid muscle or deep muscles of the neck.
Phobia, phobos – abusive pathological state in the form of extreme fear of some-
thing.
Cephalgia, cephalgia – headache which occurs at irritation of pain receptors of the
meninges, vessels, periosteum, superficial tissues of the skull, at irritation of vegeta-
tive nerves and nodes and their branches.
Exophthalmos, exophthalmos – bulging of the eyes.
Encephalitis, encephalitis – inflammation of the brain of infectious of infectious
toxic origin.
Encephalomyelitis, encephalomyelitis – inflammation in the brain and spine.
Encephalopathy, encephalopathia – organic changes in the brain tissue due to
some pathology.
Epilepsy, epilepsia – a disease characterized by periodic attacks of seizures with
loss of consciousness during the attack, with changes in the character, personality dis-
turbances.
Epiduritis, epiduritis – inflammatory disease accompanied by accumulation of pus
in the space over the dura mater.

114
 DRUGS FREQUENTLY USED IN NEUROLOGY
1. Neuroprotectors
1.1. Antioxidants: vitamin Е, unithiol, ascorbic acid, triovit, aevit, emoxipin,
mexidole, espalipon.
1.2 Antigluthamate: riluzole, Lamictal, remasemid
neuromediator amino acids (“Aminoplasmal”)
1.3 Calcium antagonists: Nimotop (nemotan), cinnarizine. stugeron,
flunarizine, dilceren.
1.4. Drugs improving cerebral metabolism: nootrops, instenon, encephabol, ac-
tovegin, cerebrolysin, tanacan, pramistan, GABA-соntaining (phenibut, am-
inalon), neuroaminoacids (glycin), semax, preparations of Ginkgo-biloba,
memory-rise, GABA-соcontaining – noophen, racitams and lucetams, glyc-
erinum, picamilon, fesam and others.
2. Drugs improving cerebral circulation
2.1. Antiagregates: clopidogrel, ticlid, curantil, aspirin, pentilin, trental, anopy-
rin, agapurin, flexital
Anticoagulants: heparin, , lasurid, bromcryptin, ronalin
2.2. МАО-В antagonists: umex, clexan, fraxiparin, rheopolyglucin, fragmin
2.3. Vasoactive drugs: sermion, euphillin, cavinton, actovegin, nicotinic acid.
2.4. angioprotectors: rhutin, dicinon, troxevasin, detrolex
3. Drugs improving and stabilizing liquocirculation:
3.1. corticosteroids: prednisolon, dexametason
3.2. venotonics: euphyllin, anavenol, aescusan, L-lysin, escinat.
3.3. saluretics: lasyx, urix, diacarb.
3.4. osmodiuretics: glycerin, mannit, manitol, including hypertonic solutions:
glucosae, magnesium, calcium chloride
4. anti-parkinsonism:
4.1 L-DOPA-containing: nacom, sinemet, madopar, sindopa
4.2 dopamine antagonists: pergolid eldeprinil, selegelin
4.4. dopamine releasing: amantadin, midantan, neomidantan
4.5. cholinolytics: parkopan, cyclodol
4.6-adrenoblockers: propranolol, anaprilin, obsidan, coreol
5. antispasmodic:
5.1. phenitoin: diphenin, phengidan, taloxa
5.2. carbamsepine: timonil, finlepsin, zeptol
5.3. valproate: depakin, orphiril, everiden
5.4. modern antiepileptic drugs:
lamotrigine, gabapentin, vigabatrin, clonasepam
5.5. phenobarbital
5.6. drugs to control of series of epileptic attacks or for treatment of epileptic
status: sibazon, relanium, phengidan, diazepam in suppositoria, barbiturats
( thyopental sodiumи and others), general anesthesia.
6. anti-migraine:
- to control the attack:
6.1. ergot drugs: dihydroergotamin, dihydergot,
nomgren, tamik
6.2. serotonin receptor agonists: sumatryptan
6.3. anticonvulsants: finlepsin, timanil, carbamazepin
- to prevent frequent attacks:
6.4. serotonin antagonists: sandomigran, nomigren

115
 6.5. calcium antagonists and -adrenoblockers (stugeron, cinnarizin, flunarizin,
propranolol, coreol, anaprilin, obsidan), vasocardin
7. vegetotropic:
7.1. -adrenoreceptor blockers: pyrroxan, coreol, sermion
7.2. -adrenoreceptor blockers: coreol, propranolol, anaprilin, obsidan, corvitol
7.3. cholonolytics and combined atropin-like drugs: atropine, platiphyllin, bel-
loid, bellaspon
7.4. antidepressants
7.4.1. tricyclic: amitriptilin, melipramin,
anafranil, gerfonal
7.4.2. quadricyclic: ludiomil
7.4.3. reverse serotonin capture inhibitors: cipramil,
avoxin, zoloft, paxil, phluoxetin (prozac)
7.4.4. combined antidepressants: eglonil
(sulpyrid)
7.5. sedative: herbion sedative drops, valerianae, novopassitum, barboval, valo-
cordin, mebicar, sedasen, notta and others.
7.6tranquilizers: benzodiazepines
8. Drugs administered in neuromuscular disorders:
8.1. improving neuromuscular conductivity: anticholinesterase - proserin,
neostigmin, amiridin (neuromidin), physostigmin, galantamin, nivalin
8.2. contributing myelin restoration: vitamin В, -lipoic acid (berlition, es-
palipon) phosphaden, lecytin, neurotransmitting aminoacids, methionin-con-
taining drugs
8.3. improving muscular metabolism: vitamin Е, retabolil, amino-acid com-
plexes
8.4antigluthamate in motoneuron diseases: rilutek ,
embryonic tissue preparations
8.5. insulin-like factor f neuron growth
9. Drugs used in autoimmune and dimyelinizing diseases:
9.1. corticosteroids: prednisolon, dexametason, methipred,
solomedrol
9.2. cytostatics: cyclophosphamid, asatioprin, imuran
9.3.hyposensibilizing: tavegil, suprastin, peritol,
claritin, phencarol, telfast.
9.4. immunomodulatorss: Т-activin, thymalin, splenin
10. drugs used in herpetic lesions of the nervous system :
10.1. antiviral drugs: zovirax, valtrex, acyclovir, medovir, proteflasid
11. drugs controlling myofascial and neuralgic pains (including tension pains):
11.1. myorelaxants: sirdalud, myolastan, baclofen, mydocalm
11.2. nonsteroid antiinflammatory drugs:
diclofenac NA, diclobru, mesulid, nemesil, sigan, naclophen,
voltaren, indomethacin, ibuprofen, ortofen, diclofenac-rapid, olfen and
others.
11.3. antiparoxysmal (carbamezepin)
11.4 drugs which control pain syndrome:
baralgin, tempalgin, sedalgin, maxigan, trigan, cetanov, spasmoveralgin,
renalgan, neurorubin and others.
12. Drugs used in muscular dystonias and hyperkinesis:
12.1. affectine muscular tone: sirdalud, baclophen ,
myolastan, disport, botox.
12.2. bensodiazepines: sibason, relanium, tranxen
116
 12.3. HAMA-containing: phenibut, noofen and others.
12.4. Deceleration amino acids: glycin and complex neuromediator amino
acids
13. antisclerotic drugs:
13.1 Vasilip (simvasatin), drugs correcting lipid metabolism
with antiatherogenic action (levostatin,
zokor, lipostabil) and others.
13.2 nicotinic acid
14. biogenic stimulators: FIBS, aloe, corpus vitrum, tinctura
ginzengi, tonic-k, herbal: rodiola, eleuterococc, leuzea and others.
15. neuroleptics: aminasin, sonapax, galoperidol, droperidol,
eglonil.
16. anabolic steroids: retabolil, nerobolil, nerobol.
17. antistress drugs: magne-В6, eglonil (sulpirid),
Novo-Passit, persen, adaptol
18. calcium-containing drugs: calcium D3 – nicomed, Са gluconas
19. interferones: rebif, -interferon.

117
 Educational edition
NEUROLOGY (in tables and pictures)

Manual
for English-medium students
edited by Prof. I.A. Grygorova

Contributors Iryna Grygorova

Konstantin Leschenko
Alina Grygorova
Elena Resnichenko
Olga Teslenko
Alexander Eskin
Ludmila Tikhonova
Elena Ibragimova

118