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DISORDERS OF CRANIAL NERVES

The motor function of muscles of the face, eye globes, soft palate,
pharynx, vocal cords and tongue, and also sensitivity of a skin of the face,
mucosa of eye, oral cavity, nasopharynx and larynx is provided with
cranial nerves. From 12 pairs of cranial nerves only sensitive are I, II and
VIII pairs, motor - III, IV, VI, VII, XI and XII pairs and the mixed - V, IX,
X pairs.
Some from them contain vegetative fibers (III, VII, IX and X pairs).
Sensory nerves form periphery departments of analyzer: olfactory (I),
visual (II), acoustical (VIII), vestibular (VIII) and gustatory (VII, IX).
These nerves are transmitters of the information on environment in basic
with the help of receptors.
Two first of cranial nerves (olfactory and visual) on a constitution
differ from others (they represent as though parts of a brain, borne on
periphery).
Others 10 steam of cranial nerves, besides an originality of each of
them, have also common features with spinal roots and nerves. We shall
not be stop on anatomy as you are know it, but we shall discuss
syndromology.

N. olfactorius.
Unilateral dropping olfactions (hyposmia) or its complete loss
(anosmia) is observed at a lesion of olfactory nerves on skull base at a
tumor, fracture, traumatic hematoma, inflammation. Also unilateral
anosmia develops at lesion of olfactory bulb, path and delta circuit and
forward substantia perforata. In hyposmia results pathological processes
on the base of a frontal lobe, in medial departments of front cranial fossa
(tumors of lobe-basal localization, hematoma at subarachnoidal
hemorrhage, focal meningitis, abscesses, cracks and fractures of bones of
the base of front cranial hole with a subdural hematoma, contusion focuses
of hemorrhagic stroke of orbital parts of frontal lobes, timorous like
formations- gummas, tuberculomas, etc.
Two-sided hyposmia or anosmia quite often has rhinogenous
character - at grippe, atrophic rhinites. Reduction of olfaction can come at
intracranial hypertension, edema and brain swelling at which cerebral
frames nestle on bones of the base of front cranial fossa.
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Hyposmia can develope at diabetes, hypothyroidism, scleroderma,

Pedget’s illness and at introduction of some medicinal preparations.
Irritation of these cortical formations can result in to original attacks
of sensations of a smell not existing actually - olfactory hallucinations.
Such paroxysms have diagnostic value, specifying on lesion of temporal
lobe of the brain. They can be combined with olfactory parastesias,
gustatory, vestibular, vegetative-visceral and other disorders. Olfactory
hallucinations show self-contained or as aura before the beginning of
epileptic attack.
Combination of olfactory and smell hallucinations with epileptic
attacks typically for a lesion of uncus hippocampus and amigdala.
Olfactory agnosias concern to crustal olfactory infringements also:
loss or decreasing of ability to identify smells and their object accessories
(at safety of elementary olfactory functions). It arises at desorder of
associative communications between hippocampus and cortical regions
surrounding it.

N. opticus.
At examination of function of vision it is necessary to spot visual
acuity under which it is meant to accept separately ability of an eye 2
points posed from each other on some distance. Weakening of visual
acuity is termed as an amblyopia, the complete loss of sight - an
amaurosis.
The important value in a neurology gets examination of a field of
vision. The field of vision is a field of space which sees fixed eye.
Dropout of one half of field of vision is termed as hemianopsia.
The lesion of a retina or one optic nerve results in decrease of visual
acuity or complete blindness. At blindness reaction of pupil on light
disappearance; concomitant response of pupil at irradiating able-bodied
eye remains because of safety efferent part of arc of this reflex. There can
be blindness in center of field of vision. At suffering of bark of occipital
lobe also there can be in sight « region of darkness », but patients of this
defect do not note, therefore such distress term as negative scotoma.
In range of decussation of optic nerves pathological process can
destroy only its central departments where pass crossed fibers from
intrinsic halves of retina. In such cases temporal halves of field of vision –
bitemporal hemianopsia - drop out. Damage only outside fields of
decussation of optic nerves is less often observed. At such patients
conductors from outside halves of retina of both eye that results in
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abaissement of nasal halves of field of vision - binasal hemianopsia are

ungeared. These are two types heteronim hemianopsias. The incomplete
compressionn of visual decussation from different directions results in
concentric narrowing of vision field.
Lesion of visual tract and lateral geniculate body the hemianopsia
produces secund homonim hemianopsia seu traktal. The same
hemianopsia arises and at lockout of visual conductors - a visual radiance
in range of intrinsic sheath or in depth parietal and occipital lobes.
At traktus hemianopsias the prime atrophy of optic nerves is found
out, cofriend response of a pupil to light is lost, frequently there is sharply
expressed asymmetry of defects of vision field. At central conduction
hemianopsia atrophy of optic nerves is not present, response of pupils to
light preserved hemianoptical, defects of field of vision are routinely
symmetrical.
At selective lesion of deep departments of parietal lobe or occipital
lobe conductors from the upper quadrant balances of the conforming
halves of retina that produces low qudrantis hemianopsia are ungeared. At
a lesion of temporal lobe or gyrus linqualis there is high quadrant
hemianopsia.
At retrochiazmal lesion of visual radiance of all medial surface of
occipital lobe vision preserved only in central fields - «macular vision».
The irritation of cortex in range calcar sulcuses is accompanied by
visual hallucinations in counter halves of vision field. As usial such
sensatins are precede of epileptic attack. At irritation of outside surface of
occipital lobe visual hallucinations are more complex, subjects seem
garbled.
Except of vision field, at patients the color perception is tested. The
complete color-blindness, except for congenital, can arise at particulate
atrophy of optic nerves.
The important value in neurologic clinic is attached examination of
eyeground. The ophthalmoscopy allows to reveal a neuritis of optic nerve,
atrophy of optic papilla - at tumour of brain - and stagnant optic disk - at
rising intracranial pressure.

N. oculomotorius.
At damage of nerve the conforming muscles only on the side are
paralyzed: there is a blepharoptosis; if this blepharon to uplift, it is visible,
that the eyeglobe is declined lateral - a divergent strabismus (strabismus
divergens), there aren’t autokinesias of eyeglobe up, medial and from top
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to bottom, there are mydriasis. The patient feels doubling subjects at view
as two eyes - diplopia. Doubled plotting miss as across, and on vertical,
i.e. settle down one above another or under an angle to each other.
At destruction of nucleus of third cranial nerve on the side of the
locus all muscle of eye will be paralysed, except for medial direct.
However on the counter side the medial direct muscle is separately
ungeared only.
Thus, the basic signs of a lesion III steams of cranial nerves are:
ptosis; divergent strabismus and impossibility of locomotions of the struck
eyeglobe medial and upwards; exophthalmia; a mydriasis with absence
direct and concomitan responses of pupil to light; paralysis of
accommodation.

N. trochlearis. At a selective lesion arise mild concurrent strabismus

and diplopia only at a view downwards.

N. abducens. At lesion of this nerve there is concurrent strabismus,

the eyeglobe cannot be voluntary removed lateral; arises diplopia,
intensifyed at view aside the struck nerve. Forking subjects are in one
horizontal plane.

Concomitant locomotions of eyeglobes.

In norm eyes move in all directions concomitant. In a back
department of the second frontal gyrus the range influencing rotational
displacements of an eye in the counter side settles down. Axons of these
central neurones pass in composition of a front leg of internal capsula,
then in pes of brain, and in pons of brain in their basic part comes over to
on the counter side to nucleus of abducent nerve.
At a lesion of a frontal oculomotor path are broken concomitant
locomotions of eyeglobes - there is a palsy of look. If the locus settles
down in one frontal lobe (a cortex, internal capsula) eyeglobes cannot be
voluntary removed on the counter side, they appear reflexly looking aside
the damage hemisphere. It is necessary to judge the locus of a lesion on
concomitant hemiplegia. If one half of brain pons suffers and is damaged
pyramidal tract eyeglobes are reflexly deviated in counter to the locus side.
At irritation of cortex of the second frontal gyrus there are convulsive
twitchings eyeglobes aside, counter to the locus.
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At lesion in the range of lamina quatrigemina combined locomotions

of eyeglobes on a vertical - a paralysis of look upwards and downwards
(set of symptoms Parino) are developed.
The particulate lesion of medial longitudinal fascicle can give to that
eyeglobes occupy various position in relation to horizontal line - a
divergent strabismus on a vertical: one eyeglobe is deviated slightly down
and medially (on the side of the locus), another - up and lateral (syndrom
Gertwig-Magandy). Besides at lesion of system of medial longitudinal
fascicle it is possible appearance of nystagmus.
The mydriasis arises at lesion of a third cranial nerve or as a result of
irritation of sympathetic nerve. Desorders of sympathetic innervation of
eye and irritation of third cranial nerve causes narrowing a pupil (miosis).
Non-uniformity of breadth of pupils is termed as anisocoria.
Narrowing of a pupil owing to infringement of sympathetic
innervation is routinely combined with enophthalmos and narrowing of a
palpebral fissure (Bernar - Gorner syndrome). The irritation of
sympathetic nerve, besides mydriasis, exophthalmia and dilating of
palpebral fissure (Pti syndrom).
At a lesion of all third cranial nerves the complete ophthalmoplegia
educes, at paralysis only external muscles – outside ophthalmoplegia, at
lockout of function of internal muscles of eye - inside (internal)
ophthalmoplegia.

N. trigeminus.
The unilateral paralysis of muscles, innervated motor root of
trigeminus, produces difficulties of mastication on the sick side. The tone
of temporal and masticatory muscles on this side is weakened. These
muscles appear atrophied. At unclosing of mouth the mandible is wedged
in the sick side as a result of predominance of tone of alary muscles over
the able-side. Mandibular reflex is not evoked. The described motorial
desorders can be combined with anaesthesia in region innervations of
mandibular nerve. Taste on front two thirds of tongue is sometimes
broken. In infrequent cases the central paralysis of masseters as constituent
of pseudobulbar syndrom is probable. This paralysis happens two-sided;
mandibular jerk increases, amyotrophias are absent.
At lesion of sensory root of trigeminal nerve the anaesthesia covers
like half of face and pilar part of head, all kinds of sensitivity suffer,
disappears mandibular reflex. Some patients has separately involved
maxilar or ophthalmic nerves, then distresses of sensitivity arise in zone
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their branchis. Lesion of these nerves leads to anaesthesia of cornea and

corneal reflex drops out.
Pathological processes in brainstem can involve different levels of
spinal path nucleus of nerve. The anaesthesia of skin of face in that case
has dissociated character and is not on projection of branches of
trigeminal, but for segmentary type. Lesion of inferior department of
nucleus anaesthesias region traps lateral ranges of the face, and at
suffering of the upper department - its medial departments around of
mouth and nose.
Lesion of talamus and back third of back leg of capsula interna
evokes contralateral lockout of all views of sensitivity on the face, trunk
and extremities (hemianaesthesia). Abaissement of sensitivity only on one
half of face arises at lesion of the inferior third of postcentral gyrus of
counter hemisphere of brain.
At irritation of trigeminus (the cicatrix, solderings, fracture etc.) arise
intensive paroxysmal pains in the face - trigeminal neuralgia. On the
localization of pain coincide routinely with projection of one of three
branches of nerve. In interspaces between attacks pain miss. At trigeminal
neuralgia on skin of face and on mucosa of oral cavity there are fields,
hiting at which results in pain attack - trigger zones.
At irritation of trigeminal nerve the tonic cramp of masseters
-masticatory spasm - educes.

N.facialis.
At lesion of nucleus of facial nerve the flaccid paralysis of mimic
muscles on the side of the locus (lagophthalmia, Bell sign, lacromoreihja)
can be combined with spastic hemiparesis on counter to the locus side -
alternating paralysis Mijar- Gubler which is connected to concomitant
lesion piramidal systems near to nucleus of facial nerve. If the
pathological locus propagates on internal genu of facial nerve function of
nucleus of abducent nerve is broken also - alternating Fovill,s syndrom
educes: -flaccid paralysis of mimic muscles and lateral direct muscle of
eye, on counter - a spastic hemiplegia.
Lesion of root of facial nerve in cerebellopontine angle leads to
paralysis of mimic muscles associating with desorder of trigeminal
function, abducent and vestibulocochlear nerve.
Lesion of facial nerve in internal acoustical passage results in the
paralysis of mimic muscles in combination with dryness of eye, lision of
taste on front two thirds of tongue and deafness on this ear.
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The lesion of facial nerve in the facial canal up to going out nervus
petrosus major shows prosoplegia, dryness of surface of conjunctiva and
cornea, hyperacusia and lision of taste on front two thirds of tongue.
The lesion of facial nerve in facial canal above level going out
n.stapedius is accompanied lacrimorheja, hyperacusia and lision of taste.
The lesion of facial nerve is higher going out chorda tympani results
in prosoplegia, lacrimorheja and to desorder of taste on front two thirds of
tongue.
At lesion of facial nerve at level of going out through stylomastoid
foramen the clinical pattern develops only of paralysis of mimic muscles
and lacrimiorheja.
Lesion of corticonuclear fibers the central paralysis only the inferior
mimic musculation on counter to the locus educes. It can be combined
with central paralysis of half of tongue, or all half of body (central
hemiplegia).
The irritation by pathological locus of cerebral cortex in zone
projections of face or some structures of extrapyramidal formations can
show paroxysms of tonic and clonic cramps (Jecsonian epilepsy), or
hyperkinesias of separate muscles of face (a facial hemispasm,
paraspasm).

N. vestibulocochlearis.
Giddiness (or vertigo) - one of the most often complaints. Other
important vestibular sign - a nystagmus, it is routine with distinctly
expressed quick and slow phases.
Infringements of vestibular response conduct to distresses of
equilibrium and coordination of locomotions. There is following cardinal
sign - vestibular ataxia. At walking and standing patient has tendency of
declination and slope aside the damaged labyrinth. If the patient who is
taking place in Romberg’s posture blindly, turns head to the left or to the
right he will fall aside of ill vestibular kettle. Vestibular ataxia it is not
characterized by intention tremor.
If there is reduction of audition (hypakusia) or its loss (anakusia) it is
necessary to spot, if depends on a lesion sound conducting (a middle ear)
or the sound-accepting nervous kettle for what use assays with tuning fork.
Use test Rhinne, Weber.
Processes in outside or middle ear reduce especially strongly
perception of low tints, and diseases of an acoustical nerve - high tints.
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N. glossopharyngeus.
Loss of taste (ageusia) or dropping (hypogeusia) arise at a lesion of
glossopharyngeal and intermediate nerves. The boring of a cortical
department of the analyzer is accompanied by false gustatory sensations
(a steam ageusia, hallucinations).
The neuralgia in region allocations of responsive branches IX steams
(tonsils, a back wall of a pharynx, a back of the tongue and outside
acoustical passage) is occasionally observed. The pain of the considerable
intensity arises paroxysmally, is prolonged from several seconds about
one minutes. Intervals between attacks are various (from several clocks
about several weeks). Routinely one nerve (dextral or left-hand) is
amazed.
At damage salivation fibers of glossopharyngeal nerve there can be
some dryness of a mucosa of oral cavity, however frequently patients do
not note it.

N. vagus.
At damage of peripheric neurone (nucleus or nerve) or at lesion of
both (dextral and left) central neurones there comes dysphagia and
phonations (aphonia). These infringements are termed bulbar paralysis.
The voice gets nasal shade. Infringement of phonatory function of
vocal cords produces hoarseness and weakening of phonation force down
to aphonia (it is possible only silent speech. The laryngoscope allows to
establish paralysis of true vocal cords. Paresis of soft palate gets the fluid
nutrition in a nose. Hit of nutrition and spit in larynx, trachea at such
patients produces choke, that can give in aspiration pneumonia.
Survey of soft palate taps its backlog at phonation on the ill side and
deflection of uvula in the able-bodied side. The palatine velum is
tightened irregularly, lagging behind on the side of paresis.
Absence or drop arch jerks on one side testifies to peripheric lesion
IX and X nerves. Two-sided absence of gag reflex and jerk from a soft
palate not always specifies presence of organic disease.
Infringements of cardiac rhythm (tachycardia), distresses of
respiration and other vegetative - visceral functions are observed at
incomplete lesions of vagus nerves. The total interruption of these nerves
incompatibles to life.
The irritation in zone innervations IX and X nerves shows as laryngs
–pharyngs piloro spasm and various vegetative distresses.
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N. accessorius.
The one side of central neurone results only to mild paresis muscles
of neck.
Lesion of nucleus or trunk of eleventh cranial nerve lead to paresis
and atrophy of sternocleidomastoid and trapezoidal muscles. The shoulder
girdle on the side of paralysis is omitted.
In innervated by XI cranial nerves muscles there are signs of irritation
- clonic twitchings of head in the counter side, tic twitchings of brachium,
nodding locomotions can be observed. The one side tonic spastic stricture
produces torticolis.

N. hypoglossus.
At one side damage of nerve the atrophy of half of tongue is
observed. Can be visible fascicular twitchings that specifies localization of
process in nucleus of XII nerves. Tongue at protrusion is wedged aside
the struck nucleus or nerve. At lesion of nucleus of hypoglossal nerve
function m. оrbicularis oris can suffer in mild degree. At diplegia of
hypoglossal nerve atrophy both halves of tongue are exposed. Tongue
becomes almost fixed (glossoplegia). Speech are stoped.
At extracranial damage of nerve functions connecting with it branches
of upper cervical nerves, in particular ansa cervicalis suffer, at swallowing
the deflection of larynx in able side is in that case observed.
The unilateral damadge of cortico-nuclear fascicle results in
deflection of tongue at protrusion in the counter side. Atrophies, fascicular
twitchings thus do not happen.

Bulbar and pseudobulbar paralyses.

It is clinically expressed by dysphagia, loss of sonority of a voice (an
aphonia}, nasal shade of speech, infringement of articulate pronunciation
of notes (dysarthria). Under the former name of myelencephalon the
complex of numbered pathological attributes has received the name
«bulbar paralysis ».
Sometimes half of diameter of myelencephalon suffers. In result
besides lesion of nucleus of cranial nerves on the side of the locus, the rest
piramidal fascicle results in development of hemiplegia on the counter
side (alternating hemiplegia). The two-sided flaccid paralysis IX, X and
XII steam of cranial nerves incompatibles to life.
The disorders of phagias, phonations and articulations occur and at
the locuses in both hemispheres of brain when central neurones to
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glossopharyngeal, vage and sublingual steams of cranial nerves are

blasted. Such paralyses are termed pseudobulbar. They occurs at
infringement of functions of cortical-nuclear parts of piramidal system.
The two-sided lesion of cortico-nuclear fascicles is accompanied by
appearance of pathological reflexis of oral automatism. Stroke by ham on
upper or under lip produces contraction circular muscle of mouth or
elongation of labiums forward - labial jerk, or as at suction - lip reflex.
The shaped boring of palm skin above eminence of major dactyl is
accompanied by hitching up skins of chin - palm-mental reflex
Marinesku-Rhadovichi.
One of precursory symptoms of two-sided lesion of central or
peripheric motoneurons of articulation musculation is the dysarthtia.
Thus signs of oral automatism are constantly taped.

SIGNS OF THE LESION OF THE brainstem

The lesion of all diameter of brainstem incompatibles to life. In
clinical practice it is necessary to meet patients with the locus of lesion in
one half of brainstem. Almost always thus the nucleus or root any of
cranial nerves is involved. Lockout of motorial nucleus or axons of its
cells produces flaccid paralysis of conforming muscles. Besides such
locus routinely damages passing in neighbourhood (pyramida,
spinnothalamic and bulbotalamik). There is paralysis of cranial nerve on
the side of the locus, hemiplegia or hemianaesthesia on counter. Such
combination of neurologic distresses has received the name «an
alternating set of symptoms » and allows to establish a lesion of cerebral
fulcrum, and the lesion of cranial nerve determines level of the locus.
Mesencephalon and symptoms of its lesion.
At lesion of nucleus or roots of third cranial nerve the outside,
intrinsic or total ophthalmoplegia educes; throchlear nerve - concurrent
strabismus, diplopia at view downwards, vertical nystagmus (spontaneous
vertical nystagmus, discoordinated locomotions of eyeglobes, an
ophthalmoplegia, horizontal nystagmus, symptoms Нотнагеля
(unbalance, audition, a paralysis of oculomotor muscles, choreic
hyperkinesias), парезы and paralyses of extremities, cerebellar distresses,
cerebrate rigidity (it is connected to lesion of mesencephalon centers of
regulating muscle tone of below red nucleus).
Parino syndrom: vertical paresis stare, infringement of convergence
of eyeglobes, particulate two-sided ptosis of blepharons. Horizontal
locomotions of eyeglobes are not limited. The set of symptoms is
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observed at lesion upper colliculus roofs of mesencephalon and at tumour

of epiphysis.
A red nucleus syndrome: intentional hemitremor, gemikiperkinesis;
Clod syndrom (the inferior red nucleus syndrome): lesion of third
cranial nerve (ptosis, divergent strabismus, mydriasis) on the side of locus;
intentional hemitremor, hemiataxia and hypomyotonia - on the counter
side.
Fua syndrom (the upper red nucleus syndrome): intentional
hemitremor, hemigyperkinesis.
Black matter syndrom: plastic muscle hypertonia, akinetic-rygidity
syndrom on countralateral side to locus.
Tegmental syndrom: on the side of the locus - ataxia, Kloda Bernard's
syndrom, tremor, myoclonias; on counter to the locus side -
hemianestesia, infringement colliculous reflexis (prompt rough
locomotions in reply to unexpected visual and annoyances - starts - jerks).
Weber syndrom: a flaccid paralysis of third cranial nerve on the side
of the locus and hemiparesis (hemiplegia) - on counter. The locus settles
down in the establishment of brain leg and breaks piramidal fibers.
Benedict’s syndrom: paralysis of third cranial nerve on the side of
locus (ptosis, divergent strabismus, mydriasis), intentional tremor and
atetoid locomotions in extremities on counter to locus side. The locus
damages fibers of third cranial nerve, red nucleus and cerebellar
conductors suitable to it dental-rubral pathes.
Lesion of one half of Pons brain the following alternating symptoms
educe:
Mijar- Gubler sindrom: flaccid paralysis of mimic muscles on the side
of locus and hemiplegia on counter side. The locus settles down in the
baze of bottom of the brain Pons, suffer nucleus n. facialis and piramidal
fascicle.
Foville syndrom: flaccid paralysis of mimic muscles and outside
direct muscle of eye (concurrent strabismus) on the side of locus,
hemiplegia - on counter. This set of symptoms arises at lesion of bottom
of the baze of Pons Varolii. Are damaged piramidal fascicle, nucleus
facial and axons of abducent nerve.
Gasperini syndrom: a flaccid paralysis of abducent and facial nerve,
weakening of audition, hypesthesia in zone of trigeminal nerve on the side
of locus and conduction hemianaesthesia on the counter side. Such
symptoms educes at unilateral locus of cover of the Pons cerebry.
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Brisso-Sikara syndrome is characterized by spastic stricture of mimic

muscles on the side of lesion (hemispasm of facial musculation from
irritation of facial nerve nucleus and spastic hemiparesis on counter to the
locus side (lesion piramidal system).
Raimon-Sestan syndrom is caused by combined lesion of medial
longitudinal fascicle and Pons center of look, medial leg of cerebellum,
medial loop and pyramidal path: are observed paresis a look aside the
lesion locus, ataxia, choroatetoid hyperkinesia - on the side of the locus;
and contralateral spastic hemiparesis and hemianaesthesia.
Graine: abaissement of surface sensitivity on the face for segmentary
type on the side of locus, conralateral hemianaesthesia of the surface
sensitivity on trunk and extremities (a lesion of nucleus V cranial nerves
and spinothalamic path).
Myelencephalon and symptoms of its lesion.
The basic alternating symptoms are the following.
Avellis syndrom: flaccid paralysis of half of tongue, soft palate and
vocal cords (IX, X, XII cranial nerves) on the side of the locus and
hemiplegia - on counter. Educes at the locus in one half of
myelencephalon.
Jackson syndrom: the flaccid paralysis of muscles of tongue on the
side of the locus and central paralysis of counter extremities arises at
lesion of one pyramid of myelencephalon and a root of XII cranial nerves.
Vallenberg – Zacharchenko syndrom: lesion of vagus nerve on the
side of the locus (unilateral paralysis of soft palate, vocal cords,
dysphagia). On same side Bernard's Gorner’s syndrom, ataxy of cerebellar
type, anaesthesia of the face, dissociated anaesthesia on the counter side
-an alternating hemianaesthesia. The symptoms arises at infringement of
circulation in an inferior back cerebellar arteria.
Schmidt's syndromset: on the side of the locus paresis of vocal cords,
soft palate, trapezoid and sternocleidomastoid muscle; on counter -
spastic hemiparesis, i.e. nucleus and fibers IX, X, XI, XII cranial nerves
and piramidal systems are damadged.
Babynsky – Naghotta Syndrom on the side of the locus - cerebellar
signs (ataxia, nystagmus, asynergia), Kloda Bernard's- Gorner syndrom,
hyperthermia; kontralateral spastic hemiparesis, dissociated
hemianaesthesia (drops out pain and a thermoesthesia).
Two-sided lesion of nucleus and roots IX, X and XII cranial nerves
educes bulbar paralysis. It is characterized by infringement of swallowing,
hit of fluid nutrition in a nose, change of voice sonority, an aphonia,
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appearance of nasal shade of speech, a dysarthtia. Are observed atrophy

and fascikular twitchings of tongue muscles. The gag reflex dissapears.
This syndrom arises at vascular and some degenerative diseases (lateral
sclerosis, syringobulbia).
Pseudobulbar paralysis is central paralysis of muscles, innervated by
IX, X, XII cranial nerves. Educes at two-sided lesion of cortic-nuclear
pathes. The locuses settle down at different levels above myelencephalon,
including in brainsteam. Clinical exhibitings are similar to those at bulbar
paralysis (infringement of swallowing, nasal shade of voice, dysarthtia).
At a pseudobulbar paralysis there are reflexis of oral automatism, violent
laughter and crying. Attributes of lesion of peripheric neurone (an atrophy,
faascicular twitchings, etc.) miss. The set of symptoms is linked to
vascular lesions of brain more often.
At infringement of function of a reticular formation distresses of
dream and a wakefulness educe.
Narcolepsy syndrom: attacks of uncontrollable tendency of the patient
to slepping in completely improper situation (during conversation, meal, at
walking, etc.) . Paroxysms of narcolepsy are frequently combined with
paroxysmal loss of a muscle tone (cataplexy), incipient at emotions. It
results to run out of movements the patient within several minutes). The
impossibility of the fissile locomotions during a short span right after
awakenings (cataplexy of awakening, or « a night paralysis ») is
sometimes observed. Thus, the reticular formation can participate in
formation of the sets of symptoms incipient at localization of the locus not
only in a fulcrum, but also in other departments of a brain. It emphasizes
existence of close functional linkages by a principle neuronal circles
including crustal, subcortical and brainsteam frames.
At the pathological locuses outside of brainstem can suffer a little bit
close posed nerves, there are characteristic syndromes. Among them it is
important to note syndrome of pontocerrebelar angle - a lesion of
acoustical, facial and trigeminal nerves.