Peripheral Nervous System Diseases

Damage of peripheral nerves is manifested by sensory disturbances (neuropathic

type of sensory disorders), motions (peripheral pareses) and vegetative-trophic
functions. Disturbance of the function of peripheral nerves possibly is as a result of
both the lesion of axon (axonal neuropathy) and its myelinic layer (demyelinating
neuropathy).

The lesion of one nerve is defined as mononeuropathy, while simultaneous lesion of

two somatical or peripheral nerves or it is more is as to polyneuropathy. Plexopathy
is lesion of nervous plexus (cervical, brachial or lumbar- sacral) as a result of injury
or other reasons (chronic compression, diabetes mellitus, and infiltration by
malignant tumor, radiation therapy and other).

Neuralgia is manifested by pain in the zone of innervations of nerve; without the

disturbances of its function. Radiculopathy is the lesion of cerebrospinal radix is
discussed in the ‘Vertebrogenic neurologic disorder’ topic.

Mononeuropathy

Mononeuropathy is manifested by the peripheral of paresis of muscles, innervated

by lesioned nerve, the mononeuropathic type of sensory disorder and by vegetative
disturbances in the zone of innervation. Mononeuropathy most frequently is caused
by injury of nerve or by its [sdavlenney] in the bone-fibrous- muscular canal (tunnel
neuropathy). It is also possible as a result of disturbance of blood circulation and
ischemia of nerve with diabetes mellitus, rheumatoid arthritis, nodular periarteritis,
amyloidosis, acromegaly, and also for the reason for direct infection with leprosy.
Facial nerve more frequently lesioned cranial nerves, and from spinal nerves, lesion
of median nerve in the region of carpal canal is the most commonly seen.

Neuropathy of facial nerve (Bell’s palsy)

Etiology and pathogenesis. The neuropathy of facial nerve in majority of the

cases is caused by ischemia, edema and compression of nerve in the narrow bone
canal, it maybe caused by idiopathic and supposedly infectious (virus, possibly,
herpetic) or infectious-allergic genesis. The frequency of disease is about 20 cases
in 100 thousand people. The symptomatic forms of neuropathy are developed with
the injury of temporal bone, tumor of pontocerebellar angle, otitis, encircling herpes
and others.

Clinical picture. Bell’s palsy frequently is provoked by supercooling. At first, pain

is frequently noted in the mastoid process region, due to acute development of
unilateral paresis or paralysis of mimic muscles. Face of patient is distorted, skin
folds are smoothed out on the side of lesion, and the angle of mouth descends.
Patient cannot raise eyebrow, shut eye, while grining, mouth displaces to the
healthy side. When eating, food frequently the stick between cheek and gum, liquid
pours out from the angle of mouth. Depending on level of lesion of facial nerve, dry
eye or epiphora, disturbance of taste on the anterior 2/3 of tongue, hyperacousia on
the side of paralysis is seen. Complete restoration of Bell’s palsy is observed in 70-
80% of patients usually for 1 month. (less frequently 2-3); the rest, paresis remains
or, less frequent (3%), paralysis of the mimetic muscles. Prognosis is worse in
elderly, with associated diabetes mellitus and/or arterial hypertonia.

Diagnosis it is based on the clinical symptoms and usually it does not cause
difficulties. If the lesion of mimetic muscles is combined with reduction in hearing,
sensory disturbance on the person (lesion of trigeminal nerve), central paresis of
extremities, cerebellar ataxia or other symptoms, which are not characteristic for
neuropathy of facial nerve, is indicated MRI of head to eliminate of ponto-cerebellar
angle tumor and other illnesses of brain.

Treatment. More rapid restoration is noted with prednisolone on 60-80 mg/day for
the first 5-7 days with the subsequent gradual cessation for 10-14 days. Possible
use of methylprednisolone (250-500 mg I/V 2 times a day for 3-5 days with the
subsequent application of prednisolone) in combination with rheopolyglucin (400 ml
of I/V of 2 times a day for 3 days, and then 1 time/day for a week) and Pentoxifyllin
(300 mg/day of I/V for 10 days) to improve microcirculation. taking into account the
assumed role of herpes simplex virus in the development of disease, it is proposed
to use acyclovir (on 200 mg of 5 times a day inward for 2-3 weeks. or the first 7
days by parenteral from the calculation 5 mg/kg of 3 times a day, and then inward).
From the first days, the gymnastics of mimic muscles, gluing from the adhesive
tape is recommended, in order to avoid the overextension of the affected muscles.
Late complications relating to the contracture of the denervated mimic muscles
may develped, which responds badly to treatment (reflexotherapy, massage,
Carbamazepine).

Mononeuropathies of peripheral nerves of the extremities

The clinical manifestations of the lesion of the peripheral nerves of extremities are
presented in the book ‘general neurology: symptoms of the lesion of spinal cord, its
radix and peripheral nerves”.

Neuropathy of median nerve. Carpal tunnel Syndrome it comprises to 2/3 of

all tunnel neuropathies. It appears as a result of compression of median nerve in the
carpal canal, formed by bones of carpal and by transverse palmar joint, which is
caused most often by thickening muscles and joints; congenital narrowing of carpal
canal plays the leading role. The syndrome of carpal canal can also be in
myxedema, acromegaly, diabetes mellitus, menopause, pregnancy, use of oral
contraceptives, rheumatoid arthritis, and also as a result of overload of radiocarpal
joint (frequent flexure- extension of fingers). Women with CTS are seen 2 times
more frequently.

Diagnosis is based on clinical data and is confirmed by the results of

electromeyromyography (decrease velocity of conducting excitation on the median
nerve in the region of carpal canal) and electromyography (presence of the
denervative changes in the innervated by median nerve muscles).

Treatment is directed toward decreasing load of radiocarpal joint, in many cases,

by bandaging of carpal at night, and when symptoms manifest, immobilization of
joint for 2-4 weeks with the aid of tire. Also NSAIDs, analgesics, anti-edematous
drugs, and compression with dimexidom are used. Corticosteroids (with or without
novocaine) can be dripped into the carpal canal. When treatment is ineffective and
progressive atrophy of muscles, surgical decompression of nerve in the region of
carpal canal is indicated.

Neuropathy of ulnar nerve appears as a result of its injury or compression in the

region of elbow or, less frequently, radiocarpal joint. In its injury, resolve the injury,
then carry out therapeutic gymnastics and massage; in tunnel neuropathy, the
treatment is the same, as carpal tunnel syndrome, and surgical decompression of
nerve is also effective.

Neuropathy of radial nerve usually appears after its injury (in fracture of
humerus) or compression at the level of the lower divisions of humeral bone. At the
level of brachial-axillary angle, compression of nerve can be caused by the incorrect
use of crutch. The lesion of nerve frequently develops acutely as a result of the
compression hand by head in the sleep, period of inconvenient pose (in alcoholic
intoxication). Restoration with the injury occurs spontaneously after 2 months, with
the use massage and therapeutic gymnastics. If after 2 months, the restoration
does not occur after injury, and also like tunnel neuropathy, surgical treatment is
recommended.

Neuropathy of ischial nerve more frequently appears in the place of its passage
through piriform muscle by mechanism of tunnel syndrome and is manifested by
pain and paresthesias of leg and foot, and disturbance of the function of nerve is
possible. The palpation of piriformis muscle is painful with propagation of pain along
the path of ischial nerve.

The syndrome of piriformis muscle can be caused by the injury of sacral-iliac or

buttock region with post-traumatic spasm of muscle, and also by reflex muscle
tension during the compression, intervertebral disk of lower lumbar and first sacral
of radix changed. In traumatic lesion, there is a possible spontaneous restoration
after 2 months, in spasm of piriformis muscle, novocaine blockade is used.

Neuropathy of femoral nerve appears usually in the region of inguinal fold, as a

result of the injury (with formation of hematoma) or spontaneous hematoma, for
example, with the use of anticoagulants. The lesion of nerve is manifested by pain
in the inguinal region, which can spread to the anterior and medial surface of thigh,
medial surface of leg and foot. The disturbance of nerve function appears in chroic
disease. Spontaneous restoration is possible after 2 months, with the use of
therapeutic gymnastics and massage.

Neuropathy of n. cutaneus lateralis femoris (Rot disease) appears in its

compression in the region of inguinal ligament, which more frequently caused by
injury, carrying of corset, bandage or tight belt or by the excess deposit of fat in the
lower division of front abdominal wall and in thighs region, less frequent by tumor,
ascites, and pregnancy. It is necessary to explain the reason for the compression of
nerve and, if possibly, then remove it. In majority of cases, the disease does not
cause serious sufferings to patient. In case of obesity, symptoms weaken with
decrease of mass of body. The introduction of local anesthetics and corticosteroids
into the region of the passage of nerve at the level of front upper iliac crest can help
with the expressed pain, in the rare cases surgical treatment is required.
Neuropathy of fibular nerve most frequently appears in its compression at the
head of the fibula, which can be caused by acute sole flexure and supination of foot,
prolonged stay in the position on haunches or sitting, after throwing far away foot to
the foot, carrying of plaster bandage. Mostly it spontaneous possible restores after
several weeks. Therapeutic gymnastics is carried out for the purpose to preserve
the contracture of talocrural joint, foot is fixed. In prolonged lesion, atrophy of
muscles of the anterior and external groups of shin is developed. If recovery does
not occur, it is recommended to do surgical decompression of nerve.

Neuropathy of tibial nerve it appears in its compression of posterior and it is

lower than medial malleolus in the region of tarsal canal, which can be caused by
edema or hematoma as a result of the injury of talocrural joint. In these cases the
pain and numbness in the sole part of foot and toes are observed, pain it is
strengthened in the position costing both with walking and also during percussion
and palpation of the place for compression. The surgical decompression of nerve is
effective.
Polyneuropathies
Polyneuropathy represents several lesion of peripheral nerves, that more frequently
manifested by symmetrical lethargic (peripheral) paresis (usually in the distal part
of extremities) and/or by sensory disturbances as polyneuropathy type, by
vegetative disorders predominantly in the distal divisions of extremities and
sometimes combining with the lesion of cranial nerves.

Etiology and pathogenesis. Polyneuropathies can be hereditary (hereditary

somatosensory and vegetative, amyloid, porphyrin and other), infectious
(diphtheria, leprous), toxic (arsenic, lead, poisoning due to organophosphorus
connected and other), dysmetabolic (in somatic diseases: diabetes mellitus, uremia,
hepatic insufficiency, hypothyroidism, hypovitaminosis B6, B12 and other); it appear
also in malignant new formations, disease of connective tissue and vasculitis
(nodular periarteritis, rheumatoid arthritis, system lupus erythematosis;
scleroderma), pregnancies, diseases of the blood, vaccinations (against
[beshestva], typhus, chickenpox and others) or iatrogenic as a result of the
complications of medicinal therapy (isoniazide, pyridoxine, diphenine and other).
Most of all (approximately in 1/__ of the cases) it is encountered as diabetic
polyneuropathy.

Clinical picture. The poly-neuropathy usually occurs gradually. Characteristically,

pain and paresthesias, sensory disturbances according to the type “socks” and
“gloves: decrease or loss of tendinous reflexes, especiallly Achilles, slow atrophic
paresis in the the distal part of extremities. As a rule, symptoms appear and prevail
in the feet. The disturbance of deep sensory can lead to sensory ataxia. Paresis of
feet produces characteristic changes in the gait ([steppazh]), in the rare cases
because of rough proximal and distal pareses the patients lose capability for
movement. Vegetative disturbances can be manifested by orthostatic hypotension,
sweating or dry skins, brittle nails, and pelvic disorders.

Diagnosis of poly-neuropathy it is based on clinical data and usually it does not

cause difficulties. Electromyography (EMG) and electroneuromyography (ENMG) can
confirm the lesion of peripheral nerves (symmetrical decrease of frequency of
conducting excitation of peripheral nerves, reduce amplitude of muscular answer,
denervation activity in the innervated muscles) and they ca be used to differentiate
between axonal degeneration (reduce amplitude of muscular answer with mild
reduction of rate of conducting excitation of nerves) and demyelination (expressed
reduction of rate of conducting excitation of nerve, and polyphase nature of
muscular answer). In the obscure cases, biopsy of nerve can have some diagnostic
value.

After revealing poly-neuropathy, it is necessary to establish its reason which

requires thorough somatic investigation of patient. Diabetic and alcoholic poly-
neuropathy is encountered mostly. In some cases, it is impossible to establish the
reason of poly-neuropathy; in elderly age patients, we should consider the
possibility of paraneoplastic syndrome, which can precede the clinical
manifestations of malignant tumor.

If poly-neuropathy occurs at young age and there are presence of cases of disease
in one family, it maybe hereditary neuropathy (Charcot-Marie-Tooth sensory
amyotrophy). it is inherited disease, usually autosomal-dominant, less frequent
autosomal recessive type. Symptoms usually appear at age up to 30 years of in the
form slowly increasing symmetrical weakness of distal divisions of feet with
development of the expressed amyotrophy and characteristic deformation of feet
(“hollow foot), in 5-10 years, it is joined with the weakness, also, in the distal
divisions of hands. While in inspection, peripheral pareses decrease or loss of
tendinous reflexes, mild sensory disturbances is seen, in a number of cases trophic
disturbances such as edema and cyanosis of the skins of extremities. Gradually,
paresis can reach the significant degree (up to plegia of feet); however, in the
majority of cases, it does not lead to the immobility of patient.

Treatment of poly-neuropathy depends on its etiology. It is necessary to remove

them with the provoking reasons (intoxication, hypovitaminosis). In the cases of
somatic disease, their treatment is the most important. In motor disturbances,
recommend therapeutic gymnastics, massage, physical therapy procedures, and in
the cases of rough paresis of extremities, orthopedic foot-wear can be suggested.

Acute inflammatory demyelinating polyradiculoneuropathy

(Guillain-Barré syndrome (GBS))
The etiology of disease is unknown, most probably due to immune disturbances,
which lead to segmental demyelination of anterior radix, proximal divisions of
peripheral nerves, plexuses and vegetative units. The frequency of disease is 1-2
cases in 100 thousand populations. Men are more likely to be ill than women.
Disease can manifests at any age, but it is encountered more frequent in 50-75
years.

Clinical picture. In 50% of patients for 1-3 weeks, the appearance of neurologic
symptoms is noted as diseases of upper respiratory tract, intestinal disorders or
angina. First neurologic disturbances are pain of paresthesia in the feet and/or
paresis of them. Later, disorders in the feet progress and connected with
disturbance of hands. Symptoms increase in 1-4 weeks. The leading manifestation
of disease is sluggish is the pair of [lich], which frequently is extended in ascending
direction, seizing muscles of legs and pelvic belt, bodies of neck and sometimes
respiratory of musculature. Investigations usually reveal muscular hypotonia,
decrease or loss of reflexes, mild sensory disturbances the form of hypoalgesia and
hyperesthesia in the distal part of extremities, the symptoms of tension. In some
cases, patient may develop fatal respiratory disturbances also disorders of
ingestion. Cranial nerves are surprised in 75% of cases, in half of them facial nerve
are affected. In many patients with expressed motor disturbances, vegetative
disorders in the form of orthostatic hypotension, tachycardia and paroxysmal
arrhythmia are developed.

The complications, caused by significant degree of immobility of the patient, are

possible: [prolelsni], pneumonia, thromboembolism of pulmonary artery, thrombosis
of veins. Lethality and the present time do not exceed 5%. In the majority of
patients the restoration begins 10-12 days after the curtailment of the progression
of disease and continues from 6 months of up to 3 years. Complete restoration is
observed in half of the cases, in majority of remaining patients remain only mild
neurologic disorders and only in 10-15% of patients remain severe pareses, which
lead to the disablement.

Diagnosis it is based on clinical data. In lumbar puncture, there is increase content

of protein with a insignificant increase of the number of cells in the cerebrospinal
liquid (protein- cellular dissociation). ENMG reveals reduction in the rate of
conducting excitation but to peripheral nerves in 90% of cases.

Treatment it is directed by mainly toward the preventive maintenance of possible

complications. Great significance has general care of patient, mechanical ventilation
of lungs (IVL) in respiratory insufficiency, parenteral nourishment if disturbed
ingestion. Restoration is accelerated by plasmaphoresis, carried out during the first
7 days of disease; it is recommended 3-5 sessions of plasmaphoresis in a day other
day with the exchange 1,5-2L of plasma for the session. Also effective is I/Vly slow
(for 6-8 h) introduction of immunoglobulin from the calculation 0,4 g/kg in 1L 0,9%
of the solution of sodium of chloride (physiological solution) for 5 days. For
preventive maintenance of thrombotic complications, it is expedient to use heparin
on 5 thousand IU under the skin of the stomach of 2 times in a 24 hour period. Also
recommended are massage of paretic muscles and therapeutic gymnastics.
Corticosteroids nowadays are not recommended.
Chronic inflammatory demyelinating of polyradiculoneuropathy is the rare
neurologic disease, similar to acute inflammatory demyelinating
polyradiculoneuropathy of Gullen-Barre, but has the chronic remitting or
continuously progressive (not less than 2 months) course. The first attacks of
disease are usually milder and are less prolonged than those following. Disease can
have both the idiopathic genesis and appear with the HIV- infection, systemic lupus
erythmatosus, malignancy and other diseases. At the basis of disease lie the
dysimmune disorders. Prednisolone 100 mg/day for 2-4 weeks is used in idiopathic
form for the treatment with the subsequent gradual decrease of dose to 5-20
mg/day. If uneffective, recommend plasmaphoresis (2 sessions in a week for 3
weeks.) or azathioprine on 50 mg of 3 times a day or of I/V introduction of
immunoglobulin. Approximately 33% of patients get better, different motor
disturbances remain in rest.

Plexopathy
Plexopathy- lesion of the nervous plexus: cervical, brachial, lumbosacralhumeral or
Lumbar- sacral.
Etiology and pathogenesis. Plexopathy appears after injury or other reasons
(chronic compression, infiltration by malignant tumor, radiation therapy).
Considerably more frequently is encountered humeral plexopathy, which is usually
caused by the injury: traumatic kinds, dislocation of humeral joint, automobile
accidents, compression of plexus in the time of narcosis, prolonged carrying of
gravity on the arm (“__________ paralysis”), knife injury, bone anomalies (neck edge
is hypertrophied transverse process Cv,|), compression by tumor of lung apex.
Lumbar- sacral plexopathy appears as a result of the volumetric formation in
retroperitoneal space (tumor, abscess, aneurysm of aorta or iliac artery),
hemorrhage in iliac-lumbar muscle (in hemophilia or overdose of anticoagulants),
fracture of pelvic bones, surgical interference on the hip joint. It Is possible also
idiopathic of plexopathy.

Clinical picture. Are separated 3 forms of humeral plexopathy. In the case of the
preferred involvement of the upper divisions of the brachial plexus (root of S5- S6)
is developed the Erb’s syndrome: paresis in the proximal divisions of hand (into the
region of humeral and elbow joints) with the gradual development of atrophy,
sensory disorder of lateral surface of arm. In lesion of lower divisions of the brachial
plexus (root of Cg- [Tts]), syndrome Dejerin -Klyumpke appears: sluggish paresis of
finger, sensory disorder over the medial surface of arm and forearm, and also
Horner's syndrome (appearing usually with in traumatic detachment of radix S8 and
Th, of spinal cord). In total lesion of the brachial plexus, paralysis of entire hand and
muscles of shoulder girdle, loss of sensory in the same zones is developed.

One of the versions of idiopathic plexopathy is Personage-Turner syndrome

(neuralgic amyotrophy): paresis in the proximal divisions of hand with the
subsequent severe atrophy without sensory disturbances developed following
intensive pain in arm; complete spontaneous restoration in 90% of cases is
observed for several months. It is possible rare family idiopathic forms of humeral
plexopathy.

The diagnosis of plexopathy is based on clinico –anamnestic data. EMG and ENMG
only to define the localization and degree of lesion. If absence of injury, it is
necessary to exclude the compression of plexus (tumor, hematoma, neck edge and
others). If injury, the prognosis is determined by its gravity, and in majority of the
cases we see complete (or partial) restoration for several months.

Treatment depends on the reason for plexopathy. The special micro-surgical sewing
of nerves is indicated in injury with complete break (for example, in knife injury).
Other remaining cases surgical treatments are recommended with absence of
restoration during 3-5 months and appear signs of axonal degeneration (according
to data of ENMG). But in all cases are expedient therapeutic gymnastics; massage
of paretic muscles is recommended, if in pain, analgesics is given, physiotherapy,
acupuncture.
Neuralgias
Neuralgia is manifested by pain in the zone of the innervation of nerve without
disturbance of its function. It can be primary (idiopathic) or by second
(symptomatic), caused tumor or by other illnesses. Most frequently encountered is
neuralgia of trigeminal nerve.
Neuralgia of trigeminal nerve. Etiology. Disease in the majority of the cases
has idiopathic genesis, assumed the compression of trigeminal nerve in its output
from pons by large artery (more frequent in the upper of cerebral artery). Idiopathic
form manifests predominantly at the age is older than 40 years, morbidity
composes 6 cases per year on 100 thousand populations, 60-70% of patients is
woman. The symptomatic form of neuralgia of trigeminal nerve can be caused by
scattered new formation (formation of sclerous platelet in the region of sensory
nucleus of trigeminal nerve), tumor of in base of skull, aneurysm, local process ain
the region, teeth, jaw or swallows.

Clinical picture. The neuralgia of trigeminal nerve is manifested by the short-term

(several seconds or 1 2 min) attack one-sided of that splitting or pressing pain
(sensation of burning or “passage of electric current”) in the second or third region,
it is less frequent than the first branch of nerve. In the time of the attack, patient
frequently lies, afraid to move and to strengthen pain, less frequent it rubs cheek
silt) it squeezes temple, trying to weaken pain. The pain attack can cause the
reflector contraction of mimic masticatory muscule on the side of pain (painful tick),
characteristically outbreak and at the end of attack, free from the pain is “bright”
spaces. The attacks of the fuss of cabins spontaneously or provoke by conversation,
ingestion by mastication, brushing teeth, shaving. Many patients see the
development of attacks during bath of cold water because they fear it will cause
attack. Patients sometimes stop cleaning teeth, rarely they bash, shave. Frequently
during start of attacks of pain have local nature, being projected the region of one
or other tooth or another or of gum, in the connection with which pain are turned for
the consultation of stomatologist. Later, region of pain increases, seizing zone of
one or not how many branches of trigeminal nerve. Pain never passes to other side;
however, in rare cases (3-5%) it’s double-sided. In many patients the attacks can
continue for months and years, repeated attacks usually appear in the same zones
of face. In some patients, spontaneous remissions never happens. In course of time,
in some patients dull pain or burning out of the attack begins. Emotional and
physical stress can increase the frequency of attacks. Inspection does not reveal
neurologic disturbances, sometimes is noted sickliness in it smelled the output of
the branches of nerve and mild hyper- or hypesthesia in the region of the interested
branch, and are revealed by hammer test which irritation provokes the attack of
pain.

Diagnosis of the neuralgia of trigeminal nerve it is based on the characteristic

attacks and the exception with its symptomatic of genesis. With the suspicion to the
tumor of the brain is indicated MRI of head.

Treatment. The basis of treatment composes medicinal therapy. Carbamazepin

(Finlepsin) is the most effective preparation, which gives positive result, also, in, the
cases. Begin treatment with 100 mg in a 24 hour period and everyday increase
dose on 100 ppm until positive result or to 600mg into 3 methods. If during the
week, 600mg of dose does not give positive effect, gradually increases dose up to
1200-1600 mg, and in cases when with these doses no positive result is seen, then
abolish preparation. Are possible application and others protium (epileptic means:
phenytoin 300-900 mg/day, myunazepam on 2-6 mg/day or gabapentine
(neurontin) 1200 mg/day. With the prolonged course of disease as die any chronic
painful syndrome, it is possible to use antidepressants, for example Amitriptylene
on 15 100 mg/day. In severe cases and medicines do not help, recommend surgical
treatment. The reposition of the blood vessel, which compresses trigeminal nerve,
most frequently is used nowadays.
Brief information about mononeuropathies of the extremities
Etiology The injury of nerve or its compression in is osteo fibrousmuscular canal (compression-
ischemic, or tunnel, neuropathy), diabetes mellitus, rheumatoid arthritis, nodular
periarteritis, amyloidosis, acromegaly, leprosy
Clinical Peripheral paresis of the muscles, innervated by the affected nerve, is mono-
manifesta neuropathic of the slimes of of sensory and the vegetative disturbances
tion
ENMG Retarding the rate of conducting excitation on notto ditch, reduce amplitude of
muscular answer
Treatmen In tunnel neuropathy, preventive maintenance of further compression of nerve, with
t uneffective of conservative therapy, surgical decompression is possible.
Brief information about neuropathy of facial nerve
Etiolo Idiopathic forms is ischemia, edema and the compression nerve in the narrow bone
gy canal (constitutional special feature), is possible the role of virus (herpetic) infection
and supercooling. Symptomatic forms is injury of temporal bone, tumor of the
pontocerebellar angle, encircling herpes
Clinica One-sided paresis or paralysis of mimic muscles, frequently pain at region of
l mammiform branch, the cartare possible dry eye or epiphora, disturbance of taste on
manif anterior 2/3 of tongue, ipsilateral hyperacousia
estati
on
Period Complete restoration in 70- 80% of patients usually in period 1-2 my., the prognosis is
worse in elderly, with associated diabetes mellitus and/or arterial the hypertonia
Treat- Prednisolone IV (1 mg/kg in 24 hour), acyclovir (1000 mg/days), therapeutic
ment gymnastics of mimetic muscles
Brief information about polyneuropathies
Etiology Diabetes, chronic alcoholism, are less frequent is hereditary, infectious
(diphtheria, leprosy), toxic, in uremia, hepatic insufficiency, hypothyroidism,
hypovitaminoses, malignant tumor, connective tissue diseases and vasculitis,
diseases of blood, after vaccinations and complication from medicines use
Clinical Symmetrical peripheral paresis of extremities, sensory disturbances of
manifestat polyneuropathic type, vegetative disorders predominantly in distal part of
ion extremities, sometimes lesion of cranial nerves
ENMG Decrease rate of conducting excitation on the peripheral nerves, reduction in the
amplitude of the muscular and sensory potentials
Treatment Therapy of basic disease or the elimination of toxic action, thiamine with the
alcoholic poly-neuropathy and the preparations of A- lipoic acid with diabetes
mellitus
Brief information about acute inflammatory demyelinizing polyradiculoneuropathy
Etiology Immune disturbances, which lead to demyelinization of anterior radix, proximal
divisions of peripheral nerves, plexuss and to vegetative units
Clinical Begin usually from pain and paresthesia in feet. Later, gradual (1-4 weeks)
manifestatio growth of peripheral paresis of extremities, frequently paresis of mimic
n muscles. Possible disorders of respiration and ingestion, vegetative
disturbances in the form of orthostatic hypotension and tachycardia
ENMG Decrease velocity of propagation of excitation of nerves of extremities
Lumbar Increased content of protein into cerebrospinal fluid
puncture
Treatment Preventive maintenance of possible complications of immobilized patients, 3-5
sessions of plasmaphoresis in a day other day (with the exchange 1,5-2L of
plasma for the session), I/V immunoglobulin (0,4 g/kg) for 5 days, therapeutic
gymnastics
Brief information about neuralgia of trigeminal nerve
Etiology In most cases idiopathic genesis, possibly cartthe compression of trigeminal nerve in
the region exit from pons by artery. Symptomatic forms is multiple sclerosis, brain
tumor and base of skull, aneurysm
Clinical Short-term (several seconds or 1-2 min) attacks of the one-sided splitting or cutting
manifesta pain in the region the second or third less frequently are less frequent than first
tion branch of nerve. Attacks appear spontaneously or they provoke by conversation,
ingestion, mastication, by cleaning teeth, by shave. Sickliness into 1 is possible the
zones of the output of the branches of nerve and light hyper- or hypesthesia in the
region of the interested branch
Treatmen Carbamazepin on 600 mg/day or other anti-epileptic means (phenytoin, gabapentin,
t antelepsin), antidepressants. If uneffective, recommend surgical treatment
(reposition of blood vessel, decompression of trigeminal nerve and other)