2. To the peripheral nervous system include:
roots and ganglia of cranial nerves,
posterior and anterior roots of the spinal cord,
intervertebral spinal ganglia,
spinal nerves their plexuses
cranial nerves.
3. • The peripheral nerve is formed by the convergence of the posterior
and anterior roots, which form the radicular nerve all the way to the
intervertebral ganglion.
• The ganglion is followed by the spinal nerve, which is divided into
anterior and posterior branches.
• The branches of the cervical, lumbar and sacral segments form the
cervical, brachial, lumbar and sacral plexuses.
4. • Peripheral spinal nerves are mostly mixed, so the symptom complex
of nerve damage is composed of motor, sensory and vasomotor-
trophic disorders.
5. Classification of diseases of the peripheral
nervous system.
Group I. Vertebrogenic lesions
• Cervical level.
• Thoracic level.
• Lumbosacral level.
Reflex syndromes and radicular syndromes are considered in each.
At the cervical and lumbosacral level, radicular vascular syndromes
(radiculoischemia) are also distinguished.
6. Group II. Lesions of nerve roots, nodes, plexuses
• Meningoradiculitis, radiculitis (usually of infectious-allergic genesis,
non-vertebrogenic).
• Radiculoganglionitis, ganglionitis
• Plexitis, plexus trauma.
7. Group III. Multiple lesions of roots, nerves.
• 1. Infectious-allergic polyradiculoneuritis (Guillain-Barré, etc.).
• 2. Infectious polyneuritis.
• 3. Polyneuropathies.
• 3.1. Toxic. lead,
• 3.1.1 Chronic domestic and industrial intoxications (alcoholic, chlorophos, etc.).
• 3.1.2 Medication.
• 3.1.3 Blastomatous: in lung cancer, gastric cancer, etc.
• 3.2. Allergic (vaccine, serum, medication)
• 3.3. Dysmetabolic: in vitamin deficiency, endocrine diseases-sugar diabetes, etc., liver disease, kidney disease, etc.
• 3.4. Dyscirculatory - in polyarteritis nodosa, rheumatic and other vasculitis.
• 3.5. Idiopathic and hereditary forms.
8. Group IV. Lesions of individual spinal nerves.
• Traumatic.
• Compression-ischemic (mononeuropathies).
• Inflammatory (mononeuritis).
Group V. Lesions of cranial nerves .
• Neuralgia of trigeminal and other cranial nerves.
• Neuritis (primary: infectious-allergic genesis: secondary - otogenic and
other genesis), neuropathies (compression-ischemic genesis) of the facial
nerve.
• Neuritis of other cranial nerves.
• Prosopalgia. Ganglionitis (ganglioneuritis) of the wing, ciliary, auricular,
submandibular and other nodes.
• Combined and other forms of prosopalgia.
• Stomatalgia, glossalgia.
9. Group I. Vertebrogenic lesions. The concept
of "vertebral motor segment"
• It consists of two adjacent vertebrae and soft tissues connecting them
(disc, intervertebral ligaments and muscles). The intervertebral disc is
formed by the glomerular nucleus, the surrounding fibrous ring and the
hyaline plates covering it.
• The structure of the glomerular nucleus includes cartilage cells, collagen
fibers. The pressure of the disc is transmitted to the annulus fibrosus and
adjacent hyaline laminae, providing cushioning and elastic mobility of the
spine.
• The annulus fibrosus is composed of crisscrossing collagen fibers. Unlike
the vascular-free glomerular core, the ring is abundantly blood supplied.
Yellow ligaments connect posteriorly mainly to the arches of adjacent
vertebrae, there are intercostal, intertransverse ligaments posterior and
anterior longitudinal ligaments.
10. • In the development of vertebrogenic reflex syndromes, pathologic
impulses from the receptors of the affected tissues of the vertebral
motor segment become the source of motor, vasomotor and other
reflexes.
• One of the most frequent reflex syndromes are lesions at the level of
the lumbosacral spine: lumbago, lumbalgia, lumboischialgia. Lumbago
- (from Latin lumbus) acute pain, "shooting" in the lumbar part of the
back
11. 1.Lumbago.
• The basis of lumbago (lumbar shooting) is the rapid movement of the
altered pulposus nucleus towards the fibrous ring and irritation of the
synovertebral nerve Luschka. Lumbago usually occurs with awkward
movement, bending, lifting weights. The patient is frozen in a forced
posture, any movement increases the pain. At rest and in a horizontal
position, the pain syndrome decreases.
• During examination, tension of paravertebral muscles in the lumbar
region is noted, knee and Achilles reflexes are not changed or
uniformly increased, paresis and paralysis are not present, sensitivity
is not disturbed, weakly expressed symptoms of tension of nerve
trunks can be determined: Lasega, Neri, Dejerina. Pain in lumbago
lasts for several hours or days, then gradually subsides.
12. • 2. Lumbalgia is caused by muscle stretching and is manifested by pain
syndrome in the lumbar region and signs of reflex-tonic protection of
the spine.
• When examining patients, painfulness of paravertebral points and
spinous processes is determined.
• Motor disorders, changes in reflexes are absent, as well as sensory
disorders.
• On spinal radiographs, 50% of patients have smooth lumbar lordosis
and Schmorl's hernia (bulging of the nucleus pulposus of the
intervertebral disc into the spongy substance of the vertebral body).
13. 3.Lumboischialgia. Symptoms of nerve trunk tension are determined,
often lumbar muscle tension.
• Sometimes mild hypoesthesia on the feet is determined, on the side
of pain there may be slight hypotonia and hypotrophy of the thigh
and shin muscles, knee and Achilles reflexes are reduced,
hyperhidrosis is noted.
• The reflex syndromes are based on muscle-tonic, neurovascular or
neurodystrophic processes.
A special role is assigned to osteochondrosis, in the genesis of which
statodynamic, autoimmune, metabolic factors are important.
14. Spinal osteochondrosis
• It begins with a dystrophic lesion of the intervertebral disc with subsequent
involvement of adjacent vertebral bodies, intervertebral joints,
ligamentous apparatus.
• In the future, bony overgrowths, bulges of the intervertebral disc begin to
have a mechanical impact on the roots, spinal cord, vessels. There are
radicular and radicular-vascular compression syndromes, which squeeze
not only the nerve fibers themselves, but also blood vessels supplying
them.
• The irritation of the radicle is accompanied by shooting pain, hypalgesia in
the zone of the corresponding dermatome and symptoms of prolapse in
the corresponding myotome (hypotrophy, hypotonia, hyporeflexia,
weakness).
15. Examination.
Examination of patients with vertebrogenic diseases of the nervous
system includes:
• radiologic examination of the spine in direct and lateral projection,
• CT or MRI examination,
• myelography,
• lumbar puncture
16. Treatment
• Treatment of patients with vertebrogenic diseases of the nervous system is carried out
conservatively and operatively.
• The main principles of therapy:
1) exclusion of statodynamic load - rest in the period of exacerbation,
2) stimulation of muscle corset activity – massage.
3) reduction of pathological impulsation - vascular, anti-inflammatory and analgesic
therapy.
Widely used physiotherapeutic treatment in the form of ultrasound and laser therapy.
An absolute indication for surgical treatment are:
• acute compression of the cauda equina or spinal cord (sphincter disorder, bilateral pain
and paresis)
• unrepaired hernia with complete liquor-dynamic and myelographic block.
Microsurgical operations are currently being developed.
17. Group II. Lesions of nerve roots, nodes,
plexuses. Duchenne-Herb's paralysis.
• Most authors divide obstetric
paralysis into 3 types. The most
common form is Duchenne-Herb's
palsy, in which the function of the
proximal arm muscle group is
disturbed. Its occurrence was
previously associated with a lesion
of the upper bundle of the brachial
plexus (segments C5-C6).
18. Distal Dejerin-Klumpke palsy.
• The second type of obstetric
paralysis is distal Dejerin-
Klumpke's palsy, caused by
damage to the lower primary
bundle of the brachial plexus, in
which the proximal muscles of
the arm are almost unaffected, in
the distal part the function is
grossly impaired - the hand
hangs down, resembling a "seal's
paw".
19. Total type of paralysis.
• A total type of paralysis is distinguished, in which the proximal and distal muscle
groups are sufficiently equally involved. Obstetric paralysis can be due to lesions
of the spinal cord, brachial plexus, or both together.
• They are caused by hemorrhage and edema of the nervous tissue due to
mechanical aids in labor, dislocation of the vertebrae, prolapse of the pen, in
polyuria, multiple pregnancy, in a large fetus, etc.
• In favor of the spinal origin of obstetric paralysis is evidenced by the absence of
sensory disturbances, paralysis of the dome of the diaphragm, pyramidal
symptoms in the lower limb on the side of obstetric paralysis, electromyography
data (rhythm of the "frequency-chamber") and radiography of the spine.
20. Diagnosis of total paralysis
In favor of the spinal origin of obstetric paralysis is evidenced by the:
• absence of sensory disturbances,
• paralysis of the dome of the diaphragm,
• pyramidal symptoms in the lower limb on the side of obstetric paralysis,
electromyography data (rhythm of the "frequency-chamber") and
• radiography of the spine.
Early recognition of obstetric paralysis is facilitated by the use of additional tests.
• If you put the newborn on the palm of the doctor's palm face down, the paretic arm
hangs down. As the child grows, the severity of the symptom decreases.
• Important for diagnosis is the symptom of "doll's arm": the paretic arm, due to the
induction and pronator position of the proximal shoulder, seems to be attached to the
torso and separated from it by a rather deep gap, a fold, which resembles the attached
arm of a doll.
• Changes in the physiologic reflexes of newborns may contribute to the recognition of
obstetric paralysis.
21. Treatment
Physiotherapeutic methods:
• electrophoresis with euphylline, nicotinic acid, with proserin;
• paraffin and ozokerite applications;
• massage, therapeutic exercises,
• drug therapy (proserin, dibasol, B vitamins).
22. Ganglionitis
• Ganglionitis in most cases is viral in nature, less often due to
intoxication.
• The clinic is characterized by vesicular rashes on an erythematous
basis (herpes zoster).
• Against the background of general malaise and increased body
temperature there is a sharp excruciating pain in the area of the
affected root, then there are usually unilateral rashes. Thoracic and
lumbar intervertebral nodes are more often affected.
23. Group II. Multiple lesions of the roots, nerves. Acute
polyradiculoneuropathy of Guillain-Barré type.
Clinical manifestations:
• pain syndrome is pronounced,
• flaccid paralysis of limbs,
• sensory disorders of peripheral type,
• autonomic disorders,
• liquor changes in the form of protein-cell dissociation are characteristic.
The disease has an autoimmune genesis
Triggers: influenza viruses, herpes measles, epidemic mumps. The disease develops 1-3
weeks after a fever, catarrhal phenomena or intestinal disorders. Pain appears in the legs,
less often - in the hands. Then flaccid paralysis develops, which spreads from distal to
proximal parts. In the ascending type of course (ascending Landry's paralysis), after the
lower limbs, the upper limbs, trunk muscles and cranial nerves are affected. The transition
to bulbar sections is dangerous for the patient's life due to the development of respiratory
and cardiovascular disorders. There is a period of increasing paralysis, which can last from 3
to 25 days, the period of stabilization, then in the 2-3rd week with a favorable course comes
a period of reverse development, which sometimes lasts for several months.
24. Diagnosis
Based on a combination of signs:
• pain syndrome with tension symptoms (Laseg, Wasserman, Neri),
• flaccid paresis, symmetrical, predominantly in the distal part with
areflexia,
• distal hypalgesia,
• presence of protein-cell diosociation in the liquor.
25. Treatment.
• Plasmapheresis
• corticosteroids (corticosteroid dose- 1-2 mg/kg)
• dehydration therapy
• analgesic therapy
Prognosis in polyradiculoneuritis is considered favorable, however,
according to current data, about 5% of patients die, 10-23% need
artificial ventilation, ~10-15% of patients remain severely disabled.
26. Group IV. Lesions of individual spinal nerves.
Mononeuropathies. Lesion of the median nerve.
• Clinical picture of the median nerve lesion (C5-C8): palmar flexion of the hand and flexion
of the I, II, III fingers, as well as extension of the middle phalanges of the II and III fingers
are impossible. Pronation of the forearm is affected. In flexion, the hand is withdrawn to
the ulnar side. Symptoms of damage to the median nerve include flattening of the palm,
the thumb is pressed, the hand resembles a "monkey's paw".
• Special tests are used to study the function
• 1) inability to hold a piece of paper with the index finger and bent thumb (paralysis of the
long flexor of the thumb);
• 2) it is impossible to oppose the thumb to the others;
• 3) when clenching the hand into a fist I and II fingers are not bent.
• Sensitivity disorder is determined mainly on the radial side of the palm surface of the
hand. Vegetative disorders are expressed, especially in the I, II, ||I fingers, there may be
pain in the last phalanges of the II and III fingers.
27. Ulnar nerve injury (C5-C6)
Occurs with wounds to the inner side of the shoulder, injuries to the
elbow joint. Complete nerve damage in the shoulder area makes it
impossible to flex the palm of the hand and withdraw it to the ulnar
side, to flex the main phalanges of the IV and V fingers, it is impossible
to fan the fingers and bring them together, to bring the thumb to the
index finger and the little finger to the ring finger. In this case, due to
the extension of the main phalanges (function of the radial nerve) and
flexion of the terminal phalanges (function of the ulnar nerve), a
characteristic position of the hand - "clawed paw" - occurs.
28. Tests:
1) inability to spread and bring the fingers, especially IV and V, if the hand
lies on the table with the palm downwards;
2) no possibility to make a scratching movement with the V finger;
3) when bending into a fist, IV and V fingers do not bend;
4) it is impossible to hold a paper between the II and straightened I finger;
5) it is impossible to oppose the little finger to the thumb.
Atrophy of interosseous muscles and sharp flattening of the hypotenar
develops in the future. Sensory disorders are expressed on the palm and
dorsal sides of the hand along its ulnar edge, the V finger and the ulnar half
of the IV finger.
29. Radial nerve lesion (C6-C7).
It occurs in fractures of the humerus, shoulder, when
using a crutch, while sleeping on the side. With high
damage to it (in the axillary fossa, in the upper third of
the shoulder), the possibility of active extension of the
forearm, hand and fingers in the main phalanges is lost.
The latter hang down, usually bent in the main
phalanges, and finger is brought to 11 due to paralysis
of the muscle that withdraws the thumb. The extensor-
lateral reflex disappears and the carporadial reflex is
weakened. Sensation is lost on the radial side of the
dorsum of the shoulder, forearm, hand and thumb.
Lesion of the radial nerve is the "dangling hand"/"seal's
paw" syndrome.
30. If the nerve in the middle third of the shoulder is damaged, the forearm can be flexed
due to the function of the triceps muscle, the ulnar extensor reflex is preserved,
sensitivity on the shoulder is not impaired. It is impossible to extend the hand, supinate
it, withdraw the thumb. Flexion in the elbow joint is weakened due to loss of function
of the brachial-lumbar muscle. There are atrophy phenomena of paralyzed muscles,
loss of nuvstivity on the dorsal surface of the thumb and in the area between the I and
II metacarpal bones.
Tests:
1. if the hand is placed on the table so that the forearm is vertical, the hand
immediately hangs down in complete paralysis;
2. the patient is offered to put the palms and fingers together and then separate
them, the fingers of the sick hand bend when the radial nerve is affected;
3. it is impossible to put the index finger on the middle finger if the hand lies palm
down;
4. it is impossible to withdraw the thumb outward and upward.
31. Tibial nerve damage (L4-S3)
There is pain, weakness of muscles flexing the foot and toes, muscles
turning the foot inward. The foot is turned to the outside, there may be
clawing of the toes. Achilles and plantar reflexes disappear. Hypesthesia is
expressed on the sole and posterior surface of the tibia. To assess the
function of this nerve, the following tests are used:
1) plantar flexion of the foot;
2) turning the bent tibia to the inside;
3) walking on socks;
4) 4) convergence and divergence of the toes.
32. Peroneal nerve damage
• In an isolated peroneal nerve lesion, there is moderate pain in the lower leg, characteristic
foot position, the foot hangs down, slightly turned to the inside, toes slightly bent. A
"peroneal" gait is observed. The patient walks, raising the leg high, cannot stand on the heel,
withdraw the foot, lift its outer edge. There is decreased sensitivity on the outer surface of
the tibia and rear of the foot, on the inner surface of the 1st and Il fingers.
• The following tests are used to diagnose the lesion:
• straighten the foot;
• raise the outer edge of the foot or take it to the outside;
• walking on the heels.
If the peroneal nerve is affected, these movements are not possible.
33. Tunnel neuropathy.
• Almost all peripheral nerves pass through anatomical constrictions,
some of which are called canals (tunnel).
• The nerve trunks and vessels passing through them are often
compressed, leading to the development of tunnel neuropathy.
• Internal compression of vessels and nerves occurs when the tunnel
lumen is reduced due to fracture or thickening of the fibrous roof of
the canal (ligament, fascia), as well as when the volume of the
structures entering the tunnel is increased.
34. Group V. Cranial nerve lesions. Facial nerve
neuropathy
• In the etiology and pathogenesis of primary facial nerve neuropathy,
disturbance of regional blood circulation during hypothermia; viral
infections; inflammatory processes in the ear; traumatic injury during
operations on the pyramid of the temporal bone and radical ear surgeries,
in case of fracture of the skull base are important. The nucleus of the piceal
nerve can be affected in poliomyelitis, tick-borne encephalitis,
disseminated encephalomyelitis; underdeveloped in Mebius syndrome.
The facial nerve is also affected in tumors of the pontocerebellar angle.
• The disease is characterized by acutely developing unpleasant sensations
behind the auricle, peripheral paresis of the mimic muscles on half of the
face. If the pathological process seizes the nerve in the pyramid of the
temporal bone, there may be taste disturbances in the anterior 2/3 of the
tongue, hyperacusis and dry eye.
35. Treatment.
• Treatment of facial nerve neuropathy is carried out taking into account the etiology,
preferably in the conditions of the hospital.
In the first days of the disease prescribed:
• dehydration (diacarb, furosemide).
• UHF,
• vitamin complex (B group, nicotinic acid),
• glucocorticoil.
• drugs that improve neuromuscular transmission (dibazol, nivalin, galantamine, proserin),
• with otogenic facial neuritis prescribe antibiotics.
Further apply therapeutic exercises, massage, electrical stimulation, heat procedures
(paraffin, ozokerite), sometimes blockade of the stellate node with 1% novocaine solution,
acupuncture.
36. Trigeminal neuralgia.
• Neuralgia of the trigeminal nerve have significance odontogenic diseases, cooling,
psychotraumas, viral infections, atherosclerosis, aneurysm, tumors of the Gasser
node and bridging node, narrowing of bone channels of the nerve branches and
other causes.
• Neuralgia of the trigeminal nerve is manifested by attacks of acute pain, more
often in the area of one branch of the nerve, can capture the entire half of the
face. Sometimes the pain is accompanied by facial redness, lacrimation,
salivation. The duration of pain can be from a few seconds to 1-2 min. The attacks
occur spontaneously or under the influence of fatigue, when chewing and talking.
The intensity of attacks varies, sometimes the pain is so unbearable that patients
lose control. Palpation of the place of exit of the nerve on the face is sharply
painful and can provoke an attack. With deep nerve damage, the pain from
paroxysmal pain becomes constant, dull, there is loss of sensation, paresis of the
masticatory muscles.
37. Treatment.
• To relieve the pain syndrome prescribe analgin, novocaine, reopirin, alcohol and
novocaine blockades in the places of trigeminal nerve exit on the face,
physiotherapeutic measures: electrophoresis with analgesics, ultrasound with
dehydrating agents. UVT, diathermy, diadynamic currents.
• With primary viral processes, hormonal therapy is prescribed, with secondary
purulent lesions, antibiotics are prescribed, as well as desensitizing agents.
• With atherosclerosis and hypertension, vasodilator therapy is prescribed.
• In trigeminal neuralgia, anti-inflammatory drugs (Tegretol, Finlepsin, trimetin),
vitamins, biogenic stimulants, ganglioblockers are used /
• If drug treatment is ineffective, novocaine blockades of the upper cervical
sympathetic or stellate node of the corresponding nerve trunks are used.
Stereotactic hydrothermal or electrical destruction of the gasser's node or
trigeminal root, as well as other surgical methods of investigation are used.
