Diseases of the peripheral nervous system. Axonal polyneuropathies (axonopathies) Axonal type neuropathy

Exam questions:

2.7. Osteochondrosis of the cervicothoracic spine: main syndromes of lesions, clinic, diagnosis, treatment.

2.8. Osteochondrosis of the lumbosacral spine: main lesion syndromes, clinic, diagnosis, treatment.

2.9. Polyradiculoneuropathy: etiology, pathogenesis, classification, clinic, diagnosis, treatment, disability examination, prevention.

Anatomical and physiological features of the peripheral nervous system

Peripheral nervous system is a part of the nervous system that connects the central nervous system with the sense organs and with voluntary muscles; two different groups of nerves are distinguished in it: cranial and spinal:

- Rootsspinal cord and brain fundamentally have a similar functional structure and include motor, sensory and autonomic fibers However, due to the peculiarities of the phylo- and ontogenesis of the head end of the body, the cranial nerves differ anatomically from the spinal ones.

- Peripheral nervous system of the head and neck (cranial nerves) includes 10 (11) cranial nerves (with the exception of I and II), discussed in the sections on the brain stem and divided into systems:

1) Analyzers: vestibular and auditory (VIII),

2) Oculomotor nerves (III, IV, VI) - ensuring the movement of the eyeball,

3) System general sensitivity faces (V) - analogue of the posterior horns of the spinal cord,

4) System facial nerve(VII) - providing facial expressions,

5) System ensure digestion- chewing (V, XII), taste and salivation (VII, IX, X), swallowing and digestion (IX, X) - and functions of internal organs- heart, lungs, etc. (X)

6) Accessory nerve(XI) - ensuring the movement of a part of the muscles of the upper shoulder girdle.

- Peripheral nervous system of the trunk and limbs includes:

1) at the cervical level - spinal nerve roots from C1 to Th1, as well as the cervical and brachial plexus,

2) at the chest level - spinal nerve roots from Th2 to Th12, do not form plexuses,

3) at the lumbosacral level - spinal nerve roots from Th12 to Co2, as well as the lumbar, sacral and coccygeal plexus.

PNS diseases: general questions

Diseases of the peripheral nervous system(PNS) make up about half in the structure of neurological morbidity in the adult population. They are the most common cause of temporary disability (76% of cases in outpatient clinics and 55.5% in neurological hospitals). Among all the causes of temporary disability, PNS diseases occupy the 4th place (Antonov I.P., Gitkina L.S., 1987). In this case, the main etiological factor is osteochondrosis of the spine (according to various sources, from 60 to 90%). Tunnel compression-ischemic lesions of nerves account for 20-40%. However, epidemiological data are fragmentary and incomplete due to the dispersion of PNS diseases in various sections of the ICD-X. In addition to class VI, they are included in the general group of diseases of the musculoskeletal system and connective tissue (class XIII), and they are in other classes.

Classification of diseases of the peripheral nervous system

- I. Vertebrogenic lesions.

- II. Damage to the nerve roots, nodes, plexuses:

1. Meningoradiculitis, radiculitis (non-vertebrogenic);

2. Radiculoanglionitis, ganglionitis, truncites;

3. Plexites;

4. Plexus injuries

- III. Multiple lesions of roots, nerves:

1. Infectious-allergic polyradiculoneuritis;

2. Infectious polyneuritis;

3. Polyneuropathies: 3.1. Toxic; 3.2. allergic; 3.3. Dysmetabolic; 3.4. Discirculatory; 3.5. Idiopathic and hereditary.

- IV. Damage to individual spinal nerves:

1. Traumatic

2. Compression-ischemic (mononeuropathies)

3. Inflammatory (mononeuritis).

- V. Damage to the cranial nerves:

1. Trigeminal neuralgia and other cranial nerves;

2. Neuritis, neuropathy of the facial nerve;

3. Neuritis of other cranial nerves;

4. Prosopalgia:

5. Dentistry, glossalgia.

Anatomical and physiological features of lesions of the spinal nerves. Root Syndrome.

The roots of the spinal cord have a strictly segmental structure. and consists of several elements:

- back spine(dendrites and axon of afferent neuron) with spinal ganglion(the body of the first neuron of any afferent pathway - the pathways of superficial and deep sensitivity, cerebellar and autonomic pathways), with damage to which occurs:

1) girdle pain in the zone of innervation of the segment,

2) violation of all types of sensitivity according to the segmental type,

3) decrease in reflexes (interruption of the afferent part of the reflex),

4) soreness at the exit points of the roots.

- front spine(axon II of the [peripheral] motor neuron, axon II of the autonomic neuron), with damage to which occurs:

1) peripheral paralysis in the zone of innervation of the segment with a decrease in the corresponding reflex

- mixed spinal nerve, formed fusion of the anterior and posterior roots the spinal cord, which, leaving the intervertebral foramen of the spinal canal, is divided into four parts:

1) front branch - forms nerve plexuses and innervates the skin and muscles of the limbs and the anterior surface of the body,

2) back- innervates the skin and muscles of the posterior surface of the body,

3) shell part- innervates the membranes of the spinal cord

4) connecting part- innervates sympathetic ganglions.

radicular syndrome- a set of symptoms that occur when compression (or other impact) of the spinal root, consists of the following symptoms:

- pain shooting character along the affected root,

- sensory disturbances- more often hypoesthesia in the zone of innervation,

- movement disorders- Peripheral paresis of a group of muscles.

Separate spinal nerves and symptoms of their defeat:

- SpineC1:

Cranio-vertebral SMS, passes between the occipital bone and the 1st cervical vertebra,

2) front branch

3) back branch- suboccipital nerve, n. suboccipitalis (CI) - under the vertebral artery, in the groove of the vertebral artery of the atlas, then passes into the triangular space formed by the posterior rectus capitis major muscle, inferior and superior oblique muscles of the head, innervates muscles- m.rectus capitis posterir major et minor, obliquus capitis superior et inferior - and then skin- parietal region of the head

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- No

5) symptoms of damage: pain- parietal region, hypoesthesia- parietal region, paresis- is compensated by C2 muscles at the expense of the connecting branch.

- SpineC2:

1) place of exit from the spine- diskless PDS C I -C II,

2) front branch- as part of the cervical plexus,

3) back branch- goes around the lower edge of the inferior oblique muscle of the head and is divided into a number of short branches to muscles- m.semispinalis capitis - and n. occipitalis major, which, accompanying the occipital artery, pierces the semispinalis muscle of the head and the tendon of the trapezius muscle, innervates skin- parieto-occipital region.

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- occipital protuberance.

5) symptoms of damage: pain hypoesthesia- parieto-occipital region, paresis- compensated by C1 muscles at the expense of the connecting branch.

- Spine C3:

1) place of exit from the spine- PDS C II -C III,

2) front branch- as part of the cervical plexus,

3) back branch- third occipital nerve, n. occipitalis tertius - located medially from the large occipital nerve, muscles- No, leather- occipital region.

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- supraclavicular fossa

5) symptoms of damage: pain- neck, sensation of swelling of the tongue (connecting branch from XII c.n.), hypoesthesia- neck, paresis- No.

- Spine C4:

1) place of exit from the spine- PDS C III -C IV,

2) front branch- as part of the cervical plexus,

3) back branch- to deep muscles neck - m.semispinales cervicis et capitis, splenius capitis - further perforates the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- acromioclavicular joint

5) symptoms of damage: pain- shoulder girdle, collarbone, in the region of the heart and liver, hiccups (participates in the formation of n.phrenicus), hypoesthesia- shoulder girdle, paresis- Difficulty in neck extension, respiratory disorders.

- SpineC5:

1) place of exit from the spine- PDSS IV -С V,

2) front branch

3) back branch - to deep muscles skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- flexion at the elbow and raising your hand to the horizontal, sensitivity zone- lateral side of cubital fossa

5) symptoms of damage:pain- the outer surface of the shoulder, the medial part of the scapula, hypoesthesia- the upper part of the outer surface of the shoulder (above the deltoid muscle), paresis- abduction and external rotation of the shoulder, partially - flexion of the forearm, weakness and hypotrophy of the deltoid muscle, areflexia- bicipital.

- SpineC6:

1) place of exit from the spine- PDSS V -C VI,

2) front branch- in the brachial plexus

3) back branch - to deep muscles neck - m.semispinales cervicis, splenius cervicis - further perforates the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- dorsiflexion of the hand , sensitivity zone- thumb,

5) symptoms of damage:pain- lateral surface of the forearm and hand, I-II fingers, hypoesthesia-lateral surface of the forearm and hand, I-II fingers, paresis- flexion and internal rotation of the forearm, partially - extension of the hand, areflexia- bicipital.

- SpineC7:

1) place of exit from the spine- PDSS VI -C VII,

2) front branch- in the brachial plexus

3) back branch - to deep muscles neck and skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- extension in the elbow joint , sensitivity zone- middle finger,

5) symptoms of damage: pain- neck, shoulder blade, shoulder girdle, back surface of the shoulder and forearm up to II-III fingers, hypoesthesia - II-III fingers, back surface of the hand and forearm, paresis - extension of the shoulder, extension of the hand and fingers, partially - flexion of the hand, areflexia- tricipal.

- SpineC8:

1) place of exit from the spine- PDSS VII -Th I,

2) front branch- in the brachial plexus

3) back branch - to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- flexion of the distal phalanx III fingers , sensitivity zone- little finger,

5) symptoms: pain- neck, inner surface of the forearm, hands up to IV-V fingers, hypoesthesia- IV-V fingers, the inner surface of the hand and forearm, paresis- flexion and spreading of the fingers, atrophy of the muscles of the elevation of the little finger, areflexia- tricipal.

- SpineTh1:

1) place of exit from the spine- PDSTh I -Th II,

2) front branch- in the brachial plexus

3) back branch - to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- abduction I finger , sensitivity zone- medial side of the cubital fossa,

5) symptoms: pain- the inner surface of the shoulder and axillary region, hypoesthesia- the inner surface of the shoulder and upper forearm, armpit, paresis- spreading fingers areflexia- No.

- SpineTh2-12:

1) place of exit from the spine- PDSTh I -Th II,

2) front branch- nn. intercostales (Th1-6); nn. thoracicoabdominal (Th7-11), n. subcostalis (Th12) - between the ribs to the intercostal muscles, the skin of the corresponding segment and the pleura, the final parts - to the abdominal muscles:

Outer group of costal muscles - mm. intercostales intimi, interni et externi (Th1-Th11), subcostale (Th12)

The inner group of costal muscles - m. transversus thoracis (Th1-Th11),

Paravertebral costal muscles - m.seratus posterior superior (Th2-5), m.serratus posterior inferior (Th9-12)

Abdominal muscles - m.obliquus abdominis extemus (Th5-12), m.obliquus abdominis internus (Th8-12), m.transversus abdominis (Th7-12), m. rectus abdominis (Th7-12), m. pyramidalis (Th12), m. quadratus lumborum (Th12);

3) back branch - to deep muscles back and mm.levatores costarum, then perforates the fascia, innervating skin in the paravertebral and scapular region,

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- For 2 - apex of the armpit 3 - 3rd intercostal space, 4 - level of nipples, 5,6,7,8,9 - 5,6,7,8,9 intercostal space, 10 - navel level 11 - 11 intercostal space, 12 - inguinal fold.

5) symptoms: pain and hypoesthesia- along the corresponding segment of the body, paresis- No, areflexia- upper abdominal (Th7-8), middle abdominal (Th9-10) and lower abdominal (Th11-12).

- SpineL1:

1) place of exit from the spine- PDSL I -L II,

2) front branch

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- No, sensitivity zone- half distance Th12-L2

5) symptoms of damage: pain And hypoesthesia- below the inguinal fold, anterior-upper-inner surface of the thigh, paresis- No, areflexia- cremaster reflex.

- SpineL2:

1) place of exit from the spine- PDSL II -L III,

2) front branch- in the lumbar plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- hip flexion ,sensitivity zone- middle of the front of the thigh

5) symptoms of damage: pain And hypoesthesia- anterior thigh paresis- No, areflexia- knee reflex.

- SpineL3:

1) place of exit from the spine- PDSL III -L IV,

2) front branch- in the lumbar plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- extension shins ,sensitivity zone- medial femoral condyle

5) symptoms of damage: pain And hypoesthesia- anterior-inferior-outer surface of the thigh and knee, paresis- flexion and adduction of the hip, extension of the lower leg, getting up from a chair, areflexia- knee reflex.

- SpineL4:

1) place of exit from the spine- PDSL IV -L V,

2) front branch- in the lumbar plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- rear bending feet ,sensitivity zone- medial malleolus

5) symptoms of damage: pain And hypoesthesia- the inner surface of the knee and the upper part of the lower leg, paresis- extension of the lower leg and abduction of the hip, areflexia- knee reflex.

- SpineL5:

1) place of exit from the spine- PDSL V -S I,

2) front branch

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group-extension big finger , hip extension, calf flexion, sensitivity zone- dorsum of the foot

5) symptoms of damage: pain And hypoesthesia- the outer surface of the lower leg and the inner surface of the foot to the first finger, paresis- dorsiflexion of the thumb and foot, inability to stand on the heels, areflexia- No.

- SpineS1:

1) place of exit from the spine- PDSS I -S II,

2) front branch- in the sacral plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group-plantar bending feet , hip extension, calf flexion, zonesensitivity- lateral surface of the heel

5) symptoms of damage: pain And hypoesthesia- outer surface of the foot, heel, sole up to the fifth toe, paresis- plantar flexion of the big toe and foot, inability to stand on toes, areflexia- Achilles reflex.

- SpineS2:

1) place of exit from the spine- PDSS II -S III,

2) front branch- in the sacral plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- No, zonesensitivity- popliteal fossa

5) symptoms of damage: pain And hypoesthesia- posterior thigh paresis- No, areflexia- Achilles reflex.

- SpineS3-5:

1) place of exit from the spine- PDSS III -S IV -S V -Co I,

2) front branch- in the sacral plexus

3) back branch- to deep muscles back, then pierces the fascia, innervating skin in the paravertebral region

4) research methods(according to the ISCSCI system): muscle group- No, zonesensitivity- ischial tuberosity (S3) and perianal area (S4-5)

5) symptoms of damage: pain And hypoesthesia- perianal area, paresis- true incontinence of urine and feces, areflexia- anal reflex.

Vertebrogenic lesions of the nervous system: general issues

Anatomy and physiology of movement in the spine:

- Anatomical components of the spine:

1) vertebral bodies,

2) intervertebral disc (IVD)- annulus fibrosus and nucleus pulposus, function: 1. connection of the vertebrae, 2. ensuring the mobility of the spinal column, 3. depreciation of the vertebrae

3) intervertebral (facet) joints- function: 1. maintaining the position of the spine; 2. movement of the vertebrae relative to each other; 3. change in the configuration of the spine and its position relative to other parts of the body,

4) main ligaments of the spine, function: 1. Protect the spinal cord by closing the holes, 2. maintaining physiological curves, 3. depreciation of the vertebrae - IVD antagonists:

Yellow (interdiscal) ligaments - connect the joints and arcs of adjacent vertebrae, have a pronounced elasticity, function: counteracting the strength of the nucleus pulposus and reducing the distance between the vertebrae,

Posterior longitudinal ligament - forms the anterior surface of the spinal canal,

Anterior longitudinal ligament - connects the anterior surfaces of the vertebral bodies and intervertebral discs,

5) additional ligaments of the spine: interspinous, intertransverse, supraspinous ligaments - connect the corresponding processes,

6) transverse muscles- consist of two independent bundles - medial-dorsal and lateral-ventral and go from bottom to top and inwards,

7) interspinous muscles- paired, directed from the bottom up, ventrally and inward.

- Vertebral motor segment (VMS)- a functional system that provides mobility of the spine.

1) Front support structure:

Anterior longitudinal ligament

The front of the disc

Anterior part of the vertebral body

2) Medium support structure:

posterior longitudinal ligament,

Back of the disc

Posterior part of the vertebral body.

3) Rear support structure:

nasty ligament,

interspinous ligament,

yellow ligament

Facet joints

- Movements in the spinal column are carried out by synergistic muscle tension of a separate SMS and the entire spinal column.

The main causes of vertebrogenic lesions of the nervous system:

Degenerative changes in the spine (disc herniation, spondylosis, osteophytes, arthrosis of the intervertebral (facet) joints),

Anomalies in the structure of the spine (anomalies of the craniovertebral transition, sacralization, lumbarization, stenosis of the spinal canal)

Instability of the spinal segment (spondylolisthesis)

Vertebral fractures

Systemic connective tissue diseases (ankylosing spondylitis, sacroiliitis),

Hormonal spondylopathy (osteoporosis)

Primary and metastatic tumors of the cauda equina, spine and surrounding tissues,

Infectious spondylitis (tuberculous)

Functional disorders of the spine.

Diagnosis of vertebrogenic lesions of the nervous system:

- Identification of the morphological substrate of the lesion

1) Radiographyspine: in the anterior-posterior, lateral (if necessary, in oblique) projections, and if indicated - tomograms, images in the position of maximum flexion and extension in the cervical region,

2) CT - state of the bone structures of the spinal segment, osteophytes, calcification of the posterior longitudinal ligament, narrowing of the spinal canal.

3) MRI- visualization (on T2-weighted tomograms) of a hernia in various parts of the spinal column, their sequestration, as well as the exclusion of other causes (tumor), the fact of spinal cord compression, its degree is determined.

4) EMG- clarification of the state of the root and spinal cord.

- Other Methods to identify the etiological factor of spinal injury

Vertebrogenic lesions of the nervous system: main syndromes

Vertebral syndrome- a set of symptoms in the area of ​​the spine, which are based on a dysfunction of one or more SMS, includes:

- change in the configuration of the spine(flattening or strengthening of lordosis or kyphosis, scoliosis, kypho- or lordoscoliosis), as well as immobility (!).

- local pain and pain with active and passive movements, as well as with palpation of the spinous processes (irritation of the sinuvertebral nerve).

- loss of spring function in the form sensations of "fatigue of the spine" and discomfort in the back, local pain with axial load, as well as changes according to x-ray: 1) thickening of the endplates, 2) reduced IVD height, 3) osteophytes, 4) neoarthrosis

Extravertebral syndromes- a set of symptoms outside the spinal zone, which are based on a dysfunction of one or more SMS, includes:

- reflex syndromes arising from the reaction of surrounding tissues to pathological impulses from PDS:

1) muscular-tonic disorders - myoadaptive reflex tension of muscle groups in order to minimize pain,

2) vasomotor and neurodystrophic disorders - vegetative disorders, foci of myoosteofibrosis as a result of prolonged muscle spasm.

- compression syndromes, caused by the impact of pathological structures (hernia, osteophyte, etc.) on:

1) spinal cord(compression myelopathy),

2) spinal root(compression radiculopathy)

3) spinal root and vessel(compression radiculo-ischemia)

"Pain syndrome"- a set of symptoms accompanying pain and arising from pathological impulses from the affected PDS, may refer to both vertebral and extravertebral manifestations:

- indicative judgment on the severity of pain:

1) light - intermittent aching pain that occurs with significant and prolonged physical exertion;

2) moderate - constant aching, boring pain in the back, aggravated by forced movements, forced position, active movements are moderately limited;

3) pronounced - constant sharp pain, aggravated with minimal movements, antalgic postures;

- objectification:

1) general form, gait, behavior of the patient;

2) tension symptoms (Lasegue, Neri, Bonnet, Spurling, Wassermann, etc.) with control - the second phase of the Lasegue symptom, the landing symptom, etc .;

4) limited mobility of the spine (!, vertebral syndrome).

Vertebrogenic lesions of the nervous system: classification and clinical picture

Syndromes in the head, neck, upper limb:

- Reflex syndromes:

1) Cervicalgia (cervicago):

- pain: acute (cervicago) or subacute / chronic (cervicalgia) in the depths of the neck, worse in the morning, after sleep, with movement, coughing, sneezing.

- myopically .

2) Cervicocranialgia (sclerotomy cervicocranialgia):

- pain: unilateral, dull/pressive, "brain", of moderate or moderate intensity, starting in the cervical-occipital region and extending to the frontal and temporal regions.

- myopically(tension of the paravertebral muscles) with restricted neck mobility.

- myodystrophic(myoosteofibrosis nodules in the muscles of the neck) And(photo/phonophobia, nausea, vomiting).

3) Cervicobrachialgia:

- pain: unilateral, aching/pulling, of moderate or medium intensity, in the back of the head with irradiation to the deep parts of the shoulder, sometimes with dysesthesia of the hands

- myopically(tension of the paravertebral muscles) with restricted neck mobility.

4) Syndrome of the inferior oblique muscle of the head:

- pain: aching / aching pain in the cervical-occipital region of a constant nature, without a tendency to paroxysmal intensification, is provoked by a prolonged static load on the muscles of the neck and during a test for rotation of the head in a healthy direction, the painful point is the attachment of the inferior oblique muscle to the spinous process of C2 along the midline of the neck in the suboccipital region.

- secondary compression (great occipital nerve):

- sensory disturbances - Hypoesthesia and periodic paresthesia in the occipital region.

- pain: aching / burning pain in the chest when abducting the arm and at night at rest.

- secondary compression (lower brachial plexus and subclavian artery):

- pain in the hand on the side of defeat

- sensory disturbances : paresthesia in the anterior chest wall and arm, hypoesthesia of the shoulder and forearm along the ulnar edge,

-movement disorders: peripheral paresis of the distal muscles of the arm, more hypothenar,

- vegetative-vascular disorders: blanching and swelling of the hand.

8) Shoulder-scapular periarthrosis (periarthropathy)- pathology of the muscles and ligaments of the rotator cuff, more often considered as a vertebrogenic neurodystrophic process - 1) tendonitis of the supraspinatus tendon, 2) calcific subacromial tendonitis and 3) complete or partial rupture of the tendon of the supraspinatus muscle,distinguish from adhesive capsulitis(constant aching pain in the shoulder, restriction of all movements, morning stiffness in the joint)

- pain: Sharp, when abducting the arm and when laying the arm behind the back in the region of the deltoid muscle, tubercles of the humerus and acromion. or spontaneous nocturnal when lying on the affected side, aggravated by movement and radiate to the neck, to the arm.

- myopically(The pectoralis major and teres major are firm and painful on palpation) with limited mobility in the shoulder joint ( frozen shoulder).

- myodystrophic(weakness and atrophy of the deltoid, supraspinatus and infraspinatus, subscapularis muscles) And vegetative-vascular disorders(blanching and swelling of the hand, in severe cases of vegetative disorders is called Steinbrokker's syndrome - "shoulder-hand").

- pain: aching / aching, in the interscapular region, more intense at night, aggravated by vibration, cooling, rotation of the body, less often when bending to the side.

- myopically(tension of the paravertebral muscles).

- myodystrophic(nodules of myoosteofibrosis of the paravertebral muscles)

- pain: in the gluteal region at rest, when moving in bed, walking, getting up from a chair, laying legs on the leg (sabraze test), reflected pain in the entire buttock, back of the thigh and lower leg,

- myodystrophic disorders(point of soreness in the region of the gluteus maximus muscle - the upper-outer sections of the outer-upper quadrant of the buttock).

4) Gluteus medius syndrome:

- pain: too, but at the moment of sitting down on a healthy buttock, pain appears in the affected side, it intensifies when standing, especially when rotating the thigh inwards, reflected pain throughout the buttock.

- myodystrophic disorders(a point of tenderness on the border with the gluteus maximus muscle, approximately in the region of the inner-upper quadrant of the buttock).

5) Syndrome of the abductors (abductor muscles) of the thigh

- pain: along the outer (lateral) and anterior surface of the thigh, the anterior outer part of the lower leg, sometimes in the area of ​​the outer ankle,

- myodystrophic disorders(point of tenderness anterior and posterior to the greater trochanter).

6) Syndrome of adductors (adductor muscles) of the thigh

- pain: in the region of the adductors of the thigh (from the groin along the inner surface of the thigh), increases with the abduction of the leg in the position on the side. When walking, the pelvis on the affected side rises, the thigh is bent and adducted, the patient steps on the toe.

- myodystrophic disorders(points of pain on the inner surface of the upper third of the thigh with irradiation of pain in the groin, along the anterior-inner surface of the thigh and lower leg).

7) Syndrome of ischiocrural muscles (back muscles) of the thigh

- pain: in the popliteal fossa with irradiation down or up.

- myopically(tension of the posterior thigh muscles) with limited mobility(limitation of the volume of bringing the knee to the chest)

- myodystrophic disorders(points of soreness of the posterior muscle group, places of origin and attachment of the ischiocrural muscles during overstretching (forward bend, extension in hip joint in the supine position).

8) Tibialis anterior syndrome

- pain: in the anterior-outer part of the lower leg, outer ankle, foot, tension of the anterior tibial muscle.

- myodystrophic disorders(points of soreness in the upper and middle third of the lower leg along the anterior surface (in the region of the tibial muscle) with pain radiating to the rear of the foot and to the big toe).

- Compression syndromes

1) Lumbar radicular syndromes, including cauda equina syndrome (see topic 3)

2) Myelopathy- signs of compression of the cone of the spinal cord

3) Piriformis syndrome andsubpiriform intermittent claudication syndrome

- pain: in the groin, knee, hip joint, are reproduced by palpation and percussion of the piriformis muscle, at the time of squatting, while sitting with an adducted thigh.

- myopically(tension of the piriformis muscle, soreness at the exit of the sciatic nerve from under the piriformis muscle)

- secondary compression (sciatic nerve):

- sensory disturbances - dull, aching pain along the posterior and posterolateral surface of the thigh and lower leg, which sharply arises / intensifies when walking (rest is necessary to stop), Lasegue's symptom, hypoesthesia of the lower leg and foot,

- motor disorders: violation of flexion of the leg. movements in the foot, decreased Achilles reflex, atrophy of the posterior muscles of the thigh, the entire lower leg and foot

Osteochondrosis of the spine with neurological manifestations

Osteocondritis of the spine- polyfactorial chronic illness, which is based on the defeat of the pulpous complex (nucleus) of the intervertebral disc, leading to the involvement in the pathological process of other parts of the spine, the musculoskeletal system and the nervous system. However, in the literature there is no single definition of the essence of the concept of osteochondrosis, and in foreign literature a syndromic approach is common, in which the concept of back pain (back pain) is used in the diagnosis of pain of the corresponding localization, often without specifying their etiopathogenetic component.

Neurological manifestations of spinal osteochondrosis- a group of clinical syndromes, pathogenetically determined reflex, compression, myoadaptive factors and emerging sensitive, motor, vegetative-trophic, vascular disorders, pain syndrome.

1. Osteochondrosis in clinical practice, it includes osteochondrosis itself (as a primary lesion of the intervertebral disc), deforming spondylosis, herniated discs and spondylarthrosis, since, as a rule, there are close pathogenetic links between these conditions:

- Herniated discs are formed as a result of prolapse of a dystrophically modified nucleus pulposus of the intervertebral disc through the fibrous ring, damaged as a result of dystrophy or trauma.

- Deforming spondylosis- manifestation of deterioration, age-related changes in the spine in the form of marginal osteophytes (bone growths) of the vertebral bodies due to primary dystrophic changes in the fibrous ring of the intervertebral disc.

- Spondylarthrosis- degenerative-dystrophic lesion of the intervertebral (facet) joints.

2. Etiology- a complex of factors:

- genetic predisposition(features of the structure of bone tissue)

- Overload and microtrauma lower lumbar and lower cervical spine, especially due to excessive static-dynamic load,

- Factors affecting normal metabolism: autoimmune, endocrine, dysmetabolic.

- Spinal anomalies

1) narrowness of the spinal canal,

2) transitional lumbosacral vertebrae (lumbarization or sacralization),

3) soldering of the cervical vertebrae (concretions, synostoses, blocks) occurs at the early stages of embryogenesis due to developmental delay (C2-C3, C3-C4).

4) hypermobility of the vertebral motor segments (retro- and antespondylolisthesis)

3. Pathogenesis consists of:

- dystrophic changes:

1) intervertebral discs(protrusion and herniation of the disc) - prolapse of the gelatinous (pulpous) nucleus through a dystrophically altered or traumatically damaged fibrous ring - irritation of the pain receptors of the outer ring, yellow and posterior longitudinal ligaments - spasm of the segmental muscles of the spine - increased pain. The displacement of the hernia into the spinal canal leads to edema and aseptic inflammation with the involvement of the corresponding root (“compression”). According to localization, they are distinguished: median, paramedian, dorsolateral, lateral.

2) changes in the vertebral bodies(deforming spondylosis) - primary dystrophic changes in the fibrous ring with rejection of its outer layer from the bone marginal border of the vertebral body - the nucleus pushes the changed fibrous ring to the side, which increases the load on the edges of the vertebral bodies and leads to tension of the anterior longitudinal ligament - in places of increased load, bone growths - osteophytes (whiskers, beaks). In addition, compaction (sclerosis) of the subchondral (terminal) plates of the vertebral bodies occurs with the spread of sclerosis deep into the body, the development of cyst-like changes, and a decrease in the height of the vertebral body.

3) intervertebral joints(spondylarthrosis) - a decrease in the height of the intervertebral disc leads to loosening of the SMS - subluxation and displacement of the vertebrae relative to each other - hypermobility in the intervertebral (facet) joints - increased wear and ankylosis of the joints.

- irritation and/or pressure ligaments, spinal nerve roots, spinal cord, cauda equina roots, spinal cord arteries:

1) aseptic inflammation and edema, provoked by IVD hernia, in rare cases, the actual compression of structures,

2) thickened yellow ligament,

3) spondylolisthesis,

4) osteophytes.

4. General clinical diagnostic criteria:

- Anamnesis: risk factors, including professional ones; typical development of the disease or exacerbation; previous episodes (reflex, compression), their nature, frequency.

- Clinical status data: presence of vertebral syndrome +/- extravertebral

- Additional methods:

1) X-ray and neuroimaging methods (CT, MRI) are performed to exclude causes that can cause back pain (the presence of "red flags" in the patient):

1) malignant tumors in history, unmotivated weight loss (oncopathology),

2) immunosuppressive conditions (long-term use of GCs) or suspected metabolic bone disorders (osteoporosis),

3) significant injury (falling from a height or severe bruising in young people, falling from a height of one's own height or lifting weights in the elderly),

4) the pain is not mechanical in nature (intensifies at night, lying on the back and does not weaken at rest - oncopathology),

5) the occurrence of pain on the background of fever or other systemic manifestations

6) tension and stiffness of the spine, prolonged stiffness in the morning (systemic diseases of the connective tissue)

7) the presence of focal neurological pathology (cauda equina syndrome),

8) lack of effect from standard treatment within a month.

5. Principles of treatment for exacerbation of the disease

1) avoid bed rest, continue normal daily activities (within reason) or resume them as soon as possible,

2) teaching the correct stereotype of movements,

3) orthopedic treatment ( orthopedic mattress, a corset for a period of acute pain).

- Systemic use of medicines:

1) Analgesics - metamizole sodium (analgin), and NSAIDs - diclofenac, meloxicam, nimesulide, ibuprofen, indomethacin.

2) Muscle relaxants - tolperisone, tizanidine.

3) Vascular, including venotonics, and metabolic drugs, chondroprotectors

- Local therapy

1) Dimexide applications

2) Novocaine blockades

- Physiotherapy, including phono- and electrophoresis of medicinal substances: lidase, caripazim

- Manual therapy, traction, massage, acupuncture

- Indications for surgical treatment:

1) acute compression of the cauda equina or spinal cord (absolute);

2) preservation of a pronounced persistent pain syndrome for 3-4 months without a tendency to a significant decrease, despite complex conservative treatment;

3) acute radiculomyeloishemia.

Anatomical and physiological features of plexuses and nerves. mononeuritic syndrome.

cervical plexus(plexus cervicalis) - anterior branches C1-C4:

- anatomy: C1 lies in the groove of the vertebral artery, then passes between the anterior and lateral rectus muscles of the head, C2-C4 - pass between the anterior and posterior transverse muscles -> 3 loops are formed on the middle scalene muscle under m.sternocleidomastoideus , has connecting branches:

1) with n.hypoglossus - ansa cervicalis (cervical loop, lies in front of the CCA) - innervation of the hyoid muscles - m.geniohyoideus (C1), thyrohyoideus (C1), sternothyroideus, sternohyoideus, omohyoideus,

2) with n.accessorius - innervation of m.sternocleidomastoideus (C2-3) et trapesius (C2-4),

3) with a sympathetic trunk.

- function: innervation of the skin and muscles occipital region and neck, diaphragm

- nerves:

1) skin:

- n.occipitalis minor(C2-3) - to the posterior edge m.s-c-m [skin behind the auricle]

- n.auricularismagnus(C3-4) - to the posterior edge m.s-c-m below the previous one - [skin of the auricle and external auditory canal].

N. transversus colli (C2-3) - to the posterior edge m.s-c-m below the previous one [skin of the anterior neck, medially from m.s-c-m]

Nn.supraclaviculares (C3-4) - to the posterior edge of m.s-c-m below the previous one [skin of the anterior-outer part of the neck, outward from m.s-c-m, shoulder girdle and chest up to 4 ribs].

2) muscle:

To m.rectus capitis anterior (C1), rectus capitis lateralis (C1), longus capitis (C2-3) [head forward flexion]

To m.longus colli (C2-4) [forward flexion of the head and neck],

To m.levator scapulae (C3-4) [raises the upper angle of the scapula, brings the lower angle to the midline]

3) mixed:

- n.phrenicus- muscular - to the diaphragm, sensitive - to the pleura, pericardium and peritoneum.

- symptoms of a complete plexus lesion:

1) pain in the neck and neck,

2) violation of sensitivity in the region of the back surface of the head, lateral and lower surfaces of the face, sub- and supraclavicular region,

3) paralysis of the diaphragm.

Brachial plexus(plexus brachialis) - anterior branches C5-Th1:

- anatomy:

1) primary bundles (truncus superior - C5-6, medius - C7, inferior - C8-Th1) follow in the interstitial space, located here behind the subclavian artery and under it, then they are located in the supraclavicular fossa outward and posterior to the lower part of m.s-c-m , crossing the lower belly of m.omohyoideus in front,

2) secondary bundles (fasciculus lateralis - C5-7, medialis - C8-Th1, posterior - C5-Th1) are located in the subclavian fossa (around a.axillaris).

- function: innervation of the skin and muscles shoulder girdle and upper limbs,

- nerves:

1) supraclavicular part of the plexus:

- muscular branches: to m.scalenus anterior (C5-C7), medius (C4-C8), posterior (C7-8)

- n.dorsalis scapulae(C4-5) - muscular - along the anterior surface of the m.levator scapulae [raises the upper angle of the scapula, brings the lower angle to the midline] to the medial edge of the scapula to m.rhomboudeus major et minor [brings the lower angle of the scapula to the midline]

- n.toracicus longus(C5-7) - muscular - down along the anterior axillary line along the lateral surface of the m.serratus anterior [pulls the scapula forward and outward - with a lesion of "pterygoid scapulae"].

- n. subclavius(C4-6) - muscular - located in front of the subclavian artery, follows to m.subclavius ​​[lowers the collarbone].

- n.suprascapularis(C5-6) - muscular - to the lower abdomen of m.omohyoideus, passes through the notch of the scapula into the supraspinatus fossa to m.supraspinatus [shoulder abduction, deltoid agonist], goes around the neck of the scapula, enters the infraspinatus fossa to m.infraspinatus [rotation of the shoulder outward ].

2) subclavian part of the plexus (lateral bundle -"L ucy L oves M e"- L ateral pectoral, L ateral root of the median nerve, M usculocutaneous ):

- n.pectoralislateralis(C5-Th1) - muscular - in front of the axillary artery, gives off branches to the deep part of m.pectoralis major [adduction and rotation of the shoulder inward].

Lateral root n.medianus(С6-7)

- n.musculocutaneus(C5-7) - mixed - down and outward, perforates m.coracobrachialis [shoulder adduction and flexion], between m.biceps brachii et brachialis [shoulder flexion, bicipital reflex], further from under the lateral edge of the distal tendon m.biceps brachii n. cutaneus antebrachii lateralis [skin of the outer surface of the forearm to thenar].

3) subclavianPartplexus(medialbeam - "M ost M edical M en U se M orphine"- M edial pectoral, M edial cutaneous nerve of arm, M edial cutaneous nerve of forearm, U lnar, M edial root of the median nerve ):

- n.pectoralismedialis(C5-8) - muscular - between the axillary artery and vein to m.pectoralis major [adduction and rotation of the shoulder inward] et minor [pulls the scapula forward and down].

- n. cutaneus brachii medialis(C8-Th1) - skin [skin of the armpit, anterior and posteromedial surfaces of the shoulder to the medial epicondyle of the humerus and olecranon].

- n. cutaneus antebrachii medialis(C8-Th1) - cutaneous - along the axillary artery, then the brachial artery to the middle of the shoulder, then gives branches to the skin [skin of the medial (palmar and dorsal) side of the forearm to the wrist joint]

- n.ulnaris(C7-8) - mixed - along the brachial artery, then in the medial intermuscular septum, then between the medial epicondyle of the humerus and the olecranon, then between the heads m.flexor carpi ulnaris [elbow flexion of the hand], lies on the anterior surface of the forearm medially from the ulnar arteries and veins to m.adductor pollicis, m.flexor pollicis brevis, hypothenar muscles (m. abductor digiti minimi, m. flexor digiti minimi brevis, m. opponens digiti minimi); middle group of muscles of the hand (mm. lumbricales III, IV) [ in defeat - the impossibility of squeezing the hand into a fist, limiting palmar flexion of the hand, adducting and spreading the fingers, atrophy of the muscles of the hand, hypothenar, IV and V fingers - "clawed paw"], then skin branches [skin of the palmar surface V and ½IV, dorsal surface V, IV and ½III fingers of the hand]

Medial spine n.medianus(C6-8) - mixed - two roots form a loop on the anterior surface of the axillary artery, then along the brachial artery to the cubital fossa, then under the m.biceps brachii aponeurosis on the forearm between the heads of m.pronator teres [forearm pronation], to m.flexor digitorum profundus, flexor pollicis longus [palmar flexion of the fingers], pronator quadratus [pronation of the forearm], flexor carpi radialis [radial flexion of the hand], then under the tendon m.flexor digitorun longus superficiallis [palmar flexion of the hand] to the area of ​​the wrist joint, then under the retainer flexors (carpal canal) to muscles middle group brushes (mm. L umbricales I, II) and thenar (m. O pponens pollicis, A bductor pollicis brevis, F lexor pollicis brevis LOAF) [in defeat - violation of palmar flexion of the I, II, III fingers of the hand, difficulty in opposing the thumb of the hand, atrophy of the tenar and forearm muscles - "monkey hand"] and skin [palmar surface of the I, II, III and ½IV fingers of the hand].

4) subclavian part of the plexus (posterior bundle - STAR - S ubscapular, T horacodorsal, A xillary, R adial ):

- n.subscapularis (C5-7) - muscular - on the anterior surface of m.subscapularis [shoulder inward rotation] to m.teres major [shoulder inward and backward rotation]

- n.thoracodorsalis(C4-7) - muscular - the water of the subscapular artery goes to m.latissimus dorsi [pronation of the shoulder, bringing back to the midline - "tying the apron"]

- n.axillaris(C5-6) - mixed - around the surgical neck of the shoulder to m.deltoideus [shoulder abduction up to 70 0 ] and m. teres minor [rotation of the shoulder outward] and to the skin n.cutaneus brachii lateralis superior [skin in the deltoid muscle]

- n.radialis(C5-8) - mixed - passes through the triangular foramen, further along the posterior surface of the brachial artery in the canalis humeromuscularis, innervates m. triceps brachii [extension of the forearm] and m. anconeus, gives cutaneous nerves - n.cutaneus brachii posterior [skin of the posterior surface of the shoulder], n.cutaneus brachii lateralis inferior [skin of the lateral surface of the shoulder], n.cutaneus anterbrachii posterior [skin of the posterior surface of the forearm], then to m.brachioradialis [flexion forearms], m.extensor carpi radialis longus et brevis [dorsal flexion of the hand], m.supinator [supination of the forearm], then the deep branch goes to the extensor muscles of the hand and fingers - m.extensor digitorum, m.extensor digiti minimi, m. extensor carpi ulnaris, m.abductor pollicis longus, m.extensor pollicis brevis, m.extensor pollicis longus [ in defeat - paralysis of the extensors of the forearm, hand and fingers, a decrease in the tricipital and carporadial reflex - "hanging hand, walrus flipper"], superficial branch - to the skin [back surface of I, II and ½III fingers of the hand].

1) complete defeat:

Pain radiating to the arm, aggravated by movement,

Loss of all types of sensitivity at the level of C5-Th2 (hand),

Peripheral paralysis of the muscles of the hand,

Decreased bicipital, tricipital and carporadial reflexes.

2) damage to the upper part of the plexus(Duchenne-Erb palsy, C5-C6):

Pain with irradiation along the outer surface of the arm,

Disorder of sensitivity on the outer surface of the hand,

Peripheral paralysis of the proximal muscles of the arm, pterygoid scapula

Decreased carporadial and bicipital reflex.

3) damage to the lower part of the plexus(Dejerine-Klumpke palsy, C7-Th1):

Pain with irradiation along the inner surface of the arm,

Sensitivity disorder on the inner surface of the hand,

Peripheral paralysis of the distal muscles of the arm,

Decreased carporadial and tricipital reflex,

Distal vegetative-trophic disorders,

Frequent development of the Bernard-Horner syndrome (C8-Th1).

Lumbar plexus(plexus lumbalis) - anterior branches Th12-L4

- anatomy: in front of the transverse processes of the lumbar vertebrae, between m.quadratus lumborum behind and m.psoas major in front.

- function: innervation of the skin and muscles anterior thigh and lower leg,

- nerves:

1) muscle:

To m.quadratus lumborum (Th12-L3)

To m.psoas major (Th12-L4)

To m.psoas minor (L1-L2)

2) n.iliohypogastricus (Th12-L1) - mixed - from top to bottom and back to front, then between m.transversus abdominis [abdominis] and m.obliquus abdominis internus [abdominal pressure] to the superficial inguinal ring [skin of the upper lateral surface of the thigh and pubis],

3) n.ilioinguinalis (L1) - mixed - from top to bottom and back to front, then between m.transversus abdominis [abdominis] and m.obliquus abdominis internus [abdominal pressure] to the superficial inguinal ring [groin skin] and scrotum,

4) n. genitofemoralis (L1-L2) - mixed - from top to bottom and back to front along m.transversus abdominis [abdominal press] to the inguinal region and then into two branches: 1) to the skin of the femoral triangle, 2) through the inguinal canal into the scrotum to m.cremaster [ elevates testis, cremaster reflex]

5) n. cutaneus femoris lateralis (L2-L3) - skin - from under the lateral edge of m.psoas major to the anterior superior iliac spine under the inguinal ligament on the thigh [skin of the anterior outer surface of the thigh]

6) n. obturatorius (L1-L5) - mixed - behind m.psoas major to the medial edge and sacroiliac joint, then to the internal opening of the obturator canal and m.obturatorius externus on the medial surface of the thigh to the adductor muscles of the thigh - m.gracilis, pectineus, adductor longus et brevis [flexion and adduction of the hip] and skin [lower parts of the medial surface of the thigh].

7) n. femoralis (L1-L4) - mixed - behind m.psoas major to m.iliacus, then through the muscle gap on the thigh to the femoral triangle to m.sartorius, m.pectineus, m.quadriceps femoris and m.arcuatus genu [hip flexion and extension lower legs, knee jerk], then there are skin branches [skin of the lower 2/3 of the anterior medial surface of the thigh to the knee joint)] and n.saphenus [skin of the medial surface of the lower leg and rear of the foot]

- plexus symptoms:

1) complete defeat:

Pain in the lower abdomen, lower back, pelvic bones,

Loss of all types of sensitivity at the level of Th12-L4 (pelvic girdle and hips),

Positive tension symptoms: Matskevich and Wasserman (n.femoralis),

Peripheral paralysis of the muscles of the pelvic girdle and thighs,

Decreased knee jerk.

sacral plexus(plexus sacralis) - anterior branches L5-S3.

- anatomy: a triangular thick plate, which is directed towards the piriform fissure with its apex, part of the plexus lies on the anterior surface of the sacrum, part on the anterior surface of m.piriformis, the fibers exit through the large sciatic foramen.

- function: innervation of the skin and muscles pelvic girdle, back of the thigh and lower leg,

- nerves:

1) obturatorius internus (S1) - muscular - under the piriformis muscle, goes around the ischial spine, approaches m.obturatorius internus [external rotation of the thigh].

2) n.piriformis (S1-2) - muscular - to m.piriformis [external rotation of the thigh]

3) n.quadratus femoris (S1) - muscular - under the piriformis muscle, gives the final branches to m.quadratus femoris, mm.gemelli superior et inferior [external rotation of the thigh]

4) n. gluteus superior (L4-S1) - muscular - above the piriformis muscle and, bending around the greater ischial notch, lies between m.gluteus minimus et medius [hip abduction], and then to m.tensor fasciae latae [internal rotation and hip flexion, supports knee extension]

5) n. gluteus inferior (L5-S2) - muscular - under the piriformis muscle in the gluteal region under m.gluteus maximus [hip extension, with damage - "duck" gait]

6) n.cutaneus femoris posterior (S1-3) - dermal - under the piriformis muscle medial to the sciatic nerve and lies under m.gluteus maximus, descends to the back of the thigh [skin of the gluteal region, medial surface of the perineum]

7) n. pudendus (L4-S4) - mixed - through the large ischial opening, goes around the ischial spine and enters the small ischial opening to the rectum and perineal muscles, forms n.dorsalis penis / clitoris [genital skin]

8) n. ischiadicus (L4-S3) - mixed - under the piriformis muscle almost in the middle of the line drawn between the ischial tuberosity and the greater trochanter of the thigh, further below the gluteal fold between m.biceps femoris [flexion of the lower leg, extension of the thigh] and m.adductor magnus [adduction of the thigh] , then between m.semimembranosus [flexion of the lower leg, extension of the thigh] and m.semitendinosus [flexion of the lower leg, extension of the thigh] to the popliteal fossa [ in defeat - dull, aching pain along the posterior and posterolateral surface of the thigh and lower leg, Lasegue's symptom, hypoesthesia of the lower leg and foot, impaired flexion of the lower leg. movements in the foot, decreased Achilles reflex, atrophy of the posterior muscles of the thigh, the entire lower leg and foot], where it is divided into n.tibialis and n.peroneus:

9) n. tibialis (L4-S3) - mixed - under m.triceps surae (m.gastrocnemius et soleus) [plantar flexion of the foot] and m.popliteus [knee flexion], further down to m.tibialis posterior [plantar flexion of the foot], m.flexor digitorum longus and m.flexor hallucis longus [flexion of the fingers], as well as to the skin - n.cutaneus surae medialis [skin of the posterior outer surface of the lower leg], then follows the medial malleolus to the skin [skin of the heel area], and then splits into [ in defeat - hypoesthesia of the foot, outward rotation of the foot, "calcaneal foot" - violation of plantar flexion of the foot and fingers, inability to stand on toes, decreased Achilles reflex]:

1) n. plantaris medialis to m. L umbricalis I, m. A bductor hallucis [abduction of the thumb], m. F lexor digitorum brevis, m. F lexor hallucis brevis [flexion of fingers] (LAFF) and sole skin [skin of medial surface and I, II, III and ½IV fingers]

2) n. plantaris lateralis to m.quadratus plantae, m.flexor digiti minimi [flexion of the fingers], m.adductor hallucis [adduction of the thumb], mm.interossei, mm.lumbricalis II-IV and m.abductor digiti minimi [abduction of the little finger] and the skin of the sole [ skin of the lateral surface of ½IV and V fingers].

10) n. peroneus (L4-S3) - mixed - under the tendon m.biceps femoris to the head of the fibula under m.peroneus longus, where it is divided into [ in defeat - hypoesthesia of the outer surface of the lower leg and rear of the foot, drooping of the foot down and rotation inward, "cock" gait (the patient raises the leg high when walking), "horse foot" - limitation of dorsiflexion of the foot and fingers, inability to stand on the heels]:

1) n.cutaneus surae lateralis - dermal - [skin of the upper outer surface of the lower leg]

2) n. peroneus superficialis - mixed - to m.peroneus longus et brevis [dorsal flexion of the foot, lateral flexion of the foot], dalle follows down to the skin [skin of the anterior surface of the lower leg and rear of the foot].

3) n.peroneus profundus - mixed - passes into the anterior muscle bed to m.tibialis anterior [dorsal flexion of the foot], m.extensor digitorum longus, m.extensor hallucis longus [toe extension], then to the foot to m.extensor digitorum brevis and m.extensor hallucis brevis [digital extension] and skin [skin of the first interdigital space]

- plexus symptoms:

coccygeal plexus- anterior branches of S5-Co1.

- anatomy: on the anterior surface of the coccyx

- function: skin innervation perineum

- nerves: nn. anococcigei - skin - [skin of the coccyx and anus]

- plexus symptoms: coccygodynia

Compression (tunnel) neuropathies

Tunnel neuropathy (TN)- local damage to the nerve trunk, due to its compression and ischemia in the anatomical channels (tunnels) or due to external mechanical influence.

The pathogenesis of TN is based on compression of the nerve (sometimes together with a nearby vessel), leading to its ischemia, and when compressed from the outside, it is predominantly mechanical stretching. Compression is carried out by the tissues surrounding the nerve that form the corresponding channel (ligaments, tendons, muscles, bone structures). Contributing factors are an increase in tissue volume and an increase in intracanal pressure, impaired blood supply to the nerve and venous outflow. A compression-traction mechanism is possible due to hyperfixation of the nerve in the tunnel (adhesions, angulation). Nerve dysfunction occurs due to both demyelination and Wallerian degeneration in the proximal nerve, sometimes with damage to the cells of the anterior horns of the spinal cord. Violation of neurotrophic control due to insufficiency of axonal transport is also important (F. A. Khabirov, M. F. Ismagilov, 1991, etc.). Recovery of functions is often significantly delayed (up to 2-3 months), especially after acute compression nerve injury (Harrison, 1976). TN can be combined with discogenic radiculopathy in osteochondrosis of the spine (variants of multilevel and multiple neuropathy). Osteochondrosis, manifested by muscular tonic and neurodystrophic syndromes, is also the direct cause of compression of the nerve or neurovascular bundle, for example, tunnel neurovascular syndrome of the anterior scalene or piriformis muscle.

Classification

1) neuropathy (neuralgia) of the cranial nerves;

2) neuropathy of the neck and shoulder girdle;

3) neuropathy of the hands;

4) neuropathy of the pelvic girdle and legs.

Polyneuropathy (polyradiculoneuropathy): general issues

Polyneuropathy (polyradiculoneuropathy)- a group of diseases caused by the influence of exogenous and endogenous factors, characterized by multiple, predominantly distal, symmetrical lesions of peripheral nerves, manifested by sensory, motor, trophic and vegetative-vascular disorders.

1. Classification of polyneuropathies(WHO, 1982; modified)

- I. Depending on the morphological features of the lesion:

1) axonopathy,

2) myelinopathy.

- II. According to the prevailing clinical signs:

1) motor polyneuropathy;

2) sensitive polyneuropathy;

3) autonomic polyneuropathy;

4) mixed polyneuropathy (sensomotor and vegetative);

- III. By the nature of the flow:

1) acute (sudden onset, rapid development);

2) subacute;

3) chronic (gradual onset and development);

4) recurrent (acute or chronic with periods of partial or complete recovery of functions).

- IV. Classification according to the etiological (pathogenetic) principle:

1) infectious and autoimmune;

2) hereditary;

3) somatogenic;

4) with diffuse diseases of the connective tissue;

5) toxic (including drugs);

6) due to the influence of physical factors (with vibration disease, etc.).

2. General features of the clinic - polyneuritic syndrome- multiple symmetrical lesions of the nerve trunks:

- Various sensory experiences in the extremities - paresthesia (burning, tingling) and pain along the nerve trunks and sensory impairment(hyper- and hyposthesia) according to the type of "socks" and "gloves", etc.,

- Peripheral paralysis predominantly distal limbs,

- Vegetative-vascular disorders: violation of trophism, sweating, cooling and swelling of the distal parts of the affected limbs.

3. Comparative characteristics depending on the morphological features of the lesion.

- Axonal:

1) start- gradual, subacute;

2) distribution of symptoms- predominantly distal parts;

3) tendon reflexes- long-term preservation;

4) muscle atrophy- early;

Pronounced changes;

6) deep sensitivity- rarely;

7) autonomic dysfunction- expressed;

8) recovery speed- low, defect rate- high;

9) ENMG- decreased M-response, denervation changes in the muscle,

- Demyelinating:

1) start- acute, subacute;

2) distribution of symptoms- proximal and distal sections;

3) tendon reflexes- fall out early;

4) muscle atrophy- late;

5) surface sensitivity- moderate changes;

6) deep sensitivity- pronounced changes;

7) autonomic dysfunction- moderate;

8) recovery speed- high, defect rate- low;

9) ENMG- Decreased conduction velocity, increased distal latency.

4 . Comparative characteristics according to the prevailing clinical signs:

- Motor:

1) symptoms:

- negative symptoms: weakness, hypotension, muscle atrophy;

- positive symptoms: tremor, cramps, fasciculations;

2) typical PNP:

- axonal: AIDP (axonal variant), Charcot-Marie-Tooth type 2, porphyria, acute alcohol intoxication, lead intoxication, vincristine;

- demyelinating: AIDP, CIDP, Charcot-Marie-Tooth type 1, intoxication with arsenic, gold, amiodarone.

- Touch:

1) symptoms:

- negative symptoms: hypoesthesia, sensitive ataxia;

- positive symptoms: hyperestheria, pain, paresthesia, restless leg syndrome;

2) typical PNP:

- with damage to thick fibers (epicritic): diabetic, diphtheria, CIDP, acute sensory (atactic) polyneuropathy,

- with damage to thin fibers (protopathic): diabetic, alcoholic, amyloid, HIV, Fabry disease.

- Vegetative:

1) symptoms:

- negative symptoms: orthostatic hypotension, fixed pulse, decreased gastrointestinal motility, hyporeflex bladder;

- positive symptoms(with porphyria): hypertension, tachycardia, intestinal colic, overactive bladder.

5. Additional research.

- Objectification of polyneuropathy syndrome

1) EMG, ENMG: type (axonopathy, myelinopathy) and prevalence of the lesion in dynamics; differential diagnosis with myasthenia gravis and myopathic syndrome

- Identification of possible causes of the disease (see for individual nosologies):

1) research of cerebrospinal fluid: protein-cell dissociation (autoimmune, Guillain-Barré syndrome),

2) genetic analyzes (with suspicion of the hereditary nature of polyneuropathy),

3) nerve biopsy.

6. Principles of treatment

- Hospitalization mandatory for AIDP, CIDP, diphtheria polyneuropathy (due to the possibility of respiratory and bulbar disorders).

- Medical treatment:

1) treatment of neuropathic pain: antidepressants (amitriptyline, imipramine), anticonvulsants (carbamazepine, gabapentin), local anesthetics (lidocaine).

2) improvement of nerve trophism: antioxidants (mildronate), antihypoxants (actovegin), microcirculation correctors (pentoxifylline), neuroprotectors (cerebrolysin)

- Non-drug treatment: hyperbaric oxygenation, magnetostimulation, laser blood irradiation, massage, physiotherapy exercises, mechanotherapy.

Polyneuropathies (polyradiculoneuropathy): separate nosological forms

1. Infectious and autoimmune.

- Acute inflammatory demyelinating polyneuropathy of Guillain-Barré(AIDP, G61.0) - post-infectious demyelinating polyneuropathy, characterized by peripheral paralysis of the muscles of the extremities and protein-cell dissociation in the cerebrospinal fluid while maintaining superficial sensitivity. Frequency - 0.6-1.9 cases per 100,000 population. The predominant sex is male, age - 20-50 years.

1) Etiology: probably an autoimmune disease that develops after or during the following conditions:

Infectious diseases: infections of the upper respiratory tract, infectious mononucleosis, mumps, CMV, herpes, influenza A, mycoplasma, HIV;

Lymphoma (especially Hodgkin's)

Vaccination, serum sickness

Operational intervention.

2) Pathogenesis : Autoimmune reaction against antigens of Schwann cells and myelin - edema, lymphocytic infiltration and diffuse primary segmental demyelination in the anterior roots and proximal spinal nerves, plexuses, limb nerves and autonomic nodes, in severe cases, peripheral nerve axon antigens are attacked (with the axonal version of the syndrome ).

3) Clinic:

Approximately 2 weeks after a viral infection or immunization, suddenly develops distal muscle weakness lower limbs, further extended upstream on the muscles of the arms, torso, neck, cranial muscles (Landry's ascending palsy) - is formed symmetrical flaccid tetraparesis.

In some cases, only the lower extremities or cranial nerves are affected.

- sensory disturbances are minimal, pain, parasthesia, hypoalgesia or hyperalgesia in the distal extremities are possible.

Often there are paresis of facial muscles and bulbar disorders(bilateral paresis of the muscles of the oropharynx), paralysis of the respiratory muscles (5-10% of cases).

4) Diagnostic criteria (Walton et al., 1994; Gecht B. M., 1996):

1) symmetrical weakness in all limbs;

2) paresthesia in the hands and feet;

3) decrease or absence of reflexes starting from the first week of the disease;

4) progression of the listed symptoms from several days to 1 month;

5) an increase in the protein content in the cerebrospinal fluid (more than 0.45 g/l) during the first three weeks from the onset of the disease;

6) a decrease in the rate of propagation of excitation along the motor and (or) sensory fibers of the nerve and the absence, especially on early stage diseases, lesions of the axial cylinder (according to ENMG).

- intoxication leading to impaired neuromuscular transmission(poisoning with heavy metals (lead, arsenic), poisoning with industrial substances (acrylamide, carbon disulfide, trichlorethylene, rapeseed oil, organophosphorus compounds), intoxication when taking drugs: gold preparations, hydralazine, disulfiram, glutethimide, phenytoin, nitrofurantoin, dapsone, metronidazole, isoniazid, pyridoxine when taken more than 2 g / day, alcohol intoxication),

- neuropathy in somatic diseases(diabetes mellitus, porphyria, polyarthritis nodosa, rheumatoid arthritis),

- vitamin B12 deficiency or folic acid

Nerve damage in oncological diseases(paraneoplastic syndrome)

- infectious diseases (acute poliomyelitis, diphtheria, botulism.)

6) Features of therapy:

IVL (in 10-23% of cases), according to indications - tracheostomy

Immunoglobulin IV 0.4 g/kg/day for 5 days

Sufficient fluid intake to maintain diuresis at a level of 1-1.5 l / day under the control of serum electrolyte concentrations, heparin 5,000 IU s / c 2 r / day - for the entire period of bed rest.

Physiotherapy to prevent contractures

Symptomatic therapy

7) Forecast: complete recovery - in 70% of cases, in 15% of patients severe residual paralysis persists .

- Chronic inflammatory demyelinating polyradiculoneuropathy(CIDP) - demyelinating polyneuropathies that have a subacute onset and a chronic (over 2 months) course, characterized in some cases by exacerbations and remissions. Frequency - 1.24-1.9 cases per 100,000 population. The predominant gender is male, age - at any age with a tendency to increase after 40 years.

1) Etiology: probably an autoimmune disease

2) Pathogenesis : see OVDP

3) Clinic:

The classic variant is characterized by symmetrical muscle weakness; a decrease in reflexes and sensory disorders that progress for more than 2 months, as well as an increase in the protein content in the cerebrospinal fluid and signs of demyelination with ENMG.

Along with the classical form of CIDP, the so-called atypical forms:

Isolated motor form

Isolated touch form,

Multifocal acquired demyelinating sensory motor neuropathy (Lewis-Sumner syndrome)

Distal acquired demyelinating symmetric neuropathy.

4) Diagnostic criteria (differences from OVDP):

1) slow (rarely subacute) onset, gradually, without previous infection, followed by progression (often with relapses) over months, sometimes many years;

2) more common after the age of 40 years;

3) in a quarter of patients, a tremor in the hands is observed, resembling an essential one, disappearing during remission and reappearing during relapse;

4) the originality of the results of the ENMG study, in particular, the presence of local areas of blockade of the conduction of excitation in various nerves and a heterogeneous block at different levels of one nerve;

5) worse prognosis and the need for special treatment tactics.

5) Differential diagnosis

Paratenemic polyneuropathies,

Hereditary motor-sensory neuropathy type I,

Multifocal motor neuropathy

6) Features of therapy:

Prednisolone up to 80-120 mg / day orally,

Plasmapheresis (in severe cases)

7) Forecast: Favorable prognostic signs are: young age (up to 45 years), female sex, subacute onset of the disease, relapsing course, pain syndrome at the onset of the disease.

- Diphtheria polyneuropathy - polyneuropathy resulting from the action of the neurotoxin of the diphtheria bacillus Corynebacterium diphtheriae (Leffler's wand).

1) Etiology: Corynebacterium diphtheriae (Gram(+) bacillus)

2) Pathogenesis : the bacterium produces a neurotoxin (polypeptide) - is absorbed into the blood, causing general intoxication, does not penetrate through the BBB (affects only the PNS) - suppression of the synthesis of proteolipids in the neuron perikaryon and myelin basic proteins in oligodendrocytes - demyelination and axonal degeneration, incubation period - 2-10 days.

3) Clinic:

- early symptoms (5-20 days)- peripheral paralysis of muscles innervated by cranial nerves:

1) bulbar group (IX and X) - bulbar paralysis,

2) oculomotor nerves - accommodation paralysis and strabismus.

- late symptoms (5-7 weeks):

1) Glanzman-Zaland syndrome("Syndrome of the 50th day") - segmental demyelination in the anterior roots of the spinal cord with the formation of lower distal polyradiculoneuropathy, with motor disorders predominating, in 90% of cases paresis is ascending, subsequently reaching tetraplegia.

2) sensitive ataxia- segmental demyelination in the posterior roots of the spinal cord

4) Features of therapy:

When early pharyngeal neuropathy using diphtheria toxoid, the best effect is achieved as a result of plasmapheresis,

At late demyelination - vasoactive drugs (trental, actovegin) and plasmapheresis;

2. Hereditary motor-sensory and autonomic neuropathies.

- Hereditary motor sensory neuropathy(peroneal muscular atrophy, HMSN-I and II, neural amyotrophy of Charcot-Marie-Tooth types 1 and 2) is the most well-known, more common heterogeneous group of polyneuropathies.

1) Type of inheritance: autosomal dominant, rarely autosomal recessive, X-linked

2) Debut age: 2nd-3rd decade (type 1), 3rd-5th decade (type 2)

3) Metabolic defect: unknown

4) Clinic:

- type and features of polyneuropathy: demyelinating distal motor neuropathy of the lower extremities, debuts with difficulty walking or running; less often loss of sensitivity, more often vibration, then pain and temperature;

- involvement of other body systems: concave foot, congenital defects of the hip joint;

3. Somatogenic polyneuropathies.

- diabetic neuropathy.

1) Etiology: diabetes mellitus, in 8% of patients during the initial diagnosis of diabetes and in 40-80% after 20 years from the onset of the disease.

2) Pathogenesis :

3) Classification (A.A.F.Sima, 1997) and clinic:

- Recurrent neuropathy(hyperglycemic neuropathy) - occurs only against the background of the development of hyperglycemia, followed by complete regression,

- Distal symmetric polyneuropathy(axonopathy, sensory-motor-vegetative type - severe paresthesia, decreased deep sensitivity, reflexes, autonomic dysfunction);

- Autonomic (autonomous) neuropathy(combined lesion of the parasympathetic and sympathetic divisions, the most common are the cardiac and gastrointestinal forms, the main development factor is chronic hyperglycemia)

- Proximal motor neuropathy(femoral or sacral plexopathy; pain in the femoral muscles (symmetrical and asymmetric), muscle weakness, atrophy of the muscles of the femoral group, difficulty getting up from a chair and climbing stairs; more often men 50-60 years old)

- Cranial mononeuropathies(usually III, less often VI, VII)

- Other mononeuropathies(femoral, obturator, sciatic, less often ulnar and median nerves).

On this moment There is no generally accepted classification of diabetic polyneuropathies. Currently, the most common and convenient to use is considered clinical classification R. Tpotav and B. TpotIshop, proposed in 1993.

I. Symmetric polyneuropathies:

1) sensory or sensorimotor polyneuropathy;

2) autonomic neuropathy;

3) symmetrical proximal motor neuropathy of the lower extremities.

II. Focal and multifocal neuropathies:

1) cranial neuropathies;

2) intercostal mononeuropathy and mononeuropathy of the extremities;

3) asymmetric motor neuropathy of the lower extremities.

III. mixed forms.

Given the long period of time that has passed since the writing of this classification, attention should also be paid to its more modern versions:

I. Symmetrical neuropathies associated with damage to long fibers:

1) diabetic polyneuropathy (symmetrical distal sensorimotor polyneuropathy with a primary lesion of the lower extremities and autonomic disorders);

2) diabetic polyneuropathy of small fibers with significant loss of body weight;

3) diabetic pandysautonomy;

4) hypoglycemic polyneuropathy.

II. Asymmetric neuropathies not associated with damage to long fibers:

1) diabetic lumbosacral plexorradicular neuropathy (proximal motor neuropathy, diabetic amyotrophy, Bruns-Garland syndrome, femoral nerve neuropathy);

2) diabetic thoracolumbar radiculoneuropathy (truncal radiculopathy, intercostal nerve mononeuropathies);

3) tunnel neuropathies;

4) brachial plexopathy;

5) neuropathy of the oculomotor nerves;

6) ischemic mononeuropathies of the lower extremities.

Differential Diagnosis

The difficulty of diagnosing diabetic neuropathy lies in the fact that none of the forms of diabetic neuropathy has unique clinical, electrophysiological and pathoanatomical signs. In addition, about 10% of diabetic patients suffer from non-diabetic neuropathies. Therefore, it is necessary to differentiate diabetic neuropathies with the following diseases:

1) inflammatory (sensory polygangliopathy: paraneoplastic or associated with systemic connective tissue diseases - Sjögren's disease, Sik-ka complex, idiopathic diseases);

2) vasculitis;

3) chronic inflammatory demyelinating polyneuropathy;

4) monoclonal gammopathy (monoclonal gammopathy unknown etiology, multiple myeloma, primary amyloidosis);

5) infectious (taxus dorsalis, leprosy, neuroborreliosis, HIV infection);

6) metabolic (uremia, hypothyroidism, chronic hepatitis);

7) alimentary (deficiency of B vitamins, alcohol intoxication);

8) toxic.

A feature of diabetic polyneuropathies is the predominance of sensory disturbances over motor ones, the predominant lesion of the lower extremities, and the presence of electrophysiological signs of axonopathy.

Diagnosis criteria for diabetic polyneuropathy

1. The presence of diabetes.

2. Prolonged chronic hypervolemia caused by the underlying disease.

3. The presence of distal symmetric sensorimotor polyneuropathy of the lower extremities.

4. Absence of signs indicating any other neurological disease.

According to the severity of diabetic polyneuropathy is divided into the following stages:

N0 - absence of clinical and electrophysiological signs of polyneuropathy;

N1a - asymptomatic polyneuropathy (violation of the conduction of excitation along two or more nerves and a decrease in the response of the heart rate to a respiratory test);

N1b - criteria N1a in combination with clinical signs of polyneuropathy or pathology detected by quantitative assessment of sensitivity;

N2a - moderate polyneuropathy with the presence of sensory, autonomic or motor disorders. Paresis of the dorsiflexors of the foot less than 50% (the patient can walk on his heels);

N2b - severe polyneuropathy with paresis of the dorsal flexors of the foot more than 50% (the patient cannot walk on his heels);

N3 - disabling polyneuropathy.

The pathogenesis of diabetic polyneuropathy

There are several mechanisms for the development of diabetic polyneuropathy.

1. Accumulation of endoneural sorbitol and fructose due to activation of the pentose phosphate pathway for glucose utilization. This leads to a competitive decrease in the concentration of axonal myoinositol, which subsequently causes a restriction of the turnover of phosphatidylinositol and a decrease in the activity of axonal Na+, K+-ATPase. As a result, axonal transport is disturbed, axonopathy develops.

2. Another consequence of hyperglycemia is an increase in the tone of the nerve vessels (vasae nervorum) due to a violation of endothelial relaxation. Violation of relaxation is caused by a decrease in the activity of nitric oxide (N0) of substance P and calcitonin-related peptide, as well as by a decrease in the formation of prostaglandin E and prostacyclin. Increased vascular tone leads to hypoxia of blood-supplying neurons, further hypoxia is exacerbated by the opening of arteriovenous shunts and a decrease in arterial inflow due to the action of insulin. As a result of hypoxia, lipid peroxidation is activated and a further increase in vascular tone occurs. As a result of all of the above, neuropathy develops.

3. In insulin-independent tissues (which include nervous tissue), due to hyperglycemia, there is an increase in the processes of non-enzymatic glycosylation of proteins, which leads to disruption of the structure and function of intracellular enzymes, pathological changes in gene expression, changes in the structure and properties of the intercellular substance and cell receptors. As a result, there is a change and perversion of biochemical reactions.

4. Decreased synthesis of neurotrophic factors in target organs and glial cells, axonal transport, impaired biological action at the receptor level, as well as the death of Schwann cells as a result of hyperglycemia.

5. Violation of the structure of cell membranes of protein receptors and myelin sheaths due to impaired metabolism of fatty acids.

6. Increasing endoneural hypoxia due to impaired prostaglandin metabolism. For example, with a decrease in the synthesis of prostaglandin E, there is a violation of endothelial-dependent relaxation of the walls of nerve vessels, as well as a violation of the propagation of the action potential due to a violation of the regulation of the activity of Na+, K+-ATPase.

7. Ischemia and local hypoxia lead to impaired axonal transport in DM, which leads to depletion of intracellular ATP reserves. Activation of the pentose phosphate pathway causes depletion of intracellular myoinositol, and non-enzymatic glycosylation of proteins (tubulin) causes a violation of the axon cytoskeleton.

4. Toxic polyneuropathies.

- Alcoholic polyneuropathy

1) Etiology: having a long period of drinking,

2) Pathogenesis : direct toxic effect of alcohol and its metabolic products, vitamin B1 deficiency - primary axonal degeneration and secondary demyelination.

3) Clinic and forms:

- symmetrical sensory polyneuropathy(alcoholic neuropathy without thiamine deficiency, progresses slowly, the dominant symptom is a violation of superficial sensitivity in combination with pain, painful paresthesias)

- symmetrical motor-sensory polyneuropathy(alcoholic neuropathy with thiamine deficiency, acute onset and rapid progression, dominated by motor disturbances in combination with symptoms of damage to deep and superficial sensitivity, weakness of the foot extensors - steppage when walking)

4) Features of therapy: exclusion of the impact of the etiotropic factor, a balanced diet rich in vitamins B1, B6, B12.

Damage to the axial cylinder of the nerve fiber causes axonal type of nerve lesion. This type of lesion occurs in toxic, dysmetabolic neuropathies, including alcoholic etiology, periarteritis nodosa, uremia, porphyria, diabetes, malignant tumors. If damage to the myelin sheath affects the reduction or blocking of the conduction of impulses along the nerve, for example, the conduction of signals of an arbitrary motor command from the cerebral cortex to the muscles, then with axonal damage, axon trophism and axonal transport are disturbed, which leads to impaired axon excitability and, accordingly, the impossibility of its activation in the affected area and distal to it. Violation of the excitability of the axon leads to the inability to conduct excitation along it. Preservation of normal values ​​of the speed of impulse conduction along the nerves in the axonal type of lesion is associated with the conductivity of the remaining unaffected fibers. Total axonal damage to all nerve fibers will lead to a complete lack of response (complete loss of nerve electrical excitability) and the inability to check the conduction velocity. Axonal damage entails a violation of axonal transport and a secondary trophic and informational effect on the muscle. In a denervated muscle with axonal damage, denervation phenomena occur. In acute denervation, there are no changes in the muscle in the first 10-14 days, since the axonal current uses the remaining resources. Further, at the first stage of denervation, the muscle, losing its organizing nervous control, tries to use humoral regulatory factors, in connection with which its sensitivity to external humoral influences increases. A decrease in the transmembrane potential of the muscle and the emergence of the possibility of quickly reaching a critical level of depolarization leads to the appearance of spontaneous activity in the form of fibrillation potentials and positive sharp waves. Fibrillation potentials occur at the first stage of denervation and reflect dystrophic processes in muscle fibers. With a continuing state of denervation, the frequency of fibrillation potentials increases, and, with death muscle cells, positive sharp waves appear. In the assessment of axonal damage, it is very important to determine three characteristics: degree of severity, reversibility and prevalence along the axon of disturbed excitability. Evaluation of all three parameters of excitability makes it possible to judge the severity, prevalence and possibility of regression of the lesion.

The severity of axon excitability disorder was determined earlier by the method of classical electrodiagnostics. The minimum intensity of an external electrical stimulus that can activate an axon (generate an action potential) characterizes its level of excitability. The intensity of the electrical stimulus is determined by 2 parameters: the magnitude of the current and the duration of its impact, i.e. the duration of the irritating impulse. Normally, at moderate current strength, the nerve is sensitive to pulses of short duration (up to 0.01-0.1 ms), the muscle is sensitive only to long-duration current (20-30 ms). It is very important that stimulation of the muscle at the motor point is not a direct stimulation of the muscle, but is mediated through the terminals of the axon and is in fact a test of the excitability of the axon, and not of the muscle. The dependence of axon excitability on the magnitude of the current and the duration of the pulse is called "Force-duration" (Fig. 13).

Rice. 13. Curve "strength-duration" - dependence of nerve excitability on

the magnitude of the current and the duration of the pulse (According to L.R. Zenkov, M.A. Ronkin, 1982).

1 - norm,

2 - partial denervation (curve with a break),

3 - complete denervation,

X 1, X 2, X 3, - chronoxia,

P 1, P 2, P 3, are rheobases.

Method of classical electrodiagnostics, previously used to diagnose muscle denervation, is based on determining the excitability of low-threshold (low-myelinated) axons, i.e. the minimum degree of muscle activation when a pulsed current is applied to it. The control of the minimum activation of the muscle was carried out visually, the current was applied at the motor point of the muscle. The strength of the acting current is from 0 to 100 mA, the pulse duration is from 0.05 ms to 300 ms, the pulsed current with a duration of 300 ms is equivalent to a constant one. The minimum current at the maximum duration (300 ms), applied at the motor point from the cathode, causing the minimum visible muscle contraction, is called rheobase. With axonal damage (denervation), the rheobase decreases, i.e. less force needed direct current for minimal muscle contraction, since it is easier to reach a critical level of depolarization. The most informative indicator of axon damage (denervation) is its excitability to a pulsed current of short duration. For this reason, the indicator chronaxies- the minimum duration of a current pulse of two rheobases, necessary for the minimum visible muscle contraction. With axonal damage (denervation), the chronaxia index increases. Comparing the indices of rheobase and chronaxy with the strength-duration curve, it can be seen that rheobase and chronaxy are the points of the curve. Thus, rheobase and chronaxia are indicative indicators in the assessment of axonal damage. Currently, the evaluation of the force-duration curve is not carried out for a number of reasons:

* the method is based on the subjective criterion of muscle activation (visual);

* significant complexity of the study;

* ambiguity in the interpretation of the results, since with partial preservation of unaffected nerve fibers in the nerve, the "strength-duration" curve will represent the sum of the excitability of the affected and unaffected fibers. The excitability of unaffected fibers will form the left side of the curve (for pulses of short duration), and the excitability of affected fibers will form the right side of the curve (for pulses of long duration);

* sufficient inertia in changing the curve when assessing the reinnervation process in comparison with needle EMG;

* lack of modern instruments for research. The previously used device UEI-1 is thoroughly outdated morally and physically, since its production has ceased more than 15 years ago.

In stimulation EMG, when studying the M-response, stimuli of 0.1 ms are more often used, while the maximum pulse duration generated by the stimulator in the EMG setup is 1.0 ms. When the M-response is registered in the supramaximal stimulation mode, all axons innervating the muscle are activated. If all axons are affected, there is no M-response. When part of the nerve axons are damaged, an M-response of reduced amplitude is recorded due to the fact that the affected axons reduce or lose their excitability. Stimulation EMG diagnostics of partial axonal lesions has advantages over classical electrodiagnostics, since it allows taking into account the contribution to the M-response not only of low-threshold axons (motor units), but also of high-threshold highly myelinated fibers. Classical electrodiagnostics allows assessing the excitability of only low-threshold, low-myelinated fibers. Taking into account the fact that the axons of highly myelinated fibers are affected when they lose connection with the body of a neuron before unmyelinated (low threshold) (E.I. Zaitsev, 1981), it can be argued that the method for assessing the parameters of the M-response is more sensitive than classical electrodiagnostics.

Reversibility of axon excitability disorder is a little-studied area, despite its great importance in the clinic. With injuries of peripheral nerves, polyneuropathies, mononeuropathies, poliomyelitis syndrome, the so-called axonal type of lesion is often recorded, i.e. a drop in the amplitude of the distal M-response with a relatively intact speed of the impulse along the nerve and the shape of the M-wave. Such a decrease in the amplitude of the M-response is combined with a decrease or loss of excitability of part of the axons. Experience in the clinic of neuroinfections of the Institute of Children's Infections shows that the violation of axonal excitability in the acute period of the lesion is in some cases irreversible and leads to the death of the axon with further compensatory reinnervation. In other cases, the disturbance of excitability is reversible, the death of the axon does not occur, and the impaired functions are quickly restored. In neurology, the term "axonal lesion" is used as a synonym for the irreversibility and severity of axon lesion, which is associated with the frequent detection of this type of lesion at a fairly late date from the onset of the disease (lesion) - 1-2 months, when the period of reversibility of the axon excitability disorder ends. An analysis of the data of patients in dynamics with neuropathy of the facial nerve, acute inflammatory polyneuropathy, experimental and clinical data from the literature allow us to speak about the following dynamics of axonal excitability disorders. Damage to the axon causes, first of all, a violation of fast axonal transport, which leads, after 5-6 days, to a partial decrease in the excitability of a part of the axons of the nerve to a pulsed current of short duration (0.1 ms) with preserved sensitivity to pulses of relatively long duration (0.5 ms). When stimulated with pulses of 0.5 ms, all axons of the nerve are activated, and the amplitude of the M-response corresponds to the standard values. These changes are reversible in the absence of further adverse effects. With the continuing and increasing impact of the damaging factor, the excitability of axons decreases to a greater extent, and it becomes insensitive to pulses with a duration of 0.5 ms. Prolongation of the damaging factor for more than 3-4 weeks leads to irreversible consequences - axon degeneration and the development of the so-called axonal lesion. Thus, the reversible stage of axonal damage (up to 3 weeks) can be called functional axonal lesion, and irreversible (over 3 weeks) - structural axonal lesion. However, the reversibility of disorders in the acute stage of the lesion depends not only on the duration and severity, but also on the speed of development of the lesions. The faster the lesion develops, the weaker the compensatory-adaptive processes. Taking into account these features, the proposed division of the reversibility of axonal damage, even when using ENMG, is rather arbitrary.

The prevalence of impaired axon excitability along the length of the nerve must be taken into account in inflammatory, dysmetabolic, toxic neuropathies. The distal type of axon lesion is more often detected in nerves with the greatest length of the nerve fiber, which is called distal neuropathy. The damaging factors affecting the body of the neuron lead to the deterioration of axonal transport, which primarily affects the distal parts of the axon (P.S. Spencer, H.H. Schaumburg, 1976). Clinically and electrophysiologically, in these cases, distal axon degeneration (structural axonal lesion) with signs of muscle denervation is detected. In the acute stage of the lesion in patients with inflammatory neuropathy, the distal type of axon excitability disorder is also detected. However, it can be detected only electrophysiologically, be reversible and not reach a clinically significant level (functional axonal lesion). The distal type of axon lesion is more often recorded in the lower extremities. In the upper extremities, with inflammatory neuropathies, the proximal part of the nerve fiber often suffers and the lesion is demyelinating in nature.

Axonal and demyelinating types of lesions almost never occur in isolation. More often, nerve damage is mixed, with a predominance of one of the types of damage. So, for example, in diabetic and alcoholic polyneuropathy, there may be lesions with both axonal and demyelinating types of disorders.

Defeat n. tibialis of traumatic, compression, dysmetabolic or inflammatory genesis, leading to dysfunction of the leg muscles responsible for plantar flexion of the foot and foot muscles, hypoesthesia of the posterior surface of the lower leg, sole and toes, the occurrence of pain syndrome and vegetative-trophic changes in the foot. In the diagnosis of pathology, the main thing is the analysis of anamnestic data and a neurological examination, auxiliary methods - EMG, ENG, ultrasound of the nerve, radiography and CT of the foot and ankle. Treatment is possible conservative (anti-inflammatory, neurometabolic, analgesic, vasoactive therapy) and surgical (neurolysis, decompression, removal of a nerve tumor).

Tibial neuropathy belongs to the group of so-called peripheral mononeuropathy of the lower extremities, which includes sciatic nerve neuropathy, femoral neuropathy, peroneal nerve neuropathy, neuropathy of the external cutaneous nerve of the thigh. Clinic similarity tibial neuropathy with symptoms of traumatic injuries of the musculoskeletal system of the lower leg and foot, as well as the traumatic etiology of most cases of the disease, makes it the subject of study and joint management of specialists in the field of neurology and traumatology. The connection of the disease with sports overload and repeated injuries determines the relevance of the problem for sports doctors.

Anatomy of the tibial nerve

The tibial nerve (n. tibialis) is a continuation of the sciatic nerve. Starting at the top of the popliteal fossa, the nerve passes it from top to bottom medially. Then, having passed between the heads of the gastrocnemius muscle, the nerve lies between the long flexor of the first finger and the long flexor of the fingers. So it reaches the medial malleolus. Approximately in the middle between the ankle and the Achilles tendon, you can feel the point of passage of the tibial nerve. Further, the nerve enters the tarsal canal, where it, together with the posterior tibial artery, is fixed by a powerful ligament - the flexor retainer. Upon exiting channel n. tibialis divides into terminal branches.

In the popliteal fossa and further, the tibial nerve gives motor branches to the triceps muscle, flexor thumb and flexor of the fingers, popliteal, posterior tibial and plantar muscles; sensory internal cutaneous nerve of the lower leg, which, together with the peroneal nerve, innervates the ankle joint, the posterolateral surface of the lower 1/3 of the lower leg, the lateral edge of the foot and the heel. Terminal branches n. tibialis - medial and lateral plantar nerves - innervate the small muscles of the foot, the skin of the inner edge of the sole, the first 3.5 fingers and the back surface of the remaining 1.5 fingers. The muscles innervated by the tibial nerve provide flexion of the lower leg and foot, raising the inner edge of the foot (i.e., internal rotation), flexion, adduction and spreading of the toes, and extension of their distal phalanges.

Causes of tibial neuropathy

Femoral neuropathy is possible as a result of nerve injury in fractures of the lower leg, an isolated fracture tibia, dislocation of the ankle joint, injuries, damage to the tendons and sprains of the foot. An etiological factor can also be repeated sports injuries of the foot, foot deformities (flat feet, hallux valgus), prolonged uncomfortable position of the lower leg or foot with compression n. tibialis (often in those suffering from alcoholism), diseases of the knee or ankle joint (rheumatoid arthritis, deforming osteoarthritis, gout), nerve tumors, metabolic disorders (in diabetes mellitus, amyloidosis, hypothyroidism, dysproteinemia), nerve vascularization disorders (for example, with vasculitis).

Most often, neuropathy of the tibial nerve is associated with its compression in the tarsal canal (the so-called tarsal tunnel syndrome). Nerve compression at this level can occur with fibrotic changes in the canal in the post-traumatic period, tendovaginitis, hematomas, bone exostoses or tumors in the canal area, as well as with neurodystrophic disorders in the ligamentous-muscular apparatus of the joint of vertebrogenic origin.

Symptoms of tibial neuropathy

Depending on the topic of the lesion n. tibialis in the clinical picture of his neuropathy, there are several syndromes.

Tibial neuropathy at the level of the popliteal fossa is manifested by a disorder of downward flexion of the foot and impaired movement in the toes. The patient cannot stand on his toes. Walking is typical with an emphasis on the heel, without rolling the foot on the toe. There is atrophy of the posterior muscle group on the lower leg and muscles on the foot. As a result of atrophy of the muscles on the foot, it becomes like a clawed paw. There is a decrease in the tendon reflex from Achilles. Sensory disorders include violations of tactile and pain sensitivity on the entire lower leg from behind and along the outer edge of its lower 1/3, on the sole, totally (on the back and plantar surface) on the skin of the first 3.5 fingers and on the back of the remaining 1.5 fingers. Neuropathy of the tibial nerve of traumatic origin is characterized by a pronounced causalgic syndrome with hyperpathy (perverted hypersensitivity), edema, trophic changes and autonomic disorders.

Tarsal tunnel syndrome in some cases is provoked by long walking or running. It is characterized by burning pains in the sole, often radiating to the calf muscle. Patients describe pain as deep, note an increase in their intensity in the standing position and when walking. There is hypoesthesia of both the inner and outer edges of the foot, some flattening of the foot and a slight "clawing" of the fingers. The motor function of the ankle joint was preserved in full, the Achilles reflex was not disturbed. Percussion of the nerve at the point between the medial malleolus and the Achilles tendon is painful, giving a positive Tinel sign.

Neuropathy at the level of the medial plantar nerve is common in long-distance runners and marathon runners. Manifests pain and paresthesia on the inner edge of the sole and in the first 2-3 toes. The presence of a point in the area of ​​the navicular bone is pathognomonic, the percussion of which leads to the appearance of burning pain in the thumb.

Defeat n. tibialis at the level of the common digital nerves is called Morton's metatarsal neuralgia. It is typical for older women who are obese and walk a lot in heels. Pain is typical, starting at the arch of the foot and going through the bases of 2-4 fingers to their tips. Walking, standing and running increase the pain syndrome. Examination reveals trigger points between 2-3 and/or 3-4 metatarsal bones, Tinel's symptom.

Calcanodynia - neuropathy of the calcaneal branches of the tibial nerve. It can be provoked by a jump on the heels from a height, long walking barefoot or in shoes with thin soles. Manifested by pain in the heel, its numbness, paresthesia, hyperpathy. With a pronounced intensity of these symptoms, the patient walks without stepping on the heel.

Diagnosis of neuropathy of the tibial nerve

An important diagnostic value is the collection of anamnesis. Establishing the fact of injury or overload, the presence of pathology of the joints, metabolic and endocrine disorders, orthopedic diseases, etc. helps to determine the nature of the damage to the tibial nerve. Conducted by a neurologist, a thorough study of the strength of various muscle groups of the lower leg and foot, the sensitive sphere of this area; identification of trigger points and Tinel's symptom allows diagnosing the level of damage.

Of auxiliary importance are electromyography and electroneurography. Determination of the nature of nerve damage can be carried out using ultrasound. According to the indications, an ankle x-ray, foot x-ray or CT of the ankle joint is performed. In controversial cases, a diagnostic blockade of trigger points is performed, the positive effect of which confirms the compression nature of neuropathy.

Treatment of tibial neuropathy

In cases where tibial neuropathy develops as a result of an underlying disease, treatment of the latter is necessary first of all. It could be wearing orthopedic shoes, therapy of arthrosis of the ankle joint, correction of endocrine imbalance, etc. With compression neuropathies, therapeutic blockades with triamcinolone, diprospan or hydrocortisone in combination with local anesthetics (lidocaine) give a good effect. It is mandatory to include drugs in the list of prescriptions to improve the metabolism and blood supply of the tibial nerve. These include injections of vit B1, vit B12, vit B6, nicotinic acid, pentoxifylline drip, alpha-lipoic acid.

According to indications, reparants (actovegin, solcoxeril), anticholinesterase agents (neostigmine, ipidacrine) can be included in therapy. With intense pain and hyperpathy, anticonvulsants (carbomazepine, pregabalin) and antidepressants (amitriptyline) are recommended. Of the physiotherapeutic methods, ultraphonophoresis with hydrocortisone ointment, shock wave therapy, magnetotherapy, electrophoresis with hyaluronidase, UHF are the most effective. To restore muscles that atrophy as a result of neuropathy n. tibialis, massage and exercise therapy are required.

Surgical treatment is necessary to remove formations that compress the trunk of the tibial nerve, as well as in case of failure of conservative therapy. The intervention is carried out by a neurosurgeon. During the operation, it is possible to carry out decompression, removal of a nerve tumor, release of the nerve from adhesions, and neurolysis.

The main clinical forms of damage to the peripheral nervous system are polyneuropathies, when there is diffuse, symmetrical damage to the peripheral nerves; mononeuropathies, when a single nerve is affected; radiculopathy - with damage to the roots; ganglionitis - nodes and plexopathy - plexus.

Pathologically, the lesion can be Wallerian - degeneration below the transverse intersection of the nerve, axonal - damage to the axonal cylinder and demyelinating - destruction of myelin.

According to the etiological basis, neuropathies can be divided into inflammatory, toxic, allergic and traumatic. The latter may be the result of a damaging effect of external causes or due to endogenous influences, for example, compression of the nerve trunks by neighboring structures (muscles, ligaments - the so-called tunnel neuropathies). This group may include injury to the spinal roots by an intervertebral disc or bone growths - osteophytes (this group of neuropathy is a particular manifestation of spinal osteochondrosis and will be discussed in a special section).

The issues of prevention and treatment of diseases of the peripheral nervous system due to the high prevalence of the latter and the defeat mainly of people of working age are becoming a problem that is relevant in medicine and is of great economic importance.

In the general structure of morbidity of the population, these diseases occupy the third place after acute respiratory infections and domestic injuries.

21.1. Polyneuropathies

Polyneuropathies(polyradiculoneuropathy) - multiple lesions of peripheral nerves, manifested by peripheral flaccid paralysis, sensory disturbances, trophic and vegetovascular disorders, mainly in the distal extremities. This is a common symmetrical pathological process, usually distal localization, gradually spreading proximally. The course of polyneuropathies is extremely diverse, depending on the etiology of the disease and the state of the organism itself. There are acute, subacute and chronic polyneuropathies, which in turn, depending on the pathomorphology of the lesion, are divided into axonal and demyelinating.

^

21.1.1. Axonal polyneuropathies (axonopathies)

Acute axonal polyneuropathies. Most often associated with suicidal or criminal poisoning and occur against the background of a picture of severe intoxication with arsenic, organophosphorus compounds, methyl alcohol, carbon monoxide, etc. The clinical picture of polyneuropathies usually unfolds within 2-4 days, and then the cure occurs within a few weeks.

^ Subacute axonal polyneuropathies. They develop within a few weeks, which is typical for many cases of toxic and metabolic neuropathies, but an even greater number of the latter take a long time (months).

^ Chronic axonal polyneuropathies. Progress for a long time: from 6 months or more. They develop most often with chronic intoxication (alcohol), beriberi (group B) and systemic diseases such as diabetes mellitus, uremia, biliary cirrhosis, amyloidosis, cancer, lymphoma, blood diseases, collagenoses. From medicines special attention should be paid to metronidazole, amiodarone, furadonin, isoniazid and apressin, which have a neurotropic effect.

^ Alcoholic polyneuropathy. It is observed in people who abuse alcohol. Alcoholic polyneuropathy develops in the late stages of the disease. In pathogenesis, the main role belongs to the toxic effect of alcohol on the nerves and the disruption of their metabolic processes. Changes develop not only in the spinal and cranial nerves, but also in other parts of the nervous system (brain and spinal cord).

Clinical manifestations. Alcoholic polyneuropathy often develops subacutely. There are paresthesias in the distal extremities, soreness in the calf muscles. Pain is aggravated by muscle compression and pressure on the nerve trunks (one of the early characteristic symptoms of alcoholic polyneuropathy). Following this, weakness and paralysis of all limbs develop, more pronounced in the legs. The extensors of the foot are predominantly affected. Atrophy develops rapidly in paretic muscles. Tendon and periosteal reflexes at the beginning of the disease may be increased, and their zones are expanded. With a pronounced clinical picture, there is muscle hypotension with a sharp decrease in muscle-joint feeling. There is a disorder of superficial sensitivity of the type of "gloves" and "socks". Disorders of deep sensitivity lead to atactic disorders, and in combination with the loss of tendon and periosteal reflexes, the clinical picture resembles a syphilitic tabes of the spinal cord and has even been called pseudotabes. However, there are no urination disorders characteristic of dryness, pain of the "lumbago" type, a positive Wasserman reaction in the cerebrospinal fluid and blood, and changes in the pupils. In some cases, alcoholic polyneuropathy can develop acutely, more often after significant hypothermia. Mental disorders are also possible.

Vasomotor, trophic and secretory disorders can be observed in the form of hyperhidrosis, edema of the distal extremities, violations of their normal color and temperature. Of the cranial nerves, the oculomotor, optic nerves can be affected, less often the vagus (acceleration of the pulse, respiratory failure) and phrenic nerves are involved in the process.

The stage of increasing painful phenomena usually lasts for weeks and even months. Then comes the stationary stage and, with treatment, the stage of reverse development. In total, the disease lasts from several months to several years. With the exclusion of alcohol consumption, the prognosis is usually favorable. The prognosis becomes serious when the cardiac branches of the vagus nerve, as well as the phrenic nerve, are involved in the process.

Treatment. Assign vitamins C, group B, metabolic agents, in the recovery period - amyridine, dibazol, physiotherapy.

Employability. In most cases, patients are unable to work, i.e. group II disabled. When motor functions are restored, disability group III can be established, taking into account the main profession, and in the future, with successful treatment, patients can be recognized as able-bodied.

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21.1.2. Demyelinating polyneuropathy (myelinopathy)

Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome). Described by the French neuropathologists G. Guillain and J. Barre in 1916. The cause of the disease remains insufficiently elucidated. It often develops after a previous acute infection. It is possible that the disease is caused by a filterable virus, but since it has not been isolated to date, most researchers consider the nature of the disease to be allergic. The disease is considered to be autoimmune with destruction of nervous tissue secondary to cellular immune responses. Inflammatory infiltrates are found in peripheral nerves, as well as roots, combined with segmental demyelination.

Clinical manifestations. The disease begins with the appearance of general weakness, an increase in body temperature to subfebrile numbers, and pain in the extremities. Sometimes the pain is excruciating in nature. chief hallmark disease is muscle weakness in the limbs. Paresthesias appear in the distal parts of the arms and legs, and sometimes around the mouth and in the tongue. Severe sensory disturbances are rare. Weakness of the facial muscles, lesions of other cranial nerves, and autonomic disturbances may occur. Damage to the nerves of the bulbar group in the absence of respiratory resuscitation can lead to death. Movement disorders first occur in the legs and then spread to the arms. Possible lesions predominantly proximal limbs; at the same time there is a symptom complex resembling a myopathy. The nerve trunks are painful on palpation. There may be symptoms of tension (Lasegue, Neri).

Vegetative disorders are especially pronounced - cold snap and chilliness of the distal extremities, acrocyanosis, hyperhidrosis phenomena, sometimes there is hyperkeratosis of the soles, brittle nails.

Typical proteinaceous cell dissociation in the cerebrospinal fluid. The protein level reaches 3–5 g/l. A high protein concentration is determined by both lumbar and occipital puncture. This criterion is very important in distinguishing Guillain-Barré syndrome from a spinal tumor, in which high concentrations of the protein are detected only with a lumbar puncture. Cytosis no more than 10 cells (lymphocytes and monocytes) in 1 µl.

The disease usually develops within 2-4 weeks, then there is a stage of stabilization, and after that - improvement. In addition to acute forms, subacute and chronic forms can occur. In the vast majority of cases, the outcome of the disease is favorable, but there are also forms that proceed according to the type of Landry's ascending paralysis with the spread of paralysis to the muscles of the trunk, arms and bulbar muscles.

Treatment. The most active method of therapy is plasmapheresis with intravenous immunoglobulin. In patients, the blood plasma is partially removed, returning the formed elements. Glucocorticoids are also used (prednisolone, 1-2 mc / kg per day), antihistamines (diphenhydramine, suprastin), vitamin therapy (group B), anticholinesterase drugs (prozerin, galantamine). It is important to care for the patient with careful monitoring of the state of the respiratory and cardiac vascular systems. Respiratory failure in severe cases can develop very quickly and lead to death in the absence of adequate therapy. If the patient's lung capacity is less than 25–30% of the estimated tidal volume or there are bulbar syndromes, intubation or tracheotomy is recommended for mechanical ventilation. Severe arterial hypertension and tachycardia are stopped by the use of calcium ion antagonists (corinfar) and beta-blockers (propranolol). With arterial hypotension, fluids are administered intravenously to increase intravascular volume. It is necessary every 1-2 hours to carefully change the position of the patient in bed. Acute urinary retention and bladder enlargement can cause reflex disturbances leading to fluctuations in blood pressure and pulse. In such cases, the use of an indwelling catheter is recommended. In the recovery period, exercise therapy is prescribed to prevent contractures, massage, ozocerite, paraffin, four-chamber baths.

^ diphtheria polyneuropathy. 1-2 weeks after the onset of the disease, signs of damage to the cranial nerves of the bulbar group may occur: paresis of the soft palate, tongue, phonation disorder, swallowing; respiratory failure is possible, especially when the phrenic nerve is involved in the process. The defeat of the vagus nerve can cause brady- or tachycardia, arrhythmia. The oculomotor nerves are often involved in the process, which is manifested by an accommodation disorder. Less common is paresis of the external eye muscles innervated by III, IV and VI cranial nerves. Polyneuropathy in the extremities usually manifests itself as late (at 3-4 weeks) flaccid paresis with a disorder of superficial and deep sensitivity, which leads to sensitive ataxia. Sometimes the only manifestation of late diphtheria polyneuropathy is the loss of tendon reflexes.

If the early manifestations of neuropathy of the cranial nerves in diphtheria are associated with the direct entry of the toxin from the lesion, then the late manifestations of neuropathies of the peripheral nerves are associated with the hematogenous spread of the toxin. Treatment is carried out according to the etiological and symptomatic principles.

^ Subacute demyelinating polyneuropathy. These are neuropathies of heterogeneous origin; have an acquired character, their course is undulating, relapsing. Clinically, they are similar to the previous form, but there are also differences in the rate of development of the disease, in its very course, as well as in the absence of clear provoking moments, triggers.

^ Chronic demyelinating polyneuropathy. Meet more often than subacute. These are hereditary, inflammatory, drug-induced neuropathies, as well as other acquired forms: in diabetes mellitus, hypothyroidism, dysproteinemia, multiple myeloma, cancer, lymphoma, etc. Most often, in these diseases, especially in diabetes mellitus, an electrodiagnostic study gives a picture of mixed axonal demyelinating processes . Very often it remains unknown which process is primary - axonal degeneration or demyelination.

^ Diabetic polyneuropathy. It develops in people with diabetes. Polyneuropathy may be the first manifestation of diabetes mellitus or occur many years after the onset of the disease. Polyneuropathy syndrome occurs in almost half of patients with diabetes mellitus.

Pathogenesis. The most significant mechanisms for the development of neuropathy are ischemia and metabolic disorders in the nerve due to hyperglycemia.

clinical picture. There are several clinical variants of polyneuropathy. An early manifestation of polyneuropathy can often be a weakening of vibrational sensitivity and Achilles reflexes. These phenomena can exist for many years. The second option is manifested by acute or subacute lesions of individual nerves: more often the femoral, sciatic, ulnar or median, as well as the oculomotor, trigeminal and abducent. At the same time, patients have pain, impaired sensitivity and paresis of the muscles innervated by the corresponding nerves. The third option is significant damage to many nerves of the limbs with sensory disorders and paresis, mainly in the legs. The pains are often aggravated by heat and at rest. Quite often the vegetative innervation is broken. If the process progresses, the pains increase, become unbearable, areas of the skin appear, painted in purple and black, mummification of gangrenous tissue. Often in such cases, itching, trophic ulcers and osteoarthropathy phenomena occur. accompanied by deformity of the feet.

The course of diabetic polyneuropathy is usually progressive. Sometimes it is accompanied by signs of the so-called visceral polyneuropathy, which can disrupt the innervation of the internal organs. Especially often at the same time orthostatic hypotension, "neurogenic" bladder, impotence develop.

A serious complication is (most often in patients older than 50 years) damage to the oculomotor nerves (III, IV and VI pairs), which leads to strabismus, anisocoria, impaired pupillary reflexes to light, accommodation and convergence.

Treatment. Effective therapy of diabetes mellitus is important to prevent the initial manifestations of diabetic polyneuropathy.

Treatment is carried out according to the general principles of neuropathy therapy. Physiotherapeutic procedures, massage and physiotherapy exercises can have a positive value. It is advisable to administer vitamins C, group B, as well as antiplatelet agents (trental, complamin, etc.), angioprotectors (anginin, zoxium), anticholinesterase drugs (amiridine and galantamine), thioctic acid preparations (thioctacid, espa lipon).

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21.2. Multifocal neuropathy

With multifocal neuropathy, individual nerve trunks are involved in the pathological process simultaneously or sequentially, partially or completely affected over several days, months or years. The main pathological process in this disease develops in several foci at once and by random "choice"; with the aggravation of the disease, there is a tendency to develop neurological defects, not so much scattered and multi-focal, but united and symmetrical. For a correct diagnosis, attention should be paid to the early symptoms of neuropathy and their dynamics, as well as the presence of somatic, skin and other disorders, since these symptoms may be a manifestation of a systemic disease. In 1/3 of adult patients there is a picture of the demyelinating process. Most often, multifocal demyelinating neuropathy is a partial manifestation of chronic inflammatory demyelinating polyradiculoneuropathy. In 2/3 of patients, multifocal mononeuropathy has an axonal origin. Most often, this form, the pathogenetic basis of which is not inflammation, but ischemia, is the result of generalized vasculitis, rheumatoid arthritis and other systemic diseases of the connective tissue.

^ Neuropathy in connective tissue diseases and vasculitis. At rheumatoid arthritis peripheral neuropathy occurs with a long and severe course of the disease. Initially, sensory disturbances occur, then severe sensorimotor neuropathy develops.

At systemic lupus erythematosus generalized polyneuropathy or multiple mononeuropathy (damage to various nerves innervating the lower and upper limbs) may develop. With mononeuropathy, the nerves that innervate the foot are more often involved in the process.

At nodular periarteritis neuropathies have the form of multiple mononeuritis. Polyneuropathy similar to Guillain-Barré syndrome may also develop.

One of the first symptoms of amyloidosis may be the so-called amyloid polyneuropathy(with familial forms occurs in 90% of cases). Pain and numbness in the arms and legs appear, peripheral sensitivity decreases, then muscle weakness, flaccid paresis of the arms and legs with distal muscle atrophy, a decrease or loss of tendon reflexes join. Sometimes trophic ulcers of the extremities are formed. Polyneuropathy is caused not only by vascular damage, but also by the deposition of amyloid in the endo- and perineurium. Also characteristic is the defeat of the mouse due to the deposition of amyloid masses in them, leading to their compaction and accompanied by significant weakness of the myopathic type. Often (in 40-75% of cases) the muscles of the tongue are affected.

At Sjögren's syndrome there is a moderately severe symmetrical distal sensory neuropathy. Isolated trigeminal neuralgia is possible. It is believed that the phenomenon of vasculitis, which is characteristic of connective tissue diseases, plays a role in the mechanism of damage to peripheral nerves.

Treatment. The underlying disease is treated, with indications - glucocorticoids; angioprotectors, antioxidants, antiaggregants are prescribed. In the recovery period - exercise therapy. Therapeutic massage, metabolic and anticholinesterase agents.

21.3. Mononeuropathies

Damage to individual nerves is most often based on direct external trauma or compression at certain levels of the nerve trunk. Predisposing factors are the superficial location of the nerve or its passage in narrow bony, muscular-ligamentous canals.

In atherosclerosis, diabetes mellitus, periarteritis nodosa and other collagenoses, mononeuropathies are associated with vascular damage. Hypothermia and infection (herpes zoster) matter.

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21.3.1. Neuropathy of the facial nerve

The disease has a different etiology. The most vulnerable segment of the nerve is the one that is located in a narrow convoluted canal 30-33 cm long, where due to swelling caused by inflammation, its compression can occur.

Provocative moments are hypothermia, trauma and infection. Neuropathy can be a complication of otitis, mesotympanitis, parotitis, inflammatory processes in the brain, but it can also be the result of a neurotropic viral infection, more often herpes zoster and poliomyelitis. Cases of poliomyelitis lesions of the facial nerve are usually noted during the epidemic.

Clinical manifestations. The clinical picture of damage to the facial nerve is mainly characterized by acutely developed paralysis or paresis of the facial muscles. Bilateral nerve damage is extremely rare. At the onset of the disease, mild or moderate pain and paresthesia in the ear and mastoid region may appear. Typically, pain occurs simultaneously or 1-2 days before the development of movement disorders. Pain is typical for damage to the facial nerve before the discharge of the drum string. Less commonly, pain occurs 2-5 days after the development of paralysis of the mimic muscles and lasts 1-2 weeks. Particularly severe pain is noted when the facial nerve is damaged at the level of the location of the knee node.

The clinical picture of neuropathy of the facial nerve depends on the level of the lesion. With damage to the nucleus of the VII cranial nerve that occurs with the pontine form of poliomyelitis, patients develop only phenomena of paresis or paralysis of the facial muscles. When the facial nerve root is damaged in the area of ​​its exit from the brain stem, the clinical picture of neuropathy of the VII nerve is combined with symptoms of damage to the VIII cranial nerve. The defeat of the facial nerve in the bone canal before the departure of the large stony nerve, in addition to paralysis of the mimic muscles, leads to a decrease in lacrimation up to dryness of the eye (xerophthalmia) and is accompanied by a decrease in the superciliary and corneal reflexes, taste disorder, salivation, hyperacusis. The defeat of this nerve before the discharge of the stapedial nerve gives the same symptomatology, but instead of dryness of the eye, lacrimation increases; if the facial nerve is affected distal to the origin of the stapedial nerve, then hyperacusis is not observed. In cases where the facial nerve is affected at the point of exit from the stylomastoid foramen, movement disorders predominate.

Forecast. In most neuropathies of the facial nerve, the clinical prognosis is favorable. Complete recovery occurs in approximately 75% of patients. It is believed that after 3 months of paralysis, the chances of recovery are significantly reduced. A more favorable prognosis is in cases where the nerve is affected after exiting the stylomastoid foramen, but only in the absence of otogenic factors, chronic inflammation of the parotid salivary gland, and inflammation of the lymph nodes located in this area. With otogenic and traumatic neuropathies, recovery may not occur at all. The course of recurrent neuropathies of the facial nerve is relatively favorable, but each subsequent relapse is more difficult than the previous one, the restoration of functions is delayed and becomes incomplete. After 2–3 months, in any form, except for poliomyelitis, contracture of the facial muscles of the face, a persistent increase in their tone, may develop. At the same time, the palpebral fissure is narrowed, mimic folds, especially the nasolabial one, are emphasized, myoclonic twitches are possible in the affected muscles.

Treatment. In acute lesions of the facial nerve, anti-inflammatory and decongestant therapy, antispasmodics and vasodilators are primarily prescribed. Large doses of nicotinic acid are shown orally (enduracin) and intravenously (complamin). For pain syndrome, analgesics are used. Of the anti-inflammatory drugs, glucocorticoids are used, in particular prednisolone and its analogues. It is noted that due to the use of glucocorticoids, facial muscle contractures usually do not develop. Non-steroidal anti-inflammatory drugs (indomethacin) can be used.

Further therapeutic measures should be aimed at accelerating the regeneration of affected nerve fibers and restoring the conductivity of the remaining ones, preventing atrophy of facial muscles, and preventing contractures. From the 5th–7th day of the disease, thermal procedures are prescribed: UHF therapy, paraffin, ozocerite and mud applications on the healthy and affected sides of the face. A good effect is given by ultrasound with hydrocortisone on the affected half of the face and the area of ​​​​the mastoid process.

If necessary, substances that affect tissue metabolism are prescribed - methandrostenolone (dianabol, nerobol), which improve metabolism (mainly protein and calcium) and reduce catabolic processes. B vitamins (B1, B6, B12, B15), glutamic acid, anticholinesterase drugs (amiridine, galantamine, nivalin), dibazol are also used. In the subacute period, therapeutic exercises, massage of mimic muscles, reflexology (acupuncture) are prescribed. Surgical intervention is possible in cases that are not amenable to conservative therapy - decompression of the nerve in the bone canal, neurolysis, suturing of the nerve, its plastic surgery, corrective operations on the mimic muscles in case of complications (contractures of the mimic muscles).

^ Knee knot syndrome. Knee knot syndrome (knee ganglionitis, knee knot neuralgia, Hunt's syndrome) is caused by a virus. It can occur in mild, severe and severe forms. It is manifested by a triad characteristic of ganglionitis: pain syndrome, herpetic eruptions and hypesthesia in the zone of innervation of the node. Periodic or constant pain occur mainly in the ear, but often spread to the back of the head, face, neck. Rashes appear, which are determined by the zone of innervation of the cranked node (tympanic cavity, tympanic membrane, external auditory canal, auricle, tragus, antitragus, auditory tube area, uvula, palate, tonsils, often the face and scalp). Motor fibers of the facial nerve pass near the geniculate node, so the syndrome also includes symptoms associated with damage to this nerve. In addition to a violation of taste in the anterior 2/3 of the tongue, patients have hyperesthesia, and later hypesthesia in the external auditory canal, the anterior third of the tongue, and, less often, the entire half of the face. Sometimes hearing is reduced, ringing in the ears, horizontal nystagmus and dizziness occur.

The illness may last for several weeks, but more often it is longer. In most cases, the prognosis for recovery is favorable, although relapses do occur.

Treatment. Start with the appointment of analgesics. Often you have to resort to injections of promedol and intravenous infusions of novocaine. Novocaine is also administered subcutaneously in front of the external auditory canal or by electrophoresis. At the same time, they are treated with B vitamins. In severe cases, the same course of treatment is recommended as for herpes zoster.

^

21.3.2. Peripheral nerve neuropathies

Neuropathy of the radial nerve. Among the nerves of the upper limb, the radial nerve is affected more often than others.

Etiology. Often the nerve is affected during sleep, when the patient sleeps with his hand under his head or under his torso, with very deep sleep, often associated with intoxication or in rare cases with great fatigue (“sleep paralysis”). Possible compression of the nerve with a crutch ("crutch" paralysis), with fractures of the humerus, compression with a tourniquet, improper injection into the outer surface of the shoulder, especially with abnormal locations of the nerve. Less commonly, the cause is infection (typhus, influenza, pneumonia, etc.) and intoxication (poisoning with lead, alcohol). The most common variant of compression is at the border of the middle and lower thirds of the shoulder at the site of perforation of the lateral intermuscular septum by the nerve.

Clinical manifestations. The clinical picture depends on the level of damage to the radial nerve. With a lesion in the axillary fossa of the upper third of the shoulder, paralysis of the muscles innervated by it occurs: when the arm is raised forward, the hand hangs down (“hanging” hand); I finger is brought to the II finger; extension of the forearm and hand, abduction of 1 finger, imposition of the second finger on the neighboring ones, supination of the forearm with an extended arm are impossible: flexion in the elbow joint is weakened; the elbow extensor reflex is lost and the carporadial reflex decreases; sensitivity disorder of I, II and partially III fingers, excluding the terminal phalanges, is not pronounced, more often in the form of paresthesia, crawling, numbness).

With damage to the radial nerve in the middle third of the shoulder, the extension of the forearm, the elbow extensor reflex are preserved; there is no sensitivity disorder on the shoulder when the remaining symptoms described above are detected. If the nerve is damaged in the lower third of the shoulder and in the upper third of the forearm, sensitivity on the back of the forearm may remain, the function of the extensors of the hand and fingers drops out, and sensitivity on the back of the hand is disturbed. Diagnostic tests can detect damage to the radial nerve: 1) in a standing position with arms down, supination of the hand and abduction of the first finger are impossible; 2) it is impossible to simultaneously touch the plane with the back of the hand and fingers; 3) if the hand lies on the table with the palm down, then it is not possible to put the third finger on the neighboring fingers; 4) when spreading the fingers (the hands are pressed against each other by the palmar surfaces), the fingers of the affected hand are not retracted, but bend and slide along the palm of a healthy hand.

^ Ulnar nerve neuropathy Among the lesions of the nerves of the brachial plexus, it ranks second in frequency

Etiology. Most often, this is nerve compression in the area of ​​the elbow joint, which occurs in people who work with their elbows on the machine, workbench, desk, and even when sitting for a long time with their hands on the armrests of chairs. Compression of the ulnar nerve at the level of the elbow joint may be localized in the ulnar groove behind the medial epicondyle or at the exit of the nerve, where it is compressed by a fibrous arch stretched between the heads of the flexor carpi ulnaris (ulnar nerve syndrome). Isolated nerve damage is observed with fractures of the internal condyle of the shoulder and with supracondylar fractures. Nerve compression can also occur at the level of the wrist. Sometimes nerve damage is observed in typhus and typhoid fever and other acute infections.

Clinical manifestations. There are numbness and paresthesia in the region of the IV and V fingers, as well as along the ulnar edge of the hand to the level of the wrist. As the disease progresses, there is a decrease in strength in the adductor and abductor muscles of the fingers. The brush at the same time resembles a “clawed paw”. Due to the preservation of the function of the radial nerve, the main phalanges of the fingers are sharply extended. In connection with the preservation of the function of the median nerve, the middle phalanges are bent, the fifth finger is usually abducted. There is hypoesthesia or anesthesia in the area of ​​the ulnar half of the IV and the entire V finger on the palmar side, as well as the V. IV and half of the III finger on the back of the hand. Small muscles of the hand atrophy - interosseous, worm-like, eminences of the little finger and the first finger. To make a diagnosis, they resort to special techniques: 1) when the hand is clenched into a fist, V, IV, and partly III, the fingers bend incompletely; 2) with a brush tightly attached to the table, “scratching” with the little finger on the table is impossible; 3) in the same position of the hand, it is impossible to spread and adduct the fingers, especially IV and V; 4) during the test, the paper is not held by the straightened 1st finger, there is no flexion of the terminal phalanx of the 1st finger (a function performed by the long flexor of the 1st finger, innervated by the median nerve).

^ Neuropathy of the median nerve. Isolated involvement of the median nerve is less common than that of the ulnar nerve.

Etiology. Injuries of the upper extremities, injuries during intravenous injections into the cubital vein, cut wounds above the wrist joint on the palmar surface, occupational overexertion of the hand (carpal tunnel syndrome) in ironers, carpenters, milkers, dentists, etc. On the shoulder, the nerve can be squeezed by a “spur” , located on the inner surface of the humerus 5–6 cm above the medial epicondyle (found on radiographs).

Clinical manifestations. Pain in fingers I, II, III, usually pronounced and causal in nature, pain on the inner surface of the forearm. Pronation suffers, palmar flexion of the hand is weakened, flexion of the I, II and III fingers and extension of the median phalanges of the II and III fingers are disturbed. The atrophy of the muscles in the area of ​​​​the elevation of the first finger is most clearly revealed, as a result of which it is installed in the same plane with the second finger; this leads to the development of a hand shape resembling a monkey's paw."

Superficial sensitivity is disturbed in the region of the radial part of the palm and on the palmar surface of the I, II, III fingers and half of the IV finger. The main tests for identifying movement disorders: 1) when the hand is clenched into a fist, I, II, and partly III, the fingers do not bend; 2) when the brush is pressed against the table with the palm of the hand, the scratching movements of the second finger do not succeed; 3) the patient cannot rotate the first finger around the other (mill symptom) with the rest of the fingers crossed; 4) opposition of I and V fingers is broken.

Treatment. Vitamins of group B, anticholinesterase drugs, dibazol, duplex are prescribed. Apply physiotherapy, massage, exercise therapy. If there are no signs of recovery within 1–2 months, surgery is indicated.

21.4. Plexopathies

Most common causes lesions of the brachial plexus (plexopathies) are trauma during dislocation of the head of the humerus, a stab wound, a tourniquet placed high on the shoulder for a long time, a plexus injury between the clavicle and the first rib or head of the shoulder during operations under inhalation anesthesia with hands behind the head, spoon pressure obstetric forceps on the plexus in newborns or stretching of the plexus during delivery manipulations. The plexus can be compressed by the callus after a fracture of the clavicle by the scalenus muscles (scalenus Nafziger syndrome), cervical ribs.

Clinical manifestations. With the defeat of the entire brachial plexus, peripheral paralysis (paresis) and anesthesia (hypesthesia) of the hand occur. Isolated damage to the upper primary trunk of the plexus leads to paralysis and atrophy of the proximal muscles of the arm - the deltoid, biceps, internal brachial, brachioradial and short supinator. As a result, it is impossible to abduct the upper limb in the shoulder joint and bend it in the elbow joint. The movements of the fingers and the hand itself are preserved. Patients complain of pain and paresthesia along the outer edge of the shoulder and forearm. In this zone, there is a decrease in sensitivity. This is the so-called upper Duchenne-Erb palsy. When the lower primary trunk of the plexus is damaged, paralysis occurs, and then atrophy of the small muscles of the hand, flexors of the hand and fingers. The movements of the shoulder and forearm are preserved in full. Hypesthesia is noted on the hand and fingers (the zone of the ulnar nerve) and along the inner surface of the forearm. This is Dejerine Klumpke's lower paralysis.

It should be borne in mind that symptoms similar to the clinical picture of lesions of the brachial plexus can be observed with cervical osteochondrosis and humeroscapular periarthritis (Dupley's syndrome). Painful restriction of movement in the shoulder joint, especially during abduction and internal rotation, is due to inflammatory changes in the periarticular tissue, sometimes accompanied by the deposition of salt in the tendon of the periosteal muscle or in the subacromial synovial sac.

Treatment. As a rule, analgesics, nootropic drugs, massage, exercise therapy, reflexology, physiotherapy are indicated. In case of traumatic damage to the trunks of the brachial plexus, there are indications for reconstructive microsurgical operations.

^

21.5. Tunnel mononeuropathies

Nerve pressure against bony prominences or incarceration in narrow channels with hard walls leads to the development of tunnel neuropathy.

^ carpal tunnel syndrome. The most common tunnel neuropathy is the syndrome of compression of the median nerve in the carpal tunnel. It often develops in individuals whose activities require repeated flexion and extension movements in the hand or prolonged bending of it (typing, playing the piano or cello, working with a jackhammer, etc.). The tendency to develop tunnel neuropathy of the median nerve is observed in persons suffering from somatic diseases, which are manifested by metabolic neuropathies (diabetes mellitus, uremia). This symptom complex can develop with rheumatoid arthritis, hypothyroidism, amyloidosis and other diseases. Women are more likely to get sick due to the natural narrowness of the canal.

Clinical manifestations. There are numbness and paresthesia of I, II, III fingers. Initially, numbness is transient, and later becomes permanent. Night pains are often noted, spreading from the hand to the forearm, sometimes to the elbow joint. Raising the arm up raises the pain and numbness. With percussion of the median nerve in the area of ​​the carpal tunnel, paresthesia occurs in the hand (positive Tinel's symptom). Flexion of the hand for 2 minutes (Phalen's sign) exacerbates symptoms. There is a moderate decrease in pain and temperature sensitivity in the first three fingers of the hand, weakness of the muscle that opposes the first finger, sometimes its atrophy. There are electromyographic signs of denervation of varying severity in the muscles innervated by the median nerve, a decrease in the speed of the impulse along its branches to the hand.

Treatment. First of all, it is necessary to treat the disease underlying the development of carpal tunnel syndrome. So, with hypothyroidism, replacement therapy is performed. In these cases, there is a rapid recovery of impaired functions.

To improve regional blood circulation, vasoactive drugs (trental, xanthinol, nicotinic acid) are prescribed in combination with anti-inflammatory and diuretic drugs (diacarb, triampur). Patients with severe paresthesias at night are shown the appointment of carbamazepine drugs (tegretol 200 mg 2-3 times a day).

In the early stages, improvement can be achieved by introducing novocaine and steroid drugs into the canal area.

In the absence of the effect of conservative therapy, there are indications for surgical treatment: dissection of the transverse ligament of the wrist. The operation is usually done openly, but can also be performed using an endoscope.

As noted earlier, tunnel syndromes also include compression of the ulnar nerve in the fascial canal between the heads of the ulnar flexor of the wrist.

^ Neuropathy of the femoral nerve. It may be due to its compression at the exit site in the region of the inguinal ligament. Patients complain of pain in the groin, which radiate along the anterointernal surface of the thigh and lower leg. Over time, sensory and motor disturbances occur, numbness of the skin occurs in the innervated area and hypotrophy, and then atrophy of the quadriceps femoris muscle.

^ Neuralgia of the external cutaneous nerve of the thigh. Neuralgia is manifested by excruciating painful sensations along the anterior outer surface of the thigh (Roth's disease). The cause is compression of the nerve in the canal formed by the inguinal fold.

^ Piriformis Syndrome. The sciatic nerve can be compressed by a spasmodic piriformis muscle. The pains are burning, severe, accompanied by paresthesias, spread along the outer surface of the lower leg and foot. Increased pain during internal rotation of the thigh, with the leg bent at the hip and knee joints is characteristic. Palpation of the piriformis also aggravates the pain.

^ Neuropathy of the tibial and peroneal nerves. The common peroneal nerve or its branches, the tibial nerve may be affected at the level of the head of the fibula. Compression occurs when the limb is in the wrong position, in particular, the streets, who like to sit with their legs crossed. Pathogenetic factors are diabetes mellitus, dysproteinemia, vasculitis, etc.

Clinically, the defeat of the common peroneal nerve is manifested by weakness of the dorsal flexor of the foot, the rotation of the foot is weakened outward. There is numbness of the outer surface of the lower leg and foot. Patients walk with slapping feet. Reduced sensitivity in the area of ​​the outer surface of the lower leg and foot. Damage to the anterior branches of the tibial nerve leads to weakness in the flexion of the foot and fingers. This nerve can be entrapped at the site of its passage behind the medial malleolus, as well as on the foot in the area of ​​the tarsal canal. There is pain, tingling along the sole and base of the toes, numbness in this area. The process may involve the medial or lateral branch of the plantar nerve. With the defeat of the first, unpleasant sensations are noted in the medial part of the foot, with the defeat of the second - along the lateral surface of the foot. There are also disorders of sensitivity in the medial or outer surface of the foot.

Surgical treatment of tunnel syndromes. In the absence of the effect of physiotherapy, blockades, local administration of hormones, there are indications for surgical decompression of the compressed nerve.

^

21.6. Traumatic injuries of peripheral nerves

As a result of nerve injury, its structural changes occur both in the axons and in the bodies of neurons. Degenerative changes in cells are characterized by chromatolysis, edema, movement of the Nissl substance to the periphery of the nerve cell, and a number of others.

In the axons distal to the site of its damage, Wallerian degeneration occurs. The axoplasm and myelin disintegrate and undergo phagocytosis, leaving empty sheaths formed by the endoneurium. Axon cells regenerating from the side grow along the preserved cases to the periphery. Myelination of newly formed fibers occurs by Schwann cells migrating into the lumen of the axonal sheaths. If, for various reasons, the regenerating axons do not penetrate into the sheaths, the latter become fibrotic, and the axons that lose their growth direction form terminal neuromes. When innervation is disturbed, inactive muscles undergo atrophy and sclerosis. and after 2 years the muscle is replaced by connective tissue scar tissue.

In connection with this pattern, when reinnervation occurs earlier than this period, a functionally significant effect can be expected. From this point of view, the consequences of damage to the proximal parts of the nerves are less favorable due to the longer regeneration of the nerve.

There are several degrees of nerve damage in trauma: I - functional conduction disorder; II - violation of the anatomical integrity of individual axons; III - violation of the anatomical integrity of the entire nerve.

Depending on the mechanism of injury, a nerve bruise, its direct damage with a sharp injuring object, and compression are distinguished.

An independent group consists of injection injuries (in case of incorrect injections of drugs directly into the nerve trunk).

When recognizing the nature of the defeat of peripheral nerves, it must be taken into account that the zone of innervation of individual sensory nerves may overlap due to other nerves.

To determine the location and nature of nerve damage great importance have neurophysiological research methods (myography, determination of the electrical excitability of the nerve and the safety of the conduction of excitation in different areas).

When roots are detached from the spinal cord, which is typical, for example, for a motorcycle injury, computed or magnetic resonance imaging is of particular importance for diagnosis, which makes it possible to detect an isolated accumulation of cerebrospinal fluid at the site of root detachment - pseudomeningocele.

^ Principles of surgical interventions for lesions of peripheral nerves. The purpose of the operation is to create conditions for the germination of axons along the sheaths of dead nerve fibers. Accurate anatomical comparison of the ends of the damaged nerves without their tension is necessary.

An indispensable condition for the success of these operations is the use of microsurgical techniques - a microscope, special instruments, atraumatic needles with the finest threads. Operations for damage to peripheral nerves should be carried out by specialists with sufficient experience. In this regard, when assisting victims with injuries to the limbs (in which we have only nerve damage), it is not necessary to simultaneously perform an operation on damaged nerves if there are no necessary conditions for its implementation.

The nature of the operation is largely determined by the characteristics of nerve damage. So, with a complete anatomical interruption of the nerve, the edges of the nerve are excised until its normal structure appears. The edges of the nerve should be brought together so that there is no tension during suturing. This can be done by mobilizing the nerve or moving it to a new, shorter bed. At the same time, it should be borne in mind that the nerve trunk can be isolated without fear of disrupting its blood supply in a section whose length is equal to 50 of its diameters. If it is not possible to match the ends of the nerve, it is necessary to use grafts - fragments of nerves that have less functional significance. For this purpose, superficial sensory nerves are usually used - the superficial peroneal, median cutaneous nerve of the forearm and some others.

Stitching of the ends of the damaged nerve is carried out in such a way that the affected fasciculae are compared with each other. Sutures may be placed on the epineurium or on the perineurium. The number of sutures should be minimal, but sufficient to achieve correct alignment of individual fasciculae. A large number of sutures leads to proliferation of connective tissue and impedes nerve regeneration. With a large distance between the ends of the nerve, as mentioned earlier, a graft is used, which is located in such a way that its internal structure, if possible, corresponds to the structure of the damaged nerve. In some cases, this requires the use of several fragments of the cutaneous nerve taken for transplantation, which can be much thinner than the damaged one.

After completion of the operation, immobilization of the limb is required for 8 weeks.

With partial damage to the nerve in its thickness, a terminal neuroma can form. In these cases, excision of the neuroma and scar tissue is performed. Restoration of the damaged part of the nerve is carried out at the expense of the graft.

In case of blunt trauma to the nerve, damage to its constituent fibers is possible with external anatomical continuity of the nerve. In these cases, it is advisable to release the nerve from the surrounding adhesions (perform neurolysis), wait for the period during which the nerve regenerates (the rate of axon regeneration is approximately 1 mm/day).

In the absence of signs of restoration of nerve function, there may be indications for excision of the affected area and its reconstruction with a graft.

When the roots are detached from the spinal cord, it is impossible to restore the continuity of the affected nerve. In these cases, it becomes necessary to use other functionally close nerves for at least partial restoration of the lost function. So, when the roots of the brachial plexus are torn off from the spinal cord, one can try to restore (at least partially) the important function of the musculocutaneous nerve of the hand with the help of the intercostal nerve. For this purpose, both nerves are crossed and the central end of the intercostal nerve is sutured to the peripheral end of the musculocutaneous. After the transition of "germination" of axons to the muscles is completed, "retraining" is necessary so that the interosseous nerve begins to perform the function of the musculocutaneous nerve.

In case of traumatic injury of the brachial plexus, there may be indications for the surgical reconstruction of damaged trunks in compliance with the principles described earlier.

To approach various nerves, including the main plexuses - the brachial and lumbosacral, various surgical approaches are used, which are described in detail in the relevant textbooks and manuals.

For the full effect after the operation, restorative treatment (special exercises, physiotherapy procedures) is necessary. During the period of nerve regeneration, electrical stimulation of the muscles in the zone of innervation is necessary, which makes it possible to prevent their degeneration and sclerosis.

The effect of the operation is determined by many factors. In addition to the technical possibility of restoring the continuity of the nerve, the time elapsed after the injury, the length of the affected nerve, the state of the blood supply (for example, the simultaneous injury of large vessels leads to disruption of the blood supply to the nerve and adversely affects the restoration of its functions) and a number of other factors are important.

^

21.7. Neuralgia of the cranial and spinal nerves

neuralgia- damage to the peripheral segment of the nerve (branch or root), manifested by symptoms of irritation. If neuropathies are characterized by symptoms of loss of nerve function, neuralgia is characterized by symptoms of irritation. There are neuralgia of the cranial (trigeminal, glossopharyngeal) and spinal (intercostal) nerves.

^ Trigeminal neuralgia. Trigeminal neuralgia is one of the most common and most excruciating pain syndromes. The disease is characterized by sudden attacks of sharp, penetrating pain in the zone of innervation of the trigeminal nerve or its individual branches. The II and III branches are most often affected. During an attack, vegetative symptoms can be observed: redness of the face, sweating, lacrimation, increased sweating. Often there is a reflex contraction of the muscles of the face. Patients take peculiar postures, hold their breath, squeeze the painful part or rub it with their fingers.

Pain attacks are short-lived, usually lasting no more than a minute. In some cases, attacks follow one after another, but long periods of remission are possible.

When examining patients, organic symptoms are usually not detected. During an attack and after it, pain can only be noted when pressed at the exit points of the branches of the trigeminal nerve.

Trigeminal neuralgia is a disease predominantly of elderly and senile people. Women are more often affected.

Previously, two types of trigeminal neuralgia were distinguished: essential - without an obvious cause, the typical clinical manifestations of which were given earlier, and symptomatic, in which it is possible to establish the cause of facial pain.

The concept of essential neuralgia has changed significantly in recent decades. Since in most cases it is possible to clarify its cause, it is believed that neuralgia is most often caused by compression of the trigeminal nerve root by a nearby vessel - an artery, a vein (for example, a loop of the superior cerebellar artery). Attacks of neuralgia of the V nerve can also be caused by volumetric formations - tumors, cholesteatoma, developing in this area.

Pain in the face, in the zone of innervation of the V nerve may be the result of an inflammatory process (neuritis of the V nerve). The source of infection in these cases is the processes in the oral cavity, paranasal sinuses, basal meningitis. However, the pains caused by these causes are more persistent, paroxysmal in nature is less typical for them, the study usually reveals a violation of sensitivity in the corresponding area of ​​the face.

Treatment. With trigeminal neuralgia, a decrease or cessation of pain can be achieved with the help of the anticonvulsant drug tegretol, the use of which is started with 200 mg per day, then the dose is increased (200 mg 3-4 times a day). Baclofen is also used (5-10 mg 3 times a day). With symptomatic neuralgia due to inflammatory process, the use of resolving therapy, physiotherapy procedures is justified.

With the ineffectiveness of drug therapy, there are indications for surgical treatment. For the treatment of neuralgia of the V nerve, many surgical methods have been proposed, both simple and complex: the intersection of the roots of the V nerve, the removal of the Gasser node.

The purpose of the operation is to block impulses that can cause an attack of neuralgia, or to eliminate the very cause of neuralgia (vascular root compression), if any.

Usually, they start with simpler interventions - blockades of individual branches of the V nerve, and last (especially in the elderly) they resort to more complex interventions.

^ Operations on peripheral branches - novocaine or alcohol blockade of the main peripheral branches.

Blockades or exercise (excision) of peripheral branches usually give a temporary effect (6–12 months).

^ Blockade of the gasser node is produced by effective and low-traumatic puncture injection of phenol, boiling water into the gasser node or by means of its radiofrequency coagulation.

^ Retrogasseral transection V nerve root with approach from the middle cranial fossa (Spiller-Freger operation) or with access from the posterior cranial fossa (Dandy operation) is very traumatic and is currently rarely used.

If the above methods of treatment are ineffective, especially in those cases in which pain persists despite the anesthesia in the face area that has come after previous operations, the Shockvist operation can be applied - the intersection of the descending nucleus of the trigeminal nerve in the medulla oblongata.

^ Vascular decompression of the V nerve root. One of the main causes of trigeminal neuralgia is compression of the V nerve root by an atypically located vessel. In old age, sclerosis and elongation of the vessels occur, as a result of which they can compress the nerve at the point of its entry into the bridge.

The goal of the operation, which is performed through a small burr hole in the scales of the occipital bone near the pyramid, is to locate this vessel (most often the superior cerebellar artery) and separate it from the nerve using a Teflon sponge or a piece of muscle.

^ Glossopharyngeal neuralgia.

Manifested by attacks of acute piercing pains (similar to those observed in trigeminal neuralgia), localized in the pharynx, tonsils, root of the tongue, ear. Pain is usually provoked by talking, swallowing and chewing.

The cause may be compression of the root of the glossopharyngeal nerve by the vascular loop. With inefficiency drug treatment decompression of the glossopharyngeal and vagus nerves is indicated.

^ Neuralgia of the cranial and spinal nerves in herpes zoster. herpes zoster (shingles) - blisters on the skin or mucous membranes on an erythematous edematous base, spreading in the zone of segmental innervation. Caused by the varicella-zoster virus, it is more common in the elderly, but can occur at any age. One or more adjacent spinal ganglia and posterior roots are affected. The first place in the structure of localization belongs to the thoracic region, the second - to the ophthalmic branch of the trigeminal nerve.

Clinical manifestations. A detailed clinical picture with rashes is quite rare. The disease begins suddenly, acutely, without warning. General infectious symptoms are noted: malaise, fever, gastrointestinal disorders. Often these phenomena are unsharply expressed. This period lasts 2-3 days. Then there are neuralgic pains in the zone of innervation of the affected nodes and roots. The pain is burning, constant, often paroxysmal intensifying. In addition to pain, there may be itching. Then hyperemia of the skin or mucous membrane develops in the zone of the corresponding dermatomes, and after 1–2 days a group of papules surrounded by a red rim appears. Papules turn into vesicles filled with serous fluid. After 3-4 days, the blisters become purulent and form yellow-brown crusts. After their separation, pigment scars remain, which may disappear. Often, whitish scars remain in their place. When the node of the trigeminal nerve is damaged, the bubbles are localized on the face in the zone of innervation of its branches, more often than the first.

The disease lasts 3-6 weeks and passes without a trace. However, often, especially in the elderly, there is postherpetic neuralgia (intercostal or trigeminal). If the bubbles pour out on the cornea, keratitis may develop, followed by a decrease in vision up to blindness.

When the crankshaft is damaged, Hunt's syndrome occurs. There are rare cases of damage to the ganglia of the IX-X cranial nerves. Serous meningitis, myelitis and meningoencephalomyelitis can be observed, which are severe. However, mild, abortive forms of the disease are more common.

Treatment. Apply antiviral drugs (acyclovir, zovirax, herpesin) inside and in the form of an ointment. Assign analgesics, acetylsalicylic acid, if necessary, in combination with antipsychotics, antihistamines, barbiturates. Antibiotic ointments are used to protect eroded areas from secondary infection. In complicated cases, corticosteroids are prescribed. In the acute stage and with postherpetic neuralgia, tranquilizers, carbamazepine (tegretol), antidepressants (amitriptyline in combination with analgesics) are prescribed.

Defeat n. tibialis of traumatic, compression, dysmetabolic or inflammatory genesis, leading to dysfunction of the leg muscles responsible for plantar flexion of the foot and foot muscles, hypoesthesia of the posterior surface of the lower leg, sole and toes, the occurrence of pain syndrome and vegetative-trophic changes in the foot. In the diagnosis of pathology, the main thing is the analysis of anamnestic data and a neurological examination, auxiliary methods - EMG, ENG, ultrasound of the nerve, radiography and CT of the foot and ankle. Treatment is possible conservative (anti-inflammatory, neurometabolic, analgesic, vasoactive therapy) and surgical (neurolysis, decompression, removal of a nerve tumor).

General information

Tibial neuropathy belongs to the group of so-called peripheral lower limb mononeuropathies, which includes sciatic nerve neuropathy, femoral neuropathy, peroneal neuropathy, neuropathy of the external cutaneous nerve of the thigh. The similarity of the clinic of tibial neuropathy with the symptoms of traumatic injuries of the musculoskeletal apparatus of the lower leg and foot, as well as the traumatic etiology of most cases of the disease, makes it the subject of study and joint management of specialists in the field of neurology and traumatology. The connection of the disease with sports overload and repeated injuries determines the relevance of the problem for sports doctors.

Anatomy of the tibial nerve

The tibial nerve (n. tibialis) is a continuation of the sciatic nerve. Starting at the top of the popliteal fossa, the nerve passes it from top to bottom medially. Then, having passed between the heads of the gastrocnemius muscle, the nerve lies between the long flexor of the first finger and the long flexor of the fingers. So it reaches the medial malleolus. Approximately in the middle between the ankle and the Achilles tendon, you can feel the point of passage of the tibial nerve. Further, the nerve enters the tarsal canal, where it, together with the posterior tibial artery, is fixed by a powerful ligament - the flexor retainer. Upon exiting channel n. tibialis divides into terminal branches.

In the popliteal fossa and further, the tibial nerve gives motor branches to the triceps muscle, flexor thumb and flexor of the fingers, popliteal, posterior tibial and plantar muscles; sensory internal cutaneous nerve of the lower leg, which, together with the peroneal nerve, innervates the ankle joint, the posterolateral surface of the lower 1/3 of the lower leg, the lateral edge of the foot and the heel. Terminal branches n. tibialis - medial and lateral plantar nerves - innervate the small muscles of the foot, the skin of the inner edge of the sole, the first 3.5 fingers and the back surface of the remaining 1.5 fingers. The muscles innervated by the tibial nerve provide flexion of the lower leg and foot, raising the inner edge of the foot (i.e., internal rotation), flexion, adduction and spreading of the toes, and extension of their distal phalanges.

Causes of tibial neuropathy

Femoral neuropathy is possible as a result of nerve injury in tibial fractures, isolated tibial fracture, ankle dislocation, wounds, tendon damage, and foot sprains. An etiological factor can also be repeated sports injuries of the foot, foot deformities (flat feet, hallux valgus), prolonged uncomfortable position of the lower leg or foot with compression n. tibialis (often in those suffering from alcoholism), diseases of the knee or ankle joint (rheumatoid arthritis, deforming osteoarthritis, gout), nerve tumors, metabolic disorders (in diabetes mellitus, amyloidosis, hypothyroidism, dysproteinemia), nerve vascularization disorders (for example, with vasculitis).

Most often, neuropathy of the tibial nerve is associated with its compression in the tarsal canal (the so-called tarsal tunnel syndrome). Nerve compression at this level can occur with fibrotic changes in the canal in the post-traumatic period, tendovaginitis, hematomas, bone exostoses or tumors in the canal area, as well as with neurodystrophic disorders in the ligamentous-muscular apparatus of the joint of vertebrogenic origin.

Symptoms of tibial neuropathy

Depending on the topic of the lesion n. tibialis in the clinical picture of his neuropathy, there are several syndromes.

Tibial neuropathy at the level of the popliteal fossa is manifested by a disorder of downward flexion of the foot and impaired movement in the toes. The patient cannot stand on his toes. Walking is typical with an emphasis on the heel, without rolling the foot on the toe. There is atrophy of the posterior muscle group on the lower leg and muscles on the foot. As a result of atrophy of the muscles on the foot, it becomes like a clawed paw. There is a decrease in the tendon reflex from Achilles. Sensory disorders include violations of tactile and pain sensitivity on the entire lower leg from behind and along the outer edge of its lower 1/3, on the sole, totally (on the back and plantar surface) on the skin of the first 3.5 fingers and on the back of the remaining 1.5 fingers. Neuropathy of the tibial nerve of traumatic origin is characterized by a pronounced causalgic syndrome with hyperpathy (perverted hypersensitivity), edema, trophic changes and autonomic disorders.

Tarsal tunnel syndrome in some cases is provoked by long walking or running. It is characterized by burning pains in the sole, often radiating to the calf muscle. Patients describe pain as deep, note an increase in their intensity in the standing position and when walking. There is hypoesthesia of both the inner and outer edges of the foot, some flattening of the foot and a slight "clawing" of the fingers. The motor function of the ankle joint was preserved in full, the Achilles reflex was not disturbed. Percussion of the nerve at the point between the medial malleolus and the Achilles tendon is painful, giving a positive Tinel sign.

Neuropathy at the level of the medial plantar nerve is common in long-distance runners and marathon runners. Manifests pain and paresthesia on the inner edge of the sole and in the first 2-3 toes. The presence of a point in the area of ​​the navicular bone is pathognomonic, the percussion of which leads to the appearance of burning pain in the thumb.

Defeat n. tibialis at the level of the common digital nerves is called Morton's metatarsal neuralgia. It is typical for older women who are obese and walk a lot in heels. Pain is typical, starting at the arch of the foot and going through the bases of 2-4 fingers to their tips. Walking, standing and running increase the pain syndrome. Examination reveals trigger points between 2-3 and/or 3-4 metatarsal bones, Tinel's symptom.

Calcanodynia - neuropathy of the calcaneal branches of the tibial nerve. It can be provoked by a jump on the heels from a height, long walking barefoot or in shoes with thin soles. Manifested by pain in the heel, its numbness, paresthesia, hyperpathy. With a pronounced intensity of these symptoms, the patient walks without stepping on the heel.

Diagnosis of neuropathy of the tibial nerve

An important diagnostic value is the collection of anamnesis. Establishing the fact of injury or overload, the presence of pathology of the joints, metabolic and endocrine disorders, orthopedic diseases, etc. helps to determine the nature of the damage to the tibial nerve. Conducted by a neurologist, a thorough study of the strength of various muscle groups of the lower leg and foot, the sensitive sphere of this area; identification of trigger points and Tinel's symptom allows diagnosing the level of damage.

Of auxiliary importance are