Nerve damage. Nervous system lesions
– this is a complete or partial disruption of the integrity of the nerve due to injury, blow or compression. Can occur with any type of injury. Accompanied by impaired sensitivity, loss of motor functions and the development of trophic disorders in the innervation zone. It is a serious injury and often causes partial or complete disability. The diagnosis is made based on clinical signs and stimulation electromyography data. Treatment is complex, combining conservative and surgical measures.
ICD-10
S44 S54 S74 S84
General information
Nerve damage is a common, severe injury caused by a complete or partial interruption nerve trunk. Nervous tissue does not regenerate well. In addition, with such injuries, Wallerian degeneration develops in the distal part of the nerve - a process in which the nerve tissue is resorbed and replaced by scar connective tissue. That's why favorable outcome treatment is difficult to guarantee even with a highly qualified surgeon and adequate restoration of the integrity of the nerve trunk. Nerve damage often causes limited ability to work and disability. Treatment of such injuries and their consequences is carried out by neurosurgeons and traumatologists.
Reasons
Closed damage nerves arise due to compression of soft tissues by a foreign object (for example, when being under a rubble), a blow with a blunt object, isolated compression of the nerve by a tumor, a fragment of bone during a fracture, or a dislocated end of a bone during a dislocation. Open nerve injuries in peacetime often result from cut wounds, during hostilities - gunshot wounds. Closed injuries, as a rule, are incomplete, and therefore proceed more favorably.
Pathogenesis
Nerve damage is accompanied by loss of sensitivity, impaired motor function and trophic disorders. In the autonomous zone of innervation, sensitivity is completely absent; in mixed zones (areas of transition of innervation from one nerve to another), areas of decreased sensitivity are detected, interspersed with areas of hyperpathy (perversion of sensitivity, in which pain, itching or other unpleasant sensations occur in response to harmless stimuli) . Motor dysfunction manifests itself flaccid paralysis innervated muscles.
In addition, skin anhidrosis and vasomotor disorders develop in the affected area. During the first three weeks, there is a hot phase (the skin is red, its temperature is increased), which is replaced by a cold phase (the skin becomes cold and acquires a bluish tint). Over time, trophic disorders occur in the affected area, characterized by thinning of the skin, a decrease in its turgor and elasticity. In the long term, joint stiffness and osteoporosis are detected.
Classification
Depending on the severity of nerve damage, the following disorders are distinguished in practical neurology and traumatology:
- Shake. There are no morphological or anatomical abnormalities. Sensitivity and motor functions are restored after 10-15 days. after injury.
- Injury(contusion). The anatomical continuity of the nerve trunk is preserved; isolated damage to the epineural sheath and hemorrhages into the nerve tissue are possible. Functions are restored approximately a month after damage.
- Compression. The severity of the disorders directly depends on the severity and duration of the compression; both minor transient disturbances and persistent loss of functions requiring treatment may be observed. surgical intervention.
- Partial damage. Loss is noted individual functions, often in combination with symptoms of irritation. Spontaneous recovery, as a rule, does not occur; surgery is necessary.
- Full break. The nerve is divided into two ends - peripheral and central. In the absence of treatment (and in some cases even with adequate treatment), the median fragment is replaced by a section of scar tissue. Spontaneous recovery is impossible; subsequently, increasing muscle atrophy, sensory disturbances and trophic disorders are observed. Required surgical treatment however, the result is not always satisfactory.
Symptoms of nerve damage
Damage ulnar nerve, primarily manifests itself as movement disorders. Active flexion, extension and abduction of the 5th and 4th and partly the 3rd fingers is impossible, muscle strength is sharply weakened. Within 1-2 months, atrophy of the interosseous muscles develops, as a result of which the contours of the metacarpal bones begin to stand out sharply on the back of the hand. In the long-term period, a characteristic claw-shaped deformation of the hand occurs. Average and distal phalanges The fifth and fourth fingers are in a state of flexion. Opposing the little finger is not possible. Sensory disorders, secretory and vasomotor disorders are observed on the ulnar side of the hand.
Damage median nerve accompanied by severe sensory impairment. In addition, already in the initial period, trophic, secretory and vasomotor disorders are clearly visible. The skin of the innervated area is flaky, shiny, cyanotic, dry, smooth and easily wounded. Nails of fingers I-III are transversely striated, subcutaneous tissue nail phalanges atrophied. Character movement disorders determined by the level of nerve damage.
Low lesions are accompanied by paralysis of the thenar muscles, high lesions are accompanied by impaired palmar flexion of the hand, pronation of the forearm, extension of the middle phalanges of the third and second fingers, and flexion of the first and third fingers. Opposition and abduction of the first finger is impossible. The muscles gradually atrophy, their fibrous degeneration develops, therefore, if the injury is more than a year old, restoration of their function becomes impossible. A “monkey hand” is formed.
Damage to the radial nerve at the level of the shoulder or axillary region is accompanied by significant motor disturbances. Paralysis of the extensors of the hand and forearm occurs, manifested by the symptom of a drooping or “falling” hand. When the underlying parts are damaged, only sensitivity disorders develop (usually of the hypoesthesia type). The dorsum of the radial side of the hand and the phalanges of the I-III fingers suffer.
Damage to the sciatic nerve is manifested by impaired flexion of the lower leg, paralysis of the fingers and foot, loss of sensation along the back of the thigh and almost the entire lower leg (with the exception of inner surface), as well as loss of the Achilles reflex. Causalgia is possible - excruciating burning pain in the area of innervation of the injured nerve, spreading to the entire limb, and sometimes to the torso. Partial damage to the nerve with loss of functions of its individual branches is often observed.
Damage to the tibial nerve is manifested by loss of the Achilles reflex, impaired sensitivity of the outer edge of the foot, sole and back of the leg. A typical deformity is formed: the foot is extended, the posterior group of muscles of the lower leg is atrophied, the toes are bent, the arch of the foot is deepened, the heel protrudes. Walking on toes, turning the foot inward, and bending the toes and toes are impossible. As in the previous case, causalgia often develops.
Damage peroneal nerve accompanied by paralysis of the extensors of the fingers and toes, as well as the muscles that ensure the outward rotation of the foot. There are sensory disturbances along the dorsum of the foot and outer surface shins. A characteristic gait is formed: the patient raises his shin high, bending the knee strongly, then lowers his leg onto his toe and only then onto the sole. Causalgia and trophic disorders, as a rule, are not expressed, the Achilles reflex is preserved.
Diagnostics
In making a diagnosis, examination, palpation and neurological examination play a vital role. During examination, pay attention to typical deformities of the limb, skin color, trophic disorders, vasomotor disorders and condition various groups muscles. All data are compared with a healthy limb. During palpation, moisture, elasticity, turgor and temperature of various parts of the limb are assessed. Then a sensitivity study is carried out, comparing sensations in a healthy and diseased limb. They determine tactile, pain and temperature sensitivity, a sense of localization of irritation, joint-muscular feeling, stereognosis (recognition of an object by touch, without visual control), as well as a sense of two-dimensional irritations (identification of figures, numbers or letters that the doctor “draws” on the patient’s skin ).
Leading additional method The current study is stimulation electromyography. This technique allows you to assess the depth and degree of nerve damage, determine the speed of impulses, functional state reflex arc, etc. Along with diagnostic value, this method has a certain prognostic value, because it allows you to identify early signs nerve restoration.
Treatment of nerve damage
Treatment is complex, using both surgical techniques and conservative therapy. Conservative measures begin from the first days after injury or surgery and continue until full recovery. Their goal is to prevent the development
Peripheral spinal nerves for the most part are mixed and consist of motor, sensory and vegetative fibers Therefore, the symptom complex of nerve damage includes motor, sensory and vasomotor-secretory-trophic disorders. Peripheral damage nervous system may be at the level of roots, plexuses and their nerves.
Damage to the spinal roots (radiculitis). The clinical picture consists of signs of simultaneous damage to the anterior (motor) and posterior (sensitive) roots, with symptoms of the disease of the posterior roots appearing first, as evidenced by the appearance of pain at the onset of the disease. The radicular symptom complex consists of symptoms of irritation and loss.
Symptoms of irritation usually predominate on early stage diseases. Clinical signs of irritation of the roots manifest themselves in the form of revitalization of tendon and periosteal reflexes, paresthesia, hyperesthesia (usually superficial types of sensitivity), pain, pain points, characteristic antalgic postures, etc. Symptoms of prolapse include weakening or complete disappearance of tendon and periosteal reflexes, segmental hypoesthesia or anesthesia of certain (or all) types of sensitivity. When the roots are damaged, muscle-tonic phenomena can be observed (symptoms of Lasegue, Bekhterev, Ne-ry, Dejerine, etc.). Disorders of sensory, movement, reflexes and trophic disorders when the roots are affected are segmental in nature. There may be changes in the cerebrospinal fluid associated with the stage of the disease and the localization of the pathological process. Thus, at the beginning of the disease, when the phenomena of irritation of the roots predominate, the number of cellular elements in the cerebrospinal fluid may be increased. At later stages of the disease, when the process moves to radicular nerve, causing its swelling, there is an increase in the amount of protein with normal or increased cytosis.
The roots are closely connected to the membranes of the spinal cord, so the clinical picture of radiculitis can be complemented by meningeal symptoms. In such cases, meningoradiculitis is diagnosed.
A characteristic feature of the clinical symptoms of radiculitis is their asymmetry. Symmetrical radicular symptoms may be observed in secondary radiculitis caused by destructive changes in the vertebrae, especially their bodies (tuberculous spondylitis, metastases to the vertebral body, etc.).
When the pathological process moves to the spinal node, they speak of ganglioradiculitis. In such cases, to clinical picture Radiculitis is combined with the picture of herpes zoster. In this case, herpetic rash is observed in the area of innervation of the affected roots and their corresponding nodes.
Damage to the roots can occur at any level, therefore cervical, thoracic and lumbosacral radiculitis are distinguished.
The nerve fibers of the roots of the lumbar and sacral regions form the sciatic and femoral nerves, so radicular pain can spread along the course of these nerves. Radicular pain intensifies with coughing, sneezing, straining during defecation and lifting, turning and bending the body, which is explained by increased intra-radicular hypertension, which is based on microcirculatory disorders and edema in the roots and their sheaths.
With artificial intensification of intraradicular hypertension, pain symptoms and points appear.
Microcirculatory and edematous phenomena in the roots and their meningeal sheaths are observed with lesions spinal column(osteochondrosis, prolapse of intervertebral discs, spondyloarthrosis, spondylolisthesis, spondylitis, etc.).
Radicular pain is often the cause of antalgic postures (scoliosis), manifested by curvature of the spinal column, often in the healthy direction. This reduces the load on the affected side and, consequently, the compression of the root-sheath complex, which helps reduce congestion and edema.
Damage to the plexuses and their nerves. Cervical plexus(plexus seri-vitalis) formed abdominal branches four cervical spinal nerves (Ci-04). It is covered by the sternocleidomastoid muscle. Nerves extending from the plexus innervate the skin and muscles of the neck, and the skin of the occipital region of the head. These include the following nerves.
Small occipital nerve(n.occipitalis minor, Ca-C3) - sensitive, innervates the skin of the outer part of the occipital region of the head and partially the auricle. Its defeat causes a sensitivity disorder in the area of innervation of the nerve, irritation is accompanied by sharp pain in the back of the head (occipital neuralgia) and the presence of pain points upon palpation along the posterior edge of the sternocleidomastoid muscle.
Greater auricular nerve (n. auricularis magnus, S3) - sensitive, partially innervates the skin of the auricle, external ear canal and mandibular region. The lesion causes sensitivity disorders in the areas of its innervation and pain in the area of the external auditory canal and the angle of the lower jaw.
Supraclavicular nerves (supraclaviculares, Sz - 04) - sensitive, innervate the skin in the area of the supraclavicular and subclavian fossa, the upper part of the scapula and shoulder. Their defeat is accompanied by sensitivity disorder and pain in these areas.
The phrenic nerve (n. phrenicus) is a mixed nerve, the most powerful nerve of the plexus. The motor branches innervate the diaphragm muscle, and the sensory branches innervate the pleura, pericardium, diaphragm and the adjacent peritoneum. Its defeat causes paralysis of the diaphragm, which manifests itself in difficulty breathing and coughing movements. Irritation is accompanied by shortness of breath, hiccups, retching, pain in the supraclavicular fossa, neck and chest.
The brachial plexus (plexuc brachialis) is formed by the anterior branches of the four lower cervical (Cs-Cs) and two upper thoracic (Thi-Th2) spinal nerves. The plexus is divided into supraclavicular (pars supraclavicularis) and subclavian (pars infraclavicularis) parts. The following nerves belong to the brachial plexus.
Axillary nerve (n. axillaris, d, - Su - mixed nerve. Its motor fibers innervate the deltoid muscle and the teres minor muscle, sensitive in the area of the upper lateral cutaneous nerve of the shoulder (n. cutaneus brachii lateralis superior) - the skin of the outer surface of the shoulder. Lesion of the axillary nerve in the supraclavicular fossa, involving the musculocutaneous nerve (n. musculocutaneus) in the process, causes Erb's palsy:
Inability to raise the shoulder as a result of paralysis rn. deltoideus and impaired sensitivity of the skin on the outer surface of the shoulder.
Musculocutaneous nerve (p. musculocutaneus, Cs-C?) - mixed. Its motor fibers innervate the biceps brachii, brachialis and coracobrachialis muscles, and the sensitive skin of the outer surface of the forearm. It consists of branches of the lateral nerve of the forearm (n. cutaneus antibrachii lateralis).
Nerve damage is accompanied by atrophy of the above muscles, loss of the flexion-ulnar reflex, and sensitivity disorder on the skin of the radial surface of the forearm and thenar.
The radial nerve (n. radialis, Cs-Cs and Thi) is mixed. Its motor fibers innervate the extensor muscles of the forearm: triceps brachii, olecranon, hand muscles:
Extensor carpi radialis longus and brevis, extensor digitorum and extensor of the little finger, abductor longus thumb hands, and an instep support, which takes part in the supination of the forearm.
Thus, the radial nerve extends the arm at the elbow joint, the hand at the wrist joint, the fingers at the main phalanges and, in addition, abducts the thumb and performs supination of the hand.
Sensitive fibers are part of the posterior cutaneous nerve of the shoulder (n. cutaneus brachii posterior), the lower lateral cutaneous nerve of the shoulder (n. cutaneus brachii lateralis inferior) and the posterior cutaneous nerve of the forearm (n. cutaneus antibrachii posterior), innervates the skin of the posterior surface of the shoulder and forearm and the radial side of the hand and partially the dorsal surface of the first, second and half of the third fingers (. 34, a, b).
When the radial nerve is damaged, a typical picture of a drooping hand is observed (. 35). The patient cannot straighten the arm at the elbow and wrist joints, the fingers in the main phalanges, abduct the thumb, and also cannot supinate the hand and forearm. Sensitivity is impaired in the zone of innervation of the nerve and most clearly on the dorsum of the hand between the main phalanges of the first and second fingers.
To detect violations of the motor function of the radial nerve, the following tests are used.
When the arms are extended forward or raised upward, a drooping of the hand is detected.
When the palms of the hands are folded apart, the fingers of the affected hand do not straighten.
Isolated damage to the radial nerve occurs when chronic intoxications lead, toxicosis of pregnancy, injuries, chronic alcohol intoxication, peripheral form multiple sclerosis.
Ulnar nerve (n. ulnaris Cg-Thi) - mixed. Its motor fibers inner-
They include the flexor carpi ulnaris, which provides flexion and abduction of the hand to the ulnar side, the deep flexor of the little finger, which provides flexion of the fourth and fifth fingers, the interosseous muscles that abduct and adduct the fingers, the muscle that adducts the thumb, and the lumbrical muscles, which provide extension of the middle and distal fingers. phalanges of fingers.
The ulnar nerve does the following: motor acts: independently bends and extends the fourth and fifth fingers in the middle and distal phalanges, spreads and adducts the second - fifth, adducts the thumb;
Together with the median nerve, it flexes the hand at the wrist joint and the second - fifth fingers in the main phalanges.
Sensitive fibers of the ulnar nerve innervate the skin of the ulnar surface of the hand, the fifth and partially fourth fingers (. 34).
If the ulnar nerve is damaged, the ability to palmar flexion of the hand, flexion of the fourth and fifth fingers, abduction and abduction of the fingers, and adduction of the thumb is lost. Due to atrophy of the small muscles of the hand and hyperextension of the main phalanges, flexion of the middle and distal phalanges of the fingers, the hand takes on the appearance of a “clawed paw” (. 36). In this case, it is impossible to bend the fourth and fifth fingers while clenching the hand into a fist, bend the distal phalanx of the little finger or scratch the last one on a smooth surface, and it is impossible to adduct the fingers, especially the first to fifth fingers. The most consistently sensitive disorders are found on the skin of the ulnar surface of the hand, in the area of the distal phalanges of the fourth and fifth fingers (autonomous zones). In addition, in the area of sensitivity disturbances, pronounced autonomic disorders are sometimes observed (cyanosis, disturbances in sweating, skin temperature). Causalgic pain is also noted.
To identify impaired motor function of the ulnar nerve, the following tests are used.
The patient is asked to spread and close the second to fifth fingers of the hand after he has placed his palm on the table.
In the same position of the hands, the patient is asked to move the distal phalanx of the little finger.
When trying to clench the hand into a fist, the middle and distal falai-gi of the fourth and fifth fingers do not bend.
They suggest stretching a strip of paper held between the thumb and forefinger. The patient cannot press a strip of paper thumb, since the adductor pollicis muscle is damaged and holds it with the bent terminal phalanx of the thumb due to the flexor pollicis longus, innervated by the median nerve (reverse Tinel test).
Isolated damage to the ulnar nerve is observed with trauma, syringomyelia and amyotrophic lateral sclerosis.
The median nerve (n. medianus) is mixed. Motor fibers innervate the flexor carpi radialis and the palmaris longus muscle, which perform palmar flexion of the hand, the deep and superficial flexors of the fingers, the long and short flexors of the thumb, which provide flexion of the fingers, especially the first three, the pronator teres and quadratus muscles, which perform pronation of the forearm, the short muscle, the abductor pollicis and the muscle that opposes the thumb to the hand.
Thanks to this, the median nerve independently innervates the following motor acts: flexion and extension of the middle and distal phalanges of the second and third fingers, flexion of the distal phalanx of the thumb, opposition of the thumb to the other fingers, pronation of the forearm; together with the ulnar nerve - palmar flexion of the hand, flexion of the proximal and middle phalanges of the fingers, with the exception of the thumb.
Sensitive fibers innervate the skin of the radial surface of the hand, the palmar surface of the first, second, third and partially fourth fingers, as well as the skin of the dorsal surface of their distal phalanges.
When the median nerve is damaged (toxic, infectious or traumatic), pronation, palmar flexion of the hand and the first three fingers and extension of the distal phalanges of the second and third fingers are impaired. In this case, the ability to bend the first, second and partially third fingers when clenching the hand into a fist is lost, and to carry out scratching movements index finger, oppose the thumb to the rest. Sensitive disorders are found in the skin of the palmar surface of the hand
And the first three (partially fourth) fingers and on the dorsal surface of the two distal phalanges of the second, third, partially fourth fingers. In addition, atrophy of the muscles of the hand is expressed, especially the elevation of the thumb of the skin (smooth, shiny, dry), vegetative-vascular disorders (cyanosis, pallor, impaired sweating, brittle nails, ulceration, etc.), and causalgic pain is quite often noted.
To determine movement disorders caused by damage to the median nerve, the following tests are used.
The patient is asked to press the hand tightly with the palm of the hand to the table and make a scratching movement with the index finger.
The patient is asked to clench his fingers into a fist. In this case, the middle and distal phalanges of the first, second and partially third fingers do not bend (“the hand of the prophet”).
The patient holds the strip of paper with a straightened thumb due to the preservation of the function of the ulnar nerve (direct Tinel test).
They ask the patient to oppose his thumb to the rest, which he cannot do.
Defeat everything brachial plexus causes peripheral paralysis of the arm muscles, loss of tendon and periosteal reflexes, a disorder of all types of sensitivity in the zone of innervation of the plexus, pain spreading throughout the arm and (with high lesions) Bernard-Horner syndrome.
Damage to the supraclavicular part of the plexus (Cs - Ce) is manifested by Duchenne-Erb palsy - dysfunction of the axillary nerve innervating the deltoid muscle, the musculocutaneous nerve innervating the biceps brachii and brachialis muscles, as well as partially the radial nerve, which is manifested by damage to the brachioradialis muscle and arch support. The function of the muscles of the forearm and hand is preserved. With such a lesion, the patient cannot move his arm to the side and raise it to the horizontal
Lines or lead to the face. The flexion-elbow reflex disappears (from the m. bisipitis brachii tendon). There is a sharp pain in the supraclavicular fossa during palpation and sensitivity disorders on the skin of the shoulder girdle.
Damage to the subclavian part of the plexus (Cy-Th^) causes Dejerine-Klumpke palsy, which occurs as a result of dysfunction of the ulnar, median and radial nerves. In this case, the muscles that perform movements in the forearm, hand and fingers are affected, but the functions of the muscles of the shoulder girdle are preserved. Tendon and periosteal reflexes in the hand disappear. Sensitivity disorders of the radicular type are found on the skin of the inner surface of the shoulder, forearm and hand. On palpation, a sharp pain occurs in the subclavian fossa, which radiates throughout the arm.
The lumbar plexus (plexuc lumbalis), formed from the anterior branches of the four lumbar spinal nerves (VI, p. 32), is located in front of the transverse processes of the lumbar vertebrae and posterior to the psoas major muscle. The lumbar plexus gives rise to the femoral and obturator nerves and the external cutaneous nerve of the thigh. When the lumbar plexus is damaged, paralysis of the muscles innervated by the above nerves is observed. The cause of the lesion is often inflammatory processes of the pelvic cavity organs, birth injuries, intoxication, etc.
Femoral nerve (p. femoralis, Lz - 1^) - mixed. Its motor fibers innervate the iliopsoas muscle, which flexes the thigh at the hip joint, the quadriceps femoris muscle, which flexes the thigh and extends the tibia, and the sartorius muscle, which is involved in flexing the leg at the knee and hip joints. Sensitive fibers in the anterior cutaneous branches (rr. cutanei anteriores) of the femoral nerve innervate the skin of the anterior surface of the lower two-thirds of the thigh and the saphenous nerve (n. saphenus) - the anterior inner surface of the leg.
Damage to the nerve below the inguinal ligament leads to impaired leg extension, loss of the knee reflex, atrophy of the quadriceps femoris muscle and sensitivity disorder in the area of innervation of the saphenous nerve.
Damage to the nerve above the inguinal ligament leads to the addition of dysfunction of the iliopsoas muscle to the phenomena described above, which makes walking and running difficult (due to the inability to bring the thigh to the abdomen), as well as sensitivity disorder on the anterior surface of the thigh.
In addition, Matskevich's symptom is noted (the appearance of pain on the front surface of the thigh when bending the lower leg in a patient lying on his stomach) and Wasserman's symptom (in a patient lying on his stomach, pain appears on the front surface of the thigh when raising the outstretched leg upward).
The sacral plexus (plexus sacralis) is the most powerful. It consists of the anterior rami of the fifth lumbar and four
Sacral spinal nerves, the fibers of which, mixing with each other, form several loops that merge into a powerful trunk of the sciatic nerve (, VII, p. 32). In front of the plexus is the piriformis muscle, behind is the sacrum. The sacral plexus is located in close proximity to the sacroiliac joint, which is often affected by various pathological processes that extend to the plexus itself.
When the sacral plexus is damaged, the functions of all nerves originating from the plexus are disrupted.
The sciatic nerve (p. ischiadicus, Ls - L^) is mixed, the largest of all peripheral nerves. Having left the pelvic cavity through the greater sciatic foramen between the greater trochanter and the ischial tuberosity, it travels along the back of the thigh into the popliteal fossa, where it divides into the tibial and peroneal nerves. Along the way, it gives off branches that innervate the biceps femoris, semitendinosus and semimembranosus muscles, which flex and internally rotate the tibia. With high damage, the function of the tibial and common peroneal nerves suffers, which is manifested by paralysis of the foot and fingers, loss of the Achilles reflex, anesthesia in the lower leg and foot. Along with this, the ability to flex the lower leg is lost. The nerve trunk contains many autonomic fibers, so its damage is accompanied by severe pain and autonomic disorders. With traumatic injuries, the pain takes on a causal nature.
Palpation along the course of the sciatic nerve and its branches, especially in places poorly covered with soft tissue, causes sharp pain spreading up and down from the site of irritation. As with damage to the lumbosacral roots, symptoms of Neri, Dejerine, Lasegue, and Bekhterev may be observed.
Tibial nerve (n. tibialis, Ln - Ls) - mixed. The motor fibers innervate the triceps surae, flexor pedalis, flexor longus and brevis, flexor hallucis longus and brevis, flexor digitorum, tibialis posterior, internal rotator, and abductor hallucis. Sensitive fibers as part of the lateral dorsal cutaneous nerve (p. taneus dorsalis lateralis) innervate the skin of the posterior surface of the leg, and as part of the lateral and medial plantar nerves (p. plantares lateralis et medialis) - the sole and fingers.
If the tibial nerve is damaged, it is impossible to plantar flex the foot and toes, as well as turn the foot inward. The foot and toes are in an extension position (calcaneal foot, pes calcaneus). In such cases, the patient cannot rise on his toes and, while walking, steps on his heel. The posterior group of muscles of the lower leg and small muscles of the foot undergo atrophy. The arch of the foot deepens. The Achilles reflex is not evoked. Sensitivity is impaired on the back of the lower leg, in the sole and toes. Lost muscle-articular feeling in the big toe.
When studying the motor function of the nerve, the patient is asked to plantar flex the foot and stand on the toe of the sore leg, which he cannot do.
TO etiological factors Nerve damage should primarily be classified as traumatic, often causing causalgic pain.
The common peroneal nerve (n. peroneus communis, 1-4-Si) - mixed, in turn, is divided into two terminal branches: deep peroneal (n. peroneus profundus) and superficial peroneal (n peroneus superficialis) nerves. Motor fibers are present in both branches; the deep peroneal nerve innervates the extensors of the foot
And the extensors of the fingers, pronating the foot, the superficial peroneal nerve - the long and short peroneal muscles, lifting the lateral edge of the foot and abducting it outward.
Sensitive fibers of the peroneal nerve innervate the skin of the outer surface of the leg and the dorsal surface of the foot.
If the peroneal nerve is damaged, it is impossible to extend the foot and toes, as well as to rotate the foot outward. In such cases, the foot hangs down, is slightly pronated and turned medially, its toes are bent, which gives the picture of a “horse foot”. The patient cannot stand on his heel and, while walking, touches the floor with the toes of his dangling foot. To avoid this, the patient raises his leg high and, when lowering it, first touches the floor with the toe, then with the lateral edge of the foot and the entire sole (peroneal, “cock”, steppage gait). Sensory disorders are found on the outer surface of the lower leg and the dorsal surface of the foot. Muscular-articular sensation in the toes is not impaired due to the preserved sensitive function of the tibial nerve. The Achilles reflex is preserved.
Superior gluteal nerve (p. gluteus superior, la, Ls-Si) - motor, innervates the gluteus medius and minimus muscles
And the muscle that pulls the fascia lata. These muscles abduct the thigh outward. If the nerve is damaged, it is difficult to abduct the hip outward. With bilateral damage, a “duck” gait occurs; the patient sways to the sides while walking
The lower gluteal nerve (n. gluteus inferior, Lo - Sa) - motor, innervates the gluteus maximus muscle, which abducts the thigh posteriorly and straightens the torso from bent position. When it is affected, the movements made by these muscles are difficult
The posterior cutaneous nerve of the thigh (p. cutaneus femoris posterior, Si - ^з) is sensitive, innervates the skin of the lower buttock and the posterior surface of the thigh. When it is damaged, sensitivity in these areas is impaired.
The coccygeal plexus (plexus coccygeus) is formed from the anterior branches of the fifth sacral root and coccygeal nerve (n. coccygeus, Ss-Coi). The anal-coccygeal nerves (nn. anococcygei) emanate from the plexus, innervating the muscles and skin of the perineum. Irritation of the plexus pathological process(inflammation, tumor, intoxication, etc.) causes neuralgia (coccygodynia).
Ulnar nerve entrapment syndrome in the elbow joint
Syndrome of entrapment of the ulnar nerve in the area of the elbow joint (cubital tunnel syndrome), as damage to the peripheral nerves. The nerve is most susceptible to damage in elbow area. Here it is located in a canal on a dense bone bed, is easily injured by a direct blow and is chronically compressed when working at a table or desk; by the same mechanism, the nerve is compressed in patients when the hand is compressed on the edge of the bed, when leaning on the elbows, on a hard mattress in a lying position on the side, after prolonged anesthesia, alcohol intoxication, coma, when sitting for a long time in a chair with uncomfortable armrests, in drivers who have the habit of hanging their arm through the window. In people with hallux valgus deformity elbow (congenital variant of the structure or consequences of injury), the nerve is injured by the wing ilium when carrying heavy loads.
The second mechanism of microtrauma of the ulnar nerve is its subluxation in the cubital canal with an anterior displacement to the anteromedial surface of the internal epicondyle of the shoulder at the moment of flexion of the arm at the elbow joint, which is facilitated by congenital or acquired weakness of the ligament covering the ulnar groove, underdevelopment or rear location epicondyle.
The third mechanism is stenosis of the cubital canal, which can occur due to developmental anomalies (hypoplasia of the epicondyle, the presence of the epicondyle-ulnar muscle, abnormal attachment with protrusion of the medial head of the triceps muscle), be congenital (constitutional narrowness of the canal), degenerative (with dystrophic changes in the elbow joint, in the medial collateral ligament lining the bottom of the canal, and the fibrous-aponeurotic triangular ligament of the roof of the canal, spreading between the medial epicondyle and olecranon) and post-traumatic. Other types of stenosis are associated with tumors (chondromatosis of the elbow joint, ganglion of the ulnar sulcus), inflammatory processes in the joint (rheumatoid and psoriatic arthritis) or neurogenic osteoarthropathy. The clinical picture of cubital tunnel syndrome is represented primarily by paresthesia, numbness along the medial surface of the forearm and hand. Here you can feel deep aching pain. Finger compression of the nerve or its percussion increases the pain. Symptoms of damage to peripheral nerves: over time, hypoesthesia develops in the innervation zone. Even intense compression of the nerve trunk at the level of the cubital canal does not cause pain. Atrophy of the first dorsal interosseous muscle, hypothenar, and small muscles of the hand becomes obvious, which is accompanied by an increase in paresis of the hand. Weakness of the palmar interosseous muscles leads to impaired finger adduction, which is often manifested by abducted little finger posture. Paresis of the adductor muscle and flexor pollicis brevis is detected when trying to bring the thumb and small fingers together, which can only be done by flexing the thumb at the interphalangeal joint. With severe paresis, the hand takes on the shape of a “clawed paw”, which is caused by weakness of the lumbrical muscles in combination with a preponderance of the extensors. Noteworthy is the relatively small impairment of hand function with severe muscle atrophy. The provoking and pathogenetic moments of this damage to the peripheral nerves are labor and sports trauma to the base of the palm, especially in mechanics, plumbers, polishers, cyclists, and gymnasts.
Compression-ischemic neuropathy syndrome
Syndrome of compression-ischemic neuropathy of the dorsal branch of the ulnar nerve occurs as a result of chronic microtrauma of the wrist 1 cm above the head ulna(the habit of leaning on the edge of the table when typing on a typewriter, while listening to a lecture), and can also be a complication of ulnar styloidosis. Diagnosis is based on the typical localization of sensory disorders on the back half of the medial surface of the hand and the main phalanges of the III-V fingers. Characteristic when peripheral nerves are affected are pain along the medial surface of the hand. Pain point that causes irritation typical pain and paresthesia, found at the styloid process of the ulna.
High compression of the radial nerve at the level of the brachioaxillary angle by a crutch, the back of a chair, the edge of the operating table, or bed leads to paresis of the extensors of the hand and fingers, weakness of the triceps muscle and hypoesthesia along the posterior surface of the shoulder and forearm, and a decrease in the reflex from the triceps muscle.
Nerve damage in spiral channel between the heads of the triceps muscle in case of blunt trauma, fracture humerus, compression by callus is accompanied by paresis of the extensor hand. At the same time, the functions of the triceps muscle and sensitivity in the shoulder are preserved. Percussion of the compression site in the projection of the radial nerve groove causes local pain and paresthesia in the area of the anatomical snuffbox. The most common localization of compression-ischemic damage to peripheral nerves is the level of the external intermuscular septum of the shoulder, where the radial nerve is compressed during deep sleep(“sleepy”, “Saturday”, “alcohol”, “anesthesia” paralysis). “Dangling hand”, hypotrophy of the dorsal muscles of the forearm, especially the brachioradialis muscle, form the basis of the clinical picture. A small zone of hypoesthesia is limited to the area of the dorsal surface of the hand between the first and second fingers. The radial nerve may be subject to compression over the lateral epicondyle of the shoulder, the fibrous arch of the lateral head of the triceps, in the area of the elbow joint and the upper third of the forearm (fractures, degenerative lesions of the joint, bursitis, benign tumors). The neurological syndrome is the same as with sleep paralysis.
Arch support syndrome
Supinator syndrome - the result of compression of the deep branch of the radial nerve in the area of the supinator or arcade of Froese - is manifested by pain in the depths of the outer parts of the elbow region and the dorsum of the hand and forearm. The pain is caused by severe handmade, worsen after sleeping on the sore arm. There is weakness in supination and extension of the main phalanges of the fingers, which causes clumsiness of the hand during work. Maximum supination of the arm, bent at an angle of 45° at the elbow joint, causes increased pain. Palpation reveals compaction and tenderness of the instep support in the median groove of the forearm.
Posterior interosseous nerve syndrome
Posterior interosseous nerve syndrome is associated with its compression below the level of the supinator. In this case, the pain is mild or completely absent. Characterized by slowly progressive weakness in the extensors of the fingers, mainly the thumb and index, and radial deviation of the hand during extension.
Damage to the superficial sensory branch of the radial nerve most often occurs in lower third forearms, on the back of the wrist; it may be associated with de Corvain's disease (ligamentosis of the dorsal carpal ligament canal) or due to traumatization of the superficial branches by a watch bracelet, handcuffs, or athletes' wristbands. Numbness and burning pain are felt on the dorsum of the radial edge of the hand and fingers I-II. The pain may radiate up the arm all the way to the shoulder. The symptom of this lesion of the peripheral nerves is sharply positive. Local thickening of the subcutaneous branch, similar to a pseudoneuroma, may be detected.
Causes and treatment of neuropathy
Polyneuropathy (polyradiculoneuropathy) is multiple damage to peripheral nerves and roots of an inflammatory and toxic nature. The cause is infection (diphtheria, measles, influenza), diabetes mellitus, obliterating endarteritis, nephrozoneuritis, as well as damage by exogenous toxic substances (lead, arsenic, mercury, organophosphorus compounds, ethanol). Viruses and toxic substances have tropism for nerve tissue- ganglia and nerve trunks are affected. There is a deterioration in microcirculation, metabolism and trophism of nervous tissue, which in turn leads to its swelling, ischemia with subsequent degenerative changes(loss of myelin sheath, proliferation of connective tissue) and changes in the bioelectrical activity of nerve fibers.
The clinical picture of the disease is dominated by pain and disturbances of all types of sensitivity (tactile, pain, muscle-articular). Sensitivity disorder occurs in a radicular, peripheral or polyneuritis type. There are also motor disorders (peripheral paresis) and autonomic-vascular trophic changes.
The main treatments for neuropathies (polyneuropathies) are anti-inflammatory drugs (antibiotics, glucocorticoids), diuretics, desensitizing drugs, vitamins B1, B6 and B12, non-steroidal anti-inflammatory drugs (analgin, ibuprofen, indomethacin, diclofenac), mediators (proserin, nevaline, galantamine) .
The objectives of physiotherapy in the treatment of neuropathies (polyneuritis) are to provide analgesic effect(analgesic and anesthetic methods), anti-inflammatory action (antiexudative, decongestant, reparative and regenerative methods), improvement of microcirculation and metabolism (vasodilator, hypocoagulant, trophostimulating methods), improvement of neuromuscular fiber function (neurostimulating methods).
Classification of diseases of the peripheral nervous system
/. Vertebrogenic lesions.
1. Cervical level.
1.1. Reflex syndromes:
1.1.1. Cervicalgia.
1.1.2. Cervicocranialgia (posterior cervical sympathetic syndrome, etc.).
1.1.3. Cervicobrachialgia with muscular-tonic or vegetative-vascular or neurodystrophic manifestations.
1.2. Radicular syndromes:
1.2.1. Discogenic (vertebrogenic) lesion (radiculitis) of the roots (specify which ones).
1.3. Radicular-vascular syndromes (radiculoischemia).
2. Thoracic level.
2.1. Reflex syndromes:
2.1.1. Thoracalgia with muscular-tonic or vegetative-visceral or neurodystrophic manifestations.
2.2. Radicular syndromes:
2.2.1. Discogenic (vertebrogenic) lesion (radiculitis) of the roots (specify which ones).
3. Lumbosacral level.
3.1. Reflex syndromes:
3.1.1. Lumbago (can be used as an initial diagnosis in outpatient practice).
3.1.2.Lumbodynia.
3.1.3. Lumboischialgia with muscular-tonic or vegetative-vascular or neurodystrophic manifestations.
3.2. Radicular syndromes:
3.2.1. Discogenic (vertebrogenic) lesion (radiculitis) of the roots (specify which ones, including cauda equina syndrome).
3.3. Radicular-vascular syndromes (radiculoischemia).
II.Lesions of nerve roots, nodes, plexuses.
1. Meningoradiculitis, radiculitis (cervical, thoracic, lumbosacral, usually of infectious-allergic origin, non-vertebrogenic).
2. Radiculangglionitis, ganglionitis (spinal sympathetic), truncitis (usually viral).
3. Plexites.
4. Plexus injuries.
4.1. Cervical.
4.2. Upper shoulder (Duchenne-Erb palsy).
4.3. Lower shoulder (Dejerine-Klumpke palsy).
4.4. Shoulder (total).
4.5. Lumbosacral (partial or total).
///. Multiple lesions of roots and nerves.
1. Infectious-allergic polyradiculoneuritis (Guillain-Barre, etc.).
2. Infectious polyneuritis.
3. Polyneuropathy.
3.1. Toxic:
3.1.1. For chronic household and industrial intoxications (alcohol, lead, chlorophos, etc.).
3.1.2. For toxic infections (diphtheria, botulism).
3.1.3. Medication.
3.1.4. Blastomatous (for lung cancer, stomach cancer, etc.).
3.2. Allergic (vaccinal, serum, medication, etc.).
3.3. Dysmetabolic: with vitamin deficiency, with endocrine diseases (diabetes mellitus, etc.), with liver, kidney diseases, etc.
3.4. Discirculatory (for periarteritis nodosa, rheumatic and other vasculitis).
3.5. Idiopathic and hereditary forms.
IV.Lesions of individual spinal nerves.
1. Traumatic:
1.1. On upper limbs: radial, ulnar, median, musculocutaneous and other nerves.
1.2. On the lower extremities: femoral, sciatic, peroneal, tibial and other nerves.
2. Compression-ischemic (mononeuropathies, more often - tunnel syndromes).
2.1. On the upper limbs:
2.1.1. Carpal tunnel syndromes (damage to the median nerve in the hand).
2.1.2. Guillain's canal syndrome (damage to the ulnar nerve in the hand area).
2.1.3. Cubital tunnel syndrome (damage to the ulnar nerve in the elbow area).
2.1.4. Damage to the radial or median nerves in the ulnar region, damage to the suprascapular, axillary nerves.
2.2. On the lower extremities: tarsal canal syndrome, peroneal nerve, lateral cutaneous nerve of the thigh (pinching under the ligament of the pupart - Roth-Bernhardt meralgia paresthetica).
3. Inflammatory (mononeuritis).
V.Lesions of the cranial nerves.
1. Neuralgia of the trigeminal and other cranial nerves.
2. Neuritis (primary, as a rule, of infectious-allergic origin; secondary - otogenic and other origins), neuropathy (compression-ischemic origin) of the facial nerve.
3. Neuritis of other cranial nerves.
4. Prosopalgia.
4.1. Ganglionitis (ganglioneuritis) of the pterygopalatine, ciliary, ear, submandibular and other nodes.
4.2. Combined and other forms of prosopalgia.
5. Dentalgia, glossalgia.
In addition to the etiology and localization of the process, the following is also indicated: 1) the nature of the course (acute, subacute or chronic), and in the case of chronic: progressive, stable (protracted), recurrent often, rarely; regredient; 2) stage (usually in the case of a recurrent course): exacerbation, regression, remission (complete, incomplete); 3) the nature and degree of dysfunction: severity of pain (mild, moderately expressed, pronounced, pronounced), localization and degree of motor disorders, severity of sensory disturbances, vegetative-vascular or trophic disorders, frequency and severity of paroxysms and attacks.
Spinal radiculopathies
Radiculitis is a lesion of the roots of the spinal cord, which is characterized by pain, sensory disturbances of the radicular type and, less commonly, paresis.
Etiology and pathogenesis
Causes: spinal osteochondrosis, discosis, disc herniation, trauma, inflammation and tumors. Traumatic lesions affect the spine itself or the intervertebral discs. Inflammation most often occurs with syphilis, meningitis, and neuroallergic processes. Neoplastic processes in neuromas, meningiomas, cancer metastases. The most common cause is degenerative changes in bone and cartilage tissue, i.e. spinal osteochondrosis. This process is chronic. The nucleus pulposus is the first to be affected. It loses moisture and becomes crumbly. Degeneration is also observed in the fibrous ring. It becomes unfibered, becomes less elastic, and the intervertebral space narrows. When a provoking factor occurs (physical stress), the fibers of the ring rupture, and part of the nucleus protrudes into the resulting gap. This is how a disc herniation occurs.
Hernial protrusion can be lateral, posterolateral, paramedian, median. With lateral protrusion, the root of the same name is compressed, with posterolateral protrusion, the underlying one is compressed.
The hernia exerts mechanical compression on the root and compresses the vessels in the root. In addition, the pathogenesis of radiculitis has an autoimmune component of inflammation. The provoking moment in the development of the disease is injury and hypothermia.
In addition, changes in the spine can affect structures rich in receptors. These are the longitudinal ligaments, the recurrent endings of the spinal nerves. In these cases, reflex syndromes occur.
Clinic depends on which root is affected.
The cervical or lumbosacral spine is most often affected.
The acute period of lumbosacral radiculitis is characterized by acute pain in the lumbar region and in the leg to the popliteal fossa or to the heel. Pain intensifies with physical activity. The L5 or S1 roots are most often affected.
L5 root syndrome is characterized by shooting pains in the upper lumbar region, along the outer surface of the thigh, the anterior outer surface of the leg and in the dorsum of the foot. Often the pain radiates to the thumb. In these same areas there may be sensations of crawling and hypoesthesia. There is weakness in the muscles that extend the big toe. The Achilles reflex is triggered.
S1 root syndrome is characterized by pain along the posterior outer surface of the thigh and lower leg, radiating to the little finger. There is weakness in the muscles that flex the foot. The Achilles reflex is lost.
Most often there is a combined lesion of both roots.
The examination reveals defence of the longitudinal muscles of the back and pain-related scoliosis of the spine. Palpation of the spinous processes of the L4, L5, S1 vertebrae is painful. On palpation, pain is detected at Vallee's points. These are the most superficial locations of the sciatic nerve - along the gluteal fold in the middle of the distance between the greater trochanter and the ischial tuberosity, behind the head of the fibula in the popliteal fossa, behind the medial malleolus.
Symptoms of tension are identified - Lasegue, Neri, Dezherina, a symptom of sitting - the inability to sit up in bed without assistance.
Cervical radiculopathy is characterized by a shooting sensation in the cervical spine. The pain can radiate to the shoulder and head. Movements in the cervical spine become limited. Paresthesia develops in the tips of the fingers. Hypoesthesia in the area of one or another root and muscle hypotonia are detected. The C6-C7 roots are most often affected. Tendon and periosteal reflexes are reduced. The duration of the pain syndrome is 1.5-2 weeks, but it can be longer.
In the cerebrospinal fluid there is protein-cell dissociation (0.4-0.9 g/l).
Flattening on x-ray lumbar lordosis, reducing the height of the disc. Accurate diagnosis using MRI.
Treatment
In the acute stage of the disease, rest and analgesics are prescribed. A bed on a backboard is recommended. Anti-inflammatory, antihistamine, vitamins, diuretics. Snake or bee venom, fastum-gel, finalgon are rubbed in locally. Physiotherapeutic procedures that are effective include DDT, electrophoresis with analgesics, and ultraviolet irradiation. Blockades relieve pain quite quickly - intradermal, subcutaneous, radicular, muscular, epidural with hydrocortisone or novocaine.
Effective in the chronic stage manual therapy, traction, physical therapy, spa treatment. For prolonged pain syndromes, antidepressants and other psychotropic drugs are added. If these measures are ineffective, surgical treatment is performed. An indication for urgent surgery is disc prolapse with the development of pelvic disorders.
Polyneuropathy – these are multiple lesions of the peripheral nerves, manifested by peripheral paralysis, sensory disturbances, trophic and autonomic-vascular disorders, localized mainly in the distal parts of the extremities. True inflammation of peripheral nerves, as a rule, does not occur, but there are metabolic, toxic, ischemic and mechanical factors that lead to changes in the connective tissue interstitium, myelin sheath and axial cylinder. Even with the infectious etiology of polyneuropathy, it is not inflammatory, but neuroallergic processes that predominate.
Etiology
The causes of polyneuropathy are various toxic substances: alcohol, arsenic, lead, mercury, thallium. Drug-induced polyneuropathy develops when taking emetine, bismuth, sulfonamides, isoniazid, imipramine, and antibiotics. Polyneuropathies occur with viral and bacterial infections, with collagenosis, after the administration of serums and vaccines, with vitamin deficiency, malignant neoplasms (cancer, lymphogranulomatosis, leukemia), with diseases of internal organs (liver, kidneys, pancreas), endocrine organs(diabetes, hyper- and hypothyroidism, hypercortisolism), with genetic enzyme defects (porphyria).
Diabetic polyneuropathy
Develops in people suffering diabetes mellitus. It can either be the first manifestation of diabetes or occur in the later stages of the disease. In the pathogenesis of the disease, metabolic and ischemic disorders in the nerve due to micro- and macroangiopathies that accompany diabetes mellitus are of greatest importance.
Among the clinical variants of diabetic polyneuropathy, several forms are distinguished:
Decreased vibration sensitivity and absence of Achilles reflexes, long-term;
Acute or infraspinatus damage to individual nerves: femoral, sciatic, ulnar, radial, median, and from the cranial nerve, oculomotor, trigeminal, abducens. Pain, sensitivity disorders, and muscle paresis predominate.
Severe damage to many nerves of the limbs with severe paresis and sensory disturbances in the legs. The pain is aggravated by exposure to heat and at rest. If the process progresses, then a change in skin color and the appearance of gangrene with mummification are possible.
Treatment
Treating diabetes. Reducing hyperglycemia leads to a decrease in symptoms of neuropathy. Pain is difficult to treat. Rest and non-narcotic analgesics (aspirin) are indicated. It is advisable to use thioctic acid preparations (thioctacid, berlition, alpha-lipoic acid).
Acute inflammatory polyradiculoneuropathy Guillain-Barré
Described by French neurologists Guillén and Barre in 1916. Most often occurs between the ages of 50-74 years. The most likely cause of the disease is a viral infection. In pathogenesis, the filtered virus penetrates the nervous system, damages the myelin sheath of nerve fibers and changes its antigenic properties. At the initial stages of disease development, ATs are produced against the virus itself; subsequently, ATs begin to be produced against altered tissues of the body’s own body, in particular myelin basic protein and other components of the sheath of nerve conductors. Thus, the disease is autoimmune in nature. Morphological changes in peripheral nerves are characterized by inflammatory changes, and even infiltrates can be detected. This is combined with the phenomena of segmental demyelination.
Clinic
The disease begins with general weakness, increased temperature to low-grade levels, pain in the extremities. A distinctive sign is muscle weakness in the legs. Sometimes the pain is girdling in nature. Paresthesia appears in the distal parts of the arms and legs, sometimes in the tongue and around the mouth. Severe sensitivity disorders are not typical for the typical course. Weakness of the facial muscles and damage to other cranial nerves may occur. Involvement of the bulbar group of the cranial nerve in the process often leads to death. Movement disorders most often and first occur in the legs, and then spread to the arms. The nerve trunks are painful on palpation. There may be symptoms of Lasegue, Neri, Bekhterev. Autonomic disorders are pronounced - chilliness, coldness of the distal parts of the arms, acrocyanosis, hyperhidrosis. There may be hyperkeratosis of the soles.
Atypical forms of Guillain-Barré polyradiculoneuritis include:
Pseudomyopathic, when there is damage not to the distal, but to the proximal parts of the limbs.
Pseudotabetic, when there are not motor, but sensory disorders with a predominance of muscle-articular sensation disorder.
Autonomic disorders in the form of heart rhythm disturbances, changes in blood pressure, and tachycardia occur quite often in this pathology.
The classic form develops up to 2-4 weeks, then a stabilization stage begins, and subsequently regression of symptoms. Sometimes it is possible to develop a severe form of Landry's ascending paralysis. In this case, death is possible.
In the cerebrospinal fluid in this disease, protein-cell dissociation is detected. The protein level reaches 3-5 g/l. High protein levels are detected during both lumbar and suboccipital punctures. Cytosis is less than 10 cells in 1 µl.
Treatment
The introduction of GCS into large doses– up to 1000 mg of prednisolone per day parenterally. Antihistamines (suprastin, diphenhydramine), vitamin therapy, proserin are prescribed.
Plasmapheresis started in the first 7 days of the disease is effective. The course includes 3-5 sessions every other day.
Immunoglobulin is used (0.4 g/kg in 1 liter of saline solution for 6-8 hours 5 days).
Maintaining breathing is one of the most important tasks in the treatment of such patients. When vital capacity decreases by 25-30%, tracheal intubation is performed. If the swallowing muscles are affected, parenteral nutrition is administered or through a nasogastric tube.
In immobilized patients, thromboembolism is prevented by administering heparin.
Empty your bowels regularly.
Prevention of contractures includes bed rest acute phase, passive movements already in the first 2-3 days.
The fight against edema includes placing it above the level of the heart, periodically squeezing the swollen limbs 2 times a day, and tightly bandaging the legs.
To reduce pain, non-narcotic analgesics are prescribed.
Brachial plexus lesion
The brachial plexus is formed by the anterior branches of the following spinal nerves: C5, C6, C7, C8, Th1. Branches C5-C6 form the upper primary trunk of the plexus. The branches of C7 form the middle primary trunk. Branches C8, Th1 form the lower primary trunk. Then all the branches intertwine and form secondary trunks: the lateral one of the branches C5, C6, C7 (the musculocutaneous nerve emerges from it). Medial trunk from branches C8, Th1 (the medial cutaneous nerve of the shoulder and forearm, as well as the ulnar nerve emerge from it). The posterior trunk is formed from all branches (the radial and axillary nerves emerge from it).
The brachial plexus provides motor, sensory, autonomic and trophic innervation to the upper limbs.
The plexus is affected by injuries, dislocation of the humerus, knife wounds, during surgical operations with hands clasped behind the head, forceps during childbirth, and cervical ribs.
IN clinical picture There are three options.
Upper Duchenne-Erb palsy. Atrophy and paralysis of the proximal limbs occurs. The deltoid muscle, biceps, internal brachialis, brachioradialis and short supinator muscles are affected. It is impossible to move the arm and bend it at the elbow joint. Pain and paresthesia occur along the outer edge of the shoulder and forearm.
Dejerine-Klumpke palsy is characterized by atrophy of the small muscles of the hand, flexors of the hand and fingers. Movement of the shoulder and forearm is preserved. Hypoesthesia occurs along the inner surface of the forearm and on the hand.
A type of lesion may occur when the entire brachial plexus is affected.
Treatment
B vitamins, anticholinesterase drugs, dibazole, vitamin E are prescribed. Massage, physiotherapy, mud therapy and exercise therapy are of particular importance.
The peripheral nervous system is a topographically conventionally distinguished extracerebral part of the nervous system, including the posterior and anterior roots of the spinal nerves, spinal nodes, cranial and spinal nerves, nerve plexuses and nerves. The function of the peripheral nervous system is to conduct nerve impulses from all extero-, proprio- and interoreceptors into the segmental apparatus of the spinal cord and brain and the removal of regulatory nerve impulses from the central nervous system to organs and tissues. Some structures of the peripheral nervous system contain only efferent fibers, others are afferent. However, most peripheral nerves are mixed and contain motor, sensory and autonomic fibers.
Symptom complexes of damage to the peripheral nervous system are composed of a number of specific signs. Switching off motor fibers (axons) leads to peripheral paralysis innervated muscles. When such fibers are irritated, convulsive contractions of these muscles occur (clonic, tonic convulsions, myokymia), and the mechanical excitability of the muscles increases (which is determined when the hammer hits the muscles).
To establish a topical diagnosis, it is necessary to remember the muscles innervated by a particular nerve and the levels of origin of the motor branches of the nerves. At the same time, many muscles are innervated by two nerves, so even with a complete break of a large nerve trunk, the motor function of individual muscles may suffer only partially. In addition, there is a rich network of anastomoses between the nerves and their individual structure in different parts of the peripheral nervous system is extremely variable - main and loose types according to V. N. Shevkunenko (1936). When assessing movement disorders, it is also necessary to keep in mind the presence of compensatory mechanisms, which compensate and mask true loss of function. However, these compensatory movements are never fully performed to a physiological extent. Typically, compensation is more achievable in the upper extremities.
Sometimes a source of incorrect volume estimation active movement there may be false movements. After contraction of the antagonist muscles and their subsequent relaxation, the limb usually passively returns to its original position. This simulates contractions of a paralyzed muscle. The force of contraction of antagonists in paralyzed muscles can be significant, which underlies muscle contractures. The latter are of other origins. For example, when nerve trunks are compressed by scars or bone fragments, intense pain is observed, the limb takes a “protective” position, in which the intensity of pain decreases. Prolonged fixation of the limb in this position can lead to the development of antalgic contracture. Contracture can also occur with prolonged immobilization of a limb (with injury to bones, muscles, tendons), as well as reflexively with mechanical irritation of a nerve (with an extensive scar-inflammatory process). This is a reflex neurogenic contracture (physiopathic contracture). Psychogenic contractures are sometimes observed. One should also keep in mind the existence of primary muscle contractures in myopathies, chronic myositis and polyneuromyositis (according to the mechanism of autoallergic immunological damage).
Contractures and joint stiffness are a big hindrance in the study of motor disorders of the limb, which depend on damage to the peripheral nerves. In the case of paralysis, due to loss of function of motor nerve fibers, the muscles become hypotonic, and their atrophy soon follows (2 to 3 weeks from the onset of paralysis). Deep and superficial reflexes carried out by the affected nerve are reduced or lost.
A valuable sign of damage to the nerve trunks is a sensitivity disorder in certain areas. Typically this area is smaller than the anatomical branching area of the cutaneous nerves. This is explained by the fact that individual areas of the skin receive additional innervation from neighboring nerves (“overlap zones”). Therefore, three zones of sensitivity impairment are distinguished. The central, autonomous zone corresponds to the area of innervation of the nerve under study. With complete disruption of nerve conduction in this area, loss of all types of sensitivity is noted. The mixed zone is supplied by both the affected and partly neighboring nerves. In this zone, sensitivity is usually only reduced or distorted. Pain sensitivity is best preserved, tactile and complex species sensitivity (localization of irritations, etc.), the ability to roughly distinguish temperatures is impaired. The accessory zone is predominantly supplied by the adjacent nerve and least of all by the affected nerve. Sensory disorders are usually not found in this zone.
The boundaries of sensory impairment vary widely and depend on variations in the “overlap” of neighboring nerves.
When sensory fibers are irritated, pain and paresthesia occur. Often, with partial damage to the sensory branches of the nerves, perception has inadequate intensity and is accompanied by extreme an unpleasant feeling(hyperpathy). Characteristic of hyperpathy is an increase in the threshold of excitability: fine differentiation of weak irritations disappears, there is no sensation of warm or cool, light tactile irritations are not perceived, there is a long latent period of perception of irritations. Painful sensations acquire an explosive, sharp character with an intense feeling of unpleasantness and a tendency to irradiate. An aftereffect is observed: pain continues for a long time after the irritation stops.
Phenomena of nerve irritation can also include a pain phenomenon such as causalgia (Pirogov-Mitchell syndrome) - burning intense pain against the background of hyperpathy and vasomotor-trophic disorders (hyperemia, marbling skin, expansion of the capillary network of blood vessels, swelling, hyperhidrosis, etc.). With causalgic syndrome, a combination of pain and anesthesia is possible. This indicates a complete break of the nerve and irritation of its central segment with a scar, hematoma, inflammatory infiltrate, or the development of a neuroma - phantom pain appears. In this case, the symptom of tapping (such as the Tinel phenomenon when tapping along the median nerve) has diagnostic value.
When nerve trunks are damaged, vegetative-trophic and vasomotor disorders appear in the form of changes in skin color (pallor, cyanosis, hyperemia, marbling), pastiness, a decrease or increase in skin temperature (this is confirmed by thermal imaging), impaired sweating, etc.
