Treatment of neuropathy of the peroneal nerve. Inflammation of the tibial nerve: the clinical picture of neuropathy

The tibial nerve (n. tibialis) is formed by the fibers of the LIV-SIII spinal roots. In the distal part of the popliteal fossa, the medial cutaneous nerve of the leg departs from the tibial nerve. It passes between the two heads of the gastrocnemius muscle and perforates the deep fascia in the middle third of the posterior surface of the lower leg. At the border of the posterior and lower thirds of the lower leg, the lateral cutaneous branch of the common peroneal nerve joins this nerve, and from this level it is called the sural nerve (n. Suralis).

Further, the nerve passes along the Achilles tendon, giving a branch to the posterior surface of the lower third of the leg. At the level of the ankle joint, it is located behind the tendons of the peroneal muscles and gives here the external calcaneal branches to the ankle joint and heel. On the foot, the sural nerve is located superficially. It gives branches to the ankle and tarsal joints and supplies the skin of the outer edge of the foot and fifth finger to the level of the terminal interphalangeal articulation. In the foot, the sural nerve also communicates with the superficial peroneal nerve. The area of ​​innervation of the gastrocnemius depends on the diameter of this anastomosis. It can include a significant part of the rear of the foot and even adjacent surfaces of the III and IV interdigital spaces.

Symptoms of damage to the sural nerve are manifested in the form of pain, paresthesia and a feeling of numbness and hypesthesia or anesthesia in the region of the outer edge of the foot and fifth toe. There is pain on palpation corresponding to the place of nerve compression (behind and below the outer ankle or on the outer part of the heel, at the outer edge of the foot). Finger pressure at this level causes or exacerbates pain at the outer edge of the foot.

The initial sections of the tibial nerve supply the following muscles: the triceps muscle of the lower leg, the long flexor of the fingers, plantar, popliteal, posterior tibial flexor longus thumb and etc.

The triceps muscle of the lower leg is formed by the gastrocnemius and soleus muscles. The gastrocnemius muscle flexes the lower limb at the knee and ankle joints.

Tests to determine the strength of the calf muscle:

1. the subject, who is in a supine position with a straightened lower limb, is asked to bend it at the ankle joint; the examiner resists this movement and palpates the contracted muscle;
2. the subject, who is in the prone position, is offered to bend the lower limb at the knee joint at an angle of 15 °; the examiner resists this movement.

The soleus muscle flexes the lower limb at the ankle joint.

Test to determine the strength of the soleus muscle: the subject, who is in the prone position with the lower limb bent at an angle of 90 ° at the knee joint, is asked to bend it at the ankle joint; the examiner resists this movement and palpates the contracted muscle and tendon.

The plantar muscle, with its tendon, is woven into the medial part of the Achilles tendon and is involved in flexion at the ankle joint.

The popliteal muscle is involved in flexion at the knee joint and rotation of the lower leg inward.

The tibialis posterior muscle adducts and elevates the inner edge of the foot (supinates) and promotes flexion at the ankle joint.

Test to determine the strength of the posterior tibial muscle: the subject is in a supine position with a straightened lower limb, flexes it at the ankle joint and simultaneously adducts and raises the inner edge of the foot; the examiner resists this movement and palpates the contracted muscle and tense tendon.

The long flexor of the fingers bends the nail phalanxes of the II - V fingers of the foot.

Test to determine the strength of the long flexor of the fingers: the subject in the supine position is asked to bend the distal phalanxes of the II - V toes in the joint; the examiner prevents this movement and holds the proximal phalanges extended with the other hand. The long flexor of the thumb flexes the first toe; its function is verified in a similar way.

From the tibial nerve, slightly above the medial malleolus, the internal calcaneal skin branches depart, which innervate the skin of the posterior calcaneal region and the posterior hour-pi sole. At the level of the ankle joint, the main trunk of the tibial nerve passes in a rigid osteofibrous tunnel - the tarsal canal. This canal goes obliquely down and forward, communicating the area of ​​the ankle joint with the sole, and is divided into 2 floors: the upper one is the ankle and the lower one is the submalleolar. The upper floor is limited from the outside by the osteoarticular wall. From the inside, the upper floor is limited by the internal annular ligament, which is formed from the superficial and deep aponeurosis of the lower leg. The lower floor is limited to the outside inner surface calcaneus, from the inside - by the adductor muscle of the thumb, enclosed in a duplication of the internal annular ligament. The tarsal canal has two openings: superior and inferior. The tendons of the posterior tibial muscle, the long flexor of the fingers and the long flexor of the thumb, as well as the posterior tibial neurovascular bundle pass through the canal. It is in a fibrous sheath and includes the tibial nerve and the posterior tibial artery with satellite veins. In the upper floor of the tarsal canal, the neurovascular bundle passes between the tendons of the long flexor of the thumb. The nerve is located outside and behind the artery and is projected at an equal distance from the calcaneal tendon to the posterior edge of the medial malleolus. In the lower floor of the canal, the neurovascular bundle is adjacent to the posterior surface of the tendon of the long flexor of the thumb. Here the tibial nerve divides into terminal branches - the internal and external plantar nerves. The first of them innervates the skin of the plantar surface of the inner part of the foot and all phalanges of the fingers, dorsal surface the terminal phalanges of the I - III and the inner half of the IV finger, as well as the short flexors of the fingers, which bend the middle phalanges of the II - V fingers, the short flexor of the thumb, the muscle that removes the big toe, and I and II worm-like muscles. The external plantar nerve supplies the skin of the outer part of the plantar surface of the foot, the plantar surface of all phalanges of the fingers and the back surface of the terminal phalanges of the V and the outer half of the IV finger. Motor fibers innervate the square muscle of the sole; flexion is facilitated by I-IV interosseous and II-IV worm-like muscles, the muscle that removes the little toe of the foot, and, in part, the short flexor of the little toe of the foot. The skin of the heel region is innervated by the internal calcaneal nerve, which arises from the common trunk of the tibial nerve just above the tarsal canal.

With damage to the common trunk of the tibial nerve in the popliteal fossa, muscle paralysis develops and the ability to flex the lower limb in the ankle joint, in the joints of the distal phalanges of the toes, middle phalanges of II - V fingers and proximal phalanx I toe. Due to the antagonistic contraction of the extensors of the foot and fingers, innervated by the peroneal nerve, the foot is in the position of extension (dorsal flexion); develops the so-called heel foot(pes calcaneus). When walking, the patient leans on the heel, lifting on the toe is impossible. Atrophy of the interosseous and worm-like muscles leads to a claw-like position of the toes (the main phalanges are unbent at the joints, and the middle and end phalanges are bent). Abduction and adduction of fingers are impossible.

With damage to the tibial nerve below the origin of the branches to calf muscles and long flexors of the fingers, only the small muscles of the plantar part of the foot are paralyzed.

For topical diagnosis of the level of damage to this nerve, the zone of sensitivity impairment is important. Sensory branches sequentially depart to innervate the skin on the posterior surface of the lower leg (medial cutaneous nerve of the calf - in the popliteal fossa), the outer surface of the heel (medial and lateral calcaneal branches - in the lower third of the lower leg and at the level of the ankle joint), on the outer edge of the foot (lateral dorsal cutaneous nerve), on the plantar surface of the foot and fingers (I - V common plantar digital nerves).

With damage to the tibial nerve at the level of the ankle joint and below, sensory disorders are localized only on the sole.

In the case of partial damage to the tibial nerve and its branches, a causalgic syndrome often occurs. Excruciating pains extend from the back of the leg to the middle of the sole. Extremely painful touch in the plantar side of the foot, which interferes with walking. The patient leans only on the outer edge of the foot and on the fingers, limping when walking. Pain can radiate throughout the lower limb and sharply intensify with a light touch on any part of the skin on this limb. Patients cannot walk even with crutches.

Often pains are combined with vasomotor, secretory and trophic disorders. Atrophy of the muscles of the back of the leg and interosseous muscles develops, as a result of which metatarsal bones clearly protrude on the back of the foot. Achilles and plantar reflexes decrease or disappear.

With damage to the terminal branches of the tibial nerve, reflex contracture is sometimes observed in the affected limb with edema, skin hyperesthesia and osteoporosis of the foot bones.

Most often, the tibial nerve is affected in the zone of the tarsal canal by the mechanism of the tunnel (compression-ischemic) syndrome.

With tarsal tunnel syndrome, pain comes to the fore. Most often they are felt in the back of the lower leg, often in the plantar part of the foot and toes, rarely radiate to the thigh. There are paresthesias along the plantar surface of the foot and toes. Here, a feeling of numbness often occurs and a decrease in sensitivity is detected within the zone of innervation of the external and / or internal plantar nerve, and sometimes in the area supplied by the calcaneal nerve. Less often than sensory disorders, motor disorders occur - paresis of the small muscles of the foot. At the same time, flexion and spreading of the fingers is difficult, and in advanced cases, due to atrophy of the muscles of the foot, it takes the form of a clawed paw. The skin becomes dry and thinner. In tarsal tunnel syndrome, light percussion or finger pressure between the medial malleolus and the Achilles tendon causes paresthesia and pain in the plantar region of the foot, which may be felt in the posterior calf. Painful sensations are also provoked during pronation and simultaneously formed extension of the foot, as well as during forced plantar flexion of the first finger against the action of the resistance force.

With this tunnel syndrome, sensitive disorders in the heel region rarely occur. Weak flexion of the lower leg and foot, as well as hypoesthesia along the posterior outer surface of the lower leg are signs of damage to the tibial nerve above the level of the tarsal canal

One of the mononeuropathies lower extremities, accompanied by dangling foot syndrome - the impossibility of dorsiflexion of the foot and extension of its fingers, as well as sensory disorders of the skin of the anterolateral region of the leg and rear of the foot. The diagnosis is made on the basis of anamnesis, neurological examination, electromyography or electroneurography data. Additionally, an ultrasound of the nerve and a study of the osteoarticular apparatus of the lower leg and foot are performed. Conservative treatment is carried out by a combination of medical, physiotherapeutic and orthopedic methods. If it fails, an operation is indicated (decompression, nerve suture, tendon transposition, etc.).

General information

Neuropathy of the peroneal nerve, or peroneal neuropathy, occupies a special position among peripheral mononeuropathies, which also include: neuropathy of the tibial nerve, neuropathy of the femoral nerve, neuropathy of the sciatic nerve, etc. Since the peroneal nerve consists of thick nerve fibers, having a larger layer of the myelin sheath, it is more susceptible to damage in metabolic disorders and anoxia. This moment probably determines the rather widespread prevalence of peroneal neuropathy. According to some data, neuropathy of the peroneal nerve is observed in 60% of patients in traumatology departments who underwent surgery and are treated with splints or plaster casts. Only in 30% of cases, neuropathy in such patients is associated with primary nerve damage.

It should also be noted that often specialists in the field of neurology have to deal with patients who have a certain amount of experience in the existence of peroneal neuropathy, including postoperative period or immobilization time. This complicates the treatment, increases its duration and worsens the result, since the earlier the therapy is started, the more effective it is.

Anatomy of the peroneal nerve

The peroneal nerve (n. peroneus) departs from sciatic nerve at the level of the lower 1/3 of the thigh. It consists predominantly of fibers LIV-LV and SI-SII of the spinal nerves. After passing through the popliteal fossa, the peroneal nerve exits to the head of the same-named bone, where its common trunk divides into deep and superficial branches. The deep peroneal nerve passes into the anterior part of the lower leg, descends, passes to the rear of the foot and is divided into internal and outer branch. It innervates the muscles responsible for extension (dorsal flexion) of the foot and fingers, pronation (raising the outer edge) of the foot.

The superficial peroneal nerve runs along the anterolateral surface of the lower leg, where it gives off a motor branch to the peroneal muscles responsible for pronation of the foot with its simultaneous plantar flexion. In the region of the medial 1/3 of the lower leg, the superficial branch of n. peroneus passes under the skin and is divided into 2 dorsal cutaneous nerves - intermediate and medial. The first innervates the skin of the lower 1/3 of the lower leg, the dorsum of the foot and III-IV, IV-V interdigital spaces. The second is responsible for the sensitivity of the medial edge of the foot, the rear of the first toe and II-III interdigital space.

Anatomically determined areas of the greatest vulnerability of the peroneal nerve are: the place of its passage in the region of the head of the fibula and the place where the nerve exits to the foot.

Causes of neuropathy of the peroneal nerve

There are several groups of triggers that can initiate the development of peroneal neuropathy: nerve injury; compression of the nerve by the surrounding musculoskeletal structures; vascular disorders leading to nerve ischemia; infectious and toxic lesions. Neuropathy of the peroneal nerve of traumatic origin is possible with knee bruises and other injuries knee joint, fracture of the lower leg, isolated fracture of the fibula, dislocation, injury to the tendons or sprain of the ankle joint, iatrogenic nerve injury during repositioning of the bones of the lower leg, operations on the knee joint or ankle.

Compressive neuropathy (so-called tunnel syndrome) n. peroneus most often develops at the level of its passage at the head of the fibula - superior tunnel syndrome. May be related to professional activity, for example, among berry pickers, parquet flooring and other people whose work involves a long stay "squatting". Such neuropathy is possible after prolonged sitting, cross-legged. With compression of the peroneal nerve at the site of its exit to the foot, inferior tunnel syndrome develops. It can be caused by wearing overly tight shoes. Often, compression of the nerve during immobilization is the cause of peroneal neuropathy of a compression nature. In addition, compression n. peroneus may have a secondary vertebrogenic character, i.e., develop in connection with changes in the musculoskeletal system and reflex muscular-tonic disorders caused by diseases and curvature of the spine (osteochondrosis, scoliosis, spondylarthrosis). Iatrogenic compression-ischemic neuropathy of the peroneal nerve is possible after its compression due to wrong position legs during various surgical interventions.

Rarer causes of peroneal neuropathy include systemic diseases accompanied by proliferation connective tissue(deforming osteoarthritis, scleroderma, gout, rheumatoid arthritis, polymyositis), metabolic disorders (dysproteinemia, diabetes mellitus), severe infections, intoxications (including alcoholism, drug addiction), local tumor processes.

Symptoms of neuropathy of the peroneal nerve

Clinical manifestations of peroneal neuropathy are determined by the type and topic of the lesion. Acute nerve injury is accompanied by a sharp almost simultaneous appearance of symptoms of its defeat. chronic injury, dysmetabolic and compression-ischemic disorders are characterized by a gradual increase in the clinic.

Damage to the common trunk of the peroneal nerve is manifested by a disorder in the extension of the foot and its fingers. As a result, the foot hangs down in plantar flexion and is slightly internally rotated. Because of this, when walking, moving the leg forward, the patient is forced to strongly bend it at the knee joint so as not to hook the toe on the floor. When lowering the leg to the floor, the patient first stands on the fingers, then leans on the lateral plantar edge, and then lowers the heel. Such a gait resembles a cock or horse and bears the appropriate names. Difficult or impossible: raising the lateral edge of the sole, standing on the heels and walking on them. Movement disorders combined with sensory disorders extending to the anterolateral surface of the lower leg and the rear of the foot. Possible pain on the outer surface of the lower leg and foot, increasing with squats. Over time, atrophy of the muscles of the anterolateral region of the leg occurs, which is clearly visible when compared with a healthy leg.

Neuropathy of the peroneal nerve with involvement of the deep branch is manifested by less pronounced drooping of the foot, decreased force of extension of the foot and toes, sensory disturbances on the dorsum of the foot and in the 1st interdigital space. The prolonged course of neuropathy is accompanied by atrophy of the small muscles on the back of the foot, which is manifested by the retraction of the interosseous spaces.

Peroneal neuropathy with lesions of the superficial branch is characterized by impaired sensory perception and pain on the lateral surface of the lower leg and the medial region of the dorsum of the foot. On examination, a weakening of the pronation of the foot is found. The extension of the fingers and foot is preserved.

Diagnosis of neuropathy of the peroneal nerve

The algorithm for diagnosing peroneal neuropathy is based on the collection of anamnestic data that may indicate the genesis of the disease, and a thorough study of the motor function and sensory sphere of the peripheral nerves of the affected limb. Special functional tests are carried out to assess the muscle strength of various muscles of the lower leg and foot. Surface sensitivity analysis is carried out using a special needle. Additionally, electromyography and electroneurography are used, which allow to determine the level of nerve damage by the speed of action potentials. Recently, nerve ultrasound has been used to study the structure of the nerve trunk and the structures located next to it.

In case of traumatic neuropathy, consultation with a traumatologist is required, according to indications - ultrasound or

Pain in the lower leg, heel and foot can be triggered by damage to the nerve fiber. Neuropathy of the tibial nerve is a common pathology, since the place of bifurcation (separation) of the sciatic nerve into the tibial and peroneal branches is not protected from negative effects except for the skin and other soft tissues. In some cases, tibial neuropathy is associated with lesions radicular nerves at the level of the lumbosacral spine. Also, such a disease can be triggered by piriformis syndrome, sciatic nerve compression and other similar pathologies.

To know detailed information about the symptoms and treatment of inflammation of the tibial nerve can be on this page - here are the main causes, Clinical signs methods of diagnosis and treatment of such diseases.

The tibial nerve (n. Tibialis) can undergo traumatic, degenerative, dystrophic, dysmetabolic, compression and inflammatory negative impact. As a result of damage to the nerve fiber, neuropathy develops - the inability to fully conduct nerve impulses and signals. As a result, secondary dystrophic processes begin in muscle tissue lower leg, vascular bed, skin.

The functional performance of the muscles of the lower leg and foot is disturbed, the internal and external arch can be flattened, which leads to the development of flat feet or clubfoot. Hypesthesia of individual areas of the leg gradually develops, the ability to bend the foot is impaired. With serious vegetative dystrophic lesions, severe pains appear in the toes, blood circulation is disturbed, trophic ulcers develop, which are difficult to sanitize and heal.

Diagnosis of the disease begins with an examination by an experienced neurologist. The doctor, when conducting special diagnostic tests, will be able to make a preliminary diagnosis. In the future, to confirm it, electromyography, electroneurography, ultrasound, X-ray of the lower leg and knee joint, CT and MRI examinations are prescribed.

In Moscow, you can sign up for a free appointment with a neurologist at our clinic manual therapy. During the appointment, the doctor will conduct an examination and diagnostic tests, make a preliminary diagnosis and recommend necessary examinations. Then, the field for clarifying the diagnosis will be developed individual course treatment. At an early stage, the disease is perfectly treatable with the help of manual therapy methods. On the late stages required in most cases surgery to restore the function of the tibial nerve.

Do not run your condition to an extreme stage, seek medical help in a timely manner.

What is tibial neuropathy?

To begin with, let's deal with the terms - what is tibial nerve neuropathy and how it develops. So, this disease belongs to the group of single neuropathies (affects only one nerve). It is very rarely bilateral, only in the case of an equivalent traumatic effect on the bifurcation point of the sciatic nerve in the popliteal fossa.

Often this disease develops at a young age in people leading active image life and involved in sports, including playing sports and weightlifting. Regular physical overload and the influence of stress factors lead to the fact that the trophism of this nerve is disturbed and the corresponding symptoms of its damage appear.

Anatomically, the tibial nerve is a kind of continuation of the sciatic nerve, which in the popliteal fossa is divided into two branches that innervate the tissues of the lower leg, ankle joint, foot and her fingers.

After separation, the branches pass along with large arteries between the muscles of the lower leg and go to the foot, then, having passed through the ankle joint, they break up into even smaller branches and innervate different parts of the foot. Therefore, with simultaneous damage to several structural parts of the foot, the doctor will always suspect damage to the tibial nerve at a higher level (in the region of the popliteal fossa or lower leg).

Neuropathy of the tibial nerve is a partial or complete loss of their functional abilities, which led to dysfunction of the muscles, skin, vascular wall etc.

Causes of tibial nerve injury

Most often, damage to the tibial nerve is traumatic or compressive in nature. This is facilitated by wearing tight clothing and shoes with high tops, the use of socks and golf with tight elastic bands, the habit of sitting with one leg crossed over the other. Other types of traumatic injury include fractures and cracks. tibia, dislocations of the knee and ankle joints, gunshot and knife wounds, torn ligaments, tendons, muscles and their fascia.

Other causes of damage to the tibial nerve include the following conditions:

• valgus and varus deformity of the foot and deviation of the thumb from the axis of the normal position when walking;
• different types of flat feet and clubfoot, which have Negative influence on the state muscle fiber shins;
• deforming osteoarthritis of the knee, hip or ankle joint;
• rheumatoid arthritis lower limbs;
• articular form of ankylosing spondylitis or gout;
• tumor neoplasms in the area of ​​passage of this nerve;
• the spread of syphilis, tuberculosis, poliomyelitis and other dangerous infections along the nerve fiber;
• diseases endocrine system such as diabetes mellitus, hypo- and hyperthyroidism, amyloidosis, etc.;
• tarsal syndrome associated with compression of the tibial nerve in the canal of the same name;
• tendovaginitis, hematomas, neurodystrophic processes;
• piriformis syndrome and other types of sciatic nerve compression;
• cauda equina syndrome;
• consequences of osteochondrosis of the lumbosacral spine and its complications, such as intervertebral protrusion and disc herniation.

The exclusion of all probable causes of the development of the disease is the most important stage in its treatment. Therefore, during the initial examination, the doctor collects anamnesis data that helps to identify and eliminate the potential cause of nephropathy.

Neuritis or inflammation of the tibial nerve (symptoms)

In the acute phase, tibial neuritis can present with several clinical syndromes. The most important of the symptoms of inflammation of the tibial nerve is pain, burning, sharp character. It appears suddenly and does not go away after changing the position of the leg. External clinical symptoms of tibial neuritis can manifest as hyperemia and slight swelling of the subcutaneous fatty tissue. Although this is not a mandatory clinical sign.

With chronic inflammation of the tibial nerve, the flexion of the foot is disturbed with its lowering down. In the future, there is a violation in the flexion of the toes. Any attempt to stand on toes ends in complete failure. If you observe the patient's gait, it will be seen that the emphasis when placing the foot is on the heel, without the typical rolling from the base of the foot.

If not carried out timely treatment, then begins atrophy of the muscular apparatus of the foot and lower leg. The foot takes on a characteristic appearance, more reminiscent of a clawed paw. Tendon reflexes in the ankle area fade away.

During the examination, the neurologist notes a significant decrease in pain sensitivity in the back of the leg and along the plantar surface of the foot. First three toes go numb. The activity of the pulse wave on the inner fold of the foot decreases. Gradually formed vascular insufficiency leading to the development of long-term non-healing trophic ulcers shins and feet.

Symptoms of a degenerative lesion of the tibial nerve

Degenerative tibial nerve disease occurs in patients with severe physical labor with prolonged standing. Significant physical activity leads to the fact that the process of impaired blood supply to the nerve fiber begins. Constant muscle spasms provoke a narrowing of the bloodstream of the capillary network. Secondary trophic neuropathy of the tibial nerve develops, the symptoms of this disease are mostly similar to neuritis.

But there are also a number of differences. For example, symptoms of a tibial nerve lesion do not include flushing of the skin and swelling. On palpation, there is a slight decrease in skin sensitivity. Flying paresthesias may appear, but they never affect the anterior surface of the lower leg.

With degeneration, dystrophy and atrophy develop very quickly. This means that numbness, loss of sensitivity and functionality of the muscles of the lower leg and arches of the foot prevail over the pain syndrome. It can be quite weak and quickly passing. Therefore, patients do not seek medical help in a timely manner, because initial stages the disease does not prevent them from living and working.

Pinching and paresis of the tibial nerve

Another type of lesion is a pinched tibial nerve, which can be traumatic, tumor, degenerative in nature. Often this disease is provoked by various neoplasms located in the soft tissues of the lower leg next to the passing nerve fiber. As they grow, they compress the nerve, provoking its dysfunction.

Complete paresis of the tibial nerve can develop with various pathogenic factors. First of all, this is the compression of its fiber by hematomas and overdeveloped muscles. With tarsal syndrome, nerve paresis occurs after 2 to 3 weeks. At the same time, the patient notes that he cannot bend the foot and fingers, skin and muscle sensitivity is completely lost.

With proper treatment, it is possible to restore all functions only in the early stages of the development of the pathological process. Therefore, when the appearance pain in the back of the lower leg and on the sole, immediately contact a neurologist for an appointment.

Treatment of tibial nerve nephropathy.

With inflammation of the tibial nerve, treatment begins with the elimination of the potential cause of the development of the disease. If this pressure is from a hematoma or tumor, then surgical intervention is necessary to eliminate them. When identified concomitant disease of the musculoskeletal system, it is necessary to simultaneously begin its therapy.

Conservative treatment of neuropathy of the tibial nerve is that it is necessary to restore it functional ability. Of the methods of manual therapy in the treatment of tibial nerve neuropathy, a combination of reflexology (acupuncture) and osteopathy is most often used. If necessary, the doctor develops an additional course therapeutic gymnastics and combines it with massage sessions.

With a traumatic lesion of the tibial nerve, treatment should include anti-edema agents and hematomas for resorption, and the use of physiotherapy, massage and osteopathy is shown to improve tissue trophism.

Treatment of tibial neuritis requires individual approach. The doctor develops a course of treatment for the tibial nerve, depending on the established type of its lesion, the general condition of the patient, and the presence of concomitant pathologies.

If you need treatment for your tibial nerve, you can book a free appointment with a neurologist at our Chiropractic Clinic. The initial consultation for all patients is free of charge. In the course of it, you will learn about whether there is a prospect of using manual therapy methods in your individual case of the disease.

2. Neuropathy of the peroneal and tibial nerves. Clinic, diagnosis, treatment.

Tibial neuropathy: 1)lesion at the level of the popliteal fossa, high - damage to all nerves: violation of flexion of the foot and fingers, rotation of the foot inward, spreading and adduction of the fingers, impaired sensitivity along the back of the leg, sole, plantar surface of the fingers, dorsal surface of the distal phalanges, articular-muscular feeling is usually preserved Atrophy of the posterior muscle group of the leg, and feet (deepened arch of the foot, retraction of the intermetatarsal spaces). The foot is in the extension position, the fingers take a clawed position, the “heel foot” is formed. The gait is difficult, support on the heel, they cannot stand on their toes. Achilles and plantar reflexes are lost. Pronounced vegetative-vascular changes, there may be a causalgic syndrome. 2 ) below the origin of the branches to the calf muscles and long flexors of the fingers (at the level of the popliteal fossa, the internal cutaneous nerve of the shin departs, which forms the sural nerve in the lower third of the shin together with a branch of the peroneal nerve) - only the small muscles of the foot, sensitive disorders on the foot will be paralyzed. 3 ) lesion at the level of the ankle joint (s-m of the tarsal canal) - Nerve compression occurs in the osteofibrous tarsal (tarsal) canal, the walls of which are formed in front by the medial malleolus, on the outside by the calcaneus, and the inner fibrous plate of the tendon retinaculum. The tarsal canal is located behind and distal to the medial malleolus. Compression of the nerve in the canal may be due to swelling of its contents or hematoma in it in case of an ankle joint injury. In some cases, the cause is unclear (idiopathic tarsal syndrome). Leading symptom - pain, paresthesia, numbness in the plantar surface of the foot and fingers that occurs while walking, radiates from the foot along the sciatic nerve to the gluteal region. Weakness of the toes, paresis of small muscles with the formation of a "clawed paw", decreased sensitivity on the plantar surface of the foot. and paresthesia in the sole. Pronation of the foot, coupled with the extensor in the ankle joint, increases pain due to tension in the flexor tendon retinaculum and flattening of the tarsal canal, supination of the foot and flexion in the ankle joint reduce pain.

4) on the foot, under the deep transverse metatarsal ligament (Morton's neuralgia) - compression and neuropathy of the common plantar digital nerves : foot deformity (wearing tight shoes with high heels, prolonged squatting). Burning paroxysmal pain in the area of ​​the plantar surface of the metatarsal bones, hypoesthesia in the distal phalanges, first while walking, later spontaneously, often at night.

For differentiation with radicular - vertebrogenic syndromes, the nature of the spread of pain, zones of sensitivity disorders. Keep in mind that simultaneous compression of the root and the nerve trunk is possible (double axoplasmic compression syndrome)

Neuropathy of the peroneal nerve 1) upper tunnel syndrome lesion common peroneal nerve (in the popliteal fossa, near the head of the fibula before dividing into superficial and deep) the extension of the foot and fingers (hanging foot), abduction and rotation of the foot is limited. The foot sags and is turned inward, the fingers are bent at the metacarpophalangeal joints - "horse foot", cock's gait, muscle atrophy along the anterior-outer surface of the lower leg. Violation of sensitivity on the lateral surface of the lower leg and on the back of the foot. The cause of the lesion is most often compression at the level of the head and neck of the fibula in case of an ankle joint injury with the foot turning inward and bending it, compression with a plaster cast, prolonged stay in a certain position - squatting, cross-legged, during deep sleep, anesthesia, coma . Predisposes to nerve compression rapid decline body weight. The nerve may be affected by ischemia, diabetes, be subjected to compression by a ganglion or cyst in the area of ​​the knee joint, lipoma, tumor of the fibula, as well as in the syndrome of the anterior muscle bed of the lower leg, requiring immediate surgical treatment.2) superficial peroneal nerve injury - violation of rotation and abduction of the foot, sensitivity - on the back of the foot, except for 1 interdigital space. 3) damage to the deep peroneal nerve in the area of ​​the ankle joint, inferior tunnel syndrome, anterior tarsal syndrome due to plaster cast, tight shoes, direct trauma. Difficulty in extension of the foot and fingers, supination of the foot, impaired sensitivity in 1 interdigital space, pain and paresthesia in 1-2 fingers.

EMG, radiography.

Treatment: fixation of the foot, prevention of contractures - active and passive movements, electrical stimulation, massage, physical therapy, exercise therapy. drug therapy (vasodilators and decongestants, vit group B, anticholinesterase drugs). In the absence of signs of recovery within 2-3 months after the injury, an increase in sensorimotor disorders is indicated for surgical treatment.

3. Transient disorders of the brain blood circulation - is a clinical syndrome characterized by the sudden onset of focal and/or cerebral symptoms due to an acute disorder of the brain blood flow with complete restoration of functions within 24 hours.

PMI account for 10-15% of all cases of stroke.

Hypertensive cerebral crisis(HCC) is defined as a condition associated with an acute, usually significant rise in blood pressure and is accompanied by the appearance cerebral symptoms in the absence of focal.

Transient neurological disorders with focal symptoms, developed as a result of short-term local ischemia of the brain, are designated as transient ischemic attacks (TIA).

HCC. A special form, the most severe form of HCC, is acute hypertensive encephalopathy - a peculiar form of damage to the nervous system in arterial hypertension of any etiology, caused by acutely developing cerebral edema. In the domestic literature, such a condition is referred to as a severe cerebral hypertensive crisis and refers to transient disorders of cerebral circulation. Main pathogenetic OGE factor- a significant increase in blood pressure (250-300 / 130-170 mm Hg). In this case, due to the disruption of the reaction of autoregulation of cerebral blood flow, the BBB is disturbed and, against the background of an increase in intravascular hydrodynamic pressure, filtration of the protein-rich plasma component into the brain tissue (vasogenic cerebral edema) occurs. Microcirculation is disturbed - worsening rheological properties due to a decrease in the plasma component and deformability of erythrocytes, an increase in platelet aggregation activity, compression of sections of the microvasculature by edematous brain tissue, which causes a reduction in local blood flow. These dysgemic disorders lead to the occurrence of areas of circulatory hypoxia of the brain and ischemia. In severe cerebral hypertensive crisis, structural disorders of the state of the vascular wall of intracerebral arterioles develop (plasmorrhagia, fibrinoid necrosis with the formation of miliary aneurysms, parietal, obstructive thrombi).

Criteria for the diagnosis of acute hypertensive encephalopathy: 1. Key clinical criteria: - increasing headache with nausea and vomiting (shell symptoms); change in consciousness, including a decrease in the level of wakefulness; - convulsive syndrome; visual disorders (photopsias, scotomas, decreased visual acuity, etc.) associated with an increase in blood pressure and rapidly regressing against a background of a decrease in blood pressure. 2. An ophthalmoscopic examination may reveal congestive changes in the optic disc with retinopathy. 3. On CT and MRI (T2 mode) - symmetrical multiple small-focal changes or confluent hypodense ischemia fields in the subcortical white matter of the parietal-occipital, occipital localization. OGE therapy: hospitalization in ICU. a) emergency decrease in blood pressure(initial decrease in blood pressure within a few minutes to 1 hour by 20% of the initial level, which does not go beyond the autoregulation of cerebral blood flow), subsequently - to blood pressure values ​​10-15% higher than the usual figures. In the absence of anamnestic data, one should be guided by a blood pressure level of 160/100 mm Hg. Means of choice - ACE inhibitors (captopril, enalapril), calcium antagonists (nifedipine), peripheral vasodilators (sodium nitroprusside). The appointment of antihypertensive drugs of central action (clonidine), ganglioblockers (pentamine, arfonad) is not excluded. With pheochromocytoma - phentolamine. The choice of these drugs is due to the rapidly onset hypotensive effect and special pharmacological properties. ACE inhibitors - optimize the tone of cerebral vessels, restore their reactivity in conditions of vasoparesis in case of disruption of autoregulatory mechanisms. Calcium antagonists prevent the reduction of cerebral blood flow due to a direct effect on the vascular wall. Peripheral vasodilators in some cases can impair venous outflow and increase cerebrospinal fluid pressure (but quickly reduce blood pressure, which is the basis of therapeutic tactics and prevails over unwanted effects. b) fight against cerebral edema(drug of choice - saluretics); in) anticonvulsant therapy; G) symptomatic treatment: maintenance of homeostasis, neuroprotection, correction of disturbed hemorheological and hemostatic parameters.

Confirmation of OGE is a rapid regression of symptoms in response to antihypertensive and decongestant therapy. If treatment is started late, then ischemic or hemorrhagic stroke may develop.

TIA in most cases is associated with cardiogenic or arterio-arterial embolism (embolic TIA), less often due to hemodynamic insufficiency (hemodynamic TIA, steal syndrome), thrombus formation, obliteration of large main vessels, vasculitis or coagulopathy. Hemodynamic TIAs occur with a decrease in blood pressure, physical activity, straining, eating, while focal neurological symptoms often appear against the background of a pre-syncope state, sometimes several times a day. The duration of focal neurological symptoms in TIA is most often 5-20 minutes, but not more than a day and ends with a complete restoration of impaired functions. Clinical significance of TIA is that they serve as a harbinger not only of stroke, but also of myocardial infarction and represent danger signals that require the doctor to take prompt diagnostic and therapeutic actions aimed at reducing the risk of these diseases.The manifestations of TIA depend on the localization of the pathological process (basin).

PNMK in the basin of the carotid arteries: hemiparesis, hemihypesthesia, aphasia and apraxia (with damage to the dominant hemisphere), confusion and ignorance of the opposite half of the space (with damage to the non-dominant hemisphere), blindness or visual impairment in one eye, paresis of the lower half of the face, etc. PNMK in the pool of vertebral arteries: dizziness, nausea, vomiting, double vision, dysarthria, dysphagia, ataxia, tetraparesis, paresis of the entire half of the face, numbness around the mouth, hearing loss, cortical blindness, global amnesia, etc.

TIA should not be diagnosed in cases where symptoms are limited to only transient loss of consciousness, isolated dizziness, incontinence of urine, feces, transient darkening of the eyes, and falling. All these manifestations are associated with general hypoperfusion of the brain and more often occur with primary pathology of the heart. In addition, rarely, TIAs are manifested by isolated double vision, tinnitus, impaired sensation in one limb or part of the face, isolated amnesia, and sudden loss of balance.

TIA has to be differentiated from other paroxysmal conditions: epileptic seizure, syncope, migraine, demyelinating disease, hyperventilation syndrome, hypoglycemia, hysteria.

You should always try to establish the cause of TIA - stenotic lesion of extracranial or large intracranial arteries, cardiac pathology, coagulopathy.

Ticket number 23

Structure and functions of the autonomic nervous system. Limbiko-hypothalamo-reticular complex. Symptoms and syndromes of injury.

The NS is subdivided into somatic (animal), which regulates relationships with the external environment, and vegetative (visceral, autonomous), which regulates internal processes.

ANS regulates the function internal organs, open and closed glands, blood and lymphatic vessels, smooth and striated muscles, as well as sensory organs, interacts with internal organs with other systems and tissues of the body, provides homeostasis.

Functions: vegetative provision of various forms of mental and physical activity and maintenance of homeostasis (homeokinesis).

Features-differences between the ANS and the SNS: autonomous to a greater extent, not controlled by consciousness, but affects the emotional background and general well-being; Connection of activity with daily biorhythms. The presence of its neurons in many parts of the body, internal organs; focal location of autonomic nuclei in the central nervous system; lack of strict segmentation and metamerism, smaller diameter of nerve fibers; slower conduction speed; three-neuron simple reflex arc, a wide representation of axonal reflexes (segmental, axonal, viscero-visceral, viscero-cutaneous, skin-visceral). The autonomic system has two parts: sympathetic and parasympathetic.

parasympathetic nervous system.

More ancient in evolutionary terms. Performs a trophotropic function, controls anabolic processes. Regulates the activity of organs responsible for maintaining homeostasis. More autonomous than sympathetic. The tone is increased at night. Cholinergic. Parasympathetic nodes - in the wall of organs or near the organ. The preganglionic fibers are longer than the postganglionic ones.

Sympathetic system: Younger in phylogenetic terms. Ergotropic functions. Controls catabolic processes. Regulates the conditions of the internal environment and organs in relation to the functions they perform. Depends on the influence of GM and the endocrine system, less autonomous than parasympathetic. The tone is increased during the day. Adrenergic. Sympathetic nodes outside the organ. The preganglionic fibers are shorter than the postganglionic ones.

Vagotonia: decrease in heart rate, blood pressure, respiratory rate, a tendency to faint, miosis, hyperhidrosis, obesity, indecision, performance is higher in the morning.

Sympathicotonia: increased heart rate, blood pressure, respiratory rate, mydriasis, eye shine, weight loss, chilliness, constipation, anxiety, increased performance in the evening, increased initiative. Reduced focus.

Amphotonia- SINS and PVNS hypertonicity.

SINS and PVNS are not 100% antagonists, 20% excitation of PVNS is SINS activation.

Structure of the ANS: suprasegmental and segmental departments.

suprasegmental department: limbicoreticular complex, "visceral brain".

There are 3 levels of suprasegmental autonomic regulation - the trunk, hypothalamus and limbic system. limbic system a takes part in the formation of motivations, emotions, regulates mnestic functions, endocrine, sleep, wakefulness, etc. Ergotropic and trophotropic systems. Functions in the limbic system are represented globally and are poorly differentiated topographically. Primary olfactory system, basal frontal and temporal lobes, hippocampus, piriform and cingulate gyrus, tonsil, hypothalamus, anterior thalamic nuclei, reticular formation. Numerous connections, and circles between various structures LRC and other departments of GM.

segmental department:

Parasympathetic (cranial region- nucleus of Yakubovich-Edinger-Westphal, Perlia, upper and lower salivary, dorsal nucleus vagus nerve and sacral– lateral horns S2-S4)

Sympathetic- sympathetic trunk - lateral horns C8-all T-L2

The defeat of the segmental department is of an organic nature, and the suprasegmental one is more often mediated by psychogenic factors.

Pathology:

Suprasegmental autonomic disorders:

Psychovegetative and neuroendocrine

Generalized and local

Primary and Secondary

Permanent and paroxysmal.

Segmental autonomic disorders:

HCV and HCV

Primary and Secondary

mixed

Primary and secondary (ISA)

The fibers leaving the sympathetic chain consist of two groups: 1) postsynaptic - sent to the executive organs, 2) presynaptic - to intermediate organs. From the superior sympathetic cervical ganglion, the fibers form the sympathetic plexus on the external and internal carotid arteries and their ramifications. From the 3rd pair of cervical sympathetic nodes, the superior cardiac nerve departs, which forms the sympathetic plexus in the heart and sends executive impulses to the myocardium. Branches from the 5 superior thoracic ganglia supply vasomotor fibers thoracic aorta, lungs and bronchi. Presynaptic fibers from the 7 lower thoracic nodes approach the celiac, superior and inferior mesenteric nodes, to the intermediate nodes in which they are interrupted. The axons of the neurons of these nodes form the celiac and hypogastric plexuses and innervate the abdominal organs. From the lumbar ganglia, they approach the lower node and the hypogastric plexus and innervates the pelvic organs.

The facial nerve contains fibers that innervate secretory lacrimal cells, submandibular and sublingual salivary glands. Parasympathetic fibers of the nuclei of the midbrain innervate the ciliary muscle and the muscles of the iris of the eye. The fibers of the nuclei of the medulla oblongata provide the heart, lungs, and digestive system. Parasympathetic formations of the sacral region spinal cord innervate urinary organs. And the rectum. Supra-segmental regulation of autonomic functions is provided by several levels. One of the main ones is the hypothalamic region, which has numerous connections with the vegetative cells of the brain stem and spinal cord, and is also associated with the cerebral cortex, especially with the limbic region, parahypocampus and orbital gyrus (limbic-hypatalamo-reticular complex).

Polyneuropathy infectious and parainfectious. Features of the course of diphtheria polyneuropathy.

Post-infectious polyneuropathy occurs in mumps, measles, infectious mononucleosis, influenza, HIV infection, neuroborreliosis).

Diphtheria polyneuropathy occurs in patients who have had diphtheria. The cranial nerves are the first to be affected - paralysis of the soft palate (dysphonia, choking), impaired sensitivity in the pharynx, a decrease in the pharyngeal reflex manifests itself at 3-4 weeks from the onset of the disease. At 4-5 weeks there is a violation of accommodation. At 5-7 weeks, paralysis of the muscles of the pharynx, larynx. Flaccid distal pair and tetraparesis with subsequent involvement of the proximal legs, arms of the body (diaphragm). Decreased and lost deep reflexes. Paresthesia in the distal extremities, hypoesthesia of the polyneuritic type. Sometimes disorders of deep sensitivity predominate, which is manifested by sensitive ataxia. Autonomic disorders - sinus tachycardia, arterial hypotension, hyperkeratosis and dry skin, sometimes there is a violation of the function of the pelvic organs. In the CSF, the protein content may increase, sometimes mild lymphocytic pleocytosis. ENMG - signs of demyelination. AT acute stage infections are injected with antidiphtheria serum. The basis of treatment is adequate supportive and symptomatic therapy. During the recovery period - therapeutic exercises, massage, PTO.

hemorrhagic stroke. Clinic, diagnosis, treatment.

Hemorrhagic stroke is a fait accompli of hemorrhage, and its pathogenesis is largely associated with the secondary influences of the outflowing blood.

Cerebral hemorrhage is a clinical form of stroke that occurs due to a rupture of an intracerebral vessel or an increase in the permeability of its wall and the penetration of blood into the brain parenchyma. In practice, hemorrhagic stroke is more often understood as a cerebral hemorrhage due to hypertension or atherosclerosis (the so-called hypertensive hematomas) . There are primary and secondary intracerebral hemorrhages. Hematoma resulting from arterial hypertension is a primary hemorrhage and is observed in 70-90%. With secondary hemorrhage, hematoma occurs due to:

Coagulopathy (10-26%) (against the background of taking anticoagulants, it develops in the 1st year of treatment, with inadequate laboratory control of the therapy and the occurrence of a pronounced hypocoagulation syndrome in the form of a decrease in the prothrombin index to 40% or an increase in INR5), with leukemia, cirrhosis liver and blood diseases)

* hemorrhages in the tumor (1-3.5%)

Rupture of an arteriovenous malformation (7%)

* vasculopathies (5%) (amyloid angiopathy, septic or mycotic arteritis).

Basic diagnostic measures

CBC, TAM, blood group, Rh factor, blood test for HIV, biochemical blood test, electrolytes, screening study of the hemostasis system, ECG, X-ray of organs chest, X-ray of the skull, consultation of a therapist, consultation of an ophthalmologist, glycemic profile, consultation of an endocrinologist, study of markers of intravascular activation of the hemostasis system, assessment of intravascular platelet aggregation

Diagnostic measures for hemorrhagic stroke:

1. Cerebral angiography

Indications:

subarachnoid hemorrhage,

Atypical localization of intracerebral hematoma (according to CT, MRI),

Ventricular hemorrhage.

Scope of study: bilateral carotid and vertebral angiography.

2. Transcranial dopplerography - to identify and assess the severity of cerebral vasospasm, its dynamics during treatment.

Clinical picture

Symptoms develop, as a rule, suddenly, usually during the day, during the period of active activity of the patient, although in isolated cases, hemorrhage may occur during rest or during sleep. The most common provoking factors are the rise in blood pressure, alcohol intake; somewhat less often - physical activity and a hot bath.

Edema of the brain substance during intracerebral hemorrhage (IC) appears after a few hours in the ipsilateral and contralateral cortex, in the basal ganglia on both sides, progresses during the first 24 hours, after which it remains constant for the first 5 days. In the future, the swelling gradually decreases.

Cerebral disorders are the leading ones in the clinical picture of VC: severe headache, nausea, vomiting, generalized epileptic seizures (in 16%), psychomotor agitation. Within 1 hour, disturbances of consciousness appear from stunning to coma.

Meningeal syndrome for the first time during the disease is manifested by hyperesthesia (primarily photophobia), Bekhterev's zygomatic symptom. Rigidity of the muscles of the neck, symptoms of Kernig, Brudzinsky are formed, as a rule, later. More than 1/3 of elderly patients have symptoms of irritation meninges are not detected.

vegetative symptoms. The skin is purple-red, breathing is hoarse, loud, stridor or of the Cheyne-Stokes type, the pulse is tense, blood pressure is elevated, hyperthermia quickly occurs.

Lobar hemorrhages, VC in the basal nuclei and the internal capsule - contralateral hemiplegia, hemianesthesia, hemianopsia, paresis of the facial muscles and tongue in the central type, aphasia (with damage to the dominant hemisphere) or a violation of the body scheme, autotopognostey, anosognosia (with damage to the subdominant hemisphere).

Hemorrhages in the thalamus - contralateral hemianesthesia, hemiataxia, hemianopsia, sometimes transient hemiparesis. Amnesia, drowsiness, apathy are possible.

Hemorrhages in the cerebellum usually develop within a few hours. They are characterized by severe dizziness, miosis, nystagmus, repeated vomiting, sharp pain in the neck and neck, hypotension or muscle atony, ataxia, and a rapid increase in intracranial hypertension.

Hemorrhages in the brainstem are observed more often in the bridge and are accompanied by the development of a deep coma within a few minutes, tetraplegia, severe decerebrate rigidity, miosis, respiratory and cardiovascular disorders. The death of patients occurs within a few hours. With a small lesion in the pontine tire, consciousness can remain preserved, and clinical symptoms are manifested by the development of an alternating syndrome.

Breakthrough of blood into the ventricular system is observed in 30-85% of cases of intracerebral hemorrhage. Most often (up to 80% of cases) a breakthrough of blood into the ventricular system is observed with thalamic hemorrhages; if their volume exceeds 10 cm3 and is characterized by: deep coma, severe hyperthermia, disappearance of tendon, pathological reflexes, instability of muscle tone with symptoms of hormetonia, impaired stem functions with respiratory and cardiac disorders.

Treatment of hemorrhagic stroke

Ensuring patency respiratory tract

Provision of oxygenation

Correction of arterial hypotension: beta-blockers, ACE inhibitors, calcium ion blockers.

Correction of convulsive syndrome and psychomotor agitation It is carried out by using benzodiazepines and barbiturates (in the absence of arterial hypotension).

Surgical treatment is advisable

Intracerebral hemispheric hemorrhages with a volume of more than 40 ml (according to CT of the head)

Putamenal and subcortical hemorrhage with a volume of more than 40 cm3. (hematoma diameter of 3 cm or more), accompanied by severe neurological deficit and / or leading to brain dislocation (displacement of median structures of more than 5 mm or deformation of brainstem cisterns);

Hemorrhage in the cerebellum with a volume of more than 15 cm3, accompanied by dislocation of the IV ventricle and / or occlusive hydrocephalus;

Hemorrhage in the thalamus, accompanied by ventricular hemotamponade and / or occlusive hydrocephalus.

Aneurysms, arterio-venous malformations, arterio-sinus fistulas, accompanied by various forms of intracranial hemorrhage and / or cerebral ischemia.

Obstructive hydrocephalus in GI.

Ticket number 24

Symptoms and syndromes of damage to the peripheral part of the autonomic nervous system. Peripheral autonomic failure.

Vegetative insufficiency is associated with a violation of the innervation of internal organs, blood vessels, secretory glands. There are primary (causes - idiopathic orthostatic hypotension, multisystem atrophy, Parkinson's disease, hereditary sensory autonomic neuropathies), secondary (in diseases of the peripheral nervous system, primarily polyneuropathies - diabetic, amyloid, porphyria, uremic, in diseases of the central nervous system - high damage to the spinal cord , tumors of the posterior cranial fossa, syringomyelia, multiple sclerosis, hydrocephalus).

Typical clinical syndromes of PVN are orthostatic hypotension, tachycardia at rest, fixed pulse, hypertension in the supine position, hypohidrosis and anhidrosis, impotence, gastroparesis, constipation, diarrhea, urinary incontinence, decreased vision at dusk and Horner's syndrome, sleep apnea.

Alcoholic polyneuropathy. Clinic, diagnosis, treatment.

Alcoholic polyneuropathy occurs only in patients with chronic alcoholism. Regular consumption of 100 ml of alcohol per day for 3 years leads to the occurrence of polyneuropathy. At the beginning, it proceeds asymptomatically, later mild symptoms of polyneuropathy appear - weight loss of leg muscles, decrease or loss of Achilles and knee reflexes, paresthesia in the legs. Weakness gradually develops, paresthesias intensify, pains of a burning nature “burning feet” appear. In the absence of treatment, the process from the distal parts extends to the proximal parts of the limbs. But there are variants with proximally pronounced weakness, as well as variants with a predominance of movement disorders (“hanging hands and feet”). The lower extremities are always affected earlier and more severely than upper limbs. Characterized by hypesthesia in the type of gloves and socks, hyperesthesia, distal hyperhidrosis, trophic disorders are possible (orthostatic hypotension, hypothermia, impaired pupillary response, impotence, sleep apnea.). Diagnosis: anamnesis - regular use of alcohol, clinics. On EMG, an axonal type of peripheral nerve damage, a decrease in SPI aff. Treatment - NSAIDs, analgesics, anticonvulsants, tricyclic antidepressants, B vitamins, detoxification therapy, with liver damage - hepatoprotectors, alpha-lipoic acid preparations (thioctacid).

Non-traumatic subarachnoid hemorrhage. Clinic, diagnosis, treatment.

Non-traumatic hemorrhage in the subarachnoid space of the brain (SAH) may be the result of a number of diseases. The main causes of non-traumatic SAH are:

ruptured cerebral aneurysms (CA): 75-80%

ruptured cerebral arteriovenous malformations (AVMs): 4-5% of cases

systemic vasculitis,

coagulation disorders,

sickle cell anemia (often from concomitant sickle cell anemia of the CA),

the use of certain drugs,

unspecified etiology (in 14-22% it is not possible to determine the specific cause of SAH).

Clinical picture of SAH. The main clinical symptom of SAH is a sudden, high-intensity headache (“like a blow to the head”), followed by irradiation to the neck (“boiling water spreading down”). Often the headache is accompanied by vomiting, photophobia, short-term or long-term loss of consciousness. Blood pressure is often elevated. A neurological examination reveals depression of the level of consciousness of various depths, cerebral symptoms, meningeal symptoms, symptoms of damage to the roots of some cranial nerves can be noted.

Survey. After the patient is admitted to a neurological or non-core hospital in the presence of a SAH clinic, it is necessary to carry out:

clinical and neurological examination,

assess the level of consciousness on the Glasgow Coma Scale (CSG) [adj. 2],

CT scan of the brain to verify the SAH and determine the anatomical form of the hemorrhage,

lumbar puncture to verify SAH, if there are no signs of hemorrhage on CT,

Classification signs of NAC (Samoilov V.I., 1990)

By etiology: 1) aneurysmal, 2) hypertonic, 3) atherosclerotic, 4) traumatic, 5) infectious-toxic, 6) blastomatous, 7) pathohemic, 8) unclear.

According to the pace of development - acute (minutes), subacute (hours, days).

According to the main neurological syndrome: 1) soporous-comatose; 2) hypothalamic; 3) meningeal-psychomotor; 4) meningeal-radicular; 5) meningeal-focal; 6) epileptic.

Soporous-comatose syndrome - a violation of consciousness by the type of stupor and coma, the absence of focal symptoms, the absence of meningeal symptoms during the first 2-6 hours (more often with a rupture of an aneurysm of the anterior communicating artery, accompanied by angiospasm).

Hypothalamic syndrome is manifested by catabolic and vasomotor reactions (rupture of arterial aneurysms).

Meningeal-psychomotor syndrome is manifested by psychomotor agitation against the background of the absence of focal neurological symptoms (more often at a young age).

Meningeal-radicular syndrome is a combination of damage to the meninges and roots of the cranial nerves (often oculomotor, abducent, less often block, 1st branch of the trigeminal), mainly when an aneurysm of the supraclinoid part of the internal carotid artery or posterior connective artery ruptures.

Meningeal-focal syndrome is a combination of meningeal symptoms and focal symptoms of brain damage (aphasia, monoparesis, anesthesia, etc.). It is typical for foci in the basins of the anterior and middle cerebral arteries.

Principles of medical tactics

Ensuring airway patency and oxygenation

In a patient with impaired consciousness on GCS 9-12 points or less (stupor - coma), tracheal intubation should be performed and auxiliary ventilation should be started. The indication for mechanical ventilation is not only respiratory, but also cerebral insufficiency.

Infusion therapy

Isoosmolal crystalloids are administered in a volume of 50-60 ml/kg per day in compliance with the principle of "two stress norms" - blood osmolality and natremia, and "two norms" - glycemia and potassium.

Sympathomimetics

The dose of sympathomimetics is selected based on the hypertensive effect and focusing on the absence of side complications: tachycardia of more than 140 beats per 1 minute and hemodynamically significant supraventricular and ventricular cardiac arrhythmias. The initial doses of dopamine are 5-6 mcg / kg-min, adrenaline - 0.06-0.1 mcg / kg-min, norepinephrine - 0.1-0.3 mcg / kg-min.

Treatment of intracranial hypertension

A universal measure is to give an elevated position of the patient's head (30-45 °). In the presence of motor activity the patient and (or) the patient's resistance to the work of the respirator, short-acting sedatives are administered so as not to exclude the possibility of a dynamic study of the neurological status for a long time. In the presence of convulsive activity, benzodiazepines and barbiturates are used (in the absence of arterial hypotension). In the absence of the effect of the measures taken, hyperosmolal preparations are used (mannitol, glycerin and hypertonic sodium solutions). Antibacterial therapy. Enteral nutrition

They start with enteral administration of glucose-salt mixtures, followed by the transition to semi-elemental or low-concentration balanced mixtures of industrial production.

Corticosteroids and metabolically active drugs

Currently, numerous drugs have been proposed that affect the pathbiochemical processes that occur during stroke: corticosteroids, antioxidants, antihypoxants, cell membrane stabilizers, regulators of choline and dopaminergic activity of the brain, vascular-active agents. Unfortunately, at present there is no convincing data on the improvement of outcomes of non-traumatic SAH with the use of these agents.

Other events

Correction of disseminated intravascular coagulation syndrome is carried out by using fresh frozen plasma or cryoprecipitate (according to coagulogram data).

For the prevention of thromboembolic complications from the third day, low molecular weight heparins or small doses (up to 20,000 IU / day) of conventional heparin are used (in the absence of signs of external and internal bleeding).

Prevention of stress ulcers is carried out by early enteral nutrition and adequate volemic support. In the presence of an ulcer history or signs of gastrointestinal bleeding, H2-blockers or proton pump inhibitors (omeprazole) are used.

Ticket number 25

Physiology of voluntary control of bladder function. The main syndromes of lesions of central and peripheral origin. Neurogenic bladder.

The act of urination has two phases - the filling phase Bladder, during which the activity of the bladder muscle that expels urine (the detrusor) is inhibited, and the internal and external sphincters are contracted, and the emptying phase, during which the detrusor contracts and the sphincters relax. Neurogenic urinary bubble- violation accumulation and evacuation of urine due to damage to the nervous system at different levels - from the cerebral cortex to the intramural apparatus of the bladder. There are two types of disorders - 1) central - In case of incomplete injuries of the spinal cord above the cone, inhibitory fibers are involved (in this case, patients experience difficulty in holding urine, there are imperative urges - early stages of multiple sclerosis) and pathways initiating an voluntary onset of urination (in case of violation of voluntary control over urination develops its delay due to the activation of inhibitory sympathetic mechanisms - in the late stages of spinal compression). After a complete break in the conduction pathways of the spinal cord - trauma, transverse injuries above the cerebral cone - in the acute phase - urinary retention, subsequently enhanced reflex activity and reflex emptying of the urinary bladder develops. bubble syndrome spinal hyperreflex bladder. Manifestations of the syndrome are 1) its spastic state and emptying with urine volumes of less than 250 ml, 2) a small amount or absence of residual urine, 3) difficulty in the voluntary onset and act of urination, 4) provoking urination by tapping in the suprapubic region or striae irritation,5 ) vegetative signs of bladder filling.

2) peripheral - a break in the sacral reflex arc leads to urinary retention due to the inhibitory effect of sympathetic mechanisms on the emptying reflex. It is observed in polyneuropathies that occur with damage to autonomic fibers.

Tibial neuropathy is characterized by damage to various etiologies, which leads to dysfunction of the muscular apparatus of the lower leg, foot, fingers. The main reason is traumatic, mechanical or infectious damage to the nerves of the lower extremities. Pathological process lead to the development of pain syndrome, the formation of swelling, increased sensitivity and spasm of the muscles of the lower leg and foot, as well as other neurotrophic disorders.

The reasons

The tibial nerve is a continuation of the sciatic nerve. Its damage is possible in the following cases:

• Injuries of the lower extremities of various etiologies (fracture, dislocation or sprain of the ankle, tendon rupture, sprain of the foot ligaments). Traumatic factors and the edema caused by them lead to direct damage or compression of the tibial nerve, which leads to impaired transmission of nerve impulses.
• Deformation changes in the foot (flat feet, valgus).
• Squeezing of the feet or their uncomfortable position for a long time, for example, when squeezing the lower extremities with a heavy object.
• Diseases of the knee joint and ankle (arthritis, arthrosis).
• Disorders in the functioning of the endocrine system, thyroid disease, diabetes mellitus.
• Tumor lesions of the tibial nerve of a benign and malignant nature.
• Violation of blood flow to the lower leg and feet of the lower extremities (vasculitis).
• Poisoning the body with toxic and chemical compounds, including alcohol-containing products.
• Inflammatory pathologies of infectious etiology of various localization, including those with damage to multiple nerve fibers.
• Long-term therapy with drugs whose action adversely affects the functioning of the central nervous system.
• decline protective properties organism.
• Harmful working conditions.
• Violation of the nutrition of the tissues of the lower leg and foot.
• Prolonged exposure to low temperatures on the lower extremities.
• Improper nutrition, resulting in a decrease in the intake of B vitamins in the body.
• Pathological processes affecting the spinal column.

People at risk are:

• professionally involved in various sports;
• with working conditions that require constant standing, including walking;
• prone to overweight or obesity - a large load on the lower limbs increases the risk of impaired functioning of the tibial nerve;
• choosing the wrong shoes: high heels, thin soles.

Symptoms

Neuropathy is accompanied by a clinical picture, the severity of which depends on the degree of damage to the nerve fibers.

Nerve dysfunction can be recognized by impaired flexion of the foot, motor ability of the fingers. When walking, the wrong setting of the foot occurs - the emphasis is on the heel. The muscular apparatus of the lower leg and foot has signs of obvious atrophy and deformation.

In the case of a traumatic origin of neuropathy, edema forms in the ankle area, blood flow is disturbed, tissue sensitivity increases, there is a pronounced pain syndrome, which intensifies when touching the damaged areas.

If the cause of nerve neuropathy is endocrine disorders, infectious lesions, the patient loses sensitivity in the lower leg and foot area. The pain syndrome persists and may have different character and degree of expression. The pain is aggravated by walking and physical activity. The patient may experience involuntary contractions of individual muscles or a convulsive syndrome covering the lower extremities.

In addition, the patient is concerned about neuro-trophic disorders, such as dryness of the epidermis in the lower leg and feet, keratinization of the upper layer of the dermis, brittle nails, pallor of the skin and decreased local temperature, increased sweating.

Diagnostics

Tibial neuropathy belongs to the group of limb mononeuropathy. The clinical picture of the pathology is typical for dysfunctions of the musculoskeletal system and has a traumatic nature, and therefore, is subject to joint monitoring and control by specialists in the field of neurology and traumatology.

The first step in making a diagnosis is to ask the patient about injuries to the lower extremities, working conditions, as well as the features of the clinical picture and the presence of other diseases that can affect the normal functioning of the nervous system. After that, the patient is examined to identify atrophic and neurotrophic changes in the lower leg and foot.

Based on the data obtained, an initial diagnosis is made, which is confirmed by instrumental studies, using one of the following methods:

• ultrasound diagnostics of the lower extremities;
• electromyography is a research method that allows you to determine the performance of the muscular apparatus of the lower leg and foot;
• X-ray diagnostics in the presence of indications, for example, in case of fractures;
• blockade of trigger points - a therapeutic and prophylactic method that involves the introduction of a drug into the affected areas of the lower extremities, which allows you to determine the degree of nerve damage;
• CT and MRI are used as additional methods diagnosis, when using other methods of data is not enough to make a diagnosis.

Therapy

The initial stage in the treatment is the therapy of the pathology that is the root cause of the dysfunction of the nerve fibers. For example, in case of endocrine disorders, the systems are prescribed hormonal preparations, with diabetes - medicines to normalize blood sugar levels. With a lack of B vitamins, intravenous administration of drugs with vitamins B1, B6 and B12 is indicated, which will improve the nutritional capacity of the tissues of the nervous system.

To reduce the severity of the feeling of pain, the resumption of motor activity, the patient is prescribed a special orthopedic shoes or insoles. The choice is made in accordance with the localization of the lesion of nerve fibers.

At severe pain, pronounced edema as a result of pinched nerve endings, blockades are carried out with the introduction of analgesics (Analgin, Novocain) and anti-inflammatory nonsteroidal drugs(Ibuprofen, Dicroberyl). Less commonly used steroid drugs(hydrocortisone) or antidepressants (amitriptyline).

In case of trophic disorders of surface tissues, reperants (Solcoseryl, Actovegin) are recommended, the action of which is aimed at updating cell structures.

To suppress nervous excitability, anticholinesterase drugs (Ipidacrine) are used.

Physiotherapeutic methods of therapy (electrophoresis, magnetotherapy, shock wave therapy), exercise therapy and massage sessions.

Surgical intervention necessary in the absence of effectiveness from conservative therapy, nerve damage, adhesion formation, impaired sensitivity of the lower extremities and severe pain syndrome. The operation is performed by a neurosurgeon.

shock wave therapy

One of the modern and effective ways physiotherapy is a shock wave method. It is carried out using a special apparatus that directs targeted acoustic waves different frequency to damaged areas. The penetration depth of such waves is up to 4 cm.

This method allows you to improve the flow of blood with nutrients to the lower leg and foot, normalize metabolic processes, loosen neoplasms and reduce the severity of pain.

Shock wave therapy is used as a preventive and therapeutic course of 5 to 10 procedures with a break of 3-7 days between them.

The advantages of this method are:

• non-invasive procedure;
• a short course of therapy;
• the duration of one session is from 10 to 20 minutes;
• the possibility of simultaneous exposure to several damaged areas;
• pain relief occurs after 2-3 sessions;
• long lasting effect.

This method is not applicable to patients with blood clotting disorders, oncology, infectious pathologies acute form, hypertension. SWT is also contraindicated in children under 14 years of age and patients with a pacemaker.

Neuropathy of the tibial nerve is characterized by a dysfunction of the muscular apparatus of the foot and lower leg, which leads to gradual tissue atrophy. It is characterized by pain, impaired walking and setting the foot. For treatment, therapy of the pathology-root cause is carried out, as well as medications are prescribed to relieve pain and physiotherapy procedures. Surgical intervention is performed according to indications.