Compression-ischemic neuropathies of the lower extremities

The functioning of the organs and systems of our body is regulated by nerve impulses - signals emanating from the brain. “Outgoing” and “incoming” impulses are transmitted along the nerves, as if through wires. Damage to the nerves disrupts this connection and can cause serious disruptions in the body's functioning. Indeed, along with disruption of nerve transmission in the affected area, cellular nutrition and blood supply deteriorate.

A condition characterized by damage to nerve fibers and accompanied by a violation of the conduction of nerve impulses along the nerve fiber is called neuropathy (neuropathy) .

If one nerve suffers, we are talking about mononeuropathy , if there is multiple symmetrical damage to peripheral nerves (for example, when the process affects both lower and/or upper limbs at once, etc.) - about polyneuropathy . The pathological process can involve both cranial and peripheral nerves.

Lesions of the peripheral nerve trunks, which are based on the infringement of a nerve enlarged as a result of inflammation and swelling in the muscle-bone tunnel, are called tunnel syndrome (there is also a name for compression-ischemic neuropathy ).

There are dozens of tunnel syndromes, the most famous of which is carpal tunnel syndrome.

1

Neuropathy. Diagnosis and treatment.

2 Neuropathy. Diagnosis and treatment.

3 Neuropathy. Diagnosis and treatment.

Causes and types of neuropathy

In 30% of cases, neuropathy is considered idiopathic (that is, arising from unknown causes).

Otherwise, the causes of the disease can be divided into internal and external.

Causes associated with various internal pathologies:

• endocrine diseases, of which diabetes mellitus accounts for about a third of all neuropathies;
• vitamin deficiency, especially deficiency of B vitamins;
• autoimmune diseases;
• multiple sclerosis;
• rheumatoid arthritis, etc.

External factors that provoke the development of neuropathy include:

• alcoholism (a common consequence is neuropathy of the lower extremities);
• injuries;
• intoxication;
• infections.

Often the cause of nerve damage is a hereditary factor. In such cases, the disease can develop independently, without any additional harmful effects.

Neuropathy is a very serious illness that requires qualified diagnosis and adequate treatment. If you are concerned about any of the symptoms listed below, consult a neurologist immediately!

Depending on the location of the disease, neuropathies of the upper, lower extremities and cranial nerves are distinguished, for example:

Facial nerve neuropathy

It can develop as a result of a traumatic brain injury, a viral infection, hypothermia, unsuccessful dental surgery, depression, pregnancy and childbirth, as well as due to a neoplasm. Signs of the disease are: weakening of the muscles on the side of the affected nerve, salivation and lacrimation, inability to completely close the eyelids.

Trigeminal neuropathy

Caused by various reasons (maxillofacial surgery, dentures, difficult childbirth, heredity) damage to the nerve endings of the gums, upper and lower lips, and chin. Patients complain of severe facial pain from the affected nerve, radiating to the upper and lower jaws, not relieved by analgesics. There is also discharge from one nostril, lacrimation and redness of the eye.

Radial nerve neuropathy

It often occurs against the background of so-called “sleep paralysis,” i.e. compression of the nerve due to incorrect position of the hand. Occurs in people who use drugs or alcohol. It also progresses with wrist fractures, bursitis or arthritis. It manifests itself as a violation of the dorsiflexion of the hand (the hand hangs), numbness of the thumb and index fingers, pain can occur on the outer surface of the forearm.

Median nerve neuropathy

Damage to this area of ​​the upper limb can occur due to sprains, fractures, diabetes mellitus, rheumatism, gout, neoplasms, as well as in the event of nerve compression. It manifests itself as severe pain (as well as numbness and burning) in the forearm, shoulder, hand, thumb, index and middle fingers.

Ulnar nerve neuropathy

The cause of this disease may be traumatic (sprain, tear and rupture) or other damage to the ulnar nerve (for example, caused by bursitis, arthritis). It manifests itself as numbness of the first and half of the fourth fingers, a decrease in the volume of the hand, and a decrease in the range of movement.

Sciatic nerve neuropathy

It usually results from a serious injury or illness (knife or gunshot wound, fracture of the hip or pelvic bones, intervertebral hernia, oncology). It manifests itself as pain along the back of the thigh, lower leg, buttock from the side of the nerve lesion.

Neuropathy of the lower extremities

It can develop due to excessive physical overload, tumors in the pelvic area, hypothermia, and also due to the use of certain drugs. Symptoms: inability to bend forward, pain in the back of the thigh, numbness in the lower leg.

Peroneal nerve neuropathy

It occurs due to bruises, dislocations and other injuries, as well as due to curvature of the spine, carpal tunnel syndrome, and wearing narrow, uncomfortable shoes. Manifestations: inability to dorsiflex the foot, cock-like gait (the patient cannot bend the foot towards himself).

1 Massage

2 Massage

3 Acupuncture

Material and methods

The study included patients aged 18 years or older with CTS who underwent median nerve decompression at the wrist in 2016–2017. at the Clinic of Nervous Diseases named after. AND I. Kozhevnikov First Moscow State Medical University named after. THEM. Sechenov. The study included 85 patients (14 men and 71 women) aged from 36 to 84 years (mean age 62±10.6 years).

When collecting anamnesis, gender and age were recorded, the nature of the patient’s professional and other activities was analyzed, and the presence of concomitant diseases and medications taken were clarified. We analyzed the diagnosis and treatment prior to the patient's visit to the Clinic for Nervous Diseases. The general somatic and neurological status was assessed, and specific Tinel and Phalen tests were performed to determine compression of the median nerve. The Tinel test was considered positive if, during percussion in the projection of the median nerve in the area of ​​the grooves of the wrist, irradiation of pain and tingling in the fingers occurred. The Phalen test was considered positive if paresthesia occurred in the fingers with maximum flexion of the hands at the wrist joints and raising the arms up for 1 minute [18].

Patients were surveyed using the Boston Carpal Tunnel Questionnaire (BCTQ), which allows assessing the severity of symptoms of the disease and functional deficit. The intensity of pain was assessed using a visual analogue scale (VAS). Among the instrumental examination methods, patients underwent ENMG of the upper extremities and ultrasound of the median nerves at the wrist level. The diagnosis was made based on patient complaints, clinical symptoms and results of instrumental studies.

Treatment of patients consisted of surgical decompression of the median nerve at the level of the wrist by completely cutting the transverse ligament.

Statistical data processing was performed using the Statistica 10.0 program

Symptoms of neuropathy

The variety of types of disease explains the huge number of specific manifestations. And yet we can identify the most characteristic signs of neuropathy :

• swelling of tissues in the affected area;
• disturbance of sensitivity (pain, numbness, coldness, burning of the skin, etc.);
• muscle weakness;
• spasms, convulsions;
• difficulty moving;
• soreness/severe pain in the affected area.

Mononeuropathies of the extremities are never accompanied by general cerebral symptoms (nausea, vomiting, dizziness, etc.); cranial neuropathies can manifest similar symptoms and, as a rule, accompany more serious diseases of the nervous system of the brain.

Polyneuropathies are manifested by impaired sensitivity, movement, and autonomic disorders. This is a serious pathology that initially manifests itself in the form of muscle weakness (paresis), and then can lead to paralysis of the lower and upper extremities. The process can also involve the trunk, cranial and facial nerves.

1 ultrasound

2 Electroneuromyography

3 Electroneuromyography

Symptoms of ischemic neuropathy

Most often, this disease affects only one eye, but approximately 1/3 of patients may also experience problems of a bilateral nature. In some cases, the pathology affects the second eye after some time (usually within 2-5 years).

As a rule, the pathology appears suddenly - after a hot bath, physical activity, or even after sleep. Visual acuity drops sharply (sometimes only light perception is preserved, and with total nerve damage, blindness occurs). Vision may deteriorate within minutes. Vision deterioration may be preceded by blurred vision, pain behind the eyeball, or headaches.

The peculiarity of this disease is that during its development, peripheral vision is always impaired. In this case, scotomas, concentric narrowing of the visual fields, and loss in various segments (lower, nasal, temporal halves) may be observed.

The duration of acute ischemia is several weeks. Then the swelling of the optic nerve head gradually subsides, and the hemorrhages resolve. Optic disc atrophy persists, with varying degrees of severity. Visual defects also remain, but may be reduced.

Diagnostics

The presence of the median nerve is indicated by the following results of functional tests:

• with the palm pressed to the table, the patient cannot make scratching movements with the 2nd finger;
• when the affected hand is clenched into a fist, bending the first three fingers is most difficult;
• the patient is unable to place the little finger and thumb on the same plane.

Additionally, various electrophysiological procedures may be prescribed. In each individual case, the neurologist working with you at the Health Workshop clinic will draw up an individual list of required examinations.

Back pain, its etiology and treatment is a problem of modern medicine, which has been repeatedly raised in scientific publications, speeches and discussions. However, despite many years of close attention to this therapeutic problem, its unambiguous solution has not been found. It must be recognized that progress in this area is still being observed - works appear [1, 2] describing the mechanisms of occurrence and consolidation of myofascial syndromes, anatomical, physiological and social features leading to an increase in morbidity are being studied, and non-drug methods of pain relief are being actively introduced. Nevertheless, the deeper the understanding of the pathophysiological processes leading to the occurrence of algic disorders becomes, the more questions specialists have. At the moment, there is not even a unity of terminology used to describe this pathological condition. The actively used terms “dorsopathy” and “dorsalgia” are a universal description of any process hidden behind the pain syndrome. At the same time, the variety of factors causing the occurrence of pain undoubtedly requires completely different therapeutic approaches, which leads to misunderstanding and lack of opportunity to streamline and standardize, as necessary, the process of diagnosing and treating back pain [3]. Thus, pain syndromes can occur with myofascial and myotonic disorders caused by a violation of the biomechanics of the motor act. In this case, the greatest attention should be paid to visual optical diagnostics and manual muscle testing, and the role of neuroimaging is secondary and optional [4]. However, often the source of pain impulses can be located in the system of the spinal motion segment and be associated with changes in the spinal column itself and nearby large joints. In this case, the therapeutic strategy should be aimed at identifying these changes and carrying out pharmacological and non-pharmacological correction of these factors [5, 6].

Thus, by now there is a need not only to change the concept of diagnostic and therapeutic methods, but also to develop terminological unity. This will make it possible to create unified methodological approaches to the treatment of pain syndromes in the back, streamline the work of specialists dealing with this problem, and, as the authors hope, will lead, as the authors hope, to a decrease in the percentage of chronicity of the disease.

Developing a treatment plan for back pain is a rather complex therapeutic task, since the disease is accompanied by a number of comorbid and concomitant disorders. One of the most common phenomena accompanying back pain is compression-ischemic neuropathies, which is not accidental - the restructuring of the motor stereotype, leading to the appearance of myotonic reactions in the back, is not an isolated process, but, as a rule, affects all parts of the motor system . Muscle spasm that occurs in the back area contributes to the restructuring of the biomechanics of all muscles involved in the act of movement. In addition, the provoking factors themselves, such as hypothermia, prolonged stay in a non-physiological position, physical inactivity, are often universal triggers leading to spasms and changes in the anatomical and topographic connections of the muscles and neurovascular bundles of the torso and limbs. Thus, it seems relevant to analyze certain types of compression-ischemic neuropathies and methods of their treatment [7, 8].

Compression-ischemic neuropathy of the sciatic nerve, or piriformis syndrome.

This type of neuropathy is caused by pinching of the sciatic nerve by a spasmed piriformis muscle. The high prevalence of the syndrome and the difficulties of its diagnosis are associated with the anatomical features of the structure of the sciatic region: the piriformis muscle has a triangular shape and is attached at one apex to the greater trochanter, then passes through the greater sciatic foramen and is attached in three uniform bundles to the sacrum, between the first and fourth sacral foramina. The capsule of the sacroiliac joint remains above the muscle, and below the muscle is the anterior surface of the sacrotuberous ligament. A bundle of blood vessels and the sciatic nerve pass through the sciatic foramen with the muscle. In this case, there are various topographic options for the location of the sciatic nerve trunk. Most often it is located under the piriformis muscle, but in some cases it can spread over the muscle or pass inside the muscle bundle. The latter option is most often accompanied by pronounced pain syndromes. The piriformis muscle is involved in a large number of movements: external rotation of the hip; bending forward with fixed and motionless lower limbs; stabilization of the hip joint and retention of the femoral head. Spasm leads to shortening and tightening of muscle fibers, which limits the rotational movements of the hip, as a result of which pain spreads to the groin area, along the leg to the knee, and to the lumbar region.

Clinically, piriformis syndrome is manifested by pain sensations both local and along the compressed sciatic nerve. Localization of pain in the gluteal muscle area is often accompanied by pain radiating not only to the leg, but also to the lower back, which forces patients to describe their sensations as back pain and complicates diagnosis. Algic phenomena in this case intensify with movements involving the piriformis muscle; the pain is neuropathic in nature and is accompanied by numbness, paresthesia, and burning in the area innervated by the sciatic nerve or its branches. With a significant degree of compression of the sciatic nerve trunk and involvement of the vascular bundle, manifestations of motor or autonomic-trophic dysfunction are also possible.

When a patient presents with such complaints, in addition to a traditional neurological examination, which allows identifying sensory or reflex disorders in the area of ​​innervation of the sciatic nerve or its branches, it is necessary to palpate the attachment points of the piriformis muscle (the area of ​​the greater trochanter of the femur and the sacroiliac joint), which will sharply painful. Dynamic testing of the condition of the iliosacral and sacrospinous ligaments is also recommended.

However, neuroimaging methods are able to identify only the primary factor in the secondary involvement of the piriformis muscle, and the appointment of an x-ray or magnetic resonance examination only leads to diagnostic inaccuracies, since in most cases it reveals degenerative-dystrophic changes in the spine of varying severity.

To confirm the diagnosis of piriformis muscle syndrome, several diagnostic tests are used, including Bonnet-Bobrovnikova's symptom (palpation of the spasmodic piriformis muscle), Vilenkin's symptom (sharp pain on percussion of the projection area of ​​the piriformis muscle), Grossman's symptom (unilateral or bilateral contraction of the piriformis muscle during percussion lower lumbar or sacral vertebrae).

The concomitant ischemic nature of the lesion can be assumed using the limb elevation test, when the patient, in a supine position, lifts first one and then the other leg. The test can be considered positive if it is possible to reproduce sensory phenomena in the form of the appearance or intensification of numbness, paresthesia, and pallor of the extremities. A patient may complain of similar symptoms when he has to stop while walking due to unpleasant sensations that occur after a short rest.

Compressive neuropathy of the ilioinguinal nerve.

The nerve can be pinched during sudden abdominal tension, for example when lifting or holding heavy objects, due to the displacement of muscle layers that deform the nerve trunk. This type of neuropathy is more common in men in whom the sensory branch of the ilioinguinal nerve reaches the base of the scrotum, exits through the outer ring of the inguinal canal and adjacent parts of the thigh. Much less frequently, this syndrome is observed in women; in this case, the inguinal branch exits in the area of ​​the uterine ligament and ends in the area of ​​the labia majora.

Compression of the ilioinguinal nerve also often occurs after or during operations for inguinal hernias, appendicitis and during nephrectomy, when the nerve trunk is compressed by adhesive scars or gets caught in a suture when suturing the abdominal wall. The most common symptom of neuropathy is pain in the groin area, often radiating to the upper inner thigh. With abdominal tension and hip extension in the hip joint, the pain intensifies, and with flexion and internal rotation of the hip, it decreases or goes away. Here hyperesthesia or hypoesthesia is sometimes detected. Upon palpation and percussion, a limited area of ​​sharp pain is determined, localized medially from the anterior superior iliac spine. This painful area corresponds to the passage of the sensory branch of the ilioinguinal nerve through the external abdominal muscle. In some cases, weakness of the abdominal muscles is detected in the hypogastric region, manifested by protrusion of the latter when the abdominal tension is tense.

Compression-ischemic neuropathy of the femoral nerve.

This nerve is mixed, its muscle branches innervate the iliopsoas muscle and the quadriceps femoris muscle; the area of ​​skin innervation is the anterior and medial surface of the thigh, leg and foot, almost up to the first finger. Thus, symptoms of neuropathy include both sensory and movement disorders. The femoral nerve originates in the lumbar plexus and exits the pelvic cavity under the inguinal ligament between the psoas major and iliacus muscles, being fixed to their fascia. Accordingly, any pathological processes in the area of ​​these muscles can cause damage to the femoral nerve. The most common cause of femoral nerve neuropathy is trauma followed by the formation of a paraneural hematoma or other pathological processes in the hip joint. Rare, but much more unfavorable prognostically, causes of compression of the femoral nerve can be tumors, abscesses and hematomas of the retroperitoneal space. A typical site of compression of the femoral nerve is the area behind the inguinal ligament, where the nerve from the retroperitoneum exits the thigh in close proximity to the hip joint capsule. With compression-ischemic neuropathy, spontaneous pain can sometimes be very intense. Patients with this syndrome can stand and walk freely, but experience severe difficulty going up and down stairs. More often, patients complain of pain under the inguinal ligament with irradiation to the anterior and inner surface of the thigh, the inner surface of the leg and foot. With prolonged disease, hypalgesia occurs in the area of ​​innervation of the femoral nerve. Motor disorders manifest themselves in the inability to straighten the leg at the knee joint and weakened hip flexion. A neurological examination in such cases reveals the absence of a knee reflex, hypoesthesia of the skin of the anterior surface of the thigh and the inner surface of the leg, and with a long course - atrophy of the quadriceps muscle. Characteristic symptoms of tension are Wasserman and Matskevich. Pain is observed when pressing on the nerve in the upper third of the thigh, under the inguinal fold, or when pressing on the muscles of the anterior surface of the thigh. Sensitive vasomotor and trophic disorders and neuropathic pain are detected in the anterior and medial surfaces of the thigh, lower leg and foot to the base of the first toe.

Compressive neuropathy of the external cutaneous nerve of the thigh (Roth disease). In neurological practice, isolated neuritis n. cutanei femoris lateralis

(LII, III), giving the clinical picture described by V.K.
Rotom (1895) under the term “ meralgia paraesthetica”
(from the Greek “
meros
” - thigh). This type of neuropathy is characterized by attacks of pain and paresthesia in the area of ​​the outer surface of the thigh and is one of the most common types of tunnel syndromes due to anatomical and topographical features. The external cutaneous nerve enters the thigh medially from the anterior superior iliac spine, where it penetrates the external bundles of the inguinal ligament. Compression of the nerve trunk in this area can be caused by banal compression by a belt, bandage or corset. Metabolic disorders or excess fat deposition in the lower anterior abdominal wall and thighs, leading to tension on the nerve trunk, increases the incidence of lesions of the external cutaneous nerve of the thigh. The main clinical manifestation of this type of neuropathy is numbness or burning pain along the anterior outer surface of the thigh. In later stages of the disease, analgesia occurs in the innervation zone. The pain in patients increases noticeably when standing and walking, but may be completely absent when lying down. Many patients experience paresthesia in the form of numbness, tingling, and burning. A characteristic symptom found in Roth's disease is increased pain and paresthesia in cases where the patient puts keys or a phone in the pants pocket on the affected side. An objective examination reveals slight hypoesthesia of the skin in the area innervated by this nerve. With a long course, symptoms of trophic skin disorders are possible, but motor disorders in the thigh area are not detected, as is muscle atrophy. Palpation and percussion of the nerve trunk medially from the anterior superior iliac spine causes local pain.

Compressive neuropathy of the saphenous nerve

(
n. saphenus
), which is the terminal branch of the femoral nerve, is most often caused by its compression in the fascial gap as it exits the adductor canal approximately 10 cm above the knee joint on the anterior inner side of the thigh. Clinically, this syndrome is manifested by pain, paresthesia and sensitivity disorder in the area of ​​the medial edge of the knee, the anterior and medial surfaces of the leg and the inner edge of the foot, and a decrease in the secretion of sweat glands is also possible. With percussion and palpation, an area of ​​pain is identified with irradiation of pain into the anterior internal region of the knee joint, the inner surfaces of the lower leg and foot. The pain increases with hip extension and adduction; at the point of exit of the saphenous nerve, the Tinel and Goldberg symptoms are positive. The patient is characterized by a gait disorder: he avoids fully extending the lower leg and walks with his leg slightly bent at the knee joint. There are no motor disorders, the knee reflex is preserved, and there is no muscle atrophy.

Compression-ischemic neuropathy of the common peroneal nerve.

In typical cases, this syndrome develops distal to the head of the fibula, where the nerve trunk or neurovascular bundle is pinched between the fibula and the fibrous edge of the peroneus longus muscle, which starts from the head of the fibula. This pathology was first described by French clinicians in 1934 as “occupational paralysis of tulip bulb diggers,” which is why in some works it bears the author’s name: Guillain-Seza-de Blondin-Walter syndrome. The disease primarily affects workers who squat and kneel, who spend a long time in a “leg-to-leg” position, and who wear a plaster cast. The peroneal nerve is the most vulnerable of all the nerve trunks of the lower extremities. It is very sensitive to injury and relatively easily causes traumatic neuritis, while the adjacent tibial nerve completely retains its function. Even in cases where the injury affects the common trunk of the sciatic nerve above its division into the tibial and peroneal nerves, the peroneal fibers may be affected selectively or predominantly. It is necessary to take into account the possibility of dividing the sciatic nerve into its main branches much above the popliteal fossa. Dislocation in the knee joint and reduction of dislocation in the hip joint can also cause peroneal nerve palsy. This type of neuropathy is clinically characterized by predominantly acute (less often subacute) development of peripheral paresis of the extensors of the foot with gait disturbance, paresthesia and hypoesthesia along the outer surface of the leg and on the dorsum of the foot. Intense pain syndrome with damage to the peroneal nerve is rare, since thin unmyelinated fibers are practically not included in its composition. Quite often this syndrome is bilateral. Peroneal nerve neuropathy causes characteristic foot drop and makes it impossible to straighten the foot and toes. The patient cannot stand on his heel, abduct the foot, or raise its outer edge. The muscles of the anterior surface of the leg atrophy. Hypoesthesia is detected, spreading to the outer surface of the lower leg, the back of the foot, and the inner surfaces of the first and second fingers. Vegetative-trophic disorders are usually minor. Palpation and percussion of the nerve at the level of the head and neck of the fibula are painful and are accompanied by paresthesia in the area of ​​innervation of the nerve. Forced plantar flexion with simultaneous supination of the foot causes or increases pain in the area of ​​the head of the fibula.

Compression-ischemic neuropathy of the tibial nerve (tarsal canal syndrome, Richet canal syndrome). This type of neuropathy is a consequence of compression of the distal part of the tibial nerve in the internal ankle fibrous canal, which connects the ankle joint with the plantar region. The Richet canal has 2 openings (superior and inferior), through which the tendons of the tibialis posterior muscle, long flexor muscles of the big and other toes, and the posterior tibial neurovascular bundle pass. The nerve lies outside the artery and projects at an equal distance between the Achilles tendon and the posterior edge of the inner malleolus. Most often, tarsal tunnel syndrome develops due to mechanical compression of the nerve by tight shoes, trauma, or repeated microtrauma of the ankle with fibrosis and thickening of the plantar fascia. In addition, it can be observed in rheumatoid arthritis, hypothyroidism and tenosynovitis. Damage to the nerve itself or the neurovascular bundle in this area makes it impossible to flex the foot towards the sole, as well as the toes. The patient cannot stand on the toe of the corresponding leg; his foot is bent to the rear. The muscles of the back of the lower leg atrophy over time. A neurological examination reveals the absence of the Achilles reflex. The impossibility of active supination of the foot develops, the toes take on a claw-like position. Sensory disorders manifest themselves in the form of intense pain. In addition, hypoesthesia of the sole and back of the leg may be observed. In some cases, pain irradiates from the foot along the sciatic nerve to the gluteal region, which makes diagnosis difficult. Vegetative-trophic disorders are sharply expressed. Compression (Goldberg test) and percussion (Tinel test) of the nerve in this area can cause characteristic pain and paresthesia in the plantar part of the foot, sometimes spreading to the posteromedial part of the leg. The same symptoms occur with simultaneous pronation and extension of the foot; Supination of the foot and flexion of the ankle joint reduce pain.

The treatment tactics for compression-ischemic neuropathies are based on an adequate combination of etiological, pathogenetic and symptomatic approaches. For effective treatment, it is necessary to identify the cause and mechanisms of compression and, if possible, eliminate these causes [9, 10]. The radical method of treating most tunnel syndromes is surgery - dissection of the tissues compressing the nerve and creation of optimal conditions for the nerve trunk, preventing its injury. However, according to numerous studies, the long-term effectiveness of surgical and conservative methods does not differ significantly [11].

The main mechanism of conservative etiotropic therapy for compression-ischemic neuropathies is the restoration of an adequate motor stereotype and biomechanics of movements. However, despite the high effectiveness of these methods in the treatment and prevention of neuropathies, they act slowly and require the indispensable addition of pathogenetic and symptomatic techniques [12].

Pathogenetic therapy for neuropathies is based on the restoration of damaged nerve tissue. Metabolic therapy of the nerve includes vitamin therapy, antioxidants, and vasoactive drugs. Relatively new in domestic neurological practice is the use of nucleotides - low-molecular structural elements that play a fundamental role in metabolic processes, are involved in energy conservation and the transfer of certain groups of molecules, and also act as intracellular signaling proteins. In addition, nucleotides are important components of nucleic acids, particularly DNA and RNA. One of the most frequently mentioned nucleotides in medicine, uridine monophosphate plays a major role in the neuronal synthesis of all necessary pyrimidine nucleotides [13, 14]. The mechanism of action of uridine in peripheral neuropathies is multifactorial in nature and includes regeneration and prevention of further degeneration of the peripheral nervous system. After penetration into the nerve cell, part of the uridine undergoes amination to form cytidine, and the remaining uridine and newly formed cytidine become fundamental components of DNA and RNA, increasing the activity of their transcription and translation processes. It is these substances that have an important enzymatic function in the biosynthesis of membrane components such as phospholipids, glycolipids and glycoproteins, which perform an important function in the formation and action of axons and their myelin sheath. In addition to the intracellular effect, pyrimidine nucleotides also have an effect on the nervous system, activating membrane receptors, which stimulates the proliferation of Schwann cells and their migration and adhesion to the axon of the damaged nerve [15, 16].

Uridine monophosphate is presented in the form of a dietary supplement (BAA) Keltican complex, which also includes vitamin B12 and folic acid. This combination was selected as the most effective stimulator of nervous tissue restoration - B12 is involved in the stages of synthesis of purine and pyrimidine nucleic bases, nucleic acids and proteins, and folic acid acts as a coenzyme in many catalytic reactions, especially in the metabolism of protein and nucleic acids (in the synthesis purine, DNA and the assembly of various amino acids), is involved in the biosynthesis of neurotransmitters, phospholipids and hemoglobin. Thus, the Keltican complex promotes nerve regeneration by replenishing the increased need of nervous tissue for the synthesis or utilization of lipids and proteins [17].

The results of numerous foreign clinical studies [18–21] have shown the effectiveness of nucleotides in various metabolic, vertebrogenic, infectious and compression-ischemic lesions of nervous tissue. In the domestic literature there are only isolated reports [22, 23] on the effectiveness of nucleotides, which is associated with the recent appearance of the dietary supplement Keltican complex on the Russian market. Nevertheless, the authors' own limited experience confirms the optimistic prospects for the use of nucleotides in patients with peripheral neuropathies.

We observed 34 patients (18 women and 16 men) with back pain and compression-ischemic neuropathies of various locations. Nucleotide therapy was used for patients with a long history of the disease (from 3.5 months to 1.5 years). Traditional pharmacotherapy was supplemented by taking 1 capsule of the dietary supplement Keltican complex with meals for 1 to 2 months. All patients receiving nucleotides experienced a more rapid recovery of motor functions, including restoration of reflex activity and improvement of vegetative-trophic function. However, the most significant was the reduction in the intensity of the pain syndrome, which made it possible, on the one hand, to reduce the dose of painkillers and thereby reduce the number of side effects; on the other hand, the reduction in pain syndrome made it possible to carry out the process of rehabilitation of motor function more actively, with the inclusion of kinesitherapy and therapeutic physical education, which made it possible to reduce the period of disability of patients. The dietary supplement Keltican complex can be used in patients with back pain as a source of additional substances and helps restore damaged nerve fibers in diseases of the spine and peripheral nerves, thereby facilitating a more rapid restoration of well-being and performance. Particular attention in this study was paid to safety issues. There was not a single patient who refused nucleotide therapy due to side effects, which is quite predictable: the components of the Keltican complex dietary supplement are organic compounds, some of them are synthesized in the human body itself. The safety of uridine (in combination with or without vitamins) was also demonstrated during large-scale foreign studies [24, 25], which involved a large number of patients. No serious adverse effects or deaths were reported.

It should be noted that therapy for back pain and compression-ischemic neuropathies must necessarily include non-drug treatment methods. Manual therapy with elements of kinesitherapy, kinesitis taping, and biofeedback methods play a leading role in the formation of the correct motor stereotype and restoration of the disturbed biomechanical pattern. Of the physiotherapeutic methods, the most effective are massage, phonophoresis with glucocorticosteroids on the area of ​​compression in the acute stage of inflammation, and for chronic scar-adhesive processes - electrophoresis with lidase and shock wave therapy of high frequency and low intensity. Reflex treatment methods are also important: acupuncture, laser, and auriculotherapy. Physical therapy exercises under the guidance of an experienced instructor, who will be able to continue to monitor the correctness of independently performed exercises, will help restore adequate movements.

Thus, back pain accompanied or caused by compression-ischemic neuropathies remains a difficult therapeutic task due to the complexity of diagnosis and the need for complex treatment. But the therapeutic options available today allow us to hope for its successful solution, since emerging new drugs have a high degree of efficiency in restoring damaged nerve fibers, good compliance and safety.

The authors declare no conflict of interest.

*e-mail; https://orcid.org/0000-0003-4364-0123

Treatment of facial nerve neuropathy

A combination of drug and non-drug methods is used for treatment. As a rule, doctors prescribe medications from these groups:

• non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen, meloxicam, nimesulide, diclofenac and other drugs; necessary to relieve pain and inflammation, eliminate swelling; used for mild to moderate neuropathy;
• glucocorticosteroids: prednisolone, hydrocortisone, dexamethasone; have an anti-inflammatory effect, relieve swelling; used for severe forms of the disease, as well as when NSAIDs are ineffective;
• diuretics: furosemide, lasix; necessary to eliminate tissue swelling;
• vascular drugs: pentoxifylline, nicotinic acid, cavinton; stimulate active blood flow in the affected area, improve tissue nutrition;
• metabolic agents: actovegin; necessary to stimulate metabolism and regenerate damaged structures;
• antiviral and antibacterial agents for the infectious nature of the pathology;
• anticholinesterase drugs: neuromidin, axamon; improve the transmission of excitation from nerve to muscle, help to quickly get rid of paralysis of facial muscles;
• B vitamins: milgamma, combilipen; stimulate nerve regeneration and improve impulse conduction.

If neuropathy has become chronic and muscle paresis has given way to spasm, muscle relaxants are prescribed: mydocalm, carbamazepine, baclofen. They replace anticholinesterase drugs and promote muscle relaxation. If these remedies are ineffective, injections based on botulinum toxin are used.

Drug treatment is complemented by physiotherapy. In the acute period the following are used:

• UHF;
• exposure to alternating magnetic field;
• phonophoresis with hormones.

After one and a half to two weeks from the onset of the disease, these methods are added:

• electrotherapy (diadynamic currents, etc.);
• electrical stimulation of muscles;
• electrophoresis;
• magnetic therapy;
• laser therapy;
• Darsonvalization.

An additional effect is provided by mud applications, therapeutic baths, and acupuncture.

During the acute period it is also recommended:

• sleep only on your side (affected side);
• tie a scarf around your face to prevent stretching of paralyzed muscles;
• carry out muscle taping: tighten the muscles using an adhesive plaster (duration from 30-60 minutes to 2-3 hours);
• tilt your head in the direction of the lesion several times a day and support the muscles with your palm; The duration of the procedure is 10-15 minutes.

After acute inflammation has subsided, it is recommended to perform therapeutic exercises to develop the affected muscles:

• frown and raise your eyebrows;
• open and close your eyes wide;
• widen the nostrils;
• puff out one's cheeks;
• smile with your mouth open and closed;
• stretch out your lips, blow out an imaginary candle, whistle;
• stick out tongue, etc.

The more the patient grimaces, the faster the muscles will recover. During the same period, a light therapeutic massage to stimulate blood circulation is acceptable.

If treatment does not bring effect within 2-3 months, doctors recommend using surgical treatment methods. Two types of operations are used:

• restoration of impulse transmission along the nerve: decompression of the nerve fiber when it is compressed in the canal of the temporal bone;
• reinnervation: replacement of the affected area with a donor nerve (segment of the hypoglossal, phrenic or accessory nerve, as well as healthy branches of the facial nerve);

The choice of a specific treatment method depends on the form of the disease, its cause, severity and level of damage.

Make an appointment