Neuropathy of the lower extremities: symptoms, causes

Neuritis

is an inflammation of the peripheral nerve trunk.

The peripheral nervous system refers to the nerve structures outside the brain and spinal cord (which are in turn called the central nervous system). Excitation (signal) is transmitted along the nerves, allowing the central nervous system to receive information about the state of all organs and systems of our body and control muscle contractions. The tissues of various organs are penetrated by nerve endings, which are connected to the brain, and in most cases to the spinal cord using bundles of nerve fibers enclosed in a sheath of connective tissue. Such bundles are called nerves, and large nerves are called nerve trunks.

With neuritis, nervous tissue is involved in the inflammatory process. This leads to the fact that the signal in some part of the nerve passes worse or does not pass at all. Accordingly, the sensitivity of any area may be lost and the mobility of the muscles innervated by the affected nerve may decrease.

Types of neuritis

A distinction is made between local neuritis and polyneuritis.

Local neuritis

is an inflammation of any one nerve (facial, auditory, oculomotor, glossopharyngeal, radial, sciatic, peroneal, femoral, etc.).
Polyneuritis
is multiple inflammation of the nerves. If the effect of the factor that caused the inflammation is local, only one nerve is affected. Polyneuritis develops under the influence of a systemic factor, which, as a rule, leads to degeneration of the nerve sheath and nerve fibers.

Classification of lower extremity neuropathy

The following types and forms of the disease are distinguished:

• inflammatory (develops due to inflammation of nerve tissue);
• toxic (occurs as a result of poisoning of the body with toxins);
• allergic (caused by individual hypersensitivity to environmental factors);
• traumatic (develops as a result of injuries to the lower extremities);
• axonal (accompanied by destruction of the axial cylinder of the nerve fiber);
• demyelinating (occurs in multiple sclerosis, encephalomyelitis).

According to the duration of its course, it can be acute and chronic, and according to the affected area - distal (affects distant parts of the legs) and proximal (affects the upper parts of the legs).

Causes of neuritis

Local neuritis is caused by:

• local infection;
• local hypothermia;
• injury. Often neuritis develops after a nerve injury;
• compression of the nerve. Thus, neuritis of the axillary nerve can develop due to prolonged use of a crutch, neuritis of the peroneal nerve - due to working in an uncomfortable position, etc.;
• arthritis (in this case the nerve of the joint may become inflamed);
• tumor (if the tumor compresses the nerve).

Multiple neuritis (polyneuritis) can be caused by such reasons as:

• infectious diseases, including measles, herpes, influenza, malaria, diphtheria and some others;
• intoxication. Poisoning with arsenic, lead, mercury, carbon monoxide, phosphorus, bismuth and other highly toxic substances can lead to the development of various types of neuritis. The most common cause of multiple neuritis is alcohol poisoning;
• systemic diseases (diabetes mellitus, rheumatism, gout);
• avitaminosis;
• vascular disorders;
• as well as some other reasons.

Sciatic nerve neuropathy. Piriformis syndrome

Diseases of the peripheral nervous system are one of the most common causes of disability in patients of working age. In the structure of these diseases, pain syndromes occupy a predominant place (N. N. Yakhno, 2003; G. R. Tabeeva, 2004). The reasons for the development of neuropathic pain syndrome can be different: diabetes mellitus, paraneoplastic processes, HIV, herpes, chronic alcoholism (A. M. Vein, 1997; I. A. Strokov, A. N. Barinov, 2002).

When the peripheral nervous system is damaged, two types of pain are distinguished: dysesthesia and truncal. Superficial dysesthetic pain is usually observed in patients with predominant damage to small nerve fibers. Truncal pain occurs with compression of the spinal roots and tunnel neuropathies.

In patients with this type of pain syndrome, it is impossible to choose the optimal treatment strategy without identifying the pathophysiological mechanisms. Therefore, when determining treatment tactics, it is necessary to take into account the localization, nature and severity of clinical manifestations of pain.

Compression-ischemic (tunnel) neuropathy refers to non-inflammatory lesions of the peripheral nerve that develop under the influence of compression or ischemic influences.

In the area of ​​compression of the corresponding nerve, painful compactions or thickening of tissue are often found, leading to a significant narrowing of the musculoskeletal sheaths through which the neurovascular trunks pass.

Currently, many variants of compression neuropathies are known. Their clinical picture consists of three syndromes: vertebral (in cases where the factor of the same name is involved), neural peripheral, reflex-myotonic or dystrophic. Vertebral syndrome at any stage of exacerbation, and even in remission, can cause changes in the walls of the “tunnel”. The myodystrophic focus, acting as a implementing link, causes neuropathy against the background of its clinical peak. The neurological picture of compression neuropathies consists of symptoms of damage of varying severity in the corresponding myo- and dermatomes. The diagnosis of compression neuropathies is made in the presence of pain and paresthesia in the area of ​​innervation of this nerve, motor and sensory disorders, as well as pain in the area of ​​the receptors of the corresponding channel and Tinel’s vibration symptom. If there are difficulties in diagnosis, electroneuromyographic studies are used: lesions of the peripheral neuron corresponding to a given nerve are determined, and the degree of decrease in the speed of impulse transmission along the nerve distal to the place of its compression. Piriformis syndrome is the most common tunnel neuropathy. Pathological tension of the piriformis muscle due to compression of the L5 or S1 root, as well as with unsuccessful injections of medicinal substances, leads to compression of the sciatic nerve (or its branches at high origin) and the accompanying vessels in the infrapiriformis space.

To choose the right treatment strategy, it is necessary to clearly know the main clinical symptoms of damage to a particular area. The main clinical manifestations of damage to the nerves of the sacral plexus:

• compression of nerves in the pelvis or above the gluteal fold;
• piriformis syndrome;
• damage to the sciatic nerve below the exit from the pelvis (at the level of the hip and below) or damage to the sciatic nerve in the pelvic cavity;
• sciatic nerve syndrome;
• tibial nerve syndrome;
• syndrome of the piriformis, internal obturator nerves and quadratus femoris nerve;
• superior gluteal nerve syndrome;
• inferior gluteal nerve syndrome.

The most difficult in terms of diagnosis are lesions in the pelvic area or above the gluteal fold - due to the presence of somatic or gynecological pathology in patients. Clinical symptoms of lesions in the pelvis or above the gluteal fold consist of the following types of disturbances of motor and sensory functions.

• Decrease and loss of function n. peroneus and n. tibialis communis, paralysis of the foot and fingers, loss of the Achilles and plantar reflexes, hypoesthesia (anesthesia) of the leg and foot.
• Reduction or loss of function of the biceps femoris, semimembranosus and semitendinosus muscles, leading to impaired flexion of the leg.
• Reduction or loss of function of the posterior cutaneous nerve of the thigh, leading to hypoesthesia (anesthesia) along the posterior surface of the thigh.
• Difficulty in external rotation of the hip.
• Presence of positive symptoms in Lasegue, Bonnet.
• The presence of vasomotor and trophic disorders (hypo-, hyperhidrosis, formation of trophic ulcers in the heel and outer edge of the foot, changes in nail growth, hypo- and hypertrichosis).

Damage to the sciatic nerve at the level of the infrapiriform foramen can be observed in two variants:

• damage to the trunk of the sciatic nerve itself;
• piriformis syndrome.

Compression of the sciatic nerve and adjacent vessels is characterized by the following clinical manifestations: a feeling of constant heaviness in the leg, dull, “cerebral” pain. There is no increase in pain when coughing or sneezing. There is no atrophy of the gluteal muscles. The zone of hypoesthesia does not extend above the knee joint.

Piriformis syndrome occurs in at least 50% of patients with discogenic lumbosacral radiculitis. If the patient is diagnosed with this, the assumption of the presence of piriformis muscle syndrome may arise in the presence of persistent pain along the sciatic nerve that does not decrease with drug treatment. It is much more difficult to determine the presence of this syndrome if there is only pain in the buttock area, which is limited in nature and associated with certain positions (movements) of the pelvis or when walking. Piriformis muscle syndrome is often recorded in gynecological practice. With piriformis syndrome it is possible:

• compression of the sciatic nerve between the altered piriformis muscle and the sacrospinous ligament;
• compression of the sciatic nerve by the altered piriformis muscle as the nerve passes through the muscle itself (a variant of the development of the sciatic nerve).

The clinical picture of piriformis syndrome consists of local symptoms and symptoms of compression of the sciatic nerve. Local includes aching, nagging, “braining” pain in the buttock, sacroiliac and hip joints, which intensifies when walking, standing, adducting the hip, and also in a squatting position; subsides somewhat when lying down and sitting with legs apart. With good relaxation of the gluteus maximus muscle, a dense and painful when stretched (Bonnet-Bobrovnikova symptom) piriformis muscle is felt underneath it. With percussion at the point of the piriformis muscle, pain appears on the back of the leg (Vilenkin's symptom). The clinical picture of compression of the vessels and the sciatic nerve in the infrapiriform space consists of the topographic-anatomical “relationship” of its tibial and fibular branches with the surrounding structures. Pain during compression of the sciatic nerve is dull, “brainy” in nature with a pronounced vegetative coloring (sensations of chilliness, burning, stiffness), with irradiation throughout the leg or mainly along the zone of innervation of the tibial and peroneal nerves. Provoking factors are heat, weather changes, and stressful situations. Sometimes the Achilles reflex and superficial sensitivity decrease. With the predominant involvement of the fibers from which the tibial nerve is formed, the pain is localized in the posterior group of muscles of the leg. Pain appears in them when walking, during the Lasègue test. Palpation reveals pain in the soleus and gastrocnemius muscles. In some patients, compression of the inferior gluteal artery and the vessels of the sciatic nerve itself is accompanied by a sharp transient spasm of the vessels of the leg, leading to intermittent claudication. The patient is forced to stop, sit down or lie down when walking. The skin of the leg turns pale. After resting, the patient can continue walking, but soon the same attack recurs. Thus, in addition to intermittent claudication with obliterating endarteritis, there is also infrapiriform intermittent claudication. An important diagnostic test is infiltration of the piriformis muscle with novocaine and assessment of the positive changes that occur. Reflex tension in the muscle and neurotrophic processes in it are caused, as a rule, by irritation not of the fifth lumbar, but of the first sacral root. Certain manual tests help recognize this syndrome.

• The presence of pain on palpation of the upper internal region of the greater trochanter of the femur (the place of attachment of the piriformis muscle).
• Pain on palpation of the lower part of the sacroiliac joint is a projection of the attachment site of the piriformis muscle.
• Passive adduction of the hip with simultaneous internal rotation (Bonnet-Bobrovnikova symptom; Bonnet symptom).
• A test to examine the sacrospinous ligament, which allows you to simultaneously diagnose the condition of the sacrospinous and iliosacral ligaments.
• Tapping the buttock (on the sore side). This causes pain that spreads along the back of the thigh.
• Grossman's sign. When struck with a hammer or folded fingers on the lower lumbar or upper sacral spinous processes, the gluteal muscles contract.

Since painful tension of the piriformis muscle is most often associated with irritation of the first sacral root, it is advisable to alternately carry out novocaine blockade of this root and novocainization of the piriformis muscle. A significant reduction or disappearance of pain along the sciatic nerve can be considered a dynamic test showing that the pain is caused by the compressive effect of the spasmed muscle.

Sciatic nerve lesions

Lesions of the sciatic nerve below the exit from the pelvis (at the level of the hip and below) or in the pelvic cavity are characterized by the following signs.

• Impaired flexion of the leg at the knee joint (paresis of the semitendinosus, semimembranosus and biceps femoris muscles).
• Specific gait: the straightened leg is carried forward when walking (due to the predominance of the tone of the antagonist muscle of the quadriceps femoris).
• Straightening the leg at the knee joint is a contraction of the antagonist (quadriceps femoris muscle).
• Lack of active movements in the foot and fingers as a result of their paresis.
• Atrophy of paralyzed muscles, which often masks the pastiness of the limb.
• Hypoesthesia along the posterior surface of the leg, dorsum of the foot, sole and toes.
• Impaired muscle-articular sensitivity in the ankle joint and interphalangeal joints of the toes.
• Lack of vibration sensitivity in the area of ​​the outer ankle.
• Pain along the sciatic nerve - at the Valle and Gar points.
• Positive Lasegue symptom.
• Reduction or disappearance of the Achilles and plantar reflexes.
• The presence of burning pain that intensifies when lowering the leg.

In addition to the clinical symptoms described above, the development of vasomotor and trophic disorders is likely: increased skin temperature on the affected leg. The lower leg and foot become cold and cyanotic. Hyperhidrosis or anhidrosis, hypotrichosis, and hyperkeratosis are often found on the sole. Changes in the color and shape of the nails, trophic disorders on the heel, dorsum of the toes, and the outer edge of the foot appear, a decrease in strength is recorded, as well as atrophy of the muscles of the foot and lower leg. The patient cannot stand on his toes or heels. The semitendinosus, semimembranosus, and biceps femoris strength tests can be used to determine initial sciatic nerve involvement.

Sciatic nerve syndrome (ischemic-compressive neuropathy of the sciatic nerve). Depending on the level (height) of the lesion, different variants of sciatic nerve syndrome are possible.

A very high level of damage (in the pelvis or above the gluteal fold) is characterized by: paralysis of the foot and toes, loss of the Achilles and plantar reflexes; anesthesia (hypoesthesia) of almost the entire lower leg and foot, except for zone n. sapheni; loss of function of the biceps femoris, semitendinosus, semimembranosus muscles; hypoesthesia (anesthesia) along the posterior surface of the thigh; inability to rotate the hip outward; the presence of positive symptoms of tension (Lasegue, Bonnet); the presence of vasomotor and trophic disorders (hyper- or hypotrichosis, hypo- or hyperhidrosis, changes in nail growth, the formation of trophic ulcers in the heel area and the outer edge of the foot).

A lesion at the level of the infrapiriformis foramen consists of two groups of symptoms - damage to the piriformis muscle itself and the sciatic nerve. The first group of symptoms includes: pain on palpation of the upper internal part of the greater trochanter of the femur (the place of attachment of the piriformis muscle to the capsule of this joint); pain on palpation in the lower part of the sacroiliac joint; Bonnet's symptom (passive adduction of the hip with its inward rotation, causing pain in the gluteal region, less often in the zone of innervation of the sciatic nerve); pain on palpation of the buttock at the point where the sciatic nerve exits from under the piriformis muscle. The second group includes symptoms of compression of the sciatic nerve and blood vessels. Painful sensations due to compression of the sciatic nerve are characterized by a feeling of constant heaviness in the leg, a dull, “cerebral” nature of the pain, no increase in pain when coughing and sneezing, as well as atrophy of the gluteal muscles; the hypoesthesia zone does not rise above the knee joint.

A lesion at the level of the hip (below the exit from the pelvis) and up to the level of division into the peroneal and tibial nerves is characterized by: impaired flexion of the leg at the knee joint; specific gait; lack of active movements in the foot and toes, which sag moderately; atrophy of paralyzed muscles that joins after 2–3 weeks, often masking the pastiness of the leg; hypoesthesia (anesthesia) on the posterior surface of the leg, dorsum of the foot, sole and toes; impairment of joint-muscular sensitivity in the ankle joint and interphalangeal joints of the toes; lack of vibration sensitivity on the outer ankle; pain along the sciatic nerve - at the points of Valle and Gar; positive Lasegue symptom; disappearance of the Achilles and plantar reflexes.

The syndrome of incomplete damage to the sciatic nerve is characterized by the presence of pain of a causalgic nature (“burning” pain, intensified when lowering the leg, provoked by a light touch); severe vasomotor and trophic disorders (for the first 2–3 weeks, the skin temperature on the affected leg is 3–5 °C higher (“hot skin”) than on the healthy leg, then the lower leg and foot become cold and cyanotic). Hyperhidrosis or anhidrosis, hypotrichosis, hyperkeratosis, changes in the shape, color and growth rate of nails are often found on the plantar surface. Sometimes trophic ulcers occur on the heel, the outer edge of the foot, and the dorsum of the toes. X-rays reveal osteoporosis and decalcification of the foot bones.

Initial sciatic nerve injury syndrome can be diagnosed by using tests to determine the strength of the semitendinosus and semimembranosus muscles.

Sciatic nerve syndrome most often appears as a result of damage to this nerve through the mechanism of tunnel syndrome when the piriformis muscle is involved in the pathological process. The trunk of the sciatic nerve can be affected by injuries, fractures of the pelvic bones, inflammatory and oncological diseases of the pelvis, lesions and diseases of the gluteal region, sacroiliac joint and hip joint. In sciatic nerve syndrome, the differential diagnosis often has to be made with discogenic compressive radiculitis LV-SII (Table).

Syndrome of the piriformis, internal obturator and quadratus femoris nerves. Complete piriformis, obturator internus, and quadratus femoris nerve syndrome is characterized by impaired lateral rotation of the hip. The syndrome of partial damage to this group of nerves can be diagnosed based on the use of tests to determine the range of motion and strength of the subject.

Superior gluteal nerve syndrome. Complete superior gluteal nerve syndrome is characterized by impaired abduction of the hip with partial impairment of hip rotation and difficulty maintaining an upright position of the torso. With bilateral paralysis of these muscles, it is difficult for the patient to stand (stands unsteadily) and walk (the so-called “duck walk” appears with waddling from side to side). Partial superior gluteal nerve syndrome can be identified with a gluteal strength test. Based on the degree of decrease in strength compared to the healthy side, a conclusion is made about partial damage to the superior gluteal nerve.

Inferior gluteal nerve syndrome. Complete inferior gluteal nerve syndrome is characterized by difficulty in straightening the leg at the hip joint, and in a standing position - difficulty in straightening a tilted pelvis (the pelvis is tilted forward, with compensatory lordosis observed in the lumbar spine). Difficulty getting up from a sitting position, climbing stairs, running, jumping. With prolonged damage to this nerve, hypotonia and hypotrophy of the gluteal muscles are observed. Partial inferior gluteal nerve syndrome can be diagnosed using a test to determine the strength of the gluteus maximus muscle. Based on the degree of decrease in the volume and strength of the indicated movement (and in comparison with the healthy side), a conclusion is made about the degree of dysfunction of the inferior gluteal nerve.

Treatment

Therapy of sciatic nerve neuropathy requires knowledge of the etiological and pathogenetic mechanisms of the development of the disease. Treatment tactics depend on the severity and rate of progression of the disease. Pathogenetic therapy should be aimed at eliminating the pathological process and its long-term consequences. In other cases, treatment should be symptomatic. Its goal is to prolong stable remission and improve the quality of life of patients. The main criterion for the optimal therapeutic effect on the patient is the combination of medicinal and non-medicinal methods. Among the latter, the leading ones are physiotherapeutic techniques and post-isometric relaxation methods.

If the function of the muscles of the pelvic girdle and lower limb is impaired, it is recommended to use one of the manual therapy techniques - post-isometric relaxation (PIR), i.e. stretching the spasmodic muscle to its physiological length after maximum tension. The basic principles of drug therapy for lesions of the peripheral nervous system are early initiation of treatment, pain relief, and a combination of pathogenetic and symptomatic therapy. Pathogenetic therapy is aimed primarily at combating oxidative stress, affecting the microvasculature, improving blood supply to the affected area, and relieving signs of neurogenic inflammation. For this purpose, antioxidant, vasoactive and nonsteroidal anti-inflammatory drugs (NSAIDs) are used. The complexity of drug therapy is associated in most cases with the intricate anatomical and physiological hierarchy of structures involved in the pathological process. This is partly due to the structure and functioning of the structures of the lumbosacral plexus. At the same time, the basic mechanism underlying the development of neuropathy is a clear correlation between compression and ischemia of the nerve and the development of oxidative stress.

Oxidative stress is an imbalance between the production of free radicals and the activity of antioxidant systems. The developed imbalance leads to increased production of compounds (neurotransmitters) released by damaged tissues: histamine, serotonin, ATP, leukotrienes, interleukins, prostaglandins, nitric oxide, etc. They lead to the development of neurogenic inflammation, increasing the permeability of the vascular wall, and also promote the release mast cells and leukocytes of prostaglandin E2, cytokines and biogenic amines, increasing the excitability of nociceptors.

Currently, clinical studies have appeared on the use of drugs that improve the rheological properties of blood and endothelium-dependent reactions of the vessel wall in patients with compression neuropathies. Drugs such as thioctic acid derivatives (thiogamma, thioctacid) and ginkgo biloba (tanakan) are successfully used to reduce the manifestations of oxidative stress. However, the use of drugs with a polyvalent mechanism of action (Cerebrolysin, Actovegin) is more pathogenetically justified.

The priority of using Actovegin is due to the possibility of its use for therapeutic blockades and its good compatibility with other drugs. For compression-ischemic neuropathies, both in the acute and subacute stages of the disease, it is advisable to use Actovegin, especially if there is no effect from other treatment methods. A drip of 200 mg of the drug is prescribed for 5 days, followed by a transition to oral administration.

In the mechanisms of development of diseases of the peripheral nervous system, an important place is occupied by hemodynamic disorders in the structures of the peripheral nervous system, ischemia, microcirculation disorders, energy exchange disorders in ischemic neurons with a decrease in aerobic energy exchange, ATP metabolism, oxygen and glucose utilization. Pathological processes occurring in nerve fibers during neuropathies require correction with vasoactive drugs. In order to improve microcirculation processes and activate metabolic and glycolysis processes in patients with tunnel neuropathies, Cavinton, Halidor, Trental, and Instenon are used.

Instenon is a combined drug with neuroprotective action, including a vasoactive agent from the group of purine derivatives, affecting the state of the ascending reticular formation and cortical-subcortical relationships, as well as the processes of tissue respiration under hypoxic conditions, physiological mechanisms of autoregulation of cerebral and systemic blood flow. For neuropathies, instenon is used intravenously, 2 ml in 200 ml of saline, for 2 hours, 5–10 procedures per course. Then oral administration of instenon forte continues, 1 tablet 3 times a day for a month. For neuropathies with sympathetic syndrome, the use of instenon 2 ml intramuscularly once a day for 10 days is indicated. For compression-ischemic (tunnel) neuropathies, a similar technique is used. This helps improve microcirculation and metabolism in the ischemic nerve. A particularly good effect is observed with the combined use of Actovegin (drops) and instenon (intramuscular injections or oral administration).

Halidor (bencyclane fumarate) is a drug with a wide spectrum of action, which is due to the blockade of phosphodiesterase, antiserotonin effect, and calcium antagonism. Halidor is prescribed in a daily dose of 400 mg for 10–14 days.

Trental (pentoxifylline) is used 400 mg 2-3 times a day orally or 100-300 mg intravenously in 250 ml of saline.

Prescribing combination drugs that include large doses of vitamin B, anti-inflammatory drugs and hormones is inappropriate.

NSAIDs remain the first-line drugs for pain relief. The main mechanism of action of NSAIDs is inhibition of cyclooxygenase (COX-1, COX-2), a key enzyme in the arachidonic acid metabolic cascade, leading to the synthesis of prostaglandins, prostacyclins and thromboxanes. Due to the fact that COX metabolism plays a major role in the induction of pain at the site of inflammation and the transmission of nociceptive impulses to the spinal cord, NSAIDs are widely used in neurological practice. There is evidence that 300 million patients take them (G. Ya. Schwartz, 2002).

All anti-inflammatory drugs have anti-inflammatory, analgesic and antipyretic effects, are able to inhibit the migration of neutrophils to the site of inflammation and platelet aggregation, and also actively bind to serum proteins. Differences in the action of NSAIDs are quantitative (G. Ya. Schwartz, 2002), but they determine the severity of the therapeutic effect, tolerability and the likelihood of side effects in patients. The high gastrotoxicity of NSAIDs, which correlates with the severity of their sanogenetic effect, is associated with indiscriminate inhibition of both isoforms of cyclooxygenase. In this regard, for the treatment of severe pain syndromes, including long-term ones, drugs are needed that have anti-inflammatory and analgesic effects with minimal gastrotoxic reactions. The most well-known and effective drug from this group is xefocam (lornoxicam).

Xefocam is a drug with a pronounced antianginal effect, which is achieved through a combination of anti-inflammatory and strong analgesic effects. It is today one of the most effective and safe modern analgesics, which has been confirmed by clinical studies. The effectiveness of oral administration according to the following regimen: 1st day - 16 and 8 mg; Days 2–4 - 8 mg 2 times a day, day 5 - 8 mg/day - for acute back pain has been reliably proven. The analgesic effect at a dose of 2–16 mg 2 times a day is several times higher than that of napraxen. For tunnel neuropathies, it is recommended to use the drug in a dose of 16–32 mg. The course of treatment is at least 5 days with a one-time daily procedure. It is recommended to use the drug Xefocam for the treatment of piriformis muscle syndrome according to the following method: in the morning - 8 mg intramuscularly, in the evening - 8-16 mg orally, for 5-10 days, which allows you to achieve a quick and accurate effect on the source of inflammation with complete anesthesia with minimal risk development of adverse reactions. It is possible to carry out regional intramuscular blockades in the paravertebral region, 8 mg per 4 ml of 5% glucose solution daily for 3–8 days. Symptomatic therapy is the method of choice for relieving algic manifestations. Most often, therapeutic blockades with anesthetics are used to treat tunnel neuropathies. Persistent pain lasting more than 3 weeks indicates a chronic process. Chronic pain is a complex therapeutic problem that requires an individual approach.

First of all, it is necessary to exclude other causes of pain, after which it is advisable to prescribe antidepressants.

M. V. Putilina , Doctor of Medical Sciences, Professor of Russian State Medical University, Moscow

Symptoms of neuritis

The main symptoms of neuritis are:

Pain along the nerve

The most common symptom of neuritis is pain along the affected nerve. The pain, as a rule, is dull in nature and intensifies in the cold, with physical activity or uncomfortable body position.

Sensory impairment

Sensory loss in the area of ​​the affected nerve is common. It can manifest itself in the form of numbness, tingling, or “pins and needles.”

Decreased muscle activity

There is a partial decrease in muscle strength (paresis), a decrease or loss of tendon reflexes, and in some cases, muscle paralysis (complete cessation of muscle activity).

Vegetative and trophic disorders

With neuritis, there may be such vegetative and trophic disorders as depigmentation of the skin, the acquisition of a bluish tint, local hair loss, increased sweating and dry skin, swelling.

What should you avoid if you have sciatica?

First of all, you should avoid hypothermia: do not stay in the cold or open wind for a long time, do not lie on cold surfaces, do not swim in cold water. To strengthen the immune system, you need to strengthen the body with exercise therapy, water treatments, yoga, and massage.

It will be important to change your occupation if it involves heavy physical work. It is also necessary to limit long stays in one position, sharp bends and turns of the body, running, fast walking, and transferring the entire body weight to the affected leg.

If you tend to be overweight, it is recommended to create a diet. Excess weight will aggravate the inflammatory process and increase pain.

Treatment methods for neuritis

Neuritis must be treated. At the first signs of the disease, you should consult a neurologist. If treatment for neuritis is not started on time, the risk of developing paresis and muscle paralysis increases.

Treatment of neuritis is aimed, first of all, at eliminating the cause that caused it. If neuritis is of infectious origin, antibacterial therapy or antiviral drugs are used. If neuritis is of toxic origin, it is important to remove toxins from the body.

Drug treatment

In addition to antibacterial or antiviral drugs, the course of treatment for neuritis usually includes:

• B vitamins
• drugs that improve blood microcirculation
• drugs that increase the conductivity of nerve fibers

Massage

Massage of the muscles innervated by the affected nerve is recommended. Massage can be combined with heat therapy (infrared sauna).

More information about the treatment method

Physiotherapy

For neuritis, physical therapy methods such as electrophoresis, diadynamic therapy, SMT therapy, ultrasound therapy, magnetic therapy, and laser therapy can be used.

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Diagnostics

Diagnosis of polyneuropathy requires a comprehensive examination, which includes:

• survey: identifying patient complaints, clarifying the time and circumstances of the occurrence of each symptom;
• taking an anamnesis: recording all past diseases, injuries, intoxications, chronic pathologies, hereditary risk factors, etc.;
• neurological examination: assessment of skin and proprioceptive (spatial) sensitivity, motor function, muscle strength, quality of reflexes;
• consultations with specialized specialists: endocrinologist, narcologist, toxicologist, nephrologist, etc.;
• general urine test, general blood test, blood biochemistry (determination of glucose levels, lipid spectrum, vitamins and microelements, kidney function indicators and other parameters);
• blood test for HIV and other infections;
• genetic and immunological studies according to indications;
• Electroneuromyography allows you to identify lesions of nerve fibers and exclude other diseases with similar symptoms;
• biopsy of nerve and muscle tissue;
• lumbar puncture (examination of cerebrospinal fluid) to exclude neuroinfections;
• Doppler ultrasound of the vessels of the lower extremities.

The list of examinations can be adjusted depending on the form of polyneuropathy and concomitant pathology.