Neuropathy. What kind of disease is polyneuropathy? Symptoms and treatment, life prognosis for polyneuropathy What is the danger of sensory diabetic neuropathy

Polyneuropathy is a group of pathologies that affects nerve endings in the human body.

This disease has a different etiology, and the factors that provoke this pathology first of all affect the fibers of the nervous system and disrupt the functionality of this system.

This is a disease that progresses and has a protracted form that becomes chronic.

Its most common manifestation is in the lower extremities.

Polyneuropathy - what is it?

Polyneuropathy is damage to blood vessels, as well as nerve fibers in the peripheral parts of the human body. This disease is often called polyneuropathy, and is also called polyradiculoneuropathy, or polyneuritis.

Polyneuritis is the name for a rather rare type of pathology, because inflammation in polyneuropathy occurs rarely, but this type of polyneuropathy is still found in medicine.

The basis of the disease neuropathy is the following conditions:

• Factor of metabolic disorders in the body (diabetic polyneuropathy;
• Ischemic factors;
• Mechanical damage to nerve fibers (morphological disturbances occur in the fibers of the nervous system);
• Infectious etiology of nerve fibers;
• Inflammatory processes in muscle and nerve cells of tissues.

If neuropathy, in addition to the nerve fibers of the peripheral part, also affects the roots of the spinal cord of the body, then polyneuroradiculopathy develops.

There are quite a few causes of polyneuropathy; any provoking factor that negatively affects the nerve fibers of the peripheral sphere of the nervous system, and also affects the peripheral vascular system, can trigger the process of inflammation in the body and develop neuropathy.

Although some types of polyneuropathy may occur with an unidentified etiology.

ICD-10 code

According to the international classification of diseases, tenth revision ICD-10, this pathology belongs to the class “Polyneuropathies and other disorders in the peripheral nervous system” and has the code:

Depending on the signs of damage and the extent of damage to the fibers of the nervous system, the following types of polyneuropathy pathology are distinguished:

• Sensory neuropathy- these are signs of pain, as well as numbness of the lower extremities with a burning sensation in these parts of the body;
• Motor sickness— develops atrophy of muscle fibers with muscle weakness;
• - simultaneous manifestation of motor signs, as well as insufficiency of the sensory functions of nerve fibers;
• Autonomic polyneuropathy- there are signs of strong sweat production by the body, dry skin, as well as constant signs of improper bowel movements, which are associated with constipation;
• Mixed pathology- with this type, signs of all types of polyneuropathy can appear simultaneously.

Causes of polyneuropathy

Polyneuropathies are a whole complex of diseases that have the same development and disorders in the peripheral parts, but have different etiologies.

The main types of etiology can be:

• Alcohol poisoning of the body (alcohol);
• Causes of poisoning by chemicals - gas, mercury poisoning, or arsenic (toxic);
• The etiology is chronic (diabetic polyneuropathy);
• Systemic diseases in the body;
• When taking medicine for a long period of medication course (medicinal type of polyneuropathy);
• Reduced immunity (autoimmune pathology);
• Etiology of genetic hereditary nature;
• The cause of polyneuropathy may be HIV or AIDS;
• Disturbances in metabolic processes in the body.

How does pathology develop?

Pathology can develop according to the following type of nature of its occurrence:

• The inflammatory process as a provocateur of polyneuropathy. There is an intensive progression of the inflammation process in the nerve fibers;
• When ingested, polyneuropathy of a toxicological nature develops, affecting the sensitivity of nerve impulses in peripheral fibers;
• Pathologies with an allergic etiology occur, and the progression of the disease occurs as allergic reactions develop;
• The traumatic nature of the disease occurs as a consequence of injury to the vascular system and fibers of the nervous system.

This disease of blood vessels and peripheral nerve endings is a very complex pathology that must be diagnosed and treated in a timely manner, because the complicated form of this pathology is dangerous to human life (this is paralysis of the body, as well as paralysis of all respiratory organs).

Types of pathology

According to the mechanism of disorder and damage, polyneuropathy is divided into:

• Pathology of demyelinating type. This disease is caused by a disruption of the metabolic process in the body and occurs with the breakdown of protein, which was inextricably linked with the membranes of nerve fibers;
• Axonal pathology. This is a violation of the functional responsibilities of the core of the nervous system and a violation of the passage of impulses through all fibers. The disease is characterized by a severe course and a long treatment process;
• Neuropathic form of the disease. With this pathology, it is the nerve fiber cells that are affected;
• Diphtheria polyneuropathy, provoked by infection entering the body;
• The diabetic type of pathology is caused by the course of diabetes mellitus in the body;
• Alcoholic type of neuropathy.

Based on the nature of the development of damage to peripheral organs, the following forms are distinguished:

• Acute form of pathology development- this is a lightning-fast emergence and development, lasting up to 4 calendar days. The treatment process lasts several calendar weeks;
• Chronic development of the disease (subacute). This form of the disease develops over several weeks. The treatment process lasts individually for each person, but on average, according to statistics, up to several calendar months.

There is also a clear classification of polyneuropathy according to its origin:

• Alimentary form of pathology development;
• Genetic hereditary etiology of the disease;
• Autoimmune polyneuropathy;
• Metabolic nature of the disease (hepatic polyneuropathy, uremic, and diabetic);
• The occurrence of pathology is of an infectious-toxic nature.

Pathology is also divided depending on the pathology process:

• Axonal nerve damage— the disease develops from damage to the nerve axon;
• Demyelinating polyneuropathy— pathology develops from demyelination of fibers of the peripheral nervous system.

Polyneuropathy during intrauterine gestation

Until recently, neuropathy was considered a postpartum pathology, but now it has been proven that Polyneuropathy during pregnancy can develop in any trimester of the baby’s intrauterine development.

The etiology of polyneuropathy in pregnant women is distinguished:

• Deficiency of B vitamins during fetal development;
• The body's sensitivity to proteins that penetrate the placental canal from the developing fetus. They become foreign to the pregnant woman’s body;
• The influence of toxic elements of food on peripheral nerves and their centers.

For pregnant women, the main method of therapy is the replenishment of B vitamins in the body, as well as desensitizing treatment.

Symptoms of polyneuropathy

The symptoms of polyneuropathy for all its types are usually the same: the symptoms are the same for the diabetic and alcoholic types, for the genetic and hereditary type, as well as for the toxic type.

The symptoms are the same with axonal demyelinating polyneuropathy.

Polyneuritic symptoms in neurology are considered:

Diagnostics

To make a correct diagnosis and determine the type of polyneuropathy, it is necessary to undergo a number of diagnostic examinations of the body:

• The first step is to go to an appointment with a neurologist, or neurologist, who will visually examine the patient;
• Also necessary for this pathology is the collection of anamnesis;
• It is very important to find out whether blood relatives have suffered from polyneuropathy;
• It is determined whether the patient is addicted to alcohol;
• After collecting anamnesis, an instrumental examination and clinical laboratory tests are prescribed;
• Biochemical blood test to detect glucose in the blood, as well as the functioning of protein metabolism, and the presence of breakdown products of toxic substances and heavy metals in the blood;
• Method of palpation of nerve fibers;
• Cerebrospinal fluid examination;
• Study of reflexes;
• Nerve fiber biopsy, which involves microscopy of the state of the peripheral nervous system;
• Instrumental diagnostics electroneuromyography is a study of the speed with which nerve impulses pass through the fibers of the system. This method allows you to identify areas where fiber damage exists;
• Radiography;
• Ultrasound (ultrasound examination);
• Examination by an endocrinologist and examination of the endocrine system as prescribed by the doctor.

Treatment of polyneuropathy

Treatment of polyneuropathy must be comprehensive, at the same time therapy should be aimed at treating the root cause of the pathology and also therapy at relieving severe symptoms of PSP.

Since PSP is a group of pathologies that have different underlying causes, therefore, drugs are selected for each group to treat this type of pathology.

With the metabolic type of polyneuropathy (secondary), it is quite difficult to choose a medication course, because this type of disease is complicated by diabetes mellitus (mostly stage 2).

Polyneuropathic syndrome in diabetes is treated by individual selection of a drug complex, taking into account destruction in the distal parts of the nerve fibers, as well as taking into account damage to the vegetative-vascular system.

If myelinopathy is diagnosed, lymph irradiation and the drug Cyclophosphamide are used. In severe cases of PSP, immunosuppressants are often prescribed with hormonal therapy.

Immunomodulatory therapy is used, which is prescribed by the attending doctor, and combines the necessary groups of therapeutic drugs. Plasmapheresis is often used in treatment. Treatment is carried out only in a hospital setting and under the strict supervision of the attending doctor.

Physiotherapeutic activities include:

• Exposure of nerve fibers to magnetic fields—magnetic therapy;
• Restoration of impulses in nerve fibers using electrical stimulation;
• Reflex therapeutic methods.

How long does it take to treat and is polyneuropathy completely curable? Treatment of this pathology takes a fairly long period of time - from several weeks (acute form of PSP) to several calendar months (with chronic type of PSP).

PSP is a pathology that cannot be completely cured, but painful symptoms can be relieved with the help of modern treatment methods, as well as stopping the destructive process of the peripheral parts of the vascular and nervous system.

Drugs for the treatment of polyneuropathy

Complications of polyneuropathy

The consequences of the development of PSP pathology are drastic, but there are not many complications of this pathology:

• Sudden cardiac arrest, resulting in death;
• Complete paralysis of the body, as consequences of impaired motor functions of the body;
• Deviations in the respiratory organs, which can lead to destruction of these organs, leading to death.

Nutrition for polyneuropathy

Food should be soft, ground, or liquid. The cooking process is only boiling and steaming; it is not allowed to use the technology of frying foods. You need to drink up to 2 liters of water.

The diet includes the following foods:

• Dried white bread;
• Soups made from vegetable broth and pureed in a blender;
• Soups made from dairy products with the addition of butter;
• Boiled lean meat and boiled vegetables;
• Low-fat steamed fish;
• Dairy products;
• Viscous porridge;
• Berry and vegetable juices;
• Steamed vegetables;
• Vegetable and fruit salads;
• The tea is not strong.

If the cause is atherosclerosis, then a cholesterol-free diet is used.

Prevention

Prevention is entirely aimed at eliminating the factors that provoke the development of polyneuropathy:

• Completely stop drinking alcoholic beverages;
• Get rid of nicotine and drug addiction;
• Do not self-medicate the root cause of the pathology, and do not select medications for yourself to treat various diseases in the body;
• To prevent any pathology from developing into a complicated form - timely treatment of the disease is necessary;
• Systematically engage in physical education;
• Take vitamins systematically, especially B vitamins;
• Constant control of blood glucose;
• Attend therapeutic massage procedures;
• Nutrition culture and diet for polyneuropathy.

Prognosis for life with polyneuropathy

If the pathology is diagnosed in a timely manner and complex therapy is prescribed to treat the disease and restore damaged organs, then the prognosis for life is more favorable.

In chronic and advanced stages of polyneuropathy, the prognosis is unfavorable, because there is no way to cure the pathology.

Neuropathy is a non-inflammatory disease of the nervous system that progresses due to damage or depletion of nerve cells. Pathology has no restrictions regarding age or gender. It is worth noting that this painful condition can affect either one nerve fiber or several at once, and they are not always located at the same point in the body.

Etiology

The manifestation of symptoms of the disease can be caused by many reasons. Among the most common are the following:

• metabolic disorder;
• traumatization of nerve fibers of any severity level;
• the presence of benign or malignant tumors;
• pathologies of blood vessels;
• intoxication of the body;
• endocrine diseases;
• decreased body reactivity;
• blood pathologies;
• chronic alcoholism;
• infections of viral and bacterial nature;
• severe hypothermia of the body;
• hereditary factor.

Varieties

In medicine, several classifications of the disease are used, which are based on the causes of occurrence and the nature of damage to nerve fibers.

Classification depending on the reasons for the progression of the pathology:

• diabetic neuropathy. This form of pathology progresses against the background of a decrease in blood glucose concentration. Usually develops with;
• post-traumatic neuropathy. The main reasons for its progression are mechanical trauma to the nerve fiber and its branches, compression of them, or surgical intervention in the affected area. In most clinical situations, this form of pathology affects the ulnar nerve, sciatic, radial, and also the nerves of the lower extremities. The most common causes of injury are neuropathy of the radial, peroneal, and ulnar nerves;
• alcoholic neuropathy. The reason for the progression is the consumption of large quantities of drinks containing high doses of alcohol. This substance, as well as its breakdown products, significantly complicate the metabolic process, in particular, the absorption of vitamins in the intestine. This, in turn, leads to, which becomes the cause of the progression of alcoholic neuropathy;
• ischemic form. This type of disease develops due to a disruption in the blood supply to the nerve endings.

Based on the nature of damage to nerve fibers, the following types of disease are distinguished:

• sensory neuropathy. It is characterized by a violation of the sensitivity of a certain organ in the human body. Manifested by the absence of pain, numbness and tingling, as well as phantom pain;
• peripheral neuropathy. Its progression is said to occur if the physiological process of transmission of nerve impulses from the central nervous system to the organs innervated by the affected nerve fibers is disrupted. As a result, peripheral neuropathy is manifested by the following symptoms: decreased or complete loss of sensitivity, muscle weakness, cramps, tics and impaired coordination of movements (usually this symptom manifests itself in the case of neuropathy of the lower extremities, neuropathy of the radial nerve, etc.);
• motor neuropathy. A characteristic symptom is inadequate motor activity. It is noteworthy that no decrease in sensitivity is observed. Characteristic symptoms: the patient makes movements with his limbs that he cannot control, some muscle reflexes disappear, muscle weakness gradually increases;
• Autonomic neuropathy. In this case, the innervation of internal organs is disrupted. This form of pathology is rightfully considered the most dangerous, since if it progresses, there is a disruption in the functioning of certain organs and systems. In particular, the patient may have problems with urination, swallowing, and defecation.

Depending on the affected nerve fiber:

• peroneal nerve neuropathy;
• ulnar nerve neuropathy;
• radial nerve neuropathy;
• damage to the trigeminal nerve;
• damage to the nerves of the lower extremities.

Symptoms

Symptoms of the disease largely depend on which nerve fiber (or fibers) were compressed or injured. In fact, there are quite a lot of signs of this disease, but most of them are not characteristic, which to a certain extent creates difficulties in making an accurate diagnosis.

Diabetic form

Diabetic neuropathy is the most common complication of diabetes mellitus. The most common manifestation of this disease is peripheral neuropathy. Manifestations of the disease are multiple, since the pathological process involves the spinal nerves, as well as the nerves responsible for the functioning of internal organs.

Symptoms of diabetic neuropathy (in case of progression of peripheral neuropathy):

• tingling in the legs;
• the muscle structures of the limbs may change their shape as diabetic neuropathy progresses;
• the patient may note that at one time he feels a strong coldness in the extremities, and at another moment a feeling of heat arises in them;
• feeling of "crawling" in the limbs;
• pain in the extremities (manifests mainly at night);
• increased sensitivity to tactile touch. Sometimes even a light touch can cause pain;
• a characteristic sign of peripheral neuropathy is the feeling of gloves or socks on the limbs, but they are bare;
• burning in the limbs;
• wounds caused by existing peripheral neuropathy take a very long time to heal.

Autonomic diabetic neuropathy manifests itself with the following symptoms:

• nausea and vomiting;
• dizziness when trying to change body position;
• heartburn;
• problems with urine output;
• , which can manifest itself even in a state of complete rest;
• erectile dysfunction;
• irregular bowel movements;
• even in the case of severe overcrowding of the bladder, there is no urge to urinate;
• loss of consciousness, despite there being no apparent reason for this;
• increased sweating;
• excessive dryness of the skin.

Facial nerve damage

Facial nerve neuropathy is very common. It is also called trigeminal neuropathy in medical literature. Usually it is provoked by hypothermia of the nerve fiber, so the disease has its own seasonality. More often it occurs in the autumn-winter period. Neuropathy of the facial nerve begins acutely - the symptoms and the degree of their severity directly depend on the location of the lesion.

Symptoms of facial nerve neuropathy:

• salivation;
• half of the face, where the affected nerve is localized, seems to freeze;
• violation of taste perception;
• with neuropathy of the facial nerve, there is severe pain from the affected nerve;
• the eye does not close fully and the person cannot blink;
• a characteristic symptom of neuropathy of the facial nerve is the front part of the tongue becomes numb;
• lacrimation;
• Sometimes severe dryness of the eye may occur.

Peroneal nerve damage

Peroneal nerve neuropathy usually affects girls between the ages of 10 and 19 years. It is worth noting that this disease has a poor prognosis. Peroneal nerve neuropathy can be triggered by injury to the knee joint or ligamentous apparatus, bone fractures, surgical intervention along the path of the nerve fiber, etc.

Symptoms of peroneal nerve neuropathy:

• the ability to rotate the foot is gradually lost;
• patients may suddenly twist their ankle while walking or running;
• inability to bend and straighten your toes normally;
• foot drop;
• a person cannot walk on his heels.

Therapeutic measures

Treatment of neuropathy should be carried out as soon as the first alarming signs of pathology progression appear. To prescribe the correct course of treatment, you must visit your doctor. Self-medication is not acceptable.

Treatment of neuropathy is performed sequentially. Necessary activities:

• elimination of the damaging factor (compression);
• elimination of inflammation;
• pain relief;
• restoration of the full functioning of the affected nerve fiber;
• stimulation of regenerative processes;
• treatment of ailments that provoked pathology (if any);
• relapse prevention.

Is everything in the article correct from a medical point of view?

Answer only if you have proven medical knowledge

Diseases with similar symptoms:

Migraine is a fairly common neurological disease accompanied by severe paroxysmal headaches. Migraine, the symptoms of which are pain, concentrated on one side of the head mainly in the area of ​​the eyes, temples and forehead, nausea, and in some cases vomiting, occurs without reference to brain tumors, stroke and serious head injuries, although and may indicate the relevance of the development of certain pathologies.

Definition
Polyneuropathies (polyradiculoneuropathies) are a large heterogeneous group of diseases caused by the influence of exogenous and endogenous factors, characterized by multiple, mainly distal, symmetrical damage to the peripheral nerves, manifested by sensory, motor, trophic and autonomic-vascular disorders.

Epidemiology
Generalized data on the epidemiology of polyneuropathies for a number of reasons (imperfect registration forms, syndromic nature of the lesion in many somatic diseases, etc.) are far from complete. The primary incidence of polyneuropathies is about 40 per 100,000 population per year. Among diseases of the peripheral nervous system, polyneuropathy ranks second after vertebrogenic lesions and is undoubtedly a common cause of temporary disability and disability. For example, of those who have undergone AIDP, 32% of patients become disabled, of which about 5% are confined to a bed or chair. About 15% of patients with diabetes have disability due to polyneuropathy. Chronic neuropathies of toxic, autoimmune, and diabetic etiology most significantly and for a long time limit the vital functions of patients and lead to social failure.

Classification
(WHO, 1982; as amended)
I.Depending on the morphological features of the lesion:
1) axonopathy: axonal degeneration of predominantly the distal part of the axon with simultaneous destruction of the myelin sheath and muscle atrophy. Functional recovery is usually slow and incomplete or does not occur. With ENMG, the speed of impulse transmission along motor fibers decreases slightly, but the number of functioning motor units decreases;
2) myelinopathy: segmental demyelination with primary damage to myelin and Schwann cells with preservation of axons and blockade of conduction along nerve fibers.
Complete or partial remyelination with restoration of function and moderate or mild residual defect is possible. The conduction velocity along motor fibers, according to ENMG data, is reduced to 20-60% of normal or less. The number of functioning motor units is reduced.
Pathomorphological differences between axonopathies and myelinopathies are not always clear; combined damage to axons and myelin sheaths is possible, which makes the clinical prognosis questionable.

II. According to the predominant clinical signs:
1) motor polyneuropathy;
2) sensitive polyneuropathy;
3) autonomic polyneuropathy;
4) mixed polyneuropathy (sensorimotor and autonomic);
5) combined: simultaneous or sequential damage to peripheral nerves, roots (polyradiculoneuropathy, multiple mono-, polyneuropathy) or the central nervous system (encephalomyelopolyradiculoneuropathy, etc.).

III. According to the nature of the flow:
1) acute (sudden onset, rapid development);
2) subacute;
3) chronic (gradual onset and development);
4) recurrent (acute or chronic with periods of partial or complete restoration of functions).

IV. Classification according to etiological (pathogenetic) principle:
1) infectious and autoimmune;
2) hereditary;
3) somatogenic;
4) for diffuse connective tissue diseases;
5) toxic (including medicinal);
6) caused by the influence of physical factors (vibration disease, cold, etc.).

Risk factors for occurrence, progression
1. General: a) unbalanced diet (vitaminosis B); b) old age; c) diabetes mellitus; d) cancer; e) hypothermia; f) insufficient or inadequate therapy for somatic and endocrine diseases.

2. Caused by the etiology of polyneuropathy: a) professional and household intoxication; b) the impact of physical factors in the process of work; c) overdose and uncontrolled use of certain medications; d) infectious diseases: diphtheria, influenza, brucellosis, HIV infection; leprosy, etc.; e) vaccination; f) history of hereditary neuropathies.

Clinic and diagnostic criteria
I. General clinical criteria:
1.Anamnesis: risk factors for polyneuropathies, including occupational ones; typical onset and development of the disease (paresthesia, pain, less often - muscle weakness in the distal lower extremities).

2. Symmetry of sensory, motor, autonomic disorders, their combination (with varying severity depending on the etiology of the disease) and ascending distribution. Isolated motor, sensory or autonomic polyneuropathy is rare.
3. A variety of sensory disorders, mostly subjective. Sympathalgic (hyperpathic) nature of pain (burning, tingling), usually intense, difficult to tolerate by patients. Distal hypalgesia, as well as a violation of deep (vibration, muscle-articular) sensitivity.
4. Common autonomic disorders, often manifested by symptoms of progressive autonomic failure, and distinct trophic disorders.

II. Features of the clinical picture due to the etiology of polyneuropathy (the forms that are most significant in neurological, including expert, practice are presented):
1. Infectious and autoimmune. A wide group of polyneuropathies, mainly secondary (parainfectious, post-vaccination). They can be caused by direct effects of an infectious agent on peripheral nerves (with rabies, brucellosis, leptospirosis, leprosy, herpes and HIV infections) and indirectly (toxic, due to an autoimmune process): primary inflammatory, with diphtheria, botulism, typhus, etc.
1.1.Acute inflammatory demyelinating polyneuropathy Guillain-Barré (AIDP).
There is reason to distinguish acute primary polyradiculopathy as an independent disease of an autoimmune nature with a trigger factor, most often in the form of a viral infection, and Guillain-Barré syndrome in various clearly defined diseases (diphtheria, primary amyloidosis, intermittent porphyria, lupus erythematosus, myeloma, etc. ). True Guillain-Barré polyradiculopathy is a common disease (1.2-1.7 per 100,000 population). It is more common at the age of 20-50 years, in men and people with manual labor. Preceding events - acute respiratory diseases, sore throat, hypothermia, fatigue. Subfibrillation is common, sometimes the temperature rises to 38-39°. Often accelerated ESR, moderate leukocytosis. The development is acute, subacute, usually begins with sensory disorders (paresthesia, pain in the legs), less often with motor ones. Symptoms increase over an average of 20 days. Motor disturbances (sluggish, sometimes mixed paresis and paralysis) are initially manifested by lower paraparesis of various distributions (usually distal, diffuse, less often proximal). Tetraparesis develops over time. Reflexes symmetrically decrease or disappear. With mixed paresis, pathological foot signs are possible. In 30% of patients, we can talk about a predominantly motor variant of the disease. In almost 30% of patients, the motor defect clearly predominates. Sensitivity disorders of the radicular, radicular-polyneuritic or polyneuritic type (in the form of “socks” and “gloves”). Radicular and distal pain with a hyperpathic component, Lasegue's symptom is observed in half of the patients at the onset of the disease. In some cases, deep sensitivity suffers, manifested by sensory ataxia. Cranial nerves are affected in 25-50% of patients (usually the facial nerve). The nerves of the bulbar group are usually involved in the process (along with the phrenic and intercostal ones) in the ascending course of the disease according to the type of Landry's palsy. Breathing problems occur, requiring respiratory assistance. Restoration of spontaneous breathing often occurs after 2-3 weeks, although death is also possible. Autonomic and trophic disorders in the extremities are typical (cyanosis and pastosity of the feet, hands, hyperhidrosis or dry skin, bedsores). In severe cases of AIDP, a typical syndrome of progressive autonomic failure often develops: orthostatic hypotension, tachycardia, paroxysmal arrhythmia with ECG changes, pelvic disorders and other characteristic symptoms. Acute cardiovascular failure due to autonomic dysfunction can cause the death of the patient. From the second week of the disease, protein-cell dissociation in the cerebrospinal fluid is constantly detected (the amount of protein is from 0.45 to 5.0 g/l).
Criteria for diagnosing ARDP: 1) symmetrical weakness in all extremities; 2) paresthesia in the hands and feet; 3) decreased or absent reflexes starting from the first week of the disease; 4) progression of the listed symptoms from several days to 1 month; 5) an increase in protein content in the cerebrospinal fluid (more than 0.45 g/l) during the first three weeks from the onset of the disease; 6) a decrease in the speed of propagation of excitation along the motor and (or) sensory fibers of the nerve and the absence, especially at the early stage of the disease, of damage to the axial cylinder (according to ENMG).
Due to the peculiarities of the clinical picture, it is advisable to distinguish between polyradiculoneuropathy and myelopolyradiculoneuropathy (Margulis variant), which occurs in 5% of patients. Possible widespread damage to the central nervous system (encephalomyelopolyradiculopathy). A predominantly axonal variant of ARDP has also been described - motor or motor-sensory axonal neuropathy with the acute development of tetraplegia, bulbar and respiratory disorders.

Depending on the severity of symptoms in the acute period, 3 degrees of severity of the disease are distinguished: a) mild (in 27% of patients): moderate severity of paresis, sensory disorders, pain syndrome; b) moderate severity (45%): para- and tetraparesis, severe pain and other sensitivity disorders; c) severe (19%): paralysis and severe paresis of the limbs, significant sensory, trophic and autonomic disorders, often an ascending course similar to Landry’s paralysis with rapidly developing damage to the respiratory muscles and bulbar nerves, which requires respiratory assistance, sometimes for 2-4 weeks

The course and prognosis are usually favorable. Lethal outcome in 5% of cases. About 70% of patients recover completely (more often with an acute onset of the disease), while the rest suffer consequences in the form of motor, less often sensory, disorders. Restoration of functions within 2-3 months or more (up to two years). In 25% of patients, relapses are observed, sometimes repeated, with more pronounced neurological deficit. In 10% of cases, a chronic course occurs with an increase in motor disorders and spontaneous improvement.

Differential diagnosis is carried out with poly-, radiculoneuropathies clinically manifested by Guillain-Barré syndrome, in particular diphtheria, porphyritic neuropathy, polyradiculoneuropathy in herpes zoster, tick-borne borreliosis, sarcoidosis, connective tissue diseases, systemic necrotizing angiitis (Degos syndrome) and other vasculitis.

1.2.Fisher syndrome. A clinical form close to AIDP, and possibly an independent disease. Clinical and diagnostic criteria: a) subacute onset and monophasic course; b) ophthalmoplegia, cerebellar ataxia, decrease or loss of tendon reflexes with preserved or slightly reduced muscle strength; c) protein-cell dissociation in the cerebrospinal fluid. There may be concomitant damage to the facial and, less commonly, other cranial nerves. ENMG, in contrast to classical OVDP. reveals changes characteristic of axonal neuropathy. The undoubted involvement of the central nervous system does not contradict the features of the autoimmune process. Fisher's syndrome is differentiated from a brain stem tumor, so-called brain stem encephalitis, myasthenia gravis. The prognosis is favorable, usually with complete restoration of function.

1.3.Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). It has common pathogenetic and clinical signs with AIDP. However, significant clinical features allow us to consider CIDP as a special nosological form. Diagnostic criteria according to the standards of the International Neuromuscular Research Group:
1) bilateral, usually symmetrical weakness in the limbs;
2) paresthesia in the feet and hands;
3) progression of the process for more than 6 weeks, accompanied by periods of increasing and decreasing weakness in the limbs for at least 3 months or slow progression from 6 weeks to several months;
4) decreased reflexes in paretic limbs, absence of Achilles reflexes;
5) an increase in protein content in the cerebrospinal fluid over 1 g/l during the period of clinical deterioration.

Differences from Guillain-Barre OVDP:
1) slow (rarely subacute) onset, gradually, without previous infection, followed by progression (often with relapses) over months, sometimes many years;
2) more common after the age of 40 years;
3) a quarter of patients have a tremor in the hands, reminiscent of an essential one, disappearing during remission and reappearing during relapse;
4) the originality of the results of the ENMG study, in particular the presence of local areas of blockade of excitation in various nerves and a heterogeneous block at different levels of one nerve; 5) worse prognosis and the need for special treatment tactics. Using CT and MRI, some patients detect foci of demyelination in the brain, which indicates a possible combination of demyelination in the central and peripheral nervous system.
The course is long, the prognosis is doubtful. About 30% of patients recover, the rest have sensorimotor disorders of varying severity (about half of them are disabled people of group II or I). Death is also possible.
Differential diagnosis with ARDP, at an early stage of the disease - with polymyositis, myasthenia.

1.4. Diphtheria polyneuropathy.
It belongs to the group of infectious and autoimmune polyneuropathies, although exposure to a neurotoxin plays a major role in the pathogenesis of early neurological complications of diphtheria. They manifest themselves in the first days of the disease as bulbar and oculomotor disorders. Severe forms of bulbar palsy, often combined with distal tetraparesis, currently occur in 55% of cases and can lead to the death of patients.
Late polyneuropathies complicate diphtheria in 8-40% of cases. In recent years, they have more often developed in adult patients not only with toxic, but also with localized forms of the disease. They are caused by an autoimmune process and are detected in the 3-10th week of the disease (“Glatsman-Zaland syndrome of the fiftieth day”), usually after the patient is discharged from the infectious diseases hospital. They manifest themselves mainly as paresis and paralysis, more pronounced in the legs. Pain syndrome, as well as distal hypoesthesia, is mild or moderate. Muscular-articular sensation is noticeably impaired, which leads to sensitive ataxia when walking. In 3% of patients, PVN syndrome is observed against the background of peripheral autonomic disorders. ENMG confirms the myelinopathic nature of polyneuropathy.
The prognosis in most cases is favorable, but there are severe forms with widespread damage to the muscles of the trunk, neck and diaphragm, breathing problems, when respiratory assistance is required and death is possible. Restoration of functions takes up to 3-6 months, sometimes 1-2 years. A year later, in 85% of those who had recovered from the disease, the motor function of the limbs is completely restored, while the rest have residual manifestations (distal paresis, hypoesthesia, autonomic-vascular disorders).
The diagnosis is based on medical history and the characteristic clinical picture of diphtheria. When judging late polyneuropathy, data on the time of onset of paresis after the acute period of the disease is important.

1.5.Herpetic neuropathies. They are the most common manifestations of herpes infection, primarily herpes zoster. An immunodeficiency state, in particular as a result of HIV infection, contributes to the disease. An obligatory component is viral ganglionitis with damage to 3-4 or more ganglia. Typical are multiple monoganglioneuritis of the thoracic, cranial, and less commonly lumbosacral and cervical localization. Spinal polyganglioneuritis is observed in 53% of cases. The clinical picture includes a typical sympathetic pain syndrome (usually against the background of herpetic eruptions), sensory and autonomic disorders, later mild or moderate paresis of the limbs and abdominal wall muscles. The area of ​​movement disorders may be wider than the localization of the rash; the proximal limbs are predominantly affected. The diagnosis is difficult when the virus is reactivated with damage to the peripheral nervous system, not accompanied by skin rashes. The outcome is generally favorable, but restoration of motor functions may take up to 3 months.
The course of the disease is complicated by postherpetic neuralgia (in 30% of cases, usually in elderly patients), which occurs with exacerbations, sometimes over many months. It is diagnosed if pain occurs more than 4-6 weeks after the rash disappears.
Regardless of the primary localization of ganglioneuritis, in the first 2 weeks from the onset of the disease, the development of polyradiculoneuropathy (Guillain-Barré syndrome) with segmental demyelination is possible, a typical clinical picture, but more severe (death was recorded in 30% of patients).

2. Hereditary motor-sensory and autonomic neuropathies.
2.1. Neural amyotrophy of Charcot-Marie-Tooth is the most famous, most common form. The disease is inherited in an autosomal dominant, less often recessive manner. It is customary to distinguish two options: 1) hypertrophic with thickening of the nerves, segmental demyelination, reduced speed of excitation along the nerves and 2) with axonal degeneration without a significant change in the speed of conduction along the motor nerve.
Clinical picture. In the first (classic) variant, the disease begins in the first (usually) or second decade of life, debuts with difficulty walking or running, and foot deformity is detected early. Amyotrophies are distal, symmetrical, and spread to the proximal lower extremities rarely and late. Moderate wasting of the muscles of the upper extremities (hands) is usually detected several years after the onset of the disease. Tendon and periosteal reflexes disappear early, primarily the Achilles. Limited muscle fasciculations are common. In 70% of patients, there is a loss of sensitivity, most often vibration, then pain and temperature. Loss of muscle-articular sensation, manifested by sensory ataxia, along with areflexia and distal muscle wasting, is considered within the framework of Roussy-Lévy syndrome. Peripheral nerves, especially the peroneal nerve, often thicken, which is determined by palpation or visually.
The severity of neurological symptoms, primarily motor disorders, varies significantly. Often there are patients with rudimentary manifestations of hereditary neuropathy (“bird shins”, “horse foot”) who have never consulted a doctor.
In the case of the second option (axonal type of lesion), the disease usually develops at a later date, often at 40-60 years of age. Clinical manifestations are similar to the first option, however, only half of the patients suffer from upper limbs and show signs of sensory impairment. As an integral part of the neurological picture, a syndrome of congenital insensitivity to pain is possible.
The course is slowly progressive, sometimes stabilization of the process occurs. The ability to move independently is rarely lost, usually after 50 years of age, although working capacity may decline at a young age. In women, the disease is usually less severe than in men.
Diagnostics. Family history, typical time of onset of the disease, clinical pattern, in particular the slowly progressive type of course, absence of pain, and ENMG data are taken into account. When making a differential diagnosis with acquired polyneuropathies, one should also keep in mind deformation of the feet, often occurring scoliosis, and hypertrophy of nerve trunks. A clinical examination, including ENMG of the patient’s relatives, helps in diagnosis, since the disease may be asymptomatic or in a rudimentary form in them.

2.2. Porphyritic polyneuropathy is observed more often in acute intermittent porphyria. A genetically determined disease, belonging to a large group of porphyrias and associated with the accumulation of porphyrins, is inherited in an autosomal dominant manner and manifests itself predominantly in women.
The pathogenesis of polyneuropathy appears to be heterogeneous: primary axonal degeneration of metabolic origin and segmental demyelination, possibly of ischemic origin. Polyneuropathy syndrome develops against the background of an acute attack of the disease, in 70% of cases provoked by the use of barbiturates, sulfonamides, antipsychotics, hormonal drugs, alcohol and manifested by severe pain in the abdomen, lower back, nausea, vomiting, stool retention, and tachycardia. There is general weakness, sometimes psychomotor agitation, and seizures. Urine is wine-red (discolored only after a few hours). Neuropathy is predominantly motor and often begins with paresis in the arms. The onset of weakness may be preceded by pain in the limbs and distal sensory disturbances. Paradoxical preservation of the Achilles reflexes is characteristic. General autonomic failure is typical (orthostatic hypotension, fixed tachycardia and other symptoms of PVN). The attack lasts 4-6 weeks or more, but recovery of motor functions can take many months, sometimes 1-2 years. In untreated patients, bulbar disorders and breathing disorders may occur due to damage to the cranial and intercostal nerves, sometimes with death. However, prevention and early treatment of attacks helps maintain a fairly high quality of life for the patient.
Diagnosis is determined by a characteristic combination of abdominal pain, cramps, psychomotor agitation with polyneuropathy. The red color of urine or the appearance of pink color when tested with Ehrlich's reagent (detection of porphobilinogen) is important. It is necessary to take into account the history of recurrence of attacks provoked by certain medications, infection, stress, remission from several months to several years, hospitalizations for acute abdomen.
Differential diagnosis with polyneuropathies of other etiologies; in particular lead, OVDP Guillain-Barre.

3.Somatogenic polyneuropathies. They belong to neuropathies that develop as a result of pathologies of internal organs, the endocrine system, blood diseases, malignant neoplasms and other diseases. Their diagnosis is often difficult, and clinical manifestations are not always taken into account in the complex of dysfunctions in internal diseases that determine the state of vital activity and ability of patients to work. Neuropathies in systemic diseases are ambiguous in etiology, morphological features, onset and course, and predominant clinical signs, which is reflected in the table, which shows the main ones.

3.1.Diabetic neuropathy. Diagnosed in 8% of patients during the initial diagnosis of diabetes and in 40-80% 20 years after the onset of the disease (Prikhozhan V.M., 1981). The rate of development of neuropathy varies; sometimes it is asymptomatic for a number of years; it is detected earlier in insulin-dependent, poorly controlled diabetes. Clinical forms:
1) distal symmetrical polyneuropathy; 2) symmetrical proximal motor neuropathy; 3) local and multiple mononeuropathy. These syndromes can occur either independently or in combination.

Distal symmetrical polyneuropathy is of the axonal type and accounts for about 70% of all diabetic neuropathies. A sensory-motor-vegetative type of lesion is typical, but sensory autonomic and motor variants are possible. The latter is much less common, especially severe paresis. In the initial stage of the disease, nocturnal paresthesia and burning pain in the distal extremities, especially in the legs, are observed. Vibration sensitivity disorders are detected early, then superficial in the form of “socks” and “gloves”. The tendon and periosteal reflexes (formerly the Achilles reflexes) decrease and then disappear. Autonomic and trophic disorders occur in a third of patients (thinning of the skin, anhidrosis, hypotrichosis, swelling of the feet). Peripheral autonomic dysfunction (autonomic neuropathy), usually developing in young patients with insulin-dependent diabetes, in severe cases fits into the clinical picture of the syndrome of progressive autonomic failure: tachycardia at rest, orthostatic hypotension, incomplete emptying of the bladder, diarrhea, impaired pupillary innervation, impotence, etc. In the late stage of the disease, flaccid paresis of the feet and pronounced distal trophic disorders are observed: ulcers, arthropathy, gangrene (diabetic foot).
The course in most cases is slowly progressive over many years. The rapid progression of polyneuropathy is facilitated by repeated hypo- or hyperglycemic comas. However, a stationary defect and partial restoration of functions are possible during treatment. Pain syndrome is often relieved more easily.
Diagnosis is difficult when symptoms of polyneuropathy appear in patients with previously undiagnosed diabetes. It is based on the typical clinical picture, the connection between the development of polyneuropathy and the duration and course of diabetes. A combination with encephalo- and myelopathy of diabetic etiology is possible (Prikhozhan V.M., 1981). EMG reveals a decrease in the amplitude of biopotentials during voluntary muscle contraction, even in the absence of obvious paresis. There is also a slight decrease in the speed of excitation along the nerve in the distal parts of the lower extremities.
Differential diagnosis is carried out with polyneuropathies of other etiologies, mainly toxic (alcohol). In this case, a possible combination of etiological factors is taken into account.
Symmetrical proximal motor neuropathy (Garland's amyotrophy) is rare, sometimes in combination with typical polyneuropathy. It manifests itself as weakness of the muscles of the pelvic girdle, mainly the hips, and aching pain. Paresis develops acutely or subacutely over several weeks. According to ENMG and EMG data, the process is neurogenic and damages the cells of the anterior horns of the spinal cord. The prognosis is relatively favorable: restoration of motor functions in a few weeks or months, subject to insulin therapy and diabetes compensation.
Local and multiple neuropathy. Acute, ischemic in nature, multiple lesions of the femoral, obturator, sciatic, less often ulnar and median nerves, sometimes occurs in elderly patients. Progression over several hours or days, severe pain and muscle atrophy are observed.
Cranial neuropathies are relatively common: oculomotor nerve (unilateral painful ophthalmoplegia, with preserved pupillary reactions, sometimes recurrent); mononeuropathy of intercostal and other nerves, in particular tunnel ones.
Differential diagnosis in the case of painful ophthalmoplegia should be made with Tolosa-Hunt syndrome, an aneurysm of the internal carotid artery. The prognosis is favorable, paralysis and pain usually regress within 6-12 months.
Distal symmetric motor neuropathy occurs in patients with repeated hypoglycemic conditions due to insulinoma. Comas with loss of consciousness and convulsions are possible. Typically decreased intelligence. Differential diagnosis with cerebral tumor, epilepsy. Treatment is surgical.

3.2. Polyneuropathies in paraneoplastic syndrome develop against the background of a malignant tumor of various locations (small cell lung cancer, breast cancer, stomach cancer, colon cancer, lymphoma, chronic lymphocytic leukemia, myeloma). More common in elderly patients. Along with other etiological factors (decrease in the level of metabolism and regeneration against the background of vitamin deficiency, somatic diseases), they are included in the group of so-called polyneuropathies of old age. They may be the first clinical manifestations of a malignant tumor; sometimes they precede the appearance of other tumor symptoms by 5 years or more. The causes of early paraneoplastic neuropathy remain unclear. Often combined with other paracarcinomatous syndromes (Lambert-Eaton, myopathy, subacute cerebellar degeneration, etc.). The main type of lesion is axonal degeneration, although myelinopathy is also possible with a recurrent course. Sensory and sensorimotor polyneuropathies predominate. Pain syndrome (burning pain, paresthesia) is moderate, although it may debut in the clinical picture of the disease. Motor disturbances (stepping), muscle wasting are more pronounced in the lower extremities. Objectively detectable sensory disorders concern all types of sensitivity.
In chronic lymphocytic leukemia, myeloma, macroglobulinemia, acute or subacute polyradiculoneuropathy such as Guillain-Barré syndrome with characteristic protein-cell dissociation can develop. It should be noted that toxic polyneuropathy also occurs in patients with lymphogranulomatosis and multiple myeloma (when treated with vincristine). Clinically, this is a typical sensory-motor symptom complex with an axonal type of lesion. Neurological deficits may worsen with repeated courses of chemotherapy. The course of paraneoplastic polyneuropathies is often progressive, although remissions are possible, in particular, after surgical removal of the tumor and corticosteroid therapy.
Differential diagnosis - with nutritional (vitamin deficiency) and toxic-nutritive neuropathies. It is difficult in elderly patients, with early onset of polyneuropathy, cancer of unknown localization. The possibility of toxic damage to nerves during chemotherapy must also be taken into account.

4.Neuropathy in diffuse connective tissue diseases. They can occur in the form of multiple mononeuropathy, tunnel neuropathy. They are caused by damage to peripheral nerves due to concomitant (secondary) vasculitis, but neuropathies are possible with so-called systemic vasculitis (periarteritis nodosa, Wegener's granulomatosis). Polyradiculopathy syndrome has also been described in systemic necrotizing angiitis Degos (Makarov A. Yu. et al., 1993). Neuropathies in collagenosis and primary vasculitis, in addition to pathology of internal organs, are often manifested by damage to the brain and spinal cord, occurring with corresponding neurological symptoms. They are more often referred to as axonopathies, but demyelinating lesions and Wallerian degeneration are possible.

4.1. Neuropathies with systemic lupus erythematosus develop in 10% of patients, usually against the background of the activity of the process, but they can also be the first clinical symptom. In the case of polyneuropathy, paresthesia appears in the distal parts of the extremities, pain and temperature sensitivity is impaired. Increased leg fatigue when walking is possible. With mononeuropathy of the lower extremities, weakness of the foot appears and deep sensitivity is lost. Bulbar symptoms occur due to damage to the caudal cranial nerves. Protein-cell dissociation is possible in the cerebrospinal fluid (with a clinical picture similar to atypical Guillain-Barré syndrome). The course is rapidly progressive, the motor defect is pronounced and persistent.

4.2. Neuropathies in rheumatoid arthritis occur in approximately 10% of patients with a long and severe course of the disease. Distal symmetrical polyneuropathy usually manifests as paresthesia and decreased sensation in the upper and lower extremities. There are no motor disorders. The course is slowly progressive, sometimes stabilization of the process or a clear progression. In the latter case, severe distal sensory-motor neuropathy may develop against the background of generalized vasculitis with a poor prognosis. There are mononeuropathies, also with a tendency to progress. The appearance of paresis is preceded by pain. Rheumatoid arthritis in such patients occurs with destructive changes in the joints and pronounced trophic disorders of the skin. Tunnel neuropathies (carpal, tarsal canal, etc.) are also widely represented.

4.3.Neuropathy with periarteritis nodosa occurs in 27% of patients. They occur against the background of a typical clinical picture (temperature, increased ESR, damage to the kidneys, gastrointestinal tract, high blood pressure, etc.). In fact, they are multiple mononeuropathies with predominant damage to the sciatic, tibial, median, and ulnar nerves, sometimes asymmetrically. First, shooting, burning pains appear, mainly in the muscles, then reflexes disappear, sensitivity is impaired, and paresis and paralysis develop. Possible damage to spinal and cranial nerves. The course is chronic over several years, improvement often occurs with hormonal therapy.

5.Toxic polyneuropathies of various etiologies. They represent a large group of diseases caused by single or chronic exposure to substances of three groups - heavy metals, toxic organic compounds and drugs. The rate of development of polyneuropathies, concomitant damage to various parts of the central nervous system, internal organs, the severity of motor, sensory, and autonomic manifestations, and the prognosis depend on the characteristics of the toxic agent. Currently, only some types of toxic polyneuropathies are relevant. Lead mononeuropathies, which were common in the past, as well as mercury polyneuropathies, are rare.

5.1.Alcoholic polyneuropathy accounts for about 30% of all polyneuropathies. Develops in 20-70% of patients with chronic alcoholism, usually with significant pathology of the digestive organs. The pathogenesis is nutritional-toxic. Vitamin B12 deficiency plays a major role. Refers to axonopathies, but segmental demyelination and a mixed type of lesion may occur.
Clinical picture. Initial manifestations in the form of paresthesia in the distal parts of the extremities and pain in the calves are usually not recorded by patients. Gradually, sometimes within several days, paresis of the muscles of the distal legs and arms is revealed, and the Achilles reflexes disappear. The most obvious weakness of the foot extensors (steppage when walking). Typical pain, hyperalgesia with symptoms of hyperpathy, especially in the feet. Subsequently, over the course of several weeks and months, muscle wasting, sensitive ataxia appear, paresis, and vegetative-trophic disorders in the limbs worsen. The latter are not uncommon at the subclinical stage of the disease. Acute development of distal paresis and hypoesthesia is possible due to poisoning with alcohol surrogates.
The current is different. Progression is possible; when you stop drinking alcohol, the process stops, but paresis and ataxia remain. A relapsing course has been described. From a diagnostic point of view, the combination with other alcoholic lesions of the central nervous system (Korsakoff psychosis, encephalomyelopathy, cerebellar degeneration) is unfavorable.
Differential diagnosis is made with alcoholic myopathy, other toxic and endogenous neuropathies, and with severe sensitive ataxia - with tabes dorsalis.

5.2. Arsenic polyneuropathy develops in acute and chronic poisoning, but the clinical picture is most pronounced in the case of acute intoxication. Distal pain syndrome is characteristic; after 1-2 weeks, sensory loss appears, including deep sensitivity, which leads to ataxia. Motor disturbances begin in the feet; in severe cases, tetraparesis develops. Atrophy of the muscles of the distal limbs is sharply expressed. In case of chronic poisoning, abortive manifestations of polyneuropathy can be observed. Functional recovery is slow (from 1 year to several years). In severe cases, paresis, amyotrophy, and contractures may remain.

5.3.Polyneuropathy from exposure to organophosphorus compounds. Poisoning with insecticides (thiophos, karbofos, chlorophos, etc.) occurs almost exclusively. The toxic effect of FOS is based on the inactivation of cholinesterase. 1-3 weeks after acute poisoning, mild distal paresthesia, muscle weakness occurs, which progresses over several days, and Achilles reflexes disappear. Typically the central motor neuron is involved in the process, and therefore the nature of the paresis is mixed. Treatment is ineffective. Spastic paraparesis often remains as a consequence.

5.4. Drug-induced polyneuropathies can develop during treatment with massive doses of isoniazid (tubazid), sulfonamides, antitumor and cytostatic drugs (azothioprine), vinca alkaloids (vinblastine, vincristine), amiodarone (cordarone), disulfiram (teturam), phenobarbital, diphenine, tricyclic antidepressants and etc. They are mainly sensory, or sensorimotor. The latter, in particular, are not uncommon during long-term treatment of tuberculosis patients with isoniazid at a dose of 5-20 mg/kg per day (due to vitamin B12 deficiency) and constant use of cordarone (400 mg per day for a year). Distal paresthesia, sensory disturbances with moderate paresis, and autonomic dysfunction are characteristic. Drug-induced polyneuropathies usually regress after discontinuation of the drug.
Diagnosis of toxic polyneuropathies is based on identifying the fact of intoxication, determining the nature of the toxic agent (using biochemical analysis methods). The clinical picture of damage to other organs and systems of the body is taken into account. Often a consultation with an occupational pathologist or hospitalization in an appropriate hospital is necessary. In order to objectify motor and autonomic disorders, and to judge the prognosis of functional restoration, EMG and ENMG, RVG, and thermal imaging are used.

6. Polyneuropathies caused by exposure to physical factors. They belong (along with some toxic ones) to occupational neuropathies. They include predominantly vegetative forms that are included in the clinical picture of vibration disease due to local or general vibration. With combined exposure, polyneuropathic syndrome is possible, affecting not only the upper but also the lower extremities. They occur in occupational “overexertion diseases” (in workers in textile and shoe production, poultry farms, seamstresses, typists, etc.). A common form (mainly among workers in meat processing plants and fishermen) is cold polyneuropathy, clinically manifested by vegetative-vascular, sensory and trophic disorders mainly in the distal parts of the upper extremities (Palchik A. B., 1988). Such polyneuropathies can be classified as angiotrophopathies due to the main pathogenetic significance of angiodystonic disorders. The type of lesion is predominantly axonal. The disease is characterized by a progressive course. In severe cases, the lower limbs are involved in the process.

III. Additional research.
1.Identification of possible causes of the disease: a) neurotoxic agents and physical factors that can cause the disease at home or at work; b) medicines; c) hereditary cause of neuropathy and type of inheritance; d) features of damage to internal organs, skin, and other formations of the peripheral and central nervous system, shedding light on the etiology of polyneuropathy.
2.EMG, ENMG: judgment about the type (axonopathy, myelinopathy) and the prevalence of the lesion over time; help in differentiation with myasthenia gravis, myopathic syndrome. It should be taken into account that regression of motor disorders is not necessarily accompanied by normalization of nerve conduction function according to ENMG data;
3.Study of cerebrospinal fluid: identification of protein-cell dissociation in order to clarify the nature of polyneuropathy (autoimmune, Guillain-Barre syndrome).
4.Sural nerve biopsy is an invasive procedure, the use of which is limited to strict indications for obtaining diagnostic information.
5. Biochemical studies of blood and urine. They are carried out for diagnostic and differential diagnostic purposes. The range of substances or their metabolites to be determined depends on the expected etiology of polyneuropathy (diabetes, porphyria, hypoglycemia, uremia, etc.).
6.Somatic, radiological, ophthalmological and other examinations, taking into account the expected etiology.
7. Bacteriological, virological, immunological research depending on the possible etiological factor.
8. Detection of peripheral vegetative-vascular disorders using additional methods: RVG, thermal imaging, etc.
9. Diagnosis of the syndrome of progressive autonomic failure, most often observed in diabetic, porphyritic, alcoholic, acute inflammatory demyelinating polyneuropathy.

Differential diagnosis
1. Between polyneuropathies of different etiologies.
2. With myopathies, damage to peripheral nerves in other diseases (noted above in the description of individual clinical forms of polyneuropathies).

Course and prognosis
Four types of polyneuropathy can be distinguished: acute (symptoms develop over several days); subacute (no more than a month); chronic (more than a month); recurrent (repeated exacerbations occur over many months or years). The prognosis, as well as the course, clearly depend on the etiology of the disease.

Principles of treatment
1. Hospitalization in the neurological department is mandatory for AIDP, CIDP, diphtheria, porphyritic polyneuropathy (due to the possibility of respiratory and bulbar disorders), and is desirable for the purpose of diagnosis and treatment in case of suspected neuropathy of any etiology.
2. Staged and comprehensive therapy, an adequate combination of pharmacological drugs (for pain - analgesics), physical and other methods (hyperbaric oxygenation, magnetic stimulation, laser blood irradiation, massage, physical therapy, mechanotherapy, etc.), patient care taking into account the period and course of the disease.

3. Features of therapy taking into account the etiological factor of polyneuropathy.
3.1. Infectious and autoimmune polyneuropathies. Treatment should be inpatient:
- for mild and moderate forms of AIDP, corticosteroids are not prescribed.
In severe forms, ascending course of the process, especially in case of respiratory failure, plasmapheresis (2-3 sessions), large doses of glucocorticoids (prednisolone, metipred - 1000 mg intravenously daily for 3 days) are used, if necessary - against the background of mechanical ventilation, which reduces the time respiratory care. There is evidence of the effectiveness of intravenous immunoglobulin.
During the recovery period, drugs are used that improve microcirculation and tissue trophism (trental, sermion, phosphaden, cerebrolysin, B vitamins, etc.), physiotherapy, massage, exercise therapy (early, but carefully). Careful care is required;
- for CIDP, prednisolone or metipred is used at a dose of 1-1.5 mg/kg per day daily. A maintenance dose of prednisolone (10-20 mg every other day) is prescribed for a long time (up to 6-8 months) and is discontinued after restoration of motor functions. When sensorimotor disorders increase, pulse therapy is performed (as with severe manifestations of AIDP). In particularly severe cases, immunosuppressants (azathioprine) may be effective. Other treatment methods are similar to those used in patients with AIDP;
- when treating diphtheria polyneuropathy, it is advisable to take into account the time of onset of neurological symptoms. In the case of early pharyngeal neuropathy, diphtheria toxoid is used, the best effect is achieved as a result of plasmapheresis, and in case of late demyelination - vasoactive drugs (Trental, Actovegin) and plasmapheresis;
- for herpetic neuropathy - etiotropic drugs: acyclovir (Zavirax) orally for 5-7 days, bonafton orally and topically in the form of an ointment, antihistamines, analgesics, B vitamins, UHF, ultrasound. For postherpetic neuralgia - famciclovir, tricyclic antidepressants, adrenergic blockers.

3.2. Hereditary neuropathies. Therapy for neural amyotrophy is ineffective. Supportive drug treatment is carried out to improve microcirculation and tissue trophism, massage, and physical therapy. Taking care of the skin of the feet, orthopedic correction of foot deformities, and special shoes for drooping feet are of great importance.
For acute intermittent porphyria, treatment is inpatient: large doses of carbohydrates (glucose or levulose) intravenously, hematin, cytochrome C for 5-7 days, analgesics, anaprilin, aminazine. In case of respiratory failure - controlled breathing, other resuscitation measures. Plasmapheresis is indicated.

3.3.Somatogenic polyneuropathies:
- in case of diabetic polyneuropathy, hospitalization in the endocrinology or neurology department is advisable for the purpose of correcting etiotropic therapy. Outpatient treatment is carried out jointly with an endocrinologist. It is necessary to normalize blood glucose levels and compensate for other manifestations of diabetes through rational dosing of long-acting insulin. Antiplatelet agents, nicotinic acid preparations, solcoseryl, trental (pentilin) ​​are used. Alpha lipoic acid is effective for non-insulin-dependent diabetes. Anabolic hormones are prescribed for proximal motor neuropathy. For intractable pain syndrome, analgesics (paracetamol), finlepsin and amitriptyline in small doses. Physiotherapeutic methods (electrophoresis of novocaine, four-chamber baths, etc.), oxygen therapy may be recommended;
- for paraneoplastic polyneuropathies, treatment is symptomatic; symptomatic regression is possible after tumor removal and corticosteroid therapy.

3.4.Neuropathy in diffuse connective tissue diseases. Treatment together with a therapist, usually in a hospital setting. Glucocorticoids (prednisolone) are required, and in severe cases, plasmapheresis. Analgesics, B vitamins, and trental are prescribed. Treatment for tunnel neuropathies is common.
3.5.Toxic polyneuropathies. The general principle is to exclude the influence of etiotropic factors. Treatment in the acute period of poisoning in an occupational pathology or neurological hospital, during the period of restoration of motor functions in the rehabilitation department, on an outpatient basis. The nature of therapy depends on the specific toxic agent. Therapy for polyneuropathies is carried out comprehensively according to the usual rules. Identification of drug-induced polyneuropathy requires discontinuation of the drug. Treatment of tuberculosis with isoniazid (tubazid) should be accompanied by the use of pyridoxine (vitamin B6). For diagnosed polyneuropathy, pyridoxine is administered parenterally.
- alcoholic polyneuropathy. Inpatient treatment is recommended in case of progression of neurological symptoms (in the neurological department, psychiatric hospital). A complete abstinence from alcohol and a balanced diet rich in vitamins are required. Vitamins B1, B6, B12 parenterally, analgesics, antidepressants, clonazepam, finlepsin (in case of persistent pain), physiotherapy, massage, corrective gymnastics.

3.6.Polyneuropathies caused by exposure to physical factors. A change in working conditions is required (temporary or permanent exclusion of the etiological factor). Treatment of neuropathy according to general principles, taking into account the predominance of peripheral vegetative-vascular disorders: ascorbic acid, indomethacin, trental, Ca blockers (nifedipine) and other drugs that improve microcirculation.

Medical and social examination Criteria of VUT
1. For infectious and autoimmune polyneuropathies:
- AIDP, Fisher's syndrome and diphtheria polyneuropathy. The timing of VL depends on the rate of recovery of motor functions. In the case of early regression of symptoms, they do not exceed 3-4 months; in case of delayed regression, it is advisable to continue treatment on sick leave according to the decision of the Institution, sometimes up to 6-8 months (if it is assumed that the patient will be able to return to work or it will be possible to determine a less severe disability group ). The duration of treatment in a hospital (including the rehabilitation therapy department) ranges from 1-2 to 3-4 months, depending on the severity of the disease. More than half of patients are discharged from the hospital after complete restoration of function. They require short-term outpatient treatment due to asthenic syndrome. Physical workers need temporary relief of working conditions on the recommendation of the VK. The pronounced consequences of the disease (in severe cases) provide grounds for referral to BMSE before the end of the recovery period, no later than 4 months of sick leave. The issue is resolved in a similar way in patients with relapses and a progressive course;
- CIDP. Usually long-term VL (up to 4 months). In case of recovery, a return to work, often with restrictions depending on the profession. If therapy is ineffective or relapses, referral to BMSE. As a rule, there are no grounds for extending treatment on sick leave;
- herpetic neuropathy. Treatment in a hospital lasts an average of 20 days. VN is most often limited to 1-2 months, but with postherpetic neuralgia the periods are longer; in addition, patients are temporarily disabled during an exacerbation. This also applies to patients with Guillain-Barré syndrome.
2. Hereditary neuropathies:
- in case of Charcot-Marie-Tous neural amyotrophy, the basis for treatment on sick leave may be decompensation of the disease, more often due to unfavorable working conditions, the need for examination, treatment (duration of VN - 1 - 2 months);
- porphyritic polyneuropathy. Patients are temporarily disabled during the attack (1.5-2 months), when inpatient treatment is necessary. In case of prolonged restoration of functions - up to 3-4 months, sometimes with an extension for another 2-3 months or referral to BMSE (in case of severe motor defect).

3.Somatogenic polyneuropathies:
- diabetic. VL is determined taking into account the course of diabetes (decompensation). Progressive polyneuropathy, especially manifested by autonomic and trophic disorders, prolongs the duration of treatment on sick leave. In the case of proximal motor neuropathy, local and multiple neuropathies, the duration of LN mainly depends on the rate of recovery of motor functions (usually 2-3 months).
- paraneoplastic polyneuropathies are the basis for VN during the primary diagnosis of cancer. In the future, the need for VN and the timing depend on the results of surgical or other treatment of the tumor.

4.Neuropathy in diffuse connective tissue diseases. The need for VN mainly depends on the clinical manifestations of the underlying disease. However, neuropathies, including tunnel ones, and Guillain-Barré syndrome may also be the main reason for treatment on sick leave. The timing of VN is determined by their curability and the nature of the flow.

5.Toxic polyneuropathies. The insufficient effectiveness of therapy and the duration of functional restoration in most forms determine long-term VL and the need to continue sick leave according to the decision of the Internal Affairs Committee. In patients with alcoholic polyneuropathy, combined damage to the central nervous system and the possibility of relapses are taken into account. Continuing VL beyond 4 months is usually not advisable. In case of arsenic, organophosphorus polyneuropathy due to the ineffectiveness of therapy, long-term (more than a year) restoration of VN functions should not exceed 4 months. Drug-induced polyneuropathies, which usually regress well after discontinuation of the drug, can themselves lead to VL within 2-3 months.

6. Polyneuropathy due to exposure to physical and toxic factors, usually occupational. Therefore, in the initial phase of the disease, it is worth limiting yourself to a temporary transfer of the patient to easier work according to the occupational bulletin (for 1.5-2 months). With persistent severe trophic and motor disorders, patients are temporarily disabled for a period of outpatient or inpatient treatment (1-2 months).
Main causes of disability
1. Motor defect due to peripheral, rarely mixed para-, tetraparesis of the limbs. Due to more pronounced and earlier occurring lower paraparesis in the residual period of polyneuropathy or in the progressive course of the disease, the ability to move and overcome obstacles is impaired to varying degrees. In the case of severe lower paraparesis, movement is possible only with the help of auxiliary means; with paraplegia, patients depend on the help of other persons. Upper paraparesis, due to predominant dysfunction of the hands, largely limits the work opportunities of patients, depending on their profession. Significant severity of paraparesis reduces the ability or makes it impossible to perform applied activities in everyday life (personal care and other tasks that require sufficient manual activity). Severe tetraparesis and tetraplegia lead to the need for constant outside care and assistance.

2. Sensitivity disorders. Pain syndrome affects the functioning of a relatively small number of patients (especially with occupational polyneuropathy, postherpetic neuralgia). Distal hypoesthesia, and especially sensory ataxia, aggravate the degree of disability and work capabilities of patients with diabetic, alcoholic and some other polyneuropathies.

3. Vegetative-vascular and trophic disorders can significantly affect the motor functions of the limbs, reduce the ability to walk and stand for long periods of time, reduce the possibility of manual operations, which leads to limited vital activity and ability to work (more often with polyneuropathies caused by exposure to physical factors).
1. General: adverse weather conditions, low temperature, high humidity, significant physical stress, contact with neurotoxic substances.
2.Individual (depending on the profession, working conditions): exposure to a specific toxic substance, functional overstrain of the upper limbs, long walking, standing, work at height, near moving mechanisms (with ataxia), associated with local and general vibration.

able-bodied patients
1. Those who have suffered acute infectious, autoimmune polyneuropathy with good (full) restoration of functions or when mild and moderate motor, sensory, and trophic disorders do not interfere with the continuation of work in the specialty.
2. Patients with diabetic polyneuropathy (in the initial stage of the disease, with compensated diabetes), mild manifestations of Charcot-Marie-Tooth neural amyotrophy, alcoholic, some other toxic (medicinal), somatogenic polyneuropathies with a regressive or stationary course of the disease (if the clinical manifestations of the underlying disease are not limit the ability of patients to work).
3. Patients with occupational polyneuropathy with moderate dysfunction, without movement disorders, a slightly progressive course of the disease, who are able to perform work in their main profession or have low qualifications, if it is necessary to change working conditions, entailing a slight decrease in earnings, or if professional work requires more stress, than before (when there is no basis for determining disability group III). A loss of 10 to 30% of professional ability to work is established.

Indications for referral to BMSE
1. Paresis and paralysis of the limbs, persistent pain syndrome, sensitive ataxia, severe autonomic and trophic disorders, manifestations of progressive autonomic failure, significantly limiting the patient’s life activity.
2. Long-term temporary disability with a poor or questionable prognosis regarding the restoration of motor and other functions.
3. Progressive course and relapses of the disease, taking into account the etiology of polyneuropathy, postherpetic neuralgia.
4. Inability to return to work in the specialty due to a motor defect and (or) contraindicated working conditions that cannot be eliminated according to the conclusion of the VC.

Minimum required examination when referring to BMSE
1. General blood and urine tests.
2. Data from the study of cerebrospinal fluid (in patients with infectious and autoimmune polyneuropathies).
3.EMG, ENMG (preferably in dynamics).
4. Somatic and ophthalmological examination data (taking into account the etiology of polyneuropathy).
5. Results of bacteriological and virological studies (depending on the etiology of polyneuropathy).
6.RVG, thermal imaging.
7. Biochemical studies of blood and urine (for toxic, porphyritic, somatic polyneuropathies).

Disability criteria
Group III: moderate motor and (or) atactic, moderate or severe vegetative-vascular, trophic, sensory disorders in stationary or slowly progressive course of the disease in the case of: a) loss of profession (the need for professional retraining for the period of its implementation); b) the need to transfer to another job, which is associated with a significant reduction in the volume of production activity (according to the criteria of limited ability to work, independent movement of the first degree).

Group II: severe limitation of life activity caused by severe motor and (or) atactic, vegetative, trophic disorders, severe and persistent pain syndrome with a progressive, recurrent or stationary course of the disease (according to the criteria of limitation of the ability to work of the second degree, to move and self-care of the second degree degrees). The uneven involvement of the upper and lower extremities in the pathological process, the frequent preservation of hand functions even with severe lower paraparesis, allows such patients to be recommended to work at home or in specially created conditions at enterprises, institutions or organizations.

Group I: pronounced limitation of life activity in patients with distal tetraparesis, lower paraplegia, often in combination with sensitive ataxia, which necessitates constant outside care (according to the criteria of third degree limitation of the ability to move and self-care).

In case of persistent severe impairment of motor functions after 4 years of observation, disability is determined indefinitely.

Causes of disability: 1) general illness; 2) occupational disease: a) in patients with polyneuropathies that developed as a result of exposure to toxic substances in production conditions; b) due to the influence of physical factors; vibration disease, cold polyneuropathy; autonomic polyneuropathy due to overexertion of the upper limbs. At the same time, the degree of loss of professional ability to work is determined as a percentage; 3) disability due to a disease acquired during military service (or occurring within 3 months from the date of discharge from the army); 4) disability since childhood.

Neuropathy refers to nerve damage. This is a common complication of diabetes.
In diabetes mellitus, the peripheral nervous system (nerves going to the arms, legs, and head) is most often affected, so the disease is called distal sensory (peripheral) diabetic neuropathy and manifests itself in damage to the nerves in the extremities.
Symptoms of neuropathy first appear in the legs (feet), and then can spread to the hands.

Stages of development of neuropathy

Stage 1 – at this stage there are no various manifestations of neuropathy. It can only be diagnosed with special equipment.
Stage 2 – developed neuropathy. It includes several stages. At this stage, a person feels all the signs of neuropathy: acute pain, burning, goosebumps, tingling, decreased sensitivity and reflexes.
Subsequently, a decrease in muscle mass occurs, which is especially acute in elderly patients and patients with type 2 diabetes.
Stage 3 – consequences of neuropathy. At this stage, patients develop ulcers, gangrene, and undergo amputations.

Feelings with developing neuropathy:

• Constantly freezing feet and hands;
• Numbness in the arms and legs;
• Swelling of the feet and hands;
• Decreased sensitivity in legs and arms;
• Burning sensation, pain in the arms and legs;
• Deformation of fingers and toes;
• Formation of chafing, calluses, ulcers.

With sensory diabetic neuropathy, a person experiences pain in the legs. Most often the pain is sharp and jerking. Less common is a dull pain. There is often a feeling of “pins and needles” and tingling in the legs.
The pain is temporary, that is, it intensifies at night.
Pain often occurs at the very beginning of diabetes, when blood glucose is high.

Screening for diabetic neuropathy

Even in the absence of any signs of neuropathy (see above), it is necessary to undergo regular examination, since the absence of pain and other unpleasant sensations does not mean that there is no neuropathy.
In the absence of a diagnosis and any signs, an examination should be performed once a year, if neuropathy is suspected and if the patient is worried about something. Then you need to see a doctor 2 times a year.

A doctor should conduct an examination to determine the degree of sensitivity reduction, namely:

• Testing knee and Achilles reflexes;
• Testing pain sensitivity by pricking with a needle;
• Testing sensory sensitivity with a special hair;
• Testing temperature sensitivity;
• Testing vibration sensitivity using a tuning fork.

To determine the degree of manifestation of sensory diabetic neuropathy, more in-depth examinations are used using special equipment.

What are the dangers of sensory diabetic neuropathy?

With distal diabetic neuropathy, the sensitivity of the limbs is greatly reduced. Therefore, a person does not notice when his shoes rub, something gets into his shoes and can injure his foot, and he does not feel cuts or other injuries. Dirt can get into the wound and inflammation will begin.

Injuries such as burns often occur. When a person with reduced sensitivity decides to steam his feet, he does not feel. That the water is very hot and gets burned. The same thing happens when heating the feet on a radiator and a heater.

Severe cases of inflammation from neuropathy lead to gangrene, which in turn can lead to amputation of the limb.

As a consequence of neuropathy, deformation of the toes and hands may begin.

What leads to the development of neuropathy?

• Poor compensation of diabetes mellitus;
• The risk of neuropathy increases with age;
• Excess body weight (especially with type 2 diabetes);
• Long experience of diabetes mellitus;
• Drinking alcohol and smoking.

Treatment for neuropathy

Today it is impossible to completely cure neuropathy, but it is possible to reduce the risk of developing late complications of neuropathy and alleviate the patient’s condition by reducing the manifestation of neuropathy.

First of all, you need to bring your glucose back to normal. This is the first and most effective thing that can and must be done.

And for drug treatment, drugs based on alpha-lipoic acid are used. The doctor prescribes which medications to use.
Your doctor may also prescribe pain medications to relieve severe pain.

It is necessary to wash your feet every evening.
After washing, feet should be dried thoroughly.
Every day, examine your feet for various cracks, injuries, and calluses. Particular attention should be paid to the plantar surface of the foot and the spaces between the toes.
You should use a moisturizer, just make sure that the cream does not get between your fingers.
It is necessary to choose the right shoes so that they do not sting, are not too big, and do not rub.

And most importantly, it is stable good compensation.