Diabetic polyneuropathy stage 2a. Sensorimotor polyneuropathy of the lower extremities. Healing Fitness

Polyneuropathies- a heterogeneous group of diseases characterized by systemic damage to the peripheral nerves. Polyneuropathies are divided into primary axonal and primary demyelinating. Regardless of the type of polyneuropathy, its clinical picture is characterized by the development of muscle weakness and atrophy, a decrease in tendon reflexes, various sensitivity disorders (paresthesia, hypo- and hyperesthesia) that occur in the distal extremities, autonomic disorders. An important diagnostic point in establishing the diagnosis of polyneuropathy is to determine the cause of its occurrence. Treatment of polyneuropathy is symptomatic, the main task is to eliminate the causative factor or compensate for the underlying disease.

Etiology and pathogenesis of polyneuropathies

Regardless of the etiological factor, two types of pathological processes are detected in polyneuropathies - axon damage and demyelination of the nerve fiber.

In axonal polyneuropathies, the transport function of the axial cylinder suffers mainly, carried out by the axoplasmic current, which carries in the direction from the motor neuron to the muscle and back a number of biological substances necessary for the normal functioning of nerve and muscle cells. First of all, the nerves containing the longest axons are involved in the process. A change in the trophic function of the axon and axonal transport leads to the appearance of denervation changes in the muscle. Denervation of muscle fibers stimulates the development of first terminal and then collateral sprouting, the growth of new terminals, and the reinnervation of muscle fibers, which leads to a change in the structure of the MU.

With demyelination, there is a violation of the saltatory conduction of the nerve impulse, resulting in a decrease in the speed of conduction along the nerve. Demyelinating nerve damage is clinically manifested by the development of muscle weakness, early loss of tendon reflexes without the development of muscle atrophy. The presence of atrophy indicates an additional axonal component. Demyelination of nerves can be caused by autoimmune aggression with the formation of antibodies to various components of the peripheral myelin protein, genetic disorders, exposure to exotoxins. Damage to the axon of the nerve may be due to the impact on the nerves of exogenous or endogenous toxins, genetic factors.

Classification of polyneuropathies

To date, there is no generally accepted classification of polyneuropathies. According to the pathogenetic basis, polyneuropathies are divided into axonal (primary damage to the axial cylinder) and demyelinating (myelin pathology). According to the nature of the clinical picture, motor, sensory and vegetative polyneuropathies are distinguished. However, in its pure form, these forms are observed very rarely; more often, a combined lesion of two or three types of nerve fibers (motor-sensory, sensory-vegetative, etc.) is detected.

According to the etiological factor, polyneuropathies are divided into hereditary (Charcot-Marie-Tooth neural amyotrophy, Roussy-Levy syndrome, Dejerine-Sott syndrome, Refsum disease, etc.), autoimmune (Miller-Flescher syndrome, axonal type of GBS, paraproteinemic polyneuropathies, paraneoplastic neuropathies and others), metabolic (diabetic polyneuropathy, uremic polyneuropathy, hepatic polyneuropathy, etc.), nutritional, toxic and infectious-toxic.

Clinical picture of polyneuropathy

In the clinical picture of polyneuropathy, as a rule, signs of damage to motor, sensory and autonomic fibers are combined. Depending on the degree of involvement of fibers of various types, motor, sensory, or vegetative symptoms may predominate in the neurological status. The defeat of motor fibers leads to the development of flaccid paresis, for most polyneuropathies, damage to the upper and lower extremities is typical with a distal distribution of muscle weakness, with prolonged damage to the axon, muscle atrophy develops. Axonal and hereditary polyneuropathies are characterized by a distal distribution of muscle weakness (more often in the lower extremities), which is more pronounced in the extensor muscles than in the flexor muscles. With severe weakness of the peroneal muscle group, steppage develops (the so-called "cock's gait").

Acquired demyelinating polyneuropathies may present with proximal muscle weakness. In severe cases, damage to the CN and respiratory muscles can be noted, which is most often observed in Guillain-Barré syndrome (GBS). Polyneuropathies are characterized by a relative symmetry of muscle weakness and atrophy. Asymmetric symptoms are characteristic of multiple mononeuropathies: multifocal motor neuropathy, Sumner-Lewis multifocal sensorimotor neuropathy. Tendon and periosteal reflexes in polyneuropathy usually decrease or disappear, first of all, Achilles tendon reflexes decrease, with further development of the process, knee and carporadial, tendon reflexes from the biceps and triceps muscles of the shoulder can remain intact for a long time.

Sensory disturbances in polyneuropathy are also most often relatively symmetrical, first appearing distally (like "gloves" and "socks") and spreading proximally. In the debut of polyneuropathy, positive sensory symptoms (paresthesia, dysesthesia, hyperesthesia) are often detected, but with the further development of the process, irritation symptoms are replaced by symptoms of loss (hypesthesia). The defeat of thick myelinated fibers leads to violations of deep muscle and vibration sensitivity, the defeat of thin myelinated fibers leads to a violation of pain and temperature sensitivity of the skin.

Violation of autonomic functions is most clearly manifested in axonal polyneuropathies, since autonomic fibers are unmyelinated. Symptoms of prolapse are more often observed: damage to sympathetic fibers that go as part of peripheral nerves is manifested by dry skin, dysregulation of vascular tone; damage to visceral autonomic fibers leads to dysautonomy (tachycardia, orthostatic hypotension, decreased erectile function, disruption of the housing and communal services).

Diagnosis of polyneuropathies

When identifying slowly progressive sensorimotor polyneuropathy, which debuted from the peroneal muscle group, it is necessary to clarify the hereditary history, especially the presence of fatigue and weakness of the leg muscles, changes in gait, deformities of the feet (high rise) in relatives.

Slowly progressive development of asymmetric muscle weakness is a clinical sign of multifocal motor polyneuropathy. Diabetic polyneuropathy is characterized by slowly progressive hypesthesia of the lower extremities, combined with a burning sensation and other manifestations in the feet. Uremic polyneuropathy occurs, as a rule, against the background of chronic kidney disease (CKD). With the development of sensory-vegetative polyneuropathy, characterized by burning, dysesthesia, against the background of a sharp decrease in body weight, it is necessary to exclude amyloid polyneuropathy.

Hereditary polyneuropathies are characterized by the predominance of weakness of the extensor muscles of the feet, steppage, the absence of Achilles tendon reflexes, and a high arch of the foot. In a later stage of the disease, knee and carporadial tendon reflexes are absent, and atrophy of the muscles of the feet and legs develops. Muscle damage corresponding to the innervation of individual nerves, without sensory disturbances, is characteristic of multiple motor polyneuropathy. In most cases, the defeat of the upper extremities predominates.

Sensory polyneuropathies are characterized by a distal distribution of hypesthesia. In the initial stages of the disease, hyperesthesia is possible. Sensorimotor axonal neuropathies are characterized by distal hypoesthesia and distal muscle weakness. With autonomic polyneuropathies, both the phenomena of loss and irritation of the autonomic nerve fibers are possible. For vibrational polyneuropathy, hyperhidrosis, impaired vascular tone of the hands are typical, for diabetic polyneuropathy, on the contrary, dry skin, trophic disorders, autonomic dysfunction of internal organs.

The study of antibodies to GM1-ganglycosides is recommended in patients with motor neuropathies. High titers (more than 1:6400) are specific for motor multifocal neuropathy. Low titers (1:400-1:800) are possible in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), Guillain-Barré syndrome and other autoimmune neuropathies. It should be remembered that an increased titer of antibodies to GM1 ganglicosides is detected in 5% of healthy people (especially the elderly). Antibodies to myelin-associated glycoprotein are detected in 50% of patients diagnosed with paraproteinemic polyneuropathy and, in some cases, other autoimmune neuropathies.

If polyneuropathy is suspected, associated with intoxication with lead, aluminum, mercury, blood and urine tests are performed for the content of heavy metals. It is possible to carry out molecular genetic analysis for all major forms of HMSN I, IVA, IVB types. Conducting needle electromyography in polyneuropathies allows you to identify signs of the current denervation-reinnervation process. First of all, it is necessary to examine the distal muscles of the upper and lower extremities, and, if necessary, the proximal muscles. Nerve biopsy is justified only if amyloid polyneuropathy is suspected (detection of amyloid deposits).

Treatment of polyneuropathies

Treatment of hereditary polyneuropathies is symptomatic. In autoimmune polyneuropathy, the goal of treatment is to achieve remission. In diabetic, alcoholic, uremic and other chronic progressive polyneuropathies, treatment is reduced to a decrease in the severity of symptoms and a slowdown in the course of the process. One of the important aspects of non-drug treatment is exercise therapy aimed at maintaining muscle tone and preventing contractures. In the case of the development of respiratory disorders in diphtheria polyneuropathy, mechanical ventilation may be required. There is no effective medical treatment for hereditary polyneuropathies. Vitamin preparations and neurotrophic agents are used as maintenance therapy. However, their effectiveness has not been fully proven.

For the treatment of porphyria polyneuropathy, glucose is prescribed, which usually causes an improvement in the patient's condition, as well as painkillers and other symptomatic drugs. Drug treatment of chronic inflammatory demyelinating polyneuropathy includes membrane plasmapheresis, the use of human immunoglobulin or prednisone. In some cases, the effectiveness of plasmapheresis and immunoglobulin is insufficient, therefore, if there are no contraindications, treatment should be started immediately with glucocorticosteroids. Improvement occurs, as a rule, in 25-30 days; after two months, you can begin a gradual reduction in the dose to maintenance. With a decrease in the dose of glucocorticosteroids, an EMG control is necessary. As a rule, it is possible to completely cancel prednisolone within 10-12 months, if necessary, you can “insure” with azathioprine (either cyclosporine or mycophenolate mofetil).

Treatment of diabetic polyneuropathy is carried out in conjunction with an endocrinologist, its main goal is to maintain a normal blood sugar level. To relieve pain, tricyclic antidepressants are used, as well as pregabalin, gabapentin, lamotrigine, carbamazepine. In most cases, thioctic acid preparations and B vitamins are used. Regression of symptoms at an early stage of uremic polyneuropathy is achieved by nephrologists by correcting the level of uremic toxins in the blood (programmed hemodialysis, kidney transplantation). Of the drugs, vitamins of group B are used, with severe pain syndrome - tricyclic antidepressants, pregabalin.

The main therapeutic approach in the treatment of toxic polyneuropathy is the cessation of contact with a toxic substance. In dose-dependent drug polyneuropathies, it is necessary to adjust the dose of the corresponding drug. With a confirmed diagnosis of diphtheria, the introduction of antitoxic serum reduces the likelihood of developing diphtheria polyneuropathy. In rare cases, due to the development of contractures and deformities of the feet, surgical treatment may be necessary. However, it should be remembered that prolonged immobility after surgery can adversely affect motor functions.

Prognosis for polyneuropathy

In chronic inflammatory demyelinating polyradiculoneuropathy, the prognosis for life is quite favorable. Mortality is very low, however, full recovery is very rare. Up to 90% of patients on the background of immunosuppressive therapy achieve complete or incomplete remission. At the same time, the disease is prone to exacerbations, the use of immunosuppressive therapy may be due to its side effects, leading to numerous complications.

With hereditary polyneuropathies, it is rarely possible to achieve improvement in the condition, since the disease progresses slowly. However, patients tend to adapt to their condition and in most cases retain the ability to self-care until the very advanced stages of the disease. With diabetic polyneuropathy, the prognosis for life is favorable, provided timely treatment and careful control of glycemia. Only in the later stages of the disease, a pronounced pain syndrome can significantly worsen the patient's quality of life.

The prognosis for life in uremic polyneuropathy depends entirely on the severity of chronic renal failure. Timely implementation of program hemodialysis or kidney transplantation can lead to complete or almost complete regression of uremic polyneuropathy.

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Clinical picture of the disease

In each case, the course of dysmetabolic polyneuropathy may be different. If the disease develops early enough and is manifested by a significant decrease in vibrational sensitivity, then knee and Achilles reflexes may be lost.

This subclinical case of polyneuropathy does not cause pain, but develops over several years in a row.

Diabetic polyneuropathy can be characterized by subacute or even acute development. In this case, certain sections of the nerve trunks are damaged. As a rule, nerve damage occurs:

1. ischial;
2. median;
3. elbow;
4. femoral.

These problems may be accompanied by paresis of the corresponding muscle groups, pain and sensitivity disorder. If the femoral nerve was affected, then in this case there is a loss of knee reflexes.

In addition, damage to the cranial nerves (abducens, trigeminal, oculomotor) was noted.

There is a third type of course of diabetic polyneuropathy. It is characterized by damage to some nerves of the limbs and the development of sensory and motor disorders (the lower limbs are especially affected).

Tendon reflexes may completely disappear, and pain in the nerve trunks is felt on palpation.

Vegetative and trophic disorders are not uncommon in polyneuropathy. Problems with urination and postural hypotension develop.

How to treat?

First of all, carbohydrate metabolism should be adjusted with insulin injections and a special balanced diet. The doctor may recommend:

• painkillers;
• B vitamins;
• finlepsin;
• ganglioblockers (gangleron);
• espa-lipon (berlition).

The schedule of measures that are used to get rid of neuropathy will be shown.

Polyneuropathy in systemic ailments

If a patient has lupus erythematosus that affects the skin, kidneys and joints, then in this case polyneuropathy is characterized by the development of paralysis or paresis of the proximal muscles, loss of some tendon reflexes. A significant decrease in susceptibility to pain is also likely.

In some cases, signs of polyneuropathy can become the first manifestations of the development of the underlying disease. Medicine knows forms with significant damage to various nerves of the arms and legs.

In this case, we will talk about mononeuropathy. In severe rheumatoid arthritis, polyneuropathy is also observed. Initially, it will manifest itself as sensory disturbances, and then quite severe sensorimotor neuropathy.

If periarteritis nodosa is present, then sequential neuropathy of individual cranial and spinal nerves develops. Such violations will be associated with severe disorders:

1. vegetative;
2. motor;
3. sensitive.

The considered form of neuropathy is often accompanied by symptoms of inflammatory angiopathy in other organs and systems.

Hereditary polyneuropathy

First of all, it is polyneuropathy, which develops with porphyria (genetic enzyme disorders). The main symptoms of this hereditary disease are:

• pain in the abdominal cavity;
• increased blood pressure;
• damage to the central nervous system;
• producing urine with a characteristic dark color.

Porphyric polyneuropathy will be manifested due to the neurological complex of symptoms. In this case, pain, weakness in the muscles, paresthesia (upper and lower extremities) occur. Motor manifestations can gradually increase, up to distal paralysis or paresis.

With this disease, the patient will feel:

1. soreness of the nerve trunks;
2. loss of all types of sensitivity.

To make an adequate diagnosis, the doctor will take into account all the symptoms of porphyrin metabolism disorders. To get rid of the disease, the doctor recommends intravenous and oral administration of glucose at a dosage of up to 400 mg (the same treatment is indicated for other forms of polyneuropathy).

Amyloid polyneuropathy

The amyloid variety of polyneuropathy develops in those patients who have a history of hereditary amyloidosis. Its main clinical symptoms are:

• stool disorders (constipation and diarrhea);
• pain in the digestive tract;
• heart failure;
• macroglossia (an increase in the size of the tongue).

With this disease, sensory disturbances predominate, for example, soreness of the limbs, loss of pain and temperature sensitivity. At later stages, paresis also joins the disorders.

As for adequate therapy, at the moment it does not exist.

Distal sensorimotor polyneuropathy

In diabetes, long nerve fibers are most often affected. Diabetic polyneuropathy is observed in 40% of diabetics. This type of disease is characterized by the absence of a feeling of pressure, changes in ambient temperature, pain, vibration and location relative to other objects.

Sensory polyneuropathy is dangerous because a diabetic may not feel any pain or high temperatures.

Ulcers appear on the lower extremities, wounds on the leg fester. Severe joint damage and fractures are not ruled out.

Sensorimotor polyneuropathy can manifest itself with active symptoms, for example, quite strong pain in the legs, which are especially aggravated at night.

As the disease progresses, there will be a violation in the work of the musculoskeletal system. When this happens:

• bone deformity;
• muscle dystrophy;
• excessive dryness of the skin;
• the appearance of age spots;
• reddish skin tone;
• sweat gland dysfunction.

The most significant symptoms of distal polyneuropathy in diabetes mellitus will be ulcers that occur between the toes and on the soles of the feet. Lesions are not capable of causing discomfort due to the absence of pain. In advanced cases, we will talk about amputation of limbs.

Autonomic polyneuropathy in diabetes

In the presence of lesions of the autonomic nervous system against the background of the course of diabetes, the patient will feel:

1. darkening in the eyes;
2. fainting when taking a vertical position;
3. dizziness.

This form of polyneuropathy will be accompanied by malfunctions in the normal functioning of the digestive tract, which is manifested by a slowdown in the intake of food by the intestines. In view of this, it is almost impossible to stabilize the concentration of glucose in the blood of a diabetic.

The cause of a sudden death can be a heart rhythm disturbance in diabetic polyneuropathy.

Those people who suffer from this disease will feel problems from the genitourinary system - urinary incontinence occurs. The bladder will lose the ability to completely empty, which becomes a prerequisite for the development of infectious diseases. In men, erectile dysfunction will be noted against the background of autonomic polyneuropathy, and in women, dyspareunia (the inability to achieve orgasm).

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Polyneuropathy - what is it?

Polyneuropathy - translated from Greek as "suffering of many nerves." These nerves can be affected by external factors that affect them for a long time and disrupt their functioning. Unlike a brain tumor or stroke, which cause a strictly defined set of symptoms depending on the location, a special clinical picture is found in polyneuropathy, which will be discussed below.

First of all, polyneuropathy is caused by diseases in which any substances that adversely affect the nerves accumulate in the body. These diseases include endocrine pathology and diabetes mellitus.

A high level of glucose in the blood, which lasts for a long time, contributes to impaired conduction of the peripheral nerves. The result is diabetic polyneuropathy. It belongs to the group of dysmetabolic disorders.

In the event that the culprit of the disease was not an ordinary substance (after all, glucose is in the blood of everyone, it’s just that there is too much of it in diabetes), but some external toxin, then there is a toxic lesion of the peripheral nerves, both sensory and motor.

This is how toxic damage to peripheral nerves develops, and the most striking example is alcoholic polyneuropathy, which occurs in people who drink heavily and for a long time.

Malignant neoplasms that poison the entire body with the products of their vital activity and decay can also cause nerve damage. Such polyneuropathy is called paraneoplastic, and it is a formidable sign of an advanced oncological disease.

Sometimes serious infections cause nerve damage. Such polyneuropathy can be attributed to both infectious and toxic - since microorganisms often use the strongest toxins, for example, diphtheria bacillus.

Finally, autoimmune polyneuropathies can occur, in which the nerves destroy the antibodies of their own body, attacking the nervous tissue “by mistake”. Such diseases include systemic scleroderma and other "large collagenoses".

Symptoms of polyneuropathy - characteristic signs

The disease has an extremely characteristic clinical picture. Before proceeding to a review of the symptoms of polyneuropathy, it should be mentioned that this nerve lesion can be of the following types:

• Sensitive or sensory form. There are predominantly sensory disorders: paresthesia, numbness, burning, tingling, sensation of discomfort or "crawling".
• Motor, or motor form. There is muscle weakness, hypotrophy and muscle atrophy.
• Most often there is their combined variant - sensorimotor polyneuropathy, which occurs in most cases, and above all in diabetes and alcoholism.
• Vegetative polyneuropathy. In this course, the autonomic nerves that “manage” the internal organs are affected.
• Finally, there is a mixed form that combines all types of disorders.

Polyneuropathy is characterized by damage to small nerves, since their myelin sheath is thinner and it is “easier to get to” them for any harmful substances. Therefore, most often there is a lesion of the hands and feet - polyneuropathy of the upper and lower extremities, the symptoms of which, as neurologists say, are like “socks and gloves”.

There is even a type of sensory disorder called the polyneuritic type. So, polyneuropathy of the upper extremities and lower extremities will have the same symptoms.

The next important symptom of polyneuropathy will be the symmetry of the lesion, since the disease-causing substance circulates in the blood.

For example, symptoms of polyneuropathy of the upper extremities may include weakness of the fingers, burning pain, a feeling of chilliness, and marbled skin on the back of the hands (vegetative disorders).

The most common signs of nerve damage are as follows:

1. Various and very diverse pains, including those with a neuropathic, "burning" shade.
2. Attachment of trembling fingers.
3. The appearance of fasciculations (or muscle twitches, which are involuntary).
4. Violations of sensitivity (not only tactile, which was written above, but also a decrease in temperature and pain sensitivity). That is why, with diabetic neuropathy, patients “feel badly” a pebble in a shoe, a badly clogged shoe stud, and other irritants.
5. Weakness in the muscles, impossibility or significant difficulty in movements with a large amplitude. Often, weakness is combined with muscle hypotension and asthenia of the patient.

A special group is made up of vegetative signs of polyneuropathy. These include hot flashes and the appearance of pallor and cold sweat, circulatory disorders (and poor wound healing, and all kinds of damage to the skin).

Not always the disease develops for a long time and gradually. So, polyneuropathy of the lower extremities, the symptoms of which indicate a decrease in sensitivity, the extinction of Achilles reflexes, the presence of trophic disorders, may indicate a long-term process, or it may appear in a matter of days and weeks, for example, with a mild degree of radiation sickness or poisoning with lead and its compounds.

Surprising complaints sometimes occur as part of polyneuropathy. So, with pernicious anemia, due to a deficiency of cyanocobalamin (vitamin B 12), posterior columnar ataxia occurs. In this case, it is not the peripheral nerves that are affected, but the spinal cord, more precisely, its posterior cords (pillars), in which the conductive bundles of the articular-muscular feeling, or Gaulle-Burdach bundles, are located.

What happens when they are defeated? Each of us, of course, with his eyes closed knows how his arms and legs are located, even if they are not moved. A patient with this type of ataxia does not know. Therefore, he cannot walk in the dark, as he gets confused and does not know where and how his legs are located. But in the light and the presence of visual control, the gait of such a person is normal.

There are special autonomic or autonomic neuropathies that disrupt the rhythm of the heart and can even lead to sudden death due to the occurrence of ventricular asystole or other fatal arrhythmias. Such polyneuropathy is a vegetative motor cardiac form of the disease.

The diagnosis is made by a neurologist, taking into account complaints, anamnesis and the development of the disease. As a rule, with polyneuropathy, the correct diagnosis is not difficult.

Neither MRI, nor CT scan, nor ultrasound help here. The most important method is ENMG - electroneuromyography, which allows you to fully identify the violation of conduction along the nerve fiber and determine what is affected - the axial cylinder of the nerve or the myelin "insulating" sheath.

Blood tests for biochemistry often show certain endocrine disorders (glucose). In extreme cases, polyneuropathy requires a biopsy of the nerve fiber, which is studied using histochemical and immune methods.

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Forms

Sensorimotor polyneuropathy differs in many ways. According to the nature of the process, acute and chronic diseases are distinguished. In addition, there are three forms:

1. Demyelinating polyneuropathy is associated with myelin breakdown. Myelin is a protein that surrounds the nerve fiber, and it also provides the process of conducting impulses. The chronic inflammatory form occurs when nerve fibers die due to their own aggression against immune forces. This happens when the immune system considers myelin to be a foreign sheath, destroying it. If treatment is carried out, then complications can be avoided and recovery can be achieved.
2. The axonal form of the pathology is associated with a violation of the functional features that the axon and the nerve shaft have. Due to malnutrition of the nerve, the symptoms of the disease are dangerous and the treatment takes a long time.
3. The neuropathic form of the disease is associated with the presence of affected nerve cell bodies.

Polyneuropathy affects nerves that have different functions, therefore, another classification of the disease is distinguished:

• The sensory form of polyneuropathy is characterized by damage to the nerves responsible for sensory function. The sensory form in the patient causes symptoms such as soreness, numbness and burning in the affected parts of the body.
• The motor form affects the motor fibers, therefore, the muscular apparatus suffers. Muscle weakness and atrophy appear.
• The vegetative form of polyneuropathy involves the nerves of the autonomic system in the process. The vegetative form disrupts the functioning of internal organs, including the heart.
• The mixed form has symptoms of other types, including a combination of all forms of the disease.

The rest of the classification is based on the causes of the formation of the disease.

Causes

The causes of the disease form several types of polyneuropathy and are associated with the influence of both external and internal factors. So, they distinguish an idiopathic type of disease that occurs when the immune system is impaired. The hereditary form is associated with a genetic predisposition and is transmitted from the father or mother.

Dysmetabolic inflammatory neuropathy appears when there are malfunctions in the metabolic processes of the body. One of the types of pathology occurs during the onset of infection. It can be a human immunodeficiency virus, infections with immunity damage, forms of diphtheria. This is how post-infectious polyneuropathy is formed.

The causes of pathology lie in the toxic effects on the body. Alcohol and its derivatives destroy the nervous system. Also, metals and toxins can affect the immune system and nervous system. It can be lead poisoning, mercury, antibiotics.

Causes such as allergic processes lead to an autoimmune reaction of the body, in which acute or chronic polyneuropathy can begin. Diseases such as scleroderma, lupus, vasculitis, affect the connective tissue, nerves and, therefore, threaten pathology.

Polyneuropathy is formed against the background of tumor processes in the body. It can be concluded that the disease can be caused by many causes and diseases that affect people. But this does not mean that everyone will get polyneuropathy. It is necessary to influence several factors, and there may also be poor-quality treatment and lifestyle disorders that allow you to catch the disease.

Symptoms

The prefix "poly" in the name of the disease means a combination of many signs and the involvement of several parts of the body and organs in the process. The symptoms of polyneuropathy are extensive and depend on the affected nerves and immune defenses.

When the nerve fibers are damaged, the limbs suffer: arms or legs. Diagnosis of pathology should begin when there is a tremor in the limbs, the presence of a tremor. In addition to tremor, symptoms of painful muscle cramps can be observed.
This is how Crumpy syndrome manifests itself.

The following symptoms are characteristic:

With damage to blood vessels and organs, symptoms of a violation in blood pressure appear. Pressure figures can reach a high point, which threatens a stroke. Effects on the heart cause symptoms of rapid heartbeat (tachycardia).

Each form of pathology manifests its own symptoms, but muscle pain and weakness are characteristic signs of the disease. If you do not start treatment, then the disease will lead a person to paralysis in the limbs and, as a result, to disability. Therapy with folk remedies without medicines will not help to cure the disease, especially since high-quality diagnostics are needed to identify the causes and not ignore the symptoms.

In most cases, the symptoms are initially minor, but over time, reduced muscle tone, atrophy, and hyperesthesia appear. So, the patient has a shaky gait, bouts of dizziness, nausea. If the disease affects the internal organs, then their work is disrupted.

Survey

Diagnosis of polyneuropathy is not carried out at home and should be comprehensive. Comorbidities are identified, and the symptoms of polyneuropathy are similar to many diseases. It is necessary to establish whether the form is acute or chronic in order to identify the neglect of the process.

Diagnosis includes the study of anamnesis, patient complaints. Also, such facts from life as the presence of injuries, alcohol consumption, peculiarities of work and rest, past diseases are revealed. This is necessary to find a treatment. It is important to establish hereditary factors, for which the history of relatives is studied.

The doctor examines and identifies neurological signs. Diagnosis requires a blood test, including for the presence of toxins. Of the hardware techniques, electroneuromyography is used, which makes it possible to determine the characteristics of impulses passing through nerve fibers. A nerve biopsy is taken. If necessary, consultations of specialists and other types of examinations are appointed.

Treatment

Treatment is aimed at eliminating the cause and getting rid of the symptoms of the disease. If there is an inflammatory reaction, an allergy, then it is necessary to carry out specific therapy. Treatment with folk remedies is allowed in combination with medicines. In diabetes, treatment is aimed at lowering blood sugar levels. With toxic effects, detoxification therapy is prescribed.

With a disease, the diet excludes alcohol, fatty foods. It is necessary to replenish the supply of vitamins and trace elements. To improve the functioning of the nerves, vitamins of group B are prescribed. Metabolic treatment improves the function of tissues and their nutrition.

The operation is prescribed to remove oncology or to restore the functioning of organs. If there is high blood pressure, then antihypertensive therapy is indicated. Treatment with folk remedies will help reduce pressure.

Pain is eliminated by analgesics, muscle relaxants, NSAIDs, hormones. Exercise therapy and physiotherapy are prescribed for recovery in combination with folk remedies.
Wearing an orthosis is recommended if necessary. It is important that the acute form of the disease does not turn into a chronic one, so the treatment must be completed completely.

ERT techniques are used in the treatment of polyneuropathy. With the help of magnetotherapy, the nerves are affected by magnetic fields. Electrical stimulation and ultrasound are used. Massage develops muscles, improves blood circulation. Reflexology, massage and gymnastics are used in treatment and prevention.

Means of prevention is the treatment of foci of infection and inflammation. To prevent illness, strengthen the immune system, nerves. And with age, you need to regularly undergo medical examinations.

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Distal

This term means that diabetes affects the nervous system located distally, that is, away from the body and internal organs. This term is opposite in meaning to the word "proximal", that is, the closest. That is, these are the “ends” of the body. There is a good figurative expression in neurology: a sock-and-glove lesion. It is in these places that elevated blood sugar levels produce the most damage to the nerves. This is because at the periphery of the nerves, the myelin sheath is thinner (because the nerves themselves are thinner, like long branches), which is the "insulator" of the nerve fiber. It is more vulnerable to the damaging effects of sugar. In addition, it is on the periphery that circulatory disorders often occur. Therefore, the distal form of the disease is the most common.

symmetrical

Symmetry is an important sign of systemic damage. If signs of polyneuropathy occur only on one leg, then this means that some kind of catastrophe has occurred with the nerves in this particular place: compression, nerve injury, or another pathological process has occurred. The symmetry of the lesion suggests that the blood is to blame, which, washing the arms and legs equally, contains a substance that is harmful. In this case, chronic, long-term hyperglycemia is to blame - high blood sugar. Patients feel that the legs and arms suffer almost equally.

sensorimotor

This word includes the meaning of defeat. Sensorimotor - means a sensory plus motor form, that is, a violation of sensitivity (sensory disorders), which is combined with motor disorders, that is, movement disorders. Of course, on the feet and ankles, as well as on the hands and fingers, various nerves "manage" the conduction of sensitivity, and also send motor impulses to the muscles. But they all equally suffer from an excess of sugar and begin to "work poorly." In particular, sensory disturbances are manifested:

• General decrease in sensitivity (hypesthesia). The patient cannot understand which toe the doctor took, unless you look and move the foot.
• Paresthesias appear (a feeling of crawling), numbness may occur.
• The most agonizing sensation is hyperpathia, a perverse sensation in which there is an excruciating sensation of heat in the feet. They don't hurt, but kind of "burn". A patient with polyneuropathy tries to stick his legs out from under the covers at night, often goes to the bathroom and wets them with cold water. As long as the feet are wet, all is well. As soon as they dry, the unpleasant sensations appear again.

Movement (motor) disorders are manifested by inhibition or complete absence of the Achilles tendon reflex, but most often there is weakness in the feet. If you ask a patient with polyneuropathy to try to walk on tiptoe, and then on his heels, then most likely he will not succeed or it will come out very unstable and clumsy: the muscles do not work. And not because they are paralyzed, but because the nerve cannot conduct a full-fledged motor impulse, since it is “poisoned” by glucose.

Actually, this term means that it is not the brain or spinal cord that is affected, but many nerves on the periphery (poly means a lot). It is this “loose” type of lesion that is characteristic of polyneuropathy. Lesions of the "socks" and "gloves" type, in addition to diabetes, are characteristic of heavy metal salt poisoning (lead) or due to prolonged alcohol abuse (alcoholic form).

lower limbs

Why are the legs involved? In fact, the symptoms of neuropathy in diabetes also appear in the hands, but they are more pronounced in the legs. There are reasons for this:

• It is in the legs, in old age, when this symptomatology usually occurs, that there are already prerequisites in the form of circulatory disorders: varicose veins, endarteritis, thrombophlebitis.
• In addition, the legs are constantly loaded in a completely different way than the arms, because when walking, the arms rest.
• Often, patients, especially those with type 2 diabetes, are overweight, which also adversely affects the health of the legs.

Now everyone knows what this complex diagnosis means. The treatment of diabetic polyneuropathy is no less complicated: it is impossible to completely eliminate the toxic damage to the nerves by glucose, which lasted for years, in one day or even a month. There are many treatment regimens. For this, for example, intravenous infusions of Berlition and other thioctic acid preparations are used.

In the treatment of polyneuropathy, agents for normalizing microcirculation (Pentoxifylline, Trental), B vitamins are of great importance, preferably in the form of a combined preparation, for example, Milgamma. Physiotherapeutic procedures are also used, for example, electrophoresis of thiamine or dibazol. With polyneuropathy, it is very important to observe foot hygiene, to prevent the appearance of wounds, cuts and calluses, since poor wound healing in diabetes in combination with polyneuropathy can lead to the appearance of a "diabetic foot", which in advanced cases is fraught with even amputation.

You can also be treated with folk remedies, but only with the permission and approval of the attending physician, since traditional medicine alone is not able to cope with this complication. It is important to know that the first and most important condition for a significant improvement in well-being in this complication of diabetes mellitus is the achievement of normoglycemia, that is, a long-term decrease in blood sugar levels to normal values.

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What is diabetic polyneuropathy

Multiple lesions of nerve fibers are observed in patients suffering from diabetes for more than one decade, in 45-54% of cases. The role of peripheral nervous regulation of the body is extremely important. This system of neurons controls the brain, heartbeat, respiration, digestion, and muscle contraction. Diabetic polyneuropathy of the lower extremities (DLN) is a pathology that begins in the feet and then spreads higher and higher.

The pathogenetic mechanism of the disease is very complex and has not been fully elucidated by scientists. Violations of the functions of the peripheral nervous system are diverse. Each type of DPN has its own clinical picture. However, all forms of this complication are dangerous and require patient treatment, otherwise a foot problem can turn a person into an invalid. Diabetic polyneuropathy is encrypted by doctors under the code G63.2 according to ICD-10, indicating the variant of the disease.

Types of neuropathy

Since the peripheral nervous system is divided into somatic and autonomic (vegetative), two types of diabetic polyneuropathy are also called. The first gives rise to multiple non-healing trophic ulcers of the lower extremities, the second - problems with urination, impotence and cardiovascular accidents, often fatal.

Another classification is based on the functions of the nervous system, which are violated as a result of the development of pathology:

• sensory polyneuropathy associated with increased pain in the lower extremities, or, conversely, with loss of tactile sensitivity;
• motor polyneuropathy, which is characterized by muscular dystrophy and loss of the ability to move;
• sensorimotor polyneuropathy, combining the features of both of these complications.

A manifestation of the latter, mixed pathology is neuropathy of the peroneal nerve. Diabetics with such an ailment do not feel pain in certain places of the foot and lower leg. These parts of the surfaces of the legs do not react to either cold or heat. In addition, patients lose the ability to control their feet. Patients are forced to walk, raising their legs unnaturally high ("cock" gait).

Diabetic distal polyneuropathy

This is a pathology that causes the death of nerve fibers. The disease leads to a complete loss of tactile sensitivity and ulceration of the most distant part of the lower extremities - the feet. Typical for diabetics with distal DPN is a dull, aching pain that is often so severe that the person cannot sleep. In addition, sometimes the shoulders begin to ache. Polyneuropathy progresses, and this leads to muscle atrophy, bone deformities, flat feet, and amputation of the feet.

Peripheral neuropathy of the lower extremities

With this type of disease, severe disorders of the sensorimotor functions of the legs occur. Diabetics have pain and numbness not only in the feet, ankles, lower legs, but also in the hands. Peripheral polyneuropathy occurs mainly when doctors prescribe strong antiviral drugs with serious side effects: Stavudine, Didanosine, Saquinavir, Zalcitabine. It is important to diagnose this pathology in a timely manner in order to immediately stop the drug.

Sensory polyneuropathy

The main feature of the pathology is the loss of sensitivity of the lower extremities, the degree of which can vary significantly. From slight tingling to complete numbness, accompanied by the formation of ulcers and deformation of the feet. At the same time, the lack of sensitivity is paradoxically combined with unbearably severe pain that occurs spontaneously. The disease first affects one leg, then often passes to the second, rising higher and higher, affecting the fingers and hands, torso, head.

Dysmetabolic polyneuropathy

The occurrence of this type of complication is often provoked, in addition to diabetes, diseases of the stomach, intestines, kidneys, liver. Many nerve plexuses of the extremities may be affected. In violation of the sciatic, femoral neurons, pain, trophic ulcers, difficulties with movement appear, knee, tendon reflexes disappear. Often damaged ulnar, trigeminal, ophthalmic nerves. Dysmetabolic polyneuropathy can occur without pain.

Why do people with diabetes develop neuropathy?

The main reason is high blood glucose levels and prolonged insulin deficiency. The deterioration of cellular metabolism has a detrimental effect on peripheral nerve fibers. In addition, diabetic polyneuropathy of the lower extremities can be caused by:

• endocrine disorders;
• severe liver or kidney disease;
• depression, weakening of the immune system;
• infections;
• abuse of alcoholic beverages;
• poisoning with toxic chemicals;
• tumors.

Symptoms of diabetic polyneuropathy of the lower extremities

The main manifestations of the disease of all types:

1. Sensitive symptoms - pain, weakening or aggravation of the perception of temperature changes, vibration.
2. Motor symptoms - convulsions, tremors, muscle atrophy of the limbs.
3. Vegetative symptoms - edema, hypotension, tachycardia, stool disorders, impotence.

Burning and tingling of the lower extremities

Sensation as if the soles of the feet are on fire, occurs when the fibers of the peripheral nerve that runs from the spine to the feet are damaged. Burning feet is not a disease, but a symptom that manifests polyneuropathy in diabetes mellitus. Damaged neurons are activated and send false pain signals to the brain, although the soles of the feet are intact, and there is no fire.

Loss of sensation in the foot

First, a diabetic experiences weakness, numbness in the feet. Then these sensations arise in the legs, hands. As the polyneuropathy of the lower extremities progresses, muscle atrophy increases and tactile sensitivity decreases. The feet become difficult to control and hang down. The hands become numb, starting from the tips of the fingers. With a long pathological process, loss of sensitivity affects part of the body in the chest and abdomen.

Diagnosis of the disease

Polyneuropathy of the lower extremities is detected using the following methods of examination of the patient:

• checking unconditioned reflexes;
• pain sensitivity test;
• vibration response test;
• thermal test;
• skin nerve biopsy;
• electroneuromyography (ENMG), which can show whether nerve impulses travel along muscle fibers.

Treatment of diabetic polyneuropathy of the lower extremities

Completely such complications cannot be cured, but their development can be slowed down. How to treat neuropathy of the lower extremities? The main condition is the normalization of glucose in the blood. Analgesics, spacious shoes, minimal walking, cool baths help reduce pain. A contrast shower relieves the burning sensation of the feet. It is necessary to use drugs that dilate peripheral vessels that affect the transmission of nerve impulses. Treatment of polyneuropathy of the lower extremities becomes more effective when taking B vitamins. It is also important to adjust the carbohydrate metabolism of the diet.

Medical therapy

The main means for the complex treatment of patients with a diagnosis of polyneuropathy of the lower extremities:

• antidepressants Amitriptyline, Imipramine, Duloxetine, blocking the reuptake of the hormones norepinephrine and serotonin;
• anticonvulsants Pregabalin, Carbamazepine, Lamotrigine;
• analgesics Targin, Tramadol (doses are strictly limited - drugs!);
• vitamin complex Milgamma;
• Berlition (thioctic or alpha lipoic acid), which has the ability to repair damaged nerves;
• Actovegin, which improves the blood supply to the nerve endings;
• Isodibut, Olrestatin, Sorbinil, protecting nerves from glucose;
• antibiotics - with the threat of gangrene development.

Treatment of neuropathy in diabetes mellitus without drugs

The hope of being cured with the help of some homemade or folk remedies is a utopia. It is necessary to take medications and actively use:

• magnetotherapy;
• electrical stimulation;
• hyperbaric oxygenation;
• acupuncture;
• massage;
• exercise therapy (physiotherapy).

vrachmedik.ru

The disease under consideration, polyneuropathy of the upper and lower extremities, begins with muscle weakness, and first of all, in the distal parts of the legs and arms. This is due to damage to the nerve fibers. With this disease, first of all, the distal parts of the limbs are affected due to the lack of sufficient protection of segments of the peripheral system (for example, the blood-brain barrier located in the brain).

Manifestations of the described pathology debut in the area of ​​the foot and spread gradually up the limb. Depending on the typology of nerve fibers that are more susceptible to destruction, all types of polyneuropathy are conventionally divided into four subgroups.

Due to the defeat, mainly, of the afferent long processes of neurons, patients have positive or negative symptoms. The first is characterized by a lack of function or its decrease, positive symptoms are those manifestations that have not been observed before.

In the first place, in patients, the disease in question is manifested by various kinds of paresthesias, such as burning, tingling, crawling, numbness. Then the clinical picture is complicated by algia of varying intensity, the susceptibility of pain stimuli increases. As symptoms increase, patients become overly sensitive to simple touch. Later, they have manifestations of sensitive ataxia, expressed in unsteadiness of gait, especially with closed eyes, and impaired coordination of movement. The negative symptoms of polyneuropathy include a decrease in sensitivity at the sites of damage to nerve fibers.

When the axons of movement neurons are damaged, polyneuropathy of the upper and lower extremities is manifested, first of all, by muscle atrophy and is found in the weakness of the legs and arms. The described symptomatology progresses to the occurrence of paralysis and paresis. Less commonly, there may be a condition manifested by unpleasant sensations in the legs, appearing mainly at rest and forcing people to make movements of a relieving nature (syndrome of "restless lower extremities"). In addition, fasciculations and convulsions may occur.

Vegetative dysfunctions are divided into trophic disorders and vascular disorders. The former include the appearance of pigmentation and peeling of the skin, the appearance of cracks and ulcers on the limbs. Vascular disorders include a feeling of cold in the damaged segments, fading of the skin (the so-called "marble pallor").

Vegetative-trophic symptoms also include changes in the structure of derivatives of the dermis (hair and nails). Due to the fact that the lower limbs can withstand more load, polyneuropathy of the legs is diagnosed much more often than the hands.

Polyneuropathy of the lower extremities

The disease under consideration, polyneuropathy of the extremities, is a degenerative destruction of nerve cells, causing a malfunction in the functioning of the peripheral nervous system. This ailment is manifested by a decrease in motor ability, a decrease in sensitivity, depending on the location of the pathological focus, any part of the limbs, muscle pain. With the disease under consideration, the patient's nerve fibers that feed the feet are damaged. As a result of structural damage to the nerve fibers, the sensitivity of the legs is lost, which affects the ability of the individual to move independently.

Treatment of polyneuropathy of the lower extremities, as a rule, is quite laborious and lengthy, since more often, this ailment is progressive in nature and develops into a chronic course.

To determine the causes provoking the development of the described disease, in the first turn, it is necessary to deal with the structure of the nervous system, in particular its separate area - the peripheral system. It is based on long processes of nerve fibers, the task of which is to transmit signals, which ensures the reproduction of motor and sensory functions. The bodies of these neurons inhabit the nuclei of the brain and spinal cord, thus forming a close connection. From a practical point of view, the peripheral segment of the nervous system combines the so-called "conductors" that connect nerve centers with receptors and functional organs.

When polyneuropathy occurs, a separate part of the peripheral nerve fibers is affected. Therefore, the manifestations of the disease are observed in certain areas. The considered pathology on the limbs manifests itself symmetrically.

It should be noted that the analyzed pathology has several varieties, which are classified depending on the functions of the damaged nerves. So, for example, if the neurons responsible for movement are affected, then the ability to move may be lost or difficult. Such polyneuropathy is called motor.

In the sensory form of the disorder in question, nerve fibers are affected, which cause sensitivity, which suffers greatly when this category of neurons is damaged.

Insufficiency of autonomic regulatory functions occurs when autonomic nerve fibers are damaged (hypothermia, atony).

Thus, the following significant factors provoking the development of this disease are distinguished: metabolic (associated with impaired metabolic processes), autoimmune, hereditary, alimentary (caused by eating disorders), toxic and infectious-toxic.

There are two forms of the described pathology, depending on the location of the lesion: demyelinating and axonal. In the first case, myelin is affected - the substance that forms the sheath of the nerves, with the axonal form, the axial cylinder is damaged.

The axonal form of polyneuropathy of the legs is observed in all types of the disease. The difference lies in the prevalence of the type of violation, for example, there may be a disorder of motor function or a decrease in sensitivity. This form appears as a result of serious metabolic disorders, intoxication with various organophosphorus compounds, lead, mercury salts, arsenic, as well as alcoholism.

There are four forms, depending on the tendency of the course: chronic and recurrent form of the course, acute and subacute.

The acute form of axonal polyneuropathy often develops in 2-4 days. More often it is provoked by severe poisoning of a suicidal or criminal nature, general intoxication due to exposure to arsenic, carbon monoxide, lead, mercury salts, methyl alcohol. The acute form can last more than ten days.

Symptoms of a subacute form of polyneuropathy increase within a couple of weeks. This form often occurs with metabolic disorders or due to toxicosis. Recovery is usually slow and can take months.

The chronic form often progresses for an extended period of time of six months or more. The disease usually appears on the background of alcoholism, diabetes mellitus, lymphoma, blood diseases, vitamin deficiency of thiamine (B1) or cyanocobalamin (B12).

Among axonal polyneuropathies, alcoholic polyneuropathy is more often diagnosed, generated by a long time and exorbitant abuse of alcohol-containing liquids. A significant role for the occurrence of the pathology under consideration is played not only by the number of “absorbed liters” of alcohol, but also by the quality of the consumed product itself, since many alcoholic beverages contain many substances that are toxic to the body.

The main factor provoking alcoholic polyneuropathy is the negative impact of toxins, which alcohol is rich in, on the nerve processes, which leads to metabolic disorders. In most cases, the pathology under consideration is characterized by a subacute course. Initially, there are sensations of numbness in the distal segments of the lower extremities, and severe pain in the calf muscles. With an increase in pressure, algia in the muscles noticeably intensifies.

At the next stage of the development of the disease, dysfunction is observed mainly in the lower extremities, which is expressed by weakness, often even paralysis. Most of all, the nerves that cause flexion-extension of the foot are damaged. In addition, the sensitivity of the surface layers of the dermis in the area of ​​\u200b\u200bthe brushes of the “glove” type and the feet of the “sock” type are disturbed.

In some cases, this disease can have an acute course. Basically, this is due to excessive hypothermia.

In addition to the above clinical symptoms, other pathological manifestations may also be present, such as a significant change in the color range of the skin of the legs and the temperature of the extremities, swelling of the distal parts of the legs (less often of the hands), and increased sweating. The disease in question can sometimes affect the cranial nerves, namely the oculomotor and optic nerves.

The described violations are usually detected and grow over several weeks / months. This disease can last for several years. With the cessation of the use of alcoholic beverages, the disease can be overcome.

The demyelinating form of polyneuropathy is considered a serious disease, accompanied by inflammation of the nerve roots and a gradual lesion of their myelin sheath.

The considered form of the disease is relatively rare. More often this disease affects the adult male population, although it can also occur in the weaker half and children. Demyelinating polyneuropathy is usually manifested by weakness of the muscles of the distal and proximal areas of the extremities, due to damage to the nerve roots.

The mechanism of development and the etiological factor of the considered form of the disease today, unfortunately, are not known for certain, however, numerous studies have shown the autoimmune nature of demyelinating polyneuropathy. For a number of reasons, the immune system begins to consider its own cells as foreign, as a result of which it is accepted to produce specific antibodies. With this form of pathology, antigens attack the cells of the nerve roots, causing the destruction of their sheath (myelin), thereby provoking an inflammatory process. As a result of such attacks, the nerve endings lose their fundamental functions, which causes a breakdown in the innervation of organs and muscles.

Since it is generally accepted that the origin of any autoimmune disease is related to heredity, a genetic factor in the occurrence of demyelinating polyneuropathy cannot be excluded. In addition, there are conditions that can change the functioning of the immune system. Such conditions or factors include metabolic and hormonal disorders, heavy physical exertion, infection of the body, emotional overstrain, vaccination, trauma, stress, severe illness, and surgery.

Thus, the treatment of polyneuropathy of the lower extremities is represented by a number of features that must be taken into account, because the violation in question does not occur on its own. Therefore, when the first manifestations and signs of the disease are detected, it is necessary to immediately establish the etiological factor, since the treatment, for example, of diabetic polyneuropathy differs from the treatment of the pathology generated by alcohol abuse.

Upper limb polyneuropathy

This violation occurs due to damage to the nervous system and leads to paralysis of the upper limbs. With this disease, symmetrical damage to the nerve fibers of the distal regions of the extremities is usually noted.

Signs of polyneuropathy of the hands are almost always the same. In patients, there is an increase in sweating, a violation of pain sensitivity, thermoregulation, skin nutrition, a change in tactile sensitivity, paresthesias appear in the form of "goosebumps". This pathology is characterized by three types of course, namely chronic, acute and subacute.

Polyneuropathy of the upper extremities is manifested, first of all, by weakness of the hands, various algias, which in their content are burning or bursting, swelling, and occasionally tingling can be felt. With this pathology, vibration sensitivity is impaired, as a result of which patients often experience difficulties in performing elementary manipulations. Sometimes in people suffering from polyneuropathy, there is a decrease in sensitivity in the hands.

Cause polyneuropathy of the hands, most often, various intoxications, for example, due to the use of alcohol, chemicals, spoiled foods. Also, the occurrence of the disease in question can be provoked by: vitamin deficiency, infectious processes (viral or bacterial etiology), collagenoses, dysfunction of the liver, kidneys, tumor or autoimmune processes, pathologies of the pancreas and endocrine glands. Often this disease appears as a consequence of diabetes.

The described disease can proceed in each patient in different ways.

According to the pathogenesis, polyneuropathy of the upper extremities can be divided into axonal and demyelinating, according to clinical manifestations into: vegetative, sensory and motor. In its pure form, it is rather difficult to meet the listed varieties of this disease, more often the disease combines the symptoms of several variations.

Treatment of polyneuropathy

Today, the methods of therapy for this disease are rather scarce. Therefore, to this day, the treatment of polyneuropathy of various forms remains a serious problem. The level of knowledge of modern physicians in the field of the pathogenetic aspect and the etiological factor of this category of diseases determined the expediency of distinguishing two areas of therapeutic action, namely, undifferentiated methods and differentiated ones.

Differentiated methods of therapeutic correction suggest treatment of the underlying disease (for example, nephropathy, diabetes) in case of endogenous intoxications; in case of pathologies of the digestive system caused by malabsorption, they require the appointment of large doses of vitamins B1 (thiamine) and B12 (cyanocobalamin).

So, for example, diabetic polyneuropathy treatment drugs and their choice is due to the maintenance of a certain glycemic level. Therapy of polyneuropathy against the background of diabetes should be phased. At the first stage, body weight and diet should be adjusted, a set of special physical exercises should be developed, and blood pressure should be monitored for compliance with the norm. Pathogenetic methods of therapy involve the use of neurotropic vitamins and the injection of alpha-lipoic acid in large doses.

Undifferentiated methods of therapeutic action are represented by glucocorticoids, immunosuppressive drugs and plasmapheresis.

Polyneuropathy treatment drugs should be administered in combination. The specificity of the choice of therapeutic measures for the pathology under consideration always depends on the etiological factor that provoked the disease and determined its course. So, for example, the symptoms of polyneuropathy, generated by an excessive content of pyridoxine (vitamin B6), disappear without a trace after normalization of its level.

Polyneuropathy caused by a cancerous process is treated by surgical intervention - the removal of a neoplasm that put pressure on the nerve endings. If the disease occurs against the background of hypothyroidism, then hormone therapy is used.

Treatment of toxic polyneuropathy, in the first place, involves detoxification measures, after which medications are prescribed to correct the disease itself.

If it is impossible to identify or eliminate the cause that provoked the development of the described disease, the main goal of treatment involves the removal of pain and the elimination of muscle weakness.

In these cases, standard physiotherapeutic methods and the appointment of a number of drugs aimed at relieving or alleviating pain caused by damage to nerve fibers are used. In addition, physiotherapy methods are actively used at all stages of rehabilitation treatment.

With the help of analgesics or non-steroidal anti-inflammatory drugs, it is quite difficult to defeat algia. Therefore, the appointment of local anesthetics, anticonvulsants and antidepressants for the relief of pain attacks is more often practiced.

The effectiveness of antidepressants lies in their ability to cause activation of the noradrenergic system. The choice of drugs in this group is set individually, since antidepressants often cause mental dependence.

The use of anticonvulsants is justified by their ability to inhibit nerve impulses emanating from the affected nerves.

Dysmetabolic polyneuropathy is an ailment that can develop against the background of the presence of somatic problems predetermined by metabolic disorders:

• diabetes mellitus;
• diseases of the kidneys, liver;
• problems of the digestive tract.

These diseases become a prerequisite for insufficiency of thiamine and other vitamins. In addition, multiple lesions of peripheral nerve endings can often be observed.

It develops in diabetes mellitus in 90% of cases. The exact number of such problems will directly depend on the duration of the course of diabetes, however, in no way depends on the degree of its severity.

Symptoms of polyneuropathy can also become harbingers of this disease.

Hypoxia with changes can become an important factor in the development of neuropathy. In view of this, the use of sugar by the peripheral nerves will be impaired.

As a result of failures of the glycolysis process, an excess of lactic acid and pyruvic acid will accumulate. Cases of changes in the process of thiamine phosphorylation have been noted.

Not the last role will be played by a violation in other types of metabolism that are present against the background of diabetes:

• water-electrolyte;
• lipid;
• protein.

Clinical picture of the disease

In each case, the course of dysmetabolic polyneuropathy may be different. If the disease develops early enough and is manifested by a significant decrease in vibrational sensitivity, then knee and Achilles reflexes may be lost.

This subclinical case of polyneuropathy does not cause pain, but develops over several years in a row.

Diabetic polyneuropathy can be characterized by subacute or even acute development. In this case, certain sections of the nerve trunks are damaged. As a rule, nerve damage occurs:

1. ischial;
2. median;
3. elbow;
4. femoral.

These problems may be accompanied by paresis of the corresponding muscle groups, pain and sensitivity disorder. If the femoral nerve was affected, then in this case there is a loss of knee reflexes.

In addition, damage to the cranial nerves (abducens, trigeminal, oculomotor) was noted.

There is a third type of course of diabetic polyneuropathy. It is characterized by damage to some nerves of the limbs and the development of sensory and motor disorders (the lower limbs are especially affected).

Tendon reflexes may completely disappear, and pain in the nerve trunks is felt on palpation.

Vegetative and trophic disorders are not uncommon in polyneuropathy. Problems with urination and postural hypotension develop.

How to treat?

First of all, carbohydrate metabolism should be adjusted with insulin injections and a special balanced diet. The doctor may recommend:

• painkillers;
• B vitamins;
• finlepsin;
• ganglioblockers (gangleron);
• espa-lipon().

The schedule of measures that are used to get rid of neuropathy will be shown.

Polyneuropathy in systemic ailments

If a patient has lupus erythematosus that affects the skin, kidneys and joints, then in this case polyneuropathy is characterized by the development of paralysis or paresis of the proximal muscles, loss of some tendon reflexes. A significant decrease in susceptibility to pain is also likely.

In some cases, signs of polyneuropathy can become the first manifestations of the development of the underlying disease. Medicine knows forms with significant damage to various nerves of the arms and legs.

In this case, we will talk about mononeuropathy. In severe rheumatoid arthritis, polyneuropathy is also observed. Initially, it will manifest itself as sensory disturbances, and then quite severe sensorimotor neuropathy.

If periarteritis nodosa is present, then sequential neuropathy of individual cranial and spinal nerves develops. Such violations will be associated with severe disorders:

1. vegetative;
2. motor;
3. sensitive.

The considered form of neuropathy is often accompanied by symptoms of inflammatory angiopathy in other organs and systems.

Hereditary polyneuropathy

First of all, it is polyneuropathy, which develops with porphyria (genetic enzyme disorders). The main symptoms of this hereditary disease are:

• pain in the abdominal cavity;
• increased blood pressure;
• damage to the central nervous system;
• producing urine with a characteristic dark color.

Porphyric polyneuropathy will be manifested due to the neurological complex of symptoms. In this case, pain, weakness in the muscles, paresthesia (upper and lower extremities) occur. Motor manifestations can gradually increase, up to distal paralysis or paresis.

With this disease, the patient will feel:

1. soreness of the nerve trunks;
2. loss of all types of sensitivity.

To make an adequate diagnosis, the doctor will take into account all the symptoms of porphyrin metabolism disorders. To get rid of the disease, the doctor recommends intravenous and oral administration of glucose at a dosage of up to 400 mg (the same treatment is indicated for other forms of polyneuropathy).

Amyloid polyneuropathy

The amyloid variety of polyneuropathy develops in those patients who have a history of hereditary amyloidosis. Its main clinical symptoms are:

• stool disorders (constipation and diarrhea);
• pain in the digestive tract;
• heart failure;
• macroglossia (an increase in the size of the tongue).

With this disease, sensory disturbances predominate, for example, soreness of the limbs, loss of pain and temperature sensitivity. At later stages, paresis also joins the disorders.

As for adequate therapy, at the moment it does not exist.

Distal sensorimotor polyneuropathy

In diabetes, long nerve fibers are most often affected. Diabetic polyneuropathy is observed in 40% of diabetics. This type of disease is characterized by the absence of a feeling of pressure, changes in ambient temperature, pain, vibration and location relative to other objects.

Sensory polyneuropathy is dangerous because a diabetic may not feel any pain or high temperatures.

Ulcers appear on the lower extremities,. Severe joint damage and fractures are not ruled out.

Sensorimotor polyneuropathy can manifest itself with active symptoms, for example, quite strong pain in the legs, which are especially aggravated at night.

As the disease progresses, there will be a violation in the work of the musculoskeletal system. When this happens:

• bone deformity;
• muscle dystrophy;
• excessive dryness of the skin;
• the appearance of age spots;
• reddish skin tone;
• sweat gland dysfunction.

The most significant symptoms of distal polyneuropathy in diabetes mellitus will be ulcers that occur between the toes and on the soles of the feet. Lesions are not capable of causing discomfort due to the absence of pain. In advanced cases, we will talk about amputation of limbs.

Autonomic polyneuropathy in diabetes

In the presence of lesions of the autonomic nervous system against the background of the course of diabetes, the patient will feel:

1. darkening in the eyes;
2. fainting when taking a vertical position;
3. dizziness.

This form of polyneuropathy will be accompanied by malfunctions in the normal functioning of the digestive tract, which is manifested by a slowdown in the intake of food by the intestines. In view of this, it is almost impossible to stabilize the concentration of glucose in the blood of a diabetic.

The cause of a sudden death can be a heart rhythm disturbance in diabetic polyneuropathy.

Those people who suffer from this disease will feel problems from the genitourinary system - urinary incontinence occurs. The bladder will lose the ability to completely empty, which becomes a prerequisite for the development of infectious diseases. In men, erectile dysfunction will be noted against the background of autonomic polyneuropathy, and in women, dyspareunia (the inability to achieve orgasm).

In this article, we will consider in detail the most common form of late neurological complication of diabetes mellitus - distal, symmetric, sensory or sensorimotor polyneuropathy.

The main symptoms of diabetic neuropathy are paresthesia, numbness, chilliness and pain in the lower extremities, as well as the hands. There are symmetrical disturbances of all types of sensitivity (pain, temperature, tactile and vibration) in the so-called zone of "socks" and "gloves". In some patients, these manifestations may be mild. In severe cases, paresthesias, pain, burning sensation of the feet and hands are characteristic that increase at night. In the absence of treatment, the pathology worsens.

Initial symptoms of neuropathy are determined in the toes, with the proximal progression of the process, signs of a decrease in sensitivity appear in the fingers. The distal parts of the upper extremities are rarely involved first.

In distal, symmetric, sensorimotor polyneuropathy, thin unmyelinated (C), weakly myelinated (Aσ) and thick myelinated nerve fibers (Aα, Aβ) suffer. For neuropathy with a predominant lesion of thin fibers, it is characteristic loss of pain and temperature (heat and cold) sensitivity. When predominantly thick fibers are involved in the process, the speed of the nerve impulse is disturbed and tactile and vibration sensitivity is reduced or lost, which in severe cases can lead to sensory ataxia. But it should be noted that signs of damage to thin nerve fibers are observed earlier than thick ones.

Symptoms of diabetic neuropathy are recorded in more than 40% of people with diabetes and about half of them have pain syndrome. Characteristic is the period of pain: at rest, with overwork, during stress and mainly at night; when walking, the intensity of pain decreases, while changing the position of the limb has no effect. Acute pain syndrome in neuropathy is described as an independent clinical unit. It is characterized by hypersensitivity and hyperalgesia. At the same time, motor nerve fibers are preserved, and sensitive functions suffer slightly. A similar phenomenon was called "diabetic cachexia" by Ellenberg. Acute pain neuropathic syndrome is noted with insulin therapy and normalization of glycemia, which Caravati describes as "insulin neuritis." In this case, pain symptoms are associated with nerve regeneration.

The progression of diabetic polyneuropathy leads to damage to motor (motor) fibers - muscle atrophy and weakness in the distal lower extremities. With the involvement of autonomic nerve fibers, sweating decreases, the skin becomes dry and prone to hyperkeratosis. The so-called "risk stop" is formed. The knee and Achilles reflexes decrease, typical bone deformities appear: protruding heads of the metatarsal bones, hammer and hook toes. A bright pink or red skin color is characteristic, symmetrical foci of hyperpigmentation are often observed on the lower leg and dorsal foot (the so-called “spotted lower leg”). Nail plates can atrophy or, on the contrary, thicken and deform, which predetermines the development of onychomycosis. Ultimately, osteoarthropathy or Charcot's foot is formed (an increase in the transverse size of the foot, transverse and longitudinal flat feet, increased deformity of the ankle joint); changes in the configuration of the foot can be unilateral or bilateral, and neuropathic edema may also occur. An important differential diagnostic sign is the preservation of pulsation in the arteries of the foot.

Prolonged pressure in places of bone deformities leads to inflammatory autolysis of the underlying tissues and the formation of neuropathic ulcers, more often on the plantar surface of the foot and in the interdigital spaces. These ulcers can be painless for a certain period of time due to reduced sensitivity, and often only infection and inflammation draw attention to the ulcer. So early detection of signs of diabetic polyneuropathy is essential to reduce the risk of ulceration and subsequent possible amputation of the limb.

Unfortunately, there is no "gold standard" for the detection of neuropathic disorders in diabetes mellitus. In 1998 in San Antonio was proposed consensus of standardized diagnostic tests for diabetic polyneuropathy who recommends the following actions:

1. Identification of clinical symptoms.
2. Clinical examination: morphological and biochemical analysis.
3. Electrodiagnostic study: determination of the speed of impulse conduction along the nerve.
4. Quantitative sensory tests.
5. Autonomous functional tests.

Often used to detect diabetic neuropathy symptom scale - NSS(Neuropathy Symptom Score) and scale of signs - VAT(Neuropathy Dysability Score). For clinical practice, this system was adapted by M. Young et al.

NSS assessment:

• burning, numbness, or crawling sensation = 2
• fatigue, cramps, or soreness = 1
• Spread:
  feet = 1
  calf muscles = 1
  other = 0
• gain:
  at night = 2
  day or night = 1
  daytime = 0
  wake up from sleep = 1
• decline:
  when walking = 2
  standing = 1
  sitting or lying down = 0

Sum of points is the value of the scale:
3-4 - minor symptoms,
5-6 - moderate symptoms,
7-9 - severe symptoms.

VAT assessment:

• knee jerk
• vibration sensitivity
• pain sensitivity
• temperature sensitivity
• reflexes:
  normal = 0
  amplify = 1
  none = 2 each side
• touch (tactile) sensitivity:
  present = 0
  reduced or absent = 1 on each side

Sum of points:
3-5 - minor signs
6-8 - moderate signs
9-10 - severe symptoms

The minimum criteria for the diagnosis of diabetic neuropathy according to the NSS and NDS are:

• moderate signs with or without symptoms (VAT = 6-8 + NSS ≥ 0)
• minor signs with moderate symptoms (VAT = 3-5 + NSS = 5-6)

To determine the severity of clinical manifestations, it is necessary neurological study of sensorimotor disorders. It includes the study of all kinds of sensitivity and reflexes.

Tactile sensitivity evaluated with 10 g of monofilament (5.07 Semmes-Weinstein). The places where it is necessary to conduct research are the plantar surface of the distal phalanx of the big toe, the plantar surface of the distal head and the fifth metatarsal bone. There should be at least 2 touches at one point. The threshold of vibration sensitivity is determined using a neurological tuning fork or biothesiometer. The study is carried out at standard points: the base of the thumb and the inner ankle. Vibration sensitivity is not reduced if the patient ceases to feel vibration when the value of the tuning fork scale corresponds to 7 EU and above. A decrease in the threshold of vibration sensitivity is considered by many researchers as the most unfavorable prognostic sign. Temperature sensitivity is determined by alternating touches of a warm and cold object to adjacent areas of the big toe, rear of the foot, inner ankle, lower leg, and knee. Pain sensitivity is studied using a blunt needle or special devices (Neuropen, Pin-wheel). To analyze the state of the motor department of the nervous system, Achilles and knee reflexes are determined using a neurological hammer. To detect autonomic neuropathy, the most accessible method in routine practice is orthostatic test.

On the basis of clinical manifestations, the following are distinguished stages of distal diabetic neuropathy(International guidelines for the outpatient management of diabetic neuropathy, 1995):

• 0 - no neuropathy, no symptoms or signs
• 1 - asymptomatic neuropathy
• 1 A - HCC = 0, normal knee jerk
• 1 B - NCC = 0, decreased knee jerk
• 2 - symptomatic neuropathy
• 2 A - HCC ≥ 1, normal knee jerk
• 2 B - HSS ≥ 1, reduced knee jerk
• 3 - severe neuropathy.

The manifestations of DP correlate:
with disease duration
with age of patients

This complication ( diabetic polyneuropathy) is heterogeneous in nature, as it affects the proximal and distal peripheral sensory and motor nerves, as well as the autonomic nervous system.

Neurological complications occur with the same frequency in all types of DM.

The most severe manifestations of DP result in:
with somatic DP to the development of ulcerative lesions of the lower extremities
with autonomous DP to high mortality of patients

Epidemiology

Frequency of development of DP:
in patients with type 1 diabetes is 13-54%
in patients with type 2 diabetes is 17-45%

According to a number of epidemiological studies, the incidence of DP in all types of diabetes mellitus varies from 5 before 100% (large data discrepancies are associated with the difficulty of diagnosis and depend on the research methods used).

Classification of polyneuropathies (I.I. Dedov et al., 2002):

1. Lesions of the central nervous system:
encephalopathy
myelopathy
2. Lesions of the peripheral nervous system:
diabetic polyneuropathy:
- sensory form (symmetrical, asymmetrical)
-motor form (symmetrical, asymmetrical)
- sensorimotor form (symmetrical, asymmetrical)
diabetic mononeuropathy(isolated lesion of the pathways of the cranial or spinal nerves)
autonomic (vegetative) neuropathy:
- cardiovascular form
- gastrointestinal form
- urogenital form
- asymptomatic hypoglycemia
- other

According to the classification of Boulton et al., 2005, the following independent types of neuropathies are distinguished:
acute sensory
chronic sensorimotor
thin and thick fibers
vegetative
hyperglycemic
focal mononeuropathies of the extremities
cranial
proximal motor (amyotrophy)
truncal radiculoneuropathy, etc.

Three more clinical varieties of diabetic neuropathy of fine fibers can be distinguished.:
true - characterized by positive neurological symptoms, including burning, tingling, signs of distal desensitization, decreased Achilles reflex
pseudosyringomyelic- characterized by a decrease in pain and temperature sensitivity in combination with neuropathy of vegetative fibers, a skin biopsy reveals a clear lesion of the axons of small fibers and a moderate lesion of large fibers
acute - acute burning pain dominates, allodynia, hypersensitivity to stabbing stimulation, weight loss, insomnia, erectile dysfunction in men, skin biopsy analysis indicates active degeneration of myelinated and unmyelinated fibers

Pathogenesis

According to modern theory pathogenesis, DP is a pathology that develops against the background of metabolic and vascular disorders characteristic of diabetes mellitus.

Absolute or relative deficiency of insulin plays a leading role in the mechanisms of the onset of DP.

DP is a consequence of violations of the structural and functional state and metabolic imbalance in the peripheral nerves.

!!! It should be noted that isolated hyperglycemia cannot underlie the formation of diabetic complications, since it has been noted that intensive control of blood glucose levels significantly reduces the manifestations of nerve and vascular lesions, but cannot completely rid the patient of them.

To date, it is assumed that the cause of the formation of diabetic complications is a complex of metabolic disorders arising from:
hyperglycemia
insulin deficiency

In this regard, the following metabolic disorders deserve the most attention, which are directly related to structural and functional damage to nerve fibers:
protein glycation
polyol metabolic pathway
sorbitol accumulation
oxidative stress
decreased activity of protein kinase C
free radical destruction of cell membranes
metabolic disorders of free fatty acids

!!! To date, it has been proven that under the condition of diabetic peripheral neuropathy, hypoxia of nerve fibers develops simultaneously with a decrease in endoneural blood flow. It is she who is the most important cause of nerve dysfunction in diabetes mellitus.

Non-fleshy nerve fibers take part in the regulation of endoneural blood flow by controlling the formation of arteriovenous anastomoses. Damage to these fibers is observed in the early phase of DP development. The lack of mechanisms to control the formation of arteriovenous anastomoses leads to increased endoneural hypoxia.

!!! One of the essential signs of DP is the stimulation of the formation of arteriovenous shunts, which is manifested by the expansion of the venous vessels of the foot and an increase in the partial pressure of oxygen in them.

A special place in the development of diabetic complications is given oxidative stress. One of its consequences is a decrease in the concentration of nitric oxide (NO), which has antiproliferative and vasodilatory effects. This leads to a deterioration in the blood supply to the nerve fibers and the development of their dysfunction.

The intensity of oxidative stress also increases due to the inhibition of the natural antioxidant system, which is recorded by a decrease in the amount of such tissue components as reduced glutathione, ascorbic acid, vitamin E, as well as a decrease in the activity of antioxidant enzymes. Oxidative stress is accompanied not only by a decrease in the content and disruption of the functioning of natural antioxidants, but also by progressive damage to the function of nerve fibers with the further development of diabetic sensory polyneuropathy.

Nutritional factors, in particular vitamin deficiencies, also play a role in the development of DP.:
impaired absorption of carbohydrates
signs of hypoglycemia are masked (the mechanisms of its counterregulation are suppressed - the glucagon phase of adaptation is inhibited and adrenergic symptoms-precursors are leveled)
altered bioavailability of oral sugar-lowering drugs

Summarizing the data regarding the pathogenesis of DP, it can be concluded that damage to nerve fibers, especially in the early stages of the development of DM, is not irreversible, but can be eliminated by improving blood supply in the neural vessels

Clinical picture of DP

Stage 0: No symptoms or signs.

Stage 1: Subclinical DP
subclinical DP at stage 1 can be diagnosed in specialized neurophysiological departments. Such diagnostic tests are not recommended for routine use.

!!! Clinical differential diagnosis between stages 0 and 1 of DP is not possible.

Stage 2: Clinical DP

1. Chronic pain form:
the presence of symptoms that worsen at night, such as burning, sharp and stabbing pain
tingling (±)
lack or impairment of sensitivity and weakening or absence of reflexes

2. Acute pain form:
poor control of diabetes, weight loss
diffuse pain (trunk)
hyperesthesia may occur
may be associated with initiation of antidiabetic therapy
minimal sensory disturbances or normal sensitivity on peripheral neurological examination

3. Amyotrophy:
usually occurs in older people with undiagnosed and poorly controlled type 2 diabetes
manifested by muscle weakness; affects, as a rule, the proximal muscles of the lower extremities; subacute onset
usually accompanied by pain, mostly at night, with minimal sensory disturbances

4. Painless DP combined with complete or partial loss of sensation:
there are no symptoms or numbness of the feet, a violation of temperature and pain sensitivity with a lack of reflexes

Stage 3: Late complications of clinical DP
foot ulcers
neuroosteoarthropathy
non-traumatic amputations

!!! For the stages of DP, see also the article Diabetic neuropathy - solving the problems of objectification in the section "Nurology and Neurosurgery" of the site website

Possible against the background of DP and focal / multifocal neuropathy (mononeuropathy):
cranial nerves
trunk nerves
limb nerves
proximal motor (amitrophy)
concomitant chronic inflammatory demyelinating neuropathies

Clinical manifestations of chronic sensorimotor diabetic polyneuropathy are:
pain (most often burning in nature, worse at night)
paresthesia
hyperesthesia
decreased sensitivity - vibration, temperature, pain, tactile
decrease or loss of reflexes
dry skin
rise or fall in temperature
the presence of callus (callus) in areas of high pressure

At the same time, it should be emphasized that complaints characteristic of neuropathy are noted only in half of the patients, and in the remaining patients, neuropathy is asymptomatic.

According to the utilitarian clinical classification, two main variants of diffuse diabetic polyneuropathy are distinguished:
acute pain (small fiber disease) neuropathy
chronic pain (damage to large and small fibers) neuropathy

Current duration acute painful diabetic neuropathy is 6-12 months, regardless of the therapy. Pathogenetic treatment for acute painful diabetic neuropathy, in particular the administration of alpha-lipoic acid preparations, is not effective.

Chronic pain diabetic neuropathy occurs much more frequently. It is characterized by a gradual onset, an intermittent course, a clear relationship between the severity of the pain syndrome and the level of glycemia, and, accordingly, a decrease in symptoms when compensation for diabetes is achieved.

Risk groups for developing DP:
patients with type 1 diabetes 1 year after the onset of the disease
patients with type 2 diabetes since the diagnosis of the disease

It should also be noted that the relationship between poor glycemic control and the severity of neuropathic manifestations is clearly seen in patients with type 1 diabetes, while it is usually absent in type 2 diabetes.

Diagnosis of DP

The most typical signs of DP:
weakening of the Achilles reflexes
decreased peripheral vibration sensitivity

The difficulty in diagnosing DP is that:
firstly, age-related changes can give a similar clinical picture
secondly, DP can often be asymptomatic and be detected only by electroneuromyography.

There are five risk factors for developing DP (according to the DCCT study):
1. SD duration
2.degree of hyperglycemia
3.age of the patient
4.male
5.higher height

DP is more common in patients with diabetic retinopathy and nephropathy.

A significant length of peripheral nerve fibers determines the high activity of metabolic processes in them, which requires their proper supply of oxygen and energy. In this regard, the lower limbs, especially the feet, are most susceptible to the development of DP.

The defeat of the central nervous system is diagnosed by a neuropathologist using special examination methods.

Methods for diagnosing damage to the peripheral nervous system

Sensory form of neuropathy
violation of vibration sensitivity
mandatory method - calibrated tuning fork (values ​​less than 4/8 of an octave of the scale on the head of the big toe)
additional method (if possible) - biotensiometry
temperature sensitivity disorder
mandatory method - touching with a warm / cold object
pain sensitivity disorder
obligatory method - pricking with a needle
impaired tactile sensation
obligatory method - touching the plantar surface of the foot with a monofilament
impairment of proprioceptive sensitivity
mandatory method - detection of sensitive ataxia (instability in the Rombeog position)
Motor form of neropathy
manifestations: muscle weakness, muscle atrophy
a mandatory method is to identify the weakening or absence of tendon reflexes (Achilles, knee)
additional method (if possible) - electroneuromyography
Autonomous form of neuropathy
cardiovascular form
mandatory method
- the manifestation of orthostatic hypotension (decrease in blood pressure is more than or equal to 30 mm Hg when changing body position from horizontal to vertical)
- lack of acceleration of heart rate on inspiration and slowing down on expiration
- Valsalva maneuver (lack of heart rate acceleration during straining)
additional method (if possible)
- 24-hour blood pressure monitoring (no nighttime blood pressure drop)
- Holter ECG monitoring (the difference between the maximum and minimum heart rate during the day is less than or equal to 14 beats / min)
- ECG recording during the Valsalva maneuver (the ratio of the maximum RR to the minimum is less than or equal to 1.2)
gastrointestinal form (enteropathy)
mandatory method - diagnosed by the clinic of alternating diarrhea and constipation, gastroparesis, biliary dyskinesia
additional method (if possible) - gastroenterological examination
urogenital form
mandatory method - diagnosed by the absence of urge to urinate, the presence of erectile dysfunction, retrograde ejaculation
additional method (if possible) - urological examination
asymptomatic form-diagnosed by the absence of clinical symptoms

Screening for Diabetic Polyneuropathy:
administered to all patients with type 1 diabetes mellitus 5 years after diagnosis and to all patients with type 2 diabetes at diagnosis, then annually
determination of temperature, pain, tactile and vibration sensitivity, tendon reflexes
careful examination of the lower extremities and feet

Treatment of DP

!!! To date, no treatment method has been developed that would become the gold standard for the treatment of DP.

primary goal to prevent DP - achieving normoglycemia

simultaneously in the presence of functional organic changes, it is necessary to prescribe drugs that affect the pathogenesis of DP and the symptoms of DP.

Pathogenic therapy includes:
measures aimed at achieving and maintaining stable compensation for DM
aldose reductase inhibitors - blockers of the polyol pathway of glucose metabolism
B vitamins - benfotiamine and cyanocobalamin - glycolysis inhibitors that block the glucotoxic effect and the formation of glycosylation end products
-lipoic acid - activates mitochondrial enzymes and glucose oxidation, inhibits gluconeogenesis
essential fatty acids - have an antioxidant effect and reduce hyperlipidemia.

Symptomatic therapy includes activities aimed at:
elimination of pain syndrome
elimination of cramps in the limbs
prevention and treatment of foot ulcers
correction of bone mineral density in the development of osteoporosis
treatment of concomitant infections, etc.

Modern approaches in the therapy of DP
Currently, two main approaches are put forward in the implementation of directed neurotropic therapy of DP, as well as in neuropharmacology in general:
the use of combined neurotropic agents containing components that affect various links in the pathogenesis of this syndrome and complement each other in pharmacodynamic and clinical terms
the use of monopreparations of a complex polytopic type of action, which have versatile and important effects from the point of view of pharmacology and clinic

It should be emphasized that such approaches not only do not contradict, but also optimally complement each other, making it possible to fully implement the strategy of complex neurotropic pharmacotherapy in DP.

The main advantages of these combined drugs include:
the possibility of using proven standard effective combinations of biologically active substances within the same dosage form (simplification of the procedure for choosing a therapeutic agent for a practitioner)
reduction of involuntary polypharmacy while maintaining or increasing the effectiveness of treatment
improvement of compliance (convenience of use for the patient and the doctor)
increasing the availability of treatment, depending on the cost of drugs

(1) To date, the most effective means in the treatment of DP are drugs thioctic (-lipoic) acid .

The main mechanisms of action of a-lipoic acid can be summarized as follows:
Impact on energy metabolism, glucose and lipid metabolism: participation in oxidative decarboxylation of a-keto acids (pyruvate and a-ketoglutarate) with activation of the Krebs cycle; increased capture and utilization of glucose by the cell, oxygen consumption; increase in basal metabolism; normalization of gluconeogenesis and ketogenesis; inhibition of cholesterol formation.
Cytoprotective action: increased antioxidant activity (direct and indirect through the systems of vitamins C, E and glutathione); stabilization of mitochondrial membranes.
Influence on the reactivity of the body: stimulation of the reticuloendothelial system; immunotropic action (decrease in IL1 and tumor necrosis factor); anti-inflammatory and analgesic activity (associated with antioxidant action).
Neurotropic effects: stimulation of axon growth; positive effect on axonal transport; reducing the harmful effects of free radicals on nerve cells; normalization of abnormal glucose supply to the nerve; prevention and reduction of nerve damage in experimental diabetes.
Hepatoprotective action: accumulation of glycogen in the liver; increased activity of a number of enzymes, optimization of liver function.
Detoxifying action(FOS, lead, arsenic, mercury, sublimate, cyanides, phenothiazides, etc.)

Alpha lipoic acid preparations are available as infusion and in tableted form (thioctacid, berlition, espalipon, thiogamma, etc.).

!!! The standard course of treatment begins with an infusion of the drug at a dose of 600 mg per day intravenously by drop infusion into 150.0 ml of a 0.9% NaCl solution for 3 weeks. (with breaks on weekends) followed by oral administration of the drug for 2-3 months at 600 mg / day. Taking into account the pharmacokinetic features of the absorption of alpha-lipoic acid tablet forms in the intestine, it is recommended to take the tablets at least 30 minutes before a meal.

An alternative scheme has also been proposed. treatment of DP, including initial therapy of 600 mg of alpha-lipoic acid 3 times a day for 3 weeks (1800 mg / day) and maintenance therapy of 600 mg 1 time per day in the morning on an empty stomach for 2-3 months

Currently, a special form has been developed - thioctacid BV, which differs from the standard one by the addition of auxiliary components to the tablet core and a change in the film coating, which ensured the optimization of the pharmacokinetics of the drug, improved bioavailability and a decrease in the coefficient of variability of the level of thioctic acid in blood plasma.

(2) neurotropic vitamins , in particular vitamin B1 (thiamine), are coenzymes in various biochemical processes, improve the energy supply of the nerve cell, and prevent the formation of end products of protein glycation.

(3) Preparations containing benfotiamine.

Benfotiamine is a lipophilic derivative of vitamin B1 that directly affects the metabolism in the nerve cell. If the penetration of conventional (water-soluble) thiamine through cell membranes is largely limited, then the bioavailability of benfotiamine is 100%. It penetrates into the nerve cells in proportion to the dose taken, reaching a high intracellular concentration. Formed from benfotiamine inside cells, biologically active thiamine is metabolized and thus becomes a coenzyme. The ability of benfotiamine to stimulate transketolase is ten times higher than that of water-soluble thiamine compounds, and is 250%.

Benfotiamine blocks four pathways of damage to target cells in diabetes (which is the advantage of benfotiamine compared to other means of pathogenetic therapy for diabetes - aldose reductase inhibitors, protein kinase C inhibitors, blockers of receptors for end products of excess glycation, affecting only one of the pathways of alternative glucose metabolism):
polyol way
glycosamine pathway
activation of protein kinase C
formation of non-enzymatic glycation products

In the painful form of DP, treatment begins with a course of 10-15 daily injections of a combination of neurotropic vitamins containing 100 mg of vitamins B1, B6 and 1000 μg of vitamin B12, and deep intramuscular lidocaine ( Milgamma, Kombilipen).

Milgamma/Combilipen- with severe manifestations, 2 ml daily for 5-7 days, then 2 ml 2-3 times a week for 2 weeks, in mild cases, 2 ml 7-10 days with a frequency of 2-3 times a week. Further switch to oral benfotiamine ( Milgamma, Benfolipen) - tablets are taken after meals, without chewing and with a small amount of liquid, 1 tablet 1-3 times a day. The duration of the course depends on the severity of the clinical manifestations of DN.

In case of severe pain syndrome (neuropathic pain) that accompanies the manifestations of DP, an effective remedy is needed to relieve it.

Until now, most often in patients with persistent severe neuropathic pain tricyclic antidepressants were prescribed for DP. Generally and currently used amitriptyline recommending starting therapy with low doses (25 mg) with a gradual increase in dose up to 150 mg per day.

However, taking these drugs is accompanied by a large number of cholinergic side effects: dry mouth, increased intraocular pressure, urinary retention, constipation, cardiac arrhythmias, etc., which limits the possibility of their use.

(4) In this regard, the emergence of new drugs among analgesics - second generation anticonvulsants(gabapentin, pregabalin) has become a new step in the treatment of neuropathic pain.

(4.1) Gabapentin belongs to the class of anticonvulsants and is structurally similar to α-aminobutyric acid, which performs a neurotransmitter function and is involved in pain modulation. Gabapentin interacts with α-amino acid transport mechanisms and binds with high specificity to the -2 subunit of voltage-gated calcium channels. The antihyperalgic properties of the drug are modulated by the mechanisms of the spinal cord. Symptomatic therapy with gabapentin is accompanied by an increase in the quality of life of patients with DM and DP.

When prescribing gabapentin, treatment should be started at a dose of 300 mg at night with a gradual increase in dose. Most patients need to prescribe the drug at a dose of 1.8 g per day for 3 doses. Monitoring should be carried out in terms of the development of side effects, primarily due to the central mechanism of action of the drug (drowsiness and others).

(4.2) In addition to gabapentin, this group includes a newer drug - pregabalin ( Lyrica), which provides an equivalent analgesic effect (up to 50%) when using significantly lower doses (150-600 mg / day) during the first week of treatment. At the same time, pregabalin improves sleep and is well tolerated. The starting dose of pregabalin - 75 mg 2 times a day - is gradually increased to 600 mg per day. After a 7-day intake and the achievement of an analgesic effect, the dose of the drug is recommended to be reduced.

(5) Anticonvulsants(carbamazepine 100 mg 2 times a day (up to 400 mg 3 times a day), phenytoin (1 tab. 2-3 times a day) also reduce pain in DP.

(6) A new anticonvulsant has been developed for the treatment of diabetic neuropathy- lacosamide, which provides selective slow inactivation of potassium channels, which distinguishes it from other anticonvulsants that can act on various types of receptors and modulate the response of the mediator collapsesin (CRMP-2). Lacosamide at a dose of 200-600 mg/day reduces pain in DN.

(7) There is evidence of the effectiveness of antiarrhythmic drugs in DP ( lidocaine and mexiletine). The mechanism of action is based on the stabilization of neuronal membranes due to the blockade of sodium channels.

Lidocaine in the form of slow intravenous infusions (30 min) at a dose of 5 mg/kg effectively reduces pain in DN.

The antinociceptive effect of the oral form of mexiletin at a dose of 450-600 mg / day has been proven in a number of double-blind, placebo-controlled studies. On a global pain scale, the improvement was insignificant, but there was a significant decrease in shooting, burning pain, tingling, and a feeling of heat. Side effects in the treatment of antiarrhythmic drugs are less pronounced compared with anticonvulsants.

(8) Some authors recommend the use of local irritants in the complex therapy of DP (finalgon, apizatron, viprosal, capsicam, etc.), especially in the treatment of burning superficial and stabbing pains. One of the mechanisms of action of these drugs is the depletion of pain mediators and other substances involved in the occurrence and maintenance of pain.

(9) An alternative to achieve an analgesic effect is to use centrally acting non-opioid analgesics, which selectively affect the level of sensitive neurons of the posterior horns of the spinal cord (soanalgesics). The mechanism of action of drugs in this group is based on indirect antagonism to NMDA receptors and agonism towards GABAergic receptors in the absence of effects on serotonin, dopamine, opiate, central muscarinergic and nicotinic receptors, as well as benzodiazepine receptors. As a result, selective activation of neuronal potassium channels occurs and an analgesic effect is provided. At the same time, there is a muscle relaxant effect, which is fundamentally important in painful forms of DN.

This group of drugs is flupirtine (katadolon), which has a proven analgesic effect in pain syndromes of various etiologies (radiculoneuritis, vertebrogenic dorsopathy, postoperative pain syndrome, cancer, diseases of the musculoskeletal system, including osteoporosis, myofascial syndromes, etc.). Assign katadolon should be 100-200 mg 3-4 times a day (daily dose of 600 mg).

(10) Aldose reductase inhibitors

The first clinical studies to evaluate the effectiveness of this group of drugs began to be conducted 25 years ago. However, to date, the only drug from this group, Epalrestat, is approved for clinical use only in Japan. Most clinical trials, for a number of reasons, have not confirmed a significant effect in terms of improving or preventing the development of diabetic neuropathy. Many of the proposed substances had a high hepatotoxicity, which limited their long-term use in clinical practice.

(11) In the structure of metabolic pathogenetic therapy, it is also advisable to use actovegina. It has antihypoxic activity and insulin-like effect, improves microcirculation. Usually actovegin is prescribed 400 mg (10 ml) intravenously by stream or intravenous drip for 10-14 days, then 1 tab. 3 times a day for 3 weeks. Actovegin is a highly active stimulator of oxygen and glucose utilization under conditions of ischemia and hypoxia, which increases the transport and accumulation of glucose in cells, which improves the aerobic synthesis of macroergic compounds and increases the energy resources of neurons, preventing their death.

Its effectiveness in the treatment of diabetic neuropathy has been confirmed in a number of double-blind, placebo-controlled studies.

(12) With concomitant severe diabetic autonomic neuropathy along with the optimization of the level of glycemia and the appointment of drugs of pathogenetic action, symptomatic therapy is also used: for example, with rest tachycardia, selective blockers(metoprolol, bisoprolol, nebivolol), calcium channel blockers(verapamil, diltiazem) or magnesium preparations(kormagnesin, magnerot).

(13) For orthostatic hypotension drinking plenty of fluids, contrast showers, elastic stockings, refusal of physical activity, cancellation of antihypertensive drugs, sleeping on a bed with a raised head edge, a slight increase in the intake of dietary salt are shown. The patient should get up slowly from the bed and chair. If such measures are unsuccessful, the volume of blood plasma can be increased by prescribing salina or fludrocortisone . In the event that orthostatic hypotension develops against the background of hypertension, it is possible to prescribe -blockers, which have intrinsic sympathomimetic activity ( pindolol, oxprenolol). Recently, an agonist has been recommended to relieve symptoms of orthostatic hypotension. -receptor midodrine .

(14) It is possible to use central muscle relaxants, but there is no evidence base regarding their higher effectiveness in DP.

Central muscle relaxants are a heterogeneous group including:
tizanidine (alpha-2-adrenergic agonist)
baclofen (GABAB receptor antagonist)
diazepam (GABAA receptor agonist)
memantine (an inhibitor of NMDA-dependent channels)
tolperisone (Na channel blocker and membrane stabilizer)

From the standpoint of the formation of pain and the preservation of the quality of life in spastic syndrome, it is important to reduce the severity of spasm, improve blood circulation in the muscle, and, finally, the absence of muscle weakness after taking the drug.

The drugs of choice are tinazidine hydrochloride (sirdalud, is prescribed 2-4 mg 3 times a day (no more than 36 mg / day) and tolperisone hydrochloride (midocalm, tolperisone is prescribed 50 (150) mg 3 times a day or intramuscularly 100 mg 2 times a day).

With muscle cramps in the legs can be prescribed magnesium preparations, including in combination With vitamin B6 (pyridoxine). Magnesium deficiency is accompanied by a violation of muscle relaxation, a decrease in the reserve pool of potassium and relative hypocalcemia, which ultimately leads to the occurrence of muscle cramps in individual muscles or muscle groups.

Magnesium preparations– magne B6, magvit, magnerot- is prescribed for cardiovascular pathology (myocardial infarction, circulatory failure, arrhythmias, vasospasms), and DP often develops in patients with initial cardiac pathology.

(15) Botulinum toxin A recent pilot, double-blind, crossover study demonstrated the efficacy of botulinum toxin type A in the treatment of pain in 18 patients with DP. Pain decreased significantly from the first week after the injection during the 12 weeks of follow-up. In 44% of patients, the reduction in pain on the visual analogue scale (VAS) was more than 3 points. An improvement in sleep was also observed starting at 4 weeks post-injection. The anti-pain effect of botulinum toxin is associated with the ability of the drug to inhibit afferent nociceptive activity in peripheral sensory nerve fibers.

(16) Glyceryl trinitrate Glyceryl trinitrate, traditionally used as a vasodilator for angina pectoris, significantly relieves the pain associated with diabetic neuropathy. It's shown
in a double-blind, placebo-controlled study evaluating the efficacy of glyceryl trinitrate spray in 48 patients with painful diabetic neuropathy. Twenty-four patients in the study group applied topical glyceryl trinitrate spray on their legs during sleep for four weeks, while the other 24 used a spray containing placebo. Glyceryl trinitrate was well tolerated and only one patient was excluded from the study due to adverse side effects. The researchers attribute the positive effect to vasodilation due to nitric oxide, a derivative of glyceryl trinitrate. Good results have been obtained when this spray is used in combination with valproic acid.

(17) Non-pharmacological methods include the use gymnastics for the legs, massage and various physiotherapeutic methods (magnetotherapy, transcutaneous electrical nerve stimulation, acupuncture, etc.).), but their effectiveness has not been proven in multicenter randomized trials.

The effectiveness of physiotherapeutic effects, confirmed in small groups and with a short observation period, allows us to recommend them for inclusion in the complex therapy of DP. At the same time, care must be taken in the choice of physiotherapeutic means of treatment, since sensory disturbances and autonomic disorders in DP predispose to the formation of burns and ulcers.

The disease has various causes. The factors that cause the appearance of the disease, first of all, irritate the nerve fibers, and only then lead to a disruption in their functioning. The characteristic signs of the disease are weakness in the muscles and pain in the affected area of ​​the body.

The disease is manifested by paralysis, impaired susceptibility to tactile touch, various disorders in the work of the upper and lower limbs of the human body. Signs of the disease and the intensity of their manifestation completely depends on the form and type of the disease. Usually polyneuropathy causes a lot of suffering to patients, the treatment is protracted. The course of the disease is progressive and the process can be chronic. Most often, this disease occurs in the lower parts of the body.

Polyneuropathy can proceed in a sluggish form, and also have lightning-fast development.

Etiology

The causes of polyneuropathy are different. The main ones include:

• poisoning with pure alcohol, gas, arsenic (chemical poisoning);
• chronic diseases (diabetes, diphtheria);
• systemic pathologies of the body;
• long-term use of certain groups of pharmaceuticals;
• alcoholism;
• impaired immunity;
• hereditary factor;
• metabolic disorder;
• HIV infection.

The pathology may be:

• inflammatory. In this case, there is intense inflammation of the nerve fibers;
• toxic. It develops as a result of the ingestion of a large amount of toxic substances;
• allergic;
• traumatic.

Nowadays, the most common type is diabetic polyneuropathy. It should be noted that polyneuropathy is a rather dangerous pathology that requires timely and adequate treatment. If it is not there, then the progression of the disease can lead to muscle atrophy and the appearance of ulcers. The most dangerous complication is paralysis of the legs or arms, followed by respiratory muscles.

Varieties

According to the mechanism of damage, the disease is divided into the following types:

• demyelinating polyneuropathy. The development of the disease is associated with the breakdown in the body of a protein that envelops the nerves and is responsible for the high speed of impulse conduction along them;
• axonal. This type is associated with a violation in the work of the nerve rod. This type is accompanied by heavy treatment and a long recovery;
• neuropathic. With it, damage is directly observed to the bodies of nerve cells;
• diphtheria and diabetic polyneuropathy;
• polyneuropathy of the lower extremities;
• alcoholic polyneuropathy.

According to the primacy of nerve damage, polyneuropathy occurs:

• touch. Manifested as numbness or pain;
• motor. Motor fibers are affected, which is accompanied by weakness in the muscles;
• sensory-motor. The characteristic symptoms of the lesion are a decrease in sensitivity and motor activity of muscle structures;
• vegetative. There is a violation in the work of internal organs due to inflammation of the nerves;
• mixed. Includes all features of the above types;
• polyneuropathy of the lower extremities.

Depending on the cause of development, polyneuropathy can be:

• idiopathic. The occurrence is associated with disorders in the immune system;
• hereditary. Passed down from one generation to another;
• dysmetabolic. Progresses due to metabolic disorders;
• toxic polyneuropathy develops from the ingestion of toxic substances;
• post-infectious. Occurs during infectious processes in the body;
• paraneoplastic. Development goes hand in hand with oncological diseases;
• in diseases of the body, develops as part of the disease;
• alcoholic polyneuropathy.

By the nature of the flow:

• acute. Development time is two to four days. Treatment lasts several weeks;
• subacute. It develops in a few weeks, the treatment takes months;
• chronic. It progresses from six months or more, has an individual treatment term for each person.

Symptoms

Regardless of what type of disease a person has, whether it is alcoholic or diabetic, hereditary or toxic polyneuropathy or demyelinating, they often have the same symptoms.

A wide range of factors that cause the disease often affect the nerve first, and then lead to a violation of the function of their work. The main symptoms of the disease are:

• weakness in the muscles of the arms and legs;
• violation of the respiratory process;
• decrease in reflexes and sensitivity, up to their complete absence;
• prolonged feeling of "goosebumps" all over the skin;
• increased sweating;
• tremor or seizures;
• swelling of the hands and feet;
• cardiopalmus;
• unsteady gait and dizziness;
• constipation.

Complications

In fact, there are not many complications of polyneuropathy, but they are all cardinal. Complications of the disease are as follows:

• sudden cardiac death;
• violation of motor functions, complete immobilization of the patient;
• violation of the respiratory processes.

Diagnostics

It is impossible to independently diagnose any of the above types of polyneuropathy only by symptoms in a person (many symptoms are similar to the manifestation of other diseases). If you find one or more of the signs, you should see a doctor as soon as possible. To make a diagnosis, specialists will conduct a wide range of studies, which include:

• initial examination and interview;
• neurological examination and testing of basic nerve reflexes;
• complete blood count;
• radiography;
• biopsy;
• consultations of the patient with such specialists as the therapist and endocrinologist.

Treatment

Primary treatment of polyneuropathy is aimed at eliminating the cause of its occurrence and symptoms. It is prescribed depending on the type of pathology:

• treatment of diabetic polyneuropathy begins with a decrease in glucose levels in the body;
• with alcoholic polyneuropathy, you must strictly refrain from taking alcoholic beverages and everything that may contain alcohol;
• cessation of all contact with chemicals to prevent the occurrence of a toxic type of disease;
• taking a large amount of fluid and antibiotics for infectious polyneuropathy;
• surgery for paraneoplastic type of disease.
• the use of painkillers for severe pain syndrome.

Among other things, you may need a complete blood purification, hormone therapy or vitamin treatment (this type of therapy, in medical circles, is considered the most effective).

Physiotherapy is a good treatment for polyneuropathy. It will be especially useful in chronic and hereditary forms of the disease.

Prevention

Preventive measures of polyneuropathy are aimed at eliminating the causes that adversely affect the nerve fibers. Prevention methods:

• complete rejection of alcoholic beverages;
• if the work is related to chemicals, perform it only in protective clothing;
• monitor the quality of food consumed;
• do not take medications without a doctor's prescription;
• timely treat diseases of any nature and complexity;
• include vitamins in your diet;
• perform physical exercises;
• constantly monitor blood sugar levels;
• periodically go for therapeutic massages.

If you think that you have Polyneuropathy and the symptoms characteristic of this disease, then a neurologist can help you.

We also suggest using our online disease diagnostic service, which, based on the symptoms entered, selects probable diseases.

Causes, symptoms and treatment of polyneuropathy of the lower extremities - what is the difference between diabetic, alcoholic and other forms of the disease

Polyneuropathy is a number of diseases, the causes of which can be varied, but their common characteristic is a violation of the normal functioning of the peripheral nervous system and individual nerves, but in large numbers throughout the body.

Often, it affects the arms and legs, manifesting itself in a symmetrical decrease in muscle performance, deterioration of blood circulation in the affected area, and a decrease in sensitivity. The legs are the most affected by this disease.

Disease classification

Polyneuropathy of the lower extremities is divided into four types, and each of them, in turn, has its own subspecies.

According to the predominant damage to the fibers

All nerve fibers are divided into three types: sensory, motor and autonomic. With the defeat of each of them, different symptoms appear. Next, consider each of the types of polyneuroglia:

1. Motor (motor). This species is characterized by weakness in the muscles, which extends from the bottom up and can lead to a complete loss of the ability to move. Deterioration of the normal state of the muscles, leading to their refusal to work and the frequent occurrence of seizures.
2. Sensory polyneuropathy of the lower extremities (sensitive). Characterized by painful sensations, stabbing sensations, a strong increase in sensitivity, even with a light touch on the foot. There are cases of decreased sensitivity.
3. Vegetative. In this case, there is profuse sweating, impotence. Problems with urination.
4. Mixed - includes all the symptoms of the above.

By damage to the cells of the nerve structures

A nerve fiber consists of axons and myelin sheaths that wrap around these axons. This species is divided into two subspecies:

1. In the case of destruction of the myelin sheaths of axons, development proceeds faster. Sensory and motor nerve fibers are more affected. The vegetative ones are destroyed slightly. Both proximal and distal regions are affected.
2. Axonal characters are the fact that development is slow. Vegetative nerve fibers are disturbed. Muscles atrophy quickly. Distribution begins with the distal sections.

By localization

1. Distilnaya - in this case, the parts of the legs that are located the farthest are affected.
2. Proximal - the parts of the legs that are located higher are affected.

Cause

1. Dysmetabolic. It develops as a result of a violation of the course of processes in the nervous tissues, which is provoked by substances produced in the body subsequently of certain diseases. After they appear in the body, these substances begin to be transported with the blood.
2. Toxic polyneuropathy of the lower extremities. Occurs with the use of toxic substances such as mercury, lead, arsenic. It often appears when

The photo shows how alcohol destroys nerve cells and polyneuropathy of the lower extremities occurs.

the use of antibiotics, but the most common type of polyneuropathy is alcoholic.

Primary and Secondary

1. Primary polyneuropathy includes hereditary and idiopathic types. This is such a disease as Guillain-Barré syndrome.
2. The secondary includes polyneuropathy resulting from poisoning, metabolic disorders, and infectious diseases.

Causes of the disease

This disease can occur for a number of reasons, but it is not always possible to accurately determine them. Polyneuropathy of the lower extremities has the following main causes:

• inherited causes;
• problems with the immune system that appear as a result of violations of the body;
• various types of tumors;
• lack of vitamins in the body;
• use of drugs unnecessarily or not according to instructions;
• disruption of the endocrine glands;
• kidney and liver problems;
• infections that cause the occurrence of processes that cause inflammation in the peripheral nerves;
• poisoning the body with all sorts of substances.

Symptoms of the disease

When the disease occurs, the functioning of the motor and sensory fibers deteriorates. In this case, the following symptoms of polyneuropathy of the lower extremities are manifested:

• partial numbness of the legs;
• swelling of the lower extremities;
• the occurrence of sensations of pain;
• stabbing sensations;
• feeling of weakness in the muscles;
• increased or decreased sensitivity.

Diagnostic methods

Diagnosis is carried out by analyzing the disease and its symptoms, while discarding diseases that can give similar symptoms.

In the process of this, the doctor must carefully examine all the external signs and changes, find out from the patient whether his immediate family had the same disease.

Polyneuropathy is also diagnosed using various procedures:

• biopsy;
• ultrasound diagnostics of internal organs;
• examination of cerebrospinal fluid;
• research using an X-ray machine;
• blood chemistry;
• study of the speed with which the reflex passes through the nerve fibers;
• study of reflexes.

Diagnosis in diabetic polyneuropathy

Pathology treatment

Treatment of polyneuropathy of the lower extremities has its own characteristics. For example, the treatment of diabetic polyneuropathy of the lower extremities will in no way depend on the refusal of alcohol, in contrast to the alcoholic form of the disease.

Features of treatment

Polyneuropathy is a disease that does not occur on its own.

Thus, at the first manifestations of its symptoms, it is necessary to find out the cause of its occurrence without delay.

And only after that to eliminate the factors that will provoke it. Thus, the treatment of polyneuropathy of the lower extremities should be comprehensive and aimed primarily at removing the very root of this problem, because other options will not give any effect.

Medical therapy

Depending on the type of disease, the following drugs are used:

• in cases of severe disease, methylprednisolone is prescribed;
• with severe pain, analgin and tramadol are prescribed;
• drugs that improve blood circulation in the vessels in the area of ​​nerve fibers: vasonite, thrintal, pentoxifylline.
• vitamins, preference is given to group B;
• medicines that improve the process of obtaining nutrients by tissues - mildronate, piracetam.

Physiotherapy

Therapy of this disease is a rather complicated process that takes a long period of time.

Especially if polyneuropathy is caused by its chronic or hereditary forms. It starts after drug treatment.

It includes the following procedures:

• massotherapy;
• exposure to magnetic fields on the peripheral nervous system;
• stimulation of the nervous system with the help of electrical appliances;
• indirect effect on organs.

In the case when the body is affected by toxic substances, for example, if the patient has alcoholic polyneuropathy of the lower extremities, treatment should be carried out by purifying the blood with a special apparatus.

Healing Fitness

Exercise therapy must be prescribed for polyneuropathy of the lower extremities, which makes it possible to maintain muscle tone.

Complications of the disease

Otherwise, it can become chronic and bring a lot of problems. In the event that you are not cured of this disease, this can lead to the fact that you will no longer feel your lower limbs, the muscles will come into terrible shape and, as a result, you may lose the ability to move.

Forecast

If treatment is started in a timely manner, then the prognosis is very favorable. There is only one exception - the treatment of chronic polyneuropathy. It is impossible to completely get rid of this disease, but there are ways to reduce the severity of its course.

Preventive measures

To eliminate the possibility of a disease such as polyneuropathy, you need to follow a number of recommendations and prescriptions.

They are associated with measures that can prevent possible damage and disruption of the normal functioning of the peripheral nervous system.

1. It is necessary to remove alcohol from your life.
2. Be sure to use protective preparations when working with toxic substances in order to prevent their penetration into the body.
3. It is recommended to monitor the quality of the products that you consume, because in case of poisoning with these products, the process of destruction and disruption of the normal functioning of nerve fibers starts. This leads to the development of polyneuropathy.
4. You should carefully monitor the doses in which you take medications and in no case use them unnecessarily. It is advisable to strictly follow the doctor's instructions and not self-medicate.
5. It is imperative to take action when you detect an infectious or viral disease. Urgently need to see a doctor and not run these diseases, which can then be the cause of the development of polyneuropathy.

As a rule, polyneuropathy cannot be prevented.

But, if you find it, you immediately consult a doctor, thereby you will be able to significantly reduce the degree of development of the disease and the period of rehabilitation. It consists in visiting a physiotherapy room and therapeutic massages.

Even if you have some kind of ailment, you must immediately inform the doctor about it, and not self-medicate, because you cannot know for sure the symptoms of this disease, confuse it with another, and start treatment for the wrong one.

And, in principle, it is easier to deal with a disease that is just beginning its development than with a disease that has been progressing for a long time, which then in the end can also lead to all sorts of complications.

Video: Diabetic polyneuropathy of the lower extremities

How to self-diagnose polyneuropathy? What is the peculiarity of the diabetic form of the disease. Why is nerve sensitivity lost?

Sensory polyneuropathy

Sensory polyneuropathy is a disease whose symptoms are caused by damage to neurons that are responsible for motor functions, due to which the functions of the motor apparatus can be severely impaired. This dangerous disease is very common in patients with diabetes. Just as in cases with other types of polyneuropathies, one of the decisive factors in the choice of treatment and its subsequent results is the timely detection of the disease.

Sensory polyneuropathy can appear due to various reasons, including due to serious autoimmune processes, intoxications, heredity and infections, while the most dangerous is the case when this disease is inherited or acquired due to a special genetic predisposition.

The main symptoms of this dangerous sensory polyneuropathy are loss of sensitivity, causeless sensations of burning, tingling and itching, a sensation of vibration in the limbs, and the patient begins to perceive heat and cold, and temperature changes worse. With sensory polyneuropathy, negative symptoms of sensory disturbance, a feeling of "gloves" and "socks", and a violation of the sensitivity of the lower abdomen are also possible.

Depending on what type of neurons is damaged, three main forms of sensory polyneuropathy can be distinguished: hyperalgesic form, atactic form and mixed form. In the atactic form of the disease, symptoms such as impaired coordination of movement, paresthesia, numbness, instability (especially with closed eyes) are noted. Muscle strength usually remains unchanged, however, when examined by a doctor and tested for strength associated with loss of deep sensation, it can decrease significantly.

The hyperalgesic form implies symptoms such as autonomic dysfunction, pain (most often burning or shooting), decreased pain sensitivity, decreased temperature sensitivity. The mixed form of sensory polyneuropathy includes symptoms characteristic of the above-mentioned forms of the disease.

With sensory polyneuropathy, the main symptoms are most often asymmetric, especially at the very beginning of the disease. So, for example, this disease can begin with one leg, while the second will remain completely healthy for a long time, but as the disease develops, the symptoms become more symmetrical. Often in the early stages of the disease, not only the legs are affected, but also the upper limbs, and sometimes even the trunk and face. Symptoms can develop within a few days or 1-2 months.

Having reached a certain point, so to speak, a maximum, many symptoms most often stabilize for a long time. It often happens that the symptoms decrease, but most often, especially in the monophasic course of the disease, they remain at the same level, which is usually quite high, or continue to grow. Unlike Guillain-Barré syndrome, sensory polyneuropathy disease is characterized by poor functional recovery.

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Loss of sensation can range from mild numbness to deep anesthesia with arthropathy and ulcers. In this disease, paresthesia and spontaneous unbearable pain are often observed. At the moment, a complete explanation for this unique disease, which combines the lack of sensitivity to painful stimuli and severe spontaneous pain, has not been found.

For the diagnosis of sensory polyneuropathy, an anamnesis is required with a thorough identification of other diseases, dietary habits, a list of medications that the patient used, descriptions of heredity, previous infectious diseases that could affect the development of polyneuropathy, an assessment of the patient's work places, to ascertain the fact of contact with toxic substances , ENMG results, as well as specific results of skin nerve biopsy, etc.

To date, the treatment of sensory polyneuropathy is rather poorly developed. The most commonly used treatments are corticosteroids, cytostatics, plasmapheresis, and immunoglobulin, but all too often treatment attempts are unsuccessful. Against the background of immunotherapy, there is a partial regression of symptoms and stabilization of the condition, but the reasons for this result are not fully understood, however, in any case, timely therapy plays the main role.

Also, as in all other types of polyneuropathies, timely diagnosis and initiation of treatment contributes, if not to recovery, then to stabilization of the patient's condition. In the case of sensory polyneuropathy, if the disease is not found at an early stage, then, after a significant part of the neurons have died, it is impossible to carry out a significant recovery, but one can hope to stop the progress of the disease and stabilize the patient's condition.

What does polyneuropathy of the lower extremities mean and what are the features of treatment?

Polyneuropathy of the lower extremities is a common pathology associated with lesions of peripheral nerves. The disease is characterized by trophic and vegetative-vascular disorders affecting the lower limbs, manifested by impaired sensitivity and flaccid paralysis.

The danger of pathology is that over time its manifestations are aggravated, there are problems with movement, which affects the ability to work and prevents a full life. Today we will talk about the symptoms and treatment of polyneuropathy of the lower extremities, and also consider methods aimed at preventing further progression of the pathology.

Polyneuropathy of the lower extremities - why does it occur?

Polyneuropathy of the lower extremities is not an independent disease. According to ICD 10, this condition is considered a neurological syndrome that accompanies a variety of diseases:

• diabetes mellitus (diabetic polyneuropathy of the lower extremities);
• chronic alcohol intoxication (alcoholic polyneuropathy of the lower extremities);
• beriberi (especially with a lack of vitamin B);
• severe poisoning with drugs, arsenic, lead, carbon monoxide, methyl alcohol (acute axonal polyneuropathy);
• systemic diseases - biliary cirrhosis, malignant tumors, lymphoma, diseases of the blood, kidneys (chronic axonal polyneuropathy);
• infectious diseases (diphtheria polyneuropathy);
• hereditary and autoimmune pathologies (demyelinating polyneuropathy).

The cause of the disease can be a variety of health disorders and chronic diseases. Cancer tumors can disrupt the functioning of the peripheral nervous system. In addition, signs of polyneuropathy may appear after a course of chemotherapy.

Infectious and inflammatory processes in the joints, any kind of intoxication of the body (drugs, alcohol, chemicals) can cause problems with impaired sensitivity and damage to nerve fibers. In children, this disease is most often hereditary, for example, the symptoms of porphyria polyneuropathy appear in a child immediately after birth.

Thus, all factors provoking the development of a pathological condition are divided into several groups by doctors:

• metabolic (associated with impaired metabolic processes);
• hereditary;
• autoimmune;
• infectious-toxic;
• toxic;
• alimentary (caused by errors in nutrition).

Polyneuropathy never occurs as an independent disease, damage to nerve fibers is always associated with an etiological factor that negatively affects the state of the peripheral nervous system.

Clinical picture

Polyneuropathy of the upper and lower extremities begins with increasing muscle weakness, which is associated with developing damage to nerve fibers. First of all, the distal parts of the limbs are damaged. In this case, a feeling of numbness occurs in the area of ​​\u200b\u200bthe feet and gradually spreads to the entire leg.

Patients with polyneuropathy complain of a burning sensation, goosebumps, tingling, numbness of the extremities. Various kinds of paresthesia are complicated by muscle pain. As symptoms increase, patients experience severe discomfort even if they accidentally touch the problem area. In the later stages of the disease, unsteadiness of gait, impaired coordination of movements, and a complete lack of sensitivity in the area of ​​\u200b\u200bdamage to nerve fibers are noted.

Muscular atrophy is expressed in the weakness of the arms and legs and in severe cases may result in paresis or paralysis. Sometimes unpleasant sensations in the limbs occur at rest, forcing them to make reflex movements. Such manifestations of physicians are characterized as "restless legs syndrome".

Pathology is accompanied by vegetative disorders, which are manifested by vascular disorders (a feeling of cold in the affected limbs, marbled pallor of the skin) or trophic lesions (ulcers and cracks, peeling and dry skin, the appearance of pigmentation).

It is difficult not to notice the manifestations of polyneuropathy; as the pathology progresses, they become obvious not only to the patient, but also to the people around them. The gait changes and becomes heavier, as the legs become "cotton", there are difficulties with movement, a person hardly overcomes even small distances that he previously walked in a few minutes. As the pathology progresses, a feeling of numbness in the limbs increases. A pain syndrome occurs, which manifests itself in different ways, one part of the patients feels only slight discomfort, while the other complains of aching or sharp, burning pains.

Patients have swelling of the extremities, impaired knee reflexes, and no response to the stimulus. In this case, only one or several characteristic symptoms may appear at once, it all depends on the severity of the lesion of a particular nerve trunk.

Classification

By the nature of the course, polyneuropathy of the lower extremities can be:

1. Acute. It develops in 2-3 days, most often against the background of severe poisoning with medicines, methyl alcohol, mercury salts, and lead. Treatment takes an average of 10 days.
2. Subacute. Symptoms of the lesion increase gradually over a couple of weeks. Pathology usually occurs against the background of toxicosis or metabolic disorders and requires long-term treatment.
3. Chronic. This form of the disease progresses against the background of diabetes mellitus, alcoholism, hypovitaminosis, blood diseases or oncology. It develops gradually, over a long period of time (from six months or more).

Given the damage to nerve fibers, polyneuropathy is divided into several types:

• Motor (motor). The neurons responsible for movement are damaged, as a result of which motor functions are difficult or completely lost.
• Sensory polyneuropathy of the lower extremities. Nerve fibers directly related to sensitivity are damaged. As a result, painful, stabbing sensations occur even with a light touch to the problem area.
• Vegetative. There is a violation of regulatory functions, which is accompanied by such manifestations as hypothermia, severe weakness, profuse sweating.
• Mixed neuropathy of the lower extremities. This form includes a variety of symptoms from all of the above conditions.

Depending on the damage to cellular nervous structures, polyneuropathy can be:

1. Axonal. The axial cylinder of nerve fibers is affected, which leads to a decrease in sensitivity and impaired motor functions.
2. Demyelinating. Myelin, which forms the sheath of the nerves, is destroyed, resulting in pain syndrome, accompanied by inflammation of the nerve roots and weakness of the muscles of the proximal and distal parts of the limbs.

The demyelinating form of polyneuropathy is the most severe form of the disease, the mechanism of development of which is still not fully understood. However, as a result of a number of studies, scientists put forward a theory about the autoimmune nature of the pathology. At the same time, the human immune system perceives its own cells as foreign and produces specific antibodies that attack the roots of nerve cells, destroying their myelin sheaths. As a result, nerve fibers lose their function and provoke innervation and muscle weakness.

Diagnostics

If polyneuropathy is suspected, the patient will have to undergo a series of diagnostic procedures, including laboratory and instrumental studies. After collecting anamnesis, the doctor will conduct an external examination, examine reflexes, and then send the patient to the laboratory for blood donation for general and biochemical analysis.

In addition, the patient will undergo an ultrasound scan of the internal organs, X-ray of the affected areas, and cerebrospinal fluid will be taken. If necessary, they will take a biopsy of nerve fibers for research. The choice of treatment regimen is started only after a full examination and diagnosis.

Treatment

The basis of therapeutic measures for polyneuropathy is a combination of medical and physiotherapeutic methods aimed at preventing the progression of the pathology and restoring the disturbed innervation of nerve fibers. Methods of therapy will largely depend on the cause contributing to the development of pathology.

If severe chronic diseases are to blame, they are primarily involved in the treatment of the underlying disease. So, in diabetic polyneuropathy, drugs are selected that will not affect the level of the glycemic index, and the therapy itself is carried out in stages. First, the diet is adjusted, body weight is normalized, and a complex of therapeutic exercises is developed for the patient. In the future, the treatment regimen includes neurotropic vitamins and injections of alpha-lipoic acid, immunosuppressive agents and glucocorticoids are prescribed.

With the toxic nature of the disease, first of all, detoxification measures are carried out, after which the necessary medications are prescribed. If the pathology develops against the background of dysfunction of the thyroid gland, hormonal preparations are used in the treatment process. Malignant neoplasms are treated surgically, removing the tumor that compresses the nerve roots.

To develop the limbs and eliminate movement disorders, methods of physiotherapy exercises (LFK) are used. Vitamins of group B help to restore sensitivity, analgesics are prescribed in the form of ointments, tablets or injections to relieve pain.

The main groups of drugs for the treatment of polyneuropathy

Metabolic agents

These are the drugs of first choice in the treatment of polyneuropathy, their therapeutic effect is aimed at improving blood circulation in the area of ​​damage, improving tissue trophism and regeneration of nerve fibers. Most often, the treatment regimen includes medicines from this list:

The action of drugs is aimed at improving neuromuscular conduction, accelerating metabolism, improving the supply of tissues with blood and oxygen. Metabolic agents are able to have an antioxidant effect, fight free radicals, stop the destruction of nervous tissue and help restore impaired functions.

Vitamin complexes

In the course of treatment, an important role is given to B vitamins (B1, B12, B6). Preference is given to combined preparations, which are produced in tablet form or in the form of injections. Among the injection forms most often prescribed:

In addition to the optimal set of vitamins, these medicines include lidocaine, which additionally provides an analgesic effect. After a course of injections, vitamin preparations are prescribed in tablet form - Neuromultivit, Neurobion, Keltikan.

Painkillers

With polyneuropathy, the use of conventional painkillers (Analgin, Pentalgin, Sedalgin) does not give the desired effect. Previously, injections of Lidocaine were prescribed to relieve pain. But its use provoked jumps in blood pressure and heart rhythm disturbances. Today, a safer option has been developed that allows the anesthetic to be applied topically. To relieve pain, it is recommended to use the Versatis patch, which is based on lidocaine. It is simply fixed on the problem area, which allows you to achieve pain relief without irritation and adverse reactions.

If the pain syndrome has a clear localization, local remedies can be used - ointments and gels with analgesic effects (for example, Kapsikam).

Anticonvulsant drugs - Gabapentin, Neurontin, Lyrica, which are produced in the form of capsules or tablets, cope well with the manifestations of the pain syndrome. The intake of such funds begins with minimal doses, gradually increasing the volume of the drug. The therapeutic effect is not instantaneous, it accumulates gradually. The effectiveness of the drug can be judged no earlier than 1-2 weeks from the start of administration.

In severe cases, when pain cannot be relieved by the above means, opioid analgesics (Tramadol) are prescribed in combination with Zaldiar. If necessary, the doctor may prescribe antidepressants. Amitriptyline is most often prescribed, with poor tolerance - Ludiomil or Venlaxor.

Medicines that improve nerve conduction

In the process of treating polyneuropathy, drugs that improve the conduction of a nerve impulse to the arms and legs are necessarily used. Tablets or injections of Aksamon, Amiridin or Neuromidin help restore sensitivity. The course of therapy with these drugs is quite long - at least a month.

In the process of treatment, the doctor can combine different groups of drugs in order to achieve the most pronounced therapeutic effect.

Physiotherapy methods

Along with the methods of physiotherapy exercises, the complex treatment of polyneuropathy necessarily includes physiotherapy procedures. Your doctor may recommend the following methods:

• darsonvalization;
• ultratonotherapy;
• taking galvanic baths;
• paraffin or ozokerite applications;
• medicinal electrophoresis;
• massotherapy;
• underwater shower-massage.

The patient will definitely be waiting for therapeutic exercises under the guidance of an experienced instructor who will individually select a rehabilitation program and conduct wellness classes.

Regular courses of physiotherapy will help restore muscle tone, restore lost sensitivity, improve the supply of oxygen and nutrients to tissues, activate nerve conduction and literally put the patient on his feet.

Dysmetabolic (autonomous, hereditary, distal, sensorimotor, amyloid) polyneuropathy

Dysmetabolic polyneuropathy is an ailment that can develop against the background of the presence of somatic problems predetermined by metabolic disorders:

• diabetes mellitus;
• diseases of the kidneys, liver;
• problems of the digestive tract.

These diseases become a prerequisite for insufficiency of thiamine and other vitamins. In addition, multiple lesions of peripheral nerve endings can often be observed.

Diabetic polyneuropathy develops in diabetes mellitus in 90% of cases. The exact number of such problems will directly depend on the duration of the course of diabetes, however, in no way depends on the degree of its severity.

Symptoms of polyneuropathy can also become harbingers of this disease.

Hypoxia with changes can become an important factor in the development of neuropathy. In view of this, the use of sugar by the peripheral nerves will be impaired.

As a result of failures of the glycolysis process, an excess of lactic acid and pyruvic acid will accumulate. Cases of changes in the process of thiamine phosphorylation have been noted.

Not the last role will be played by a violation in other types of metabolism that are present against the background of diabetes:

Clinical picture of the disease

In each case, the course of dysmetabolic polyneuropathy may be different. If the disease develops early enough and is manifested by a significant decrease in vibrational sensitivity, then knee and Achilles reflexes may be lost.

This subclinical case of polyneuropathy does not cause pain, but develops over several years in a row.

Diabetic polyneuropathy can be characterized by subacute or even acute development. In this case, certain sections of the nerve trunks are damaged. As a rule, nerve damage occurs:

These problems may be accompanied by paresis of the corresponding muscle groups, pain and sensitivity disorder. If the femoral nerve was affected, then in this case there is a loss of knee reflexes.

In addition, damage to the cranial nerves (abducens, trigeminal, oculomotor) was noted.

There is a third type of course of diabetic polyneuropathy. It is characterized by damage to some nerves of the limbs and the development of sensory and motor disorders (the lower limbs are especially affected).

Tendon reflexes may completely disappear, and pain in the nerve trunks is felt on palpation.

Vegetative and trophic disorders are not uncommon in polyneuropathy. Problems with urination and postural hypotension develop.

How to treat?

First of all, carbohydrate metabolism should be adjusted with insulin injections and a special balanced diet. The doctor may recommend:

The schedule of measures that are used to get rid of neuropathy will be shown.

Polyneuropathy in systemic ailments

If a patient has lupus erythematosus that affects the skin, kidneys and joints, then in this case polyneuropathy is characterized by the development of paralysis or paresis of the proximal muscles, loss of some tendon reflexes. A significant decrease in susceptibility to pain is also likely.

In some cases, signs of polyneuropathy can become the first manifestations of the development of the underlying disease. Medicine knows forms with significant damage to various nerves of the arms and legs.

In this case, we will talk about mononeuropathy. In severe rheumatoid arthritis, polyneuropathy is also observed. Initially, it will manifest itself as sensory disturbances, and then quite severe sensorimotor neuropathy.

If periarteritis nodosa is present, then sequential neuropathy of individual cranial and spinal nerves develops. Such violations will be associated with severe disorders:

The considered form of neuropathy is often accompanied by symptoms of inflammatory angiopathy in other organs and systems.

Hereditary polyneuropathy

First of all, it is polyneuropathy, which develops with porphyria (genetic enzyme disorders). The main symptoms of this hereditary disease are:

• pain in the abdominal cavity;
• increased blood pressure;
• damage to the central nervous system;
• producing urine with a characteristic dark color.

Porphyric polyneuropathy will be manifested due to the neurological complex of symptoms. In this case, pain, weakness in the muscles, paresthesia (upper and lower extremities) occur. Motor manifestations can gradually increase, up to distal paralysis or paresis.

With this disease, the patient will feel:

1. soreness of the nerve trunks;
2. loss of all types of sensitivity.

To make an adequate diagnosis, the doctor will take into account all the symptoms of porphyrin metabolism disorders. To get rid of the disease, the doctor recommends intravenous and oral administration of glucose at a dosage of up to 400 mg (the same treatment is indicated for other forms of polyneuropathy).

Amyloid polyneuropathy

The amyloid variety of polyneuropathy develops in those patients who have a history of hereditary amyloidosis. Its main clinical symptoms are:

• stool disorders (constipation and diarrhea);
• pain in the digestive tract;
• heart failure;
• macroglossia (an increase in the size of the tongue).

With this disease, sensory disturbances predominate, for example, soreness of the limbs, loss of pain and temperature sensitivity. At later stages, paresis also joins the disorders.

As for adequate therapy, at the moment it does not exist.

Distal sensorimotor polyneuropathy

In diabetes, long nerve fibers are most often affected. Diabetic polyneuropathy is observed in 40% of diabetics. This type of disease is characterized by the absence of a feeling of pressure, changes in ambient temperature, pain, vibration and location relative to other objects.

Sensory polyneuropathy is dangerous because a diabetic may not feel any pain or high temperatures.

Ulcers appear on the lower extremities, wounds on the leg fester. Severe joint damage and fractures are not ruled out.

Sensorimotor polyneuropathy can manifest itself with active symptoms, for example, quite strong pain in the legs, which are especially aggravated at night.

As the disease progresses, there will be a violation in the work of the musculoskeletal system. When this happens:

• bone deformity;
• muscle dystrophy;
• excessive dryness of the skin;
• the appearance of age spots;
• reddish skin tone;
• sweat gland dysfunction.

The most significant symptoms of distal polyneuropathy in diabetes mellitus will be ulcers that occur between the toes and on the soles of the feet. Lesions are not capable of causing discomfort due to the absence of pain. In advanced cases, we will talk about amputation of limbs.

Autonomic polyneuropathy in diabetes

In the presence of lesions of the autonomic nervous system against the background of the course of diabetes, the patient will feel:

1. darkening in the eyes;
2. fainting when taking a vertical position;
3. dizziness.

This form of polyneuropathy will be accompanied by malfunctions in the normal functioning of the digestive tract, which is manifested by a slowdown in the intake of food by the intestines. In view of this, it is almost impossible to stabilize the concentration of glucose in the blood of a diabetic.

The cause of a sudden death can be a heart rhythm disturbance in diabetic polyneuropathy.

Those people who suffer from this disease will feel problems from the genitourinary system - urinary incontinence occurs. The bladder will lose the ability to completely empty, which becomes a prerequisite for the development of infectious diseases. In men, erectile dysfunction will be noted against the background of autonomic polyneuropathy, and in women, dyspareunia (the inability to achieve orgasm).

Polyneuropathy: diabetic, lower extremities, alcoholic (toxic) and others

Polyneuropathy is a lesion of the peripheral nerves and blood vessels that provide them with nutrition. This pathological process is sometimes called polyneuropathy, changing one letter, neuropathy, polyradiculoneuropathy or polyneuritis, but the latter (polyneuritis) is perceived as inflammation, and for peripheral nerves, the true inflammatory process is somehow not characteristic, if it occurs, it is very rare.

The basis of polyneuropathies are other factors: metabolic disorders (a vivid example is diabetic polyneuropathy), ischemic factors, mechanical damage, which give morphological changes in nerve fibers. And even an infection that has got into the nerve fibers does not give a typical inflammation, but manifests itself as an allergic reaction. That is why the word "polyneuritis" is gradually leaving the terminology.

If, in addition to peripheral nerves, disorders affect the roots of the spinal cord, the disease is called polyradiculoneuropathy. The pathological process is most noticeable when the distal parts of the legs are affected (polyneuropathy of the lower extremities) - it is given out by the patient's characteristic "cock's gait".

The reasons for the development of this pathology are very diverse, almost any factor that has had a negative effect on the body at least once can lead to the onset of the disease, while individual cases of the disease remain a mystery forever.

How to understand the diagnosis?

In most cases, patients in the "diagnosis" see not just the word "polyneuropathy", usually some definition is added to it. And if the words "alcoholic" or "toxic" are more or less clear to people, then other terms ("axonal" and "demyelinating") raise questions. In order for the reader to understand the meaning of these definitions, it will be necessary, based on data from various sources, to make an attempt to somehow classify this pathology, since a generally accepted version of the classification has not yet been developed.

By origin, the following forms of polyneuropathy are distinguished:

• Alimentary.
• Hereditary.
• Autoimmune.
• Metabolic (hepatic, uremic, diabetic polyneuropathy).
• Toxic.
• Infectious-toxic.

Meanwhile, in the literature, one can also find another division of the disease according to the etiological factor, where they distinguish: inflammatory, although true inflammation is classified as extremely rare, toxic, allergic and traumatic variants.

demyelination in neuropathy

Depending on the type of pathological process, two forms of the disease have been distinguished and, it seems, opinions do not differ here:

1. Axonal polyneuropathy - it occurs when the axon is damaged;
2. Demyelination - is formed from the demyelination of nerve fibers.

It should be noted that these two forms do not exist for long, and therefore not always, in their pure form: with a primary lesion of the axon, a demyelinating component joins as a secondary pathology, and with demyelination, an axonal one.

There is no particular disagreement regarding the classification of polyneuropathy according to the nature of the course, therefore, in the description of the disease, you can find:

In addition, depending on the prevalence of symptoms of a particular type of neuropathy, motor, sensory vegetative forms are distinguished, which, however, occur quite rarely in an isolated form, motor-sensory or sensory-vegetative types of the disease are more often noted.

It is quite difficult to describe (or just list) all types of neuropathy - there are a lot of them, however, it should be borne in mind that, regardless of the etiological factor, all forms have common clinical manifestations, which, to the same extent as the origin, determine the therapeutic approach and prognosis of the disease. .

Symptoms of polyneuropathy

typical lesions in polyneuropathy

Systemic damage to the peripheral nerves is referred to the main clinical manifestations characteristic of the entire group of neuropathies and it is not so important: what type it belongs to and in what direction the pathological process is moving - the main symptoms will be present:

1. Muscle weakness and atrophy;
2. Decreased tendon reflexes;
3. Peripheral paresis;
4. Sensitivity disorder in the distal extremities (hypoesthesia, parasthesia, hyperesthesia);
5. Trophic vegetative-vascular disorders.

Demyelinating PNP are manifested mainly by the suffering of large myelinated (motor and sensory) nerve fibers, while non-myelinated autonomic and sensory nerves that provide superficial sensitivity, without being particularly involved in the process, remain intact. This variant of the disease is manifested by a loss of deep reflexes and a violation of vibrational sensations with a relative preservation of surface sensitivity. Demyelination, affecting not only the distal extremities, over time expands the boundaries and begins to spread to the roots, manifesting itself:

• Peripheral paresis;
• Weakness of the limbs (distal sections);
• Thickening of the nerves in the case of a chronic course.

Such polyneuropathy of the lower extremities does not belong to irreversible processes. If the etiological factor is eliminated and adequate treatment is carried out, the myelin sheaths are restored and neurological symptoms regress within 1.5–2 months.

Axonal neuropathies can affect fibers of various types with the gradual development of a pathological condition. Typical symptoms of this type of PNP include:

1. Sensitive (pain, temperature) disorders;
2. Vegetative disorders;
3. The absence of violations of deep reflexes at an early stage of the disease.

It is hardly possible to expect a complete restoration of the lost functional abilities in the case of axonopathy. Axons regenerate slowly, and the processes of the surviving axons, although they try to compensate for the loss, do not have the ability to do so in full.

However, given that in order to obtain a good effect from therapeutic measures, first of all, the causal factor is important, special attention is paid to its search.

What factors cause peripheral nerves to suffer?

NK damage in diabetes

Diabetes is the main reason

Most often, neuropathy is meant when they talk about the complications of a very common disease all over the globe - diabetes mellitus (diabetic neuropathy, diabetic foot), so one cannot but emphasize its leading position in the list of causes. The defeat of small vessels in diabetes mellitus is observed in half or more of patients with diabetes mellitus. It is difficult to predict when the disease manifests itself, it can happen even at the beginning of the disease and become the first symptoms of diabetes, or the development of the disease can be delayed for an indefinite period, calculated for many years.

The main factor triggering the mechanism for the development of diabetic neuropathy is the ischemic component and metabolic disorders in the nerve fiber.

The appearance of the first neurological signs of diabetic polyneuropathy (the sensation of vibration at the ankles is shortened, the Achilles reflexes are reduced) does not give reason to believe that the disease will begin to develop rapidly. With these symptoms, a diabetic can live for many years without presenting other complaints until the progression of the process begins, when the clinical picture acquires a color typical of neuropathy:

• There is a strong, very painful soreness in the feet and legs, which, in warmth and at rest, becomes even more acute;
• Feet become weak;
• Vegetative innervation begins to suffer;
• The intensity of pain continues to increase over time - they become unbearable;
• Simultaneously with the increase in pain, itching appears (not always, but very often), the color of the skin changes (from purple to black);
• A diabetic foot is formed, which leads not only to a decrease in the functionality of the lower extremities, but is often the cause of their amputation.

Polyneuropathy of the lower extremities, which develops against the background of diabetes mellitus, is the most common serious complication of type 2 diabetes mellitus and a headache for endocrinologists, therefore, an established diagnosis (DM) is already a reason for preventing damage to nerve fibers, and the appearance of the first signs is for reviewing therapy in direction of increasing efficiency. In addition to measures aimed at compensating for the underlying disease (DM), treatment is prescribed to improve blood circulation, relieve swelling, and prevent infection (topical antibiotic therapy).

Diabetic neuropathy, video program "Live healthy!"

In addition to diabetes, other diseases can also trigger the formation of neuropathy and make it concomitant: hematological pathology, collagenoses, biliary cirrhosis, neoplasms, hypothyroidism, multiple myeloma, etc.

Vitamin B deficiency

Deficiency of certain vitamins from the B group (B1, B12, B6), which naturally have a neurotropic effect (positive effect on the central nervous system and peripheral nerves), therefore, in a medicinal form, they are used as important means of pathogenetic treatment. Naturally, if for some reason there is a lack of these vitamins in the body, which will not be quickly replenished, then symptoms of chronic axonal polyneuropathy will soon manifest themselves:

1. Deficiency of vitamin B1 (thiamine) causes neuropathy of the lower extremities, reminiscent of diabetic or alcoholic;
2. Lack of B6 (pyridoxine) - forms mainly sensory disturbances, manifested by numbness and tingling;
3. Lack of B12 (cyanocobalomin) - most often leads to degeneration of the spinal cord and damage to the posterior cords, sometimes to the development of sensory disturbances with numbness and tingling.

The main treatment for this type of polyneuropathy is the introduction of B vitamins and ascorbic acid in therapeutic doses, as well as a diet rich in these beneficial substances.

toxic form

The toxic form of the disease with damage to the cranial nerves can develop as a complication of the infectious process caused by agents such as Leffler's bacillus (diphtheria bacillus - diphtheria neuropathy), herpes virus, human immunodeficiency virus (HIV).

Severe intoxications that develop as a result of the penetration into the blood of substances alien to the human body that enter there accidentally or intentionally in order to commit suicide: arsenic, methanol, which is confused with ethanol, carbon monoxide, dichlorvos and other organophosphorus (or simply toxic) chemical compounds. Chronic use of alcoholic beverages also forms toxic polyneuropathy, the only difference is that the above poisons act very quickly and affect the nerves in 2-4 days, causing acute axonal polyneuropathy, and an alcoholic poisons his body for months and years, creating the ground for the progression of the pathological process. In most cases, within six months, a person suffering from alcoholism "uses his chances" to get this disease.

Alcoholic polyneuropathy develops in 2 - 3% of people who do not know the measure in strong drinks, and is in second place after diabetic. The main role in the formation of the pathological process is played by 2 factors: 1) the toxic effect of ethanol on the nervous system, 2) metabolic disorders in the nerves. Not only peripheral nerves suffer from the influence of alcohol, certain changes also affect the brain and spinal cord.

Symptoms of alcoholic polyneuropathy develop gradually:

• Pain in the calves, aggravated by pressure, and paresthesias in the distal parts appear first;
• A little later comes weakness and paralysis, which concern both the upper limbs and the lower ones;
• Paretic muscles quickly begin to atrophy;
• Deep reflexes increase, their zones expand;
• A violation of superficial sensitivity begins to appear, like socks and gloves;
• The deepening of clinical manifestations in the absence of treatment can lead to the fact that the external signs of PNP begin to resemble dorsal dryness in syphilis, however, the absence of characteristic symptoms (RW - positive, urinary incontinence, "backache") indicates a different causative factor and a different type of neuropathy, nothing in common with syphilis without.

Sometimes alcoholic polyneuropathy develops rapidly and this usually happens after severe hypothermia. This type is characterized by a wide range of changes in the nervous system, patients, as a rule, have an "eloquent" appearance and present a lot of complaints. Vasomotor, secretory and trophic disorders cause increased sweating, swelling of the distal parts of the lower and upper extremities, changes in temperature and skin color.

Pain in alcoholic polyneuropathy can increase over several months. Meanwhile, timely treatment, which includes vitamin therapy, nootropics, physiotherapy, prozerin, can reverse the development of the process.

In conclusion of this section, we should recall the neuropathy that develops from the use of substances intended for the treatment and prevention of diseases. Drug-induced polyneuropathy develops against the background of treatment with drugs that are difficult to attribute to simple ones: gold salts, bismuth, sulfonamides, anticonvulsants, antibacterial and chemotherapy drugs. In other cases, peripheral nerves may be affected after going for vaccination (administration of vaccines and sera).

Injuries, compression, hypothermia and an unknown factor

In this subsection, we have collected somewhat similar reasons, because it is often possible to hear that the manifestations of the disease developed after a bruise or hypothermia, sometimes signs of polyneuropathy appeared as a result of an infection or due to compression syndromes, which are so rich in osteochondrosis of the spine.

Thus, the cause of neuropathy is often:

1. Injuries. Mechanical damage to the nerves as a result of injuries (bruises, dislocations, open and closed fractures, unsuccessful surgical interventions) can cause neuropathy of the lower or upper extremities with paresthesia, numbness, tingling. For example, a traumatic disruption of the integrity of the ulnar nerve of one of the upper extremities gives a typical picture of ulnar neuropathy: bent lifeless fingers, a hand with signs of muscle atrophy, loss of functional ability.

relationship between the level of spinal injury and organs

Compression of the nerve roots. Compression syndrome in osteochondrosis or herniated discs, where the symptoms of peripheral nerve suffering are more often transient, can cause radiculopathy of both the upper and lower extremities, accompanied by motor, sensory and autonomic disorders. Degenerative-dystrophic changes mostly concern the lower parts of the spine (osteochondrosis and its consequences) and, in the absence or ineffectiveness of treatment, often lead to compression of the nerve roots, which can easily turn into the development of neuropathy of the lower extremities. Compression syndrome resulting from the progression of rheumatoid arthritis, the development of a tumor, medical manipulations, threatens to pinch the nerves of the upper extremities, which often results in brachial plexus neuropathy (brachial plexitis) or ulnar neuropathy.

Of particular interest is polyneuropathy, which was originally called postpartum polyneuritis. Upon further study of this pathological condition, it turned out that it is not so postpartum and can develop at any stage of pregnancy, so now the disease has been given a different name - polyneuropathy of pregnant women.

The origin of PNP of pregnant women is associated with:

• With a lack of vitamins (group B - in particular) during pregnancy;
• With hypersensitivity to proteins that enter the body of a woman from the placenta and fetus and are foreign to her;
• With the toxic effect of metabolic products on peripheral nerves.

Symptoms of polyneuropathy of the lower extremities (paresthesia, paresis, paralysis and pain) appear against the background of complete well-being, but often the development of the disease does not end there and signs of intoxication (general weakness, nausea, vomiting, etc.) join the symptoms of PNP.

The main treatment for this pathology is the appointment of vitamin complexes containing B vitamins, desensitizing therapy.

Heredity

Hereditary neuropathies represent a heterogeneous group of pathological conditions: some gene mutations cause one single sign, while others, on the contrary, give a lot of different symptoms, among which peripheral nerve damage manifests itself.

Metabolic neuropathies include inherited amyloidoses, as well as porphyrias and lipid metabolism disorders of the same origin. Mysterious forms represent hereditary motor-sensory (Charcot-Marie-Tooth syndrome) and sensory-vegetative types (Fabry disease). An example of hereditary PNP is Fabry disease (sex-linked trait, lysosomal storage disease), in which neuropathy is one of the many symptoms. Since the gene that controls this pathology is located on the X chromosome, men are predominantly affected, which is understandable - they have only one X chromosome, and if it turns out to be defective, the disease is inevitable. However, cases of women's disease are known, but why this happens - geneticists have not yet given a clear answer. The disease has a rich symptomatology (intolerance to exercise, decreased sweating, damage to internal organs) and a characteristic appearance of the patient (acromegaly). Manifestations of neuropathy can equally affect both the lower and upper limbs: the feet and palms experience constant burning, numbness, and soreness. Symptoms are aggravated by a crisis, which is provoked by stress, cold or heat exposure.

Treatment

Although the treatment of polyneuropathy is determined taking into account the causative factor and involves the treatment of the underlying disease that caused the damage to the peripheral nerves, therapeutic measures should be comprehensive while simultaneously focusing on eliminating the symptoms of PNP.

The problem of treating metabolic forms of ANP, which are primarily the most common types: diabetic polyneuropathy (a complication of type 2 diabetes mellitus) and alcoholic polyneuropathy (a consequence of chronic alcohol intoxication). As a rule, these, and often others, neuropathies are accompanied by an intense pain syndrome and a pronounced violation of sensitivity. To reduce clinical manifestations, modern medicine offers various methods of treatment:

1. Vitamin therapy. Combined preparations containing vitamins B1, B6, B12 (neuromultivit, milgamma) in pharmaceutical doses are among the first. They give a good analgesic effect, eliminate sensitivity disorders by improving the ability of nerves to restore their structural components, and provide antioxidant protection. Natural forms of the listed vitamins are involved in the treatment of PNP, combining them, as well as other drugs of this pharmacological group (vitamins A, C, E).
2. Painkillers. For pain relief, mainly non-narcotic analgesics (aspirin, tramal) and non-steroidal anti-inflammatory drugs (NSAIDs) are used, but in other cases codeine and even morphine are prescribed for severe pain. It is considered appropriate to add Magne B6 to analgesic therapy, which increases the effectiveness of analgesic treatment.
3. Glucocorticoids, plasmapheresis, immunosuppressants. Recent results of scientific research have shown that in the pathogenesis of some PNP, the main role belongs to failures in tissue immunity, so long-term immunomodulation with the help of medications is very justified. In these cases, drugs such as azathioprine, cyclosporine, irradiation of the lymphatic system + cyclophosphamide are used. However, when the patient is in a serious condition, immunosuppressants are often combined with hormones or plasmapheresis (azathioprine + prednisolone, azathioprine + plasmapheresis). Erbisol is often prescribed as an auxiliary drug, which is a complex of natural organic compounds with a multidirectional effect (immunomodulatory, anti-inflammatory, antioxidant, membrane-stabilizing). Meanwhile, hormone therapy regimens (prednisolone, methylprednisolone) with increasing and decreasing doses (taking into account the patient's condition) are determined only by the doctor. He also combines hormone therapy with immunoglobulins (normal human immunoglobulin, sandoglobulin) or plasmapheresis. These activities are carried out in stationary conditions.
4. Other drugs. In case of polyneuropathy, other drugs are also prescribed: those that accelerate the utilization of glucose, improve tissue nutrition and the rheological properties of blood, which have a diuretic, vasodilating, venotonic effect (all these qualities contain instenon), as well as drugs that improve cellular metabolism (actovegin) and neuromuscular - muscle conductivity (prozerin), normalizing blood flow in the microvasculature (trental), regulating redox reactions in tissues (phosphaden). In some cases, detoxification or desensitizing therapy is carried out. In the list of prescriptions for a patient with PNP, you can find a wide range of drugs from various pharmacological groups: cerebrolysin, oxypin, picamelon, encad, calcium pantothenate ... What to prescribe and how to justify it - the doctor will think.

Polyneuropathy (depending on its origin and clinical manifestations) can sometimes tie the patient to bed for a long time. And he himself, and especially his relatives, must remember that not everyone is in the power of chemical compounds called drugs. A significant role is played by proper nutrition, rehabilitation measures and, especially, care and concern.