Diabetic distal symmetric sensorimotor polyneuropathy. What is diabetic polyneuropathy of the lower extremities. Diabetic polyneuropathy: symptoms, classification and directions of treatment

Diabetic polyneuropathy is a serious pathology accompanied by damage to the structures of the peripheral nervous system. The disease is a complication of diabetes; its first signs appear several years after the diagnosis of diabetes mellitus. It progresses slowly, firstly the distal and then the proximal parts of the nervous system are involved in the pathological process.

Polyneuropathy is detected in 70% of patients with diabetes and, as a rule, already at a stage when therapy is often ineffective. Untimely treatment leads to the appearance of severe pain, performance is lost. There is a risk of death. Consider how to treat polyneuropathy in diabetes.

Causes, pathogenesis of polyneuropathy

The main reason that triggers the mechanism for the onset of neuropathy is an increased concentration of glucose in the blood. The result is an increase in the intensity of oxidative processes. Free radicals accumulate in the body, which negatively affect neurons, disrupting their functions.

Excessive sugar content leads to the activation of autoimmune processes that destroy nerve tissue. The accumulation of glucose causes disturbances in the osmolarity of the intracellular space, the nerve tissues swell, and the conduction between cells is disturbed. The growth of nerve fiber cells slows down. Constant hyperglycemia reduces the intensity of energy metabolism, impulse conductivity worsens. The endings of nerve cells experience hypoxia (oxygen starvation).

Factors provoking the development of neuropathy:

• Long course of diabetes;
• Elderly age;
• The presence of bad habits;
• Intoxication with chemical compounds, drugs.

Pathology can develop against the background of systemic diseases:

• Ischemia;
• Uremia.

The risk of polyneuropathy is increased in diabetics with arterial hypertension, obesity, and hyperlipidemia.

Classification

Depending on which part of the nervous system is damaged, several forms of polyneuropathy are distinguished:

1. Autonomous. It is characterized by disruption of the work of individual organs or systems. It also comes in several forms:

• Cardiac;
• Gastrointestinal;
• Respiratory;
• Urogenital.

1. Somatic. In this form, the disease affects the entire body.

According to the localization of the lesions, 3 types of neuropathy are distinguished:

1. Sensory. The patient's sensitivity to stimuli decreases.
2. Motor. The motor function is impaired.
3. Distal (sensorimotor) form. The disease combines type 1 and type 2 symptoms.

Autonomic, diabetic sensory, distal polyneuropathy (mixed form) is most often detected.

Damage to the nervous system provokes the onset of symptoms of diabetic polyneuropathy. The manifestations of the disease depend on which nerve fibers are involved in the process: small or large. In the first case, the patient:

• Limbs grow numb (lower, upper);
• There is a burning sensation, tingling sensation;
• The skin becomes insensitive to high and low ambient temperatures;
• The skin of the feet turns red;
• Hands, feet are freezing;
• The feet are swollen, sweat a lot;
• The skin on the legs flakes off, becomes dry;
• Pains appear in the limbs at night;
• Calluses and painful cracks form on the feet.

If large nerve fibers are affected, the manifestations of the disease will be as follows:

• Balance when walking is disturbed;
• Are concerned about joint pain;
• The skin of the lower extremities becomes even more sensitive;
• With light touches, painful sensations appear;
• There is insensitivity to finger movements.

In addition, polyneuropathy is accompanied by nonspecific manifestations. These include:

• Dizziness;
• Speech disorders;
• Deterioration of vision.

Consider the symptoms characteristic of those forms of polyneuropathy that are most often detected. With lesions of the autonomic nervous system (autonomous form), the digestive function worsens, dizziness appears. If a person gets up, his eyes darken, he may faint. With this form of neuropathy, the risk of genitourinary infections is high. Myocardial dysfunction sometimes causes sudden death.

Diabetic distal polyneuropathy usually affects the lower extremities, the upper ones are very rare. There are 3 stages in the development of pathology:

1. Subclinical. There are no particular complaints, only the sensitivity of the limbs to pain, high and low temperature decreases.
2. Clinical. Patients complain of pain in various parts of the body, numbness of the extremities, deterioration of sensitivity. With the further development of the process, severe tingling, burning, pain appears. Symptoms become more intense at night. There is a painless form, it is characterized by: numbness of the feet, severe impairment of sensitivity, muscle weakness, impaired motor function.
3. Complications. Ulcers form on the legs, in some they are accompanied by mild pain. The disease at this stage can provoke the development of gangrene, then a decision is made about amputation.

Diabetic sensory neuropathy usually occurs in late-stage diabetes and is characterized by sensory disturbances and pain in the legs.

The pain symptom usually appears at night. This form is characterized by persistent paresthesias. They are characterized by a feeling of numbness, the appearance of "goose bumps", tingling.

Doctors also distinguish between positive and negative symptoms of diabetic polyneuropathy. Positive ones appear in the early stages, they include:

1. Burning sensation (on the 1st limb or throughout the body). Most noticeably, if the person is as relaxed as possible, as well as at night.
2. Sharp pains in the region of the pharynx, abdomen, in the right hypochondrium.
3. Lumbago, similar electric shocks.
4. Painful sensations (allodynia) with light touches.
5. Hypersensitivity to pain of any intensity.

Negative symptoms:

• Stiffness of the limbs;
• Pain with any movements of the legs, arms;
• Tingling;
• Numbness of the limbs.

The function of the vestibular apparatus is impaired, the patient has poor stability when walking. The appearance of negative symptoms indicates the onset of a late stage of the disease, when the changes have become irreversible.

Diagnostics

If you suspect polyneuropathy, you should consult an endocrinologist, neurologist, surgeon. The diagnosis is made on the basis of complaints, examination of the patient and the results of laboratory and instrumental studies. Condition, limb sensitivity, reflexes are assessed. Laboratory tests include determining:

• Cholesterol levels;
• The amount of sugar in the blood, urine;
• Glycosylated hemoglobin, C-peptide;
• Insulin level in the blood.

Additionally, ECG, ultrasound is performed, electroneuromyography, MRI are performed.

Treatment

With a timely diagnosis, adequate therapy for polyneuropathy in the early stages, the prognosis for recovery will be positive in most patients.

An important condition is maintaining blood sugar levels.

Treatment of diabetic polyneuropathy of the lower extremities is complex, it is necessary to influence the causes and symptoms of the pathology. Therapeutic activities include:

1. Removal of excess glucose from nerve tissues, restoration of damaged cells with the help of alpha-lipoic acid preparations. The substance belongs to antioxidants, is involved in metabolic processes. Alpha lipoic acid neutralizes the action of free radicals, promotes the breakdown of glucose, and stimulates the processes of its transportation.
2. Restoring the process of passing impulses, reducing the negative effect of excess sugar on nerve cells. For this purpose, the patient is prescribed B vitamins, which have a positive effect on the state of the central nervous system, the musculoskeletal system. Vitamin E is useful, neutralizing the negative effect of glucose on neurons.
3. Restoration of normal metabolism in nerve tissues by taking antioxidant drugs. Actovegin gives good results, which does not give side effects. The agent has an antihypoxic effect, positively affecting the absorption and utilization of oxygen. The drug exhibits an insulin-like effect, since it improves the processes of oxidation, glucose transport. Taking Actovegin will allow you to replenish energy reserves in neurons.
4. Weakening the process of glucose synthesis, reducing its negative effect on the structures of the nervous system by taking drugs that inhibit aldose reductase (Olredaza, Izodibut, Sorbinil). Medicines reduce the manifestations of neuropathy: they eliminate the pain symptom, restore the sensitivity of the limbs, and accelerate the healing process of ulcers.
5. Relief of pain symptoms with non-steroidal anti-inflammatory drugs (Diclofenac, Ibuprofen).
6. Elimination of numbness, seizures with drugs, which include potassium, calcium, magnesium.
7. When ulcers appear on the extremities, a course of antibiotics and local wound-healing agents are prescribed.

To increase the effectiveness of treatment, taking medications must be combined with non-drug methods. To improve blood circulation and maintain muscle tone, the patient is prescribed physiotherapy (electrophoresis, magnetotherapy). The motor function of the lower extremities is restored with the help of therapeutic massage, acupuncture.

Swimming and exercise therapy have a good effect. Exercise daily for 10-20 minutes.

Phytotherapy

In addition to medical treatments prescribed by your doctor, you can be treated with traditional medicine. Herbal medicine will help reduce the intensity of symptoms.

You can normalize sugar levels with a decoction, which includes:

• Peppermint - 30 g;
• Corn silk - 60 g;
• Galega (goat's rue) - 100 g;
• Bean shells - 100 g.

Pour 6 table. l. collecting 1 liter of boiling water and put on low heat for 5 minutes. Strain the broth before use and take before meals. A single amount is 100 ml.

To provide your neurons with nutrients, consume a vitamin shake daily. You will need:

• Kefir - 1 tbsp.;
• Sunflower seeds - 2 tablespoons. l .;
• Parsley to taste.

Peel and grind sunflower seeds, add to kefir. Add greens and stir. Drink a cocktail 1 r. / Day half an hour before breakfast (on an empty stomach).

Clove (spice) exhibits a good antioxidant effect. To prepare the infusion you will need:

• Cloves - 30-35 g;
• Water - 3 tbsp.

- a complex of diseases of the nervous system, proceeding slowly and resulting from an excess amount of sugar in the body. In order to understand what diabetic polyneuropathy is, one must remember that diabetes mellitus belongs to the category of serious metabolic disorders that negatively affect the functioning of the nervous system.

In the event that competent therapeutic therapy has not been carried out, an increased level of sugar in the blood begins to inhibit the vital processes of the whole organism. Not only kidneys, liver, blood vessels suffer, but also peripheral nerves, which is manifested by various symptoms of damage to the nervous system. Due to fluctuations in the level of glucose in the blood, the work of the autonomic and autonomic nervous system is disrupted, which is manifested by difficulty breathing, disturbed heart rhythm, and dizziness.

Diabetic polyneuropathy occurs in almost all patients with diabetes mellitus, it is diagnosed in 70% of cases. Most often, it is found in the later stages, however, with regular preventive examinations and an attentive attitude to the state of the body, it can be diagnosed in the early stages. This makes it possible to suspend the development of the disease and avoid complications. Most often, diabetic polyneuropathy of the lower extremities is manifested by a violation of the sensitivity of the skin and pain, which most often occurs at night.

• Excess blood sugar increases oxidative stress, leading to the production of large amounts of free radicals. They have a toxic effect on cells, disrupting their normal functioning.
• An excess of glucose activates autoimmune processes that inhibit the growth of cells that form conductive nerve fibers and have a destructive effect on nerve tissue.
• Disruption of fructose metabolism leads to excess production of glucose, which accumulates in large volumes and disrupts the osmolarity of the intracellular space. This, in turn, provokes edema of the nervous tissue and impaired conduction between neurons.
• The reduced content of myoinositol in the cell inhibits the production of phosphoinositol, which is the most important component of the nerve cell. As a result, the activity of energy metabolism and an absolute violation of the impulse conduction process decrease.

How to recognize diabetic polyneuropathy: initial manifestations

Dysfunctions of the nervous system, developing against the background of diabetes, are manifested by a variety of symptoms. Depending on which nerve fibers are affected, they emit specific symptoms that occur when small nerve fibers are damaged, and symptoms of damage to large nerve fibers.

1. Symptoms that develop with damage to small nerve fibers:

• numbness of the lower and upper extremities;
• tingling and burning sensation in the limbs;
• loss of sensitivity of the skin to temperature fluctuations;
• chills of the limbs;
• redness of the skin of the feet;
• swelling in the feet;
• painful sensations that bother the patient at night;
• increased sweating of the feet;
• peeling and dry skin on the legs;
• the appearance of calluses, wounds and non-healing cracks in the area of ​​\ u200b \ u200bthe feet.

2. Symptoms arising from damage to large nerve fibers:

• balance disorders;
• damage to large and small joints;
• pathologically increased sensitivity of the skin of the lower extremities;
• painful sensations arising from light touch;
• insensitivity to finger movements.

In addition to the listed symptoms, the following non-specific manifestations of diabetic polyneuropathy are also observed:

• urinary incontinence;
• stool disorders;
• general muscle weakness;
• decreased visual acuity;
• convulsive syndrome;
• sagging skin and muscles around the face and neck;
• speech disorders;
• dizziness;
• violations of the swallowing reflex;
• sexual disorders: anorgasmia in women, erectile dysfunction in men.

Classification

Depending on the location of the affected nerves and symptoms, there are several classifications of diabetic polyneuropathy. The classical classification is based on which part of the nervous system is most affected by metabolic disorders.

The following types of disease are distinguished:

• Damage to the central parts of the nervous system, leading to the development of encephalopathy and myelopathy.
• Damage to the peripheral nervous system, leading to the development of pathologies such as:
  - diabetic polyneuropathy of the motor form;
  - diabetic polyneuropathy of the sensory form;
  - mixed sensorimotor diabetic polyneuropathy.
• Damage to the conducting nerve pathways, leading to the development of diabetic mononeuropathy.
• Diabetic polyneuropathy resulting from damage to the autonomic nervous system:
  - urogenital form;
  - asymptomatic glycemia;
  - cardiovascular form;
  - gastrointestinal form.

They also distinguish diabetic alcoholic polyneuropathy, which develops against the background of regular alcohol consumption. It also manifests itself as a burning and tingling sensation, pain, muscle weakness, and complete numbness in the upper and lower extremities. Gradually, the disease progresses and deprives a person of the ability to move freely.

The modern classification of diabetic polyneuropathy includes the following forms:

• Generalized symmetric polyneuropathy.
• Hyperglycemic neuropathy.
• Multifocal and focal neuropathies.
• Lumbar-thoracic radiculoneuropathy.
• Diabetic polyneuropathy: acute sensory form.
• Diabetic polyneuropathy: a chronic sensorimotor form.
• Autonomic neuropathy.
• Cranial neuropathy.
• Tunnel focal neuropathies.
• Amyotrophy.
• Chronic inflammatory demyelinating neuropathy.

What are the most common forms?

Distal diabetic polyneuropathy or mixed polyneuropathy.

This form is the most common and occurs in about half of patients with chronic diabetes mellitus. Due to excess sugar in the blood, long nerve fibers suffer, which provokes damage to the upper or lower extremities.

The main symptoms are:

• loss of the ability to feel pressure on the skin;
• pathological dryness of the skin, pronounced reddish skin tone;
• disruption of the sweat glands;
• insensitivity to temperature fluctuations;
• lack of pain threshold;
• inability to feel a change in body position in space and vibration.

The danger of this form of the disease is that a person suffering from an ailment can seriously injure a leg or get a burn without even feeling it. As a result, wounds, cracks, abrasions, ulcers appear on the lower extremities, and more serious injuries of the lower extremities are also possible - joint fractures, dislocations, severe bruises.

All this further leads to disruptions in the work of the musculoskeletal system, muscular dystrophy, and bone deformation. A dangerous symptom is the presence of ulcers that form between the toes and on the soles of the feet. Ulcerative formations do not cause harm, since the patient does not experience pain, however, a developing inflammatory focus can provoke amputation of the limbs.

Diabetic polyneuropathy is a sensory form.

This type of ailment develops in the late stages of diabetes mellitus, when neurological complications are pronounced. As a rule, sensory impairments are observed 5-7 years after the diagnosis of diabetes mellitus. From other forms of dibetic polyneuropathy, the sensory form differs in specific pronounced symptoms:

• persistent parasthesias;
• feeling of numbness of the skin;
• sensitivity disorders in any modality;
• symmetrical pain in the lower extremities that occur at night.

Autonomous diabetic polyneuropathy.

The cause of autonomic disorders is an excess of sugar in the blood - a person experiences fatigue, apathy, headache, dizziness, tachycardia attacks, increased sweating, darkening in the eyes with a sharp change in body position also often occur.

In addition, the autonomous form is characterized by digestive disorders, which slows down the flow of nutrients into the intestines. Digestive disorders complicate antidiabetic therapy: it is difficult to stabilize blood sugar levels. Cardiac arrhythmias, often associated with autonomic diabetic polyneuropathy, can be fatal due to sudden cardiac arrest.

Treatment: main directions of therapy

Treatment of diabetes mellitus is always complex and aims to control blood sugar levels, as well as neutralize the symptoms of diseases that are secondary. Modern combined drugs affect not only metabolic disorders, but also concomitant diseases. Initially, you need to bring the sugar level back to normal - sometimes this is enough to stop the further progression of the disease.

Treatment for diabetic polyneuropathy includes:

• The use of drugs to stabilize blood sugar levels.
• Taking vitamin complexes that necessarily contain vitamin E, which improves the conductivity of nerve fibers and neutralizes the negative effect of high blood sugar concentration.
• Taking B vitamins, which have a beneficial effect on the functioning of the nervous system and musculoskeletal system.
• Taking antioxidants, especially lipoic and alpha acids, which prevent the accumulation of excess glucose in the intracellular space and help restore damaged nerves.
• Taking painkillers - analgesics and local anesthetics, which neutralize pain in the extremities.
• Taking antibiotics, which may be needed in case of infection of ulcers on the legs.
• Prescribing magnesium preparations for seizures, as well as muscle relaxants for spasms.
• Prescribing drugs that correct heart rate in persistent tachycardia.
• Prescribing a minimum dose of antidepressants.
• The purpose of Actovegin is a drug that replenishes the energy resources of nerve cells.
• Local wound healing agents: capsicam, finalgon, apizartron, etc.
• Non-drug therapy: therapeutic massage, special gymnastics, physiotherapy.

Timely, based on regular preventive examinations, carrying out competent therapeutic therapy and adherence to preventive measures - all this allows you to smooth the symptoms of diabetic polyneuropathy, as well as prevent the further development of the disease. A person suffering from such a serious metabolic disorder as diabetes should be extremely attentive to their health. The presence of initial neurological symptoms, even the most insignificant ones, is a reason for urgent medical attention.

Bolgova Lyudmila Vasilievna

Moscow State University M.V. Lomonosov

Diabetic polyneuropathy: symptoms, classification and directions of treatment

Diabetes mellitus may not always manifest itself with classic, textbook symptoms such as emaciation, thirst, itching, increased urination and fatigue. This is how type 1 diabetes usually manifests itself. These are the main symptoms of the disease caused by hyperglycemia, which cannot be overlooked. But there is a more smoothed form of diabetes. For example, with type 2 diabetes, the symptoms may not be as pronounced. After many years of a sluggish course, the disease can manifest itself as complications, among which diabetic polyneuropathy of the lower extremities stands out. What does the occurrence of this complication indicate, and how is it treated?

Polyneuropathy - what is it? The very particle "neuro" in the name of the diagnosis, as it were, hints that this complication is associated with nerves. This is true, but the full name of this complication is: distal symmetric sensorimotor diabetic polyneuropathy. By this name, you can arrange walks like in a museum. Every word and even part of it carries important information to doctors. In order to understand what kind of complication it is, you can parse the meaning of the diagnosis in the literal sense of the words.

Distal

This term means that diabetes mellitus 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 nearest. That is, these are the "endings" of the body. In neurology, there is a good figurative expression: a lesion in the type of socks and gloves. It is in these areas that elevated blood sugar levels do the most damage to the nerves. This is because the myelin sheath is thinner at the periphery of the nerves (because the nerves themselves are thinner, like long branches), which is the "insulator" of the nerve fiber. She is more vulnerable to the harmful effects of sugar. In addition, it is in the periphery that blood supply disturbances 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 appear only on one leg, then this means that some kind of catastrophe with the nerves has occurred in this particular place: compression, nerve injury or other pathological process has occurred. The symmetry of the lesion suggests that the blood is to blame, which, washing hands and feet 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 are affected in almost the same way.

Sensorimotor

This word includes the meaning of defeat. Sensomotor - means 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 in the area of ​​the ankle joint, as well as on the hands and fingers, various nerves "manage" the conduction of sensitivity, and also send motor impulses to the muscles. But all of them equally suffer from excess sugar and begin to "work poorly". In particular, sensitive disorders are manifested:

• General decrease in sensitivity (hypesthesia). The patient cannot understand which toe the doctor took him by, if he does not look and move the foot.
• Paresthesias (creeping sensation) appear, and numbness may occur.
• The most excruciating sensation is hyperpathy - a perverted sensitivity in which there is an excruciating sensation of heat in the feet. They do not hurt, but rather “burn”. A patient with polyneuropathy tries to stick his legs out from under a blanket at night, often goes to the bathroom and moistens them with cold water. As long as the feet are wet, everything is fine. As soon as they dry out, unpleasant sensations appear again.

Movement (motor) disorders are manifested by suppression or complete absence of the Achilles tendon reflex, but weakness in the feet is most common. If you ask a patient with polyneuropathy to try to walk on tiptoe, and then on the 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 motor impulse, since it is "poisoned" by glucose.

Polyneuropathy

Actually, this term means that it is not the brain or spinal cord that is affected, but many nerves in 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 poisoning with salts of heavy metals (lead) or as a result of prolonged alcohol abuse (alcoholic form).

Lower limbs

Why are the legs involved? In fact, the symptoms of diabetic neuropathy 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 from the hands, because when walking, the hands are resting.
• Often patients, especially those with type 2 diabetes mellitus, are overweight, which also adversely affects the health of the legs.

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

In the treatment of polyneuropathy, means for the normalization of microcirculation ("Pentoxifylline", "Trental"), vitamins of the "B" group, preferably in the form of a combined preparation, for example, "Milgamma", are of great importance. Physiotherapeutic procedures are also used, for example, electrophoresis of thiamine or dibazol. In case of 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 is fraught with even amputation in advanced cases.

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 with this complication of diabetes mellitus is the achievement of normoglycemia, that is, a long-term decrease in blood sugar levels to normal values.

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

This complication ( diabetic polyneuropathy) is heterogeneous in nature, since 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 diabetes.

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

Epidemiology

The incidence 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 PD in all types of diabetes mellitus varies from 5 before 100% (large discrepancies in the data 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 shape (symmetrical, asymmetrical)
-motor shape (symmetrical, asymmetrical)
- sensorimotor form (symmetrical, asymmetrical)
diabetic mononeuropathy(isolated lesion of the pathways of the cranial or spinal nerves)
autonomic (autonomic) 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 radiculoneuropathies, etc.

There are three more clinical types of diabetic neuropathies of fine fibers.:
true - characterized by positive neurological symptoms, including burning, tingling, signs of distal decreased sensitivity, decreased Achilles reflex
pseudosyringomyelic- characterized by a decrease in pain and temperature sensitivity in combination with neuropathy of autonomic fibers, skin biopsy reveals a clear damage to the axons of small fibers and moderate damage to 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 inherent in diabetes mellitus.

Absolute or relative insulin deficiency is of leading importance in the mechanisms of DP.

DP is a consequence of structural and functional disorders and metabolic imbalance in 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 eliminate them from the patient.

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 greatest attention, which are directly related to structural and functional damage to nerve fibers:
glycation of proteins
polyol metabolic pathway
accumulation of sorbitol
oxidative stress
decreased activity of protein kinase C
free radical destruction of cell membranes
impaired metabolism 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 to 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 suppression 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 by a decrease in the activity of antioxidant enzymes. Oxidative stress is accompanied not only by a decrease in the content and dysfunction of natural antioxidants, but also by progressive damage to the function of nerve fibers with the further development of diabetic sensory polyneuropathy.

A nutritional factor, in particular a lack of vitamins, also plays a role in the development of DP.:
absorption of carbohydrates is impaired
signs of hypoglycemia are masked (the mechanisms of its counterregulation are suppressed - the glucagon phase of adaptation is inhibited and adrenergic precursor symptoms are leveled)
changes in the 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 diabetes development, 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.

Stage1: Subclinical DP
Stage 1 subclinical DP can be diagnosed in specialized neurophysiological departments. Such diagnostic tests are not recommended for daily use.

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

Stage 2: Clinical DP

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

2. Acute painful form:
poor diabetes control, weight loss
diffuse pain (trunk)
hyperesthesia may occur
may be associated with the initiation of antihyperglycemic therapy
minimal sensory disturbances or normal sensitivity on peripheral neurologic 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 painful, mostly at night, with minimal sensory disturbances

4. Painless DP in combination with complete or partial loss of sensitivity:
there are no symptoms or numbness of the feet, violation of temperature and pain sensitivity with the absence of reflexes

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

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

Possible on the background of DP and focal / multifocal neuropathies (mononeuropathies):
cranial nerves
torso nerves
limb nerves
proximal motor (amitrophy)
concomitant chronic inflammatory demyelinating neuropathies

The clinical manifestations of chronic sensory-motor diabetic polyneuropathy are:
pain (most often burning in nature, worse at night)
paresthesias
hyperesthesia
decreased sensitivity - vibration, temperature, pain, tactile
decreased or lost reflexes
dry skin
increase or decrease in temperature
the presence of callus (callus) in areas of high pressure

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

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

Duration of flow 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 painful diabetic neuropathy is much more common. It is characterized by a gradual onset, an intermittent course, the presence of a clear connection 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 insufficient glycemic control and the severity of neuropathic manifestations is clearly seen in patients with type 1 diabetes, while in type 2 diabetes, it is usually absent.

Diagnosis of DP

The most common signs of DP:
weakening of 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 can only be detected by electroneuromyographic examination

There are five risk factors for PD (according to the DCCT study):
1.duration of SD
2.degree of hyperglycemia
3.the patient's age
4.male gender
5.taller height

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

The considerable length of the peripheral nerve fibers predetermines the high activity of metabolic processes in them, for which they must be properly supplied with oxygen and energy. In this regard, the lower extremities, especially the feet, are most susceptible to the development of DP.

Damage to the central nervous system is diagnosed by a neuropathologist using special examination methods.

Methods for diagnosing lesions of the peripheral nervous system

Senor neuropathy
violation of vibration sensitivity
the obligatory method is a calibrated tuning fork (values ​​less than 4/8 octave of the scale on the head of the big toe)
additional method (if possible) - biotensiometry
violation of temperature sensitivity
mandatory method - touching with a warm / cold object
violation of pain sensitivity
obligatory method - tingling with a needle
violation of tactile sensitivity
obligatory method - touching the plantar surface of the foot with the monofilament
impaired proprioceptive sensitivity
an obligatory method is to identify sensitive ataxia (instability in the Rombeog position)
Motor form of neuropathy
manifestations: muscle weakness, muscle atrophy
a mandatory method - identifying the weakening or absence of tendon reflexes (Achilles, knee)
additional method (if possible) - electroneuromyography
Autonomous form of neuropathy
cardiovascular form
required method
- the manifestation of orthostatic hypotension (a decrease in blood pressure is more than or equal to 30 mm Hg with a change in body position from horizontal to vertical)
- lack of acceleration of heart rate on inspiration and deceleration on expiration
- prba Valsalva (no acceleration of heart rate when straining)
additional method (if possible)
- 24-hour monitoring of blood pressure (absence of a night decrease in blood pressure)
- 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 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 according to 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:
is performed for all patients with type 1 diabetes mellitus 5 years after the detection of the disease and for all patients with type 2 diabetes mellitus at diagnosis, then annually
determination of temperature, pain, tactile and vibration sensitivity, tendon reflexes
careful examination of the lower limbs and feet

DP treatment

!!! Until now, no treatment method has been developed that would become the gold standard for DP therapy.

primary goal to prevent DP - reaching normoglycemia

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

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

Symptomatic therapy includes measures 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 DP therapy
Currently, two main approaches have been put forward to the fore in the implementation of targeted neurotropic therapy for LTP, as in neuropharmacology in general:
the use of combined neurotropic drugs 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 from the point of view of pharmacology and clinic effects

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

The main advantages of the aforementioned combination drugs include:
the possibility of using proven standard effective combinations of biologically active substances within one dosage form (simplifying the procedure for choosing a therapeutic agent for a practitioner)
reduction of forced polypharmacy while maintaining or increasing the effectiveness of treatment
improved compliance (ease 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 (α-lipoic) acid .

The main mechanisms of action of α-lipoic acid can be summarized as follows:
Impact on energy metabolism, glucose and lipid metabolism: participation in the oxidative decarboxylation of a-keto acids (pyruvate and a-ketoglutarate) with the activation of the Krebs cycle; enhancing the uptake and utilization of glucose by the cell, oxygen consumption; increased 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 (reduction of IL1 and tumor necrosis factor); anti-inflammatory and analgesic activity (associated with antioxidant action).
Neurotropic effects: stimulation of axonal growth; positive effect on axonal transport; reducing the harmful effect 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; increasing the activity of a number of enzymes, optimizing liver function.
Detoxification effect(FOS, lead, arsenic, mercury, mercuric chloride, cyanides, phenothiazides, etc.)

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

!!! The standard course of treatment begins with the infusion of the drug at a dose of 600 mg per day intravenously drip in 150.0 ml of 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 the tabletted forms of alpha-lipoic acid in the intestine, it is recommended to take the tablets at least 30 minutes before a meal.

So an alternative scheme is 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 a 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 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) The drugs containing benfotiamine.

Benfotiamine is a lipophilic derivative of vitamin B1, which directly affects the metabolism in the nerve cell. If the penetration of ordinary (water-soluble) thiamine through cell membranes is largely limited, then the bioavailability of benfotiamine is 100%. It penetrates into nerve cells in proportion to the dose taken, reaching a high intracellular concentration. The biologically active thiamine formed from benfotiamine inside the cells 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 amounts to 250%.

Benfotiamine blocks four pathways of target cell damage with diabetes (which is the advantage of benfotiamine in comparison with other means of pathogenetic therapy of diabetes - aldose reductase inhibitors, protein kinase C inhibitors, blockers of receptors for the end products of excessive glycation, affecting only one of the pathways of alternative glucose metabolism):
polyol route
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 / Kombilipen- with pronounced manifestations, 2 ml daily for 5-7 days, then 2 ml 2-3 times a week for 2 weeks, in mild cases, 2 ml for 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 drinking 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.

With severe pain syndrome (neuropathic pain) accompanying the manifestations of DP, an effective remedy is needed to stop it.

Until now, the most common in patients with persistent severe neuropathic pain for DP, tricyclic antidepressants were prescribed. As a rule, they still use amitriptyline recommending starting therapy with low doses (25 mg) with a gradual increase in the dose 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 their use.

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

(4.1) Gabapentin belongs to the class of anticonvulsant drugs and is structurally similar to α-aminobutyric acid, which performs a neurotransmitter function and is involved in pain modulation. Gabapentin interacts with the mechanisms of transport of α-amino acids 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 diabetes mellitus with DP.

When gabapentin is prescribed, treatment should be initiated 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 in 3 doses. Monitoring should be carried out in terms of the development of side effects due primarily 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 promotes better 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 7 days of taking and achieving an analgesic effect, it is recommended to reduce the dose of the drug.

(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 compares favorably with other anticonvulsants capable of acting on various types of receptors and modulating the response of the collapsin mediator (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 oral mexiletine at a dose of 450-600 mg / day has been proven in a number of double-blind, placebo-controlled studies. On the general pain assessment scale, the improvement was not significant, but there was a significant decrease in shooting, burning pains, tingling sensations and sensations of heat. Side effects in the treatment of antiarrhythmic drugs are less pronounced compared with anticonvulsants.

(8) Some authors recommend the use of locally irritating agents 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 in achieving an analgesic effect is to use centrally acting non-opioid analgesics, which selectively affect the level of sensory neurons in the dorsal horns of the spinal cord (co-analgesics). The mechanism of action of drugs in this group is based on indirect antagonism to NMDA receptors and agonism in relation to GABA-ergic receptors in the absence of influence on receptors of serotonin, dopamine, opiates, central muscarinergic and nicotinergic, as well as benzodiazepine receptors. As a result, neuronal potassium channels are selectively activated and an analgesic effect is provided. At the same time, there is a muscle relaxant effect at the same time, which is fundamentally important in painful forms of DN.

A representative of this group of drugs is flupirtine (katadolon), which has a proven analgesic effect in pain syndromes of various etiologies (radiculoneuritis, vertebral dorsopathies, postoperative pain syndrome, oncological diseases, diseases of the musculoskeletal system, including osteoporosis, myofascial syndromes, etc.). Prescribe katadolon 100-200 mg 3-4 times a day (daily dose 600 mg).

(10) Aldose reductase inhibitors

The first clinical studies to assess the effectiveness of this group of drugs began 25 years ago. However, to date, the only drug of 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 were highly hepatotoxic, which limited their long-term use in clinical practice.

(11) In the structure of metabolic pathogenetic therapy, it is also advisable to use actovegin... It has antihypoxic activity and insulin-like effect, improves microcirculation. Usually Actovegin is prescribed at 400 mg (10 ml) intravenous stream or intravenous drip for 10-14 days, then 1 table. 3 times a day for 3 weeks. Actovegin is a highly active stimulator of oxygen and glucose utilization under conditions of ischemia and hypoxia, increasing the transport and accumulation of glucose in cells, which improves aerobic synthesis of high-energy 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 glycemic level and the prescription of drugs of pathogenetic action, symptomatic therapy is also used: for example, in case of rest tachycardia, selective β-blockers(metoprolol, bisoprolol, nebivolol), calcium channel blockers(verapamil, diltiazem) or magnesium preparations(feed magnesin, magnerot).

(13) With orthostatic hypotension shows abundant drinking, a contrast shower, elastic stockings, refusal of physical activity, abolition of antihypertensive drugs, sleeping on a bed with a raised head edge, a slight increase in salt intake. The patient needs to get up slowly from the bed and chair. If such measures are unsuccessful, the blood plasma volume 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 with intrinsic sympathomimetic activity ( pindolol, oxprenolol). Recently, an agonist has been recommended to reduce the manifestations of orthostatic hypotension. -receptors of midodrine .

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

Central muscle relaxants are a heterogeneous group that includes:
tizanidine (an alpha 2-adrenergic receptor agonist)
baclofen (GABAB receptor antagonist)
diazepam (GABAA receptor agonist)
memantine (NMDA-dependent channel inhibitor)
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, it is prescribed 2-4 mg 3 times a day (no more than 36 mg / day) and tolperisone hydrochloride (midocalm, tolperisone is prescribed at 50 (150) mg 3 times a day or intramuscularly 100 mg 2 times a day).

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

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

(15) Botulism toxin In a recent pilot, double-blind, crossover study, botulism toxin type A was shown to be effective in treating pain in 18 patients with DP. Pain reliably decreased starting from the first week after injection during 12 weeks of observation. In 44% of patients, pain reduction according to the visual analogue scale (VAS) was more than 3 points. There was also an improvement in sleep starting at 4 weeks after injection. The anti-pain effect of botulism toxin is associated with the drug's ability 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 pain associated with diabetic neuropathy. This is shown
in a double-blind, placebo-controlled study evaluating the efficacy of a spray with glyceryl trinitrate in 48 patients with painful diabetic neuropathy. Twenty-four patients in the study group applied topical glyceryl trinitrate spray to their legs during sleep for four weeks, while the other 24 used a placebo spray. Glyceryl trinitrate was well tolerated and only one patient was excluded from the study due to adverse side effects. The researchers associate the positive effect with vasodilation due to nitric oxide, a derivative of glyceryl trinitrate. Good results have been obtained with this spray in combination with valproic acid.

(17) Non-drug methods include the use of gymnastics for legs, massage and various physiotherapeutic methods (magnetotherapy, transcutaneous electroneurostimulation, 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 follow-up period, makes it possible to recommend them for inclusion in the complex therapy of DP. At the same time, care must be taken in the choice of physiotherapeutic treatment, as sensitivity disorders and autonomic disorders in DP predispose to the formation of burns and ulcers.

& nbsp & nbsp & nbsp & nbsp & nbsp & nbsp & nbsp & nbsp & nbsp13225
Date of publication: September 18, 2012

& nbsp & nbsp & nbsp & nbsp

Sensomotor polyneuropathy results in decreased ability to move or strange feelings due to nerve damage.

Causes

Neuropathy means disease or damage to the nerves. When this occurs outside of the spinal cord, it is called peripheral neuropathy. Mononeuropathy means that only one nerve is affected. Polyneuropathy means that many nerves are damaged in different parts of the body. Neuropathy can affect the nerves that provide feeling (sensory neuropathy) or the cause of movement (motor neuropathy). It can also affect movement - sensorimotor neuropathy. Sensomotor polyneuropathy is a systemic process that damages nerve cells, nerve fibers (axons), and nerve lining (myelin sheath). Damage to the coating of nerve cells causes slowing of nerve signals. Damage to nerve fibers or whole nerve cells can cause a loss of nerve robotic capacity.

Nerve damage can be caused by:

• Autoimmune disorders
• Conditions that put pressure on the nerves
• Decreased blood flow to the nervous systems
• Diseases that destroy the connective tissue that holds cells and tissues together
• Swelling (inflammation) of the nerves

Some diseases lead to polyneuropathy. Possible causes of sensorimotor polyneuropathy include:

• Alcoholic neuropathy
• Cancer (called paraneoplastic neuropathy)
• Chronic inflammatory neuropathies
• Diabetic neuropathy
• Drug-related neuropathies
• Guillain-Barré Syndrome
• Hereditary neuropathy
• Vitamin deficiency (vitamins B12, B1 and E)

Symptoms

• Decreased feeling in any area of ​​the body
• Difficulty swallowing
• Difficulty using hands
• Difficulty walking
• Pain, burning, tingling, or abnormal sensations in any part of the body (called neuralgia)
• Weakness in the face, arm, or leg, or any part of the body

Symptoms can develop rapidly (like Guillain-Barré syndrome) or slowly over several weeks to several years. Symptoms usually appear on both sides of the body. Most often, they start at the ends of the fingers.

Tests

The test can show:

• Decreased feeling (may affect touch, pain, vibration, or posture)
• Slowing down reflexes
• Muscles atrophy
• Muscles twitch
• Muscle weakness
• Paralysis

Tests can include:

• Biopsy
• Blood tests
• Electrical Muscle Test (EMG)
• Electrical tests of nerve conduction
• X-rays or other imaging tests

Treatment

Treatment goals include:

• Finding the cause
• Symptom management

Depending on the cause, treatment may include:

• Changing medicines if they cause a problem
• Blood sugar control
• Refusal of alcohol
• Nutritional supplements

Controlling symptoms

Safety is an important consideration for people with neuropathy. Lack of muscle control and decreased sensation can increase the risk of falls or other injuries. If you have movement difficulties, consider the following safety precautions:

• Remove obstructions (such as carpets on the floor that might slide on the floor).
• Water temperature test before bathing.
• Use a railing.
• Wear safety shoes (for example, closed toes and low heels).
• Wear shoes that have non-slippery soles.

Medicines used to treat this condition:

• Pain relievers to relieve stabbing pain (neuralgia)
• Anticonvulsants (gabapentin, carbamazepine, phenytoin, pregabalin)
• Antidepressants (duloxetine, amitriptyline, nortriptyline, venlafaxine)
• Lotions, creams

Avoid pain relievers whenever possible, or use only when needed. Maintain your body in the correct position.

Perspectives

You can fully recover from peripheral neuropathy if your doctor can find the cause and treat it successfully. The amount of disability is changing. Some people do not have a disability, while others have partial or complete loss of movement, function, or feeling. Nerve pain can be uncomfortable and can last for a long time. Sometimes sensorimotor polyneuropathy causes severe, life-threatening symptoms.