What is diabetic sensory polyneuropathy. Diabetic polyneuropathy

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

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

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

In distal, symmetrical, sensorimotor polyneuropathy, thin unmyelinated (C), weakly myelinated (Aσ) and thick myelinated nerve fibers (Aα, Aβ) are affected. Neuropathy predominantly affecting small fibers is characterized by loss of pain and temperature (heat and cold) sensitivity. When predominantly thick fibers are involved in the process, the speed of nerve impulse conduction is disrupted 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. The period of occurrence of pain is characteristic: at rest, during overwork, during stress and mainly at night; when walking, the pain intensity decreases, while changing the position of the limb has no effect. Acute pain syndrome due to neuropathy is described as an independent clinical entity. It is characterized by hypersensitivity and hyperalgesia. In this case, motor nerve fibers are preserved, and sensory functions are slightly affected. A similar phenomenon was called “diabetic cachexia” by Ellenberg. Acute neuropathic pain syndrome is observed 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 fibers - muscle atrophy and weakness in the distal lower extremities. When autonomic nerve fibers are involved, sweating decreases, the skin becomes dry and prone to hyperkeratosis. A so-called “risk stop” is formed. The knee and Achilles reflexes are reduced, and typical bone deformities appear: protruding heads of the metatarsal bones, hammertoes and hooked toes. The skin color is bright pink or red, and symmetrical areas of hyperpigmentation are often observed on the lower leg and dorsum of the foot (the so-called “spotted shin”). The 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 deformation of the ankle joint); changes in the configuration of the foot can be unilateral or bilateral, and the appearance of neuropathic edema is also possible. An important differential diagnostic feature is the persistence of pulsation in the arteries of the foot.

Prolonged pressure in areas of bone deformation leads to inflammatory autolysis of the underlying tissues and the formation of neuropathic ulcers, most often on the plantar surface of the foot and in the interdigital spaces. These ulcers may be painless for a certain period of time due to decreased sensitivity, and often only infection and the inflammatory process attract attention to the ulcerative defect. That's why early detection of signs of diabetic polyneuropathy is extremely important to reduce the risk of ulceration and subsequent possible amputation of the limb.

Unfortunately, there is no “gold standard” for identifying neuropathic disorders in diabetes mellitus. In 1998, San Antonio proposed consensus of standardized methods for diagnosing diabetic polyneuropathy, which recommends the following activities:

1. Identification of clinical symptoms.
2. Clinical examination: morphological and biochemical analysis.
3. Electrodiagnostic study: determination of the speed of impulse transmission 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 characteristics - VAT(Neuropathy Dysability Score). For clinical practice, this system was adapted by M. Young et al.

NSS assessment:

• burning, numbness (numbness) or crawling sensation = 2
• fatigue, cramping or soreness = 1
• spreading:
  feet = 1
  calf muscles = 1
  other = 0
• gain:
  at night = 2
  day or night = 1
  daytime = 0
  awakening from sleep = 1
• reduction:
  when walking = 2
  standing = 1
  sitting or lying down = 0

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

VAT assessment:

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

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

The minimum criteria for diagnosing diabetic neuropathy according to the NSS and VAT 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 examination of sensorimotor disorders. It includes the study of all types of sensitivity and reflexes.

Tactile sensitivity assessed using 10 g monofilament (5.07 Semmes-Weinstein). The areas to be examined 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 must be at least 2 touches at one point. The vibration sensitivity threshold is determined using a neurological tuning fork or biothesiometer. The examination is carried out at standard points: the base of the big toe and the inner ankle. Vibration sensitivity is not reduced if the patient stops feeling vibration when the tuning fork scale value corresponds to 7 UE and above. A decrease in the vibration sensitivity threshold is assessed 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, dorsum of the foot, inner ankle, shin and knee. Pain sensitivity is studied using a blunt needle or special devices (Neuropen, Pin-wheel). To analyze the state of the motor part of the nervous system, the Achilles and knee reflexes are determined using a neurological hammer. To identify autonomic neuropathy, the most accessible method in routine practice is orthostatic test.

Based on 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 - NSS = 0, normal knee reflex
• 1 B - NSS = 0, reduced knee reflex
• 2 - symptomatic neuropathy
• 2 A - NSS ≥ 1, normal knee reflex
• 2 B - NSS ≥ 1, decreased knee reflex
• 3 - severe neuropathy.

Content

A prolonged excess of glucose in the blood, having a destructive effect on blood vessels, is no less destructive for the nervous system. Polyneuropathy is a severe complication of diabetes mellitus, which can affect several large plexuses of peripheral nerves that control the functions of the lower extremities.

What is diabetic polyneuropathy

Multiple lesions of nerve fibers are observed in patients suffering from diabetes mellitus 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, breathing, digestion, and muscle contraction. Diabetic polyneuropathy of the lower extremities (DPN) is a pathology that begins in the feet and then spreads higher and higher.

The pathogenetic mechanism of the disease is very complex and is not fully understood by scientists. Disorders 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 the leg problem can turn a person into a disabled person. 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 with fatal outcomes.

Another classification is based on the functions of the nervous system that are disrupted as a result of the development of pathology:

• sensory polyneuropathy associated with increased pain in the legs, or, conversely, 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 this disease do not feel pain in certain places of the foot and lower leg. These same 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 ("rooster" 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 farthest part of the lower extremities - the feet. The typical condition for diabetics with distal DPN is a dull, aching pain, which is often so severe that the person cannot sleep. In addition, sometimes my shoulders begin to ache. Polyneuropathy progresses, and this leads to muscle atrophy, bone deformation, flat feet, and foot amputation.

Peripheral

With this type of disease, severe disorders of the sensorimotor functions of the legs occur. Diabetics suffer from pain and numbness not only in their feet, ankles, lower legs, but also in their hands. Peripheral polyneuropathy occurs mainly when doctors prescribe potent 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 discontinue the drug.

Sensory polyneuropathy

The main feature of the pathology is loss of sensation in the legs, the degree of which can vary significantly. From minor 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 moves to the second, rising higher and higher, affecting the fingers and hands, torso, and head.

Dysmetabolic

The occurrence of this type of complication is often provoked, in addition to diabetes, by diseases of the stomach, intestines, kidneys, and liver. Many nerve plexuses of the extremities may be affected. When the sciatic and femoral neurons are disturbed, pain, trophic ulcers, difficulties with movement appear, knee and tendon reflexes disappear. The ulnar, trigeminal, and optic nerves are often damaged. 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 leg polyneuropathy can be caused by:

• endocrine disorders;
• severe liver or kidney diseases;
• depression, weakened immunity;
• infections;
• alcohol abuse;
• poisoning with toxic chemicals;
• tumors.

Symptoms

The main manifestations of the disease of all types:

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

Burning and tingling in the legs

The feeling that the soles of the feet are on fire occurs when the peripheral nerve fibers that run from the spine to the feet are damaged. Burning feet are not a disease, but a symptom that manifests itself in 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

At first, the diabetic experiences weakness and numbness in the feet. Then these sensations arise in the legs and hands. As lower extremity polyneuropathy progresses, muscle atrophy increases and tactile sensitivity decreases. The feet become difficult to control and droop. The hands become numb, starting from the fingertips. With a long-term 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 examining the patient:

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

Treatment of diabetic polyneuropathy of the lower extremities

Such complications cannot be completely cured, but their development can be slowed down. How to treat neuropathy of the lower extremities? The main condition is the normalization of blood glucose. Analgesics, loose shoes, minimal walking, and cool baths help reduce pain. A contrast shower relieves burning feet. It is necessary to use drugs that dilate peripheral vessels and 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 correct carbohydrate metabolism with diet.

Drug therapy

The main means for the complex treatment of patients diagnosed with 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 restore damaged nerves;
• Actovegin, which improves blood supply to nerve endings;
• Isodibut, Olrestatin, Sorbinil, protecting nerves from glucose;
• antibiotics - if there is a threat of gangrene development.

Treatment without drugs

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

• magnetic therapy;
• electrical stimulation;
• hyperbaric oxygen therapy;
• acupuncture;
• massage;
• Exercise therapy (physical therapy).

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Among the complications of diabetes, one of the most painful and difficult to tolerate is diabetic polyneuropathy. Due to nerve damage, the patient feels muscle weakness, legs burn or burn, and there may be a feeling of numbness, severe itching, and acute long-term pain. These sensations are poorly relieved by antihistamines and simple painkillers. As a rule, symptoms intensify at night, the patient is practically deprived of normal sleep, so depression, panic attacks, and mental disorders are added to polyneuropathy.

Diabetic polyneuropathy accounts for one third of all neuropathies. The likelihood of a complication depends on the duration of diabetes: after 5 years of experience, neuropathy is diagnosed in every seventh patient; living with diabetes for 30 years increases the likelihood of nerve damage to 90%.

What is diabetic polyneuropathy

Disorders of carbohydrate and other types of metabolism in diabetes mellitus negatively affect the entire nervous system, from the brain to the endings on the skin. Damage to the central nervous system is called, peripheral -.

Neuropathy is divided into:

• sensory – with impaired sensitivity;
• motor – with damage to the nerves serving the muscles;
• autonomic, when the nerves serving a human organ are damaged.

Sensorimotor neuropathy is the most common type, most often it begins in the areas furthest from the central nervous system, usually in the lower extremities. That’s why it’s called distal, from the Latin disto – to settle. Usually changes begin on both legs at once, and they also progress symmetrically. Distal symmetric sensorimotor neuropathy is called “diabetic polyneuropathy”; it ranks first among neuropathies in prevalence, accounting for up to 70% of peripheral nerve lesions.

Thus, diabetic polyneuropathy is usually called damage to the motor fibers of skeletal muscles, mechanoreceptors of the skin, tendons, pain receptors, which occurs in diabetes mellitus in remote areas of the body.

ICD-10 code –G63.2 E10.4 – E14.4 depending on the type of diabetes.

Polyneuropathy is one of the fundamental factors in the development of the syndrome, in which infection is added to nerve damage and, as a result, deep, poorly healing ulcers form on the limb.

Types of diabetic polyneuropathy

There are 3 types of diabetic polyneuropathy:

1. Touch type. The destruction of sensory peripheral nerves predominates, which are nerve fibers of different diameters that collect information about our sensations and transmit it to the brain.
2. Motor type. There is greater destruction of the motor nerves, which are needed to transmit information to the muscles about the need to contract and relax.
3. Mixed type. In the body, all nerves work together: sensory nerves detect that the iron is hot, motor nerves carry the command to withdraw your hand to avoid a burn. Nerves are also most often damaged in a complex manner, which is why sensorimotor polyneuropathy is the most common.

Causes of the disease

The development of polyneuropathy directly depends on the level of glycemia of a diabetic patient. It has been clinically proven that the more often high sugar is observed in the blood of a diabetic, the faster all complications will progress, including polyneuropathy. If blood glucose is stably normal, 15 years after diabetes, signs of polyneuropathy are recorded in only 15% of patients, all of them in a mild form.

Causes of damage to nerve cells under conditions of hyperglycemia:

1. Metabolic disorder.

• chronic causes the body to use other ways of utilizing glucose, in which sorbitol and fructose accumulate, including in and around nerve cells. The nerve sheath, which is directly involved in the transmission of impulses, suffers from this;
• glycation of nerve cells;
• destruction of their shell by free radicals;
• lack of myelin in the nerve due to blocking the transport of myoinositol.

1. Damage to blood vessels. Due to diabetic microangiopathy, the vessels supplying the peripheral nerves are damaged.
2. Heredity. A predisposition to diabetic polyneuropathy has been identified. There is evidence that some people experience nerve damage within a few years of diabetes diagnosis, while others live for decades without this complication, despite high sugar levels.
3. Immunity disorders- the most poorly studied reason. There are versions that polyneuropathy can be provoked by antibodies to nerve growth factors, which are produced by the patient’s body itself.

Distinctive symptoms and signs

With polyneuropathy, the sensory fibers are usually the first to suffer, then the motor fibers begin to be damaged. Most often, the first symptoms are observed on the feet, and then gradually spread to all lower extremities, involving the hands and forearms, and in severe cases, the abdomen and chest.

Type of polyneuropathy	Characteristic symptoms
Sensory	Increased sensitivity, discomfort from ordinary touches or clothing. Goosebumps, numbness, superficial pain at rest for no reason. An uncharacteristic reaction of the body to an irritant, for example, itching when stroking. Decreased sensitivity. A patient with diabetic polyneuropathy ceases to feel previously familiar things: surface roughness when walking barefoot, pain when stepping on small objects. The ability of the skin to determine the temperature of water is impaired; usually hot water seems barely warm.
Motor	Fatigue sets in faster when walking, and the strength of the hands decreases. Mobility in the joints decreases, first on the fingers of the upper and lower extremities, it becomes difficult to bend them strongly and straighten them completely. Coordination of movements deteriorates, fine motor skills suffer, for example, it is impossible to thread a needle. In the future, a shaky gait, instability in a standing position is added, and muscle volume decreases. All symptoms are brighter after rest.
Sensomotor	The complex of the above symptoms; at the onset of polyneuropathy, sensory ones predominate. All signs are better felt at night or immediately after waking up.

Diabetic distal polyneuropathy

The longest nerve fibers in the human body are located in the legs. Damage to them in any area means loss of nerve function, so polyneuropathy is most often distal, localized in the lower extremities. The most serious changes are observed in the so-called “toe area” - on the feet and ankles. First of all, tactile, temperature, and then pain sensitivity are impaired.

Subsequently, changes begin in the muscles, as a result of which the appearance of the foot changes - the toes bend and overlap each other, the arch flattens. Skin that is deprived of sensitivity becomes an excellent target for various damages, which, due to concomitant nutritional disorders and the outflow of metabolic products, gradually cease to heal, forming. Constant local inflammation destroys bone tissue. As a result, distal polyneuropathy can turn into gangrene and osteomyelitis with loss of the ability to move independently.

Diabetic polyneuropathy of the lower extremities at the initial stage has symptoms such as numbness, tingling, heaviness in the feet at night, the inability to feel a light touch, a constant feeling of coldness in the toes, decreased sweating on the feet or, conversely, constantly moist skin, peeling and redness in places friction.

How to treat polyneuropathy in diabetic patients

Treatment of diabetic polyneuropathy of the lower extremities at the first stage is the achievement of permanently normal blood sugar. It has been proven that good glycemic control leads to regression of newly diagnosed neuropathy and is a prerequisite for effective treatment of severe forms of the disease.

To normalize glucose levels in the bloodstream consultation with a competent endocrinologist is necessary, who will prescribe a new treatment regimen and select more effective medications. At this stage, the patient is required to strictly follow the specialist’s recommendations, which, in addition to medications, include physical exercise and significant dietary restrictions - usually completely excluded from the diet.

Treatment without drugs

You can improve blood circulation, and therefore the nutrition of tissues in the feet, using simple non-drug methods. Several times a day you need to do a light self-massage of your feet. If the skin is dry, be sure to use a moisturizer during massage. Heating pads and hot baths are prohibited due to the danger of a burn, which a diabetic with polyneuropathy may not even feel, since the receptors on the surface of the skin are destroyed.

Under no circumstances should activity be limited. Be sure to walk for a long time every day, but at the same time make sure that your legs do not become overtired.

A simple set of exercises will be useful to improve blood circulation:

1. Sit on a chair.
2. Bend and straighten your toes.
3. Perform circular movements with your feet in different directions.
4. Pull your toes away from you and towards you.
5. Roll round objects with your feet on the floor - balls, pieces of pipe, a rolling pin.

In physiotherapy rooms, electrophoresis, paraffin baths, ultratonotherapy, radon and hydrogen sulfide baths can be prescribed to reduce pain.

Use of medications

Direction of treatment	Drugs	Dosages and course of treatment
Neutralization of free radicals	Antioxidants, most often lipoic acid: Thioctacid, Thiogamma, Neurolipon.	600 mg per day. First intravenously, then orally. From 3 weeks to six months.
Metabolism correction	Vitamins, especially group B: Vitagamma, Milgamma, Neuromultivit.	3-5 weeks, dosage is indicated in the instructions.
	Angioprotectors and circulation correctors: Actovegin	Intravenously up to 10 ml per day – 3 weeks. Orally, one tablet three times a day for at least 6 weeks.
Anesthesia	Antidepressants: Amitriptyline.	From 10 mg and above, course for at least 2 months.
	Local remedies: Capsicam, Finalgon.	Use before bedtime.
	Centrally acting analgesics: Katadolon.	100-200 mg three times a day.
	Opioids: Tramadol.	Only as prescribed by a doctor.

Popular folk remedies

There is no evidence of the effectiveness of treating diabetic polyneuropathy with folk remedies, so such therapy can be considered solely as an additional treatment to traditional methods of treatment.

Recipe No. 1

Most often, compresses made from green or blue clay are used to treat feet in diabetics. 100 g of clay is diluted to a paste with chamomile infusion (brew a bag of chamomile in a glass of water). The clay is applied to the skin slightly warm and waited for complete drying. Compresses are repeated daily for two weeks, followed by a break of the same duration.

Recipe No. 2

A popular recipe for reducing sugar using folk remedies: take equal parts of dandelion root, bean leaves, nettle leaves and galega, mix. Every morning, brew a tablespoon of this mixture in a glass of water. Drink the decoction throughout the day.

Recipe No. 3

Clove powder has antioxidant properties. It is brewed with ginger and cardamom and drunk as tea for diabetes. Proportions: a quarter teaspoon of all ingredients per mug of water.

Prevention

To prevent polyneuropathy, immediately after diagnosing diabetes mellitus, you need to completely restructure your lifestyle: control your diet, undergo training, learn how to accurately calculate the dose of insulin, and independently correct hyperglycemia. Compensation for diabetes reduces the risk of complications in the nervous system tenfold; it is possible only if the patient is active and follows all doctor’s orders.

Regular courses of vitamins (multivitamins or only group B) and lipoic acid, playing sports or simply an active lifestyle will be useful for the prevention of diabetic polyneuropathy.

Due to its toxic effect on the nervous system, you should never drink alcohol. Diabetic and alcoholic polyneuropathy in combination greatly worsens the prognosis of treatment, complications develop much faster. In addition, regular drinking makes it impossible to achieve normoglycemia.

Content

This disease is a common ailment, the symptoms of which cover a wide range of clinical manifestations. Autonomic innervation affects the most important parts of the peripheral nervous system, responsible for controlling organs and muscles. Their unstable work has a direct impact on the vital functions of the body.

What is diabetic polyneuropathy

Damage to the nerves of the peripheral system can lead to the most unpredictable consequences, ranging from foot deformation to sudden death. Diabetic neuropathy (ICD 10 code: G63.2) is rightfully considered one of the most dangerous diseases requiring urgent medical intervention. The disease affects both the somatic and autonomic nervous systems, so the failure of any of them threatens the patient with death. Simultaneous damage to the brain and spinal cord doubles the risk of sudden death.

Autonomic polyneuropathy

The disease has several forms, each of which concerns a specific area in the human body. Autonomic neuropathy in diabetes mellitus is characterized by dysfunction of certain organs or entire systems, which can lead to the development of diseases such as orthostatic hypotension or osteoarthropathy. There are different types of visceral neuropathy among patients, the most common of which are:

• urogenital form;
• respiratory form;
• cardiovascular form;
• sudomotor form;
• gastrointestinal form.

Somatic polyneuropathy

Neurological complications affecting the functioning of the peripheral system are identified in medical circles as a disease that affects the entire body. Somatic polyneuropathy is still an incompletely studied phenomenon, since it is not possible for even the most famous scientific institutions to identify the causes of its occurrence in 25% of cases.

Causes of polyneuropathy

Diabetic polyneuropathy can appear due to various factors, the most important of which is sugar decompensation. According to recent studies, therapy aimed at reducing the concentration of this substance helps stop the development of complications. However, there are other causes of diabetic polyneuropathy, for example, poisoning with chemical compounds or drugs. Often there are cases caused by chronic intoxication (vitaminosis). The following systemic pathologies can lead to the onset of the disease:

• collagenoses;
• ischemia;
• oncological diseases;
• uremia;
• hypothyroidism;
• cirrhosis.

Classification of polyneuropathy

The disease stimulates the development of a pathological process in the body, which triggers a number of complications, ranging from paralysis of the upper limbs to autonomic disorders. Such manifestations can be divided not only by etiological factor. There is a separate classification of diabetic polyneuropathy, which includes two types - the mechanism of damage and the type of nerve fiber cell.

Each of them is divided into several subtypes, for example, according to the mechanism of damage, they distinguish between neuropathic, demyelinating or axonal disease. There are several more pathologies related to the type of nerve fiber; these include: mixed, sensory, autonomic, motor and sensorimotor. The most common is sensory diabetic polyneuropathy, which causes a weakening of vibration sensitivity.

Motor polyneuropathy

Diabetes mellitus is fertile ground for the development of many serious diseases, such as axonal motor polyneuropathy. The disease is considered a very common problem among people suffering from lesions of the peripheral system or cancer. Medicine also knows other factors that influence the development of pathology - this is a hereditary predisposition or a lack of vitamin B.

Diabetic polyneuropathy is often accompanied by discomfort in the lower extremities, however, sometimes the disease also affects the hands. The skin of such patients loses its former elasticity, becomes dry and rough, as can be seen by looking at several photos on the Internet.

Sensory form of polyneuropathy

If the zone of neurons responsible for the motor functions of the body is damaged, the functioning of the motor system may be disrupted. The sensory form of diabetic polyneuropathy is considered a consequence of these complications, the main cause of which is elevated blood sugar levels. However, there are cases of other etiologies, such as neurogenic bladder or mummification of gangrenized tissue.

The most dangerous form of pathology is considered to be genetic deviations of a hereditary nature, because it is almost impossible to cure such a disease. Loss of sensation in the limbs and muscle paresis are among the main symptoms indicating the development of the disease. The patient may experience a burning, itching or tingling sensation that occurs for no apparent reason.

Distal polyneuropathy

There are several types of central nervous system lesions, such as distal or sensory-motor polyneuropathy. The first form is a very common complication that leads to the death of nerve fibers. Ultimately, the process may cause sensory loss in the lower or upper extremities, anisocoria, or strabismus. Characteristic signs of pathology include:

• muscle cramps;
• uremic itching;
• impaired pupillary reflexes;
• severe pain in the feet;
• mummification of gangrenized tissue.

The pain syndrome can reach critical conditions when the patient is unable to move or carry out other activities. During the development of a distal complication, symptoms of paresthesia are noted, covering the thighs, upper legs and even shoulders. The fingers of the lower extremities are the first to suffer, because the progression of the negative manifestations of diabetes mellitus begins with them.

Stages of diabetic polyneuropathy

Some diseases are so difficult to detect in the early stages of development that only with the help of special equipment is it possible to confirm the diagnosis. Neuropathy in diabetes mellitus has three stages of development, each of which includes certain symptoms. At first, the manifestations are completely absent, but at the second stage all the signs of the development of pathology become obvious - acute or subacute damage to some brain fibers:

• femoral;
• sciatic;
• oculomotor;
• trigeminal.

Most patients experience decreased reflexes, severe pain, burning, tingling, etc. Elderly people begin to lose weight sharply, which is also typical for patients with progressive diabetes. The third stage of the disease already requires urgent therapeutic procedures. In some cases, there is a need for surgical intervention to remove trophic ulcers or gangrene, which are initially localized on the lower extremities of the body.

Diagnosis of diabetic polyneuropathy

It will not be possible to identify the form of a complication and attribute it to a specific group of diseases without special equipment. The patient must give detailed answers regarding his state of health or make complaints regarding the functioning of organ systems. After the anamnesis, you will need to use a neurologist's kit for diagnosing diabetic neuropathy to determine blood glucose levels and perform additional procedures:

• encephalopolyneuropathy;
• study of Achilles reflexes;
• electromyography;
• EchoCG;
• general urinalysis.

How to treat neuropathy

Therapy includes an integrated approach to solving the problem after clarifying all previous measures. It is very important to determine the cause of the disease, after which treatment for polyneuropathy in diabetes mellitus can begin. Doctors prescribe glucocorticoid drugs to combat autoimmune processes in the body; in addition, patients take drugs based on potassium salts and adhere to a protein diet. All medications contain large amounts of vitamins B and C, and detoxification therapy is carried out in parallel.

Reduced blood sugar levels

There are several known methods of lowering human blood sugar levels, which are used to treat patients suffering from diabetes. Doctors recommend using not only medications to lower blood sugar, but also completely changing your diet. Food consumed during the day should exclude large amounts of easily digestible carbohydrates from entering the body. Patients are prohibited from eating foods such as pasta or potatoes. Their place should be taken by vegetables that can reduce sugar levels.

Alpha lipoic acid for diabetes

Thioctic acid is directly involved in the processes of metabolism and energy production by the body. This substance is considered the most powerful antioxidant, helps break down glucose and neutralizes the effects of free radicals. Alpha lipoic acid is sold as a dietary supplement and is used therapeutically for serious heart or liver disease. The antioxidant stimulates the processes of glucose transport, due to which their absorption occurs.

Inhibitors for diabetes mellitus

This group of substances is effectively used to treat patients suffering from hypertension. ACE inhibitors for diabetes mellitus are drugs that have a protective effect on the patient’s body. They prevent further progression of the disease, therefore they are the first choice drugs for people at any stage of diabetes. However, taking ACE inhibitors can cause negative reactions such as asymptomatic glycemia or hyperglycemia.

Nonsteroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs are often used in medicine for pain relief. The medicine is considered the most effective among other therapeutic agents, however, uncontrolled use of NSAIDs for pain can cause serious adverse reactions on the part of the patient. To prevent the development of circulatory problems, doctors conduct regular examinations of the patient's condition.

Actovegin for polyneuropathy

Antioxidant drugs help normalize metabolic disorders in the nerve; over the past few years they have been used to treat diabetes mellitus. Treatment of diabetic polyneuropathy with Actovegin is an absolutely safe procedure due to the fact that the substance does not cause side effects. For several years, not a single negative precedent involving this drug has been registered; its composition includes exclusively physiological components.

Treatment of diabetic polyneuropathy of the lower extremities

Complications caused by high blood glucose levels can lead to a variety of consequences; one of the most common cases is diabetic neuropathy of the lower extremities. With such a diagnosis, complex treatment is necessary, which will consist of medicinal and non-medicinal components. To normalize sugar levels, doctors prescribe a special diet, including taking special medications.

Treatment of polyneuropathy of the lower extremities with folk remedies

Drug therapy, with the approval of a doctor, can be supported by traditional methods of treatment as additional procedures. There are several effective recipes, some of which are intended for internal use, while others are exclusively for external application. The most extreme is considered to be trampling on the leaves and stems of nettles with bare feet. Treatment of polyneuropathy with folk home remedies can only be used under the supervision of a specialist.

Prevention of polyneuropathy

The appearance of hereditary diseases cannot be prevented, however, in all other cases, the prevention of diabetic neuropathy is an important therapeutic measure. The main points of treatment are aimed at eliminating the causes of the disease. To achieve a favorable prognosis, the patient must adhere to a special diet and lead an active lifestyle, which includes playing sports or gymnastics.

Discuss

Diabetic polyneuropathy - types, stages and treatment

Polyneuropathy- a heterogeneous group of diseases characterized by systemic damage to 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, decreased tendon reflexes, various sensory disturbances (paresthesia, hypo- and hyperesthesia) occurring in the distal limbs, and autonomic disorders. An important diagnostic point when making a diagnosis of polyneuropathy is to determine the cause of its occurrence. Treatment of polyneuropathy is symptomatic; the main goal 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 identified in polyneuropathies - axon damage and demyelination of the nerve fiber.

and the axonal type of lesion, secondary demyelination occurs; with a demyelinating lesion, the axonal component is secondary. The majority of toxic polyneuropathies, axonal type GBS, NMSN type II are primarily axonal. Primary demyelinating polyneuropathies include the classic version of GBS, CIDP, paraproteinemic polyneuropathies, and NMSF type I.

In axonal polyneuropathies, the transport function of the axial cylinder suffers mainly, carried out by the axoplasmic current, which carries a number of biological substances necessary for the normal functioning of nerve and muscle cells in the direction from the motor neuron to the muscle and back. The process involves first the nerves containing the longest axons. 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 reinnervation of muscle fibers, which leads to a change in the structure of the motor unit.

With demyelination, saltatory conduction of the nerve impulse is disrupted, 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 atrophies 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, and exposure to exotoxins. Damage to a nerve axon can be caused by exposure of nerves to exogenous or endogenous toxins or genetic factors.

Classification of polyneuropathies

To date, there is no generally accepted classification of polyneuropathies. Based on pathogenetic characteristics, polyneuropathies are divided into axonal (primarily damage to the axial cylinder) and demyelinating (myelin pathology). Based on the nature of the clinical picture, motor, sensory and autonomic polyneuropathies are distinguished. However, in their 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-Levi syndrome, Dejerine-Sotta syndrome, Refsum disease, etc.), autoimmune (Miller-Flesher syndrome, axonal type of GBS, paraproteinemic polyneuropathies, paraneoplastic neuropathies and etc.), metabolic (diabetic polyneuropathy, uremic polyneuropathy, hepatic polyneuropathy, etc.), nutritional, toxic and infectious-toxic.

Clinical picture of polyneuropathy

The clinical picture of polyneuropathy, as a rule, combines signs of damage to motor, sensory and autonomic fibers. Depending on the degree of involvement of different types of fibers, motor, sensory or autonomic symptoms may predominate in the neurological status. Damage to motor fibers leads to the development of flaccid paresis; for most polyneuropathies, damage to the upper and lower extremities with a distal distribution of muscle weakness is typical; with prolonged damage to the axon, muscle atrophy develops. Axonal and hereditary polyneuropathies are characterized by a distal distribution of muscle weakness (usually 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, stepping develops (the so-called “cock gait”).

Acquired demyelinating polyneuropathies may present with proximal muscle weakness. In severe cases, damage to the CN and respiratory muscles may occur, 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, multifocal sensorimotor neuropathy Sumner-Lewis. Tendon and periosteal reflexes with polyneuropathy usually decrease or disappear; first of all, the Achilles tendon reflexes decrease; with further development of the process, knee and carporadial reflexes; 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 occurring in the distal regions (like “gloves” and “socks”) and spreading proximally. At the onset of polyneuropathy, positive sensory symptoms (paresthesia, dysesthesia, hyperesthesia) are often detected, but with further development of the process, symptoms of irritation are replaced by symptoms of prolapse (hypoesthesia). Damage to thick myelinated fibers leads to impairment of deep muscle and vibration sensitivity, while damage to thin myelinated fibers leads to impairment of pain and temperature sensitivity of the skin.

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

Diagnosis of polyneuropathies

When identifying a slowly progressing sensorimotor polyneuropathy that begins with the peroneal muscle group, it is necessary to clarify the hereditary history, especially the presence of fatigue and weakness of the leg muscles, gait changes, and foot deformities (high instep) in relatives.

and the development of symmetrical weakness of the wrist extensors, it is necessary to exclude lead intoxication. As a rule, toxic polyneuropathies are characterized, in addition to neurological symptoms, by general weakness, increased fatigue and rarely abdominal complaints. In addition, it is necessary to find out what medications the patient has taken/is taking in order to exclude drug-induced polyneuropathy.

Slowly progressive development of asymmetric muscle weakness is the clinical feature of multifocal motor polyneuropathy. Diabetic polyneuropathy is characterized by slowly progressive hypoesthesia of the lower extremities in combination with a burning sensation and other manifestations in the feet. Uremic polyneuropathy usually occurs 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 a predominance of weakness of the extensor muscles of the feet, stepping, 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 impairment, is characteristic of multiple motor polyneuropathy. In most cases, damage to the upper extremities predominates.

Sensory polyneuropathies are characterized by a distal distribution of hypoesthesia. 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 loss and irritation of autonomic nerve fibers are possible. For vibrational polyneuropathy, hyperhidrosis and disturbances in the vascular tone of the hands are typical; for diabetic polyneuropathy, on the contrary, dry skin, trophic disorders, and autonomic dysfunction of internal organs are typical.

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 of other autoimmune neuropathies.

If polyneuropathy associated with intoxication with lead, aluminum, or mercury is suspected, blood and urine tests are performed to determine the content of heavy metals. It is possible to carry out molecular genetic analysis for all main forms of NMSI types I, IVA, IVB. Carrying out needle electromyography for polyneuropathies allows us to identify signs of the ongoing 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. A nerve biopsy is justified only if amyloid polyneuropathy is suspected (detection of amyloid deposits).

Treatment of polyneuropathies

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

To treat porphyritic 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 prednisolone. In some cases, the effectiveness of plasmapheresis and immunoglobulin is insufficient, therefore, if there are no contraindications, treatment should immediately begin with glucocorticosteroids. Improvement usually occurs within 25-30 days; After two months, you can begin to gradually reduce the dose to a maintenance dose. When reducing the dose of glucocorticosteroids, EMG monitoring is necessary. As a rule, it is possible to completely stop prednisolone within 10-12 months; if necessary, you can “insure yourself” with azathioprine (either cyclosporine or mycophenolate mofetil).

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

The main therapeutic approach in the treatment of toxic polyneuropathy is to stop contact with the toxic substance. For dose-dependent drug-induced polyneuropathies, it is necessary to adjust the dose of the appropriate drug. If the diagnosis of diphtheria is confirmed, the administration of antitoxic serum reduces the likelihood of developing diphtheria polyneuropathy. In rare cases, surgical treatment may be necessary due to the development of contractures and foot deformities. However, it should be remembered that prolonged immobility after surgery can negatively affect motor functions.

Prognosis for polyneuropathy

With chronic inflammatory demyelinating polyradiculoneuropathy, the prognosis for life is quite favorable. Mortality is very low, however, complete recovery is very rare. Up to 90% of patients achieve complete or incomplete remission during immunosuppressive therapy. 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 an improvement in the condition, since the disease progresses slowly. However, patients, as a rule, adapt to their condition and in most cases retain the ability to self-care until the very late stages of the disease. With diabetic polyneuropathy, the prognosis for life is favorable, subject to timely treatment and careful glycemic control. Only in the later stages of the disease can severe pain syndrome significantly worsen the patient’s quality of life.

The prognosis for life with uremic polyneuropathy completely depends 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 specific case, the course of dysmetabolic polyneuropathy may be different. If the disease develops early enough and manifests itself as a significant decrease in vibration sensitivity, then loss of the knee and Achilles reflexes may be observed.

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, damage to individual sections of the nerve trunks occurs. As a rule, nerve damage occurs:

1. sciatic;
2. middle;
3. elbow;
4. femoral

These problems may be accompanied by paresis of the corresponding muscle groups, pain and sensitivity disorders. If the femoral nerve has been affected, then loss of knee reflexes is observed.

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

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

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

Autonomic and trophic disorders are common in polyneuropathy. Problems with urination and postural hypotension develop.

How to treat?

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

• painkillers;
• B vitamins;
• finlepsin;
• ganglion blockers (gangleron);
• espa-lipone (berlition).

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

Polyneuropathy in systemic diseases

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

In some cases, signs of polyneuropathy may 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 cases of rheumatoid arthritis, polyneuropathy is also observed. Initially, it will manifest itself as sensory disturbances, and then as 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.

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

Hereditary polyneuropathy

First of all, this 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.

Porphyritic polyneuropathy will manifest itself due to a neurological complex of symptoms. In this case, pain, muscle weakness, and paresthesia (upper and lower extremities) occur. Motor manifestations can gradually increase, up to distal paralysis or paresis.

With this illness, 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 existing symptoms of porphyrin metabolism disorders. To get rid of the disease, the doctor recommends intravenous and oral administration of glucose in a dosage of up to 400 mg (the same treatment is indicated for other forms of polyneuropathy).

Amyloid polyneuropathy

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

• bowel disorders (constipation and diarrhea);
• pain in the digestive tract;
• heart failure;
• macroglossia (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, it does not exist at the moment.

Distal sensorimotor polyneuropathy

In diabetes mellitus, long nerve fibers are most often affected. Diabetic polyneuropathy occurs in 40% of diabetics. This type of illness 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 pain or high temperatures.

Ulcers appear on the lower extremities, and wounds on the leg fester. Serious joint damage and fractures cannot be ruled out.

Sensorimotor polyneuropathy can manifest itself with active symptoms, for example, quite severe pain in the legs, which is especially worse at night.

As the disease progresses, disturbances in the functioning of the musculoskeletal system will be observed. This happens:

• bone deformation;
• muscle dystrophy;
• excessive dryness of the skin;
• the appearance of pigment spots;
• reddish skin tone;
• dysfunction of the sweat glands.

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. The 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

If there are lesions of the autonomic nervous system against the background of diabetes mellitus, the patient will feel:

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

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

The cause of sudden death may be cardiac arrhythmia due to diabetic polyneuropathy.

Those people who suffer from this disease will experience problems with the genitourinary system - urinary incontinence occurs. The bladder will lose the ability to completely empty itself, 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 (inability to achieve orgasm).

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Polyneuropathy - what is it?

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

First of all, polyneuropathy is caused by diseases in which any substances that have a harmful effect on the nerves accumulate in the body. Such diseases include endocrine pathology and diabetes mellitus.

High levels of glucose in the blood, which last for a long time, contribute to impaired conduction of peripheral nerves. The result is diabetic polyneuropathy. It belongs to the group of dysmetabolic disorders.

If the culprit of the disease is not an ordinary substance (after all, everyone has glucose in their blood, there is simply too much of it in diabetes), but some external toxin, then toxic damage to the peripheral nerves, both sensory and motor, occurs.

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, which poison the entire body with the products of their metabolic activity and decay, can also cause nerve damage. This polyneuropathy is called paraneoplastic, and it is a serious sign of advanced cancer.

Sometimes serious infections cause nerve damage. Such polyneuropathies can be classified as both infectious and toxic - since microorganisms often use strong toxins, for example, diphtheria bacillus.

Finally, autoimmune polyneuropathies may 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 “major collagenoses”.

Symptoms of polyneuropathy - characteristic signs

The disease has an extremely characteristic clinical picture. Before reviewing the symptoms of polyneuropathy, it should be mentioned that this nerve damage can be of the following types:

• Sensitive or sensory form. Mostly sensory disorders occur: paresthesia, numbness, burning, tingling, a feeling of discomfort or “crawling.”
• Motor or motor form. Muscle weakness, muscle wasting and atrophy occurs.
• Most often there is a combined version of them - sensorimotor polyneuropathy, which occurs in most cases, and especially in diabetes and alcoholism.
• Autonomic polyneuropathy. With this course, the autonomic nerves, which “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 for all harmful substances to reach them. Therefore, most often there is damage to the hands and feet - polyneuropathy of the upper and lower extremities, the symptoms of which, as neurologists say, are of the “socks and gloves” type.

There is even a type of sensitivity disorder called the polyneuritic type. Thus, polyneuropathy of the upper 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 marbling of the skin on the back of the hands (autonomic disorders).

The most common signs of nerve damage are as follows:

1. Various and very varied pains, including those with a neuropathic, “burning” tinge.
2. Attachment of trembling of fingers.
3. The appearance of fasciculations (or muscle twitches that are involuntary).
4. Impaired sensitivity (not only tactile, which was described above, but also a decrease in temperature and pain sensitivity). That is why, with diabetic neuropathy, patients “badly feel” a pebble in a shoe, a poorly driven shoe stud and other irritants.
5. Muscle weakness, inability or significant difficulty in moving with a large amplitude. Weakness is often combined with muscle hypotonia and asthenia of the patient.

A special group consists of autonomic signs of polyneuropathy. These include hot flashes and the appearance of pallor and cold sweat, poor circulation (and poor healing of wounds and all kinds of damage to the skin).

The disease does not always develop over a long period of time and gradually. Thus, polyneuropathy of the lower extremities, the symptoms of which indicate a decrease in sensitivity, extinction of Achilles reflexes, and the presence of trophic disorders, may indicate a long-term process, or 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.

Sometimes surprising complaints arise as part of polyneuropathy. Thus, with pernicious anemia, due to a deficiency of cyanocobalamin (vitamin B 12), posterior column ataxia occurs. In this case, it is not the peripheral nerves that are affected, but the spinal cord, more precisely, its posterior cords (columns), in which the conductive bundles of joint-muscular sense, or Gaulle-Burdach bundles, are located.

What happens when they are defeated? Each of us, undoubtedly, with our eyes closed, knows how our arms and legs are positioned, even if we don’t move them. But the patient with this type of ataxia does not know. Therefore, he cannot walk in the dark, because he gets confused and does not know where and how his legs are located. But in the presence of light and visual control, such a person’s gait is normal.

There are special autonomic or autonomic neuropathies that disrupt the heart rhythm and can even lead to sudden death due to ventricular asystole or other fatal arrhythmias. This polyneuropathy is an autonomic 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, making the correct diagnosis does not cause difficulties.

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

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

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Forms

Sensorimotor polyneuropathy varies according to many criteria. According to the nature of the process, acute and chronic disease are distinguished. In addition, there are three forms:

1. Demyelinating polyneuropathy is associated with myelin breakdown. Myelin is the protein that surrounds the nerve fiber and also mediates 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 a foreign membrane, destroying it. If you carry out treatment, you can avoid complications and achieve recovery.
2. The axonal form of pathology is associated with a violation of the functional characteristics of the axon and the nerve shaft. Due to the disruption of nerve nutrition, the symptoms of the disease are dangerous and 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, there is another classification of the disease:

• The sensory form of polyneuropathy is characterized by damage to the nerves responsible for sensory function. The sensory form causes symptoms in the patient such as soreness, numbness and burning in the affected parts of the body.
• The motor form affects the motor fibers, therefore the muscular system suffers. Symptoms of muscle weakness and atrophy appear.
• The autonomic form of polyneuropathy involves the nerves of the autonomic system. 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 disease.

Reasons

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

Dysmetabolic inflammatory neuropathy occurs when there are disruptions in the body's metabolic processes. One type of pathology occurs during the onset of infection. This could be the human immunodeficiency virus, infections that damage the immune system, or forms of diphtheria. This is how post-infectious polyneuropathy is formed.

The causes of the pathology lie in the toxic effect on the body. Alcohol and its derivatives destroy the nervous system. Metals and toxins can also affect the immune system and nervous system. This could be lead, mercury, or antibiotic poisoning.

Causes such as allergic processes lead to an autoimmune reaction of the body, which can lead to acute or chronic polyneuropathy. Diseases such as scleroderma, lupus, vasculitis affect connective tissue and 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. Several factors are required; there may also be poor quality treatment and lifestyle changes that allow one to contract the disease.

Symptoms

The prefix “poly” in the name of the disease means a combination of many symptoms and the involvement of several parts of the body and organs in the process. The symptoms of polyneuropathy are wide-ranging and depend on the nerves affected and the immune defenses.

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

The following symptoms are typical:

When blood vessels and organs are damaged, symptoms of blood pressure disorders appear. Blood pressure numbers can reach high levels, which threatens a stroke. The effect on the heart is caused by symptoms of rapid heartbeat (tachycardia).

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

In most cases, at first the symptoms are minor, but over time, decreased muscle tone, atrophy, and hypersthesia appear. So, the patient experiences an unsteady gait, attacks of dizziness, and nausea. If the disease affects internal organs, their functioning is disrupted.

Survey

Diagnosis of polyneuropathy is not carried out at home and must be comprehensive. Concomitant pathologies 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 studying the patient's history and complaints. Also, such facts from life as the presence of injuries, alcohol consumption, work and leisure habits, and past illnesses are revealed. This is necessary to select treatment. It is important to establish hereditary factors, for which the anamnesis of relatives is studied.

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

Treatment

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

In case of illness, the diet excludes alcohol and fatty foods. It is necessary to replenish the supply of vitamins and microelements. To improve nerve function, B vitamins are prescribed. Metabolic treatment can improve tissue function and nutrition.

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

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

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

Prevention means treating foci of infection and inflammation. To prevent illness, they strengthen the immune system and nerves. And as you age, you need to undergo regular medical examinations.

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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 the opposite in meaning to the word “proximal,” that is, closest. That is, these are the “endings” of the body. In neurology, there is a good figurative expression: a sock-and-glove lesion. It is in these places that elevated blood sugar levels do the most damage to the nerves. This happens because at the periphery of the nerves the myelin sheath is thinner (because the nerves themselves are thinner, like long branches), which is an “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 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 causes harm. In this case, chronic, long-term hyperglycemia—high blood sugar—is to blame. Patients feel that their legs and arms suffer almost equally.

Sensorimotor

This word includes the meaning of defeat. Sensorimotor - means sensory plus motor form, that is, a sensitivity disorder (sensory disorders), which is combined with motor disorders, that is, movement disorders. Of course, on the feet and in the ankle area, 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 suffer equally from excess sugar and begin to “perform poorly.” In particular, sensory disorders manifest themselves:

• General decrease in sensitivity (hypoesthesia). The patient cannot understand which toe the doctor grabbed unless he looks and moves his foot.
• Paresthesia (a crawling sensation) appears, and numbness may occur.
• The most painful sensation is hyperpathy - a perverted sensitivity that causes a painful sensation of heat in the feet. They do not hurt, but seem to “burn.” A patient with polyneuropathy tries to stick his legs out from under the blanket at night, often goes to the bathroom and wets them with cold water. As long as your feet are wet, everything is fine. As soon as they dry out, the unpleasant sensations appear again.

Movement (motor) disorders are manifested by depression or complete absence of the Achilles tendon reflex, but weakness in the feet most often occurs. If you ask a patient with polyneuropathy to try to walk on tiptoes, and then on his heels, then most likely he will not succeed or it will turn 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” with glucose.

Actually, this term means that it is not the brain or spinal cord that is affected, but many nerves in the periphery (poly means many). It is this “scattered” 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 due to prolonged abuse of alcohol (alcoholic form).

Lower limbs

Why are the legs involved? In fact, the symptoms of neuropathy in diabetes also appear in the arms, 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 prerequisites already exist 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 their legs.

Now everyone knows what this complex diagnosis means. Treatment of diabetic polyneuropathy is no less complex: it is impossible in one day or even a month to completely eliminate toxic damage to the nerves by glucose, which has lasted for years. 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, preferably in the form of a combination drug, for example, Milgamma, are of great importance. Physiotherapeutic procedures are also used, for example, electrophoresis of thiamine or dibazole. With polyneuropathy, it is very important to maintain 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 “diabetic foot”, which can even lead to 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 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 mellitus 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, breathing, digestion, and muscle contraction. Diabetic polyneuropathy of the lower extremities (DPN) is a pathology that begins in the feet and then spreads higher and higher.

The pathogenetic mechanism of the disease is very complex and is not fully understood by scientists. Disorders 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 the leg problem can turn a person into a disabled person. 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 that are disrupted as a result of the development of pathology:

• sensory polyneuropathy associated with increased pain in the lower extremities, or, conversely, 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 this disease do not feel pain in certain places of the foot and lower leg. These same 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 ("rooster" 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 farthest part of the lower extremities - the feet. The typical condition for diabetics with distal DPN is a dull, aching pain, which is often so severe that the person cannot sleep. In addition, sometimes my shoulders begin to ache. Polyneuropathy progresses, and this leads to muscle atrophy, bone deformation, flat feet, and foot amputation.

Peripheral neuropathy of the lower extremities

With this type of disease, severe disorders of the sensorimotor functions of the legs occur. Diabetics suffer from pain and numbness not only in their feet, ankles, lower legs, but also in their hands. Peripheral polyneuropathy occurs mainly when doctors prescribe potent 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 discontinue the drug.

Sensory polyneuropathy

The main feature of the pathology is loss of sensation in the lower extremities, the degree of which can vary significantly. From minor 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 moves to the second, rising higher and higher, affecting the fingers and hands, torso, and head.

Dysmetabolic polyneuropathy

The occurrence of this type of complication is often provoked, in addition to diabetes, by diseases of the stomach, intestines, kidneys, and liver. Many nerve plexuses of the extremities may be affected. When the sciatic and femoral neurons are disturbed, pain, trophic ulcers, difficulties with movement appear, knee and tendon reflexes disappear. The ulnar, trigeminal, and optic nerves are often damaged. 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 lower extremity polyneuropathy can be caused by:

• endocrine disorders;
• severe liver or kidney diseases;
• depression, weakened immunity;
• infections;
• alcohol abuse;
• 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 worsening of the perception of temperature changes, vibration.
2. Motor symptoms - convulsions, tremor, muscular atrophy of the limbs.
3. Autonomic symptoms - edema, hypotension, tachycardia, stool disorders, impotence.

Burning and tingling of the lower extremities

The feeling that the soles of the feet are on fire occurs when the peripheral nerve fibers that run from the spine to the feet are damaged. Burning feet are not a disease, but a symptom that manifests itself in 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

At first, the diabetic experiences weakness and numbness in the feet. Then these sensations arise in the legs and hands. As lower extremity polyneuropathy progresses, muscle atrophy increases and tactile sensitivity decreases. The feet become difficult to control and droop. The hands become numb, starting from the fingertips. With a long-term 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 examining the patient:

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

Treatment of diabetic polyneuropathy of the lower extremities

Such complications cannot be completely cured, but their development can be slowed down. How to treat neuropathy of the lower extremities? The main condition is the normalization of blood glucose. Analgesics, loose shoes, minimal walking, and cool baths help reduce pain. A contrast shower relieves burning feet. It is necessary to use drugs that dilate peripheral vessels and 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 correct carbohydrate metabolism with diet.

Drug therapy

The main means for the complex treatment of patients diagnosed with 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 restore damaged nerves;
• Actovegin, which improves blood supply to nerve endings;
• Isodibut, Olrestatin, Sorbinil, protecting nerves from glucose;
• antibiotics - if there is a threat of gangrene development.

Treatment of neuropathy in diabetes without drugs

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

• magnetic therapy;
• electrical stimulation;
• hyperbaric oxygen therapy;
• acupuncture;
• massage;
• Exercise therapy (physical therapy).

vrachmedik.ru

The disease in question, 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, the distal parts of the limbs are primarily 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 foot area and gradually spread up the limb. Depending on the typology of nerve fibers that are subject to destruction to a greater extent, all types of polyneuropathy are conventionally divided into four subgroups.

Due to damage mainly to the afferent long processes of neurons, patients experience positive or negative symptoms. The first is characterized by the absence of function or its decrease; positive symptoms are those manifestations that have not previously been observed.

In the first turn, in patients with the disease in question, various types of paresthesia are manifested, such as burning, tingling, crawling, and numbness. Then the clinical picture is complicated by algias of varying intensity, and the susceptibility to painful stimuli increases. As symptoms increase, patients become overly sensitive to simple touches. Later, they experience manifestations of sensitive ataxia, expressed in unsteady gait, especially with closed eyes, and impaired coordination of movement. Negative symptoms of polyneuropathy include decreased sensitivity in areas where nerve fibers are damaged.

When the axons of movement neurons are damaged, polyneuropathy of the upper and lower extremities manifests itself, firstly, as muscle atrophy and is found in weakness of the legs and arms. The described symptoms progress to the occurrence of paralysis and paresis. Less commonly, a condition can be observed that is manifested by unpleasant sensations in the legs, appearing mainly at rest and forcing people to make movements of a relieving nature (restless lower limbs syndrome). In addition, fasciculations and convulsions may occur.

Autonomic dysfunctions are divided into trophic disorders and vascular disorders. The first include the appearance of pigmentation and peeling of the skin, the appearance of cracks and ulcers on the extremities. Vascular disorders include a feeling of cold in the damaged segments, dullness of the skin (the so-called “marble pallor”).

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

Polyneuropathy of the lower extremities

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

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

To determine the reasons that provoke the development of the described illness, first of all, it is necessary to understand 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 live in 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, manifestations of the disease are observed in certain areas. The pathology in question on the limbs manifests itself symmetrically.

It should be noted that the pathology under consideration has several varieties, which are classified depending on the functions of the damaged nerves. For example, if the neurons responsible for movement are damaged, the ability to move may be lost or impaired. This type of polyneuropathy is called motor polyneuropathy.

In the sensory form of the disorder in question, the nerve fibers that cause sensitivity are affected, which greatly suffers 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 that provoke the development of this disease are identified: metabolic (associated with metabolic disorders), autoimmune, hereditary, nutritional (caused by nutritional 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, myelin, the substance that forms the sheath of nerves, is affected; in the axonal form, the axial cylinder is damaged.

The axonal form of leg polyneuropathy is observed in all types of the disease. The difference lies in the prevalence of the type of disorder, 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 within 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, and methyl alcohol. The acute form can last more than ten days.

Symptoms of the subacute form of polyneuropathy increase over a couple of weeks. This form often occurs with metabolic disorders or due to toxicosis. Recovery usually occurs slowly and may take many months.

The chronic form often progresses over a long period of time, six months or more. The disease usually appears against the background of alcoholism, diabetes, lymphoma, blood diseases, and deficiency of vitamins thiamine (B1) or cyanocobalamin (B12).

Among axonal polyneuropathies, alcoholic polyneuropathy, caused by prolonged and excessive abuse of alcohol-containing liquids, is most often diagnosed. A significant role for the occurrence of the pathology in question is played not only by the number of “absorbed liters” of alcohol, but also by the quality of the product consumed, since many alcoholic drinks contain many substances toxic to the body.

The main factor provoking alcoholic polyneuropathy is the negative impact of toxins that alcohol is rich in on nerve processes, which leads to metabolic disorders. In most cases, the pathology in question is characterized by a subacute course. Initially, numbness occurs in the distal segments of the lower extremities, and severe pain occurs in the calf muscles. As pressure increases, pain in the muscles increases noticeably.

At the next stage of development of the disease, dysfunction of mainly the lower extremities is observed, which is expressed by weakness, often even paralysis. The nerves that cause flexion and extension of the foot are the most damaged. In addition, the sensitivity of the superficial layers of the dermis in the area of ​​the hands, like a “glove,” and the feet, like a “sock,” is disrupted.

In some cases, this disease can have an acute course. This mainly occurs 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 of the skin of the legs and the temperature of the extremities, swelling of the distal parts of the legs (less often the arms), and increased sweating. The disease in question can sometimes affect the cranial nerves, namely the oculomotor and optic nerves.

The described disturbances are usually detected and increase over several weeks/months. This disease can last for several years. When you stop drinking alcohol, the disease can be overcome.

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

This form of the disease is relatively rare. Most often, this disease affects the adult male population, although it can also occur in the weaker half and children. Demyelinating polyneuropathy usually manifests itself as 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 etiological factor of this form of the disease are, unfortunately, not known for certain today, 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 begins to produce specific antibodies. In this form of pathology, antigens attack the cells of the nerve roots, causing destruction of their membrane (myelin), thereby provoking an inflammatory process. As a result of such attacks, nerve endings lose their fundamental functions, which causes disruption of 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 activity, infection of the body, emotional stress, vaccination, injury, 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 disorder in question does not arise independently. Therefore, when the first manifestations and signs of the disease are detected, it is necessary to immediately establish the etiological factor, since treatment, for example, of diabetic polyneuropathy differs from the treatment of pathology caused by alcohol abuse.

Polyneuropathy of the upper extremities

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

Signs of hand polyneuropathy are almost always the same. Patients experience increased sweating, impaired pain sensitivity, thermoregulation, skin nutrition, changes in tactile sensitivity, and paresthesia in the form of “goosebumps” appears. 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 arms, various algias, which in their content are burning or bursting, swelling, and occasionally tingling may be felt. With this pathology, vibration sensitivity is impaired, as a result of which patients often experience difficulties in performing basic manipulations. Sometimes people suffering from polyneuropathy experience decreased sensitivity in their hands.

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

The described disease can occur differently in each patient.

According to pathogenesis, polyneuropathy of the upper extremities can be divided into axonal and demyelinating, and according to clinical manifestations into: vegetative, sensory and motor. It is quite difficult to encounter the listed varieties of this disease in their pure form; more often the disease combines the symptoms of several variations.

Treatment of polyneuropathy

Today, treatment methods for the disease in question are quite scarce. Therefore, to this day, the treatment of polyneuropathies of various forms remains a serious problem. The level of knowledge of modern physicians in the field of the pathogenetic aspect and etiological factor of this category of diseases has determined the advisability of identifying two areas of therapeutic intervention, namely undifferentiated methods and differentiated ones.

Differentiated methods of therapeutic correction involve treatment of the underlying ailment (for example, nephropathy, diabetes) for endogenous intoxications; for pathologies of the digestive system caused by malabsorption, they require the administration of large dosages of vitamins B1 (thiamine) and B12 (cyanocobalamin).

For example, diabetic polyneuropathy is treated with drugs and their choice is determined by maintaining a certain glycemic level. Therapy for polyneuropathy due to diabetes should be gradual. At the first stage, you should adjust your body weight and diet, develop a set of special physical exercises, and monitor your blood pressure levels to normal. Pathogenetic methods of therapy involve the use of neurotropic vitamins and the injection of alpha-lipoic acid in large dosages.

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

Polyneuropathy treatment drugs should be prescribed in combination. The specificity of the choice of therapeutic measures for the pathology in question always depends on the etiological factor that provoked the disease and determined its course. For example, the symptoms of polyneuropathy caused by excess levels of pyridoxine (vitamin B6) disappear without a trace after its level is normalized.

Polyneuropathy caused by a cancerous process is treated by surgery - removal of the tumor that was putting pressure on the nerve endings. If the disease occurs against the background of hypothyroidism, then hormonal therapy is used.

Treatment of toxic polyneuropathy, first of all, 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 relieving pain and eliminating muscle weakness.

In these cases, standard physiotherapeutic methods and the prescription of a number of medications are used to relieve or relieve pain caused by damage to nerve fibers. In addition, physiotherapy methods are actively used at all stages of rehabilitation treatment.

It is quite difficult to overcome algia with the help of analgesic drugs or non-steroidal anti-inflammatory drugs. Therefore, it is more common to prescribe local anesthetics, anticonvulsants and antidepressants to relieve attacks of pain.

The effectiveness of antidepressants lies in their ability to activate the noradrenergic system. The choice of drugs in this group is determined 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.