Diabetes mellitus is a common disease throughout the world. The clinical course of the disease is often accompanied by the development of chronic complications. One of the complications of the disease is diabetic polyneuropathy.
Chronic diabetic (sensomotor) polyneuropathy is a common form of neuropathy that is accompanied by sensory, autonomic and motor disorders.
ICD-10 code
E 10.42 diabetic polyneuropathy in type 1 diabetes,
E11.42 diabetic polyneuropathy in type 2 diabetes,
G 63.2 diabetic distal polyneuropathy.
Diabetic polyneuropathy is accompanied by pain and significantly reduces the standard of living of patients.
The development of the disease can lead to even more serious complications. Such as: ataxia, Charcot's joint, diabetic foot syndrome, diabetic osteoarthropathy.
Diabetic polyneuropathy of the extremities can lead to gangrene and subsequent amputation.
Therefore, it is important to prevent development, and start effective treatment already at the first signs in patients with diabetes mellitus.
The main etiological factors that provoke the development of diabetic polyneuropathy are considered to be:
Numerous studies indicate that constant monitoring of glucose levels and blood pressure significantly reduces the development of pathology. And the timely use of insulin therapy reduces the risk of development by half.
Symptoms of diabetic polyneuropathy are manifested by pain in the lower extremities. Burning, dull or itching pain, less often sharp, stabbing and penetrating. It often occurs in the foot and intensifies in the evening. In the future, pain may appear in the lower third of the lower leg and arms.
Patients complain of frequent muscle numbness, joint pain, gait disturbance. This is due to the development of disorders in the nervous system. Temperature sensitivity is lost, trophic ulcers may appear.
The patient experiences discomfort from the touch of clothing. The pain syndrome in such cases is permanent and significantly worsens the general well-being of the patient.
How to identify and clarify the diagnosis?
Diagnosis of polyneuropathy begins with a visit to a doctor who carefully collects an anamnesis and prescribes the necessary types of research.
As the main study, preference is given to electroneuromyography. In addition, studies of VKSP (vegetative skin sympathetic potentials) can be used.
After the diagnosis of diabetic polyneuropathy is established, treatment begins with etiotropic therapy. It is important to normalize the level of glucose in the blood. After constant monitoring, in 70% of cases, pain is reduced. In some cases, insulin therapy is prescribed.
In the treatment regimen for oxidative stress, to restore the affected, prescribe medications with a pronounced antioxidant effect. The drugs are taken in courses for quite a long time. During this period, the patient is monitored and monitored.
Analgesics and anti-inflammatory drugs are prescribed to relieve pain. But, as experts point out, they are not able to completely get rid of pain, and long-term use can harm the proper functioning of the stomach.
For symptoms of chronic neuropathic pain, anesthetics, antidepressants, and antiepileptic drugs are prescribed. As an addition to the drugs, it is recommended to use patches with lidocaine, gels, ointments and creams.
As a consolidation of the complex treatment of diabetic polyneuropathy, depending on the patient's condition, the following is prescribed:
Treatment folk remedies allowed only with the consent of the attending physician. As an addition to traditional methods of treatment, herbal medicine and the use of healing ointments can be used.
Effective treatment of diabetic polyneuropathy is considered to be an individual approach of a doctor to each patient with a complex of conservative methods of treatment.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
Alcoholic polyneuropathy is a neurological disease that causes dysfunction of many peripheral nerves. The disease occurs in people who abuse alcohol in the later stages of the development of alcoholism. Due to the toxic effect on the nerves of alcohol and its metabolites and the subsequent disruption of metabolic processes, pathological changes develop in the nerve fibers. The disease is classified as an axonopathy with secondary demyelination.
Clinical signs of the disease and their connection with excessive alcohol consumption were described in 1787 by Lettsom, and in 1822 by Jackson.
Alcoholic polyneuropathy is detected in people who drink alcohol of any age and gender (with a slight predominance in women), and does not depend on race and nationality. On average, the frequency of distribution is 1-2 cases per thousand. population (about 9% of all diseases that occur with alcohol abuse).
Depending on the clinical picture of the disease, there are:
Depending on the course of the disease, there are:
Asymptomatic forms of the disease are also found in patients with chronic alcoholism.
The etiology of the disease is not fully understood. According to existing data, about 76% of all cases of the disease are provoked by the reactivity of the body in the presence of alcohol dependence for 5 years or more. Alcoholic polyneuropathy develops as a result of hypothermia and other provoking factors in women more often than in men.
Also, the development of the disease is influenced by autoimmune processes, and certain viruses and bacteria are the triggering factor.
Causes liver disease and dysfunction.
All forms of the disease develop as a result of the direct influence of ethyl alcohol and its metabolites on the peripheral nerves. The development of the motor and mixed forms is also affected by a deficiency in the body of thiamine (vitamin B1).
Hypovitaminosis of thiamine in alcohol-dependent patients occurs as a result of:
At the same time, the utilization of alcohol requires a large amount of thiamine, so drinking alcohol increases thiamine deficiency.
Ethanol and its metabolites increase glutamate neurotoxicity (glutamate is the main excitatory neurotransmitter of the central nervous system).
The toxic effects of alcohol have been confirmed by studies that demonstrate a direct relationship between the severity of alcoholic polyneuropathy and the amount of ethanol taken.
A condition for the development of a severe form of the disease is an increased vulnerability of the nervous tissue resulting from a hereditary predisposition.
Although the pathogenesis of the disease is not fully understood, it is known that the main target in the acute form of alcoholic polyneuropathy are axons (transmitting impulses, cylindrical processes of nerve cells). The lesion affects thick myelinated and thin weakly myelinated or unmyelinated nerve fibers.
The increased vulnerability of the nervous tissue is the result of the high sensitivity of neurons to various metabolic disorders, and especially to thiamine deficiency. Hypovitaminosis of thiamine and insufficient formation of thiamine pyrophosphate causes a decrease in the activity of a number of enzymes (PDH, a-CGCH and transketolase) involved in carbohydrate catabolism, the biosynthesis of certain cell elements and the synthesis of nucleic acid precursors. Infectious diseases, bleeding and a number of other factors that increase the energy needs of the body exacerbate the deficiency of B vitamins, ascorbic and nicotinic acid, reduce the level of magnesium and potassium in the blood, and provoke protein deficiency.
With chronic alcohol consumption, the release of p-endorphins from hypothalamic neurons decreases, and the p-endorphin response to ethanol decreases.
Chronic alcohol intoxication causes an increase in the concentration of protein kinase, which increases the excitability of primary afferent neurons and increases the sensitivity of peripheral endings.
Alcoholic damage to the peripheral nervous system also causes excessive formation of free oxygen radicals, which disrupt the activity of the endothelium (a layer of flat cells lining the inner surface of the vessels that perform endocrine functions), cause endoneural hypoxia (endoneural cells cover the myelin sheath of the nerve fibers of the spinal cord) and lead to cell damage .
The pathological process can also affect Schwann cells, which are located along the axons of nerve fibers and perform a supporting (supporting) and nutritional function. These support cells of the nervous tissue create the myelin sheath of neurons, but in some cases they destroy it.
In the acute form of alcoholic polyneuropathy, under the influence of pathogens, antigen-specific T- and B-cells are activated, which cause the appearance of anti-glycolipid or anti-ganglioside antibodies. Under the influence of these antibodies, local inflammatory reactions develop, the set of blood plasma proteins involved in the immune response (complement) is activated, and a membranolytic attack complex is deposited in the area of Ranvier's interception on the myelin sheath. The result of the deposition of this complex is a rapidly increasing infection of the myelin sheath with hypersensitive macrophages, and the subsequent destruction of the sheath.
In most cases, alcoholic polyneuropathy is manifested by motor or sensory disorders in the limbs, and in some cases, muscle pain of various localization. Pain can occur simultaneously with movement disorders, numbness, tingling, and crawling (paresthesia).
The first symptoms of the disease are manifested in paresthesia and muscle weakness. In half of the cases, the disorders initially affect the lower extremities, and after a few hours or days they spread to the upper ones. Sometimes in patients, the arms and legs are affected at the same time.
Most patients experience:
Violation of mimic muscles is possible, and in severe forms of the disease - urinary retention. These symptoms persist for 3-5 days, and then they disappear.
Alcoholic polyneuropathy in the advanced stage of the disease is characterized by the presence of:
For severe cases of the disease is also characteristic:
Pain in alcoholic polyneuropathy is more common in forms of the disease that are not associated with thiamine deficiency. It can be aching or burning in nature and localized in the foot area, but its radicular character is more often observed, in which pain sensations are localized along the affected nerve.
In severe cases of the disease, damage to the II, III and X pairs of cranial nerves is observed.
The most severe cases are characterized by mental disorders.
Alcoholic polyneuropathy of the lower extremities is accompanied by:
Painful phenomena can increase for weeks or even months, after which the stationary stage begins. With adequate treatment, the stage of reverse development of the disease begins.
Alcoholic polyneuropathy is diagnosed based on:
In doubtful cases, MRI and CT are performed to rule out other diseases.
Treatment for alcoholic polyneuropathy of the lower extremities includes:
With medical treatment are prescribed:
In the presence of toxic liver damage, hepatoprotectors are used.
Symptomatic therapy is used to correct autonomic disorders.
Alcoholic polyneuropathy is a common complication of alcohol abuse. As a doctor, I can say that this is a very dangerous complication. And it is dangerous, among other things, that it sneaks up unnoticed and often until the last patient does not understand that he is already sick. It is no longer worth doing sports, especially active ones - only exercise therapy, swimming, massages, physiotherapy. Mandatory drug therapy - B vitamins such as neuromultivit or combilipen, thioctic acid preparations (thioctacid bv), possibly neuromedin, if indicated.
Doctor Belyaeva, my sister is sick, she has fear, frequent urges (sometimes with an interval of 2 minutes), but naturally she doesn’t go to the toilet, she is afraid to eat, she constantly says that she is dying, but she eats everything, walks along the wall (to the toilet), what do you recommend?
My sister is sick, she has fear, frequent urges, although she doesn’t want to go to the toilet and immediately forgets, she walks “on the wall”.
Polyneuropathy (polyradiculoneuropathy) is a multiple lesion of peripheral nerves, manifested by peripheral flaccid paralysis, sensory disturbances, trophic and vegetovascular disorders, mainly in the distal extremities. This is a common symmetrical pathological process, usually distal localization, gradually spreading proximally.
Most often associated with suicidal or criminal poisoning and occur against the background of a picture of severe intoxication with arsenic, organophosphorus compounds, methyl alcohol, carbon monoxide, etc. The clinical picture of polyneuropathies usually unfolds within 2-4 days, and then the cure occurs within a few weeks .
They develop within a few weeks, which is typical for many cases of toxic and metabolic neuropathies, but an even greater number of the latter last for months.
Progress over a long time: from 6 months or more. It develops most often in chronic alcohol intoxication (alcoholic polyneuropathy), beriberi (group B) and systemic diseases such as diabetes mellitus, uremia, biliary cirrhosis, amyloidosis, cancer, lymphoma, blood diseases, collagenoses. Of the drugs, special attention should be paid to metronidazole, amiodarone, furadonin, isoniazid and apressin, which have a neurotropic effect.
Described by the French neuropathologists G. Guillain and J. Barre in 1916. The cause of the disease remains insufficiently elucidated. It often develops after a previous acute infection. It is possible that the disease is caused by a filterable virus, but since it has not been isolated to date, most researchers consider the nature of the disease to be allergic. The disease is considered to be autoimmune with destruction of nervous tissue secondary to cellular immune responses. Inflammatory infiltrates are found in peripheral nerves, as well as roots, combined with segmental demyelination.
1-2 weeks after the onset of the disease, signs of damage to the cranial nerves of the bulbar group may occur: paresis of the soft palate, tongue, phonation disorder, swallowing; breathing disorders are possible, especially when the phrenic nerve is involved in the process. The defeat of the vagus nerve can cause brady- and tachycardia, arrhythmia. The oculomotor nerves are often involved in the process, which is manifested by an accommodation disorder. Less common is paresis of the external eye muscles innervated by III, IV and VI cranial nerves. Polyneuropathy in the extremities is usually manifested by late (on the 3-4th week) flaccid paresis with a disorder of superficial and deep sensitivity, which leads to sensitive ataxia. Sometimes the only manifestation of late diphtheria polyneuropathy is the loss of tendon reflexes.
If the early manifestations of neuropathy of the cranial nerves in diphtheria are associated with the direct entry of the toxin from the lesion, then the late manifestations of neuropathy of the peripheral nerves are associated with the hematogenous spread of the toxin. Treatment is carried out according to the etiological and symptomatic principles.
These are neuropathies of heterogeneous origin; have an acquired character, their course is undulating, relapsing. Clinically, they are similar to the previous form, but there are also differences in the rate of development of the disease, in its very course, as well as in the absence of clear provocative moments, triggers.
Meet more often than subacute. These are hereditary, inflammatory, drug-induced neuropathies, as well as other acquired forms: in diabetes mellitus, hypothyroidism, dysproteinemia, multiple myeloma, cancer, lymphoma, etc. processes. Very often it remains unknown which process is primary - axonal degeneration or demyelination.
It develops in people with diabetes. Polyneuropathy may be the first manifestation of diabetes mellitus or occur many years after the onset of the disease. Polyneuropathy syndrome occurs in almost half of patients with diabetes mellitus.
Treatment of polyneuropathies depends on their type. Alphalipolic acid preparations (thiogamma, thioctacid, berlition, espolidon, etc.) and vitamin B complexes are often used. These drugs maximally stimulate the potential for reinnervation. For the treatment of demyelinating polyneuropathy, in addition to pharmacotherapy, agents are used that block pathological autoimmune mechanisms: the administration of immunoglobulins and plasmapheresis. In the period of remission of the disease, complex rehabilitation plays an important role.
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Polyneuropathy is a complex of diseases, including multiple lesions of peripheral nerves. The disease most often passes into the chronic stage and has an ascending path of spread, that is, the process initially affects small fibers and gradually covers larger and larger branches.
The classification of polyneuropathy according to ICD 10 is officially recognized, but does not take into account the individual characteristics of the course and does not describe treatment tactics.
The clinical picture is primarily based on disorders of the musculoskeletal system and the cardiovascular system. The patient complains of pain in the muscles, their weakness, convulsions and lack of ability to move normally (paresis of the lower extremities). To the general symptoms is added an increase in the heart rate (tachycardia), jumps in blood pressure, dizziness and headaches due to changes in vascular tone and improper blood supply to the organs of the central nervous system.
With the deterioration of the health of the patient, the muscles completely atrophy, the person mostly lies, which negatively affects the nutrition of soft tissues. Sometimes necrosis develops.
Initially, the doctor is obliged to listen to all the patient's complaints, conduct a general examination, check tendon reflexes and skin sensitivity with the help of special tools.
Laboratory diagnostics of blood is effective in the case of determining concomitant pathologies and the causes of the development of the underlying disease. There may be an increase in the concentration of glucose or toxic compounds, salts of heavy metals.
Of the modern instrumental methods, electroneuromyography and nerve biopsy are preferable.
An international committee has developed a whole system for the treatment of polyneuropathy. First of all, the influence of the main causative factor is excluded - organisms are destroyed with the help of antibiotics, diseases of the endocrine system are compensated by hormonal therapy, the place of work changes, alcohol intake is completely excluded, neoplasms are removed by surgery.
In order to avoid the development of complications, a high-calorie diet is prescribed (in the absence of contraindications), a complex of vitamins and minerals that restore the immune system and cell trophism.
Pain medications, antihypertensive drugs, and muscle stimulants are used to relieve symptoms.
The information on the site is provided for informational purposes only, does not claim to be reference and medical accuracy, and is not a guide to action. Do not self-medicate. Consult with your physician.
Polyneuropathy of the lower extremities is a common pathology associated with lesions of peripheral nerves. The disease is characterized by trophic and vegetative-vascular disorders affecting the lower limbs, manifested by impaired sensitivity and flaccid paralysis.
The danger of pathology is that over time its manifestations are aggravated, there are problems with movement, which affects the ability to work and prevents a full life. Today we will talk about the symptoms and treatment of polyneuropathy of the lower extremities, and also consider methods aimed at preventing further progression of the pathology.
Polyneuropathy of the lower extremities is not an independent disease. According to ICD 10, this condition is considered a neurological syndrome that accompanies a variety of diseases:
The cause of the disease can be a variety of health disorders and chronic diseases. Cancer tumors can disrupt the functioning of the peripheral nervous system. In addition, signs of polyneuropathy may appear after a course of chemotherapy.
Infectious and inflammatory processes in the joints, any kind of intoxication of the body (drugs, alcohol, chemicals) can cause problems with impaired sensitivity and damage to nerve fibers. In children, this disease is most often hereditary, for example, the symptoms of porphyria polyneuropathy appear in a child immediately after birth.
Thus, all factors provoking the development of a pathological condition are divided into several groups by doctors:
Polyneuropathy never occurs as an independent disease, damage to nerve fibers is always associated with an etiological factor that negatively affects the state of the peripheral nervous system.
Polyneuropathy of the upper and lower extremities begins with increasing muscle weakness, which is associated with developing damage to nerve fibers. First of all, the distal parts of the limbs are damaged. In this case, a feeling of numbness occurs in the area of \u200b\u200bthe feet and gradually spreads to the entire leg.
Patients with polyneuropathy complain of a burning sensation, goosebumps, tingling, numbness of the extremities. Various kinds of paresthesia are complicated by muscle pain. As symptoms increase, patients experience severe discomfort even if they accidentally touch the problem area. In the later stages of the disease, unsteadiness of gait, impaired coordination of movements, and a complete lack of sensitivity in the area of \u200b\u200bdamage to nerve fibers are noted.
Muscular atrophy is expressed in the weakness of the arms and legs and in severe cases may result in paresis or paralysis. Sometimes unpleasant sensations in the limbs occur at rest, forcing them to make reflex movements. Such manifestations of physicians are characterized as "restless legs syndrome".
Pathology is accompanied by autonomic disorders, which are manifested by vascular disorders (feeling of cold in the affected limbs, marbled pallor of the skin) or trophic lesions (ulcers and cracks, peeling and dry skin, the appearance of pigmentation).
It is difficult not to notice the manifestations of polyneuropathy; as the pathology progresses, they become obvious not only to the patient, but also to the people around them. The gait changes and becomes heavier, as the legs become "cotton", there are difficulties with movement, a person hardly overcomes even small distances that he previously walked in a few minutes. As the pathology progresses, a feeling of numbness in the limbs increases. A pain syndrome occurs, which manifests itself in different ways, one part of the patients feels only slight discomfort, while the other complains of aching or sharp, burning pains.
Patients have swelling of the extremities, impaired knee reflexes, and no response to the stimulus. In this case, only one or several characteristic symptoms may appear at once, it all depends on the severity of the lesion of a particular nerve trunk.
By the nature of the course, polyneuropathy of the lower extremities can be:
Given the damage to nerve fibers, polyneuropathy is divided into several types:
Depending on the damage to cellular nervous structures, polyneuropathy can be:
The demyelinating form of polyneuropathy is the most severe form of the disease, the mechanism of development of which is still not fully understood. However, as a result of a number of studies, scientists put forward a theory about the autoimmune nature of the pathology. At the same time, the human immune system perceives its own cells as foreign and produces specific antibodies that attack the roots of nerve cells, destroying their myelin sheaths. As a result, nerve fibers lose their function and provoke innervation and muscle weakness.
If polyneuropathy is suspected, the patient will have to undergo a series of diagnostic procedures, including laboratory and instrumental studies. After collecting anamnesis, the doctor will conduct an external examination, examine reflexes, and then send the patient to the laboratory for blood donation for general and biochemical analysis.
In addition, the patient will undergo an ultrasound scan of the internal organs, X-ray of the affected areas, and cerebrospinal fluid will be taken. If necessary, they will take a biopsy of nerve fibers for research. The choice of treatment regimen is started only after a full examination and diagnosis.
The basis of therapeutic measures for polyneuropathy is a combination of medical and physiotherapeutic methods aimed at preventing the progression of the pathology and restoring the disturbed innervation of nerve fibers. Methods of therapy will largely depend on the cause contributing to the development of pathology.
If severe chronic diseases are to blame, they are primarily involved in the treatment of the underlying disease. So, in diabetic polyneuropathy, drugs are selected that will not affect the level of the glycemic index, and the therapy itself is carried out in stages. First, the diet is adjusted, body weight is normalized, and a complex of therapeutic exercises is developed for the patient. In the future, neurotropic vitamins and injections of alpha-lipoic acid are included in the treatment regimen, immunosuppressive agents and glucocorticoids are prescribed.
With the toxic nature of the disease, first of all, detoxification measures are carried out, after which the necessary medications are prescribed. If the pathology develops against the background of dysfunction of the thyroid gland, hormonal preparations are used in the treatment process. Malignant neoplasms are treated surgically, removing the tumor that compresses the nerve roots.
To develop the limbs and eliminate movement disorders, methods of physiotherapy exercises (LFK) are used. Vitamins of group B help to restore sensitivity, analgesics are prescribed in the form of ointments, tablets or injections to relieve pain.
These are the drugs of first choice in the treatment of polyneuropathy, their therapeutic effect is aimed at improving blood circulation in the area of damage, improving tissue trophism and regeneration of nerve fibers. Most often, the treatment regimen includes medicines from this list:
The action of drugs is aimed at improving neuromuscular conduction, accelerating metabolism, improving the supply of tissues with blood and oxygen. Metabolic agents are able to have an antioxidant effect, fight free radicals, stop the destruction of nervous tissue and help restore impaired functions.
In the course of treatment, an important role is given to B vitamins (B1, B12, B6). Preference is given to combined preparations, which are produced in tablet form or in the form of injections. Among the injection forms most often prescribed:
In addition to the optimal set of vitamins, these medicines include lidocaine, which additionally provides an analgesic effect. After a course of injections, vitamin preparations are prescribed in tablet form - Neuromultivit, Neurobion, Keltikan.
With polyneuropathy, the use of conventional painkillers (Analgin, Pentalgin, Sedalgin) does not give the desired effect. Previously, injections of Lidocaine were prescribed to relieve pain. But its use provoked jumps in blood pressure and heart rhythm disturbances. Today, a safer option has been developed that allows the anesthetic to be applied topically. To relieve pain, it is recommended to use the Versatis patch, which is based on lidocaine. It is simply fixed on the problem area, which allows you to achieve pain relief without irritation and adverse reactions.
If the pain syndrome has a clear localization, local remedies can be used - ointments and gels with analgesic action (for example, Kapsikam).
Anticonvulsant drugs - Gabapentin, Neurontin, Lyrica, which are produced in the form of capsules or tablets, cope well with the manifestations of the pain syndrome. The intake of such funds begins with minimal doses, gradually increasing the volume of the drug. The therapeutic effect is not instantaneous, it accumulates gradually. The effectiveness of the drug can be judged no earlier than 1-2 weeks from the start of administration.
In severe cases, when pain cannot be relieved by the above means, opioid analgesics (Tramadol) are prescribed in combination with Zaldiar. If necessary, the doctor may prescribe antidepressants. Amitriptyline is most often prescribed, with poor tolerance - Ludiomil or Venlaxor.
In the process of treating polyneuropathy, drugs that improve the conduction of a nerve impulse to the arms and legs are necessarily involved. Tablets or injections of Aksamon, Amiridin or Neuromidin help restore sensitivity. The course of therapy with these drugs is quite long - at least a month.
In the process of treatment, the doctor can combine different groups of drugs in order to achieve the most pronounced therapeutic effect.
Along with the methods of physiotherapy exercises, the complex treatment of polyneuropathy necessarily includes physiotherapy procedures. Your doctor may recommend the following methods:
The patient will definitely be waiting for therapeutic exercises under the guidance of an experienced instructor who will individually select a rehabilitation program and conduct wellness classes.
Regular courses of physiotherapy will help restore muscle tone, restore lost sensitivity, improve the supply of oxygen and nutrients to tissues, activate nerve conduction and literally put the patient on his feet.
Before using medications, consult your doctor!
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
Such a pathology as neuropathy is quite common. It is manifested by severe nerve damage. In post-traumatic neuropathy, damage occurs due to cuts, bruises, and fractures. Despite the fact that the nerve itself was not damaged as a result of direct exposure, cicatricial processes occur in the wound healing area, which compress the nerves. As a rule, most often such a pathology is characterized for the elbow, median and radial nerve.
In the canal itself, the nerve can be compressed directly by the thickened wall of the canal, which often occurs against the background of arthrosis of the bone wall of the canal, deforming arthrosis of the muscles, or after a fracture. This disorder is characterized by symptoms such as muscle atrophy, numbness, or decreased sensation. Many patients sometimes complain of very unpleasant sensations in the fingers, which usually increase at night. Also, the grip strength of the hand decreases, paresthesia, hyperesthesia changes, and a noticeable swelling of the hand is noted.
First of all, to make a diagnosis, a visual examination will be required to identify areas of increased or decreased sensitivity. It is also necessary to determine the presence of Tinel's syndrome and violations of the existing discriminatory sensitivity, which is the ability to distinguish and perceive the same stimuli when applied to the skin.
Along with this, during the examination, it is necessary to identify muscle atrophy or increased numbness during flexion. It should be noted that more often such motor disorders appear somewhat later in sensory disorders. In the future, the first examination and the collection of the necessary anamnesis should be followed by the necessary instrumental examination. by the most effective method in modern diagnostics, electroneuromyography is considered, which determines the exact passage of an impulse along a nerve.
In addition, in most cases, ultrasonography and ultrasound are performed for clear visualization. The best way to diagnose is a variant of magnetic resonance imaging, which helps to get a complete picture of the size, type and location of a specific localization of the disorder. Then, based on the data obtained, the specialist, if necessary, selects the type of necessary surgical treatment for post-traumatic neuropathy.
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It has been proven that the successful treatment of the presented disorder directly depends on the duration and type of damage. Significant damage to a specific nerve trunk on any forearm (radial, ulnar and median nerves) should preferably be treated as soon as possible by modern restoration of anatomical integrity. In this case, first of all, neurolysis is indicated, which is a simple surgical operation aimed only at releasing a certain nerve from severe compression by scar tissue.
It should be noted that it is necessary to contact specialists with post-traumatic neuropathy as early as possible so that the entire treatment process goes smoothly and there are a minimum of complications. When more than two months have passed since the onset of the development of the existing lesion, then a specific surgical intervention has a more voluminous character.
The likelihood of developing a dangerous neurogenic contracture of the hand depends directly on the period of time elapsed after the injury. Irreversible changes occur, due to which the nerve practically ceases to properly innervate certain muscles. In this case, all kinds of orthopedic operations are prescribed, in which the necessary transposition of the tendons and muscles is carried out. The rapid restoration of the lost innervation of the necessary muscles is also a fairly popular method of surgical intervention.
Additional treatment in a certain postoperative period includes immobilization of the operated limb in the correct physiological position. In addition, fixation in a forced position is sometimes advisable, when the tension of the nerve is the smallest.
Regardless of the cause of the lesion, in the process of treating post-traumatic neuropathy, the necessary drug therapy is also used. In addition, a suitable complex of vitamin preparations is prescribed. Treatment is always accompanied by immobilization of the specific operated limb. This period is up to three weeks, so that scars in the operated area appear minimally. Along with this, immobilization is also important to reduce the risk of possible suture ruptures in the further postoperative period.
Adequate physical therapy is also necessary. Its purpose is to prevent the dangerous development of contractures in this operated limb. Physiotherapy is also shown, which is mainly aimed at quickly reducing the formation of existing scar tissue.
G50-G59 Disorders of individual nerves, nerve roots and plexuses
G60-G64 Polyneuropathies and other disorders of the peripheral nervous system
G70-G73 Diseases of the neuromuscular junction and muscles
G80-G83 Cerebral palsy and other paralytic syndromes
The following categories are marked with an asterisk:
G55* Compression of nerve roots and plexuses in diseases classified elsewhere
G73* Disorders of the neuromuscular junction and muscles in diseases classified elsewhere
G94* Other disorders of the brain in diseases classified elsewhere
G99* Other disorders of the nervous system in diseases classified elsewhere
Excludes: current traumatic lesions of nerves, nerve roots
and plexuses - see nerve injury by area of the body
Includes: 5th cranial nerve lesions
G50.0 Trigeminal neuralgia. Paroxysmal facial pain syndrome, painful tic
G50.1 Atypical facial pain
G50.8 Other disorders of trigeminal nerve
G50.9 Disorder of trigeminal nerve, unspecified
Includes: 7th cranial nerve lesions
G51.0 Bell's palsy. facial paralysis
G51.1 Inflammation of the node of the knee
Excludes: postherpetic inflammation of the knee node (B02.2)
G51.2 Rossolimo-Melkersson syndrome. Rossolimo-Melkersson-Rosenthal syndrome
G51.3 Clonic hemifacial spasm
G51.8 Other disorders of facial nerve
G51.9 Disorder of facial nerve, unspecified
G52.0 Disorders of the olfactory nerve. 1st cranial nerve lesion
G52.1 Glossopharyngeal nerve disorders. Damage to the 9th cranial nerve. Glossopharyngeal neuralgia
G52.2 Disorders of the vagus nerve. Damage to the pneumogastric (10th) nerve
G52.3 Hypoglossal nerve disorders. Damage to the 12th cranial nerve
G52.7 Multiple lesions of cranial nerves. Polyneuritis of the cranial nerves
G52.8 Disorders of other specified cranial nerves
G52.9 Disorder of cranial nerve, unspecified
Inflammation of the ganglion node of the knee
trigeminal neuralgia
G53.2* Multiple cranial nerve lesions in sarcoidosis (D86.8+)
G53.3* Multiple lesions of cranial nerves in neoplasms (C00-D48+)
G53.8* Other disorders of cranial nerves in other diseases classified elsewhere
Excludes: current traumatic lesions of nerve roots and plexuses - see nerve injury by body region
neuralgia or neuritis NOS (M79.2)
neuritis or sciatica:
G54.0 Lesions of the brachial plexus. Infrathoracic syndrome
G54.1 Disorders of the lumbosacral plexus
G54.2 Disorders of cervical roots, not elsewhere classified
G54.3 Disorders of thoracic roots, not elsewhere classified
G54.4 Disorders of lumbosacral roots, not elsewhere classified
G54.5 Neuralgic amyotrophy. Parsonage-Aldren-Turner syndrome. Shoulder neuritis
G54.6 Phantom limb syndrome with pain
G54.7 Phantom limb syndrome without pain. Phantom limb syndrome NOS
G54.8 Other nerve root and plexus disorders
G54.9 Nerve root and plexus disorder, unspecified
G55.0* Compression of nerve roots and plexuses in neoplasms (C00-D48+)
G55.1* Compression of nerve roots and plexuses in disorders of intervertebral discs (M50-M51+)
G55.2* Compression of nerve roots and plexuses in spondylosis (M47.-+)
G55.8* Compression of nerve roots and plexuses in other diseases classified elsewhere
G56.0 Carpal tunnel syndrome
G56.1 Other disorders of median nerve
G56.2 Damage to the ulnar nerve. Late ulnar palsy
G56.3 Involvement of radial nerve
G56.8 Other mononeuropathies of the upper limb Interdigital neuroma of the upper limb
G56.9 Mononeuropathy of upper limb, unspecified
Excludes: current traumatic nerve injury - see nerve injury by body region
G57.0 Involvement of sciatic nerve
Associated with intervertebral disc disease (M51.1)
G57.1 Meralgia paresthetic. Lateral femoral cutaneous nerve syndrome
G57.2 Involvement of femoral nerve
G57.3 Damage to the lateral popliteal nerve. Peroneal (peroneal) nerve palsy
G57.4 Median popliteal nerve lesion
G57.5 Tarsal tunnel syndrome
G57.6 Damage to the plantar nerve. Morton's metatarsalgia
G57.8 Other mononeuralgias of the lower limb. Interdigital neuroma of the lower limb
G57.9 Mononeuropathy of lower limb, unspecified
G58.0 Intercostal neuropathy
G58.7 Multiple mononeuritis
G58.8 Other specified mononeuropathy
G58.9 Mononeuropathy, unspecified
G59.0* Diabetic mononeuropathy (E10-E14+ with common fourth character.4)
G59.8* Other mononeuropathies in diseases classified elsewhere
Excl.: neuralgia NOS (M79.2)
peripheral neuritis of pregnancy (O26.8)
G60.0 Hereditary motor and sensory neuropathy
Hereditary motor and sensory neuropathy, types I-IY. Hypertrophic neuropathy in children
Peroneal muscular atrophy (axonal type) (hypertrophic type). Russi-Levi Syndrome
G60.2 Neuropathy associated with hereditary ataxia
G60.3 Idiopathic progressive neuropathy
G60.8 Other hereditary and idiopathic neuropathies Morvan's disease. Nelaton's syndrome
G60.9 Hereditary and idiopathic neuropathy, unspecified
G61.0 Guillain-Barré syndrome. Acute (post-) infectious polyneuritis
G61.1 Serum neuropathy. If it is necessary to identify the cause, use an additional code of external causes (class XX).
G61.8 Other inflammatory polyneuropathies
G61.9 Inflammatory polyneuropathy, unspecified
G62.0 Drug-induced polyneuropathy
G62.1 Alcoholic polyneuropathy
G62.2 Polyneuropathy due to other toxic substances
G62.8 Other specified polyneuropathy Radiation polyneuropathy
If it is necessary to identify the cause, use an additional code of external causes (class XX).
G62.9 Polyneuropathy, unspecified Neuropathy NOS
G63.2* Diabetic polyneuropathy (E10-E14+ with common fourth character.4)
G63.5* Polyneuropathy in systemic lesions of connective tissue (M30-M35+)
G63.8* Polyneuropathy in other diseases classified elsewhere. Uremic neuropathy (N18.8+)
Peripheral nervous system disorder NOS
transient neonatal Myasthenia gravis (P94.0)
If the disease is caused by a drug, an additional external cause code is used to identify it.
G70.1 Toxic disorders of neuromuscular junction
If it is necessary to identify a toxic substance, use an additional code of external causes (class XX).
G70.2 Congenital or acquired myasthenia gravis
G70.8 Other disorders of neuromuscular junction
G70.9 Disorder of neuromuscular junction, unspecified
Excludes: congenital arthrogryposis multiple (Q74.3)
Autosomal recessive childhood type, resembling
Duchenne or Becker dystrophy
Benign scapular-peroneal with early contractures [Emery-Dreyfus]
Excludes: congenital muscular dystrophy:
With specified morphological lesions of the muscle fiber (G71.2)
G71.1 Myotonic disorders. Myotonic dystrophy [Steiner]
Dominant inheritance [Thomsen]
Recessive inheritance [Becker]
Neuromyotonia [Isaacs]. Paramyotonia is congenital. pseudomyotonia
If necessary, to identify the drug that caused the lesion, use an additional external cause code (class XX).
Congenital muscular dystrophy:
With specific morphological lesions of the muscular
Disproportion of fiber types
Non-raspberry [non-raspberry body disease]
G71.3 Mitochondrial myopathy, not elsewhere classified
G71.8 Other primary muscle disorders
G71.9 Primary lesion of muscle, unspecified Hereditary myopathy NOS
Excludes: congenital arthrogryposis multiplex (Q74.3)
ischemic infarction of muscle (M62.2)
G72.0 Drug-induced myopathy
If necessary, to identify the drug, use an additional code of external causes (class XX).
G72.1 Alcoholic myopathy
G72.2 Myopathy due to other toxic substance
If it is necessary to identify a toxic substance, use an additional code of external causes (class XX).
G72.3 Periodic paralysis
Periodic paralysis (familial):
G72.4 Inflammatory myopathy, not elsewhere classified
G72.8 Other specified myopathies
G72.9 Myopathy, unspecified
G73.0* Myasthenic syndromes in endocrine diseases
Myasthenic syndromes with:
G73.2* Other myasthenic syndromes in neoplastic lesions (C00-D48+)
G73.3* Myasthenic syndromes in other diseases classified elsewhere
G73.5* Myopathy in endocrine diseases
G73.6* Myopathy in metabolic disorders
G73.7* Myopathy in other diseases classified elsewhere
Includes: Little's disease
Excludes: hereditary spastic paraplegia (G11.4)
G80.0 Spastic cerebral palsy. Congenital spastic palsy (cerebral)
G80.1 Spastic diplegia
G80.3 Dyskinetic cerebral palsy Athetoid cerebral palsy
G80.4 Ataxic cerebral palsy
G80.8 Other type of cerebral palsy Mixed syndromes of cerebral palsy
G80.9 Cerebral palsy, unspecified Cerebral palsy NOS
Note For primary coding, this category should only be used when hemiplegia (complete)
(incomplete) reported without further specification, or stated to be long-standing or long-standing but unspecified. This category is also used in multi-cause coding to identify types of hemiplegia due to any cause.
Excl.: congenital and infantile cerebral palsy (G80.-)
G81.1 Spastic hemiplegia
G81.9 Hemiplegia, unspecified
Excl.: congenital or infantile cerebral palsy (G80.-)
G82.1 Spastic paraplegia
G82.2 Paraplegia, unspecified Paralysis of both lower limbs NOS. Paraplegia (inferior) NOS
G82.4 Spastic tetraplegia
G82.5 Tetraplegia, unspecified Quadriplegia NOS
Note For primary coding, this category should only be used when the listed conditions are reported without further specification, or are stated to be long-standing or long-standing, but their cause is not specified. This category is also used when coding for multiple reasons for identification of these conditions caused by any cause.
Incl.: paralysis (complete) (incomplete) other than that specified under G80-G82
G83.0 Diplegia of upper limbs. Diplegia (upper). Paralysis of both upper limbs
G83.1 Monoplegia of the lower limb. Paralysis of the lower limb
G83.2 Monoplegia of the upper limb. Paralysis of the upper limb
G83.3 Monoplegia, unspecified
G83.4 Cauda equina syndrome Neurogenic bladder associated with cauda equina syndrome
Excludes: spinal bladder NOS (G95.8)
G83.8 Other specified paralytic syndromes Todd's palsy (post-epileptic)
G83.9 Paralytic syndrome, unspecified
Excludes: alcohol-induced autonomic nervous system disorder (G31.2)
G90.0 Idiopathic peripheral autonomic neuropathy Syncope associated with irritation of the carotid sinus
G90.1 Familial dysautonomy [Riley-Day]
G90.2 Horner's syndrome. Bernard(-Horner) Syndrome
G90.3 Multisystem degeneration. Neurogenic orthostatic hypotension [Shy-Drager]
Excludes: orthostatic hypotension NOS (I95.1)
G90.8 Other autonomic [autonomic] nervous system disorders
G90.9 Autonomic [autonomic] nervous system disorder, unspecified
Includes: acquired hydrocephalus
G91.0 Communicating hydrocephalus
G91.1 Obstructive hydrocephalus
G91.2 Normal pressure hydrocephalus
G91.3 Post-traumatic hydrocephalus, unspecified
G91.8 Other hydrocephalus
G91.9 Hydrocephalus, unspecified
If necessary, identify the toxic substance using
additional external cause code (class XX).
G93.0 Cerebral cyst. Arachnoid cyst. Porencephalic cyst, acquired
Excludes: periventricular acquired cyst of newborn (P91.1)
congenital cerebral cyst (Q04.6)
G93.1 Anoxic disorder of brain, not elsewhere classified
G93.2 Benign intracranial hypertension
Excludes: hypertensive encephalopathy (I67.4)
G93.3 Fatigue syndrome after a viral illness. Benign myalgic encephalomyelitis
G93.4 Encephalopathy, unspecified
G93.5 Compression of the brain
Infringement > brain (trunk)
Excludes: traumatic compression of brain (S06.2)
Excludes: cerebral edema:
G93.8 Other specified disorders of brain Radiation-induced encephalopathy
If it is necessary to identify an external factor, use an additional external cause code (class XX).
G93.9 Disorder of brain, unspecified
G94.2* Hydrocephalus in other diseases classified elsewhere
G94.8* Other specified disorders of brain in diseases classified elsewhere
G95.0 Syringomyelia and syringobulbia
G95.1 Vascular myelopathy Acute spinal cord infarction (embolic) (non-embolic). Thrombosis of the arteries of the spinal cord. Hepatomyelia. Non-pyogenic spinal phlebitis and thrombophlebitis. Spinal edema
Subacute necrotizing myelopathy
Excludes: spinal phlebitis and thrombophlebitis other than non-pyogenic (G08)
G95.2 Compression of spinal cord, unspecified
G95.8 Other specified diseases of spinal cord Spinal bladder NOS
If it is necessary to identify an external factor, use an additional external cause code (class XX).
Excludes: neurogenic bladder:
neuromuscular dysfunction of the bladder without mention of spinal cord injury (N31.-)
G95.9 Disease of spinal cord, unspecified Myelopathy NOS
G96.0 Leakage of cerebrospinal fluid [liquorrhea]
Excludes: on lumbar puncture (G97.0)
G96.1 Meningeal disorders, not elsewhere classified
Meningeal adhesions (cerebral) (spinal)
G96.8 Other specified disorders of central nervous system
G96.9 Disorder of central nervous system, unspecified
G97.0 Leakage of cerebrospinal fluid on lumbar puncture
G97.1 Other reaction to lumbar puncture
G97.2 Intracranial hypertension after ventricular bypass
G97.8 Other disorders of nervous system following medical procedures
G97.9 Disorder of nervous system after medical procedures, unspecified
Nervous system disorder NOS
G99.0* Autonomic neuropathy in endocrine and metabolic diseases
Amyloid autonomic neuropathy (E85. -+)
Diabetic autonomic neuropathy (E10-E14+ with common fourth character.4)
G99.1* Other disorders of the autonomic [autonomic] nervous system in other diseases classified elsewhere
G99.2* Myelopathy in diseases classified elsewhere
Compression syndromes of anterior spinal and vertebral artery (M47.0*)
G99.8* Other specified disorders of nervous system in diseases classified elsewhere
Neuropathy of the radial nerve (syn. neuritis of the radial nerve) is a lesion of a similar segment, namely: metabolic, post-traumatic, ischemic or compression, localized in any of its areas. The disease is considered the most common among all peripheral mononeuropathies.
In the vast majority of cases, the predisposing factor is pathological causes. However, there are a number of physiological sources, such as incorrect hand posture during sleep.
The clinical picture includes specific manifestations, namely: a symptom of a “hanging hand”, a decrease or complete absence of sensitivity in the area from the shoulder to the back surface of the middle and ring fingers, as well as the little finger.
A neurological examination is often sufficient to establish the correct diagnosis. However, a wide range of instrumental diagnostic procedures may be required.
Treatment is very often limited to the use of conservative therapeutic methods, including: taking medications and performing therapeutic exercises.
Based on the international classification of diseases of the tenth revision, such a pathology has a separate code - ICD-10 code: G56.3.
The main reason against which neuropathy of the radial nerve most often develops is its prolonged compression, and this is due to the influence of the following factors:
However, such a disease can also develop due to pathological sources, namely:
It follows from this that not only a neurologist can diagnose and treat neuropathy, but also a traumatologist, orthopedist and sports physician.
Depending on the site of localization, neuropathy of the radial nerve of the hand can damage such areas of neurofibers as:
The clinical picture of such a pathology depends on the place of nerve compression.
Based on the above etiological factors, there are several types of the disease, differing in origin:
As mentioned above, the symptoms of such a disorder are largely determined by the location of the nerve compression. The defeat in the armpit zone develops quite rarely and has a second name - "crutch paralysis".
This form has the following features:
If the middle third of the shoulder is damaged, then the symptoms will be presented:
Damage to the radial nerve in the elbow area contributes to the appearance of such external signs as:
Neuropathy of the radial nerve in the wrist area has the following clinical picture:
Such external manifestations during the course of such an ailment can occur in absolutely every person, regardless of gender and age category.
The main method of diagnosis is a neurological examination. Nevertheless, only a comprehensive examination of the body will help to accurately confirm the diagnosis, as well as to establish its causes.
First of all, the clinician should independently perform several manipulations:
As for laboratory research, they are limited to the implementation of:
Instrumental diagnostic measures include:
Additional diagnostic measures are consultations with an orthopedist, endocrinologist and traumatologist.
Radial neuropathy must be differentiated from:
Therapy of such a disease is carried out mainly by conservative methods, including:
Medical treatment involves the use of:
Novocaine and cortisone blockades may also be required.
Among the physiotherapy procedures it is worth highlighting:
Good results in complex therapy are shown by therapeutic massage. It is important to take into account that for the entire duration of treatment it is necessary to limit the functionality of the diseased upper limb.
With the normalization of the patient's condition, clinicians recommend carrying out therapeutic exercises.
The most effective exercises:
No less effective is gymnastics carried out in water, in which all movements are repeated 10 times.
Surgical intervention is addressed only when the cause of the disease was any injury or for other individual indications. In this case, neurolysis or plastic surgery of the nerve is performed.
With timely therapy, it is possible to fully restore the functioning of the radial nerve in 1-2 months.
Recovery time is dictated by the following factors:
Very rarely, the pathology becomes chronic.
In order to prevent radial nerve neuropathy, you must follow a few simple recommendations.
Preventive measures include:
The prognosis of the described pathology is predominantly favorable, especially when conducting complex therapy and following all the recommendations of the attending physician. The disease does not lead to complications, however, this does not mean that the consequences of the provocative disease will not arise.
If you think that you have Radial Neuropathy and the symptoms characteristic of this disease, then doctors can help you: a neurologist, an orthopedist, an orthopedic traumatologist.
We also suggest using our online disease diagnostic service, which, based on the symptoms entered, selects probable diseases.
Neuritis is a neurological inflammatory disease. Experts distinguish its several varieties depending on the location. If the disease affects the upper limbs of the patient, then he is diagnosed with neuropathy of the radial nerve.
The reasons for its development are manifold. According to medical data, this ailment is the most common among other diseases of the upper extremities.
This disease can develop due to various reasons. For example, one of the most common is nerve compression at the moment when a person is sleeping.
Neuritis of the radial nerve occurs due to excessive numbness of the patient's hand while he takes a certain position and stays in it for a long time. Usually the upper limb is located either under the head or under the body.
Sleep must be very deep. This often happens when the sleeper is either very tired or intoxicated.
Neuritis of the radial nerve can develop due to its compression with a crutch. This is the so-called crutch paralysis.
The disease can occur if the crutches were not properly sized for height or they do not have a soft padding on the armpit. Excessive compression of the radial nerve leads to the development of the disease.
The third cause of the disease is trauma, for example, a serious injury to the humerus. It can also develop due to excessive compression of the tourniquet. In some cases, the disease occurs with a sudden contraction of the nerve.
Traumatic cases of neuritis development also include:
Quite rarely, the disease appears after infections: influenza, pneumonia, typhus, etc. Intoxication, for example, alcohol poisoning, can cause the development of radial nerve neuritis.
The main preventive measures include the need to avoid injury, hypothermia and infection.
The manifestation of the disease will directly depend on the degree of damage and the area of damage localization.
But for any neuritis, the following symptoms are characteristic:
Other symptoms will depend on the location of the damage.
So, if the armpit or the upper third of the shoulder is affected, then the disease is characterized by the following manifestations:
When the middle third of the shoulder is affected, the patient has similar symptoms. However, the patient is able to extend the forearm and the sensitivity of the back of the shoulder is preserved.
In this case, a characteristic feature is a "falling" brush. In addition, the patient cannot straighten his fingers in the metacarpophalangeal joints.
If the lower third of the shoulder or the upper third of the forearm is affected, then, as a rule, the shoulder and forearm retain their motor functions. Violations occur exclusively with the extension of the hand and fingers.
Symptoms of alcoholic neuropathy: numbness and weakness in the legs with damage to the nerves of the lower extremities.
Symptoms of inflammation of the occipital nerve are listed here.
The doctor can make a preliminary diagnosis based on the patient's complaints and a specific clinical picture. Be sure to apply diagnostic tests that help assess the level of damaged nerve and the degree of impairment.
The patient, at the request of the doctor, performs several light exercises.
The doctor draws conclusions about the presence of an ailment based on the following characteristic features:
To confirm the diagnosis, the patient is sent for electroneuromyography. With the help of this procedure, the final diagnosis is made. To assess the degree of nerve recovery after a course of therapy, the patient is re-sent to electroneuromyography.
Treatment of neuritis of the radial nerve is determined in accordance with the cause that caused its development. So, if the disease appeared due to infections, then the patient is prescribed antibiotic therapy, antiviral and vascular drugs.
In traumatic neuritis, the patient is prescribed anti-inflammatory drugs, analgesics. Treatment begins with immobilization of the limb, then anti-edematous therapy is prescribed.
In both cases, the patient is prescribed vitamins B, C and E. This is necessary in order to restore blood circulation.
Drug treatment of radial neuritis is used in combination with additional methods that allow you to quickly and efficiently cope with the disease.
So, the patient is prescribed physiotherapy:
Their main goal is the return of sensitivity, as well as an increase in muscle tone. Usually they are prescribed not immediately, but at the end of the first week of treatment.
In addition, the following procedures apply:
Symptoms of neuropathy are determined by the nature of nerve damage and their location. Most often it occurs with general diseases, various intoxications, sometimes due to various injuries.
The most common forms of neuropathy are diabetic, toxic, and post-traumatic.
The damage to the nerve branches in diabetes mellitus is promoted by an increased level of sugar and lipids in the blood, and the initial damage as a result of this to the smallest vessels that feed the nerve fibers.
Post-traumatic neuropathy develops as a result of compression and malnutrition of nerve fibers. Often, the conduction of the nerve is disturbed due to an acute injury, for example, a strong blow, which leads to a violation of the integrity of the nerve sheaths.
In addition, arthritis, renal and hepatic insufficiency, hypothyroidism, tumors, and other diseases can contribute to the development of neuropathy.
The most typical form of neuropathy occurs in diabetes mellitus. In diabetes, first of all, the smallest vessels suffer, including those that supply nerve fibers with blood. The main distinguishing feature of this form of neuropathy is a decrease in sensitivity in the affected areas. As a result, the risk of injury and infection of the skin in the area of the disease increases. In diabetes, this picture is most typical for the lower extremities.
Most patients diagnosed with diabetes have some form of neuropathy:
Peripheral: in this case, when the nerves responsible for the innervation of the upper or lower extremities are damaged, there is a feeling of numbness or tingling on the side of the affected nerve; patients note a violation of the sensitivity of the toes or hands, as well as a feeling of numbness.
Proximal: there is a violation of sensitivity in the lower leg, thighs and buttocks.
Autonomous: the activity of the digestive, urinary or genital organs is disturbed.
General weakness in the muscles also often accompanies any form of diabetic neuropathy. At the same time, the muscles gradually atrophy, and violations of the integument develop.
Clinic of toxic neuropathies.
The cause of this form of the disease is various kinds intoxication. Nerve damage can be observed both in infectious diseases (diphtheria, HIV, herpes infection), and in case of poisoning with chemicals (alcohol, lead, arsenic), as well as when certain medications are taken incorrectly.
Alcoholic neuropathy is a severe lesion of the peripheral nervous system, which is the most common complication of the excessive use of alcohol and its surrogates. Asymptomatic forms of alcoholic neuropathy are found in almost all alcohol abusers.
At the moment, it is known that both the effect of the toxic substance itself on the nerve fiber, and the violation of metabolic processes due to poisoning of the body contribute to the development of neuropathy.
The nerves of the extremities are most often affected. Regardless of the cause of poisoning, neuropathy is manifested by a violation of sensitivity in the feet and hands, the appearance of a burning sensation and tingling on the skin, and hyperemia of the skin of the extremities. Also, in the later stages of the disease, swelling of the tissues of the lower extremities may appear. This disease has a protracted course, requiring preventive measures, in particular, spa treatment.
Clinic of post-traumatic neuropathy.
The cause of post-traumatic damage to nerve fibers is their compression as a result of fractures, tissue edema, improper formation of post-traumatic scars, and other neoplasms. More frequent forms of this disease are lesions of the ulnar, sciatic and radial nerve. At the same time, muscle atrophy develops, a violation of their contractility and a decrease in reflexes. There is also a decrease in sensitivity to painful stimuli.
In case of toxic damage, it is necessary to stop the toxic effect (cancel the drug, exclude the use of toxic substances). Treatment of the diabetic form of the disease is reduced, first of all, to maintaining normal blood sugar levels. With post-traumatic lesions of nerve fibers, it is necessary to get rid of the consequences of the traumatic factor in the best way.
Regardless of the form of the disease, painkillers, special groups of vitamins, and other drugs that improve metabolic processes and stimulate regeneration are prescribed to the patient. Later, according to the doctor's prescription, physiotherapy treatment is carried out.
An important role is played by the prevention of neuropathies. It comes down to the normalization of metabolic processes, the timely treatment of systemic and infectious diseases, and timely muscle stimulation during orthopedic treatment is also important.
Given that this disease often becomes chronic, it is necessary to take all measures to prevent exacerbation. For this, patients with neuropathy are referred for sanatorium treatment. In sanatoriums for the treatment of neuropathy, the following procedures are used:
Exercise therapy and massage with acupuncture techniques;
During spa treatment, patients are also recommended diet therapy rich in vitamins of groups B, C and E. It should be remembered that only diseases in remission with a chronic process are subject to treatment in sanatoriums.
Polyneuropathy is the clinical manifestation of multiple lesions of peripheral nerves of various nature.
Often, toxic substances of exogenous or endogenous origin act as a damaging factor in polyneuropathy.
The resulting toxic polyneuropathies (TP) have a common clinic and treatment approaches. Depending on the time of exposure and the characteristics of contact with a toxic agent, an acute or chronic form of the disease develops.
The relevance of toxic damage to the nervous system is due to the expansion of human contacts with harmful production factors, the progressive deterioration of the environmental situation and the decrease in the quality of food products produced using new technologies.
The proportion of TP caused by uncontrolled drug intake is growing. In addition, the cause of the pathology of peripheral nerves is often infectious pathogens that implement neurotropic effects through toxins.
According to the 10th revision of the International Classifier of Diseases and Related Health Problems, toxic polyneuropathies are included in the block of headings "Polyneuropathies and other lesions of the peripheral nervous system", belonging to the class of diseases of the nervous system.
Since the classifier does not provide for a separate subheading summarizing the varieties of toxic polyneuropathies, they are all encoded with separate four-digit ciphers from the heading G62 "Other polyneuropathies". So, alcoholic polyneuritis is assigned the code G62.1, and drug TP is encrypted as G62.0, indicating an additional code for identifying the drug.
For polyneuropathies caused by toxic agents not mentioned, code G62.2 is provided. In the case of an unspecified nature of toxic substances, the diagnosis is Polyneuropathy, unspecified (G62.9).
Is it possible to cure polyneuropathy and what drugs are used for therapy, you will learn in the following topic:. Details about the methods of drug therapy.
Fundamentally important for the diagnosis and treatment of AFL is the allocation of chronic, subacute and acute forms of the disease. The first of them involve the development of pathological changes for 60 or more days, with a subacute form, the process develops in terms of 40 to 60 days. And acute toxic damage to peripheral nerves is diagnosed when the clinic of the disease manifests itself up to 40 days from the moment of contact with the causative factor.
Depending on the origin of the toxic substance, two large groups of TP are distinguished:
The first group of TP is represented by diphtheria polyneuropathy, lesions of the peripheral nervous system in herpetic and HIV infections, lead, arsenic and organophosphorus polyneuropathies, as well as alcoholic and drug-induced polyneuritis.
The group of endogenous TP includes polyneuropathies that have developed against the background of diabetes mellitus, connective tissue diseases, dysproteinemia, uremia, liver failure and diseases of the gastrointestinal tract.
The cause of toxic polyneuropathy of the lower extremities are various intoxications of the whole organism with the development of a specific pathological process in the peripheral nerves.
The pathological mechanism of AFL is based on the toxic effects of certain external or internal factors, leading to the destruction of the myelin sheath and the axial cylinder of the nerve trunks.
The lesion affects mainly the distal extremities due to a number of predisposing factors:
The points of application of various neurotoxicants may be different. For example, organophosphate poisons cause diffuse damage to the central and peripheral nervous system. Arsenic, mercury, organic solvents and carbon disulfide act selectively on sensitive nerve endings.
Hexochlorafen, lead, arsenic, tellurium, and thallium generally interfere with the motor functions of the peripheral nerves.
The clinic of TP is determined by the degree of involvement in the pathological process of sensitive, motor and autonomic branches of the nerve trunks.
Typical symptoms of movement disorders are:
Patients have difficulty moving, in severe cases they cannot walk, stand and hold objects on their own. With damage to the diaphragmatic muscles, respiratory disorders and a decrease in lung volume are possible.
Sensitivity disorders are represented by:
In some cases, TP shows signs of a disorder of autonomic innervation:
The symptomatology of certain types of TP has characteristic differences, depending on the etiological factor that caused the damage to the nerve trunks, the time of its exposure, and the degree of the body's reactivity to a particular neurotoxicant.
Diphtheria TP adults who have had a toxic form of infection are more likely to get sick. Typically, the defeat of the cranial - cerebral nerves, manifested by paralysis of accommodation, impaired swallowing, nasal voice and tachycardia. A dangerous complication of diphtheria AFL can be diaphragmatic paralysis, disorders of respiratory function and cardiac activity.
For lead TS characteristic damage to the radial and peroneal nerve, manifested by symptoms of "hanging feet and hands" and "cock's gait". Severe pain syndrome is accompanied by vegetative disorders, while sensitivity practically does not suffer. The clinical picture of lead polyneuritis unfolds against the background of intoxication symptoms: increased fatigue, decreased memory and attention, anemia and spastic colitis.
Manifestations of alcoholic TP have a pathogenetic relationship with impaired absorption of vitamin B 1 and associated thiamine deficiency. In patients, the sensitivity of the feet is disturbed, soreness of the calf muscles is noted, distal tendon reflexes fade away. In severe cases, against the background of shooting pains in the legs, muscle atrophy and symmetrical paresis of the flexor muscles develop, and sensitive disorders of the “gloves and socks” type develop.
Symptoms of drug-induced polyneuropathy may appear on the background of taking gold preparations, antibacterial agents, isoniazid, perhexylen, teturam, cordarone, vinca alkaloids or platinum preparations, vitamins E and group B. The clinic is dominated by sensitivity disorders, paresthesia and loss of muscular-articular sensations (ataxia). Moderate paresis (perhexylen), muscle weakness (vitamin preparations), as well as their combination with damage to the optic nerves (teturam) are possible.
To determine the cause of AFL and prescribe adequate treatment, it is necessary to determine the type of neurotoxicant and the timing of its effect on the body.
Of great help in this is a thorough history taking, including the nature of the patient's work, his place of residence and the presence of harmful addictions (alcoholism, substance abuse).
In addition, they clarify information about existing diseases and medications taken.
Diagnostic information about:
The main role in the diagnosis of atrial fibrillation is assigned to an objective examination of the patient with special tests to detect dysfunction of the peripheral nerves.
As additional types of research, analyzes for toxins, hormones, sugar levels and antibodies to infectious pathogens (herpes, HIV) are used. Porphyrins and salts of heavy metals are determined in urine.
Additional electrophysiological research methods, in particular electromyography (EMG), help to confirm the diagnosis.
The main therapeutic measure for toxic polyneuropathy of the lower extremities is the termination of contact with the neurotoxicant. In the acute form of poisoning, detoxification agents and antidotes are administered intravenously:
Pharmacotherapy of toxic polyneuropathy against the background of alcohol includes courses of amino acids (methionine, glutamic acid), lipoic and thioctic acid, thiamine bromate, as well as vegetotropic agents, nootropics and tranquilizers. Limit dietary fats. With viral lesions of peripheral nerves, acyclovir is effective.
In all forms of TP, eufillin, vitamins of group B, actovegin, xanthinol nicotinate, preparations ascorbic acid, funds to improve microcirculation (trental). With severe trophic disorders, ATP and anabolic steroids are indicated.
In addition to drug therapy, physiotherapy methods are prescribed - massage, electromyostimulation, therapeutic exercises, balneotherapy.
In most cases, TP have a favorable prognosis for recovery.
When contact with a toxic substance is stopped, paresis and sensory disturbances regress within weeks or months.
In some cases of infectious AFL, relapses of skeletal muscle weakness are possible.
The prognosis for alcoholic polyneuropathies depends on the refusal or return to alcohol. A rather serious prognosis for toxic damage to FOS is due to poor recovery of paralysis.
Untimely diagnosis and treatment of AFL can be complicated by paresis and paralysis of the limbs. The progressive dynamics of the disease is often accompanied by diffuse muscle atrophy. In the case of a severe course of diphtheria polyneuropathy, cardiac arrest is possible.
