Alcoholic polyneuropathy is a multiple lesion of peripheral nerves in alcoholism. Usually occurs in the late stages of alcoholic illness. It is accompanied by muscle weakness, sensitivity disorders and ataxia. Excessive sweating is possible. Edema, changes in temperature and coloration of the distal extremities are often observed. In some cases, mental disorders occur. Develops gradually, less often acutely. With treatment, symptoms are reduced within a few months or years. Vitamin therapy, metabolic therapy and physiotherapy are carried out. If you refuse alcohol, the prognosis is quite favorable.
ICD 10
G62.1 Alcoholic polyneuropathy
General information
Alcoholic polyneuropathy is a disease accompanied by simultaneous damage to a large number of peripheral nerves. According to statistics, polyneuropathy, accompanied by neurological symptoms, is detected in 10-30% of patients suffering from alcoholism. When conducting a comprehensive electromyographic study, certain disorders indicating the presence of an asymptomatic form of alcoholic polyneuropathy are detected in most chronic alcoholics.
Men suffer from clinical forms of polyneuropathy more often than women. In most cases, there is a chronic or subacute course. Sometimes the disease develops acutely, against the background of binge drinking or hypothermia. The duration of the disease can vary significantly and ranges from several months to several years. The outcome largely depends on timely treatment and abstinence from alcohol consumption. Alcoholic polyneuropathy often causes disability, which can later be removed in case of satisfactory treatment results. The treatment of this disease is carried out by neurologists in cooperation with specialists in the field of narcology.
Causes of alcoholic polyneuropathy
The main causes of the development of alcoholic polyneuropathy are: the toxic effect of alcohol on the body, a lack of B vitamins, nutritional disorders, an increase in blood sugar and hereditary features of the patient’s metabolism. Pathology, as a rule, occurs in patients with the third, less often – with the second stage of alcoholism. The likelihood of symptoms of polyneuropathy increases when taking low-quality alcohol, denaturates and all kinds of chemical liquids containing ethyl alcohol.
With the constant use of alcohol, a toxic intermediate of ethanol decomposition, acetaldehyde, accumulates in the patient’s body. It has a destructive effect on all organs and tissues, including the axons of nerve cells. The rate of accumulation of acetaldehyde is largely determined by hereditary features of metabolism – the ability of the body to produce acetaldehyde dehydrogenase and alcohol dehydrogenase (enzymes involved in the processing of ethanol).
The situation is aggravated by a deficiency of vitamin B1, which is involved in the transmission of nerve impulses, acts as an antioxidant, prevents the destruction of cells (including nerve tissue cells) and affects the processing of alcohol in the liver. Vitamin B1 deficiency is caused by a whole complex of reasons, including insufficient or unbalanced nutrition associated with decreased appetite, binge drinking, financial difficulties and inattention to one’s health; deterioration of vitamin B1 absorption in the intestine; impaired liver cell function, etc.
Classification
All disorders develop gradually, pathological changes in the peripheral nervous system occur long before the first clinical symptoms appear. Taking into account the severity of these changes, as well as the presence or absence of clinical symptoms, there are 4 stages of polyneuropathy:
- Stage 0 – there is no polyneuropathy. Signs of pathology are not detected even during special studies (electromyography, quantitative vegetative and sensory testing).
- Stage 1 – asymptomatic polyneuropathy. There are no clinical signs, but special studies indicate the presence of pathological changes.
- Stage 2 – clinically significant polyneuropathy. The disease can be diagnosed on the basis of complaints and objective research, there is no pronounced functional defect.
- Stage 3 – polyneuropathy with severe functional disorders. The ability to work is reduced or lost.
Symptoms of alcoholic polyneuropathy
The first manifestations of alcoholic polyneuropathy usually become paresthesia – sensitivity disorders, manifested by a feeling of slight numbness, crawling goosebumps and tingling. Patients complain that they “sat out the leg” during a long stay in a sitting position or “lay down the arm” in a dream. In the initial stages of polyneuropathy, paresthesias appear only when they are in an uncomfortable position for a long time, therefore they often do not cause special anxiety in patients.
Subsequently, the frequency and severity of paresthesia increases. Temperature and pain sensitivity decrease, numbness becomes permanent and gradually spreads in the proximal direction. Patients with severe polyneuropathy say that their hands and feet seem to be wearing gloves and socks that reduce sensitivity. When walking, a feeling of movement “on an air cushion” is created. When working with hands, objects are poorly perceived by touch. The symptom can progress both sharply (for about a month) and gradually (for a year or more).
Paresthesia can be combined with progressive muscle weakness, which also spreads in an upward direction. In some cases, muscle weakness prevails in the clinical picture, and paresthesia fades into the background. Sensory and muscular disorders in the lower extremities are detected in almost all patients. The upper limbs are involved in the process in about 50% of cases. With the defeat of thick fast-conducting nerve fibers, not only temperature and pain, but also vibration sensitivity, as well as muscle-joint feeling, suffer. In severe cases, paralysis occurs.
Diagnostics
Neurological examination reveals an increase in tendon reflexes in the early stages, and a decrease in the later stages. Skin and pain sensitivity is reduced. Muscle tone is reduced, and atrophy develops rapidly in the presence of muscle disorders. Sometimes contractures form in the distal parts of the limbs. Often there is a lesion of the calf muscles, accompanied by increased pain during palpation of the muscles and pressure on the area of passage of the nerves innervating this anatomical area. Electromyography, quantitative vegetative and sensory testing are used as an additional method to confirm the diagnosis of polyneuropathy.
Treatment of alcoholic polyneuropathy
Treatment includes a complete refusal to take alcoholic beverages and proper nutrition. Patients are prescribed B vitamins in tablets and injections, antioxidants, antihypoxants, means to improve microcirculation and nerve conduction. With intense pain syndrome, analgesics are used, sometimes anticonvulsants and antidepressants. Massage and physical therapy are carried out, aimed at preventing contractures and strengthening the affected muscles.
An important part of the treatment is psychotherapeutic work to explain the causes of the development of alcoholic polyneuropathy and the importance of maintaining a sober lifestyle. In addition, the psychotherapist helps the patient cope with psychological difficulties arising from the cessation of alcohol intake. If necessary, the patient is referred to a narcologist who conducts drug treatment of alcoholism, implant insertion, Dovzhenko coding or hypnosuggestive therapy.
Forecast
The prognosis for polyneuropathy depends on the severity of the disease, the presence or absence of treatment and the patient’s willingness to give up alcohol. At the height of the disease, pronounced disability is observed, but subsequently the manifestations of polyneuropathy are gradually reduced. In the active phase, most patients receive group II disability, as their condition improves, they are transferred to group III. Subsequently, in mild cases, complete elimination of symptoms and restoration of working capacity is possible, in other patients residual phenomena of varying severity are observed. Alcohol intake and eating disorders in patients who have undergone alcoholic polyneuropathy can provoke an exacerbation of the disease with the development of even more vivid clinical symptoms.
