Alcoholic encephalopathy is a lesion of brain cells as a result of alcohol consumption. It usually develops at the end of stage II – beginning of stage III of alcoholism, although an earlier onset is possible. It can occur acutely or chronically. It is accompanied by mental, somatic and neurological disorders. It is characterized by a deterioration in appetite, weight loss, impaired coordination of movements, constant fatigue, anxiety, mood instability and memory disorders. Delusional and hallucinatory disorders are possible. The treatment is conservative.
ICD 10
G31.2 Degeneration of the nervous system caused by alcohol
General information
Alcoholic encephalopathy is a disease accompanied by the destruction of brain cells under the influence of alcohol. The disease, as a rule, occurs shortly before the transition or after the transition of the II stage of alcoholism to the III. The duration of constant alcohol consumption before the appearance of the first symptoms ranges from 7 to 20 years, but an earlier onset of the disease is also possible. In some cases, symptoms may occur in the absence of alcoholism against the background of periodic alcohol consumption.
Alcoholic encephalopathy is a serious disease and requires early qualified treatment. The number of deaths in this pathology according to various experts in the field of narcology is 30-70%. In other cases, the outcome, as a rule, is mental disorders of varying severity. It is possible to develop a psycho-organic syndrome, a pseudoparalytic syndrome or dementia. Treatment of alcoholic encephalopathy is long-term, carried out in a narcological hospital.
Causes of alcoholic encephalopathy
The cause of the development of this disease in the vast majority of cases is the prolonged use of large doses of alcohol. As a rule, the appearance of the first symptoms is preceded by binge drinking, which lasts for weeks or months, or the usual daily intake of alcohol for many years. The risk of the disease increases with the use of technical liquids and alcohol surrogates. Sometimes, due to the individual characteristics of the patient’s body, the disease develops in the absence of alcoholism, against the background of regular consumption of small doses of alcohol or rare alcoholic excesses.
The disease is based on metabolic disorders characteristic of alcoholism. The leading role is played by the lack of vitamins (first of all, group B). With constant alcohol consumption, the body’s need for vitamin B1 increases, and its level decreases. This is due to irregular monotonous diet, lack of appetite during binge drinking, deterioration of vitamin B1 absorption in the intestine and impaired liver function. The consequence of B1 deficiency is metabolic disorders in the brain. The problem is compounded by a lack of vitamin P and B6. Due to the deficiency of these vitamins, the functions of the digestive system are further disrupted, and the capillaries in the brain become more permeable, which can lead to cerebral edema.
Classification of alcoholic encephalopathy
Depending on the rate of development, prevailing symptoms, course characteristics and outcome options, two groups of alcoholic encephalopathies are distinguished: acute and chronic.
Acute encephalopathies include:
- hemorrhagic polyencephalitis (Gaye-Wernicke syndrome);
- mitigated acute encephalopathy;
- encephalopathy with a lightning course.
In the anamnesis of patients suffering from chronic encephalopathy, as a rule, severe alcoholic psychoses or acute encephalopathy are detected. There are two forms of chronic alcoholic encephalopathy:
- Korsakov psychosis (alcoholic paralysis, polyneuritic psychosis);
- alcoholic pseudoparalysis.
Acute alcoholic encephalopathies
Initially, symptoms appear-harbingers of the disease. Asthenia occurs in combination with sleep and appetite disorders. Patients feel aversion to foods rich in fats and proteins, and prefer foods with a high carbohydrate content, which contributes to the aggravation of metabolic disorders that have already occurred. Sometimes anorexia develops. Disorders of the gastrointestinal tract are detected. Nausea and vomiting often occur (especially in the morning). Abdominal pain, belching, heartburn and stool disorders are possible. The physical condition of patients deteriorates rapidly, weight decreases, exhaustion increases. Signs of alcoholic polyneuropathy may be detected.
Gaye-Wernicke encephalopathy
In the classic version, it begins with a delirium of moderate severity. Patients develop monotonous fragmentary visual illusions and hallucinations in combination with complex repetitive movements. Periods of excitement are replaced by short episodes of immobility, muscle tone during such episodes remains elevated. Patients mumble or shout something, productive communication becomes impossible.
There is swelling of the face in combination with general exhaustion. Ataxia occurs, multiple neurological disorders are detected (nystagmus, different pupil sizes, indistinct paresis, etc.). Body temperature is elevated, pulse and breathing are accelerated, there is a tendency to decrease blood pressure with deterioration of the general condition. On the part of the digestive system, a change in the color of the tongue (crimson) and an increase in the liver are detected. Possible violations of the chair. As the clinical symptoms worsen, progressive disturbances of consciousness occur – from mild stun to stupor. In severe cases, a coma develops.
Death may occur 10-15 days after the first symptoms of delirium appear. The probability of a fatal outcome increases with the addition of intercurrent diseases – pneumonia, bedsores, etc. With a favorable development of events, delirium lasts from 3 weeks to 1.5 months. The outcome of the disease is a psycho-organic syndrome, which is expressed in mental helplessness, memory impairment and loss of the ability to adapt to ordinary everyday life. In patients, the volitional sphere suffers, the ability to work and the level of resistance to stress decreases. The transition of acute alcoholic encephalopathy to chronic is possible.
Mitigated acute encephalopathy
It begins with harbingers in the form of asthenia, mood deterioration, loss of appetite and sleep disorders. There is a pronounced anxiety and a tendency to hypochondria. Neurological disorders are represented by mild neuritis. The prodromal period lasts 1-2 months, then delirium develops. After coming out of psychosis, there are residual phenomena in the form of asthenia and prolonged, poorly amenable to medical correction of memory disorders.
Super – acute form
It is characterized by rapid development and unfavorable course with frequent fatal outcomes. The duration of the harbinger period is about 3 weeks. Then severe psychosis occurs, accompanied by pronounced neurological and somatic disorders. The body temperature rises to 40-41 degrees, progressive disturbances of consciousness are observed. Within a few days, a coma occurs, and then death. The surviving patients develop a pseudoparalytic syndrome after the end of delirium – carelessness, a feeling of complete satisfaction with themselves and others, combined with a lack of criticism, overestimation of their capabilities and ridiculous behavior.
Chronic alcoholic encephalopathy
Korsakov ‘s psychosis
It is more often observed in women, manifested by memory disorders, false memories and disorientation. Patients do not remember new information well, they hardly remember what happened to them before the onset of the disease. In a conversation with patients, it turns out that they often “remember” events that did not happen in reality. Orientation in space, place and time is difficult. There is a poverty of speech and motor reactions. Neurological disorders in the form of neuritis are detected. With the abolition of alcohol, the symptoms of the disease can be reduced.
Alcoholic pseudoparalysis
Usually occurs in men. Both gradual development and rapid progression of symptoms after acute alcoholic psychosis are possible. Dementia is characterized by the loss of previous knowledge and skills, memory disorders and a decrease in criticism of their condition. There is coarsening (rudeness, cynicism) in combination with sudden mood swings. Neurological symptoms are represented by polyneuritis, speech disorders, trembling of the muscles of the hands and face.
Diagnostics
The diagnosis is made on the basis of anamnesis and clinical symptoms, differential diagnosis is carried out with other forms of psychosis, schizophrenia, malignant and benign neoplasms of the brain.
Treatment of alcoholic encephalopathy
Treatment involves the selection of a balanced menu with a high content of proteins and vitamins. Patients are prescribed high doses of vitamin B1, nootropics, drugs to improve cerebral circulation and activate metabolism in the brain. Concomitant somatic pathology is being treated.
The most important role in the successful treatment of alcoholic encephalopathies, minimizing residual effects and preventing the transition of the acute form of the disease into chronic encephalopathy is played by complete abstinence from alcohol. The choice of tactics and methods of treatment of alcohol dependence is determined by the narcologist individually, depending on the specific case. It is possible to insert an implant, use medical methods of treatment, hypnosuggestive therapy or coding according to Dovzhenko. It is advisable to conduct comprehensive rehabilitation with the subsequent supervision of a specialist, a visit to a psychotherapist or support groups.
