Alcoholic epilepsy

Alcohol refers to substances toxic to the human body, and alcohol epilepsy is one of the manifestations of its negative effect on the central nervous system. This condition is characterized by the development of convulsive and non-convulsive epileptiform seizures associated with alcohol abuse. It is attributed to one of the manifestations of alcoholic brain disease.

Causes of seizures

Single or episodic use of even a large dose of alcohol will not cause the development of convulsive syndrome, unless acute toxic cerebral edema develops. Attacks of alcoholic epilepsy are peculiar to people with a formed dependence, which is accompanied by a the defeat of many internal organs and the brain and dysmetabolic disorders.

The reasons for the appearance of convulsive syndrome with alcoholism are few, they usually combine and mutually reinforce each other's influence on the work of the central nervous system. The main components of the pathogenesis of alcohol epilepsy:

• excitotoxic activity of glutamate, which is released in excess from the association with specific NMDA receptors in the first few days of alcohol withdrawal;
• deficiency of vitamin B1 (thiamine) of nutritional origin, due to lack of its intake with food and disruption of digestion processes in the gastrointestinal tract;
• decrease in the amount and activity of the GABA neurotransmitter (gamma-aminobutyric acid), which leads to the predominance of neuronal excitation processes and increased convulsive readiness of the brain;
• deficiency of potassium and magnesium ions, associated with inadequate intake from food;
• direct damaging effect of ethanol on nerve tissue;
• increase in the permeability of the blood-brain barrier and vascular wall, which results in the arrival of toxic metabolic products and swelling of tissues to the nerve cells.

In addition, the risk of developing convulsive syndrome with alcoholism is increased by other factors. They have an indirect effect, leading to a disruption in the nutrition of neurons. For example, alcohol abusers often suffer from a decrease in glucose tolerance due to impaired pancreatic function and complex cascading disgomonal disorders. As a result, a subhypoglycemic condition may develop in a hangover period, which, in combination with other factors, may become one of the components of the pathogenesis of an epileptic attack.

A certain effect is also on the inhibition of the detoxification function of the liver together with the impairment of bilirubin metabolism. Also in the withdrawal period there is a thickening of the blood, leading to a disturbance of the microcirculation and aggravating the hypoxia of the nervous tissue.

With the passage of time, alcoholism leads to an increase in irreversible changes in the brain. There is an uneven atrophy of the cortex, various-caliber degenerative and ischemic foci appear in various subcortical structures, and neurotransmitter systems are depleted. At the same time they speak of alcoholic encephalopathy, accompanied by a progressive intellectual-mnestic decline and characteristic changes in personality. During this period, the appearance of convulsive seizures, not related to the time with the use of alcohol.

How is alcoholic epilepsy manifested?

Alcoholic epilepsy is characterized mainly by convulsive attacks that develop without a prior aura. They are generalized, that is, accompanied by deep oppression of consciousness. But it is possible to develop non-convulsive seizures of a different nature.

Initially, seizures develop during the withdrawal period, when an alcoholic person completely exits a drinking-bout or drastically reduces the dose of alcohol consumption. Seizures may appear by the end of the first day of alcohol withdrawal, but most often they are observed on day 2-3 of the interruption of the drinking-bout. Sometimes during life a person suffers only one attack, although he continues to alcoholize. But most often episodes of seizures are repeated. And in process of aggravation of a lesion of a nervous tissue with development of focal changes in a brain attacks can become frequent, vary on character and to lose direct connection with abstinent syndrome.

Features of convulsive paroxysms in alcohol epilepsy:

• generalized character;
• the sudden onset of an attack, the absence of harbingers (auras), although some authors refer to them appearance during the period of abstinence hallucinations, confusion, severe headache, dizziness and impaired coordination of movements;
• predominance of the tonic phase;
• symmetry of muscle contractions;
• the absence of the so-called march with the spread of seizures from one part of the body to the other;
• most often the absence of prolonged post-stupid stunning and sleep;
• withdrawal from the attack is often confused, within the next 24 hours hypnagogic hallucinations, insomnia and symptoms of a psychotic state ("fever") may appear.

At the expressed metabolic disturbances development of an epileptic status is possible: a series of consecutive convulsive attacks, between which a person does not come into clear consciousness and usually is in a state of deep sopor or coma.

In addition to the typical course of convulsive syndrome, a small number of alcohol sufferers may develop other forms of epilepsy. For example, less than 5% of cases are accompanied by focal seizures. Possible absences, dysphoria attacks and other non-convulsive paroxysmal conditions.

The picture of convulsive syndrome with alcoholism

The seizure attack with alcoholic epilepsy develops against the backdrop of increasing mental and somatic manifestations of withdrawal syndrome. It begins with a sudden loss of consciousness and the fall of a man, often because of spasm of muscles of the larynx, there is a characteristic scream. The resulting continuous tonic convulsions of all muscle groups lead to a head tilt, a temporary stop of breathing (apnea). Skin sharply turns pale, often marked cyanosis of the face and neck, pupils usually expand. The body arches, the limbs take a forced deformed position due to the uneven toning of flexors and extensors.

The subsequent, clonic seizure phase is usually poorly expressed. When you leave the attack, breathing is restored, at first it becomes noisy and uneven, then acquires a frequency and depth that is characteristic earlier. Perhaps involuntary urination and even defecation, caused by a sharp relaxation of sphincters. The person who has undergone a convulsive fit is usually not structurally disoriented, not critical and does not remember what happened, can be in a state of psychomotor agitation and show aggression towards those trying to help him. In contrast to the classic epileptic seizure, alcohol-related convulsions may not result in deep sleep and asthenic conditions. Within a few days a person can note burning or aching pain in the muscles.

Diagnostics

When there are seizures associated with drinking, you should exclude other possible causes of their occurrence. For example, it can be true epilepsy, hypoglycemia, poisoning with alcohol substitutes or taking medications, acute renal-hepatic insufficiency, subdural or subarachnoid hemorrhage, and a number of other pathologies. Therefore, a number of tests are recommended: a biochemical blood test, a radiograph of the skull, and if necessary also CT or MRI of the brain. An important diagnostic method is the EEG, in the case of alcoholic epilepsy, it does not reveal typical epileptic signs.

Often, patients who have suffered a seizure attack, after independent withdrawal from it, refuse further examination. Inpatient examinations are often only hospitalized with serial seizures or epileptic status, and also undergoing treatment for alcoholism and its consequences.

Currently used by doctors ICD-10 allows attributing alcoholic epilepsy to different headings, there is no separate nosological unit with this name. Diagnoses can be established: an organic brain disease of alcoholic origin with convulsive syndrome (F 06), withdrawal syndrome with convulsive seizure (F 10).

Treatment and prognosis

Specific and preventive treatment of alcohol epilepsy does not exist, the only prevention of the development of seizures is a complete refusal to drink alcohol. To stop the convulsive syndrome, use intravenous tranquilizers (preferably seduksen) and hypertensive glucose solution, in the case of epileptic status, injections of thiopental sodium and hexenal are indicated. It is possible to use anticonvulsants of different groups, mainly carbamazepine and valproate. In some cases, a decision is made to conduct a medical-diagnostic spinal cord puncture with the removal of up to 10 ml of fluid. This allows you to reduce the pressure of the cerebrospinal fluid, but increases the risk of brain wedging when it swells. Therefore such manipulation is carried out only in stationary conditions.

Pathogenetic treatment includes the administration of a thiamine solution, replenishment of the BCC deficiency (circulating blood volume) and elimination of blood clotting, correction of electrolyte and endocrine disorders. They also take measures to maintain the functioning of the liver and kidneys, improve microcirculation and increase trophism of tissues.

The prognosis of alcoholic epilepsy depends on the patient's further behavior. Complete refusal of alcohol prevents further progression of encephalopathy and is the best prevention of repeated convulsive syndrome. Continuation of alcoholization will lead to an increase in signs of brain damage with a decrease in cognitive functions, depletion emotions and needs, the appearance of polymorphic neurological disorders and the possible repetition of convulsive attacks.