Anticonvulsants for alcoholic epilepsy

Treatment of alcoholic epilepsy at the Brain Clinic is carried out on the basis of strict anonymity.

To treat alcoholic epilepsy, our specialists use the most advanced, gentle methods of restorative medicine, using special intensive hospital replacement therapy. This gives a quick and lasting effect. At the same time, for the full treatment of alcoholic epilepsy in our clinic, inpatient treatment of alcoholic epilepsy is offered extremely rarely, only in the most severe cases.

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Alcoholic epilepsy - what is it?

Alcoholic epilepsy is a severe brain damage caused by prolonged use of large doses of alcohol. The disease can manifest itself both in the form of classic convulsive seizures and in the form of non-convulsive epilepsy.

For reference. The development of symptoms of alcoholic epilepsy (AE) is associated with the toxic effects of ethanol on the nervous system.

Systematic drinking of alcohol leads to damage to nerve cells, the development of alcoholic encephalopathy and alcoholic dementia . AE occurs in 10-30% of patients suffering from chronic alcoholism. At the same time, in patients who have previously suffered from alcoholic delirium, the incidence of alcoholic epilepsy increases to 42%.

Alcoholic epilepsy most often develops in patients 26-46 years old after 7-10 years of drinking alcohol (the end of the 2nd or the beginning of the 3rd stage of alcoholism).

With severe alcohol intoxication, as well as in the presence of concomitant diseases, alcoholic epilepsy can develop much earlier (2-3 years after the onset of chronic alcohol consumption).

Initially, symptoms of epilepsy in alcoholics appear after drinking alcohol, but as the disease progresses, seizures begin to bother the patient even in a sober state.

Our specialists

Yushina Maria Alexandrovna
Head of the Center for Epilepsy and Paroxysmal Conditions.
The doctor is a neurologist. Epileptologist. Ozone therapist. Experience: 6 years.
Kordonskaya Irina Sergeevna
Pediatric neurologist of the highest category. Epileptologist. Neurophysiologist (EEG diagnostic doctor). Experience: 23 years.
Volkova Svetlana Anatolevna
The doctor is a neurologist of the highest category. Epileptologist. Ozone therapist. Physiotherapist. Experience: 25 years.
Derevianko Leonid Sergeevich
Head of the Center for Diagnostics and Treatment of Sleep Disorders.
The doctor is a neurologist of the highest category. Vertebrologist. Somnologist. Epileptologist. Botulinum therapist. Physiotherapist. Experience: 22 years.
Tarasova Svetlana Vitalievna
Expert No. 1 in the treatment of headaches and migraines. Head of the Center for the Treatment of Pain and Multiple Sclerosis.
Somnologist.
Epileptologist. Botulinum therapist. The doctor is a neurologist of the highest category. Physiotherapist. Doctor of Medical Sciences.
Experience: 22 years.
Palagin Maxim Anatolievich
The doctor is a neurologist. Somnologist. Epileptologist. Botulinum therapist. Physiotherapist. Experience: 5 years.

Causes of alcoholic epilepsy

The main cause of alcoholic epilepsy is intoxication and damage to brain tissue as a result of prolonged consumption of large amounts of alcohol.

The pathogenesis of the development of symptoms of alcoholic epilepsy includes:

progressive deficiency of vitamin B1, magnesium and potassium, caused by chronic alcohol intoxication, impaired absorption processes in the intestines, as well as a deficiency of vitamins and minerals in food (patients with chronic alcoholism have no appetite, so they develop exhaustion, vitamin deficiency and a deficiency of useful macro- and microelements);
damage to nerve tissue by alcohol and its breakdown products;
disruption of the liver, leading to inhibition of its detoxification and protein synthetic functions;
pathological excitation of brain neurons and increased convulsive readiness due to a decrease in the level of gamma-aminobutyric acid;
intoxication and pathological excitation of neurons due to an excess of toxic glutamate and the development of withdrawal syndrome after stopping alcohol consumption;
blood thickening and increased risk of thrombosis during the hangover period;
oxygen starvation of the brain and impaired cerebral circulation .

For reference. Gradually, as alcoholism progresses, the severity, area and depth of damage to brain tissue increases. Against the background of the gradual death of neurons and destruction of the cortex and subcortical structures of the brain, the development of alcoholic encephalopathy, dementia, and alcoholic epilepsy is noted.

Characteristic

Epilepsy and alcohol are interrelated. Epilepsy after chronic binge drinking is a common complication that leads to epileptic seizures with or without convulsions. Seizures reflect the reaction of the central nervous system to ethyl alcohol poisoning. Initially, epileptic seizures develop after taking a dose of alcohol and then giving it up. Later, against the background of chronic alcoholism, episodes of convulsive seizures occur spontaneously, regardless of the fact of alcohol consumption.

Alcoholic epilepsy is a condition characterized by repeated episodes of loss of consciousness and tonic-clonic seizures, often accompanied by dilated pupils and other characteristic signs. The attack consists of 2 phases. In the first (tonic) phase, the patient suddenly loses consciousness, falls, the face is distorted by a grimace, the skeletal muscles tense, the eyeballs involuntarily move upward.

Due to increased muscle tone, the head tilts back. The arms are bent at the elbow joints, often pressed to the chest. The fingers are clenched into a fist. The legs are bent at the knee joints, often pulled towards the abdominal area or spread in different directions. Another variant of the posture of a patient who is in the tonic phase is that the spine is in a state of retroflexion (turning in the opposite direction), arches back, and the arms are extended in the forward direction.

The forced position of the limbs is often associated with injuries - dislocation of the femoral neck (with a sharp spread of the legs to the sides), a fracture of the spinal column in the lumbar or thoracic region (with retroflexion of the spine). Traumatic injuries to the tongue and inner surface of the cheeks are common consequences of an epileptic attack that occurs while drinking large amounts of alcohol. Usually the patient bites the tongue and mucous membranes of the cheeks, causing blood-colored foam to come out of the mouth.

There are frequent cases of amputation of the tip of the tongue as a result of a sharp clenching of the jaws due to convulsive contraction of the muscles of the maxillofacial apparatus. Foam protruding from the mouth is a mixture of saliva, bronchial secretions, and blood that appears due to mechanical damage to the mucous membranes of the oral cavity and tongue. Due to muscle spasms located in the chest, diaphragm and abdominal area, the breathing process is disrupted or suspended.

At the beginning of a convulsive attack, paleness of the skin is observed. Impaired breathing results in a bluish discoloration of the skin. At the same time, cardiac activity may cease for a short time. Staying in the tonic phase is accompanied by total areflexia - the absence of reflexes, provoked by a violation of the regulatory function of the central nervous system.

The patient has no reaction to external stimuli at all. In the event of an unsuccessful fall, colliding with hard, sharp, hot objects, the patient often receives damage to the bone structures of the limbs, skull and brain matter of the head, skin and other parts of the body. Usually the duration of the tonic phase does not exceed 30 seconds.

In the second (clonic) phase, alternation of convulsions and a state of relaxation of skeletal muscles occurs. Convulsions are involuntary pathological contractions of muscle groups, relaxation is relaxation of skeletal muscles. Rhythmic twitching is initiated in the eyelids and distal fingers. With increasing strength, the spasms spread towards the muscles of the head, neck, arms and legs, and body. Then the generalized seizure subsides.

The amplitude of flexion and extension movements is greater in the upper extremities compared to the lower extremities. During the clonic phase, the head turns from side to side, the eyeballs rotate, and involuntary, frequent chewing movements occur in the area of the lower jaw. Various facial grimaces alternate with each other and arise due to random contraction of the facial muscles. During the clonic phase, patients experience spontaneous urination and defecation.

The duration of the phase varies between 1-3 minutes. At the final stage, the amplitude and frequency of muscle contractions decrease, respiratory activity is restored, and manifestations of cyanosis (bluish tint of the skin) are eliminated. Some time after the end of the attack, a number of patients experience residual, unexpressed signs of respiratory dysfunction (delays, intermittent breathing), and a slight increase in muscle tone.

A convulsive attack ends in a coma, which is manifested by areflexia, relaxation of skeletal muscles, and increased sweating. A state of stupor then occurs, which later transforms into deep sleep or a state of wakefulness with clear consciousness. A person who has suffered an attack experiences increased salivation, excessive sweating, and hypersecretion of the bronchial membranes.

Risk factors for developing alcoholic epilepsy

The risk of developing alcoholic epilepsy, as well as more intense progression of the disease, is observed when drinking low-quality alcoholic beverages containing large amounts of toxic impurities.

Also, the development of alcoholic epilepsy is promoted by:

the presence of a genetic predisposition (the presence of chronic forms of alcoholism, epilepsy or psychoneurological diseases in close relatives);
traumatic brain injuries, tumors, cysts, aneurysms in the brain;
previous neuroinfections;
cerebrovascular accident (atherosclerosis of the neck and brain vessels, severe cervical osteochondrosis);
the presence of concomitant dementia or severe liver disease;
onset of alcohol abuse at a young age;
drug use;
long-term use of psychotropic drugs.

Symptoms

Sometimes an attack of epilepsy in drunk people is preceded by a state of nervousness, psychomotor agitation and other signs characteristic of a hangover (withdrawal) syndrome. The patient becomes aggressive and irritable, reacts emotionally and painfully to harmless remarks. He has sleep disorders and speech disorders (incoherent muttering, illogical phrases). Restless sleep is often accompanied by hallucinations and unpleasant dreams, in which the theme of nightmares prevails.

More often, the symptoms of alcoholic epilepsy do not appear immediately before the attack. Loss of consciousness and subsequent fall occur suddenly. Typically, an episode of falling is accompanied by a cry, forced movement of the head back or to the side. In 70% of cases, unprovoked seizures occur during the day, in 30% of cases - at night. After the seizure ends, the patient becomes lethargic and drowsy. In 80-90% of cases, patients do not remember the onset and fact of the attack.

After the end of an epileptic attack associated with a hangover, symptoms appear - sleep disturbance, delirium (a mental disorder manifested by confusion, impaired perception, emotional disturbance, deterioration of concentration and mental activity). At the same time, hallucinations are observed, which after the end of the attack and exit from the binge state become pronounced and intense.

The later stages of alcoholism are dangerous due to irreversible changes that occur in the brain. It is impossible to completely cure a long-term pathological process - changes in the morphological structure of nervous tissue, disruption of neural connections and mechanisms are irreversible.

Alcoholic epilepsy - classification

Depending on the symptoms, alcoholic epilepsy is divided into: convulsive and non-convulsive (absence seizures). The convulsive form of alcoholic epilepsy is more common.

This type of disease is especially common among binge alcoholics.

For reference. Drinking large amounts of alcohol, as well as subsequent withdrawal from binge drinking, can provoke the development of an extensive convulsive attack, accompanied by loss of consciousness and clonic convulsions.

Also, seizures in AE are divided into: epileptic reactions, epileptic syndromes and classic alcoholic epilepsy.

Epileptic reactions include single or episodic convulsive attacks associated with alcohol consumption in persons who do not suffer from chronic alcoholism. Epileptic reactions most often develop when consuming low-quality alcohol, large doses of alcohol, as well as in the presence of concomitant neurological diseases.

Epileptic syndrome is a precursor to alcoholic epilepsy. It develops in people suffering from chronic alcoholism and manifests itself in the form of recurrent epileptic seizures. The symptoms of this condition are similar to those of alcoholic epilepsy.

Alcoholic epilepsy develops against the background of chronic alcoholism and is manifested by an epileptic aura, the appearance of convulsions against the background of deep depression of consciousness (non-convulsive absence seizures are less common), symmetrical clonic convulsions, deep sleep after a convulsive attack.

It should be noted that the symptoms of alcoholic epilepsy are combined with other manifestations of chronic alcoholism:

limb tremors,
lack of appetite,
weight loss,
decreased intelligence,
degradation and disintegration of personality,
nervousness and increased aggressiveness,
frequent mood changes.

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Alcoholic epilepsy - symptoms

The first signs of alcoholic epilepsy most often develop at the end of the second or at the beginning of the third stage of chronic alcoholism.

Alcoholic epilepsy is characterized by the presence of an aura (harbingers) of an attack. Most often during the aura period, patients are concerned about:

mood swings,
emotional instability,
feeling of fear or panic attacks,
increased anxiety,
negative intrusive thoughts,
headache,
increased fatigue.

Pathological psychomotor agitation (often combined with delusions or hallucinations), increased aggressiveness and irritability, and incoherent speech are also often observed.

During periods of heavy drinking, large convulsive seizures most often develop (in this case, the aura may be absent or last several seconds). As the disease progresses, non-convulsive absence seizures or convulsive epileptic seizures may occur during the period of sobriety.

For reference. Classically, a major attack of AE usually begins with the patient losing consciousness and falling. Due to spasm of the glottis, the fall is often accompanied by a specific cry.

Then a tonic muscle spasm develops, manifested by spasm of the jaw muscles, forced throwing back of the head, and stretching of the limbs along the body.

Tonic convulsions, manifested by twitching of the limbs, eyes, and lower jaw, may be mild.

Also characterized by deep depression of consciousness, the appearance of involuntary urination and defecation, hallucinations, and delusions.

For reference. After an attack, the patient does not remember what happened (post-attack amnesia).

In severe cases, a convulsive attack can develop into status epilepticus (convulsions lasting more than half an hour).

Absences (non-convulsive seizures) are manifested by a temporary switching off of the patient’s consciousness. In this case, the patient freezes, lacks a reaction to external stimuli, and has a blank gaze directed at one point.

After the absence seizure stops (10-20 seconds), the patient continues his activities without remembering that he had an attack.

Distinctive signs of alcoholic epilepsy

Alcoholic epilepsy almost always occurs with an aura (much less often there are no previous symptoms), accompanied by headaches, hallucinations, and irritability.
A convulsive attack develops against the background of deep depression of consciousness.
Short nonconvulsive seizures develop less frequently than convulsive seizures.
Alcoholic epilepsy is characterized by symmetrical clonic and tonic muscle contractions.
The clonic phase of convulsions (muscle twitching) is less pronounced than the tonic phase (spasm, muscle tension).
After the attack, the patient is in a lethargic, stunned state. Hallucinations and delusions may occur.
After the end of the attack, a long, deep sleep is often observed.
After returning to a normal state, the patient does not remember the attack.

Symptoms and features of the disease

Doctors understand a seizure as a convulsive reflex that occurs against the background of overexcitation of the neural system of the brain.

Doctors understand a seizure as a convulsive reflex that occurs against the background of overexcitation of the neural system of the brain. The seizure is accompanied by foam at the mouth, erratic movements, and loss of consciousness. Sometimes the movements become too sharp, and the patient can damage his own body. The alcoholic must understand that such seizures will be repeated more often; the occurrence of seizures cannot be determined periodically. But you can understand when epilepsy occurs:

A seizure most often occurs the day after binge drinking.
Before the onset of an attack, the patient experiences pressure in the legs, arms, and a burning sensation.
There is a sharp change in mood towards aggression, uncontrollable anger.
Confusion of speech, fragmentation, fog of consciousness.
Dreams are often accompanied by nightmares, turning into delirium delirium.
Constant auditory, visual and olfactory hallucinations appear. The patient sees what is not really there, taking everything that happens as reality.

Important! An ECG procedure will not show the presence of the disease. Hardware examination does not reveal attacks of ordinary non-alcoholic epilepsy.

The patient screams in pain.
There is a bluish discoloration of the nasolabial triangle.
The head is thrown back, the skin turns pale and covered with perspiration.
Saliva is produced profusely.

The duration of the condition is up to several minutes, leaving behind obvious signs of the disease: hallucinations, tremors. Hallucinations have their own “picture” - most often they are crawling insects and mythological monsters. The patient’s condition at such a moment is dangerous for others.

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Alcoholic epilepsy - consequences

A convulsive attack can be complicated by transition to status epilepticus, sudden death syndrome, the patient falling into a coma, severe cardiac arrhythmia, circulatory arrest, impaired blood supply to internal organs, severe injuries from a fall, neurogenic edema of the lungs and brain, and aspiration pneumonia.

For reference. When an attack of alcoholic epilepsy transitions into status epilepticus, the development of malignant hyperthermia (increased body temperature), electrolyte disturbances, and severe oxygen starvation of the brain is possible.

Also, during an attack, the patient may choke on vomit or die from suffocation due to the retraction of the tongue.

After the end of the attack, hallucinations, psychotic disorders, aggressive behavior, and a tendency to autotraumatization and suicide may appear.

It is also important to consider that alcoholic epilepsy is accompanied by progressive dementia, personality decay, decreased intelligence, and the appearance of mental disorders.

For reference. The most common causes of death in alcoholic epilepsy are trauma, cerebral edema, life-threatening arrhythmias, asphyxia due to tongue retraction or aspiration of vomit.

Symptoms

This is how a typical attack of alcoholic epilepsy can proceed. Against the background of the onset of sobriety, the person suddenly turns pale, acrocyanosis, cyanosis of the skin of the upper body and face develops. The head is thrown back (or lowered to the chest), the hands are bent inward, the arms are bent at the elbows and brought towards the body. The legs are pulled up at the knees, the teeth close tightly, their grinding is often heard, and the patient emits a lowing groan. Possible involuntary urination, apnea.

Breathing slows down to 8-10 per minute, pulse increases to critical numbers - 120-170 per minute, pressure rises, pupils are constricted, the person does not respond to someone addressing him, reflexes are sharply reduced or depressed.

Sometimes, against the background of a similar condition, a person does not experience tonic convulsions; instead, he notices how convulsions, starting in one place (usually in a limb or on the face), spread in a wave further, covering the entire half of the body. You can see how his muscles twitch near his mouth, followed by cramps in his arm or on the anterior abdominal wall.

Sometimes patients experience so-called precursors of an epileptic attack. Those suffering from alcoholic epilepsy also have them, and are most often expressed in the form of a sudden increase in anxiety, aggressiveness, and negativism. As a rule, you can expect a convulsive attack within 1-2 days after this. Unfortunately, against the background of alcohol withdrawal, these signs often remain unrecognized because they are confused with signs of recovery from binge drinking.

First aid for alcoholic epilepsy

When an aura appears, it is necessary to lay the patient on a flat surface. If possible, place the edge of a blanket or a low pillow under your head.

To facilitate oxygen access, the patient should be freed from constricting clothing (remove the scarf, unbutton the top buttons of the shirt).

You should also turn the patient's head to the side so that he does not choke on vomit and call an ambulance.

Attention. Treatment of a patient with alcoholic epilepsy should be carried out in a narcological hospital.

First aid

The main commandment of first aid during attacks of alcoholic epilepsy (as well as any other convulsive seizures) is the refusal to forcibly restrain a person. It is necessary to create all the conditions to prevent injuries during an attack, but you cannot fix it, try to “bring it to your senses,” or hold a convulsively twitching muscle.

Alcoholic epilepsy or a similar condition that appears in a person for the first time requires calling an ambulance. Before her arrival, the patient must be laid on the floor or seated on a wide bench or bed, thus eliminating the possibility of falling and additional injuries. Unbutton your shirt collar, loosen your belt or waistband, and support your head by gently holding it on your lap or adjusting it on a pillow. It is better to turn your head (and, if possible, fix the whole body) on its side, this will prevent suffocation with a sunken tongue and choking on saliva.

There is no need to try to “start” breathing during apnea - neither by artificial respiration, nor by blows to the chest or cheeks. After the end of the convulsions, you need to monitor the victim for at least half an hour - during this period they may recur.

It is prohibited to give any medications, dietary supplements, herbs or any forms of them.

The arriving ambulance must be given a complete picture of the medical history, without hiding the past binge, and describe the nature, duration, and intensity of the convulsive attack (or other manifestations).

If an attack lasts more than 3 minutes, if a person does not regain consciousness within half an hour after the end of the convulsions, calling an ambulance is necessary, regardless of whether this is the first case or epileptic seizures have been noted before.

Alcoholic epilepsy - treatment

Anticonvulsant therapy is used to relieve an acute attack. Detoxification therapy is also carried out, antioxidants, vitamin C and B vitamins are introduced. Additionally, symptomatic therapy is carried out.

The basis of treatment for alcoholic epilepsy is complete abstinence from drinking alcohol.

Attention. If the patient continues to drink alcohol, any treatment will not be effective. Anticonvulsants will only have a temporary effect, but the disease will still continue to progress.

In addition to the symptoms of AE, liver dysfunction, signs of alcoholic encephalopathy and dementia will continue to progress.

What it is?

Epilepsy is a neurological disorder accompanied by sudden seizures and further degenerative personality changes. Alcoholic epilepsy manifests itself in convulsive and non-convulsive seizures that occur in people suffering from alcohol dependence.

Similar disorders can also be observed in persons who do not have a morbid addiction to ethanol after a single use of alcohol or pharmaceutical preparations containing alcohol. In fact, there is no separate nosological form (the diagnosis of “Alcoholic epilepsy”). This disease is a complex of various pathological conditions that have similar developmental mechanics.

The International Classification of Diseases interprets a similar group of symptoms as the occurrence of convulsive seizures provoked by alcohol intoxication or withdrawal syndrome accompanied by organic damage to the brain and nervous system. According to official statistics, epileptic seizures are observed in approximately 1–2% of chronic alcoholics.

A condition such as a grand mal seizure, provoked by ethanol, occurs in several phases: tonic is accompanied by loss of consciousness; during clonic, the muscles of the face, limbs and torso contract convulsively

The disease is usually accompanied by a high fever, and after an attack, the patient most often falls into a state of prostration and disorientation, from which it takes at least several days and the support of his close circle to recover. Epilepsy and alcohol have a close relationship, so the occurrence of a pathological disorder can only be prevented by completely abstaining from alcohol.

Literature

Maksimova Irina Viktorovna, Berezovskaya Marina Albertovna, Korobitsina Tatyana Valerievna Clinical and psychopathological features of patients with alcoholism with convulsive syndrome // Siberian Medical Review. 2020. No. 5 (95).
Donskoy V.V., Sukhanova N.S., Gusev A.M., Kolontai M.V. Convulsive syndrome in alcoholism // Omsk Psychiatric Journal. 2014. No. 2 (2).
Kushnir G.M., Ioshina N.N. Epileptic seizures in patients with alcoholism // Tauride Journal of Psychiatry. – 2020. – T. 19. – No. 2 (71).

Diagnostics

The majority of patients have a history of episodes of blackouts, which are accompanied by tonic-clonic seizures and are not associated with the consumption of alcoholic beverages. Often, epilepsy attacks occur several years after treatment for alcohol dependence and complete abstinence from alcohol. The main method of instrumental research is electroencephalography, during which the following signs are revealed in patients with alcoholism:

Increased epileptic activity during sleep compared to wakefulness in patients with a history of epileptic seizures.
Areas of epileptic activity in patients with a history of epileptic seizures are predominantly detected in the hippocampus (part of the limbic system responsible for the formation of emotions and the integration of short-term and long-term memory).
An increase in epileptic activity (a decrease in the seizure threshold) in patients who drink alcohol without a history of epileptic seizures, which indicates a high risk of developing epilepsy of alcohol origin in the future.

Based on the results of the encephalogram, an alcoholic seizure is regarded as partial (correlating with damage to nerve cells in a separate zone in one of the cerebral hemispheres) with secondary generalization (characterized by the spread of an epileptic discharge to both hemispheres of the brain, which leads to the development of a generalized seizure).

During the physical examination and neuropsychiatric testing, the neurological status of the patient is revealed, including such characteristics as stability in the Romberg position, results of the Barany finger-finger test, the presence of tremor of the head and extremities, and headache.