Gaie-Wernicke syndrome is named after the French doctor Gaie and the German neuropsychologist Wernicke. The first described the disease, which he called "diffuse encephalopathy", the second - gave a description of a similar clinical picture called "upper acute polioencephalitis", because he believed that it was based on inflammatory processes. Gaie-Wernicke encephalopathy occurs mainly in men aged 30-50 years, most often in the period from 35 to 45 years. However, in the modern literature on neurology, one can find single descriptions of the development of the syndrome before the age of 30. Although alcohol abuse is not the only cause, most often Gaie-Wernicke syndrome occurs precisely on the basis of alcoholism, in connection with which it is classified as acute alcoholic encephalopathy.
Causes of Gaie-Wernicke syndrome
According to modern ideas, Gaie-Wernicke syndrome is caused by a pronounced deficiency in the body of thiamine (vitamin B1).
the latter is a cofactor of several enzymes involved in various metabolic processes human body... As a result of B1 deficiency, biochemical reactions provided by these enzymes are inhibited. The consequence is a decrease in the utilization of glucose by nerve cells, that is, their energy starvation, and extracellular accumulation of glutamate. Glutamate acts as an activator of ion channel receptors in cerebral neurons. Its increased concentration leads to hyperactivation of the channels through which calcium ions enter the nerve cell. An excess of intracellular calcium entails the activation of a number of enzymes that destroy the structural elements of the cell, primarily mitochondria, and initiate apoptosis (self-destruction) of neurons.
Characteristic is periventrivular lesion of cerebral tissues in the region of the III and IV ventricles, sylvian aqueduct. Structures of the brain stem and diencephalon, the cerebellar worm, mediodorsal nucleus of the thalamus are mainly affected. Memory disorders accompanying Gaie-Wernicke syndrome are associated with the pathology of the latter.
Any pathological processes leading to thiamine deficiency can be the cause of the disease. For example, hypovitaminosis, gastrointestinal diseases with malabsorption syndrome, prolonged fasting, inadequate parenteral nutrition, constant vomiting, AIDS, some helminthiasis, oncological diseases leading to cancer cachexia, etc.
However, in most cases Gaie-Wernicke syndrome is associated with chronic alcoholism. The duration of alcohol abuse before the onset of the syndrome varies from 6 to 20 years, in women it can be only 3-4 years. As a rule, Gaie-Wernicke syndrome manifests itself in the third or at the end of the second stage of alcoholism, when daily alcohol consumption lasts for months. At the same time, 30-50% of patients already have a history of alcoholic psychosis.
As a rule, Gaie-Wernicke syndrome debuts after a prodromal period, the duration of which ranges on average from several weeks to months. Asthenia, anorexia with aversion to certain foods, stool instability (constipation alternating with diarrhea), nausea and vomiting, abdominalgia, sleep disturbances, cramps in the fingers and calf muscles, decreased vision, dizziness. In some cases Gaie-Wernicke syndrome debuts without a prodrome against the background of acute somatic or infectious pathology, withdrawal symptoms.
The characteristic triad of the manifestation of Gaie-Wernicke's acute encephalopathy is: confusion, ataxia, oculomotor disorders (ophthalmoplegia). However, it is observed in only 35% of patients. In most cases, there is an inability to concentrate, apathy, disorientation, lack of coherent thinking, disorder of understanding and perception.
whether Gaje-Wernicke syndrome debuts against the background of withdrawal symptoms, alcoholic delirium is possible, accompanied by psychomotor agitation. Ataxia is usually expressed to the degree of abasia - the inability to walk on their own and even stand. It is mixed: cerebellar, vestibular and sensitive. The latter is caused by polyneuropathy, the presence of which is stated in 80% of cases. Eye disorders include strabismus, horizontal nystagmus, drooping of the upper eyelid, discoordination of friendly eye movements; in the later stages - miosis.
Gaie-Wernicke encephalopathy is often coma and fatal if left untreated. Against the background of the therapy, there is a gradual regression of the above symptoms. First of all, ophthalmoplegia disappears. This can happen a few hours after the start of the introduction of vitamin B1, in some cases - after 2-3 days. In the absence of such dynamics, the diagnosis should be revised. Consciousness disorders regress more slowly. Against this background, problems with the assimilation of new information and memory impairments (fixation amnesia, false memories), which make up the clinic of the Korsakov syndrome, are gradually emerging.
Of the oculomotor disorders, in half of the patients, horizontal nystagmus persists, which occurs when the gaze is shifted to the side. A similar vertical nystagmus can be observed for 2-4 months. Reverse development of ataxia and vestibular disorders can take weeks to months. In about 50% of patients, persistent residual ataxia remains, and walking remains awkward and slow.
A neurologist can diagnose Gaie-Wernicke syndrome by anamnesis data, a characteristic clinical picture, regression of symptoms during thiamine therapy. On examination, attention is paid to the signs of chronic nutritional disorders (low body weight, dry skin and decreased elasticity, deformation of the nails, etc.). In the neurological status, a disorder of consciousness, mixed ataxia, ophthalmoplegia, polyneuropathy, signs of autonomic dysfunction (hyperhidrosis, tachycardia, arterial hypotension, orthostatic collapse) are noted.
In a biochemical blood test, a significant decrease in the activity of transketolase and an increase in the concentration of pyruvate are possible. After a lumbar puncture, a study of the cerebrospinal fluid determines that it is normal. If pleocytosis or a protein content of more than 1000 g / l is detected, one should think about the development of complications. The caloric test diagnoses the presence of almost symmetrical bilateral vestibular disorders.
In half of the cases, Gaie-Wernicke syndrome is accompanied by a generalized slowing down of EEG waves. REG often determines a diffuse decrease in cerebral blood flow.
the brain, as a rule, does not register pathological changes in cerebral tissues. MRI of the brain reveals hyperintense areas in the medial nuclei of the thalamus, mammillary bodies, walls of the third ventricle, reticular formation, gray matter surrounding the sylvian aqueduct, roof of the midbrain. The affected areas tend to accumulate the contrast introduced during additional contrast enhancement during MRI. In these areas, petechial hemorrhages and signs of cytotoxic edema can be determined.
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Gaia Wernicke syndrome - what is it?
Gaie Wernicke (wernicke's encephalopathy) Is an acute lesion of the midbrain and hypothalamus as a result of thiamine deficiency in the human body, which occurs during the chronic use of alcoholic beverages.
The disease is associated with a decrease in the number of neurons, gliosis and demyelination in the periventricular gray matter. This problem belongs to organic-toxic psychoses and often occurs in conjunction with Korsakoff's syndrome. The disease proceeds acutely, subacutely or chronically.
The reasons
Gaia Wernicke's disease most often due to vitamin B1 deficiency, alcoholism, complete exhaustion of the body. Fasting, hemodialysis, malignant tumor formations, AIDS also predispose to the onset of this disease.
Other causes of Gaie-Wernicke encephalopathy are:
- gastrointestinal diseases;
- vomiting during pregnancy;
- vomiting in case of poisoning with digitalis drugs.
Symptoms characteristic of Gaje Wernicke's encephalopathy are:
- ataxia (impaired coordination of movements);
- confusion of consciousness;
- ophthalmoplegia (paralysis of the muscles of the eye due to damage to the oculomotor nerves);
- disorientation;
- apathy;
- irritability.
Diagnostics
Gaie-Wernicke syndrome is diagnosed by a neurologist. Laboratory tests of blood, cerebrospinal fluid, MRI and computed tomography of the brain are prescribed.
Patients with the syndrome have such deviations:
- macrocytic anemia - in the peripheral blood;
- in the cerebrospinal fluid - increased protein content (<90 мг%);
- mastoid atrophy on CT and MRI.
Treatment for Gaie-Wernicke syndrome
Treatment for Gaje-Wernicke syndrome includes:
- taking vitamin B (thiamine);
- intake of vitamins B2, B6, nicotinic and ascorbic acid, anabolic steroids;
- taking magnesium sulfate 25 solution;
- psychological therapy.
Danger
If Gaie-Wernicke Syndrome is not promptly treated, this can lead to the following negative consequences:
- changes in human behavior and life;
- the inability to restore the work of the brain;
- amnesia or partial memory loss;
- drowsiness;
- loss of consciousness;
- persistent heartburn;
- schizophrenia;
- brain tumor;
- complete atrophy of brain activity.
In case of untimely treatment, a coma may occur, and then death.
Risk group
The main risk group is made up of men aged 35 to 65 years who abuse alcoholic beverages. Women between the ages of 30 and 65 are also at risk.
Prevention
- give up the abuse of low-alcohol and strong alcoholic beverages;
- establish regular and nutritious meals;
- ensure adequate sleep;
- exercise regularly.
medcentr.online
Gaie-Wernicke syndrome (Wernicke's disease, upper acute hemorrhagic Wernicke polioencephalitis) is an acute form of alcoholic encephalopathy. It usually occurs in men aged 35-45 years.
Gaye-Wernicke ndrom is classified as alcoholic encephalopathy, severe damage to the central nervous system resulting from alcohol abuse. There is also a chronic form of alcoholic encephalopathy, Korsakov's psychosis. For all forms of encephalopathy, a period of pre-disease of varying degrees of duration is characteristic: from several weeks to a year or more, it is the shortest in the hyperacute form of 2-3 weeks. This period is characterized by the development of asthenia with a predominance of adynamia, decreased appetite up to complete anorexia, aversion to fatty and protein-containing foods. Quite a common symptom of vomiting, mainly in the morning. Heartburn, belching, abdominal pain, and unstable stools are often noted. Physical exhaustion increases. For the state of the prodrome, sleep disturbances, difficulty falling asleep, shallow superficial sleep with vivid nightmares, frequent awakenings, and early waking up are typical. There may be a perverse sleep-wake cycle: sleepiness during the day and insomnia at night. More often, there are sensations of chills or heat, which are accompanied by sweating, palpitations, pain in the region of the heart, feeling short of breath, usually at night. In various areas of the body, usually in the extremities, skin sensitivity is disturbed, and convulsions are noted in the muscles of the calves, fingers or toes.
Clinical picture
The onset of the disease, as a rule, is delirium with scanty, fragmentary, monotonous hallucinations and illusions.
undermine anxiety and fear. Motor arousal is observed mainly in the form of stereotyped actions (as in everyday or professional activities). Periodically, the development of short-term states of immobility with increased muscle tone is possible. Patients can mumble something, shout out monotonous words, while speech contact with them is impossible. After a few days, a state of stunnedness develops, which can then turn into a stupor, and with an unfavorable course in a coma. In more rare cases, the soporous state is preceded by an apathetic stupor.
Deterioration of the mental state is facilitated by the aggravation of somatic and neurological disorders; the latter are very diverse. Fibrillar twitching of the tongue, lips, and facial muscles is common. Complex involuntary movements are constantly noted, including tremors, alternating with twitching, choreimorphic, athetoid and other types of movements. Muscle tone can be either increased or decreased. Ataxia soon develops. Nystagmus, ptosis, strabismus, immobility of the gaze, as well as pupillary disorders (anisocoria, miosis, weakening of the reaction to light up to its complete disappearance) and impaired convergence are determined. Quite often, polyneuritis, mild paresis, the presence of pyramidal signs are noted, and the rigidity of the occipital muscles can be determined from the meningeal symptoms. Patients are physically exhausted, look older than their age. The face is swollen. The tongue is crimson, its papillae are smoothed. There is an increased temperature. Tachycardia and arrhythmia are constant, blood pressure decreases with worsening of the condition, there is a tendency to hypotension and collapse. Hepatomegaly is noted, diarrhea is often found.
A hyperacute course is characterized by the fact that at first severe forms of delirium (professional or exaggerating) develop. The vegetative and neurological symptoms of the prodromal period increase sharply. Body temperature reaches 40-41 C. After one or several days, a state of stunnedness develops with a transition to comatose. Death occurs more often on the 3-6th day.
In the outcome of Gaie-Wernicke syndrome, the development of a psychoorganic syndrome is possible. Mortality is often associated with the addition of concomitant diseases, usually pneumonia, to which these patients are prone.
neurology.com.ua
The role of vitamin B1 in the pathogenesis of the disease
Vitamin B1 is an essential trace mineral. It plays the role of a cofactor - a non-protein substance for several enzymes (alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, transketolase). With its deficiency in the body, mitochondria are damaged and the utilization of glucose by neurons is significantly reduced. The periventricular parts of the brain are also affected.
Vitamin B1 is a white crystalline powder. Well soluble in water, it is unstable in an alkaline environment, when exposed to an oxidizing agent it turns into thiochrome. The maximum content of this vitamin is observed in cereals and yeast.
Wernicke's encephalopathy is accompanied by punctate hemorrhages, atrophy of the mastoid bodies. The most common signs of this disease are neuropil disintegration, endothelial proliferation, demyelination, and death of some neurons.
We highly recommend that you read this video if you think that drinking a glass of red wine a day is the norm:
Causes of occurrence
First of all, Wernicke's disease is caused by a deficiency of thiamine, depletion of the body, as well as alcoholism. Other reasons for the development of this condition include:
- unbalanced diet;
- avitaminosis;
- oncological diseases;
- starvation;
- poisoning with digitalis drugs;
- gastrointestinal pathology;
- pregnancy.
Clinical picture
Alcoholic encephalopathy, or rather its acute form, Gaie-Wernicke syndrome, is accompanied by a number of symptoms that make it possible to identify and recognize this disease. Deteriorating health, an increase in the number of various disorders from nervous to mental, exacerbation of other diseases - all these factors together indicate the development of Wernicke's syndrome. They characterize the initial stage, the time frame of which can vary from several weeks to several months.
Wernicke's encephalopathy has three main features: ataxia, ophthalmoplegia, and impaired consciousness.
- Ataxia. Translated from the Greek language "ataxia" means "disorder". It indicates a violation of balance and coordination of movements.
- Ophthalmoplegia. This phenomenon is characterized by paralysis of the main muscles as a result of damage to the oculomotor nerves.
- Impaired consciousness. This concept is a general name for disorders of integral brain activity, which are expressed in a violation of the ability to adequately comprehend and perceive reality, respond to the environment, remember the events taking place in it, enter into speech contact and much more.
In Gaie-Wernicke syndrome, most patients are apathetic, disoriented, and unable to concentrate. There are oculomotor disorders and impaired coordination of movements. Without proper treatment, a coma can occur with further death.
Alcoholic encephalopathy has the following symptoms, depending on the period and form of Gaie-Wernicke syndrome. 
Symptoms of the initial period include:
- increased sleepiness;
- earlier and frequent awakening;
- a long period of falling asleep;
- nightmares;
- deafening.
Other symptoms of this disease include conditions such as:
- decreased appetite and the appearance of aversion to fatty and protein-containing foods;
- vomiting and nausea;
- belching and heartburn;
- pain in the abdomen;
- increased physical exhaustion;
- unstable stools;
- asthenia - a painful condition, which is manifested by exhaustion and increased fatigue, loss of the ability to prolonged physical and mental stress;
- meaningless and incoherent chatter;
- hallucinations and clouding of consciousness;
- movement disorders.
Signs of an advanced stage of Wernicke's disease include such phenomena as:
- chills and fever;
- heart palpitations;
- pain in the heart area;
- excessive sweating;
- limb cramps;
- feeling short of breath;
- violation of sensitivity in the muscles on the skin;
- increased body temperature;
- arrhythmia;
- feeling of causeless anxiety and fear;
- tachycardia.
If you find 3 - 4 signs of Gaie-Wernicke syndrome, immediately consult a neurologist in order to avoid the dire consequences of this disease.
Diagnostics
In order to diagnose Wernicke's disease, consultation of a therapist, neurologist, psychotherapist and ophthalmologist is required. Specialists confirm the diagnosis of Wernicke's encephalopathy based on the results of the examination and the initial examination. As a rule, doctors prescribe the following types of research:
- analysis of urine and blood;
- electrocardiography;
- standard caloric test;
- magnetic resonance imaging;
- analysis of cerebrospinal fluid;
- computed tomography.
Difficulties in the diagnosis of this pathology are that it is necessary to differentiate this syndrome from brain tumors, various psychoses and schizophrenia.
Effects
In the absence of timely diagnosis and treatment of Gaie-Wernicke syndrome, the following negative consequences may occur:
- partial memory loss;
- uncontrolled changes in the behavior and life of the patient;
- constant sleepiness;
- heartburn;
- the inability to restore the functioning of the brain at the previous level;
- tumors;
- atrophy of brain activity;
- schizophrenia and other mental illness;
- coma;
- in the worst case, death.
Treatment and prognosis
Alcoholic encephalopathy has a very poor prognosis, according to which the mortality rate of patients is 50%. This is due to the acute course of the disease, exacerbation of concomitant pathologies: diabetes mellitus, liver cirrhosis, etc.
In order to avoid the development of such a prognosis, it is important to immediately start treating the syndrome. If a patient has alcoholic encephalopathy, then doctors recommend:
- psychological therapy;
- consumption of vitamins B1, B2 and B6;
- taking ascorbic and nicotinic acid, as well as anabolic steroids;
- the introduction of magnesium sulfate 25th solution.
It is important to remember that it is possible to improve the prognosis in this pathological condition only with its timely and correct treatment.
A poor prognosis suggests that Gaie-Wernicke syndrome is much easier to prevent than to cure. As a preventive measure, doctors recommend giving up alcoholic beverages, getting adequate and regular sleep, playing sports and eating right.
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What is Wernicke's encephalopathy
Wernicke's encephalopathy (acute upper hemorrhagic Gaie-Wernicke polioencephalitis) is a brain damage as a result of thiamine deficiency, which usually occurs with chronic alcoholism, less often with indomitable vomiting, unbalanced parenteral nutrition.
Wernicke's encephalopathy and Korsakov's syndrome are relatively common conditions due to vitamin B1 deficiency. In SSA, they are predominantly affected by alcoholics, but other causes of exhaustion and vitamin deficiency also predispose them to them: constant vomiting, starvation, hemodialysis, malignant neoplasms, AIDS.
What provokes Wernicke's encephalopathy
Wernicke's encephalopathy and Korsakov's syndrome are caused by vitamin B1 deficiency.
Pathogenesis (what happens?) During Wernicke's encephalopathy
Vitamin B1 serves as a cofactor for several enzymes, including transketolase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase. With avitaminosis B1, glucose utilization by neurons decreases and mitochondria are damaged. The accumulation of glutamate as a result of a decrease in the activity of alpha-ketoglutarate dehydrogenase against the background of energy deficiency has a neurotoxic effect. In rats with vitamin B1 deficiency, electron microscopy shows morphological signs of the neurotoxic effect of excitatory mediators: destruction of mitochondria, aggregation of chromatin, and swelling of neurons with signs of degeneration in the nuclei of the diencephalon. Neuronal degeneration can be stopped by the administration of NMDA glutamate receptor antagonists.
Pathological anatomy. The periventricular parts of the diencephalon, the brainstem and the upper part of the cerebellar worm are affected: the areas of the brain around the third ventricle, the Sylvian aqueduct and the fourth ventricle are discolored, in acute cases, punctate hemorrhages are sometimes visible, for chronic cases, atrophy of the mastoid bodies is typical. Common signs are endothelial proliferation, demyelination, neuropil disintegration and the death of some neurons. In some cases, these changes are visible on MRI). Amnesia is associated with damage to the mediodorsal nucleus of the thalamus.
Symptoms of Wernicke's encephalopathy
The classic triad of symptoms - ophthalmoplegia, ataxia, confusion - is present in only a third of cases. Most patients are deeply disoriented, apathetic, unable to concentrate, sometimes delirium with agitation is observed as a manifestation of alcohol withdrawal syndrome. Without treatment, stupor and coma may develop and death may occur. Oculomotor disorders include horizontal nystagmus when looking to the sides, paralysis of the external rectus muscle of the eye (usually bilateral), disorder of friendly eye movements, and occasionally ptosis. Ataxia (mainly abasia) is caused by a combination of polyneuropathy, cerebellar and vestibular ataxia. The pupils, as a rule, are not changed, but in the later stages of the disease they can be narrowed.
With the timely administration of thiamine IV or IM, oculomotor disorders quickly disappear, only nystagmus is persistent.
Wernicke's encephalopathy is usually accompanied by other manifestations of nutritional disorders - in particular, 80% of patients have polyneuropathy. Amblyopia and spinal spastic ataxia are much less common. Tachycardia and orthostatic hypotension are frequent, which can result from damage to the autonomic nervous system or be symptoms of the wet form of beriberi. Oculomotor disorders disappear a few hours after the administration of thiamine, while ataxia lasts longer, and in about half of patients, full recovery does not occur and the gait remains slow, shuffling, with legs wide apart. Apathy, drowsiness, confusion of consciousness also disappear gradually. As these disorders regress, fixation amnesia - the Korsakov syndrome - may come to the fore. It is a frequent companion of Wernicke's encephalopathy; in fact, we are talking about one disease - Wernicke-Korsakoff syndrome. Often, Korsakov's syndrome stays firm, patients have memory lapses, confabulations, confusion of the sequence of events.
Course of the disease. About 15-20% of hospitalized patients die, and this is usually due to intercurrent infections (most often pneumonia, pulmonary tuberculosis and septicemia) or liver failure.
If the patient begins to recover, it usually happens as follows. Paralysis of the oculomotor muscles can begin to regress within a few hours after the appointment of thiamine and almost always - after a few days. If the patient does not respond to treatment in this way, then doubts arise about the diagnosis of Wernicke's disease. Paralysis of the abducens nerve, ptosis and paresis of the vertical gaze regress completely within 1-2 weeks, but the vertical nystagmus provoked by the translation of gaze sometimes persists for up to several months. Horizontal gaze paralysis usually recovers completely, but in more than 50% of patients, clear horizontal nystagmus caused by a combined rotation of the eyeballs persists as a persistent consequence of the disease.
Diagnosis of Wernicke's encephalopathy
When studying the reaction to a standard caloric test in the acute stages of Wernicke's disease, bilateral, more or less symmetrical vestibular disorders are always found. CSF is normal or the protein content in it is slightly increased; if protein levels exceed 1000 mg / L or pleocytosis is present, complications should be suspected. In untreated patients, the content of pyruvate in the blood is increased, and the activity of blood transketolase (thiamine-dependent enzyme of the hexosomonophosphate shunt) is significantly reduced. Approximately 50% of patients on the EEG note a diffuse slowing down of mild to moderate waves. On the other hand, the total cerebral blood flow and the consumption of oxygen and glucose by the brain can be sharply reduced in the acute stages of the disease and remain so for several weeks after starting treatment.
Treatment of Wernicke's Encephalopathy
Wernicke's encephalopathy is an emergency condition. Thiamine, 50 mg IV or IM, is urgently administered. Further, the drug in the same dose is administered daily until the patient switches to a normal diet. Thiamine must be administered before glucose IV, since it can provoke Wernicke's encephalopathy or fulminant (cardiac) form of beriberi, and at the initial stage of these conditions, it can make them heavier. Therefore, when prescribing IV glucose to a patient with alcoholism, it is imperative to first introduce thiamine.
It is necessary to constantly monitor the functions of the cardiovascular system.
Which doctors should you contact if you have Wernicke's encephalopathy?
Neurologist
Therapist
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Causes of encephalopathy
Malnutrition for 2-3 weeks can already cause a lack of thiamine enough to show the first signs of Wernicke's encephalopathy. However, there are a number of other causes of this condition:
- systematic abuse of alcoholic beverages;
- diseases of the digestive system (recurrent vomiting, repeated diarrhea, pyloric stenosis, gastric ulcer and duodenal ulcer, intestinal obstruction or perforation, pancreatitis, etc.);
- diarrhea as a result of medication (for example, treatment of depression with lithium drugs or high doses of intravenous nitroglycerin);
- lack of magnesium, which is necessary for the absorption of thiamine, with Crohn's disease, bowel resection, or with prolonged use of diuretics;
- indomitable vomiting in pregnant women;
- oncological diseases and chemotherapy courses;
- the transferred surgical interventions (gastrectomy, colectomy, bypass anastomosis, etc.);
- polished rice as a food base;
- spontaneous refusal to eat (anorexia nervosa);
- there may be a genetic predisposition to the development of such encephalopathy.
Despite the fact that Wernicke's encephalopathy can occur for any of the above reasons, in practice, this type of pathology most often occurs as a result of the patient's alcohol abuse.
Clinical picture
Gaie-Wernicke's acute encephalopathy is characterized by the following triad of symptoms:
- Ophthalmoplegia and nystagmus. Oculomotor disorders are the most obvious and their absence, due to various reasons, can significantly complicate the diagnostic process. On examination, bilateral paresis of the abducens nerve (horizontal double vision), converging strabismus and nystagmus caused by turning the gaze in the horizontal plane are determined.
- Ataxia. Balance disorders manifest themselves primarily when standing and moving. Sometimes the patient is unable to maintain a standing posture and move without additional support.
- Clouding of consciousness. The patient is lethargic, does not manifest himself in any way, is indifferent to what is happening around him. He does not answer questions, he can fall asleep right during a conversation. A person does not orientate himself in space and time, he hardly recognizes familiar faces. In many patients, upon examination, the doctor determines the impairment of long-term memory as a manifestation of Korsakov's amnestic syndrome. Further deterioration of the condition can lead to depression of consciousness and coma.
Along with this symptomatology, body temperature also decreases, severe weakness appears and tachycardia develops at rest.
The condition usually develops in combination with malnutrition and obvious depletion of the body, accompanied by signs of peripheral polyneuropathy. In some patients, signs of alcohol withdrawal can be detected.
Late symptoms include fever, spastic paresis, hyperkinesis.
Korsakov syndrome
Acute alcoholic encephalopathy and Korsakov's syndrome, which often go hand in hand, are united by one common name - Gaie-Wernicke-Korsakoff syndrome. Wernicke-Korsakoff syndrome is manifested by an inability to remember new information (while old events are remembered better than new ones), which is often combined with problems with long-term memory.
However, if Wernicke's encephalopathy most often has temporary metabolic disorders that are completely reversible with adequate treatment, then with Korsakov's syndrome structural damage has already developed and its prognosis is not so favorable. Thus, the Korsakov syndrome is already the next, more severe stage in the development of the disease, which is already more difficult to treat.
Wernicke-Korsakoff syndrome can also have a non-alcoholic origin. In addition to the conditions associated with acute thiamine deficiency described earlier, it can rarely occur as a result of traumatic brain injury or even intravenous anesthesia.
Diagnostics
The standard for diagnosing alcoholic encephalopathy is MRI. It is this diagnostic method that makes it possible to identify the main morphological substrate of Gaie-Wernicke encephalopathy ─ necrosis of the mammillary bodies.
The disease can often proceed without symptoms, so the doctor is faced with the task of assessing the possibility of developing this pathology in persons suffering from alcoholism. In such people, it is necessary to assume the presence of multivitamin (and primarily vitamin B1 - thiamine) deficiency and fight it in time.
Treatment approaches
In the first few days (up to 72 hours) from the onset of the first symptoms, encephalopathy responds well to replacement therapy with vitamin B1 ─ thiamine. Moreover, the introduction of the vitamin must be intravenous, to create a high concentration in the body. On the first day, thiamine is administered at a dose of more than 1000 mg. After 5-7 days of injections, the patient is transferred to oral medication, which continues for several more weeks. The dosage of the vitamin is gradually reduced after 2 weeks of oral administration.
The total duration of thiamine use varies depending on the severity of the patient's condition, on average it is about 3 months, with the development of Korsakov's syndrome it can last for several years.
Also, thiamine intramuscularly in a short course with a subsequent transition to oral administration can be prescribed to patients who are at risk for the development of this pathology.
With the timely intravenous administration of the necessary vitamins:
- oculomotor disorders quickly subside, although nystagmus may persist;
- the patient's ability to maintain balance at rest returns, but gait remains unsteady.
Together with vitamin B1 therapy, it is important to avoid dehydration and electrolyte deficiency, to maintain a satisfactory water-electrolyte balance.
In addition to replenishing the thiamine deficiency, the prevention of the development of Wernicke's encephalopathy is to reduce the amount of carbohydrates in the diet, since they require an increased consumption of vitamin B1 from the body. You should also avoid the administration of glucose solutions to persons suffering from alcoholism, as this increases the risk of developing encephalopathy.
Thus, Wernicke's encephalopathy is a disease that is sometimes difficult to diagnose, but the outcome of the entire treatment often depends on its efficiency.
golovalab.ru
Concept and classification
Many people have only a vague idea of \u200b\u200bwhat alcoholic encephalopathy is. In medical terminology, this phenomenon is characterized as alcoholic psychosis, which is extremely severe. The disease is characterized by poisoning and death of brain cells due to the systematic use of alcohol. As a rule, it combines several diseases, which are united by a single clinical picture, symptoms and etiology. According to the International Classification of Diseases (ICD), alcoholic encephalopathy belongs to class 6 out of 10.
In addition to pathological changes in the brain, the disease is characterized by severe exhaustion of the body, intoxication with alcohol metabolism products (cirrhosis of the liver, hepatitis, etc.), deficiency of vitamins and microelements, oxidative stress.
Alcoholic encephalopathy of the brain is often diagnosed in people who abuse alcoholic surrogates. It is these people who most often end up in medical institutions with various poisonings, alcohol delirium (delirium tremens) and other mental disorders, as well as diseases of the internal organs caused by alcohol.
Alcoholic encephalopathy has two forms of the disease - acute and chronic. Other types are much less common, and it is customary to attribute the abuse of certain wines to the reasons for their appearance.
The acute alcoholic stage includes Gaie-Wernicke syndrome (Wernicke encephalopathy), which affects the stronger sex in adulthood (from 35 to 45 years), but sometimes cases are diagnosed when young people also suffer from it.
The chronic form includes Korsakov's psychosis (observed mainly in women), alcoholic pseudo-paralysis (diagnosed in persons of both sexes aged 30 to 65 years, but in women it is much less common).
Let's consider each stage in detail.
Acute encephalopathy (Gaie-Wernicke syndrome)
If we talk about the time frame for the course of the stage, then for each patient it is individual. For some, it lasts several weeks, for others, it lasts for months. But in any case, the acute stage is characterized by a sharp deterioration in health.
A person has a number of disorders of both nervous and somatic nature, as well as the development of certain diseases characteristic of chronic alcoholics (pancreatitis, hepatitis, liver cirrhosis).
Wernicke's encephalopathy has the following symptoms:
- weakness, arrhythmia, shortness of breath even with minor physical exertion;
- poor appetite and, as a result, weight loss;
- nausea, vomiting;
- diarrhea;
- palpitations, headaches;
- trembling limbs, incoordination of movements;
- swelling, blue discoloration of the skin on the arms and legs;
- burning sensation in the chest;
- psychological abnormalities manifested in depression, fear, anxiety, hallucinations;
- serious speech impairment (the person cannot speak);
- insomnia or sleep disturbances accompanied by nightmares;
- delirium tremens;
- decreased muscle tone;
- fever, hyperthermia, sweating, peeling of the skin (in some cases - the formation of bedsores).
Gaie-Wernicke encephalopathy is characterized by a rather striking symptom - a person's lack of satisfaction from drinking.
A patient with an acute alcoholic form should be immediately provided with medical care, otherwise he will have a syndrome of depression of consciousness - stunning, stupor, coma. Even if a person manages to survive, the prognosis is unfavorable: in most cases it is dementia.
Chronic stage of encephalopathy
Korsakov's psychosis is also called polyneuritic. It is characterized by fixation or retrograde amnesia, disorientation in space, time and place. A person loses the ability to move, cannot talk, he has muscle atrophy, polyneuritis of the extremities, skin sensitivity decreases. Sometimes the patient experiences confabulation - false memories of events that never happened in his life.
Another form of the chronic stage of encephalopathy is alcoholic pseudoparalysis. It is diagnosed much less often than Korsakov's psychosis.
The signs are in many ways similar to Korsakov's psychosis, but not so pronounced:
- manic and delusional states, partial or complete memory loss;
- trembling limbs, impaired facial expressions.
If the patient was treated correctly and in a timely manner, then the above mental pathologies disappear without leaving consequences, in contrast to the acute stage of encephalopathy, which in most cases leads to irreversible consequences, disability and death.
Diagnostic measures
Toxic encephalopathy in alcoholism, which is characterized by multidirectional symptoms, is dangerous in that it can be easily confused with some diseases: schizophrenia, delirium tremens, acute psychosis (non-alcoholic etiology), brain tumors, as well as an acute form of vitamin deficiency that has developed as a result of anorexia.
That is why the decisive factor in the fight against alcoholic encephalopathy is the collection of anamnesis, the study of the medical history. These actions will allow the specialist to make correct assumptions about what exactly led to such a clinical picture. The doctor specifies when exactly the disease began, the drinks consumed by the patient. If consciousness is not impaired, the doctor speaks directly with the patient, but if he has a depression of consciousness, then a survey of relatives or people who were in the immediate vicinity of the victim is conducted.
Additional diagnostic measures - ultrasound, MRI, CT.
Diagnostic measures should be carried out as early as possible, otherwise the patient may experience heart failure, cerebral edema and other irreversible phenomena, up to and including death.
First aid
If alcoholic encephalopathy is suspected, a person should immediately call an ambulance. Before the arrival of the medical team, it is necessary to cover the patient with a blanket in order to keep the body warm. In this case, it is necessary to observe so that a person does not choke on vomit - unfortunately, such cases take place in medical practice.
If the patient falls into a coma, then all that remains is to trust the doctors, since this state can only be overcome with the help of medication and appropriate procedures. It should be noted that such a state is a powerful stress, therefore, it is unlikely to do without consequences for all organs and body systems.
What methods are treated
There is no single treatment regimen for alcoholic encephalopathy, it all depends on the form of the disease and the patient's condition. The requirement for successful treatment is a complete rejection of alcohol. The treatment is continuous and long-term. Its length ranges from several weeks to months.
Treatment of alcoholic encephalopathy includes the following steps:
- removal of alcohol metabolism products from the body (detoxification);
- the formation of persistent gag reflexes to the smell and taste of alcohol (conditioned reflex therapy);
- elimination of cravings for hot drinks (sensitization);
- psychotherapy (individual and group);
- hypnotherapy.
If a patient has Wernicke's encephalopathy, he needs immediate medical attention. Therapy includes taking vitamins of the B1, B6, PP groups (3 times a day, the dosage is set by the doctor), magnesium sulfate, nootropic drugs (if there are brain disorders). In some cases, therapeutic measures may be required, the purpose of which is to normalize intracranial pressure. Treatment is used similar to severe forms of delirium tremens, psychological support.
Chronic stages of alcoholic psychosis are treated based on the extent to which the brain is affected - in the future, this will determine the possibilities of a full life of the patient.
Therapy for Korsakov's psychosis includes fortification (intake of vital vitamins B, C, P, K). An appropriate diet is prescribed without fail. Measures are taken to cleanse the blood from toxins, physiotherapy procedures.
Alcoholic pseudoparalysis should be treated with the same methods as for Korsakov's psychosis. This also includes drugs to maintain liver function, drugs aimed at eliminating pain.
Connection to a ventilator, hemodialysis, parenteral nutrition, that is, the use of life support systems is advisable in severe cases. To prevent the appearance of brain tumors, Furosedin is used.
Particular attention is paid to the rehabilitation process, since there is a high risk of irreversible changes in the body and serious complications: disorders of cardiovascular activity, brain tumors, paralysis of the limbs, dementia and others.
If we talk about the effectiveness of folk methods for alcoholic encephalopathy, then they are advisable in the acute stage. They can be used, but only in combination with the main treatment and after consulting a specialist. Self-medication is dangerous and fraught with complications.
To create a lasting effect of aversion to alcohol and support the body in the rehabilitation period, you can use thyme, sea buckthorn, wormwood.
Forecasts and preventive measures
It is difficult to predict what consequences alcoholic encephalopathy will have, it all depends on the timing of the course of the disease, the frequency of alcohol consumption (mostly surrogates), the patient's environment, heredity.
In advanced cases, the risk of disability, both physical and mental, is very high due to disruption of the activity of all organs and systems.
Prevention measures include identifying alcoholism in the early stages and voluntary refusal from alcoholic beverages of any strength, support for loved ones, a healthy lifestyle, a balanced diet, and reasonable sports training.
The abuse of alcoholic beverages for a long period of time leads to serious consequences associated with impaired functioning of the brain and central nervous system. Gaje-Wernicke syndrome plays a special role in the transformed state of the body - a disease that develops against the background of alcohol intoxication. A predisposition to it was revealed in representatives of the stronger sex of the age category from 35 to 45 years.
Wernicke's encephalopathy is an acute lesion of the hypothalamus and midbrain as a result of a lack of vitamin B1. This disease is based on a decrease in the number of gliosis and neurons, as well as demyelination in the periventricular gray matter zone.
Note! Demyelination of the brain is a pathological process characterized by thinning of the insulating layer by myelinated nerve fibers. It disrupts the conduction of impulses along the pathways of the white matter of the spinal cord and brain.
With Gaje-Wernicke syndrome, vascular-dystrophic changes occur in the brain tissue. The defeat mainly covers the substance from those parts of the brain that are located at the bottom of the 4th ventricle, near the 3rd ventricle and the Sylvian aqueduct - the channel connecting the above noted ventricles. Despite the fact that vascular pathologies accompany chronic alcoholism, Wernicke's disease can develop due to prolonged vitamin deficiency and exhaustion, which is preceded by fasting, constant vomiting, malignant tumors, AIDS and other factors.
Before discussing in detail the topic of Wernicke's alcoholic encephalopathy, we recommend you as a preventive measure.
The role of vitamin B1 in the pathogenesis of the disease
Vitamin B1 is an essential trace mineral. It plays the role of a cofactor - a non-protein substance for several enzymes (alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, transketolase). With its deficiency in the body, mitochondria are damaged and the utilization of glucose by neurons is significantly reduced. The periventricular parts of the brain are also affected.
Vitamin B1 is a white crystalline powder. Well soluble in water, it is unstable in an alkaline environment, when exposed to an oxidizing agent it turns into thiochrome. The maximum content of this vitamin is observed in cereals and yeast.
Wernicke's encephalopathy is accompanied by punctate hemorrhages, atrophy of the mastoid bodies. The most common signs of this disease are neuropil disintegration, endothelial proliferation, demyelination, and death of some neurons.
We highly recommend that you read this video if you think that drinking a glass of red wine a day is the norm:
Causes of occurrence
First of all, Wernicke's disease is caused by a deficiency of thiamine, depletion of the body, as well as alcoholism. Other reasons for the development of this condition include:
- unbalanced diet;
- avitaminosis;
- oncological diseases;
- starvation;
- poisoning with digitalis drugs;
- gastrointestinal pathology;
- pregnancy.
Clinical picture
Alcoholic encephalopathy, or rather its acute form, Gaie-Wernicke syndrome, is accompanied by a number of symptoms that make it possible to identify and recognize this disease. Deteriorating health, an increase in the number of various disorders from nervous to mental, exacerbation of other diseases - all these factors together indicate the development of Wernicke's syndrome. They characterize the initial stage, the time frame of which can vary from several weeks to several months.
Wernicke's encephalopathy has three main features: ataxia, ophthalmoplegia, and impaired consciousness.
- Ataxia. Translated from the Greek language "ataxia" means "disorder". It indicates a violation of balance and coordination of movements.
- Ophthalmoplegia. This phenomenon is characterized by paralysis of the main muscles as a result of damage to the oculomotor nerves.
- Impaired consciousness. This concept is a general name for disorders of integral brain activity, which are expressed in a violation of the ability to adequately comprehend and perceive reality, respond to the environment, remember the events taking place in it, enter into speech contact and much more.
In Gaie-Wernicke syndrome, most patients are apathetic, disoriented, and unable to concentrate. There are oculomotor disorders and impaired coordination of movements. Without proper treatment, a coma can occur with further death.
Alcoholic encephalopathy has the following symptoms, depending on the period and form of Gaie-Wernicke syndrome. 
Symptoms of the initial period include:
- increased sleepiness;
- earlier and frequent awakening;
- a long period of falling asleep;
- nightmares;
- deafening.
Other symptoms of this disease include conditions such as:
- decreased appetite and the appearance of aversion to fatty and protein-containing foods;
- vomiting and nausea;
- belching and heartburn;
- pain in the abdomen;
- increased physical exhaustion;
- unstable stools;
- asthenia - a painful condition, which is manifested by exhaustion and increased fatigue, loss of the ability to prolonged physical and mental stress;
- meaningless and incoherent chatter;
- hallucinations and clouding of consciousness;
- movement disorders.
Signs of an advanced stage of Wernicke's disease include such phenomena as:
- chills and fever;
- heart palpitations;
- pain in the heart area;
- excessive sweating;
- limb cramps;
- feeling short of breath;
- violation of sensitivity in the muscles on the skin;
- increased body temperature;
- arrhythmia;
- feeling of causeless anxiety and fear;
- tachycardia.
If you find 3 - 4 signs of Gaie-Wernicke syndrome, immediately consult a neurologist in order to avoid the dire consequences of this disease.
Diagnostics
In order to diagnose Wernicke's disease, consultation of a therapist, neurologist, psychotherapist and ophthalmologist is required. Specialists confirm the diagnosis of Wernicke's encephalopathy based on the results of the examination and the initial examination. As a rule, doctors prescribe the following types of research:
- analysis of urine and blood;
- electrocardiography;
- standard caloric test;
- magnetic resonance imaging;
- analysis of cerebrospinal fluid;
- computed tomography.
Difficulties in the diagnosis of this pathology are that it is necessary to differentiate this syndrome from brain tumors, various psychoses and schizophrenia.
Effects
In the absence of timely diagnosis and treatment of Gaie-Wernicke syndrome, the following negative consequences may occur:
- partial memory loss;
- uncontrolled changes in the behavior and life of the patient;
- constant sleepiness;
- heartburn;
- the inability to restore the functioning of the brain at the previous level;
- tumors;
- atrophy of brain activity;
- schizophrenia and other mental illness;
- coma;
- in the worst case, death.
Treatment and prognosis
Alcoholic encephalopathy has a very poor prognosis, according to which the mortality rate of patients is 50%. This is due to the acute course of the disease, exacerbation of concomitant pathologies: diabetes mellitus, liver cirrhosis, etc.
In order to avoid the development of such a prognosis, it is important to immediately start treating the syndrome. If a patient has alcoholic encephalopathy, then doctors recommend:
- psychological therapy;
- consumption of vitamins B1, B2 and B6;
- taking ascorbic and nicotinic acid, as well as anabolic steroids;
- the introduction of magnesium sulfate 25th solution.
It is important to remember that it is possible to improve the prognosis in this pathological condition only with its timely and correct treatment.
A poor prognosis suggests that Gaie-Wernicke syndrome is much easier to prevent than to cure. As a preventive measure, doctors recommend giving up alcoholic beverages, getting adequate and regular sleep, playing sports and eating right.
Gaie-Wernicke encephalopathy is a dangerous but reversible neurometabolic disorder caused by a deficiency of thiamine (vitamin B1).
Vitamin B1 is an essential coenzyme and is involved in many biochemical processes, such as the decarboxylation of ketonic acids. The presence of this vitamin is especially important for the functioning of the central nervous system. With its deficiency, the ability of neurons to utilize glucose (their main nutrient substrate) worsens and their mitochondria are damaged. Moreover, thiamine is most important in the metabolism of the diencephalon and brainstem, which means that with a lack of vitamin B1, these areas suffer earlier than others.
Thiamine molecule model
For the first time, the condition caused by acute thiamine deficiency was described by Karl Wernicke in Germany and received the name "upper hemorrhagic encephalitis." In the International Classification of Diseases of the 10th revision (ICD-10), encephalopathy, named after Gaie-Wernicke, is referred to as diseases of the endocrine system, nutritional disorders and metabolic disorders (code E51).
Causes of encephalopathy
Malnutrition for 2-3 weeks can already cause a lack of thiamine enough to show the first signs of Wernicke's encephalopathy. However, there are a number of other causes of this condition:
- systematic abuse of alcoholic beverages;
- diseases of the digestive system (recurrent vomiting, repeated diarrhea, pyloric stenosis, gastric ulcer and duodenal ulcer, intestinal obstruction or perforation, pancreatitis, etc.);
- diarrhea as a result of medication (for example, treatment of depression with lithium drugs or high doses of intravenous nitroglycerin);
- lack of magnesium, which is necessary for the absorption of thiamine, with Crohn's disease, bowel resection, or with prolonged use of diuretics;
- indomitable vomiting in pregnant women;
- oncological diseases and chemotherapy courses;
- the transferred surgical interventions (gastrectomy, colectomy, bypass anastomosis, etc.);
- polished rice as a food base;
- spontaneous refusal to eat (anorexia nervosa);
- there may be a genetic predisposition to the development of such encephalopathy.
Despite the fact that Wernicke's encephalopathy can occur for any of the above reasons, in practice, this type of pathology most often occurs as a result of the patient's alcohol abuse.
Chronic alcohol intoxication is the main risk factor for the development of Wernicke's encephalopathy
Clinical picture
Gaie-Wernicke's acute encephalopathy is characterized by the following triad of symptoms:
- Ophthalmoplegia and nystagmus. Oculomotor disorders are the most obvious and their absence, due to various reasons, can significantly complicate the diagnostic process. On examination, bilateral paresis of the abducens nerve (horizontal double vision), converging strabismus and nystagmus caused by turning the gaze in the horizontal plane are determined.
- Ataxia. Balance disorders manifest themselves primarily when standing and moving. Sometimes the patient is unable to maintain a standing posture and move without additional support.
- Clouding of consciousness. The patient is lethargic, does not manifest himself in any way, is indifferent to what is happening around him. He does not answer questions, he can fall asleep right during a conversation. A person does not orientate himself in space and time, he hardly recognizes familiar faces. In many patients, upon examination, the doctor determines the impairment of long-term memory as a manifestation of Korsakov's amnestic syndrome. Further deterioration of the condition can lead to depression of consciousness and coma.
The most common manifestation of Wernicke's encephalopathy is confusion.
Along with this symptomatology, body temperature also decreases, severe weakness appears and tachycardia develops at rest.
The condition usually develops in combination with malnutrition and obvious depletion of the body, accompanied by signs of peripheral polyneuropathy. In some patients, signs of alcohol withdrawal can be detected.
Late symptoms include fever, spastic paresis, hyperkinesis.
Korsakov syndrome
Acute alcoholic encephalopathy and Korsakov's syndrome, which often go hand in hand, are united by one common name - Gaie-Wernicke-Korsakoff syndrome. Wernicke-Korsakoff syndrome is manifested by an inability to remember new information (while old events are remembered better than new ones), which is often combined with problems with long-term memory.
However, if Wernicke's encephalopathy most often has temporary metabolic disorders that are completely reversible with adequate treatment, then with Korsakov's syndrome structural damage has already developed and its prognosis is not so favorable. Thus, the Korsakov syndrome is already the next, more severe stage in the development of the disease, which is already more difficult to treat.
Wernicke-Korsakoff syndrome can also have a non-alcoholic origin. In addition to the conditions associated with acute thiamine deficiency described earlier, it can rarely occur as a result of traumatic brain injury or even intravenous anesthesia.
Diagnostics
The standard for diagnosing alcoholic encephalopathy is MRI. It is this diagnostic method that makes it possible to identify the main morphological substrate of Gaie-Wernicke encephalopathy ─ necrosis of the mammillary bodies.
The disease can often proceed without symptoms, so the doctor is faced with the task of assessing the possibility of developing this pathology in persons suffering from alcoholism. In such people, it is necessary to assume the presence of multivitamin (and primarily vitamin B1 - thiamine) deficiency and fight it in time.
Treatment approaches
In the first few days (up to 72 hours) from the onset of the first symptoms, encephalopathy responds well to replacement therapy with vitamin B1 ─ thiamine. Moreover, the introduction of the vitamin must be intravenous, to create a high concentration in the body. On the first day, thiamine is administered at a dose of more than 1000 mg. After 5-7 days of injections, the patient is transferred to oral medication, which continues for several more weeks. The dosage of the vitamin is gradually reduced after 2 weeks of oral administration.
Treatment of patients with Wernicke encephalopathy is the administration of Thiamin
The total duration of thiamine use varies depending on the severity of the patient's condition, on average it is about 3 months, with the development of Korsakov's syndrome it can last for several years.
Also, thiamine intramuscularly in a short course with a subsequent transition to oral administration can be prescribed to patients who are at risk for the development of this pathology.
Vitamin B1 for oral administration
With the timely intravenous administration of the necessary vitamins:
- oculomotor disorders quickly subside, although nystagmus may persist;
- the patient's ability to maintain balance at rest returns, but gait remains unsteady.
Together with vitamin B1 therapy, it is important to avoid dehydration and electrolyte deficiency, to maintain a satisfactory water-electrolyte balance.
In addition to replenishing the thiamine deficiency, the prevention of the development of Wernicke's encephalopathy is to reduce the amount of carbohydrates in the diet, since they require an increased consumption of vitamin B1 from the body. You should also avoid the administration of glucose solutions to persons suffering from alcoholism, as this increases the risk of developing encephalopathy.
Thus, Wernicke's encephalopathy is a disease that is sometimes difficult to diagnose, but the outcome of the entire treatment often depends on its efficiency.
Shoshina Vera Nikolaevna
Therapist, education: Northern Medical University. Work experience 10 years.
Articles written
Today alcoholism is not just a disease of an individual, it is a social problem of the whole society as a whole. Medical research has proven that there is a relationship between an irresistible craving for alcohol and various neuropsychiatric pathologies. - one of the most common and very dangerous phenomena leading to the occurrence of irreversible processes in the brain.
Many people have only a vague idea of \u200b\u200bwhat alcoholic encephalopathy is. In medical terminology, this phenomenon is characterized as alcoholic psychosis, which is extremely severe. The disease is characterized by poisoning and death of brain cells due to the systematic use of alcohol. As a rule, it combines several diseases, which are united by a single clinical picture, symptoms and etiology. According to the International Classification of Diseases (ICD), alcoholic encephalopathy belongs to class 6 out of 10.
In addition to pathological changes in the brain, the disease is characterized by severe exhaustion of the body, intoxication with alcohol metabolism products (cirrhosis of the liver, hepatitis, etc.), deficiency of vitamins and microelements, oxidative stress.
Alcoholic encephalopathy of the brain is often diagnosed in people who abuse alcoholic surrogates. It is these people who most often end up in medical institutions with various poisonings, alcohol delirium (delirium tremens) and other mental disorders, as well as diseases of the internal organs caused by alcohol.
Alcoholic encephalopathy has two forms of the disease - acute and chronic. Other types are much less common, and it is customary to attribute the abuse of certain wines to the reasons for their appearance.
The acute alcoholic stage includes Gaie-Wernicke syndrome (Wernicke encephalopathy), which affects the stronger sex in adulthood (from 35 to 45 years), but sometimes cases are diagnosed when young people also suffer from it.
The chronic form includes Korsakov's psychosis (observed mainly in women), alcoholic pseudo-paralysis (diagnosed in persons of both sexes aged 30 to 65 years, but in women it is much less common).
Let's consider each stage in detail.
Acute encephalopathy (Gaie-Wernicke syndrome)
If we talk about the time frame for the course of the stage, then for each patient it is individual. For some, it lasts several weeks, for others, it lasts for months. But in any case, the acute stage is characterized by a sharp deterioration in health.
A person has a number of disorders of both nervous and somatic nature, as well as the development of certain diseases characteristic of chronic alcoholics (pancreatitis, hepatitis, liver cirrhosis).
Wernicke's encephalopathy has the following symptoms:
- weakness, arrhythmia, shortness of breath even with minor physical exertion;
- poor appetite and, as a result, weight loss;
- nausea, vomiting;
- diarrhea;
- palpitations, headaches;
- trembling limbs, incoordination of movements;
- swelling, blue discoloration of the skin on the arms and legs;
- burning sensation in the chest;
- psychological abnormalities manifested in depression, fear, anxiety, hallucinations;
- serious speech impairment (the person cannot speak);
- insomnia or sleep disturbances accompanied by nightmares;
- delirium tremens;
- decreased muscle tone;
- fever, hyperthermia, sweating, peeling of the skin (in some cases - the formation of bedsores).
Gaie-Wernicke encephalopathy is characterized by a rather striking symptom - a person's lack of satisfaction from drinking.
A patient with an acute alcoholic form should be immediately provided with medical care, otherwise he will have a syndrome of depression of consciousness - stunning, stupor, coma. Even if a person manages to survive, the prognosis is unfavorable: in most cases it is dementia.
Chronic stage of encephalopathy
Korsakov's psychosis is also called polyneuritic. It is characterized by fixation or retrograde amnesia, disorientation in space, time and place. A person loses the ability to move, cannot talk, he has muscle atrophy, polyneuritis of the extremities, skin sensitivity decreases. Sometimes the patient experiences confabulation - false memories of events that never happened in his life.
Another form of the chronic stage of encephalopathy is alcoholic pseudoparalysis. It is diagnosed much less often than Korsakov's psychosis.
The signs are in many ways similar to Korsakov's psychosis, but not so pronounced:
- manic and delusional states, partial or complete memory loss;
- trembling limbs, impaired facial expressions.
If the patient was treated correctly and in a timely manner, then the above mental pathologies disappear without leaving consequences, in contrast to the acute stage of encephalopathy, which in most cases leads to irreversible consequences, disability and death.
Diagnostic measures
Toxic encephalopathy in alcoholism, which is characterized by multidirectional symptoms, is dangerous in that it can be easily confused with some diseases: schizophrenia, delirium tremens, acute psychosis (non-alcoholic etiology), brain tumors, as well as an acute form of vitamin deficiency that has developed as a result of anorexia.
That is why the decisive factor in the fight against alcoholic encephalopathy is the collection of anamnesis, the study of the medical history. These actions will allow the specialist to make correct assumptions about what exactly led to such a clinical picture. The doctor specifies when exactly the disease began, the drinks consumed by the patient. If consciousness is not impaired, the doctor speaks directly with the patient, but if he has a depression of consciousness, then a survey of relatives or people who were in the immediate vicinity of the victim is conducted.
Additional diagnostic measures -,.
Diagnostic measures should be carried out as early as possible, otherwise the patient may experience heart failure, cerebral edema and other irreversible phenomena, up to and including death.
First aid
If alcoholic encephalopathy is suspected, a person should immediately call an ambulance. Before the arrival of the medical team, it is necessary to cover the patient with a blanket in order to keep the body warm. In this case, it is necessary to observe so that a person does not choke on vomit - unfortunately, such cases take place in medical practice.
If the patient falls into a coma, then all that remains is to trust the doctors, since this state can only be overcome with the help of medication and appropriate procedures. It should be noted that such a state is a powerful stress, therefore, it is unlikely to do without consequences for all organs and body systems.
What methods are treated
There is no single treatment regimen for alcoholic encephalopathy, it all depends on the form of the disease and the patient's condition. The requirement for successful treatment is a complete rejection of alcohol. The treatment is continuous and long-term. Its length ranges from several weeks to months.
Treatment of alcoholic encephalopathy includes the following steps:
- removal of alcohol metabolism products from the body (detoxification);
- the formation of persistent gag reflexes to the smell and taste of alcohol (conditioned reflex therapy);
- elimination of cravings for hot drinks (sensitization);
- psychotherapy (individual and group);
- hypnotherapy.
If the patient has Wernicke's encephalopathy, he needs immediate medical attention. Therapy includes taking vitamins of the B1, B6, PP groups (3 times a day, the dosage is set by the doctor), magnesium sulfate (if there are disorders of the brain). In some cases, therapeutic measures may be required, the purpose of which is to normalize intracranial pressure. Treatment is used similar to severe forms of delirium tremens, psychological support.
Chronic stages of alcoholic psychosis are treated based on the extent to which the brain is affected - in the future, this will determine the possibilities of a full life of the patient.
Therapy for Korsakov's psychosis includes fortification (intake of vital vitamins B, C, P, K). An appropriate diet is prescribed without fail. Measures are taken to cleanse the blood from toxins, physiotherapy procedures.
Alcoholic pseudoparalysis should be treated with the same methods as for Korsakov's psychosis. This also includes drugs to maintain liver function, drugs aimed at eliminating pain.
Connection to a ventilator, hemodialysis, parenteral nutrition, that is, the use of life support systems is advisable in severe cases. To prevent the appearance, Furosedin is used.
Particular attention is paid to the rehabilitation process, since there is a high risk of irreversible changes in the body and serious complications: disorders of cardiovascular activity, the occurrence of brain tumors, paralysis of the limbs, and others.
If we talk about the effectiveness of folk methods for alcoholic encephalopathy, then they are advisable in the acute stage. They can be used, but only in combination with the main treatment and after consulting a specialist. Self-medication is dangerous and fraught with complications.
To create a lasting effect of aversion to alcohol and support the body in the rehabilitation period, you can use thyme, sea buckthorn, wormwood.
Forecasts and preventive measures
It is difficult to predict what consequences alcoholic encephalopathy will have, it all depends on the timing of the course of the disease, the frequency of alcohol consumption (mostly surrogates), the patient's environment, heredity.
In advanced cases, the risk of disability, both physical and mental, is very high due to disruption of the activity of all organs and systems.
Prevention measures include identifying alcoholism in the early stages and voluntary refusal from alcoholic beverages of any strength, support for loved ones, a healthy lifestyle, a balanced diet, and reasonable sports training.
Gaie Wernicke (Wernicke's encephalopathy)- This is an acute lesion of the midbrain and hypothalamus as a result of thiamine deficiency in the human body, which occurs during the chronic use of alcoholic beverages.
The disease is associated with a decrease in the number of neurons, gliosis and demyelination in the periventricular gray matter. This problem belongs to organic-toxic psychoses and often occurs in conjunction with Korsakoff's syndrome. The disease proceeds acutely, subacutely or chronically.
The reasons
Gaia Wernicke's disease is most often caused by vitamin B1 deficiency, alcoholism, complete exhaustion of the body. Fasting, hemodialysis, malignant tumor formations, AIDS also predispose to the onset of this disease.
Other causes of Gaie-Wernicke encephalopathy are:
- gastrointestinal diseases;
- vomiting during pregnancy;
- vomiting in case of poisoning with digitalis drugs.
Gaie-Wernicke syndrome symptoms
Symptoms characteristic of Gaje Wernicke's encephalopathy are:
- ataxia (impaired coordination of movements);
- confusion of consciousness;
- ophthalmoplegia (paralysis of the muscles of the eye due to damage to the oculomotor nerves);
- disorientation;
- apathy;
- irritability.
If you find similar symptoms in yourself, be sure to consult a specialist. It is easier to prevent a disease than to deal with its consequences.
Best Doctors for Gaie Wernicke Syndrome Treatment
Patients with the syndrome have such deviations:
- macrocytic anemia - in the peripheral blood;
- in the cerebrospinal fluid - increased protein content (<90 мг%);
- mastoid atrophy on CT and MRI.
Treatment for Gaie-Wernicke syndrome
Treatment for Gaje-Wernicke syndrome includes:
- taking vitamin B (thiamine);
- intake of vitamins B2, B6, nicotinic and ascorbic acid, anabolic steroids;
- taking magnesium sulfate 25 solution;
- psychological therapy.
Danger
If Gaie-Wernicke Syndrome is not promptly treated, this can lead to the following negative consequences:
- changes in human behavior and life;
- the inability to restore the work of the brain;
- amnesia or partial memory loss;
- drowsiness;
- loss of consciousness;
- persistent heartburn;
- schizophrenia;
- brain tumor;
- complete atrophy of brain activity.
In case of untimely treatment, a coma may occur, and then death.
Risk group
The main risk group is made up of men aged 35 to 65 who abuse alcoholic beverages. Women between the ages of 30 and 65 are also at risk.
Prevention
- give up the abuse of low-alcohol and strong alcoholic beverages;
- establish regular and nutritious meals;
- ensure adequate sleep;
- exercise regularly.
This article is posted for educational purposes only and does not constitute scientific material or professional medical advice.
