Wernicke's disease. Wernicke encephalopathy treatment methods

30.12.202027.05.2017

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. Gaie-Wernicke syndrome refers to 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. Anxiety and fear dominate. 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.

The 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 interspersed with twitchings, 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. The patients are physically exhausted and 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.

Wernicke's encephalopathy is a severe brain damage that occurs due to a deficiency of thiamine (vitamin B1). Most often it occurs with chronic alcoholism and unbalanced diet. Vitamin B1 is essential for the metabolism of cerebral cells. With its deficiency, three clinical symptoms of Wernicke's encephalopathy arise: disorder of the oculomotor function, mixed ataxia and impaired integrative function of the central nervous system.

Wernicke's encephalopathy most often affects men between the ages of 30 and 50 and appears due to vitamin B1 deficiency

This disease is often referred to as Gaie-Wernicke syndrome. It is named after its discoverers, the German neuropsychiatrist Wernicke and the French physician Gaie. Both of them, independently of each other, described the disease, which was based on disorders of the metabolism of nerve cells.

This syndrome is characterized by an acute deficiency in the body of vitamin B1, or thiamine. This component is involved in a number of metabolic processes, and its deficiency leads to the inhibition of some biochemical reactions. The result is a decrease in glucose utilization by nerve cells. Energy starvation develops, due to which extracellular accumulation of glutamate occurs.

An increased concentration of this substance leads to the fact that an increased amount of calcium ions begins to enter the cellular structure. As a result, a number of enzymes are activated that sequentially destroy the structure of the cell. The pathological process takes place in the brain stem, affecting the cerebellum and the nucleus of the thalamus.

As a result of the progression of Wernicke's syndrome, memory disorders are possible.

Wernicke's encephalopathy most commonly affects men between the ages of 30 and 50. It is extremely rare that the disease affects patients under the age of 30. Most often, the disease manifests itself on the basis of alcoholism, which is why modern medicine classifies it as an acute form of alcoholic encephalopathy. However, alcohol abuse is not the only reason for the development of pathology.

Autopsy data indicate a low prevalence of Wernicke's encephalopathy. There are only 2 cases of the disease per 100 thousand of the population. Most often, the disease is diagnosed posthumously - during the patient's life, the diagnosis is established in less than 20% of cases. This is due to the fact that most patients with Wernicke's encephalopathy have problems with alcohol dependence and do not monitor their health.

Causes

The main reason for the development of this disease is alcoholism. In men, the syndrome can develop at 6-8 years of alcohol abuse. For women, the period of development of pathology is only 3 years.

As a rule, the disease manifests itself in the second or third stage of alcoholism. Moreover, half of the patients have alcoholic psychoses.

In addition to alcohol abuse, this disease can develop for a variety of reasons. The most common ones are:

prolonged fasting;
AIDS;
diseases of the gastrointestinal tract, in which malabsorption is observed (impaired absorption of nutrients);
improper parenteral nutrition;
persistent vomiting;
oncological ailments that lead to the development of cancer cachexia;
some types of helminthiasis.

Symptoms

Most patients are deeply disoriented, unable to concentrate, delirium with excitement is observed as a manifestation of alcohol withdrawal syndrome

The classic triad of symptoms of Wernicke's encephalopathy includes the following:

Ataxia (loss of coordination of movements). As a rule, it is represented by a combination of vestibular and cerebellar ataxia, as well as polyneuropathy.
Ophthalmoplegia (paralysis of the eye muscles). Presented by various oculomotor disorders. When looking to the sides, patients have horizontal nystagmus, bilateral paralysis of the rectus muscle of the eye. In rare cases, ptosis is observed.
Confusion of consciousness. Most patients with Gaie-Wernicke encephalopathy are disoriented and apathetic. They are unable to concentrate and carry out any serious assignment. Very often, the patient's speech is incoherent, and the conclusions have no logical background. In some cases, delirium is observed.

Only in a third of cases the patient has all the above symptoms of Gaie-Wernicke syndrome. Most often, there is only one, maximum two symptoms.

Oculomotor disorders quickly disappear when thiamine is prescribed.

Nystagmus is more difficult to treat and requires the development of an individual course of therapy, taking into account the individual characteristics of the patient's body. Ataxia is also difficult to treat, and half of the patients never recover completely. They retain a slow, shuffling gait.

In most cases, Wernicke's encephalopathy develops in parallel with the following disorders:

polyneuropathy, which occurs in 80% of patients;
spinal ataxia of the spastic type;
amblyopia;
orthostatic hypotension;
tachycardia.

The last two pathological symptoms develop as a result of damage to the autonomic nervous system.

Complications and consequences

Gaie-Wernicke encephalopathy is a serious disease that often leads to adverse consequences, including death. About 20% of hospitalized patients die. Most often, death occurs due to concomitant pathologies caused by alcoholism. We are talking about liver failure, pulmonary tuberculosis and pneumonia.

Approximately half of the surviving patients never recover from treatment. Their motor, and sometimes brain, activity remains limited for life. If the disease is left untreated, the patient may develop stupor over time. Coma and death follow.

Diagnostics

The unsatisfactory detection of Wernicke's encephalopathy is explained by the fact that many doctors traditionally believe that the disease develops exclusively in patients with alcoholism, without taking into account the possibility of its non-alcoholic origin

If the above symptoms are found, the patient should consult a specialist. A neurologist can identify this disease. When making a diagnosis, the doctor relies on data from anamnesis, features of the clinical picture and regression of symptoms during treatment with thiamine.

When examining a patient, a specialist records the following signs of the disease:

The patient has signs of a serious malnutrition. We are talking about a low body mass index, a decrease in skin elasticity, the presence of deformation of the nails.
There are signs of autonomic dysfunction, such as hypotension, tachycardia, and excessive sweating.
The neurologist notes mixed ataxia and consciousness disorder.

After the examination, the patient is sent to undergo laboratory and instrumental diagnostics. Laboratory tests involve donating blood for biochemical analysis.

Instrumental diagnostics usually gives the following results:

REG records a diffuse decrease in cerebral blood flow.
EEG in 50% of cases shows generalized slowing of waves.
MRI of the brain helps to identify hyperintense areas in some areas of the brain. In the affected areas, there is an accumulation of contrast introduced during MRI.
CT scan does not reveal changes in cerebral tissues.

Also, the patient can be directed to a lumbar puncture followed by analysis of cerebrospinal fluid (CSF).

Treatment

Take orally half an hour before meals 2 times a day, 2 tablets, without chewing, drinking 100 ml of water, the interval between doses should be 8-10 hours

This syndrome requires urgent care. The patient should be urgently hospitalized in order to start therapy with vitamin B1.

Typically, thiamine is given by intravenous drip. After some time, you can switch to intramuscular injection. The standard treatment regimen involves the introduction of the vitamin twice a day.

Vitamins such as PP, B6 and C can be used as supportive therapy. If a patient has delirium, then the following drugs are prescribed to him:

Chlorpromazine;
Barbamil;
Diazepam;
Haloperidol.

If necessary, the use of other psychotropic drugs is possible. The dosage and course of treatment is determined by the doctor on an individual basis.

As part of antioxidant therapy, cytoflavin infusions are used. In order to improve memory functions, the patient can be prescribed courses of nootropics and drugs that support vascular tone. At the same time, treatment with thiamine is periodically repeated.

Important! If the patient is diagnosed with a serious mental disorder, then treatment should be carried out with the participation of a narcologist or psychiatrist.

Forecast

With the timely start of treatment and the absence of serious complications, the prognosis is favorable. However, in most cases, Wernicke's encephalopathy develops in avid alcoholics who neglect treatment, and therefore often die from manifestations of concomitant diseases.

If the disease is of an alcoholic nature, then it most often turns into the Korsakov syndrome. It often occurs against the background of this disease. It should be noted that it is very difficult to overcome this ailment, and the patient often retains residual phenomena in the form of memory lapses, confusion, false memories, etc.

If the disease was not provoked by alcohol addiction, then, subject to timely treatment, the patient can count on a complete recovery. The complexity and duration of therapy directly depends on the neglect of the disease and the patient's health. Therefore, the sooner professional therapy begins, the better.

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 concepts, 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 in the 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, i.e., 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. Moreover, 30-50% of patients already have a history of alcoholic psychoses.

As a rule, Gaie-Wernicke syndrome debuts after a prodromal period, the duration of which ranges on average from several weeks to months. In the prodrome, asthenia, anorexia with aversion to certain dishes, instability of the stool (constipation alternating with diarrhea), nausea and vomiting, abdominalgia, sleep disturbances, cramps in the fingers and calf muscles, decreased vision, dizziness can be observed. 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, gradually emerge.

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.

To establish the diagnosis of Gaie-Wernicke syndrome to a neurologist, the data of anamnesis, a characteristic clinical picture, regression of symptoms during therapy with thiamine allow. On examination, attention is paid to the signs of chronic malnutrition (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 cases, Gaie-Wernicke syndrome is accompanied by a generalized slowing down of waves in the EEG. 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 area. This problem belongs to organic-toxic psychoses and often occurs in conjunction with Korsakoff's syndrome. The disease proceeds acutely, subacutely or chronically.

Causes

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

Gaia-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 referred to 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-illness 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, and 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, difficulties in 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.

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 thiamine deficiency, depletion of the body, and also 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. Deterioration of 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, react 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 appropriate 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 the 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 death rate of patients is 50% of cases. 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 the 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 enough sleep and getting enough sleep, playing sports and eating right.

prosindrom.com

What is Wernicke's encephalopathy

Wernicke's encephalopathy (Gaye-Wernicke's acute upper hemorrhagic polioencephalitis) is a brain damage as a result of thiamine deficiency, usually occurring in 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 alcoholic patients, 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 avitaminosis B1, electron microscopy shows morphological signs of the neurotoxic action 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 excitement 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 introduction 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 administration 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.

Diagnostics of the Wernicke 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 its protein content 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, as 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 most often this type of pathology 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, during 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

MRI is the standard for diagnosing alcoholic encephalopathy. 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 disturbances 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.

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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 Gaje-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, the sensitivity of the skin 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 frequently 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 psychoses (non-alcoholic etiology), brain tumors, as well as an acute form of vitamin deficiency that 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 talks directly with the patient, but if he has a depression of consciousness, then a survey of relatives or people who were in close proximity to 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 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, nootropic drugs (if there are brain disorders). In some cases, therapeutic measures may be required, the purpose of which is to normalize intracranial pressure. The treatment used is 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.

Alcohol 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 during 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 early detection of alcoholism and voluntary refusal from alcoholic beverages of any strength, support of loved ones, a healthy lifestyle, a balanced diet, and reasonable sports training.

Wernicke's encephalopathy (EV) is a rare but severe neurological syndrome (an acute brain disorder characterized by severe cerebral and mental disorders and high mortality) caused by a deficiency of thiamine (vitamin B1). EV was first described by C. Wernicke in 1881 under the name polyoencephalitis haemorrhagica superior acuta - acute upper hemorrhagic polioencephalitis.

According to autopsy data, the prevalence of EV in the general population ranges from 0.4 to 2.8 per 100 thousand of the population, and in people who abuse alcohol, the disease occurs much more often than in those leading a healthy lifestyle. In most cases, EV is diagnosed posthumously; during life, the diagnosis was made in less than 20% of cases. The incidence of EV does not depend on race, and women get sick less often than men (the ratio of men and women is 1.7: 1).

Terminology issues... In various scientific sources, there is a different eponymous designation of encephalopathy caused by thiamine deficiency - Wernicke encephalopathy: encephalopathy (syndrome) "Gaia [Gaia] - Wernicke" and syndrome "Wernicke - Korsakoff" (eponym [in science] is the name of the phenomenon [for example, disease], concept, structure or method by the name of the person who first discovered or described them [for example, Quincke's edema]). "Gaye-Wernicke syndrome" is a complete "clinical synonym" for Wernicke's encephalopathy, and "Wernicke-Korsakoff syndrome" is used to denote brain damage in alcoholism, which occurs initially with a picture of [Gaye-] Wernicke encephalopathy, and then, as the patient's condition improves , with a known reverse development of pathological symptoms, with the identification of signs of Korsakov's syndrome ( those. : absence or significant decrease in the ability to memorize new information [with the relative preservation of other mental functions that distinguish this disorder from alcohol dementia]). The presence of such conditions does not give any reason to consider Gaie-Wernicke encephalopathy and Korsakoff's syndrome as a single disorder.

The daily requirement of an adult for thiamine reaches 1 - 2 mg (depending on the amount of carbohydrates consumed). Vitamin reserves in the body are only 30-50 mg, so any condition that causes an insufficient intake of thiamine and lasts more than 3-4 weeks can cause a complete depletion of the vitamin reserve.

In the case of thiamine deficiency, there is a lack of intracellular thiamine diphosphate, which leads to a number of metabolic changes in the central nervous system. The gradient of ion concentration on both sides of the cell membrane is disrupted, which causes cytotoxic edema. The integrity of the blood-brain barrier is also disrupted, with the subsequent development of vasogenic edema of the brain substance. The biochemical mechanism of the development of clinical manifestations in EV is due to a dysregulation of thiamine-dependent metabolic processes. However, early cellular changes are reversible with adequate and timely (before cell necrosis) replenishment of vitamin B1 deficiency - the concept of "reversible biochemical damage".

The most common cause of thiamine deficiency is chronic alcohol abuse. In this case, hypovitaminosis develops not due to alcoholism, but due to the low absorption at the level of the mucous membrane of the gastrointestinal tract and insufficient intake of nutrients associated with alcoholic cirrhosis of the liver. In addition to alcoholism, there are many conditions accompanied by malabsorption syndrome and, as a consequence, a decrease in the absorption of vitamin B1: operations on the organs of the gastrointestinal tract (including gastric bypass surgery, gastrojejunostomy, gastrectomy, colectomy), installation of an intragastric balloon, vomiting of pregnant women, terminal tumors, chemotherapy, allogeneic stem cell transplantation, AIDS, anorexia nervosa, dietary restrictions during fasting, fasting, hemodialysis, pancreatitis, unbalanced nutrition, parenteral nutrition, overeating, long-term intravenous glucose infusions. All these conditions can be considered as predisposing factors.

Histological changes in acute EV include intra- and extracellular edema with swelling of astrocytes and oligodendrocytes, an increase in the number of microglia cells, various stages of the necrotic process, demyelination, angiogenesis, petechial hemorrhages, damage to the blood-brain barrier. The most pronounced changes occur in structures adjacent to the third ventricle [ mRI scans ]: on the medial surface of the thalamus, in the periaqueductal gray matter, the mastoid bodies, the plate of the quadruple of the midbrain. The defeat of these areas is typical for EV, since these structures are characterized by a high level of oxidative metabolism and, therefore, are most susceptible to thiamine deficiency. Less commonly, changes are found in the cerebellum, the dentate nucleus, the nuclei of the cranial nerves, the red nucleus, the caudate nucleus, the corpus callosum, the cortex of the cerebral hemispheres.

The classic debut of EV is the sudden appearance of a typical triad of symptoms: a change in mental status, ophthalmoplegia and ataxia (according to the recommendations of some authors, in accordance with classical descriptions, EV is manifested in a tetrad of the following main symptoms: ophthalmoplegia, nystagmus, ataxia, confusion; possible additional ophthalmological symptoms of EV - edema of the optic nerve discs and retinal hemorrhage). However, this clinical picture occurs in only one third of patients. The most common manifestation is a change in mental status: confusion, spatial disorientation, dizziness, drowsiness, apathy, cognitive impairment with memory loss, inability to concentrate, [with severe EV] coma and death; these symptoms are due to damage to the nuclei of the thalamus and mastoid bodies.

note! The combination of depression of consciousness, ophthalmoplegia, ataxia and hyperreflexia is also characteristic of Bickerstaff stem encephalitis [SEB] (the autoimmune mechanism of SEB development today is beyond doubt: the state in 23% of cases is associated with diarrhea caused by Campylobacter jejuni, or is often associated pneumoniae; anti-GQ1b IgG antibodies are detected in 66 - 68% of patients with SEB). More about SEB [ 1 ] in the article “Bickerstaff stem encephalitis, acute transverse myelitis and acute axonal motor neuropathy: difficulties in diagnosis and treatment of patients with overlapping syndromes. Clinical observation "A.F. Murtazina, E.S. Naumova, S.S. Nikitin, L.M. Boriskina, A.V. Lagutin; Medical Center "Practical Neurology", Moscow; LLC "Normodent Clinic Central", Moscow; Federal State Budgetary Institution "Central Clinical Hospital with Polyclinic" of the Administrative Department of the President of the Russian Federation, Moscow (journal "Neuromuscular Diseases" No. 3, 2017) [read] and [ 2 ] in the article "Clinical manifestations in Bickerstaff encephalitis" Valikova TA, Pugachenko NV, Golikova NB, Alifirova VM, Azhermacheva MN; Siberian State Medical University, Tomsk; OGUZ "Tomsk Regional Clinical Hospital", Tomsk (journal "Bulletin of Siberian Medicine" No. 2, 2011) [read].

The clinical manifestations of EV are often non-obvious, which significantly complicates its timely diagnosis and, therefore, prevents the provision of the necessary medical care to patients. The above classic tetrad of symptoms is determined in no more than every tenth case, therefore the disease often (according to some sources, in 80% of cases) remains unrecognized, often being detected only during autopsy or, in much more rare cases, as an accidental finding in neuroimaging research.

With regard to visual disturbances, complete ophthalmoplegia is rare, the most common symptom being nystagmus (usually horizontal). Balance disorder is manifested by ataxia when walking, and the latter can range from mild to complete inability to stand. This is the result of damage to the cerebellar vermis and vestibular dysfunction. In some cases, polyneuropathy and dysarthria are observed. Sometimes the onset of the disease may look different: heart failure with arterial hypotension and tachycardia, gastrointestinal symptoms (abdominal pain and nausea), hypothermia due to damage to the posterior lobe of the hypothalamus, deafness when the thalamus is involved, epileptic seizures in case of increased activity of the glutamatergic system. Our patient had oculomotor disorders (nystagmus), ataxia, nausea and vomiting.

Considering the variety of clinical manifestations of EV, in 1997 D. Caine et al. developed two groups of diagnostic criteria for this disease: for patients suffering from chronic alcoholism and for patients who do not abuse alcohol. For the first group, at least 2 of the following criteria are required: malnutrition, oculomotor disorders, signs of cerebellar damage and changes in mental status. The second group is most characterized by a change in mental status without other symptoms, which is the main reason for late diagnosis.

Differential diagnosis should be carried out with stroke and intracranial hemorrhage, meningitis and encephalitis, brain tumor, poisoning, liver failure, Markiafawa-Bignami disease, metronidazole-induced encephalopathy.

REFERENCE INFORMATION... Markjafava-Bignami disease (primary degeneration of the corpus callosum) occurs exclusively in alcoholics with intense and prolonged (more than 20 years) alcohol abuse. It is based on necrosis of the corpus callosum, commissures. Clinical symptoms are highly variable. In severe cases, a coma develops acutely; with a subacute course, there is a progressive development of frontal symptoms, pelvic disorders, and gait apraxia. Some patients may have dysarthria, hemiparesis, or aphatic disorders. A neuroimaging study (CT / MRI) reveals changes in the corpus callosum and commissures, sometimes changes in the semi-oval center are also noted. Symptoms may improve with stopping alcohol and eating well, but dementia is irreversible.

EV is essentially a clinical diagnosis, and the determination of the concentration of thiamine in the blood and the activity of erythrocyte transketolase play only an auxiliary role in its confirmation. Computed tomography (CT) can identify areas of low density at the level of the periaqueductal gray matter and the medial part of the thalamus, but in most cases this method does not reveal focal pathology in acute EV. Currently, MRI is a highly specific and most effective method for diagnosing EV. In such patients, MRI usually identifies bilateral symmetric hyperintense pathological foci in T2W and FLAIR modes, their typical localization is the thalamus (scans 2 and 3), mastoid bodies (scans 1 and 4), quadruple plate (scan 1) and periaqueductal zone (scan one). Atypical localization includes findings in the medulla oblongata and pons, the dentate nucleus of the cerebellum, the red nucleus, the substantia nigra of the midbrain, in the nuclei of the cranial nerves, in the vermis and the intermediate part of the cerebellar hemispheres, the corpus callosum, the fornix, the head of the caudate nucleus, the frontal parietal bark. Typically, atypically located foci are identified along with changes in typical sites. Against the background of effective treatment with vitamin B1, along with the gradual reverse development of clinical symptoms, focal MRI changes.

A change in the signal intensity in the cerebellar region is observed both in patients with chronic alcoholism and in cases of EV that is not associated with alcohol consumption. According to the literature, involvement of the cerebral cortex in the pathological process is prognostically unfavorable, as it indicates the irreversibility of the pathological process (however, recently N.W. Cui et al. Described a case of EV not associated with alcohol consumption: a patient with lesions of the cerebral cortex after 45 days of vegetative state regained consciousness thanks to parenteral administration of thiamine). However, the absence of pathological changes on MRI does not exclude the diagnosis of EV, in this case, a study with intravenous administration of gadolinium can help (see also MRI scans for EV on the RADIOMED.RU portal).

The fundamental differences between "alcoholic" and "non-alcoholic" EV are described in the literature. First, in patients with alcohol dependence, typical lesions in EV are combined with atrophy of the mastoid bodies and cerebellar vermis, which is a sign of previous exacerbations of EV. On the contrary, in patients with “non-alcoholic” EV, there are no atrophic disorders, and the change in the signal intensity on MRI is primarily due to a disorder in the regulation of thiamine-dependent metabolic processes. It is believed that atypical localization of focal changes in the substance of the brain (but always in association with typical) is also more characteristic of "non-alcoholic" EV (however, in 2012, KS Liou et al. Described an interesting case: a patient with "alcoholic »EV damage was found in olives, in the nuclei of the cranial nerves in the medulla oblongata and in the dentate nuclei of the cerebellum in the absence of foci with typical localization).

Differential diagnosis of symmetric focal changes in the medial thalamus using MRI should be carried out with the following diseases: cerebral venous thrombosis, paramedian thalamic syndrome, upper basilar syndrome, viral encephalitis, acute disseminated encephalomyelitis, atypical course of Creutzfeldt's disease, primary jacob flu virus Ah, West Nile meningoencephalitis. Differential diagnosis of symmetric lesions in the dentate nuclei, cranial nerve nuclei, red nuclei, and corpus callosum ridge should be performed with metronidazole-induced encephalopathy.

EV refers to emergency medical conditions, and any delay leads to irreversible neurological damage and death. If EV or its onset is suspected, treatment consists in the appointment of thiamine. To date, there is no consensus about the optimal dose of thiamine, the route of administration and the timing of treatment. Traditionally, at least 100 mg of vitamin per day is recommended for parenteral administration; recently, some authors have recommended the appointment of thiamine 200 mg 3 times a day. Thiamine is prescribed before taking any carbohydrates or simultaneously with them, since a separate administration of glucose can aggravate the course of the disease. The first signs of improvement in acute EV appear within 1 week, but usually the period of stabilization of the state takes from 1 to 3 months. Nevertheless, persistence of neurological deficits in the form of nystagmus and ataxia during walking is widespread. In the absence of treatment or in the case of the appointment of low doses of thiamine, EV leads to irreversible damage to the brain substance and, as a consequence, to death in 20% of patients and to the formation of Korsakov's syndrome in 85% of survivors.

ENCEPHALOPATHY WERNIKE: OPTIONS FOR ATYPICAL COURSE

Wernicke encephalopathy (Guy-Wernicke) develops in patients with long-term massive alcohol abuse as a result of severe alcoholic delirium and, less often, gradually, without prior fever (Delirium tremens). The risk of Wernicke's encephalopathy increases with malnutrition, general exhaustion, internal diseases with metabolic disorders and previously suffered alcoholic psychoses. The disease is characterized by an unfavorable course with high mortality and a frequent outcome in Korsakov's psychosis in surviving patients.

The essence of Wernicke's acute alcoholic encephalopathy disease is that it is one of the types of severe alcoholic brain damage, the significance of which is determined by the high (over 40% of clinically outlined cases) mortality and the possibility of an outcome in Korsakov psychosis, hemorrhagic lesions of the midbrain and diencephalon against the background of prolonged severe alcoholic intoxication, the cause of which [hemorrhagic damage] is a lack of thiamine (vitamin B1), leading to insufficient formation of thiamine pyrophosphate (TPP) and a decrease in the activity of TPP-dependent enzymes that catalyze a number of metabolic reactions in brain tissue. The decrease in the activity of TPP-dependent enzymes is one of the reasons for the decrease in the cerebral content of gamma-aminobutyric acid (GABA) and aspartate. The neurometabolic shifts resulting from these factors increase the susceptibility of neurons to the excitotoxic action of glutamate, the massive release of which from the connection with NMDA receptors is observed in acute alcohol withdrawal in addicts. In addition, a change in the activity of monoamines and acetylcholine, an increase in the permeability of the blood-brain barrier and a decrease in liver function play a certain role in the development of metal-alcoholic psychoses. Similar neurometabolic processes underlie alcoholic peripheral polyneuropathy. The clinical symptoms of Wernicke's encephalopathy are as follows:

1 ... oculomotor disorders that are bilateral and asymmetrical (ophthalmoparesis, strabismus, external ophthalmoplegia, decreased photoreactions, horizontal and rotator nystagmus);
2 ... severe cerebellar ataxia (up to astasia, abasia);
3 ... mental disorders (3.1. a state of global disorientation and indifference; 3.2. predominance of impairments in long-term memory, i.e., Korsakov's amnestic syndrome (see below); 3.3. less than 20% of them have alcoholic delirium, symptoms of alcohol withdrawal, or their variants ).

1st An atypical feature of Wernicke's encephalopathy is the possibility that the classic triad of symptoms of Wernicke's encephalopathy (see above): confusion of consciousness, predominantly of the amentive type, ataxia and ophthalmoplegia, is detected, according to some authors, only in 10% of patients. Due to the frequent erased or asymptomatic course, Wernicke's encephalopathy often remains unrecognized and is detected during autopsy or during neuroimaging studies (including as an accidental finding). It is noteworthy that a characteristic morphological (MRI) sign of Wernicke's encephalopathy, indicating its presence in the absence of obvious clinical symptoms, is multiple lesions of the mammillary bodies, periaqueductal (and in some cases, cortical) gray matter, medial portions of the optic tubercle, walls of the third ventricle, pons , medulla oblongata and basal ganglia. It is assumed that Wernicke's encephalopathy (including its unrecognized forms) and other alcoholic lesions of the central nervous system can cause deterioration in the processes of normal aging of the brain and cognitive dysfunction in old age.

2nd An atypical feature of Wernicke's encephalopathy is the following fact: a number of authors believe that one of the reliable criteria for the unfavorable course and outcome of metal alcohol psychosis is the shift in the ratio between psychopathological and neurological symptoms towards the prevalence of the latter (neurological). The most benign, in the prognostic sense, are cases of delirium, the clinical manifestations of which are practically exhausted by psychopathological symptoms, and neurological symptoms are reduced to autonomic disorders (albeit rapidly flowing). Even the most acute forms of alcoholic delirium tremens, occurring with extremely profuse hallucinatory disorders and severe psychomotor agitation, but not accompanied by severe neurological disorders and damage to internal organs, with timely and adequate treatment, almost do not pose a danger of an unfavorable outcome. The acute course of the disease is considered a favorable sign not only for metal-alcohol psychosis, but can also be considered a general rule of psychiatry. The acute onset of mental disorders is considered as a criterion for a favorable prognosis in schizophrenia. A sign of an aggravation of the course of metal-alcoholic psychoses is a change in delirious stupefaction by a simple (so-called quantitative) decrease in its level by the type of stunning or stupor. An even more formidable symptom is the transformation of delirious clouding of consciousness into amentive. If persistent fever insomnia is replaced by drowsiness, and motor frenzy is replaced by lethargy or agitation within the bed, we can state the transition of delirium into an unfavorable stage of acute encephalopathy, requiring a fundamental change in therapeutic measures in connection with the onset of serious threats to the life of patients.

3rd an atypical (feature) form of Wernicke's encephalopathy are those cases when Korsakov's syndrome dominates in the advanced stage of Wernicke's encephalopathy, including amnesia for current events, when the patient cannot assimilate new information while retaining memory for distant events, disorientation in time and space, confabulation, and pseudo-reminiscences (distorted memories of actual events). Therefore, the entire symptom complex is designated as Wernicke's disease, if the state of amnesia is absent, or as Wernicke-Korsakoff syndrome, if amnestic symptoms are found along with oculomotor disorders and ataxia. The outcome of Korsakov's psychosis is different. Complete or nearly complete recovery occurs in less than 20% of patients. In other patients, recovery is usually slow and incomplete. Depending on the severity of the residual symptoms, some patients may be cared for outside the clinic, while others must be in a hospital. The residual state of the psyche is characterized by significant memory lapses without confabulations, the patient is not able to distribute events in the correct time sequence. This last stage of the disease, by the time of the onset of which the severity of oculomotor disorders and ataxia decreases or they cannot be recognized at all, is often indistinctly referred to as a state of alcohol degradation, or alcoholic dementia.

4th An atypical feature of Wernicke's encephalopathy is that its subacute forms can pose a serious threat to the health and life of alcoholics. Along with the considered cognitive disorders and specific forms of encephalopathy, long-term alcohol abuse in a number of cases is characterized by varying degrees of decline in the level of the personality according to the organic type, the significance of which is determined by a variety of adverse effects on health, interpersonal relationships, as well as on professional fitness and social adaptation.

sources: 1. article "Clinical observation of a favorable outcome of Wernicke's encephalopathy" Yu.P. Sivolap, V.A. Savchenkov, M.V. Yanushkevich, A.M. Yakovchuk (Moscow Medical Academy named after IM Sechenov, Moscow City Clinical Hospital N№33 named after AA Ostroumov); 2. article "Mental disorders in alcohol abusers" Yu.P. Sivolap; GBOU VPO First MGMU them. IM Sechenov of the Ministry of Health and Social Development of the Russian Federation (journal "Psychiatry and psychopharmacotherapy" No. 6 - 2011; 3. article "Alcoholic brain disease (on the systematics of metal-alcoholic psychoses)" YP Sivolap (Journal of Neurology and Psychiatry named after S.S. Korsakov No. 5 - 2006); 4. "Review. Wernicke's encephalopathy (disease)" Site of radiation diagnostics doctors RADIOMED.RU v 2.0.

Fixation amnesia in Korsakov's psychosis is vividly illustrated by a classic description belonging to S.S. Korsakov (1954): “From one patient I had to hear almost constantly the following:“ I’m lying in bed today, I’m going to get up — only this minute my legs are somehow bent — as soon as they disperse, I’ll get up ”. He had a long contracture in his knees, but he, not remembering its existence, believed that it was only a matter of the moment. The same patient categorically asserted that he had no pains in his legs, but meanwhile he had very strong shooting pains: when he fires, he will scream, and then immediately answer a question that he has absolutely no pains. ... This same patient, reading a newspaper, could read the same line ten times in a row as something completely new; it happened that by chance his eyes would stop on something interesting, and he would read this line aloud to his mother and laugh; but at this time, of course, for a few seconds he will tear his eyes from the place that he was reading, and then, when his eyes attack this place again, at least now, he again with the same words: "listen, mother" - reads this passage, and thus can be repeated many times ... ".

In severe cases, manifestations of fixative amnesia can reach a degree of amnestic disorientation. The fundamental difference between Korsakov's psychosis and dementia is the selective nature of mental disorders, which practically do not go beyond the limits of cognitive impairment, while the personality is preserved. Symptoms of amnesia in patients with Korsakov's psychosis are sometimes accompanied by confabulations, the compensatory role of which is to fill the memory gaps with events that did not actually occur (filling in amnestic "gaps"). Additional symptoms of Korsakoff psychosis include apathy and other mood disorders.

The proposed mechanisms of amnestic disorders in patients with Korsakov's psychosis are associated with a critical disturbance of the conduction of the mamillary-thalamic pathways, which is of decisive importance in the formation and consolidation of memory, and, apparently, for this reason, damage to the mamillary bodies and nuclei of the visual tubercle plays a key role in the development of clinical symptoms of the disease. Also, according to some authors, the change in the prefrontal cerebral cortex and especially its ventromedial and orbitofrontal areas is of particular importance for the emergence of a specific unconsciousness characteristic of Korsakov's psychosis. The main cause of damage to the pathways in the central nervous system in Korsakov's syndrome is a deficiency of thiamine (vitamin B1) associated with malnutrition, insufficient intake of thiamine (like other vitamins) from food, a decrease in its absorption and, finally, difficulty in converting thiamine into thiamine pyrophosphate (TPP), which plays the role of an active part of the so-called TPP-dependent enzymes (alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase and transketolase), catalyzing biochemical reactions aimed at maintaining normal metabolism of the nervous tissue. Lack of thiamine, along with alcohol abuse, which disrupts vitamin overcoming of the blood-brain barrier and its cellular transport, leads to its insufficient content in the brain tissue and a decrease in the activity of TPP-dependent enzymes, which entails the development of local lactate acidosis, dysfunction of mitochondria, inhibition of tissue respiration processes, a decrease in the energy potential of neurons and neuroglia cells [

Wernicke-Korsakoff syndrome is a complex of related neuropsychiatric symptoms caused by vitamin B1 (Thiamine) deficiency. Develops with prolonged alcoholism, poor absorption of nutrients. The disease manifests itself in the form of movement disorders, eye paralysis, delirium.

Reasons for the development of Wernicke-Korsakov syndrome

Gaie-Wernicke-Korsakoff syndrome is a set of clinical manifestations caused by a deficiency of vitamin B1 with further hemorrhage in the brain. This phenomenon was first discovered in patients with chronic alcoholism. The symptoms of the syndrome were described in a woman suffering from persistent vomiting after a burn with sulfuric acid of the stomach.

It develops under the following conditions:

Fasting for gastrointestinal oncology to avoid pain.
Anorexia.
Lack of Thiamine in food.
Diseases of the gastrointestinal tract that reduce the intake of vitamin B1 with food.
Chronic alcoholism.
Indomitable vomiting in case of poisoning, pregnancy, alcoholism with Mallory-Weiss syndrome.
Acquired secondary immunodeficiency.
Hemodialysis in patients with impaired renal function.
Helminthic invasions.

Disease development

Wernicke's syndrome is an encephalopathy that develops against the background of small hemorrhages, as a rule, in the subcortical formations: the optic tubercle, mastoid bodies. The midbrain and the medial part of the hypothalamus are also involved in the pathological process. Degradation of the white matter occurs - demyelination of the pathways connecting nerve cells to each other.

The intercellular substance of the optic hillock, hypothalamus, midbrain suffers from thiamine deficiency due to the fact that it is in these areas that the vitamin is used as a cofactor for transketolase. The lack of this nutritional element leads to an energy deficit in the brain, and especially in the above-mentioned areas.

Vitamin B1 hypovitaminosis leads to the accumulation of an excitotoxic substance - glutamic acid, which has an exciting effect on neurons. Its excessive influence is the reason for further disruption of the functioning of nerve cells and their death.

It is useful to know what caused: the main causes and treatment of alcoholic amnesia.

Important: and what diseases alcohol provokes.

The hypothalamus regulates the autonomic function, which is responsible for vascular tone. Its defeat in Wernicke's syndrome leads to cerebral edema and hemorrhages. The dead cells and white nerve fibers are subsequently replaced by glia, that is, by the intercellular substance.

It also affects the cerebellar vermis, the centers of the oculomotor, abducens and vestibular cochlear nerves.

Symptoms of Wernicke-Korsakov's disease

Damage to various structures of the brain leads to impairment of their function. Wernicke-Korsakoff syndrome includes the following clinical symptoms:

, nystagmus (trembling of the eyeballs).
Headache.
Nervous, motor excitement.
Amnesia, confabulation (confusion of memory).
Delirium: delirium, hallucinations.
Asthenia, weakness.
Nausea, vomiting, heartburn, stool disorders.
Autonomic disorders: sweating, chills, facial flushing.

The defeat of the cerebellum causes ataxia, which is expressed in an unstable gait, impaired coordination of movements. Hemorrhage in the area where the nucleus of the oculomotor nerve is located leads to ophthalmoplegia, i.e., paralysis of the eyeballs.

Changes in pupillary reflexes, their asymmetric response to light are possible. The results of the cold test are often reduced in comparison with the norm.

The defeat of the hypothalamus and its nuclei causes autonomic disorders:

increased body temperature or chills;
expansion or narrowing of skin vessels;
change in complexion.

In the stem part, the nuclei of the vagus nerve are located, so edema and hemorrhages in this place lead to disorders of the digestive system, which it controls. This is manifested by diarrhea or unstable stools, vomiting.

With a deficiency of vitamin B1, not only the central, but also the peripheral nervous system suffers, and polyneuropathy develops.

Korsakov's syndrome, which occurs after hemorrhage, includes mental disorders, as well as partial memory loss. In this case, amnesia may increase. Damage to the connections between nerve cells leads to a change in memories, a person can confuse the time of the event. Delirium is a delusional disorder. Often a person is in a state of stupor, that is, stunning.

Diagnostics and treatment of Wernicke-Korsakoff syndrome

The patient needs to be examined by a neurologist and psychiatrist. Differential diagnostics is carried out with pathologies such as schizophrenia, brain neoplasms, psychosis against the background of drug intoxication.

Timely treatment will prevent amnesia from getting worse. Delay in providing an ambulance can lead to the death of the patient. For treatment, vitamin B1 is used, administered parenterally (subcutaneous, intravenous injections). Thiamin therapy is carried out until clinical improvement. It should be remembered that this drug, despite its harmlessness, can cause anaphylactic shock in the patient. Other B vitamins are also introduced: Pyridoxine, Cobalamin, Nicotinic acid.

Patients are also shown:

When exhausted, anabolic steroids are used to gain weight.
Treat the underlying disease that caused these disorders: alcoholism, Malory-Weiss syndrome, vomiting.
Antihypoxic drugs are used to protect cells from oxygen starvation: Mexidol,.
Angioprotector Actovegin improves blood circulation, rheological properties of blood.
Nootropic drugs are used to preserve memory: Noopept, Aniracetam.

Conclusion

Vitamin B1 is an essential nutrient, deficiency of which leads to Wernicke's encephalopathy and Korsakoff's mental syndrome. The earlier the treatment of the disease is started, the more favorable its prognosis. In case of untimely assistance, disability and even death are possible. With deep-seated Wernicke-Korsakov encephalopathy, residual manifestations in the form of unsteadiness of gait, memory impairment are possible.

Causes

Symptoms

Complications and consequences

Diagnostics

Treatment

Forecast

Causes of Gaie-Wernicke syndrome

Gaia Wernicke syndrome - what is it?

Causes

Diagnostics

Treatment for Gaie-Wernicke syndrome

Danger

Risk group

Prevention

The role of vitamin B1 in the pathogenesis of the disease

Causes of occurrence

Clinical picture

Diagnostics

Effects

Treatment and prognosis

What is Wernicke's encephalopathy

What provokes Wernicke's encephalopathy

Pathogenesis (what happens?) During Wernicke's encephalopathy

Symptoms of Wernicke's encephalopathy

Diagnostics of the Wernicke encephalopathy

Treatment of Wernicke's Encephalopathy

Which doctors should you contact if you have Wernicke's encephalopathy

Causes of encephalopathy

Clinical picture

Korsakov syndrome

Diagnostics

Treatment approaches

Concept and classification

Acute encephalopathy (Gaie-Wernicke syndrome)

Chronic stage of encephalopathy

Diagnostic measures

Additional diagnostic measures - ultrasound, MRI, CT.

First aid

What methods are treated

Forecasts and preventive measures

Reasons for the development of Wernicke-Korsakov syndrome

Disease development

Symptoms of Wernicke-Korsakov's disease

Diagnostics and treatment of Wernicke-Korsakoff syndrome

Conclusion

Meaning of symbols and methods of decoding

Explanation of the meaning of the figures received

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