Gaia Wernicke encephalopathy symptoms. Gaie-Wernicke encephalopathy

Gaie Wernicke (Wernicke 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.

Causes

Gaia Wernicke's disease is most often caused by B1 vitamin 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 years old 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.

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:

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

Disease development

Wernicke's syndrome is an encephalopathy that develops against the background of small hemorrhages, usually 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 food 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 hemorrhage. The dead cells and white nerve fibers are subsequently replaced by glia, that is, by the intercellular substance.

It also affects the cerebellar worm, 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:

  1. , nystagmus (trembling of the eyeballs).
  2. Headache.
  3. Nervous, motor excitement.
  4. Amnesia, confabulation (confusion of memory).
  5. Delirium: delirium, hallucinations.
  6. Asthenia, weakness.
  7. Nausea, vomiting, heartburn, stool disorders.
  8. 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.

It is possible to change pupillary reflexes, their asymmetric reaction to light. 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:

  1. When exhausted, anabolic steroids are used to gain weight.
  2. Treat the underlying disease that caused these disorders: alcoholism, Malory-Weiss syndrome, vomiting.
  3. Antihypoxic drugs are used to protect cells from oxygen starvation: Mexidol,.
  4. Angioprotector Actovegin improves blood circulation, rheological properties of blood.
  5. 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.

Wernicke's encephalopathy is a brain damage due to an acute shortage of thiamine - vitamin B1 in the body, against the background of chronic alcoholism, malnutrition, and incessant vomiting.

The systematic use of alcohol for a long time can lead to disastrous consequences that arise from dysfunction of the brain and central nervous system.

Gaie-Wernicke syndrome develops as a result of alcohol intoxication. Statistics claim that there is also a certain predisposition to this disease, especially in men after thirty years.

Pathogenesis and causes of violation

Gaia-Wernicke encephalopathy is characterized by acute lesions of the hypothalamus, brainstem, and cerebellum. The development of the pathology mechanism is based on a decrease in the number of nerve cells and the destruction of myelin in the white matter area.

The defeat extends to the substances of those parts of the brain that are located in the 4th ventricle, near the 3rd ventricle and the Sylvian aqueduct - the channel connecting these divisions. In acute cases, punctate hemorrhages are diagnosed. In chronic cases, atrophy of the mastoid bodies.

Despite the fact that the disease is mainly accompanied by chronic alcoholism, the syndrome can develop as a result of vitamin deficiency and exhaustion after prolonged fasting, continuous vomiting, malignant tumors and other factors. Also given pathological condition, vascular-dystrophic changes occur.

With a deficiency of vitamin B1, the processing of glucose by neurons decreases and mitochondria are damaged. Excessive accumulation of glutamate due to decreased activity of the enzyme alpha-ketoglutaradehydrogenase due to lack of energy has neurotoxic effects.

Not only people who abuse alcoholic beverages or have a lack of thiamine in the body can develop this disease. There are a number of other factors that can provoke pathology, so Wernicke's encephalopathy develops in the following conditions:

  • malnutrition;
  • avitaminosis;
  • tumors;
  • prolonged fasting;
  • poisoning with medications that contain digitalis extract;
  • gastrointestinal diseases;
  • pregnancy.

What will indicate the disease?

The acute form is accompanied by a number of signs that make it possible to identify and diagnose this violation.

Deterioration of the general physical condition, the appearance of various nervous and mental disorders, exacerbation of other ailments - all this together will indicate the presence of Gaie-Wernicke syndrome.

First of all, pathology is characterized by a triad of symptoms:

  • - impaired coordination of movements and a sense of balance;
  • ophthalmoplegia - paralysis of the eye muscles due to damage to the oculomotor nerves;
  • disorder of consciousness - inability to adequately perceive the surrounding reality, think and react to external stimuli.

Patients with Wernicke's encephalopathy become apathetic, disoriented, unable to concentrate on anything.

The initial stage of the disease can last from several weeks to months and is manifested by the following symptoms:

  • a strong feeling of drowsiness;
  • systematic premature awakening;
  • inability to fall asleep quickly;
  • sleep is accompanied by nightmares;
  • feeling overwhelmed.

Other symptoms include the following conditions:

  • loss of appetite;
  • a gradual aversion to fatty foods and foods containing proteins;
  • the appearance of frequent nausea with vomiting;
  • belching and heartburn;
  • pain in the abdomen;
  • feeling physically tired;
  • upset stool;
  • increased fatigue;
  • inability to endure prolonged physical and mental stress;
  • violation of speech - the appearance of incoherence and lack of meaning in the patient's conversation;
  • hallucinations;
  • movement disorders.

Symptoms of the advanced stage of Wernicke's encephalopathy include:

  • chills and fever;
  • tachycardia;
  • pain in the region of the heart;
  • increased sweating;
  • seizures in the limbs;
  • feeling of suffocation;
  • violation of tactile reactions;
  • high body temperature;
  • arrhythmia;
  • the appearance of a feeling of fear and anxiety.

Establishing diagnosis

To diagnose encephalopathy, consultation of a neurologist, therapist, ophthalmologist and psychotherapist is required. Diagnosis confirmed on the basis of the results of the survey, which is carried out using the following methods:

  • analysis of urine and blood;
  • electrocardiography;
  • analysis of the caloric response;
  • MRI and CT;
  • analysis of cerebrospinal fluid.

Difficulties in making a diagnosis may arise against the background of the fact that the disease must be differentiated from various pathologies, such as schizophrenia and other psychoses.

Therapies

This disease is referred to as an emergency. If even a few symptoms are detected, the patient requires urgent hospitalization.

Without proper and timely treatment, coma and further death can occur.

The essence of the general treatment consists in replenishing the water balance in the body, correcting electrolyte disturbances, replenishing thiamine deficiency, and returning the patient to a normal diet.

For this, the following drugs are prescribed:

  • - injected intravenously or intramuscularly at a dose of 100 mg, the course of treatment is at least 5 days;
  • magnesium sulfate - injections are carried out every 6-8 hours at a dose of 1-2 g;
  • magnesium oxide - applied orally at a dose of 400-800 mg once a day;
  • complex of vitamins B2, B6;
  • ascorbic and nicotinic acid;
  • anabolic steroid;
  • glucose - it is injected intravenously after the introduction of thiamine, otherwise, if glucose is used incorrectly, the condition may worsen with lightning speed.

Reception of thiamine in such a dosage continues until the patient completely transitions to a normal diet. In addition to the above drugs, the patient is prescribed a course of multivitamins. Along with this, the work of the cardiovascular system is constantly monitored.

A prerequisite for successful therapy is a complete rejection of alcoholic beverages.

Prognosis and complications

The forecast in this case can be quite unfavorable. As practice shows, half of the cases are fatal. Such a high percentage of mortality is associated with an acute course of the disease and exacerbation of concomitant ailments, such as diabetes mellitus, cirrhosis of the liver.

A very important role is played by timely seeking medical help and qualified treatment. Among the severe complications of Wernicke's encephalopathy, the following conditions can be distinguished:

  • partial memory loss;
  • disorders of the cognitive sphere and human life in general;
  • constant sleepiness;
  • the impossibility of restoring the full functioning of brain activity as before the disease against the background of brain atrophy;
  • mental disorders;
  • high probability of coma and death.

Preventing this disease is much easier than treating it. Prevention of pathology is as follows:

  • complete refusal to take alcohol;
  • maintaining a healthy and active lifestyle;
  • adherence to proper sleep patterns;
  • good balanced nutrition;
  • timely access to a doctor.

Wernicke encephalopathy (Gaie-Wernicke syndrome or Gaie-Wernicke acute hemorrhagic polioencephalitis) is a brain disease that occurs against the background of a deficiency, for various reasons, of thiamine (vitamin B1).

As a consequence of the disease, the midbrain, cerebellum and hypothalamus are primarily affected, which causes confusion, hallucinations, delirium and other severe symptoms associated with the central nervous system and the brain.

The main factor influencing the development of this disease is a pronounced lack of vitamin B1. This affects the metabolism and the level of enzymes in the brain cells.

Thiamine deficiency lowers the level of biochemical processes in neurons, which causes a decrease in the level of glucose necessary for cell nutrition, but at the same time, an accumulation of an enzyme called glutamate occurs. This enzyme serves as a catalyst for the activity of receptors in cerebral neurons, which leads to an influx of calcium ions.

In turn, calcium ions contribute to the activation of many enzymes that destroy brain cells already weakened due to a lack of glucose. Taken together, all factors have a strong destructive effect, which affects both the functioning of the brain and the general state of the nervous system.

Despite the large number of reasons, most often it is chronic alcoholism that is the main factor in the development of vitamin B1 deficiency in most patients.

The duration of alcohol consumption varies from 5 to 20 years for men, for women the numbers are much lower, which is associated with the characteristics of the female body, which is more susceptible to the effects of alcoholic beverages.

Gaie-Wernicke syndrome symptoms

At the initial stage preceding the disease itself, when the level of vitamin B1 falls below normal, so-called prodromal symptoms are observed, which are characterized by the following manifestations:

  • sharp weight loss;
  • asthenia;
  • sleep disturbance;
  • muscle cramps;
  • frequent constipation, alternating with diarrhea;
  • unreasonable nausea or vomiting;
  • visual impairment;
  • dizziness and weakness;
  • increased fatigue.

This prodromal period can last from several weeks to months, depending on the state of the body and lifestyle at this time.

  • confusion of consciousness;
  • ophthalmoplegia (disorders of the motor functions of the eyes);
  • inability to concentrate;
  • disorientation in space;
  • apathy and depression;
  • decreased mental ability;
  • disorder of perception and understanding of reality;
  • hallucinations;
  • rave;
  • frustration;
  • loss of motor functions.

The main symptoms indicating illness should be sudden squint and lack of coordination. There may also be a drooping of the eyelid and polyneuropathy (impaired motor function). The patient is unable to move independently and is often lost in space, which, according to statistics, is present in 80% of patients.

In the most advanced stages, the patient may have coma and death if the brain damage is not compatible with life.

Diagnostics

This disease is dealt with by a neurologist. He first examines the history (cumulative information about the patient's condition), based on personal questions, symptoms and clinical presentation.

Additionally, analyzes and studies are prescribed:

  • biochemical blood test (for pyruvate and transketolase);
  • lumbar puncture of the spinal cord (increased protein levels indicate complications);
  • EEG (generalized slowing down of waves should be observed);
  • REG (for a diffuse decrease in cerebral blood flow);
  • CT scan of the brain;
  • MRI of the brain.

After carrying out all the necessary procedures to determine the nature and stage of the disease, the doctor prescribes a course of treatment.

Elderly age, physical inactivity, overweight - all these are risk factors for the development of encephalopathy of mixed origin. In this article, you will find out what consequences this pathology can lead to.

Treatment

This disease can only be cured in a clinical setting, that is, hospitalization is necessary. No self-medication is appropriate here. First, therapy with thiamine (vitamin B1) is used intravenously 2 times a day. Then the patient is gradually transferred to intramuscular injections.

Additionally, other vitamins are prescribed (PP, B6 and vitamin C).

Psychotropic drugs are used for treatment:

  • Haloperidol;
  • Aminazine;
  • Seduxen;
  • Barbambil;
  • and etc.

The choice of drug depends on the nature of the mental and neurological disorders. The drugs are prescribed only by the attending physician under the complete supervision of the patient on his part.

Antioxidants may be prescribed, such as Cytoflavin, which is used to reduce oxidative reactions in the body.

For the treatment of disorders of the brain, nootropic drugs are prescribed (Piracetam, Piracesin, Aminalon, Gammalon), which help to restore lost abilities faster, and vascular drugs to improve blood circulation (Cavinton, Trental).

In parallel with the use of medicines, a narcologist and a psychiatrist should work.

This therapy is aimed at eliminating the root cause of the disease - alcoholism, as well as the return and adaptation of a person in society, since the patient will have to radically change his lifestyle after recovery, if he, of course, wants it himself.

Complications

In case of untimely treatment or its complete absence, the patient may experience irreversible disturbances in the work of the brain, and therefore the body as a whole:

  • irreversible decrease in mental capacity;
  • the occurrence of tumors;
  • atrophy of brain tissue;
  • personality change;
  • development of mental disorders (schizophrenia, psychosis, etc.);
  • metabolic disease;
  • dysfunction of internal organs;
  • complete loss of motor functions;
  • coma.

The level of possible complications is determined by the amount of damage to the brain tissue. Depending on which part of the patient's brain has undergone the most damage, such symptoms will be observed.

If no treatment is carried out, then the patient's condition will worsen from a larger amount of dead brain tissue. The most extreme case is death.

Forecast

Gaie-Wernicke syndrome has a very high mortality rate - about 50% of cases in the acute stage. This is due to a large number of disorders in the body associated with disease, such as diabetes mellitus or cirrhosis of the liver. All pathologies are greatly aggravated and patients cannot always tolerate it.

After starting treatment with thiamine, the patient will experience significant improvement in his condition.

If the level of damage was not critical, then after a course of therapy, the patient will be discharged from the hospital. However, this does not mean that he is completely healthy.

We'll have to return the lost mental and other abilities, and for this, special programs are provided that depend on the complications caused by the disease.

The main cause of the disease is chronic alcoholism, therefore, when observing the symptoms of Wernicke's encephalopathy, one should completely abandon alcohol and consult a doctor.

Only emergency help from medical specialists will help stop the development of the disease, and then cure the patient. It must be remembered that the sooner you seek help, the faster and easier the treatment will be. There is no need to hesitate, as the disease can cause irreversible health consequences.

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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:

  1. 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.
  2. There are signs of autonomic dysfunction, such as hypotension, tachycardia, and excessive sweating.
  3. The neurologist notes mixed ataxia and disturbance of consciousness.

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:

  1. REG records a diffuse decrease in cerebral blood flow.
  2. EEG in 50% of cases shows generalized slowing of waves.
  3. 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.
  4. 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 effects 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.