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Alcoholic encephalopathy
Last reviewed: 07.07.2025
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Alcoholic encephalopathy is divided into acute and chronic forms. Transitional variants are possible between them, but this has no determining clinical significance. In encephalopathies, mental disorders are always combined with systemic somatic and neurological disorders, which occupy a leading place in the clinical picture.
Acute alcoholic encephalopathy
An organic lesion of the central nervous system of a dystrophic nature that occurs as a result of the toxic effects of alcohol.
Reasons
- Use of alcohol substitutes and technical liquids.
- Heavy and prolonged binges.
- Organic brain damage.
Pathogenesis
The pathogenesis of acute alcoholic delirium is not fully known; it is believed that a disruption in the metabolism of CNS neurotransmitters and severe, primarily endogenous, intoxication are involved.
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Symptoms
These conditions are characterized by clouding of consciousness up to amentia, delirium and severe neurological disorders.
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Wernicke's encephalopathy
Hemorrhagic encephalopathy with subacute course, which is rarely observed nowadays. The main role in the pathogenesis of this condition is played by the disturbance of vitamin B1 metabolism. Prodromal phenomena usually occur 3-6 months before the development of psychosis and are manifested by rapid asthenia of the patient, weight loss, and a sharp decrease in tolerance to alcohol.
The onset of the disease is acute, usually after delirious clouding of consciousness. At the onset of the disease, periods of drowsiness or stereotypical excitement prevail, manifested in a limited space, as well as scanty, fragmentary, static visual hallucinations and illusions. The patient may periodically shout out individual words, mumble something indistinctly, short-term states of immobility, "freezing" with tension of all muscle groups are possible. Fragmentary delirious and hallucinatory experiences, phenomena of amnestic disorientation are observed. After a few days, a change in the clinical picture occurs, drowsiness develops during the day, stupefaction of consciousness increases, as the condition worsens, sopor develops - a pseudoencephalitic syndrome, which can, in turn, develop into a coma.
Neurological symptoms in the clinical picture of Wernicke-Gaiet encephalopathy are in the first place. From the very beginning of occurrence, complex hyperkinesis (tremors, twitching, choreoathetoid movements), attacks of torsion spasm are characteristic, unstable muscle hypertonus can be expressed up to decerebrate rigidity, involuntary movements of the limbs are observed. The most common pathological reflexes are proboscis, spontaneous lip pursing, grasping. Pathological eye reflexes are nystagmus, ptosis, double vision, strabismus, fixed gaze, Gudden's symptom - miosis, anisocoria, weakening of the reaction to light up to its complete disappearance, convergence disorders. Cerebellar disorders, meningeal symptoms (rigidity of the occipital muscles) are also characteristic. Hyperpathy and polyneuritis accompanied by mild paresis are always present.
The appearance of patients is characteristic; they are usually emaciated, their complexion is earthy-gray or yellowish with a dirty tint, their face is puffy, and a peculiar oiliness of the skin of the face is also noted.
The skin of the body is dry, flabby, flaky, the limbs are cyanotic, often edematous, and extensive necrotic bedsores easily form on them (with insufficient care). Breathing is shallow and clear. Arterial hypertension at the onset of psychosis, as the condition worsens, turns into hypotension or collapse. Water and electrolyte disorders increase, shortness of breath, arrhythmia, and leukocytosis in the blood occur. As the condition worsens, body temperature rises - an unfavorable prognostic sign. The liver is enlarged and painful.
The disease can proceed in attacks. After the development of manifest symptoms, an improvement in the patient's somatoneurological condition is observed in 3-7 days, a favorable sign is the normalization of sleep. In the future, attacks can be repeated, but each subsequent one is less severe and shorter than the previous one. If during light intervals, symptoms of confabulatory confusion appear, this indicates the possibility of transition to the chronic form of Karsakov's syndrome.
Fatal outcome in acute encephalopathy is not uncommon, death usually occurs in the middle or by the end of the second week from the onset of psychosis. Legal outcome is facilitated by intercurrent diseases, most clearly pneumonia. Psychosis that does not lead to death lasts 3-6 weeks. Outcomes psychoorganic syndrome of varying depth, structure and severity: Korsakov's syndrome, symptoms of pseudo-paralysis.
Mitigated acute encephalopathy (moderate encephalopathy)
First described by S.S. Korsakov in 1887. The prodromal period lasts 1-2 months, marked asthenia with irritability, depressed mood, sleep and appetite disorders prevail. Manifest symptoms are represented by shallow delirious disorders at night, drowsiness during the day. Affective disorders in the form of anxiety-hypochondriacal depression are constant. signs of dysphoria. Neurological symptoms are constant, represented mainly by neuritis of a shallow degree of severity. The exit from acute psychosis is accompanied by pronounced asthenic symptoms. Memory impairment is constant, long-term, slowly passing. The duration of the described variant is up to 2-3 months.
Encephalopathy with a hyperacute, fulminant course
The most unfavorable variant of psychosis, usually ending fatally. As a rule, only men are ill. The prodromal period lasts up to 3 weeks, the course is without features, adynamic asthenia prevails. In this case, vegetative and neurological disorders are expressed from the very beginning, their intensity increases already in the initial period of psychosis. Impaired consciousness is represented by severe forms of delirium - professional or muttering. Hyperthermia is significant - 40-41 ° C. After a few days, stupor develops, quickly turning into a coma. Death occurs in a maximum of 1 week, usually - in 3-5 days. With timely adequate professional treatment, the development of pseudo-paralytic syndrome can be noted as an outcome.
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Chronic alcoholic encephalopathy
Persistent dystrophic lesion of the central nervous system of toxic (alcoholic) origin.
Reasons
Chronic encephalopathy is a consequence of long-term, systematic alcohol intoxication.
Pathogenesis
Organic changes in the central nervous system at the biochemical and cellular level, including persistent disturbances of homeostasis, processes of degeneration, demyelination, and apoptosis.
The clinical picture includes the development of dementia, neuritis of the extremities, sensory disturbances, weakening of tendon reflexes, Korsakov's syndrome (fixation, retrograde and anterograde amnesia, euphoria, amnestic disorientation and confabulations - false memories), and other disorders.
Korsakoff's psychosis (alcoholic paralysis, polyneuritic psychosis)
In his dissertation "On Alcoholic Paralysis" (1KH7), G.S. Korsak was the first to describe a peculiar psychosis in patients with alcoholism combined with polyneuritis, characterized mainly by memory disorders for current and recent events, retrograde amnesia, and a tendency to confabulation. At that time, the nosological independence of this disease was disputed. Subsequently, Korsakoff clarified and refined the symptoms of this disease. At present, the name Korsakoff's psychosis (in contrast to Korsakoff's syndrome, which is also encountered in other diseases) is retained for cases that have alcoholic myology and a pronounced clinical picture described by Korsakoff.
And today it is rarely encountered in clinical practice. Women are more often ill, the general picture of alcoholism, the age of patients, predisposing factors are similar to those in acute alcoholic encephalopathy and are described in the general part.
As a rule, Korsakov's psychosis develops after complex or severe delirium, acute Gayet-Wernicke encephalopathy, much less often - gradually, without previous states of clouding of consciousness. Mental disorders and the advanced stage of psychosis are determined by a triad of symptoms: amnesia, disorientation and confabulation.
Along with fixation, retrograde amnesia (memory impairment for events preceding the disease) is observed, covering several months or even years. The patient confuses the temporal sequence of events. The assessment of the time section suffers.
Confabulations do not appear spontaneously, but only when the patient is questioned. He talks about events in everyday life that seem to have just happened to him, or about situations related to his professional activities (for example, a patient who has not left the clinic for several weeks talks about a trip to the country, where he dug, planted seedlings, etc.). Confabulations of a fantastic or adventure nature are rarely observed. Since patients are highly suggestible, the doctor can change or direct the content of confabulations during questioning. The severity of amnestic disorders and the number of confabulations do not correlate with each other.
Disorientation is often amnestic, for example, the patient claims that he is writing or is currently in a place where he once lived.
Consciousness of the disease is always present, manifested, first of all, by memory disorder. The patient complains of poor memory, its progressive deterioration, but tries to hide it with the help of certain tricks, often childish, primitive.
Neuritis of the lower extremities is constant and obligatory. The relationship between the severity of mental and neurological disorders is also not traced
In Korsakov's psychosis, a regressive course is possible with a relative improvement in mental state within a year, cases of recovery are very rare. In more severe cases, a pronounced organic defect with dementia is formed. In the most malignant cases, a fatal outcome is possible due to hemorrhagic changes leading to extensive defects in the cerebral hemispheres.
Alcoholic pseudoparalysis
Nowadays it is encountered even less frequently than Korsakov's psychosis. It got its name due to the similarity of the clinical picture with progressive paralysis. However, it should not be forgotten that these are different diseases by etiology. Alcoholic pseudoparalysis develops mainly in men with a long history of the disease, who preferred denatured, low-quality alcoholic beverages, emaciated patients with severe nutritional disorders in the presence of hypovitaminosis or avitaminosis. It develops both after acute severe delirium and acute encephalopathy, and gradually, against the background of pronounced alcoholic degradation. Mental and neurological disorders are similar to dementia or expansive form of progressive paralysis. Mood - from complacently elevated, euphoric to agitated and angry.
They observe lush, absurd, excessive and senseless ideas of grandeur, there is a complete loss of criticism, disinhibition of lower drives, a tendency to rude, cynical jokes appears. Ideas of grandeur are often confabulatory. Occasionally they observe states of anxious depression, reaching agitation, with elements of Cotard's delirium. Memory disorders are increasing, severe. Neurological symptoms are represented by tremor of the facial muscles, tongue, fingers, dysarthria, polyneuritis, altered tendon reflexes.
If pseudoparalysis developed after acute psychosis, the further course is usually regressive, but organic decline remains. If the disease developed gradually, then the course is progressive, with an outcome in dementia. Lethal outcomes are rare.
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Rare forms of alcoholic encephalopathy
There are a significant number of other encephalopathies that have acute and chronic course, favorable and unfavorable outcomes. These forms are not distinguished in ICD-10 as nosological units.
Alcoholic encephalopathy with pellagra features
Occurs due to chronic deficiency of vitamin PP (nicotinic acid). Distinctive features: changes in the skin of the hands (the appearance of symmetrical red or gray-brown inflamed areas, then peeling begins), damage to the digestive tract (stomatitis, gastritis, enteritis, loose stools), minor memory disorders.
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Alcoholic encephalopathy with beriberi features
Develops as a result of chronic deficiency of vitamin B1 (thiamine). Features: neurological disorders prevail, polyneuritis of the lower extremities dominates - pain and paresthesia or muscle weakness with loss of sensitivity. Sometimes - myocardial dystrophy with symptoms of right ventricular failure. An asthenic symptom complex is expressed.
Encephalopathy with symptoms of retrobulbar neuritis (alcoholic, vitamin amblyopia)
Features: impairment of central or central-marginal vision, more pronounced in relation to objects of red and white color. Neurological symptoms are significant: paresthesia, unsteadiness when walking, dysphonia, spastic paralysis. Asthenic manifestations predominate. The course is protracted from 1.5 to 4-10 months.
Alcoholic encephalopathy due to stenosis of the superior vena cava
Characteristic of patients with chronic alcoholism suffering from liver cirrhosis. Features: acute development of disorders of consciousness - from stupor to coma. Hand tremor with successive flexion and extension of the fingers, muscle hypotonia are typical. Fatal outcomes are frequent. With a favorable course, the indicated disorders quickly disappear, but have a tendency to recur.
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Alcoholic cerebellar atrophy
It is necessary to differentiate from acute transient disorders due to a single severe alcohol poisoning. The disease develops slowly, neurological disorders, balance disorders during walking, in the Romberg pose, intention tremor, adiadochokinesis, muscle hypotonia, vestibular disorders predominate. Psychoorganic syndrome of varying severity develops. Not everyone recognizes the nosological specificity.
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Marchiafava-Bignami encephalopathy (Marchiafava-Bignami syndrome, central degeneration of the corpus callosum)
It was first described by Italian psychiatrists Marchiafava E. Bignami A. (1903) in peasants who drank homemade red wine in large quantities. Mostly men are affected. The disease develops over many years, and its manifestations resemble severe degradation. It usually manifests itself with delirious disorders, which are later followed by significant neurological disorders similar to acute Gayet-Wernicke encephalopathy. Mental disorders are similar to those in pseudoparalysis, with fixation amnesia and confabulation. The prognosis is unfavorable. Death occurs 2-3 months after the onset of symptoms, in a state of coma or mental and physical insanity. The nosological specificity is questionable.
Central pontine necrosis (central pontine myelinosis)
Described by Adams K. (1959). Mental disorders are similar in state to apathetic stupor: the patient does not react to external, even painful stimuli, while pain sensitivity is preserved. Neurological symptoms are pronounced, represented by eye symptoms, tetraparesis, pseudobulbar disorders, and forced crying. Not everyone recognizes the nosological specificity.