Alcohol encephalopathy

Alcohol encephalopathy is divided into acute and chronic forms. Between them, transitional variants are possible, but it does not have a determining clinical significance. With encephalopathy, mental disorders are always combined with systemic somatic and neurological disorders, which occupy a leading place in the clinical picture. 

[1], [2], [3], [4], [5], [6]

Acute alcoholic encephalopathies

The organic lesion of the central nervous system is of a dystrophic nature, which is due to the toxic effect of alcohol.

Causes

• The use of surrogates of alcohol and technical liquids.
• Heavy and long binges.
• Organic damage to the brain.

Pathogenesis

The pathogenesis of acute alcohol delirium is not completely known, presumably the metabolism of the neurotransmitters of the central nervous system and the severe, especially endogenous intoxication, are important.

[7], [8], [9], [10], [11]

Symptoms

For these states, the confusion of consciousness up to amenia, delirium and pronounced neurological disorders is characteristic.

[12],

Encephalopathy of Gaye-Wernicke

Hemorrhagic encephalopathy with a subacute current is rare. In the pathogenesis of this condition, the main role is played by the violation of vitamin B1 metabolism. Prodromal phenomena occur, as a rule, for 3-6 months. Before development of a psychosis and are shown by fast astenizatsiej the patient, weight loss, sharp depression of tolerance to alcohol.

The onset of the disease is acute, usually after the delirious confusion of consciousness. At the onset of the disease, periods of drowsiness or stereotyped excitement occur in limited space, as well as meager, fragmentary, static visual hallucinations and illusions. The patient may occasionally shout out individual words, mutter something inaudibly, short-term conditions of immobility, "congealing" with the tension of all muscle groups, are possible. Observe fragmentary delusional and hallucinatory experiences, phenomena of amnestic disorientation. After a few days, the clinical picture changes, drowsiness develops during the day, the stunning of consciousness increases, when the condition becomes heavier, sopor develops, a pseudoencephalitic syndrome capable of switching to a coma.

Neurological symptoms in the clinical picture of encephalopathy Gaia-Wernicke come first. From the very beginning of the occurrence, complex hyperkineses are characteristic (trembling, twitching, choreoathetoid movements), torsion spasm attacks, unstable muscle hypertension can be expressed up to a decerebral rigidity, observe involuntary limb movements. The most frequent pathological reflexes are proboscis, spontaneous stretching of the lips, grasping. Pathological eye reflexes - nystagmus, ptosis, doubling, strabismus, motionless glance, Gudden's symptom - miosis, anisocoria, weakening of reaction to light until its complete disappearance, violation of convergence. Characteristic are also cerebellar disorders, meningeal symptoms (neck stiffness). There is always hyperpathy and polyneuritis accompanied by mild paresis.

The appearance of the patients is typical, they are usually depleted, the complexion is earthy gray or yellowish with a dirty shade, the face is puffy, they also note the peculiar greasiness of the facial skin.

The skin of the trunk is dry, flabby, flaky, the limbs are cyanotic, often swollen, they are easily formed extensive necrotic bedsores (with insufficient care). Breathing is superficial clean. Arterial hypertension in the beginning of psychosis, as the state worsens, goes into hypotension or collapse. Water-electrolyte disorders increase, dyspnea, arrhythmia, in the blood - leukocytosis. If the condition worsens, the body temperature increases, an unfavorable prognostic sign. The liver is enlarged, painful.

The disease can proceed paroxysmally. After the development of manifest symptoms after 3-7 days, the patient's somato-neurologic condition is improved, a favorable sign of sleep normalization. In the future, seizures may recur, but each subsequent - less severe and less prolonged than the previous one. If symptoms of confabulation confusion appear during light intervals. This indicates the possibility of transition and the chronic form of the Karsakov syndrome.

The fatal outcome in acute encephalopathy is not uncommon, death usually occurs in the middle or towards the end of the second week from the onset of psychosis. The legal outcome is facilitated by acceding intercurrent illnesses, most commonly pneumonia. A psychosis that does not lead to death lasts 3-6 weeks. Outcomes of the psychoorganic syndrome of different depth, structure and degree of severity: Korsakov syndrome, symptoms of pseudoparachy.

[13], [14]

Mitigated acute encephalopathy (medium-severity encephalopathy)

First described by S.S. Korsakov in 1887. The prodromal period lasts 1-2 months, the severe asthenia with irritability, the lowered background of mood prevails, disturbances of a dream and appetite prevail. Manifest symptoms are represented by shallow delirious disorders at night, daytime drowsiness. Constant affective disorders in the form of anxious-hypochondriacal depression. Signs of dysphoria. Neurological symptoms are constant, mainly represented by neurites of a shallow degree. The way out of acute psychosis is accompanied by severe asthenic symptoms. Memory irregularities are permanent, long, slow. The duration of the described variant is up to 2-3 months.

[15], [16]

Encephalopathy with a fast, lightning course

The most unfavorable version of psychosis, ending, as a rule, lethal. As a rule, only men are ill. The prodromal period lasts up to 3 weeks, the course 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. Disorders of consciousness are represented by severe forms of delirium - professional or exaggerating. Hyperthermia is significant - 40-41 ° C. A few days later the stunning is developing, quickly turning into a coma. Death occurs a maximum of 1 week, usually in 3-5 days. With timely adequate professional treatment, the development of a pseudo-paralytic syndrome can be noted as an outcome.

[17], [18], [19], [20], [21],

Chronic alcoholic encephalopathy

Persistent dystrophic CNS damage of toxic (alcoholic) origin.

Causes

Chronic encephalopathy is the result of a long, systematic alcohol intoxication.

Pathogenesis

Organic changes in the CNS at the biochemical and cellular level, including persistent violations of homeostasis, processes of degeneration, demyelination, apoptosis.

In the clinical picture, the development of dementia, neuritis of limbs, sensitivity disorders, weakening of tendon reflexes, Korsakov's syndrome (fixative, retrograde and anterograde amnesia, euphoria, amnestic disorientation and confabulation - false memories), other disorders are noted.

[22], [23], [24]

Korsakov's psychosis (alcoholic paralysis, polyneuric psychosis)

In the dissertation "On alcoholic paralysis" (1КН7) G .. With Korsak for the first time described a kind of psychosis in patients with alcoholism in combination with polyneuritis, characterized mainly by memory disorders for current and recent events, retrograde amnesia, propensity to confabulation. At that time the nosological independence of the disease was disputed. Subsequently, Korsakov clarified and finalized the symptoms of this disease. At the present time, the name of Korsakov's psychosis (unlike Korsakov's syndrome, found in other diseases) is reserved for cases with alcoholic mythology and a pronounced clinical picture described by Korsakov.

And clinical practice today is rare. Women suffer more often, the general picture of alcoholism, the age of patients, predisposing factors are similar to those in acute alcoholic encephalopathy and are set out in the general part.

As a rule, Korsakov's psychosis develops after complex or severe delirium, acute encephalopathy of Gaye-Wernicke, much less often - gradually, without previous states of obscuration of consciousness. Mental disorders and the unfolded stage of psychosis define a triad of symptoms: amnesia, disorientation and confabulation.

Together with the fixation, retrograde amnesia (memory impairment at the events preceding the disease) is observed, covering several months and even years. The patient confuses the temporal sequence of events. Suffices the estimation of the cross section of time.

Confabulations are not manifested spontaneously, but only when the patient is questioned. He talks about the events of everyday life that have just happened to him, or about situations connected with his professional activities (for example, a patient who does not leave the clinic for several weeks, talks about a trip to the dacha where he dug, planted seedlings, etc.). Seldom observe confabulations of fantastic or adventure content. Since patients are highly suggestible, during interrogations the doctor can change or direct the content of the confabulation. The severity of amnestic disorders and the number of confabulations do not correlate with each other.

Disorientation is more often amnestic, for example, the patient claims to be writing or is currently in the place where he once lived.

Consciousness of the disease is always present, manifested, first of all, by a memory disorder. The patient complains of bad memory, its progressive deterioration, but tries to hide it with the help of certain tricks, often childish, primitive.

Neuritis of the lower limbs are permanent, mandatory. The relationship between the severity of mental and neurological disorders also does not follow

Under Korsakov's psychosis, there may be a regentive course with a relative improvement in the mental state during the year, very rarely there are cases of recovery. In more severe cases, a pronounced organic defect with dementia is formed. In the most malignant cases, a lethal outcome is possible due to hemorrhagic changes leading to extensive defects in the cerebral hemispheres.

Alcoholic pseudo-paralysis

At the present time they meet even less often than Korsakov's psychosis. Got its name in the link with the similarity of the clinical picture with progressive paralysis. However, do not forget that the etiology is a different disease. Alcoholic pseudo-paralysis develops mainly in men with a long history of illness, who prefer denatured, low-quality alcoholic beverages, depleted patients with severe eating disorders with hypovitaminosis or vitamin deficiency. It develops after acute severe delirium and acute encephalopathy, and gradually, against the background of pronounced alcoholic degradation. Mental and neurological disorders are similar to a dementic or expansive form of progressive paralysis. The mood is from graciously uplifted, euphoric to agitated and angry.

Observe the lush, absurd, excessive and its senselessness ideas of greatness, there comes a complete loss of criticism, the dissolution of the lower drives, a tendency to rough, cynical jokes. Ideas of greatness are often confabulation. Occasionally, the state of anxious depression, reaching the agitation, with elements of delirium Kotar. Memory disorders are increasing, heavy. Neurological symptoms are represented by tremors of mimic muscles, tongue, fingers, dysarthria, polyneuritis, altered tendon reflexes.

If the pseudo-paralysis has developed after acute psychosis, further flow is usually regentive, but organic decline remains. If the disease spreads gradually, the flow is progressive, with the outcome of dementia. Lethal outcomes are rare.

[25], [26], [27], [28], [29], [30],

Rare forms of alcoholic encephalopathy

There is a significant number of other encephalopathies with acute and chronic course, favorable and unfavorable outcomes. These forms are not identified in the ICD-10 as nosological units.

Alcohol encephalopathy with a picture of pellagra

It occurs in connection with chronic insufficiency of vitamin РР (nicotinic acid). Distinctive features: changes in the skin of hands (the appearance of symmetrical red or gray-brown inflamed areas, then begins peeling), defeat of the digestive tract (stomatitis, gastritis, enteritis, liquid stool), superficial memory disorders.

[31], [32], [33], [34], [35]

Alcohol encephalopathy with the picture beriberi

It develops as a result of chronic insufficiency of vitamin B1 (thiamine). Features: neurological disorders predominate, polyneuritis of the lower extremities dominates - pain and paresthesia or muscle weakness with loss of sensation. Sometimes - myocardial dystrophy with the phenomena of right ventricular failure. The asthenic symptom complex is expressed.

[36], [37], [38]

Encephalopathy with symptoms of retrobulbaric neuritis (alcoholic, vitaminic amblyopia)

Features: violation of central or central-edge vision, expressed more strongly in relation to objects of red and white color. Neurological symptoms are significant: paresthesia, instability in walking, dysphonia, spastic paralysis. Asthenic manifestations predominate. The flow is prolonged from 1.5 to 4-10 months.

Alcoholic encephalopathy caused by stenosis of the superior vena cava

It is characteristic for patients with chronic alcoholism, suffering from cirrhosis of the liver. Features: acute development of disorders of consciousness - from deafness to coma. Typical tremor of the hands with consecutive flexion and extension of the fingers, muscle hypotension. Deaths are frequent. With a favorable course, these disorders quickly disappear, but tend to recur.

[39], [40], [41], [42], [43], [44]

Alcoholic cerebellar atrophy

It is necessary to differentiate with acute transient disorders due to a single heavy alcohol poisoning. The disease develops slowly, neurological disorders prevail, balance disorders in walking, Romberg pose, intentional tremor, adioadichokinesis, muscle hypotension, vestibular disorders. The psycho-organic syndrome of different degrees of severity develops. Not all are recognizing nosological specificity.

[45], [46], [47], [48],

Encephalopathy of Marietaafa-Binyami (Markiafawa-Binyamy syndrome, central degeneration of the corpus callosum)

For the first time described by Italian psychiatrists Marchiafava E. Bignami A. (1903) from peasants who used homemade red wines in large quantities. Mostly men are ill. The disease develops over many years, in manifestations resembles severe degradation. Manifests, as a rule, delirious disorders, subsequently there are significant neurological disorders similar to acute encephalopathy of Gaye-Wernicke. Mental disorders are similar to those with a pseudoparache, there is fixative amnesia, confabulation. The outlook is unfavorable. Death occurs 2-3 months after the manifest symptoms, in a state of coma or mental and physical senility. Nosological specificity is questioned.

Central necrosis of the bridge (central bridge myelinosis)

Described by Adams K. (1959). Mental disorders are close to an apathetic stupor: the patient does not react to external, even painful stimuli, while the pain sensitivity is preserved. Neurological symptoms are expressed, represented by eye symptoms, tetraparesis, pseudobulbar disorders, violent crying. Not all are recognizing nosological specificity.

[49], [50], [51], [52], [53], [54]