Alcoholic psychosis

In recent years, the incidence of chronic alcoholism (alcohol dependence) has been increasing in our country, there has been a noticeable increase in the incidence of a condition such as alcoholic psychosis that most accurately reflects the prevalence and severity of the course of chronic alcoholism (alcohol dependence).

The frequency of alcoholic psychosis development is clearly correlated with the level of alcohol consumption and on average is about 10%. It is believed that the higher this level, the higher the incidence of alcoholic psychosis.

There is also a certain pathomorphism of chronic alcoholism towards increasing the number of heavy and atypical alcohol delirium, the early development of the first delirium (3-5 years after the onset of the disease), the development of alcoholic psychosis among adolescents.

Many modern authors rightly believe that the appearance of psychotic disorders in a patient with chronic alcoholism testifies to the transition of the disease to an extended, difficult stage. According to different authors, there is no alcohol abstinence syndrome, and accordingly, alcoholism without psychosis.

Alcohol delirium in case of incorrect treatment can result in death, the probability of a lethal outcome is 1-2%. Mortality in alcoholic encephalopathies, according to different authors, reaches 30-70%.

All of the above allows us to conclude that the importance of timely and correct diagnosis of alcoholic psychosis.

[1], [2],

Causes of alcoholic psychosis

The cause (s) and mechanisms for the development of alcoholic psychosis remain open, but it has been actively studied in recent years in view of the urgency of this problem. The development of alcoholic psychosis does not depend on the direct, even prolonged, action of alcohol, but is related to the influence of the products of its disintegration and disturbed metabolism. The most common psychoses - alcoholic delirium and hallucinosis - do not arise during binge drinking, but against the background of the developed abstinence syndrome (with a decrease in the alcohol content in the blood). Often the occurrence of psychosis is preceded by trauma, acute infectious diseases, acute poisoning (eg, alcohol substitutes, drugs, etc.), concomitant somatic pathology, stress. This is why the term "metal psychosis" is often encountered in the literature, emphasizing their development as a result of prolonged, chronic alcohol intoxication, which affects internal organs and disrupts metabolism in general.

Currently, it is believed that the combination of several factors plays an important role in the development of alcoholic psychosis: endogenous and exogenous intoxication, metabolic disorders (primarily neurotransmitters of the central nervous system), immune disorders. Indeed, psychoses develop, as a rule, in patients with chronic alcoholism of II-III stage with pronounced disturbances of homeostasis.

According to the results of numerous studies, the systematic use of alcohol disrupts metabolic processes in the central nervous system, the most active alcohol affects the function of the GABA system and N-methyl-D-aspartic acid receptors. GABA is a neurotransmitter that reduces the sensitivity of neurons to external signals. A single intake of alcohol increases the activity of GABA receptors, chronic alcohol intoxication leads to a decrease in their sensitivity and a drop in the level of GABA in the central nervous system, which explains the excitation of the nervous system observed in alcoholic AC.

One of the main stimulating neurotransmitters in the central nervous system is glutamate, which interacts with three types of receptors, including N-methyl-D-aspartic acid, and plays an important role in the implementation of learning processes. The participation of I-methyl-D-aspartic acid in the pathogenesis of convulsive seizures has also been demonstrated. A single intake of alcohol inhibits the activity of N-methyl-D-aspartic acid receptors, with the systematic use of ethanol, their amount increases. Accordingly, in the alcoholic AU, the activating effect of glutamate increases.

The acute effect of alcohol has an inhibitory effect on the calcium channels of neurons, which leads to an increase in the number of potential-dependent channels in chronic alcohol intoxication. That is why, during the period of ethanol deprivation, calcium transport to the cell increases, accompanied by an increase in the excitability of neurons.

Great importance in the pathogenesis of alcoholic AU belongs to the exchange of dopamine, endorphins, serotonin and acetylcholine. According to modern ideas, changes in the exchange of classical neurotransmitters are secondary (monoamine) or compensatory (acetylcholine).

Dopamine coordinates the motor functions of the central nervous system, plays an important role in the implementation of mechanisms of motivation and behavior. A single injection of alcohol causes an increase, and a chronic introduction of a decrease in extracellular dopamine in n. Assumbens. It is believed that there is a direct relationship between the level of the given neurotransmitter and the severity of alcohol delirium: in patients with developed psychosis, the concentration of dopamine reached 300%. Nevertheless, dopamine receptor blockers (neuroleptics) in case of alcoholic delirium are ineffective. Apparently, this can be explained by the effect of a less obvious disruption in the metabolism of other neurotransmitters and modulators of the central nervous system (serotonin, endorphins, etc.), as well as changes in the biological effect of dopamine in the interaction of the neurotransmitter with catabolism products and pathologically altered neuropeptides.

The leading factor of pathogenesis in alcoholic delirium, apparently, is the violation of metabolic and neurovegetative processes. The defeat of the liver leads to a violation of detoxification function, inhibition of the synthesis of protein fractions of blood and other important compounds. As a result, the toxic lesion of the central nervous system develops, primarily its diencephalic parts, which leads to the breakdown of neurohumoral compensatory mechanisms. Decrease in detoxification reserves of the liver disrupts and slows down the processes of alcohol oxidation, resulting in the formation of more toxic under-oxidized products of its transformation. Another important predisposing factor in the development of delirium is the violation of electrolyte metabolism, especially the redistribution of electrolytes between cells and extracellular fluid. The triggering mechanism in delirium is considered to be a sharp change in internal homeostasis, the development of AS, associated somatic diseases, possibly local circulatory disturbances and a decrease in the permeability of vessels for toxic substances.

The mechanisms of the onset of alcoholic delirium and acute encephalopathies seem to be close. In the pathogenesis of alcoholic encephalopathies, along with the disorders inherent in delirium, an important place is given to violations of vitamin metabolism, especially the lack of vitamins B1, B6 and PP.

Among the exogenously-organic hazards, the consequences of craniocerebral injuries, chronic physical illnesses are the most important. One can not deny a certain role of the hereditary factor, possibly, determining the imperfection of the mechanisms of homeostasis.

The pathogenesis of alcoholic hallucinosis and delusional psychosis is now virtually unknown.

[3], [4], [5], [6], [7]

Clinical forms of alcoholic psychosis

There are different approaches to the classification of alcoholic psychosis. From the clinical point of view, acute, prolonged and chronic psychoses, as well as psychopathological syndromes leading in the clinical picture are distinguished: delirious, hallucinatory, delusional, etc.

The length of alcoholic psychosis is characterized by the phases of development of clinical manifestations, often combined with their polymorphism (ie, in the structure there are simultaneously or alternately different psychotic disorders).

Mixed mixed psychosis is said if the symptoms of one form, for example, delirium, are combined with hallucinosis or paranoid symptoms.

In atypical psychoses, the symptomatology of the basic forms is combined with endorphic disorders, for example, with the onyroid obscuration of consciousness or psychic automatisms.

With complex structure of the metal psychosis, a consistent change of one psychosis to another is observed, for example, delirium hallucinosis, hallucinosis paranoid, etc.

In the development of acute psychoses, it is very important to take into account the severity of the condition, since in such patients, in addition to psychotic disorders, violations of neurohormonal regulation, dysfunctions of internal organs and systems, immunodeficiency states, expressed neurological disorders (convulsive seizures, progressive encephalopathy with edema of the brain, etc.)

Against the background of modern therapy, the duration of alcohol delirium lasts no more than 8-10 days, hallucinosis and crazy alcoholic psychoses are considered acute if they are reduced within a month; prolonged (subacute) psychosis lasts up to 6, and chronic - more than 6 months.

According to the type of current, alcoholic psychosis happens:

• transient one-time arisen;
• relapsing repeated two or more times after remission;
• mixed - transitory or relapsing, the current is replaced by a chronic psychotic state;
• with a continuous course immediately after an acute psychotic state, or a periodically exacerbated chronic psychosis occurs on its own.

Types of alcoholic (metal-alcoholic) psychoses:

• Alcoholic delirium.
• Alcoholic hallucinations.
• Alcohol crazy psychosis.
• Alcoholic encephalopathy.
• Rare forms of alcoholic psychosis.

Also, alcoholic psychosis is traditionally attributed to alcoholic depression, alcoholic epilepsy and dipsomania. However, this point of view is not recognized by all authors, since it causes a sufficient number of disputes. According to the peculiarities of development, alcoholic depression and epilepsy can be classified as intermediate syndromes. Arising on the background of chronic alcohol intoxication. For example. G.V. Morozov (1983) classifies this controversial group as psychopathological conditions that arise during alcoholism (depression, epilepsy) and in alcoholic excesses (dipsomania).

At present, these conditions are usually considered within the framework of withdrawal disorders (alcoholic depression) as a manifestation of pathological attraction to alcohol (dipsoomania or drunkenness) or as a special disease, the cause of which is chronic alcoholism (alcoholic epilepsy).

Nevertheless, these states are identified here in a separate group - "Special forms of alcoholic psychosis."

[8], [9],

Special forms of alcoholic psychosis

Despite the ambiguous points of view of different researchers and the controversy of joining alcoholic psychoses of alcoholic epilepsy, alcohol of my depression and dipsomania, for a more complete coverage of the topic, this time describes the clinical manifestations of these conditions, not isolated and MKB-10.

Alcoholic epilepsy

Alcoholic epilepsy (epileptiform syndrome with alcoholism, alcohol-epilepsy) is a kind of symptomatic epilepsy that occurred with alcoholism and its complications.

In 1852, M. Guss described the occurrence of convulsive seizures in chronic alcoholism and pointed to their toxic origin. However, there is still no general consensus on the terminology and nosological delineation of epileptiform disorders in chronic alcoholism. To denote these disorders, most authors use the term "alcoholic epilepsy", proposed by Manyan in 1859.

The fullest definition of alcoholic epilepsy was given by SG. Zhislin: "Under alcoholic epilepsy one must understand one of the varieties of symptomatic and precisely toxic epilepsy, i.e. Those forms in which it can be shown that every seizure without exception is the result of intoxication and in which after the elimination of the factor of intoxication these seizures and other epileptic phenomena disappear. "

The frequency of alcoholic seizures, with both alcoholic alcoholism and its complications, is about 10% on average. Describing epileptiform seizures in chronic alcoholism, the researchers note some of their characteristics.

Differential diagnosis of genoein epilepsy and epileptiform seizures in alcohol dependence

Epileptiform seizures in alcohol dependence	Genuine epilepsy
The emergence is associated with a prolonged heavy intake of alcoholic beverages. Most epileptiform seizures are formed on stage II or III of alcoholism (take into account the clinical symptoms of alcoholism)	The occurrence of epileptic seizures is not associated with taking alcohol, the first seizures can form long before the first intake of alcohol or occur when it is taken in small amounts
Occur only in certain cases: on the 2-4th day of development of alcoholic AU; in the debut or in the period of the manifest phenomena of delirium and encephalopathy of Gaia-Wernicke	The development of seizures does not depend on the stage and period of coexisting alcoholism
The most common are convulsive seizures without transformation of the picture, there are abortive seizures	At the first occurrence of a seizure, small epileptic seizures are transformed into large
There are no small seizures, postpositive oligophasia, twilight obscurations of consciousness - very rarely, there is almost no	The structure of seizures is different, diverse
The aura is not typical, sometimes vegetative	The aura is characteristic - a "visiting card" of every clinical case, a wide variety of clinical manifestations
Absence of seizures during remission and in a state of intoxication	Regardless of the duration and amount of alcohol consumption
Alcohol-related personality changes	Personality changes by epileptic type (epileptic degradation)
Changes in the electroencephalogram nonspecific or absent	Frequently diagnose specific changes in the electroencephalogram

[10], [11]

Alcohol Depression

Alcoholic melancholia is a group of conditions that unites various depressive disorders in patients with chronic alcoholism, different in clinical picture and duration.

Depressive disorders occur, as a rule, with the development of alcoholic AO, can persist after its arrest, less often they are observed after the transferred delirium or hallucinosis. In the latter case, alcoholic depression can be attributed to transitional syndromes, replacing psychosis with productive symptoms.

At present, the variants of the development of affective pathology in patients with alcoholism are clearly delineated. The first is associated with a deepening of premorbid features with a tendency to form different affective disorders at the level of cyclothymia or affective psychosis; the second is acquired affective disorders, which are a sign of toxic damage to the brain and emerging encephalopathy. In the first case, patients have deeper and more intense affective disorders, vital components have a large specific gravity, frequent ideas of self-abasement, elements of depressive depersonalization. Suicide attempts may occur. In the second variant, shallow anxious depression predominates with hypochondriacal inclusions, tearfulness, emotional lability. Often in clinical practice, there are dysphoric depressions. Patients complain of depressed mood, a sense of hopelessness, tearful, but after a short time they can be seen animatedly chatting with neighbors in the ward. The structure of alcoholic depression is dominated by psychogenic formations, hysterical and dysphoric manifestations, exhaustion. The duration of these disorders varies from 1-2 weeks to 1 month or more.

[12], [13]

True drinking

Dipsomania (true drinking) is very rare. Observe in people who do not suffer from chronic alcoholism. For the first time it was described in 1817 in Moscow by the doctor Silyvatori. Hufeland in 1819 proposed this form of drunkenness to be called dipsoomania. Dipsomania develops mainly in psychopathic individuals, mainly epileptoid circle, in persons suffering from manic-depressive psychosis, with schizophrenia, and also against the background of the endocrine psychosyndrome.

For the clinical picture is characterized by several mandatory features. True depressing is preceded by a depressed-anxious mood background, a dysphoric component is significantly expressed, fatigue increased, poor sleep, anxiety, a sense of fear. In other words, affective tension and infection are necessarily present. There arises a passionate, irresistible desire to consume alcohol. Components of craving for alcohol (ideator, sensory, affective, behavioral and vegetative) are expressed to a large extent. Attraction to alcohol is so strong that the patient, despite no obstacles, starts to drink and comes to a serious degree of intoxication. Alcohol is absorbed in a variety of forms and in huge amounts up to 2-4 liters. Nevertheless, the symptoms of intoxication are insignificant or absent. During such a binge, the patient gives up work, all his business, his family, he is out of the house, can drink all his money and clothes. Appetite is not present, the patient practically nothing eats. Many researchers note the development during the drinking-bout drumming. The duration of this condition is from several days to 2 3 weeks. The end of the binge is usually sudden, with persistent extinction and treatment for alcohol, often - an aversion to it. Gradual decrease in the doses of alcohol, as is the case with pseudo-dust, is not observed. After kurtosis, the mood often accompanied by indefatigable activity. This fact, according to SG. Zhislina (1965), testifies to the relationship between the binge and the altered affect. Drinking can end with a long sleep, sometimes mark a partial amnesia of the drinking-bout period. In light intervals, patients lead a sober lifestyle and do not consume alcoholic beverages.

Since the middle of the current century, dipsomania is increasingly referred to as an independent nosological form. Probably, it would be more correct to classify dipso- mony as a special form of symptomatic alcoholism.

In the III stage of alcoholism, a form of alcohol abuse is identified as a true binge. Spontaneously there is an intense attraction to alcohol, there are characteristic changes in the mental and physical state, the end of the binge is associated with intolerance and the development of aversion to alcohol, the emergence of binges - a cyclic.

Treatment of alcoholic psychosis

Intensive therapy of acute alcoholic psychoses is based on the correction of metabolic disorders that arise due to the systematic intake of alcoholic beverages. However, due to the lack of understanding of the pathogenetic mechanisms of these diseases, the variety and complexity of the metabolic changes developing in them, the drugs used cause adverse side effects, which leads to a worsening of the course of the disease. That is why they constantly search for new therapeutic approaches and optimize traditional methods aimed at speeding up patients' exit from the psychotic state, minimizing losses and preparing patients for qualitative and long-term remissions.

Course, pathomorphosis and prognosis of alcoholic psychoses

Psychoses with alcoholism can occur only once and repeatedly. Repeated development of psychosis is due only to one reason - the continued abuse of alcoholic beverages. However, the feedback is not tracked: the transferred psychosis can be the only one even with the continued use of alcohol.

Alcoholic psychosis in one and the same patient can proceed in different ways: like delirium, auditory hallucinosis, paranoid. Such clinical observations undoubtedly testify to the proximity of "independent" forms of alcoholic psychosis.

Type of course of alcoholic psychosis and further prognosis in many ways determine the severity of alcoholic encephalopathy, features of the constitutional background and additional exogenous harmfulness.

The occurrence of single alcoholic psychoses is completely dependent on chronic alcohol intoxication, in particular, on the duration of drinking periods. Single psychoses are more characteristic for the II stage of alcoholism, with a lower severity of chronic alcoholic encephalopathy. As a rule, in this case, we observe delirium with sufficiently deep darkening of consciousness, auditory hallucinosis with symptoms of white fever, on the one hand, and transitory clinical symptoms, on the other. In the clinical picture of the experienced single psychoses (delirium and hallucinosis), there are practically no psychological automatisms, elements of the Kandinsky-Clerambo syndrome, deceptions of the perception of erotic content, delusions of jealousy, imperative hallucinations. The above features of the psychopathological structure of the transferred psychoses are regarded as prognostically favorable. Thus, if the above clinical features are observed, the probability of a single development of AP without a tendency to further recurrence is high.

Alcoholic psychosis with unfavorable protracted course develops, as a rule, in the II-III stages of alcoholism, with the intermittent or constant form of alcohol abuse, against the background of significant personality degradation by alcohol type. An important role is played by constitutional moments - premorbid personality anomalies of the paranoiac and schizoid circle. Prognostically unfavorable signs include the inclusion in a clinical picture of psychosis of complex hallucinatory-paranoid phenomena, systematized delirium, the presence in the psychopathological structure of delirium or hallucinosis of ideas of jealousy, the appearance of deceptions of perception of erotic content.

Relapse of alcoholic psychosis most often occurs 1-2 years after the first attack. This is directly related to the progression of the disease itself and alcoholic encephalopathy - increased pathological craving for alcohol, heavier drinking, deepening personality changes. Between the first and second psychoses, the interval is always the greatest, in the future the intervals are shortened. Repeated psychosis occurs after long, heavy drinking bouts and after short (1-2 days) alcoholic excesses. According to MS. Udaltsova (1974), the recurrence of delirium is preceded by a significant but short alcoholic kurtosis, and the hallucinosis is continued use of low doses of alcohol.

More than half of the cases with repeated alcoholic psychoses retain the previous clinical picture, it can only be slightly complicated or simplified. At the same time, the exogenous type of reactions necessarily takes the leading place. In other cases, there is a transformation of the clinical picture, the number of hallucinosis and paranoid increases, and a variety of endoform patterns arise.

In the dynamics of alcoholic psychosis, a rigid pattern is revealed: with the progression of alcoholism, with the increase in the severity of alcoholic encephalopathy, the clinical picture changes from delirium to hallucinosis and delusional states. Endogenization of the clinical picture, the increasing dominance of schizophrenic psychopathological disorders are accompanied by a decrease or even disappearance of the obligate syndrome of exogenous psychoses of obscuration of consciousness. In these cases, differential diagnosis with schizophrenia is very difficult. Crucial importance for the diagnosis of alcoholic psychosis is attributed to chronic alcoholism and the clinical picture of psychosis (including the dynamics of mental disorders).

The addition of psychosis causes the severity of the further course of alcoholism: an increase in the progression of the disease is observed, remissions are shorter, and relapses are more prolonged and more severe.

The transferred alcoholic psychoses, undoubtedly, strengthen manifestations of chronic alcoholic encephalopathy. First of all, this is evidenced by a decrease in professional qualifications, the commission of antisocial actions, illegal actions. At the same time acute psychosis can be replaced by atypical (endogenous), and then psycho-organic.

[14], [15]

What is the prognosis of alcoholic psychosis?

The forecast of alcoholic psychosis largely depends on the form of alcohol use and such factors as heredity, premorbid state, additional exogenous harmfulness, the presence of concomitant somatic and neurological diseases.