Psychiatry - O. K. Napreyenko 2001

Clinical Psychiatry
Alcoholism. Alcoholic Psychoses

Alcoholism (alcohol use disorder) is a progressive disease that develops As a result of systematic alcohol consumption and is accompanied by psychological and physical dependence on it. It leads to dysfunctions in virtually all Organs and systems, specific personality Changes in the patient, and can be complicated by alcoholic (metalcoholic) psychoses.

The term "chronic alcoholism" was proposed by the Swedish researcher M. Huss in 1852. Significant contributions to The Study of alcohol-related disease and psychoses were made by E. Kraepelin, S. S. Korsakow, V. A. Sikorsky, E. M. Jellinek, A. A. Portnov, I. N. Pyatnitskaya, and other scientists. Today, alongside the term "alcoholism," The concepts of "alcohol use disorder" and "alcohol dependence" are widely used.

Given the numerous inconsistencies in the terminology and Classification of alcohol-related disorders arising from various methodological approaches, it is advisable to clearly outline the core concepts.

CORE CONCEPTS

Intoxication — a complex of emotional, cognitive, behavioral, and somato-neurological changes that occur upon The Use of a psychoactive substance and disappear after its elimination from the body.

Alcohol abuse (heavy drinking) — excessive alcohol consumption accompanied by a violation of social norms. It is primarily non-medical in nature, although some researchers view heavy drinking as a pre-nosological stage of alcoholism. It differs from alcohol use disorder in that it does not involve dependence.

Chemical dependence (addiction) — an individual's reliance on a specific chemical agent, manifested by a compulsive need for its continuous use. This term encompasses tobacco smoking, alcoholism, and drug addiction. The Development of chemical dependence is accompanied by a significant increase in tolerance. Interruptions in the systematic use of a psychoactive substance trigger specific painful states, namely withdrawal syndrome (hangover). Psychological and physical levels of chemical dependence are distinguished.

Psychological dependence — a continuous or periodic desire to consume a psychoactive substance. At the behavioral level, it manifests as an inability to control the intake of alcohol or drugs.

Physical dependence — a reliance on any chemical agent (drug, alcohol, tobacco) caused by its incorporation into the metabolic processes of The Human Body.    

CLASSIFICATION OF ALCOHOLISM

In this section, we present the three most common classifications used in Ukraine: the traditional clinical classification, ICD-10, and DSM-IV.

The traditional domestic clinical classification includes three stages, which are discussed in detail below.

According to ICD-10

F 10.0 Acute intoxication

F 10.1 Harmful use

F 10.2 Dependence syndrome

F 10.3 Withdrawal state

F 10.4 Withdrawal state with delirium

F 10.5 Psychotic disorder

F 10.6 Amnestic syndrome

F 10.7 Residual and late-onset psychotic disorder (incl. F 10.73 — dementia)

F 10.8 Other psychotic and behavioral disorders

F 10.9 Unspecified psychotic and behavioral disorders

According to DSM-IV

303.00 Alcohol intoxication

303.90 Alcohol Dependence

305.00 Alcohol Abuse

291.0 Alcohol-Induced Delirium

291.0 Alcohol Withdrawal Delirium

291.1 Alcohol-Induced Persisting Amnestic Disorder

291.2 Alcohol-Induced Persisting Dementia

291.3 Alcohol-Induced Psychotic Disorder with Hallucinations

291.5 Alcohol-Induced Psychotic Disorder with Delusions

291.8 Alcohol Withdrawal with Perceptual Disturbance

291.8 Alcohol-Induced Mood Disorder

291.8 Alcohol-Induced Anxiety Disorder

291.8 Alcohol-Induced Sexual Dysfunction

291.9 Alcohol-Induced Sleep Disorder

291.9 Unspecified Alcohol-Related Disorder

Epidemiology

The Study of the epidemiology of alcoholism is complicated by the fact that A large number of patients remain unaccounted for ("hidden alcoholism", "home drinkers"). Attempts to investigate this issue based on the volume of alcohol sold or the number of deaths from Liver disease are considered insufficiently effective. Anonymous questionnaire surveys tend to reflect the level of alcohol consumption rather than the actual prevalence of alcoholism among respondents.

Numerous studies have demonstrated that the prevalence of alcoholism ranges from 6.2% to 14.8% of the adult population (E. A. Babayan, M. H. Gonopolsky, 1987; H. Kaplan, B. Sadock, 1996). This figure varies across different social groups.

Throughout the 20th century, fairly consistent epidemiological trends regarding alcoholism have been identified:

✵ an increase in the number of cases (both absolute and relative);

✵ a downward shift in the age of onset;

✵ female alcoholism outpacing male alcoholism in its rate of development.

Effects of Ethanol on the Body

The human body synthesizes 1–9 g of endogenous ethanol daily. Depending on emotional state, its concentration ranges from 0 to 0.16 mg/L. This serves as one of the substrates for the synthesis of endogenous acetaldehyde, which is involved in the turnover of catecholamines, dopamine, and endogenous opioids (enkephalins and endorphins). These substances are synthesized in the Hypothalamus and the limbic System of the Brain, where they modulate the turnover of many other Neurotransmitters and activate the reward pathways (Olds' pleasure centers).

When exogenous ethanol is consumed, rapid absorption causes its concentration to increase thousands of times, peaking at 40–80 minutes on an empty Stomach and 90–120 minutes after a meal. Alcohol is absorbed primarily in the Small Intestine (80%) and The Stomach (20%). Foods such as potatoes, meat, and animal fat counteract this process; when consumed together, alcohol may remain in the stomach for up to 3 hours. Individual physiological characteristics also influence absorption rates. In patients with alcoholism or PEPTIC ULCER DISEASE, this process occurs more rapidly. During absorption, Blood alcohol levels begin to rise, reaching a maximum at 40–50 minutes (following a single dose of alcohol).

Approximately 10% of ethanol is excreted unchanged (primarily via urine and exhaled air), while the remainder is metabolized in the liver. Alcohol is broken down by the enzyme Alcohol dehydrogenase (ADH) in the presence of acetyl-coenzyme A (acetyl-CoA) as a coenzyme and nicotinamide adenine dinucleotide (NAD). In this process, ethanol is oxidized to acetaldehyde (AcA). During heavy alcohol consumption, additional Metabolic pathways are recruited: the microsomal ethanol-oxidizing system (MEOS) and the catalase pathway. Both pathways also result in The production of AcA. It should be noted that the Toxic Effect of AcA is hundreds of times greater than that of ethyl alcohol. Subsequently, the enzyme aldehyde dehydrogenase (ALDH) comes into play, dehydrogenating AcA in the presence of NAD and converting it into non-toxic acetate.

The processes of alcohol detoxification are genetically programmed and exhibit significant individual Variability. The rate of alcohol elimination depends on the functional state of the body, particularly the liver, and increases during the development of chronic alcoholism. This creates the biological foundation for the development of tolerance.

Upon entering the body, ethanol rapidly disrupts the blood-brain barrier and penetrates the brain. Its highest concentrations are found in the Cerebral Cortex AND certain subcortical structures.

SIMPLE ALCOHOL INTOXICATION

The depth of intoxication depends on numerous factors, including personality type, psychophysiological state, and the quality and strength of the alcoholic beverages consumed. Three degrees of alcohol intoxication are distinguished.

Mild intoxication is characterized by a sense of well-being and a diminished self-критика regarding one's actions and capabilities. Thinking speed increases, though this is driven by superficial associations and a decline in the quality of mental performance. Cognitive Functions are impaired, error rates rise, and work quality deteriorates. Personality traits that are subdued in a sober state become prominent. Facial Skin flushes, mild dysarthria appears, and gait becomes unsteady. Occasionally, pupillary dilation and moderate bradycardia are observed. Blood alcohol concentration typically ranges from 0.5 to 1.5 %₀.

Moderate intoxication manifests as a further decline in task performance, cognitive processes, and motor coordination. Sharp mood swings are characteristic, reflecting the individual's traits and cultural Background. Blood alcohol concentration ranges from 1.5 to 2.5 %₀.

Severe intoxication involves disorientation and blunted emotions. A soporous or comatose state is possible. Blood alcohol concentration ranges from 2.5 to 3.0 %₀ or higher, with a lethal dose considered to be 5–6 %₀.

Laboratory Diagnostics

Occasionally, There is a need to objectify the Diagnosis, for which various Methods are employed.

Rapoport's reaction: Bubbling exhaled air through a solution of potassium permanganate and sulfuric acid. If alcohol vapor is present in the air, the solution changes color.

Mokhov-Shinkarenko reaction: When exhaled air containing alcohol vapor is passed through a special indicator tube, the reagent changes color.

The limitation of these reactions is their non-Specificity. The indicators react positively to acetone, ether, methyl alcohol, etc. Therefore, in contentious situations (e.g., when driving a vehicle), the diagnosis of alcohol intoxication can only be established by a physician, who also verifies the blood alcohol concentration.

Differential diagnosis

Alcohol intoxication must be differentiated from several other conditions.

Methanol poisoning occurs due to the accidental ingestion of methyl alcohol. Diagnosis is complicated by its similar odor. Ingesting even a small amount of methanol leads to metabolic acidosis (the lethal dose is 1–5 g/kg). Initial symptoms include vomiting after consuming a small amount and visual impairment, potentially progressing to complete blindness. Treatment: immediately administer an ethanol solution to the patient at a loading dose of 0.6 g/kg followed by 10 g hourly to inhibit methanol METABOLISM.

Coma. Diagnostic errors occur most frequently with diabetic and hepatic comas. This is due to the patients' presentation: unconsciousness, specific breath odor, and vomiting. Differentiation is based on medical history, physical examination findings, and blood test results.

Subarachnoid and subdural hematomas manifest 2–3 days following trauma. Patients appear lethargic and confused, superficially resembling individuals who are intoxicated. Consciousness is impaired (most frequently presenting as obnubilation). The resemblance to drunkenness is further heightened by the fact that vomiting frequently accompanies intracranial hematomas. Differential signs include persistent impairment of consciousness, elevated intracranial pressure, and a history of HEAD trauma (particularly to the occipital region). In severe cases, spontaneous urination and defecation may occur, necessitating the immediate transfer of the patient to a neurosurgical department. To confirm the diagnosis, instrumental examinations can be performed, such as Skull radiography in two projections, cranial ultrasound (USS), and lumbar puncture (presence of blood in the CEREBROSPINAL FLUID).

Treatment

Treatment of acute alcohol intoxication should begin with the removal of alcohol from the stomach. This is achieved through gastric lavage—either with or without a tube—using large volumes of Water (to dilute the stomach contents and prevent chemical Burns to the Pharynx). Additionally, activated charcoal can be administered if the alcohol was consumed recently. To support cardiac function, cardiotonic agents should be administered. For sobering up, massive doses of B-complex Vitamins, particularly thiamine (up to 100 mg), are prescribed along with a 40% glucose solution. In severe cases, patients are transferred for hemodialysis and mechanical ventilation.

ATYPICAL ALCOHOL INTOXICATION

Atypical alcohol intoxication occurs when alcohol is consumed by individuals with underlying psychiatric pathology, such as organic Central Nervous system disorders, psychopathies, or Affective Disorders. Based on Clinical presentation, several types of intoxication are distinguished.

Dysphoric intoxication occurs in individuals with organic CNS lesions or explosive (epileptoid) psychopathy. During intoxication, aggressiveness and belligerence increase. Affected individuals are prone to picking fights, starting conflicts over trivial matters, and committing acts of vandalism; sexual assault may also occur.

Depressive intoxication is more commonly observed in individuals with cyclothymia and neurotic disorders who often consume alcohol to elevate their mood. The clinical picture is dominated by depression with continuous rumination over psychotraumatic events. Patients tend to exaggerate the consequences and harbor distorted ideas regarding their own self-worth. During episodes of severe depression, suicide attempts are possible.

Hebephrenic intoxication. Intoxicated individuals behave like children, making inappropriate jokes; their behavior is characterized by primitive vital drives and flattened emotions and urges.

Hysterical intoxication. This most frequently occurs in histrionic psychopathy. Behavior is characterized by efforts to attract maximum attention, and alcohol is often consumed publicly and ostentatiously. In such cases, the subject attempts to appear significantly more intoxicated than they actually are.

Expertise

Labor. Patients in a state of intoxication are temporarily disabled.

Forensic psychiatric. Patients are sane during alcohol intoxication. If a crime is committed in a state of pathological alcohol intoxication, patients are considered legally insane.

CHRONIC ALCOHOLISM

Etiology of Alcoholism

Regarding THE ORIGIN OF alcohol-related disease (chronic alcoholism), various, sometimes curious, hypotheses and theories exist. Today, it is widely accepted that the development of alcohol craving involves a combination of genetic, biochemical, psychological, and social factors. The risk factors for developing alcoholism include the following:

✵ psychological (childhood hyperactivity, emotional lability, impulsivity, selfishness, attention deficit, heightened anxiety);

✵ characterological (attempts to compensate for character accentuations);

✵ neurophysiological (decreased amplitude and prolonged latency of the P300 component during evoked potential testing);

✵ hormonal (low androgen levels);

✵ biochemical (low monoamine oxidase activity);

✵ social (family history of alcohol problems, adolescent antisocial behavior).

Stages of Alcoholism Progression

There are numerous Perspectives and classifications concerning the stages of alcoholism. In Ukraine, the most widespread clinical classification divides alcoholism into three stages:

I — psychological dependence;

II — physical dependence (addictive);

III — decompensation (encephalopathic).

Two intermediate stages (I–II and II–III) are also distinguished, along with the so-called pre-nosological stage, i.e., heavy drinking. In our view, the term "heavy drinking" carries more of a social than a clinical connotation. However, since it very frequently precedes alcoholism, we will examine it separately.

HEAVY DRINKING

The term "heavy drinking" refers to alcohol consumption that exceeds socially acceptable norms. There are standards dictating the frequency and dosage of alcohol consumption for each demographic group (men, women, youth) or social stratum (workers, military personnel, intellectuals). Naturally, these vary greatly depending on local conditions. For instance, socially acceptable alcohol consumption in countries with a developed winemaking culture (Georgia, Moldova, France, Italy) may be regarded as excessive in other regions. The same applies to socio-group norms.

Heavy drinking differs from alcoholism in that there is no dependence yet, significant fluctuations in The amount of alcohol consumed are observed, and periods of sobriety are relatively prolonged when circumstances change.

Heavy drinking can be conditionally divided into two types. The first is associated with peer pressure in drinking groups and habitual drinking typical of individuals with an amorphous personality Structure ("out of boredom"). The second type is more dangerous regarding the development of alcoholism. The first type of heavy drinking is situationally determined. Upon changing one's environment (changing jobs, relocating), the level of alcohol consumption decreases.

The literature distinguishes between the so-called French and Scandinavian types of heavy drinking. The former is characterized by daily consumption of small amounts of alcohol, while the latter involves heavier, episodic drinking (once or twice a month punctuated by periods of sobriety).

The intensity of heavy drinking may increase during stressful situations and decrease once the problems are resolved.

Certain psychological defense mechanisms may develop during heavy drinking.

Stages of Alcoholism

The First stage of alcoholism is characterized by the development of psychological dependence on alcohol. Intoxication becomes a desired state.

Drinking sprees become more frequent, and alcohol tolerance gradually increases.

The patient's thoughts become entirely focused on alcohol. If circumstances prevent them from drinking, the individual experiences irritation, the true cause of which they cannot understand. Since drinking at this stage remains more or less socially acceptable, patients invent various excuses and motives for drinking. At this stage, a system of psychological defense is finally established.

One of its manifestations is the so-called system of pledges (self-imposed limitations). This involves the patient, having realized their dependence on alcohol, attempting to somehow control their drinking. For example, they may avoid alcohol for a certain period (until 6:00 PM) or until completing a specific task (finishing a work assignment). Patients frequently break these pledges, trying to consciously circumvent them ("I promised not to drink alcohol, but beer isn't alcohol").

Another manifestation is the rationalization of drinking. Every drinking bout is justified by various reasons, such as celebrating a holiday, following a tradition (receiving a paycheck, meeting friends), or responding to circumstances (feeling cold, having a toothache, etc.).

Drinking sprees become more frequent, and tolerance gradually increases. Total amnesias and palimpsests appear (amnesias lasting short periods of 15–30 minutes, associated with rising blood alcohol levels). Post-intoxication states emerge after drinking bouts and are gradually replaced by withdrawal symptoms, signaling the transition to the Second Stage. These states differ in the individual's attitude toward alcohol. In a post-intoxication state, not only consuming alcohol, but even its smell or the mere thought of it causes revulsion (nausea and vomiting), whereas during withdrawal, alcohol is the only way to feel better.

The second stage is characterized by developed physical dependence on alcohol.

Its manifestations include: a compulsive (irresistible) craving for alcohol; an abstinence (hangover) syndrome and secondary craving for alcohol (an irresistible desire to drink after a small dose of alcohol); increased alcohol tolerance (The ability to consume significantly larger amounts than before the illness); and the disappearance of the gag reflex.

The craving for alcohol intensifies and eventually becomes irresistible. In other words, once the thought of alcohol arises in the patient's mind, it must be acted upon. This can manifest at the subconscious level through the activation of the alcoholic dynamic stereotype when something triggers the memory of drinking (a situation, meeting friends, specific food, etc.). This is reflected in the facial-gustatory symptom (Zaviliansky's symptom): upon the mention of alcohol, the patient becomes animated, rejoices, and salivates excessively. To enhance the effects of alcohol, patients drink on an empty stomach and without appetizers (anorexia of intoxication) or wash it down with soda or beer. These symptoms indicate a malignant progression of the disease.

Withdrawal syndrome appears the day after alcohol consumption. The primary sign of its development is the absence of aversion to alcohol and nausea on the day after a drinking bout. This is followed by a symptom complex of somatic (palpitations, nausea, retching, tremors, headache, etc.), neurological (autonomic disorders, paresthesias, hyperesthesia of visual and auditory analyzers), and psychopathological (irritability, asthenia, cognitive-mnestic impairments) disorders. Alcohol psychosis very frequently develops against the background of withdrawal syndrome. All these symptoms disappear after partaking in "Hair of the dog" drinking (remedying a hangover). Typically, large amounts of strong tea, coffee, or cold water are used initially for this purpose (nonspecific hangover relief), followed by low-alcohol beverages, and by the end of the second stage, patients relieve their hangover with vodka. If social conditions prevent morning drinking, it is done later in the day.

Withdrawal syndrome frequently precedes alcoholic psychosis or alcohol-related Epilepsy. Symptomatic toxic epilepsy manifests as convulsive seizures, which most commonly occur on the 1st or 2nd day of sobriety. Sometimes these may be combined with alcoholic psychosis or occur at the peak of a heavy drinking bout (spree). A characteristic feature of these seizures is the absence of an aura.

Typical manifestations of secondary pathological craving for alcohol include two symptoms: impairment of situational control (drinking under any circumstances) and quantitative control (the inability to stop after consuming small doses of alcohol). When drinking in company, this is reflected in the symptom of anticipating the toast (consuming alcohol in larger quantities than others).

CHARACTERISTICS OF THE second stage include pseudo-binge or continuous drinking patterns, and the development of various medical conditions alongside alcoholism. The rate of degradation depends on the pattern of alcohol abuse. The most malignant variant is continuous drinking lasting months or years. Most commonly, pseudo-binges lasting 3 to 14 days are observed. These are characterized by morning hangover relief transitioning into daytime drinking. Such episodes end under three circumstances: satiation (absence of craving for alcohol), inability to continue drinking due to deteriorating physical health, and social limitations (lack of money, isolation, etc.). A period of sobriety follows a pseudo-binge.

Furthermore, at this stage, the patient undergoes both social and moral-ethical degradation. They begin consuming low-quality and excessively strong beverages, neglect professional and family responsibilities, become deceitful, and run afoul of the law. Attention and memory functions become impaired. Intellectual activity revolves entirely around alcohol. Speech typically becomes primitive, incorporating profanity, and its thematic content is exclusively tied to alcohol consumption. Affective reactions are unrestrained, unpredictable, polar, following an "all-or-nothing" principle. A mismatch between the stimulus and the reaction is typical. So-called black humor (gallows humor) emerges. A specific alcoholic anosognosia is also characteristic, meaning the patient is firmly convinced they can stop at any moment of their own will, without treatment. Family life is marked by scandals and quarrels, frequently leading to numerous psychological problems and, in many cases, The breakdown of the family.

Personality degradation and alcoholic dementia can develop along four main pathways: autistic, explosive, hysterical, and hebephrenic.

Autistic. Patients are withdrawn or communicate exclusively within their own circle. External communication is driven solely by The Need for alcohol. They very frequently drink alone. Their self-esteem is low, and they perceive no other Prospects in life than continuing alcohol abuse until death.

Explosive. Patients are brutal, pick fights with everyone, and provoke conflicts. Their behavior is often antisocial and, in the Cytology/cytology/16.html">Early stages of alcohol dependence, may form part of their psychological defense mechanism: a conflict situation serves as a motive for drinking. This form of alcoholic degradation is most typical of psychopaths and individuals with organic CNS pathology.

Hystericoid. Patients openly display their drinking, boast about it, and exaggerate the amounts and scale of their consumption. They may harass others, provoke verbal conflicts, or plead for help. They tend to blame others for all their problems (including alcoholism). This type of degradation is characteristic of women.

Hebephrenic. Patients try to appear cheerful and lively, exhibiting childish behavioral traits. They convince everyone that this is the exact life they wanted, and so on. Their speech is saturated with alcoholic jargon, and their jokes lean toward "black humor" (often directed at themselves).

Alcoholic dementia, which begins to manifest at this stage, predominantly assumes a global character, fixed entirely around alcoholic themes.

Several types of specific alcoholic dementia are distinguished: Korsakoff's psychosis, Wernicke–Korsakoff syndrome (Wernicke's encephalopathy), and Marchiafava–Bignami disease.

Numerous somato-neurological complications develop during the second stage of alcoholism.

The Third Stage is characterized by a decrease in ethanol tolerance and bouts of heavy drinking (binges) during which the individual drinks at short intervals and remains in a constant state of withdrawal. Severe personality degradation occurs. Patients are brutal, deceitful, and interested in nothing other than alcohol. Socially, they lose everything—family, job, and home. At this stage, the disease reaches its absolute peak of severity. Quite often, it culminates in alcoholic encephalopathy.

Remissions and Relapses

During the development of alcohol use disorder, more or less prolonged remissions may occur—both spontaneous and post-treatment. These are most commonly observed in the early stages of alcoholism, specifically stages I and II. Such remissions can be broadly divided into two categories: a conscious refusal of further alcohol consumption, and the inability to drink due to the exacerbation of somatic illnesses. Remissions in alcoholism should not be equated with recovery, because if alcohol is consumed even after a long period of remission (10–20 years), symptoms of physical dependence rapidly reappear. Consequently, some researchers consider alcoholism to be an incurable disease. The stability of remission is enhanced when sobriety holds personal value for the patient, when they recognize their inability to consume alcoholic beverages in moderation, and when they fill their time with other meaningful activities (work, hobbies, sports, etc.).

Relapses of the disease stem from both external and internal causes. External causes include The Influence of a drinking social circle (sometimes taking the form of overt pressure) and constant reminders from others about the patient's alcoholism (at home, at work, or from former friends). Internal causes include hormonal fluctuations (especially in women), affective mood swings (toward both pleasant and unpleasant sensations), states of hunger, and physical or mental exhaustion.

A separate Discussion is warranted regarding spontaneous craving for Alcohol and the reactivation of the alcohol-related dynamic stereotype. This most frequently manifests as an "influx" of thoughts about wanting to drink (typically in the evening and at night) and alcohol-themed dreams. These dreams are usually vivid and thematically tied to the preparation for alcohol consumption. In the early stages of sobriety, such experiences can trigger a pseudo-abstinence syndrome—psychopathological and somato-vegetative disorders that mimic withdrawal symptoms. The reactivation of the alcoholic dynamic stereotype can be triggered by any memory of drinking: a familiar place, a situation, a visit to a grocery store, etc.

It should be noted that relapse triggers never exist in isolation and are not always recognized by the patient. To prevent relapses, specialized psychotherapeutic treatment should be administered in courses lasting from 0.5 to 2 years.

Specific features of Alcoholism in Women

In women, the progression of alcohol-related disease is generally faster than in men. Some authors attribute this to the hormonal cycle. Furthermore, women exhibit a tendency toward bravado regarding drinking, which leads to heavy alcoholization and ethanol dependence. Often, women begin drinking heavily with the goal of "controlling their husband's drinking."

Additionally, the disease relapses more frequently in women. This may be due to the clinical and psychological similarities between premenstrual tension and withdrawal syndrome.

Specific Features of Adolescent Alcoholism

Adolescence marks a person's first exposure to the effects of alcohol. Heavy drinking in the early stages can manifest as specific adolescent reactions, such as emancipation and grouping. Alcohol is most frequently tried for the first time in the company of peers, where members copy the leader. This can lead to heavy alcoholization with a conscious suppression of the gag reflex in the early Stages of the disease, resulting in the symptom of "a hangover without a hangover."

Occasionally, alcohol consumption may form part of a protest reaction. In such cases, it is temporally linked to a conflict (most often within the family) and decreases significantly once the situation improves.

The earlier systematic alcohol consumption begins, the more malignant the course of the disease.

Quite often, alcohol is consumed concurrently with barbiturates, cannabinoids, and inhalants. A transition to other narcotic substances is also possible.

SYMPTOMATIC ALCOHOLISM

Heavy alcohol consumption can also be caused by other psychiatric disorders, and sometimes alcohol dependence even develops. However, alcohol consumption and the symptomatology of the disease in such patients differ somewhat.

For instance, heavy drinking is frequently observed during the manic phase of manic-depressive (bipolar) psychosis. In these cases, alcohol tolerance increases significantly over a short period, and such patients do not appear intoxicated. Often, heavy alcoholization lasts for 1.5–2 months and ceases abruptly. This phenomenon is not typical of the depressive phase. It is dangerous because under the influence of alcohol, depression can intensify and suicidal ideation may emerge.

Alcoholization in patients with epilepsy and organic central nervous system lesions is most frequently observed during dysphoric states and is accompanied by aggression. Atypical and pathological forms of intoxication occur, as well as convulsive seizures during abstinence. Overall, during dysphoria, alcoholization is excessively intense, and patients attempt to get drunk as quickly as possible. Binging episodes are short-lived due to a deterioration in somatic and neurological status. Amnestic forms of intoxication develop very rapidly, and the progression of the disease is high. Alcoholism comorbid with Schizophrenia has the following features: patients abuse alcohol only during exacerbations of schizophrenia. During remissions, patients practically do not drink. Even in the early stages, alcoholization occurs in solitude. Psychoses are merely triggered by alcohol and take the form of typical schizophrenic psychoses. Alcoholic degradation is not typical, even with prolonged heavy drinking. Schizophrenic patients do not exhibit abstinence states.

Treatment of Chronic Alcoholism

Patients with alcoholism are usually treated in inpatient settings, although outpatient therapy is possible in the early stages of the disease.

Several stages can be distinguished in the treatment of alcohol-related disease.

Cessation of the binge and alleviation of the withdrawal syndrome. To achieve this, anxiolytics, hypnotics, cardiotonics, and osmotic Diuretics are employed.

Detoxification therapy aims to clear alcohol breakdown products from the body. It is carried out for 1–2 weeks, depending on the patient's condition. It must be more intensive in cases involving surrogate alcohol, moonshine (samogon), and liqueurs made from stone fruit berries.

Conditioned reflex therapy aims to establish a persistent conditioned vomiting reflex to alcohol. For this purpose, alcohol is administered along with emetics (such as club moss decoction or apomorphine), or a disulfiram-alcohol reaction (DAR) is provoked. The drawback of this method is the relatively rapid extinction of the conditioned reflex.

Alcohol-sensitizing therapy involves the use of medications that are incompatible with alcohol (disulfiram, phthalazol, metronidazole). Disulfiram is primarily used in the form of "Eperaute" (Esperal) implantable tablets. Its action is based on blocking aldehyde dehydrogenase and causing acetaldehyde intoxication. Esperal is implanted subfascially, most often beneath the scapula. Following the Procedure, alcohol consumption within 8–12 months can lead to severe somato-neurological complications and even the patient's death. In such cases, the medication must be immediately removed surgically, and intensive detoxification therapy must be administered.

Psychotherapy for alcoholism should be aimed at achieving complete, lifelong abstinence from alcohol. It is advisable to conduct it in several stages: immediately after sobering up and over the course of 1–2 years to gradually resolve problems that will confront the patient. It is also recommended to conduct psychotherapeutic work with the patient's relatives.

Social rehabilitation in Ukraine is carried out by non-governmental structures that support sober living communities for individuals with alcohol and drug dependencies, as well as Alcoholics Anonymous (AA), Al-Anon (for relatives of individuals with alcoholism), and Alateen (for their children). The goal of AA, Al-Anon, and Alateen is to support a sober lifestyle and help resolve the psychological problems of their members.

ALCOHOLIC PSYCHOSES

Alcoholic psychoses encompass psychotic disorders that develop as a consequence of alcohol abuse in stages II–III of chronic alcoholism. These psychoses are categorized into distinct forms based on their clinical presentation. The recognized forms include alcoholic delirium, encephalopathy (including Korsakoff's psychosis), hallucinosis, paranoid disorders, and acute transitory alcoholic psychosis (pathological intoxication).

Alcoholic psychoses are also referred to as meta-alcoholic conditions, as they are triggered not only by the direct neurotoxic effects of alcohol, but also by somatocerebral and metabolic disturbances driven by chronic alcohol intoxication.

DELIRIUM TREMENS (ALCOHOLIC DELIRIUM — DELIRIUM TREMENS POTATORUM)

Acute alcoholic psychosis, or delirium tremens, typically develops in patients with stage II–III chronic alcoholism (with a disease history of at least 5 years). This usually occurs several hours or days after cessation of alcohol intake against a backdrop of pronounced hangover symptoms. The onset of alcoholic delirium is often precipitated by somatic illnesses, head injuries, acute infections, or surgical Procedures.

During the prodromal period, which lasts for several days or weeks, patients experience headaches, sleep and appetite disturbances, chills, and precordial pain. The psychopathological symptoms of withdrawal progressively intensify—manifesting as anxiety, emotional lability, attention deficits, and subdepressive or depressive affective disorders. Illusions and fragmentary hallucinatory phenomena emerge, accompanied by sleep disturbances involving terrifying nightmares and frequent awakenings. Alcoholic delirium is occasionally preceded by major epileptic seizures or, less commonly, abortive ones.

The core Clinical Features of alcoholic delirium include: clouded consciousness with disorientation in time and space while self-awareness (personal orientation) remains intact; true visual, tactile, auditory, olfactory, and gustatory hallucinations; perceptual fragmentation; delusional interpretation of the environment (delusions of reference, persecution, physical influence, and jealousy); intense fear; and psychomotor agitation.

Typically, in the evening, the patient experiences escalating general restlessness, accelerated speech, motor activity, and facial expressions. All gestures become markedly animated, and patients are unable to remain still. They experience a flood of vivid, scene-like mental imagery and memories. Hyperesthesia is frequently observed. External stimuli, even minor ones, readily capture the patient's attention. Mood becomes extremely labile; the withdrawal syndrome is characterized by an anxious-depressive mood coloration, where dejection, anxiety, and fear easily shift into euphoria, gaiety, and excitement. Concurrently, autonomic symptoms and insomnia progressively worsen.

In the fully developed stage of alcoholic delirium, the patient suffers from total insomnia, and illusions and hallucinations become the dominant Features of the clinical picture. These illusions, predominantly visual, take the form of multiple fantastic pareidolias or mundane everyday scenes. Alongside illusions, visual hallucinations occur, most commonly of a zoological nature (insects, small animals, lizards, mice, rats, snakes). Terrifying images of humanoid creatures, corpses, or devils may also appear. Hallucinatory tableaus drift before the patient's eyes in continuous succession, resembling a "cinema on the wall."

These visual hallucinations change in scale, receding or advancing, and depict various life situations (such as banquets or erotic scenes). A distinctive characteristic of these visual hallucinations is that they are "silent."

The Emergence of auditory, tactile, olfactory, or other sensory hallucinations indicates a deeper level of delirious clouding of consciousness.

Body schema disorders and sensations of altered spatial body positioning are frequently observed. The content of these hallucinatory experiences dictates the patient's behavior (affective reactions, delusional statements). Motor agitation dominates, driven by an impulse to escape or hide. Speech consists of short, disconnected phrases or isolated words. The patients' attention cannot be sustained on any single object. The patient responds to everything with brief remarks, facial expressions, and gestures. Expressions of surprise alternate with complacency and bewilderment, though a pervasive sense of fear predominates. Vivid delusions of persecution, physical destruction, and jealousy are present. Patients are highly suggestible: by applying pressure to closed eyes and asking leading questions, a physician can elicit visual hallucinations that the patient then describes in detail (Lipmann's symptom). Furthermore, the patient will converse with an imaginary interlocutor when the physician hands them a disconnected telephone receiver (Aschaffenburg's symptom).

Under the influence of distracting stimuli, such as a conversation with a physician, the symptoms of alcoholic delirium may temporarily vanish spontaneously. A characteristic feature is the intensification of symptoms in the evening and, especially, at night.

Alcoholic delirium is invariably accompanied by neurological and somatic disorders, predominantly autonomic. Characteristic signs include rhythmic tremors, ataxia, muscular hypotonia, and hyperreflexia. Profuse sweating (hyperhidrosis), cutaneous hyperemia (especially of the face), tachycardia, blood pressure fluctuations (mostly hypotension), and tachypnea are frequently observed. The hepatomegaly is present, and the sclerae are icteric. Body Temperature is most often subfebrile, but occasionally reaches high levels of 39–40 °C. Blood tests reveal leukocytosis, a left shift in the leukocyte differential, and an elevated ESR. In a subset of patients, epileptic seizures occur during alcoholic delirium.

With clinical deterioration, the psychosis may transition into alcoholic delirium with professional delirium (occupational delirium) or muttering delirium (murmuring delirium). The harbingers of occupational delirium include a deepening of consciousness disturbances, the disappearance of lucid intervals, and a waning of prior hallucinatory phenomena. Misidentifications arise: strangers entering the field of Vision are mistaken for relatives, acquaintances, or colleagues. Affective disturbances become monotonous, dominated by a persistent anxiety that gives way to fear. Vivid delusions of persecution subside and vanish. The diverse, coordinated motor disturbances are replaced by a uniform agitation dominated by relatively simple motor acts, frequently reflecting routine daily activities, including those related to the patient's profession. Communication with the patient becomes impossible. As the intensity of the psychosis escalates, it leads to pronounced stupor and the development of muttering delirium.

In muttering delirium, patients are inaccessible for verbal contact. Agitation, characterized by rudimentary motor acts—such as groping, grasping, picking at fingers, and pulling or smoothing the bedcovers—is confined within the BOUNDARIES OF THE bed. Speech degrades into a series of isolated syllables, sounds, or brief words uttered in a low, unmodulated voice.

Both variants of severe delirium are accompanied by pronounced somatoneurological disorders, the intensity of which correlates with the severity of the mental status impairment. Marked tachycardia or, conversely, bradycardia with muffled Heart sounds, alongside shallow, irregular, intermittent, and accelerated breathing, is observed. Profuse sweating is accompanied by dehydration and oliguria. Blood clotting disorders and increased capillary permeability lead to The formation of subcutaneous hematomas. Hyperthermia reaches 40–41 °C. Neurological signs include ataxia, dysarthria, tremor, hyperkinesia, oral primitive Reflexes, Muscle tone abnormalities, pathological plantar reflexes, nuchal rigidity, Kernig's sign, and pelvic organ dysfunction.

The most common causes of death are superimposed intercurrent infections, acute cardiovascular failure, and cerebral edema. In cases of recovery, unlike classical delirium, the entire period of occupational and muttering delirium is completely amnesesed.

ACUTE ALCOHOLIC HALLUCINOSIS

Acute alcoholic hallucinosis develops during stages II–III of chronic alcoholism, which typically has lasted for over 10 years. The clinical picture is dominated by auditory (verbal) hallucinations, hallucinatory-delusional ideas, and affective disorders occurring against a background of clear, unclouded consciousness. This condition primarily manifests During the first days of hangover symptoms, and less frequently in the final days of a drinking binge or during the abatement of withdrawal symptoms. The onset of acute hallucinosis is often preceded by anxiety, occasionally accompanied by a paranoid mood, and depressive disorders. Initial auditory hallucinations—taking the form of akoasmas and phonemes (noise, whistling, knocking, coughing, whispering, music, isolated words and phrases)—appear in the evening or amidst nighttime insomnia. Perceptual disturbances occur periodically, accompanied by anxiety, restlessness, a diffuse delusional mood, and bewilderment. Autonomic symptoms, particularly hyperhidrosis, are also present. Initially, auditory verbal hallucinations are neutral in content, indistinct, and manifest as functional hallucinations that coincide with various external acoustic stimuli (such as the sound of running tap water or engine noise). The progression of hallucinosis into multiple verbal hallucinations is accompanied by disorientation, anxiety, fear, and motor disturbances. Typically, the patient hears the voices of a multitude of people, less often just one or two. These voices can vary in intensity and spatial localization. At times, they converse and argue among themselves about the patient; at other times, they address the patient directly, accusing, insulting, threatening, and scolding them for heavy drinking and immoral behavior. The voices often assume an imperative character. Naturally, the patient does not consider themselves entirely blameless, but the accusations they "hear" seem vastly exaggerated and unjust. Voices defending the patient frequently join in as well. Overwhelmed by hallucinatory experiences, the patient develops secondary delusional ideas, most commonly delusions of persecution, physical destruction, accusation, and jealousy. At the peak of hallucinosis, the predominant affects are fear, anxiety, and despair. Patient behavior generally corresponds to the content of the hallucinations and delusions: they barricade themselves in the rooms where the voices found them, seek help from the police, attempt to flee, or exhibit suicidal tendencies. Psychotic symptoms intensify in the evening and at night, subsiding during the day when the patient may exhibit semi-critical or critical insight into their hallucinatory experiences. Recovery from this psychotic state is gradual. Concurrently with the fading of hallucinatory symptoms—or slightly later—affective disturbances resolve, and delusional ideas regress. A fully critical attitude toward the experienced psychosis does not appear immediately; patients may retain residual delusions and a subdepressive or depressive mood. Acute alcoholic hallucinosis lasts from several days to a month.

Subacute (protracted, prolonged) alcoholic halluncinoses, characterized by a slow regression of psychotic symptoms, last from 1 to 6 months.

CHRONIC ALCOHOLIC HALLUCINOSIS

Chronic alcoholic halluncinoses comprise forms of psychosis lasting longer than 6 months. The development of chronic alcoholic hallucinosis may be preceded by acute hallucinosis with depressive-paranoid symptoms.

The most common presentation is chronic verbal hallucinosis without delusions, often termed "pure hallucinosis." Auditory hallucinations, especially at the onset of the disorder, are persistent. Voices discuss all the patient's actions and desires, threaten them, condemn them, or, conversely, defend them. In the first months and years, this elicits reactions of protest, anger, and indignation from the patients. They argue, scold the voices, and plead for help. Over time, the intensity of these experiences wanes, and patients appear to grow accustomed to what they hear. Outwardly, patient behavior normalizes; they are able to fulfill their daily and sometimes professional duties. Critical awareness of perceptual distortions emerges, along with a desire to conceal them from others. Noticeable impairments in remote memory are absent, whereas memory for recent events is significantly more impaired. Upon the resumption of drinking, hallucinosis symptoms exacerbate, and behavioral disturbances return, making the clinical picture resemble that of acute alcoholic hallucinosis.

In cases of chronic alcoholic hallucinosis with delusions, patients experience, alongside auditory hallucinations, unsystematized delusional ideas of persecution and influence.

In chronic alcoholic hallucinosis accompanied by psychic automatisms and a paranoid transformation of delusions, these phenomena—particularly alcoholic paraphrenia—emerge during the later stages of the disease. Megalomanic ideas, combined with automatisms and hallucinosis, do not tend toward systematization. A progressive organic personality defect gradually develops.

ALCOHOLIC DELUSIONAL PSYCHOSES

Based on their psychopathological features, delusional psychoses in chronic alcoholism are classified into alcoholic paranoid disorder and alcoholic delusion of marital infidelity.

ALCOHOLIC PARANOID DISORDER

Alcoholic paranoid disorder, much like delirium and hallucinosis, most commonly develops during states of abstinence. Occasionally, there is a brief prodromal period characterized by insomnia, unmotivated anxiety and fear, and a delusional mood. The clinical picture of the fully developed psychosis is predominantly defined by persecutory delusions. The patient is suddenly struck by the conviction that their life is in mortal danger. This threat is perceived to originate from people in their immediate environment, with new pursuers appearing in every situation. Although the patient cannot specify who is threatening them or why, they remain certain that everything happening around them is aimed at their destruction. This delusional interpretation of the environment is accompanied by illusory-hallucinatory perceptions. Threatening remarks are heard in conversations, and the patient may even visualize specific murder weapons (such as knives, pistols, or brass knuckles) in the hands of their "pursuers." An affect of fear dominates, reaching the level of panic terror and despair. Brief bursts of impulsive motor agitation occur: patients suddenly attempt to flee, jump out of vehicles, throw themselves out of windows, seek help from the police, or commit suicide. In the evening and at night, elementary illusions and hallucinations (visual and auditory) appear. The psychosis lasts from several days and weeks to several months in protracted cases.

Alcoholic Delusion of Marital Infidelity (Alcoholic Delusion of Jealousy, Alcoholic Paranoia)

Alcoholic delusion of jealousy is a chronic form of psychosis that occurs exclusively in men. It does not include cases of residual jealousy delusions resulting from alcoholic delirium or hallucinosis. The psychosis typically arises in individuals with psychopathic personality traits and a predisposition toward overvalued ideas, which becomes especially pronounced during periods of alcoholic excess. In most cases, the psychosis is preceded by chronic alcohol intoxication accompanied by signs of degradation. The delusion of jealousy develops slowly and insidiously. Initially, isolated delusional statements appear during intoxication or against the background of a hangover, but eventually they persist even in a sober state. Delusional interpretations emerge, while the content of the delusional constructs maintains a semblance of plausibility, often causing people in the patient's environment to misinterpret the condition as non-pathological. Gradually, The connection between these delusional interpretations and real facts dissolves, leading to the systematization and progressive crystallization of the delusion. This process is frequently accompanied by verbal illusions—in casual remarks about family matters, the patient perceives hints, ridicule, and insults. Their behavior becomes increasingly driven by this delusional concept, directed entirely at proving the wife's infidelity and exposing her. Various checks and investigations are initiated, and "proofs" of betrayal are accumulated. Patients even lodge Complaints with public organizations, demanding help to save their marriage.

Further progression of the psychosis involves the emergence of retrospective delusions: the patient begins to claim that the wife has been unfaithful for a long time, dating back to the early years of their marriage, and that the children were not fathered by him. He cites "evidence" to support this, leading to a corresponding shift in his attitude toward the children.

Occasionally, the transformation of monothematic jealousy delusions becomes complicated by persecutory, poisoning, or magical harm delusions. The malignant affect that frequently accompanies this can result in acts of aggression directed at the wife.

Upon cessation of alcohol consumption, the intensity of the delusional ideas diminishes significantly, and they assume a residual character. Patients assert that they are trying to forget the past and have forgiven their wives; however, a full critical evaluation of their previous delusional statements and behavior is lacking.

PATHOLOGICAL ALCOHOLIC INTOXICATION

Pathological alcoholic intoxication is an acute transient psychosis resulting from a single ingestion of a small or moderate dose of alcohol by individuals who do not chronically abuse alcoholic beverages. The primary symptom of pathological intoxication is a sudden twilight state of consciousness, culminating in profound psychological and physical exhaustion. This condition is invariably accompanied by complete or partial amnesia of the psychotic episode.

Two forms of pathological intoxication are distinguished: the epileptoid and the hallucinatory-paranoid forms. In the epileptoid form, the clinical picture is dominated by intense motor agitation manifested as chaotic, aggressive actions. The affect of rage and malice, along with motor stereotypies, predominates. Speech is impoverished, consisting of isolated words, sounds, or repetitions thereof.

In the hallucinatory-paranoid form of pathological intoxication, figurative delusions predominate, centered around situations of danger and life-threatening danger. The environment is perceived delusionally, and misidentifications occur constantly. Affective disturbances are defined by fear, anxiety, and anger. Despite motor agitation, patients retain the ability to perform complex, sequential actions that externally appear purposeful. Their vocabulary is somewhat richer than in the epileptoid form, consisting of isolated words and short phrases framed as questions, warnings, or appeals. Less frequently, the clinical picture of the hallucinatory-paranoid form is dominated not by delusions, but by terrifying visual hallucinations.

Pathological intoxication occurs most frequently in individuals with underlying organic brain pathology.

ENCEPHALOPATHIES

This group of alcoholic psychoses develops against the background of a malignant course of stage II–III chronic alcoholism lasting from 7 to 20 years.

The clinical picture of alcoholic encephalopathies combines psychiatric disorders with severe neurological and somatic disturbances. Depending on the acuteness of the course, psychiatric impairments manifest as severe delirium, stupor, or the symptomatology of a profound psycho-organic syndrome.

Acute Wernicke-Korsakoff Alcoholic Encephalopathy

The initial and, particularly, manifest manifestations of the psychosis share many similarities with severe forms of delirium. The onset features an anxious-depressive or depressive-delusional state with elements of figurative delusions and verbal hallucinations. However, within a few days, symptoms of delirium supervene. Further clinical deterioration is marked by professional or muttering delirium. The subsequent Evolution of the clinical picture is defined by daytime deepening of stupor, which is sometimes preceded by an apathetic stupor—patients lie motionlessly on their backs with open eyes, unresponsive to their environment, and providing brief, monosyllabic Answers TO QUESTIONS. At night, professional or muttering delirium recurs. As the condition worsens, apathetic stupor transitions into true stupor, accompanied by the disappearance of nocturnal delirious disturbances. The psychiatric symptoms of acute alcoholic encephalopathy are invariably intertwined with neurological and somatic ones. Autonomic dysfunctions are consistently observed. Patients are exhausted and appear prematurely aged. Their face and limbs are edematous, the skin and mucous membranes are pale, and the sclerae are icteric. Trophic disturbances lead to the formation of extensive necrotic bedsores. Body temperature typically ranges from 37 to 38 °C, though in severe cases it may spike to 40–41 °C. A constant feature is cardiac rhythm disturbance in the form of tachycardia and arrhythmia. ARTERIAL BLOOD PRESSURE is slightly elevated at the onset of the psychosis but drops as the patient's condition deteriorates, with hypotension and collapse-like states predominating. Respiration is rapid and shallow. Fibrillary twitchings of facial Muscles are observed, alongside complex hyperkinesias featuring tremor, choreiform, athetoid, myoclonic, and ballistic movements. Muscle tone ranges from hypertonia to hypotonia, with muscular hypertonia occasionally reaching the intensity of decerebrate rigidity.

Signs of oral automatism, horizontal nystagmus, and ataxia are constant findings. Alongside nystagmus, clinicians may observe ptosis, diplopia, strabismus, visual field constriction, anisocoria, sluggish pupillary light reflexes, and impaired convergence (Gudden's sign). Against a background of hyperreflexia, Babinski and Rossolimo signs can be elicited, alongside meningeal signs and nuchal rigidity.

The fatal outcome of acute alcoholic encephalopathy is frequently associated with secondary intercurrent infections and typically occurs toward the end of the second week of psychosis. The earliest sign of recovery is the normalization of sleep; during this period, patients may exhibit confabulatory confusion with the potential development of Korsakoff's syndrome.

Pathoanatomical examinations reveal petechial hemorrhages and perivasculitis in the Midbrain and around the third and fourth ventricles. Korsakoff's Amnestic Alcoholic Psychosis (Alcoholic Paralysis, Polyneuritic Psychosis)

This form of psychosis was first described by S. S. Korsakoff in 1887. It most frequently develops following severe alcoholic delirium or Wernicke's encephalopathy. Considerably less often (predominantly in older patients), Korsakoff's psychosis arises without a preceding state of clouded consciousness.

The clinical picture of the psychosis is defined by pronounced psychiatric and neurological alterations. The psychiatric component comprises severe organic memory impairments, amnestic disorientation, confabulations, and pseudoreminiscences. Impairments in registering current events—fixation amnesia—are evident, alongside retrograde and anterograde amnesia. The gaps in the patient's memory are filled with confabulations and pseudoreminiscences, which most frequently pertain to everyday life events and, much less commonly, take the form of fantastic confabulations.

Fixation amnesia, confabulations, and pseudoreminiscences lead to amnestic disorientation or impaired orientation regarding place, time, and surroundings. Patients exhibit sluggishness, passivity, increased fatigue, irritability, and anxious restlessness accompanied by hypochondriacal ideas. The patient retains partial awareness of their illness, as evidenced not only by their complaints but also by attempts to conceal memory deficits.

Neurological disorders in patients with Korsakoff's amnestic alcoholic psychosis typically manifest as neuritis accompanied by muscular atrophy, impaired limb sensation, and diminished or absent deep tendon reflexes.

Korsakoff's psychosis tends to be regredient. Upon recovery from this acute state, persistent impairments in memory and cognitive processes remain.

Pathoanatomical findings reveal diffuse alterations and neuronal loss in the cerebral cortex, petechial hemorrhages in the cortex, Brainstem, around the Third ventricle, as well as in the Spinal Cord and peripheral nerves.

Marchiafava–Bignami–Nazari encephalopathy develops gradually over the course of 2–6 years. Against a background of passivity, mild memory decline, and sleep disturbances, isolated visual hallucinations emerge that resemble delirium in content (frightening hallucinations and zoopsia) yet are perceived without emotional coloring. Neurologically, symptoms include limb tremor, hyporeflexia, gait ataxia, and sluggish pupillary light reflexes.

Pathoanatomical examination reveals necrosis within the corpus callosum and the cerebral White matter.

Treatment of Alcoholic Psychoses

Patients suffering from alcoholic psychosis, particularly acute forms, require emergency care. This is provided in specialized units or intensive care departments. Treatment strategy depends on the course of the disorder. For mild to moderate alcohol delirium without severe somatic complications, patients are prescribed hypnotics for 7–10 days (5–10 ml of a 5% barbamil solution; Popov's mixture; Ravkin's mixture), neuroleptics (chlorpromazine or levomepromazine at 2–3 ml of a 2.5% solution 2–3 times daily intramuscularly or via intravenous drip with 400–500 ml of a 5% glucose solution; haloperidol at 1–2 ml of a 0.5% solution intramuscularly; Clopixol Acuphase at 200–300 mg intramuscularly; flupenthixol injections at 20 mg daily, provided there is no alcohol intoxication), and tranquilizers—2–4 ml of a 0.5% sibazon (seduxen, relanium) solution intramuscularly or intravenously with 10–15 ml of a 40% glucose solution.

In cases of severe alcohol delirium, these methods prove ineffective, and treatment with neuroleptic agents frequently results in severe collapse, physical deterioration, and worsening neurological symptoms.

The treatment of acute alcoholic psychoses and encephalopathies is based on pathogenetic principles and aims at intensive detoxification, restoration of acid-base balance and metabolism, and the Prevention of Hypoxia and cerebral edema.

Treatment begins with the elimination of psychomotor agitation. Seduxen is administered intravenously (60–70 mg/day) in a 40% glucose solution; sodium oxybutyrate is given orally 3–4 times daily, having dissolved 2–4 g of the drug in 20 ml of a 5% glucose solution, or administered intravenously as a 20% solution. Barbamil (500–600 mg 2–3 times daily), phenobarbital (300 mg 1–2 times daily), raderorm (5–10 mg/day), and rudotel (10–30 mg/day) are prescribed orally. In cases of prolonged agitation, 25 mg of chlorpromazine in 500 ml of isotonic sodium chloride solution is administered via intravenous drip, alongside intramuscular seduxen (50 mg) or diphenhydramine (10–30 mg).

In the presence of dehydration, detoxification therapy utilizes low-molecular-weight plasma substitutes (hemodes, rheopolyglucukin), isotonic sodium chloride solution, and a 5% glucose solution. If symptoms of hyperhydration are present (edema, venous congestion), a hypertonic glucose solution with Insulin, potassium chloride, and diuretics (furosemide, mannitol, urea) is administered.

Ensuring adequate Circulation is crucial. In Heart Failure, cardiotonic agents (strophanthidin, corglycon) are indicated; for hypotension resulting from dehydration, a 5% glucose solution and rheopolyglucukin are administered via intravenous drip; for acute vascular failure, adrenaline or noradrenaline is given. In all cases of collapse, glucocorticoid medications are prescribed: prednisolone (50–150 mg/day intramuscularly) and hydrocortisone (75–125 mg/day intramuscularly). These are tapered gradually over 3 days following the normalization of blood pressure.

If pulmonary edema is diagnosed, therapy begins with oxygen inhalation. Alongside strophanthin and corglycon, cocarboxylase (100–150 mg), calcium chloride (10 ml of a 10% solution intravenously), antihistamines (diphenhydramine, suprastin), aminophylline, and glucocorticoids are prescribed. Adrenaline and noradrenaline are contraindicated as they increase peripheral vascular resistance. In the event of respiratory impairment, oxygenation via a nasal catheter is required. For symptoms of cerebral edema, provided renal function is intact, a 30% urea solution or 20% mannitol solution is administered intravenously. To prevent renal failure, patient diuresis is continuously monitored, and efforts are made to correct acidosis and hypoxia; furosemide is administered in cases of oliguria.

When the liver is affected, concentrated glucose solution is used in combination with insulin, ascorbic acid, B-group vitamins, cocarboxylase, Methionine, sirepar, and hormonal agents such as prednisolone and hydrocortisone. If intercurrent diseases develop, appropriate treatment is administered.

The aforementioned therapeutic measures are implemented to a greater or lesser extent in all forms of delirium and acute encephalopathies. For Korsakoff's psychosis and acute Wernicke-Korsakoff syndrome, thiamine (500–1000 mg), pyridoxine (500–1000 mg), ascorbic acid (1000 mg), and nicotinic acid (300–500 mg) are additionally administered daily via intramuscular injection for a month.

In the treatment of alcoholic hallucinosis and paranoia, neuroleptic agents play the primary role: haloperidol (10–30 mg/day), stelazine (20–50 mg), chlorpromazine (150–300 mg), levomepromazine (50–150 mg), clopixol (200–400 mg), flupenthixol (20–40 mg), zyprexa (5–20 mg), and risperidone (4–6 mg). Administration begins parenterally, transitioning to oral intake as symptoms subside. When depressive affect is prominent, antidepressants are employed: amitriptyline (50–100 mg/day), citalopram (20–40 mg), fluoxetine (20–40 mg), and sertraline (50–220 mg). Psychotropic treatment for both acute and chronic alcoholic psychoses is continued until productive psychopathological symptoms completely disappear and a critical insight into the illness is established.

To prevent epileptic seizures and other neuropsychiatric disorders during alcohol withdrawal syndrome, carbamazepine is prescribed at 600–800 mg/day divided into 2–3 doses for 2–4 weeks.

Prognosis

Without treatment, the prognosis for life is unfavorable. Patients most frequently die In the second and third stages of the disease due to trauma and comorbid pathologies (most commonly liver and cardiovascular diseases). If the patient's history indicates prolonged spontaneous or therapeutic remissions, cognitive decline slows down.

Prevention

Prevention of alcohol-related disorders is carried out in three stages (according to WHO classification). Primary prevention involves counteracting the Development of the disease and is conducted simultaneously in several directions. From an informational standpoint, this entails fostering healthy lifestyle habits and direct anti-alcohol propaganda. Socially, it involves reducing the demand for alcoholic beverages through The regulation of their production and sale, increasing alcohol prices via taxation (excise duties), and improving product quality. Legally, it involves combating the counterfeiting of alcoholic beverages and enforcing bans on alcohol consumption at specific times and in certain locations. Medically, it involves identifying high-risk groups.

Secondary prevention aims to slow down the progression of the disease. This encompasses early detection of the disorder, adequate treatment, anti-relapse measures, and social rehabilitation of individuals with alcoholism.

Tertiary prevention measures include reducing the risk of disability and other manifestations of impaired social functioning among patients through rehabilitation programs.

Expert Evaluation

Medical and social expertise. During the course of treatment, patients are temporarily incapacitated, as certified by issued medical certificates. In cases of alcoholic dementia and severe somatic complications, they are considered permanently disabled and may be referred for disability status.

Other manifestations of patients' social maladaptation (such as inability to move or communicate) are assessed, and a comprehensive readaptation plan is developed.

Military expertise. Patients registered at addiction clinics are unfit for military service in peacetime and conditionally fit during wartime (Article 19, paragraphs b and c). In cases of significant mental disorders, they are exempt from military registration entirely (Article 19, paragraph a).

Forensic psychiatric expertise. If a crime is committed in a psychotic state, patients are deemed not guilty by reason of insanity (insane). Individuals with alcoholic dementia may also be declared legally insane.

Review Questions

1. Definition of the concept of "alcoholism". Prevalence. ETIOLOGY AND Pathogenesis.

2. Clinical signs and stages of alcoholism.

3. Age and gender characteristics of alcoholism.

4. Methods of alcoholism treatment. Prevention. Rehabilitation.

5. Clinical manifestations of alcoholic delirium.

6. Alcoholic hallucinosis and paranoid syndromes.

7. Acute alcoholic encephalopathy.

8. Korsakoff's alcoholic psychosis.

9. Pathological intoxication.

10. Treatment and prevention of alcoholic psychoses.