Psychiatry: A Course of Lectures - V. S. Bitensky 2004

Mental and behavioral disorders due to psychoactive substance use

The combination of mental and behavioral disorders resulting from The Use of psychoactive substances is the subject of addictology. In other words, addictology is a scientific discipline that investigates the Etiology and mechanisms underlying The Development of substance use disorders (SUDs), alongside their toxic effects, with the ultimate goal of establishing effective Methods for the Diagnosis, Treatment, and Prevention of these conditions.

The core syndrome in addictive disorders—whether alcoholism, drug addiction, or substance abuse—is the pathological craving for psychoactive substances. The term "psychoactive substances," coined by the World Health Organization (WHO), is particularly apt as it encompasses categories such as alcohol and illicit drugs, thereby avoiding The Need for strict differentiation between them.

Alcohol and drugs exert a distinct adverse effect on The Human Body. Chronic use of psychoactive substances compromises all internal systems and Organs, most notably The Heart and Liver. Furthermore, individuals struggling with substance abuse frequently develop gastrointestinal pathologies (such as pancreatitis, gastritis, and peptic ulcers), respiratory disorders including tuberculosis, and cardiovascular complications. As a rule, these are chronic conditions requiring prolonged and, in some cases, inpatient care. It is important to note that somatic impairments manifest in the Cytology/cytology/16.html">Early stages of the disease—typically within the first 4 to 5 years—while their frequency, severity, and reversibility correlate directly with clinical and dynamic parameters such as disease duration and stage.

When discussing the etiology of addictive disorders, one must always consider multiple interacting components, including social, psychological, and, undoubtedly, biological factors, given the robust modern consensus regarding an individual's biological predisposition to dependency. The fundamental biological mechanisms of addictive disorders have now been elucidated, leading to a contemporary theory of substance dependence that highlights the pivotal role of the catecholamine system in its Pathogenesis. Elevated catecholamine levels are directly linked to the activation of pathological cravings for psychoactive substances. This theoretical framework underpins the development of comprehensive, differentiated treatment, diagnostic, and preventative programs for alcoholism and drug addiction.

Epidemiological research plays a vital role in addictology, pursuing broad-scale objectives. The planning of an epidemiological study involves assembling a representative population sample and designing a research protocol that accounts for numerous variables, primarily socio-psychological and clinical parameters. The social spectrum of factors evaluated in these studies encompasses economic and legal aspects, as well as the cultural and ethnic traits of the cohort—such as varying traditions of alcohol consumption—along with geographical and climatic conditions. In essence, the Specific characteristics of the regions under investigation are factored in to the greatest extent possible. Statistical data serve as the foundation for epidemiological analysis, enabling researchers to grasp the core of the problem and draw valid Conclusions.

As previously noted, the pathogenesis of addictive disorders—specifically the biological mechanisms driving dependence—has now been mapped out, revealing several General Principles. First, a commonality has been established between the biological mechanisms of alcohol and drug dependence, regardless of the specific psychoactive substance involved (whether alcohol, opiates, cannabinoids, or cocaine). While variations exist among specific forms of drug addiction, the overarching biological mechanisms of their formation are well understood. Second, the core mechanisms of psychoactive substance dependence have been identified; without a detailed understanding of these central biological drivers, determining the correct therapeutic strategy is virtually impossible. The advancements of addictology as a biological science are largely attributable to experimental modeling—the creation of models for alcohol and drug dependence in rats, mice, rabbits, and primates. These fundamental experimental studies made it possible to formulate The Theory of dependence development. Moreover, such research serves a strictly practical purpose: identifying targets for therapeutic intervention (pharmacological, non-pharmacological, and psychotherapeutic).

A defining objective of addictology is the treatment of individuals suffering from alcoholism, drug addiction, and substance abuse. Treatment primarily focuses on stabilizing remission and preventing relapse. This is achieved through an integrated multimodal approach combining pharmacological, psychotherapeutic, and social interventions, the relative weights of which may vary. Systematic treatment and rehabilitation are anchored in controlling pathological cravings for alcohol and drugs, treating concurrent somatic conditions, and repairing the patient's interpersonal relationships. Beyond the intensive management of alcohol withdrawal syndrome during the initial phase of therapy, prolonged symptomatic treatment—specifically the correction of somatic pathology—is essential. Without addressing this, achieving the primary objective remains exceedingly difficult.

Treating substance addictions is considerably more complex. In these cases, the social, psychological, and rehabilitative dimensions are substantially more labor-intensive and intricate—a reality that must be acknowledged and incorporated into any therapeutic program.

Another key mission of addictology is disease prevention. The WHO has outlined several stages of preventive intervention: primary prevention, secondary prevention, and others. Primary prevention entails modifying the social conditions that give rise to the disease. At present, this remains a non-medical priority, meaning physicians cannot directly engage in primary prevention. Theoretically, primary prevention could fall within the purview of an addictologist if a comprehensive panel of biological markers for predisposition to alcoholism and drug addiction were identified. Such markers could pave the way for pharmacological toolkits designed to correct innate biochemical abnormalities.

Fundamental biological mechanisms of alcohol and drug dependence

Today, alcohol and drug dependence has emerged as one of the most critical biomedical and social challenges. While our country has traditionally experienced high rates of alcohol abuse, recent years have witnessed a sharp surge in the prevalence of Various Forms of drug addiction, with growth rates far outpacing those in most other nations. An increasing number of chemical substances capable of triggering dependence syndrome are entering Circulation. Consequently, it was proposed to group all these agents together under the designation of psychoactive substances.

Mass abuse of psychoactive substances leads to a rise in poisoning incidents, traumatic injuries, violent crimes, and other societal harms. Of particular concern is the fact that drug use is most prevalent among youth, including adolescents and children, while alcohol abuse is also frequently detected at a very early age. Undoubtedly, these factors profoundly shape personality development, personal interests, and social status.

Intravenous drug use accelerates the transmission of viral infections, including AIDS and hepatitis. The majority of individuals dependent on opioids unfortunately die at a young age.

One of the paramount tasks is investigating the biological mechanisms of psychoactive substance dependence, as a thorough understanding of pathogenesis is the sole foundation upon which effective treatments and preventive strategies can be built for any disease.

The impact of drugs, alcohol, and other psychoactive substances on the human body, its vital activity, and its Functions manifests across three distinct directions.

First, psychoactive substances exert a specific effect on particular Brain systems and structures, thereby triggering the development of dependence syndrome. This very syndrome serves as the leading, core component in the clinical picture of addictive disorders.

Second, drugs and alcohol exert a toxic impact on virtually all Internal Organs and systems. It must be emphasized that toxic organ damage is not directly tied to the manifestations of dependence syndrome. At the same time, temporary disability, invalidism, and mortality among individuals with alcoholism and drug addiction (including premature death) are most frequently driven precisely by the consequences and complications of psychoactive toxicity.

Finally, third, contemporary science has definitively proven the profound impact of parental addiction pathology on offspring. Numerous biomedical and genetic studies confirm that children born to parents with alcoholism or drug addiction face a significantly elevated risk of developing these same disorders. Furthermore, the majority of such children exhibit various characterological and behavioral abnormalities: heightened excitability, aggressiveness, risk-taking tendencies, predisposition to depressive states, and more. Maternal alcohol consumption during Pregnancy leads to fetal alcohol syndrome, whereas drug use can result in a newborn entering the world with established drug dependence.

The findings of numerous studies lead to the Conclusion that the impact of psychoactive substances on neurochemical brain processes is the foundation upon which dependence syndrome develops. It should be noted that the massive disruption caused by narcotic agents leads to the dysfunction of nearly all neurochemical brain systems, though not all of these disturbances are linked to the pathogenesis of drug dependence. Investigations into the Mechanisms of action of psychoactive drugs have demonstrated that each possesses a distinct pharmacological spectrum. However, all substances capable of inducing dependence share a common pharmacological nexus: a characteristic effect on catecholaminergic neurotransmission within limbic brain structures, particularly the "reward system." The action of psychoactive substances triggers an intensive release of catecholamine Neurotransmitters—primarily dopamine (DA)—from synaptic stores within these brain regions, resulting in a profound hyperstimulation of the reward system. This disruption is frequently accompanied by positively valenced emotional experiences. Free catecholamines are subsequently targeted by metabolic Enzymes and rapidly degraded. A portion of the free neurotransmitter is recovered into storage via reuptake mechanisms. Repeated use of psychoactive substances depletes neurotransmitter reserves, manifesting clinically as an inadequate response of the reward system to "normal" physiological stimuli. Psychophysically, this is experienced by the individual as depressed mood, lethargy, weakness, boredom, emotional discomfort, and depressive symptoms. Consuming psychoactive substances against this backdrop once again provokes an additional release of neurotransmitters from storage, temporarily compensating for their deficit within the synaptic cleft and normalizing The activity of limbic brain structures. This process is accompanied by a subjective sense of recovery, emotional relief, and psychological comfort. However, the free catecholamines are rapidly degraded once again, leading to a subsequent drop in their levels, a worsening of the psycho-emotional state, and, consequently, a renewed compulsion to use the drug.

This "vicious circle" underlies The formation of psychological dependence on alcohol and drugs. While the mechanisms described are primary, they are accompanied by numerous other disruptions in neurochemical processes, brain functions, and behavior.

Prolonged use of alcohol and drugs can precipitate a neurotransmitter deficit severe enough to threaten the Organism's viability. As a compensatory mechanism, the body responds by upregulating catecholamine synthesis while suppressing the activity of metabolic enzymes, primarily monoamine oxidase (MAO) and dopamine beta-hydroxylase (DBH), the enzyme that controls The conversion of dopamine to norepinephrine. Thus, the catecholamine surge triggered by another dose of psychoactive substances, along with its accelerated and excessive degradation, is coupled with a compensatory enhancement in neurotransmitter synthesis. This establishes an accelerated turnover of catecholamines. Consequently, upon drug cessation—namely during withdrawal—the typical massive release of catecholamines from storage does not occur, but their accelerated synthesis persists. Due to altered enzyme activity, one specific catecholamine—dopamine—accumulates within biological fluids and Tissues (primarily the brain). It is this very process that drives the Development of the primary clinical signs of withdrawal syndrome: severe anxiety, tension, discomfort, elevated Blood pressure, tachycardia, various autonomic disorders, Sleep disturbances, and the onset of psychotic states.

The aforementioned alterations in neurochemical brain functions constitute the foundation for physical dependence on psychoactive substances.

Blood dopamine levels correlate closely with the clinical severity of withdrawal syndrome (WS); levels double the baseline are associated with severe withdrawal, while a threefold increase typically precipitates an acute psychotic state, specifically alcohol delirium.

Throughout the dynamics of remission in individuals with established physical dependence, typical fluctuations in dopamine levels are observed: in the early stages, dopamine is slightly elevated, after which it generally remains below normal. Evidently, the dopamine deficit within the brain's reward structures underlies the persistent pathological craving for drugs and alcohol, carrying a high probability of relapse.

During the course of remission, researchers have recorded biochemical correlates of so-called "dry withdrawal," wherein symptoms of withdrawal syndrome—such as insomnia, anxiety, irritability, and aches—temporarily recur against the backdrop of long-term remission. In these instances, a spontaneous elevation of blood dopamine has been detected, matching the NEUROCHEMICAL MECHANISMS OF acute withdrawal.

Acute alcohol intoxication (alcohol intoxication)

According to ICD-10, acute alcohol intoxication is a transient condition that occurs after alcohol consumption, causing disturbances or changes in physiological, psychological, and behavioral functions and responses. Since alcohol is a neurotoxin, these primarily involve Central Nervous system (CNS) functions. For practical convenience, it is best to divide these functions into mental, neurological, and autonomic categories.

Regardless of the severity of acute alcohol intoxication, all three mentioned functional spheres are impaired or altered, but first and foremost and to the greatest extent — the mental sphere. Therefore, in a purely clinical sense, alcohol intoxication can be defined as a psychopathological syndrome whose Structure depends on the dose of alcohol consumed, the time elapsed since its intake, as well as the biological and psychological CHARACTERISTICS OF THE individual subjected to intoxication. The degrees of alcohol intoxication represent stages in the dynamics of this psychopathological syndrome and are directly related to blood alcohol concentration.

Acute alcohol intoxication may manifest as simple alcohol intoxication, modified forms of simple alcohol intoxication, and pathological intoxication.

Simple alcohol intoxication

The aforementioned narrow clinical definition of alcohol intoxication as a psychopathological syndrome differs markedly from its less common interpretation as inappropriate behavior or a state in which "normal responses to the surrounding external environment change." The fact is that the exact same behavior can be adequate in some circumstances and inadequate in others. The assessment of behavior and its degree of appropriateness depend largely on the specific environmental conditions, and whether they are familiar or, conversely, extreme. For example, at very low blood alcohol concentrations, when there are no clinical signs of intoxication, drivers' skill levels decrease by 32%. It is easy to imagine that the degree of inadequate reaction will increase dramatically when dealing with ultra-high speeds and emergency situations. Conversely, during routine and unhurried human activity, finding any deviations in reactions after consuming, say, a Glass of beer is hardly possible.

Thus, the clinical diagnosis of simple alcohol intoxication, which is syndromal in nature, does not coincide with the assessment of behavioral appropriateness, which is usually carried out through special testing and on The basis of departmental instructions.

Although simple alcohol intoxication represents a mental pathology in a clinical sense, it is not considered such in a legal sense and does not release a person from liability.

Degrees of alcohol intoxication

By conventionally dividing cerebral functions into mental, neurological, and autonomic, we can assume even more conditionally that mild simple alcohol intoxication manifests primarily through mental disorders, moderate intoxication through The Emergence of obvious neurological disorders In addition to the mental ones, and severe intoxication through the disruption of vital autonomic functions. However, as already noted, all these functions are impaired to some degree even at the mild stage of intoxication.

Mild alcohol intoxication

Mild alcohol intoxication (blood alcohol concentration from 0.5 to 1.5 %o) is typically characterized by elevated mood, talkativeness, accelerated association processes, reduced self-criticism, increased amplitude of emotional reactions, attention instability, impatience, and other signs of mental excitation prevailing over inhibition. At the same time, certain neurological (impaired coordination of fine motor skills, nystagmus) and autonomic (facial flushing, tachycardia, accelerated Respiration, hypersalivation) disorders are observed.

Moderate alcohol intoxication

In moderate intoxication (blood alcohol concentration from 1.5 to 2.5 %o), mental reactions lose their liveliness, thinking becomes slowed and unproductive, speech becomes perseverative and slurred, attention weakens, and orientation in the surroundings is impaired. Understanding and correctly assessing what is happening around becomes sharply difficult. Emotional reactions coarsen, acquire a brutal character, and mood leans toward gloominess, irritability, or dull indifference. Gross neurological disorders emerge: ataxia, incoordination of movements, unsteady gait, dysarthria, and reduced pain and Temperature sensitivity. Facial flushing is replaced by cyanotic coloring and pallor; nausea and vomiting frequently occur.

Severe alcohol intoxication

Severe alcohol intoxication (blood alcohol concentration from 2.5 to 4 %) is expressed by suppression of consciousness — ranging from somnolence to coma, a passive body position, sometimes with aimless chaotic movements, lack of response to painful stimuli, pupil constriction, and sluggish pupillary light Reflexes. At higher blood alcohol concentrations, death from respiratory paralysis may occur.

The maximum tolerated concentration of alcohol is variable. While a blood alcohol concentration of 4 to 5 % threatens asphyxia in an individual unaccustomed to alcohol, patients with alcoholism at such body alcohol levels are often able to communicate and provide more or less coherent Answers TO QUESTIONS. A case has been described where a person remained alert and capable of participating in a conversation at a blood alcohol concentration exceeding 7.8 %o.

The duration of alcohol intoxication depends on many factors (gender, age, racial characteristics, tolerance to alcohol), but most of all on The amount of alcohol consumed and The rate of its metabolic breakdown. Normally, the amount of ethanol in the body decreases by 7-8 g per hour, whereas in patients with alcoholism, it decreases by 11-12 g.

Following moderate and especially severe alcohol intoxication, post-intoxication disorders are observed the next day over the course of several hours: headache, dizziness, tremor, malaise, thirst, abdominal bloating, nausea, vomiting, sweating, and palpitations. Work capacity is reduced to varying degrees depending on the individual characteristics of the person and The Nature of their work.

With age, as well as in The process of systematic alcohol abuse, the time required for full recovery to a normal state increases, while the disorders become more severe and diverse. With continued systematic alcohol abuse, a "symptom of well-being decompensation" is formed. In these cases, general well-being remains poor for 1-2 days after intoxication. The next stage may be the transformation of the post-Intoxication syndrome into alcohol withdrawal syndrome.

Modified forms of simple alcohol intoxication

The symptomatology of acute alcohol intoxication largely depends on the "terrain" upon which alcohol acts. The presence of a pathological terrain (psychopathy, consequences of prior brain illnesses and injuries, as well as the development of cerebral pathology) leads to the emergence of modified forms of alcohol intoxication. Among them, the following can be distinguished.

The dysphoric variant of intoxication is a state in which, instead of the euphoria characteristic of simple alcohol intoxication, a gloomy mood emerges from the very beginning, accompanied by irritability, anger, conflict behavior, and a tendency toward aggression. In other words, the mild stage of intoxication resembles its moderate stage in its emotional Background, meaning it essentially contains elements of a more severe condition. Such features of alcohol intoxication are frequently observed in patients with chronic alcoholism, as well as with various types of organic brain insufficiency.

The paranoid variant of intoxication is characterized by the appearance of suspiciousness, vulnerability, fault-finding, and a tendency to interpret the words and actions of others as an attempt to humiliate, mock, deceive, or gain the upper hand in rivalry; jealous feelings and associated aggression are possible. Such behavioral traits during intoxication are found in certain psychopathic personalities — paranoid, epileptoid, and primitive ones (especially if they suffer from chronic alcoholism).

Alcohol intoxication with hebephrenic features manifests as mischief, stereotypies, clowning, chaotic horseplay, monotonous echolalia, and senseless rampages. Such pictures can be observed in the presence of a latent schizophrenic process, as well as in adolescents and young adults.

Alcohol intoxication with hysterical features occurs when certain personality prerequisites are present (egocentrism, a craving to be the center of attention, a tendency to "exploit" the sympathy of others, a desire to make a striking impression, and ambition outweighing actual abilities. In such cases, acute alcohol intoxication triggers hysterical mechanisms that most commonly manifest as demonstrative suicide attempts, theatrical emotional reactions, violent outbursts of despair, "madness," and the like.

Pathological Intoxication

The term "pathological intoxication" does not quite accurately capture The Essence of this phenomenon: it represents not so much the result of alcohol intoxication as a manifestation of a peculiar idiosyncrasy to alcohol, which can arise under a specific combination of factors (fatigue, enforced sleep deprivation, psychogenic factors, organic cerebral insufficiency, etc.). Outwardly, the clinical picture of pathological intoxication bears little resemblance to typical drunkenness, as there are no impairments in stance and motor coordination, nor the characteristic pantomimic features typical of an intoxicated person.

Strictly speaking, pathological intoxication is a transient psychosis and, from a syndromological perspective, a twilight state of consciousness. Two forms are distinguished—epileptoid and paranoid—which differ in the predominance of specific disorders.

In the epileptoid form, pathological symptoms are represented by total disorientation, a complete lack of contact with the surrounding reality, acute motor agitation, an affect of fear, malice, and rage, accompanied by silent, senseless, and rigid aggression that occasionally takes the form of automatic and stereotyped actions.

In the paranoid form, the patient's behavior reflects delusional and hallucinogenic experiences of a frightening nature. This is indicated by isolated words, exclamations, commands, and threats, although speech on the whole remains sparse and barely intelligible. Motor activity is relatively organized, taking the form of complex, goal-directed actions (escaping using transport, defense, or attack, executed with immense force).

Pathological intoxication arises suddenly and subsides just as abruptly, frequently terminating in a deep sleep. It lasts from a few minutes to several hours, leaving behind asthenia, headaches, and total or partial amnesia. Complete amnesia is more characteristic of the epileptoid form, whereas partial amnesia—featuring fragmentary and sometimes vivid memories—is typical of the paranoid form.

Clinical Aspects of Alcoholism

General provisions, Definitions, Classification

Alcoholism is, first and foremost, a disease. Like any illness, alcoholism is a process with a beginning, stages, and an endpoint, and it progresses at varying speeds. Similar to other diseases, alcoholism emerges and develops as a combined (in varying proportions) result of environmental and biological factors.

Alcoholism is a chronic mental disorder caused by the abuse of alcoholic beverages, characterized by a pathological craving for Alcohol and the associated, progressively severe consequences of alcohol intoxication.

The premise contained in this definition regarding the two Components of the clinical picture of alcoholism implies that all clinical syndromes of the disorder—whether the neurasthenoid syndrome in The First stage, the withdrawal syndrome In the second stage, or personality degradation in the Third Stage—develop according to a single pattern: they are formed by a pathological craving for alcohol framed by various post-intoxication disorders. The reference to the increasing severity of the consequences of chronic alcohol intoxication as the disease progresses clearly reflects its progradient nature. Ultimately, differences in the severity and persistence of the consequences of alcohol intoxication form the basis of the stages of alcoholism, constituting the essence of the qualitative features of its individual stages.

Most dynamic classifications identify three stages of alcoholism under various names: the first, second, and third stages.

The dynamics of alcoholism are characterized not only by changing symptoms but also by the rate of these changes, which can be rapid or, conversely, barely noticeable. Accordingly, high, medium, and low rates of alcoholism progradience are distinguished, each of which is typically inherent to a particular patient from the outset. As it turns out, the varying rates of symptom development are closely linked to crucial parameters of the disease, such as heredity, premorbid status, the severity of the clinical picture, and curability. This underscores the necessity of including the rate of progradience among the classified features of alcoholism.

Since alcohol abuse in patients with alcoholism is a direct manifestation of a pathological craving for alcohol, its clinical forms also constitute essential characteristics of the disease. Distinctions among types of alcohol abuse are important from a practical standpoint, particularly regarding therapeutic strategies.

Clinical symptoms of Alcoholism

The signs of alcoholism are diverse and vary in Specificity, and consequently, in diagnostic value. Some of these signs, due to their optional nature, can hardly be called symptoms of alcoholism per se, yet they suggest the presence of alcohol-related problems: consumption of alcohol surrogates, cigarette Burns between the index and middle fingers, arcus senilis along the corneal margin, palmar erythema, facial puffiness and a cyanotic Skin tint, decreased cutaneous sensitivity in the distal lower extremities, lower limb Muscle weakness, painless hepatomegaly, and elevated mean corpuscular volume (MCV) of erythrocytes, along with increased plasma levels of triglycerides, uric acid, gamma-glutamyl transpeptidase, aspartate aminotransferase, Alanine aminotransferase, and others. These signs evolve into true disease symptoms and acquire diagnostic reliability when they appear as part of clinical syndromes whose definition and consistency are rooted in core pathogenetic mechanisms. Therefore, the Discussion below will focus on the cardinal clinical syndromes of alcoholism: pathological craving for alcohol, the alcohol withdrawal syndrome, and alcoholic degradation.

Pathological Craving for Alcohol

The conventional phrase "pathological craving for alcohol" seemingly implies the existence of a non-pathological, i.e., normal, craving for alcohol.

Unlike a normal desire, a pathological craving for alcohol is self-sufficient and serves as the dominant motive for behavior; consuming alcohol ceases to serve any purpose other than achieving a state of intoxication—meaning that alcohol intoxication becomes an end in itself. In this process, alcohol is consumed in quantities that preclude the successful execution of any other activity. It follows that a pathological craving for alcohol cannot be comprehended through common sense; it is psychologically incomprehensible, and various "motivational" explanations do not apply to it (of course, the transition from normal alcohol consumption to pathological forms does not happen suddenly, but through mutual alternation; we are referring here solely to the extreme manifestations of both).

A pathological craving for alcohol exhibits pronounced dominant properties, which means, among other things, that it takes precedence over other motivations, regardless of their objective importance and significance to the individual's core interests. As a result, alcohol is consumed not so much for a specific purpose, but in spite of numerous negative consequences—among them the disruption of sexual, social, and occupational relationships, legal conflicts, deteriorating health, and severe hangover states. The continuation of systematic alcohol drinking despite these circumstances remains the most reliable diagnostic criterion for a pathological craving for alcohol.

Against the backdrop of weakened cerebral functions—particularly higher mental functions associated with systematic alcohol intoxication—the dominance of the pathological focus that dictates the craving for alcohol in patients with alcoholism becomes indisputable and exaggerated. This provides a useful "hint" for formulating a rational therapeutic program aimed at suppressing the pathological craving for alcohol.

From the foregoing, the most critical clinical sign of alcoholism follows quite naturally: the loss of quantitative and situational control. The loss of situational control manifests as the individual's persistence in consuming alcohol in their habitual manner, disregarding external circumstances—inappropriate surroundings, a workday, potential negative consequences, and so on. Loss of control is a manifestational form of a pathological craving for alcohol.

It should be noted that loss of control does not always automatically stem from the presence of a pathological craving for alcohol: on the path toward extreme manifestations of control loss, entirely acceptable forms of alcohol consumption may still be observed episodically, though these subsequently become increasingly rare.

Behavioral manifestations of a pathological craving for alcohol, much like human behavior in general, are highly individualized. Nevertheless, a patient's actions invariably reflect this morbid craving in one way or another. The presence of a productive psychopathological radical underlying the craving for alcohol secures alcoholism's "legitimate" place among mental disorders.

Alcohol Withdrawal Syndrome

Alcohol withdrawal syndrome (AWS) is a complex of autonomic, somatic, neurological, and psychiatric disturbances that occur in patients with alcoholism following the cessation or sharp reduction of a more or less prolonged and heavy drinking bout.

Structure of AWS (Withdrawal Syndrome)

Many of the symptoms that make up the clinical picture of AWS—such as headache, dizziness, asthenia, malaise, thirst, coated Tongue, nausea, bloating, loose stools, elevated blood pressure, discomfort or pain in the cardiac region, and low mood—occur not only in patients with alcoholism, but also in individuals experiencing a hangover, that is, the period following alcohol abuse. Both within a simple hangover (post-intoxication) state and in patients with alcoholism (i.e., within AWS), these disturbances are more severe, diverse, and frequent the older the person is and the poorer their baseline somatoneurological status (which, in patients with alcoholism, is also a consequence of the severity and chronicity of the underlying disease). All of these disturbances are nosologically non-specific, although they constitute a significant proportion of the AWS structure.

At the opposite pole of the clinical picture of AWS are disturbances that fundamentally distinguish alcohol withdrawal syndrome from a post-intoxication state. These include a whole range of signs of secondary pathological craving for alcohol which, as already noted, is observed only in patients with alcoholism, becoming exacerbated under METABOLISM/18.html">The Influence of impulses from the body's internal environment associated with alcoholic and non-alcoholic intoxication. These include an intense desire to drink alcohol (to "take a Hair of the dog"), inner tension, irritability, dysphoria, depression, and motor restlessness.

An intermediate position between non-specific and nosologically specific disorders is occupied by disturbances primarily associated with chronic alcohol intoxication and, therefore, only relatively specific to patients with alcoholism. These include intermittent, superficial, and anxious sleep; vivid, disturbing, and frightening dreams; ideas of reference and guilt; hyperacusis; isolated auditory and visual hallucinations; hypnagogic hallucinations; significant tremor of the entire body or hands, and tongue; nystagmus, sweating, tachycardia, epileptic seizures, and others. Sometimes, when patients with alcoholism are very young and possess sufficient compensatory capabilities, and the disease is of relatively short duration, AWS symptoms are limited to a secondary pathological craving for alcohol and mildly expressed autonomic disturbances (sweating, tachycardia, enhanced dermographism). This has provided grounds for asserting that AWS is frequently absent in adolescents and during the early stages of alcoholism.

On the other hand, in some patients—even against the background of months of abstinence from alcohol—states occasionally arise that completely or partially replicate the picture of AWS. In these cases, the symptoms are also limited to signs of an exacerbated pathological craving for alcohol, now primary in nature ("dry withdrawal"), which testifies to the relativity of the distinction between Primary and secondary pathological cravings.

Thus, AWS consists essentially of two components: a group of signs of pathological alcohol craving that possess nosological specificity, and a variety of non-specific or marginally specific disorders that arise as a result of the toxic action of alcohol combined with other pathogenic factors, determining the individual features of AWS in a specific patient.

Clinical Variants of AWS (Withdrawal Syndrome)

On this basis, several clinical variants of AWS are distinguished, depending on the predominance of certain disturbances. The basic variant, present in any case of AWS but prone to "acquiring" additional symptomatology, is the neurovegetative variant (poor sleep, asthenia, lethargy, sweating, facial puffiness, poor appetite, thirst, dry Mouth, elevated or lowered blood pressure, tachycardia, finger tremor). If neurovegetative disturbances are accompanied by severe headache with nausea, dizziness, hyperacusis, sharp startling, fainting spells, and epileptiform seizures, we are dealing with the cerebral variant. If abdominal pain, nausea, vomiting, flatulence, loose stools, subicteric sclerae, angina pectoris, cardiac arrhythmia, and shortness of breath predominate, the visceral (somatic) variant of AWS is identified. The presence of pronounced mental disorders (suicidal thoughts and behavior, anxiety, fear, depression, dysphoria, ideas of reference and guilt, total insomnia, hypnagogic hallucinations, auditory and visual illusions, vivid "adventurous" dreams, confusional states with temporary disorientation in the environment) indicates the psychopathological variant of AWS.

The identification of different clinical variants is of substantial practical importance, as it points to the impairment of corresponding organs and systems and facilitates the Selection of differentiated restorative therapy.

Alcohol withdrawal syndrome occurs within 6 to 48 hours after the last alcohol consumption and lasts from 2–3 days to 2–3 weeks. Despite its transient nature, it is accompanied by severe pathogenic effects on vital organs and systems. In particular, Impairment of the Sympathetic division of the Autonomic nervous system and Excessive production of Adrenal Hormones damage brain Neurons, especially Cells of the hippocampus, which affects memory processes and the emotional sphere; a sharp increase in catecholamine levels exerts a toxic effect on the myocardium, manifesting as reduced contractility, arrhythmias, fibrillation, and frequently causing sudden death. This is reason enough to pay serious attention to the Diagnosis and treatment of AWS.

Alcoholic Degradation

All types of mental degradation, regardless of their nosological affiliation, share a common feature: intellectual decline. At the same time, they differ in their specific accents—on impaired critical judgment, memory loss, or decreased mental flexibility, among others. A hallmark of alcoholic degradation is the emphasis on moral and ethical decline: lightheartedness, weakening of conscience and a sense of duty, loss of diverse interests, egoism, parasitic tendencies, emotional blunting, shallowness, untruthfulness, and others.

It is important to note that, firstly, these traits manifest in patients with alcoholism very early, practically from the very onset of the disease, and secondly, they are relatively changeable and dynamic, undergoing significant, though incomplete, regression during remissions of alcoholism. It follows that moral and ethical decline constantly accompanies or is even directly linked to the presence and severity of the pathological craving for alcohol. This is all the more logical since signs of moral and ethical decline are an exact expression of the dominant Properties of the pathological craving for alcohol—that is, its reflection and aspect. Thus, the cardinal syndrome of alcoholism—pathological craving for alcohol—is incorporated into The structure of another crucial syndrome, alcoholic degradation, imparting nosological specificity to it.

Another component of alcoholic degradation—intellectual decline associated with the Toxic Effect of alcohol on brain neurons—appears comparatively late; it is proportional to the duration and severity of alcohol intoxication and the total volume of alcohol consumed.

Studies using pneumoencephalography and computed tomography have demonstrated that brain tissue atrophy is observed in patients with alcoholism in the late Stages of the disease. It manifests as an enlargement of the brain ventricles (indicating subcortical involvement) and sulci (the latter resulting from Cerebral Cortex atrophy). The cerebral cortex is more sensitive to the damaging effects of alcohol, as sulcal widening is noted not only in elderly patients but also in younger ones, whereas ventricular enlargement is observed only in the elderly.

Perhaps the mind-weakening process in alcoholism is caused not only by the direct action of alcohol on the brain, but also indirectly—via alcohol-induced liver damage, which in turn leads to toxic encephalopathy.

The disease process that ultimately leads to alcoholic dementia is manifested in the earlier stages of alcoholism by neurosis-like and psychopath-like disorders.

Neurosis-like disorders in patients with alcoholism differ from genuinely neurotic ones by the absence of psychogenic features, the predominance of asthenia, lower emotional intensity, less fixation on them, diffuseness, a multitude of distressing autonomic sensations that patients attempt to combat with alcohol. Initially, they demonstrate adequate social and occupational adaptation based on professional experience and knowledge, preserved social and personal connections, a system of alcoholic "alibis," and the exploitation of job specifics and work schedules. However, poor sleep, fatigue, impatience, inattention, irritability combined with a pathological craving for alcohol—all this determines the "formulaic" Nature of the work performed, the lack of creative search and striving for novelty, inattentiveness and negligence, passivity and laziness, indifference, evasion of family and household duties, and the loss of former hobbies and interests. Such behavioral and mental status traits are precursors to future decline and impoverishment of the personality in the event of further disease progression. This indicates a progression from neurosis-like disorders in patients with alcoholism in the first stage of the disease to alcoholic degradation with dementia in its third stage.

The same dynamics are observed in psychopath-like disturbances. They arise during the Initial Stages of alcoholic personality deterioration; throughout this process, various characterological traits that were once merely personal idiosyncrasies without disrupting psychological harmony become manifested, exaggerated, and exacerbated. As a result, personality anomalies emerge in individuals who were previously practically healthy. Psychopathization formed in this manner differs from genuine psychopathy by the imprint of general decline: thinking becomes unproductive, judgments superficial and standard, and the personality

—much more coarse and primitive.

Among psychopath-like patients with alcoholism, unstable, excitable, and hysterical personalities predominate. Epileptoid, asthenic, and schizoid personalities are less common.

Psychopath-like manifestations generally intensify during states of intoxication and hangover. Subsequently, with the deepening of the alcoholic mental defect, these psychopath-like personality changes smooth out, their distinct boundaries blur, giving way to the clinical picture of alcoholic encephalopathy.

Summarizing the review of the main clinical syndromes of alcoholism, it must be emphasized that a definite interrelationship exists between them: the first of these (pathological craving for alcohol) is incorporated into the STRUCTURE OF THE other two—AWS and alcoholic degradation—determining their nosological specificity. The remaining symptomatology in these two syndromes is nosologically non-specific or marginally specific, although it is formed as a result of alcohol intoxication.

Clinical Dynamics of Alcoholism

Stages of Alcoholism

The clinical dynamics and process-like nature of alcoholism manifest as distinct stages of the disease. These stages differ in their qualitative features and the severity of disorders. The degree of severity is characterized by progressive alcoholic degradation, which is not always apparent during a standard clinical examination. An important diagnostic tool in this regard is the evaluation of intoxication symptomatology in a specific patient—specifically, the identification of altered or atypical forms of intoxication. These emerge as a result of a "terrain altered by alcoholism" and serve as a harbinger of future persistent and overt personality changes. Furthermore, these altered forms of intoxication, while atypical for one stage of the disease, eventually become typical for subsequent stages.

The greatest diagnostic challenge is presented by the first (initial) stage of the disease: it lies on the borderline between illness and health, and this boundary is blurred due to the very gradual transition from mere alcohol abuse (social drinking) to pathological craving.

In Addition to a pathological craving for alcohol, the first stage of alcoholism is characterized by neurosis-like disorders, as well as Changes in the patient's behavior and social appearance.

The symptomatology of alcohol intoxication shifts toward a shorter duration and diminished intensity of euphoria; irritability, rudeness, aggressiveness, and fault-finding emerge. During intoxication, other premorbid personality traits are also exacerbated—such as a tendency toward boasting, egocentrism, vulnerability, and rigidity. A significant increase in alcohol tolerance is observed, being 2 to 3 times higher than the baseline level, which is associated both with enhanced ethanol metabolism and decreased sensitivity of neural tissue to it.

Already in the first stage of alcoholism, distinct changes in the functional state of peripheral nerves occur in all patients: electroneuromyography reveals a sharp decrease in Nerve Impulse Conduction velocity and amplitude.

Despite the absence of overt signs of alcohol withdrawal syndrome, all of this indicates the genuine existence of the first stage of alcoholism and underscores the need to improve early Diagnostics for this condition.

The Second Stage of alcoholism differs from the first by the presence of alcohol withdrawal syndrome. The secondary pathological craving for alcohol inherent in the structure of this syndrome alters the nature of alcohol abuse: regular hangover drinking increasingly leads to subsequent uncontrolled alcohol consumption and further daily drinking—thus forming binge or continuous patterns of alcohol abuse. Binge drinking episodes are facilitated by deepening emotional disturbances manifested as preceding depressive-dysphoric or depressive-apathetic states. The primary pathological craving for alcohol gradually loses its connection to external circumstances and becomes "biologized." Alcohol tolerance rises to its maximum, reaching 5 to 6 times the baseline level. Signs of moral and ethical decline and coarsening, which were previously observed mainly during intoxication, become noticeable. Psychopath-like states form or premorbid personality traits become exacerbated. In the clinical picture of alcohol intoxication, alongside the deepening of the changes noted in the first stage, an "organic" undertone appears: mental rigidity, aggression, affective brutality, and memory lapses during intoxication—manifested either as alcohol palimpsests (fragments of more or less blurred memories) or total memory loss regarding events that occurred during that time.

The third stage of alcoholism is characterized primarily by a mental deficit, the clinical picture of which is dominated by the absence of subtle emotions and the intensification of primitive ones, the disappearance of genuine attachments and interests, the prevalence and uncontrollability of lower drives, euphoria, lack of critical insight, inactivity, impairment of intellectual-mnestic functions, and other signs of alcoholic degradation. These are accompanied by various somatic and neurological disorders—polyneuropathy, cerebellar disorders, liver, pancreatic, and gastrointestinal diseases, among others—creating a clinical picture of general Aging and decline. Unlike the first two stages, alcohol tolerance decreases significantly; with a combination of severe and varied withdrawal symptoms, a constant need for a hangover, and low tolerance, the patient remains in a state of continuous alcohol intoxication. Its symptomatology is entirely devoid of euphoric coloring, at times resembling psychotic disorders—patients mutter incoherently, address unseen interlocutors, make threats, and gesticulate.

With this pattern of alcohol consumption, withdrawal symptoms appear blurred because they are combined with alcohol intoxication. If alcohol consumption is ceased or the dose is significantly reduced, the withdrawal syndrome proceeds very severely and includes pronounced psychopathological disturbances—fear, insomnia, illusory and hallucinatory disorders, ideas of reference, guilt, and persecution. Psychoorganic symptomatology is frequently observed in the clinical picture of the withdrawal syndrome—intellectual helplessness, elements of amnestic disorientation, impaired control over pelvic sphincters with involuntary urination, and possible epileptic seizures.

In some patients in the third stage of alcoholism, along with a decrease in tolerance to alcohol, the pathological craving for alcohol also diminishes; having lost its euphorigenic effect, it becomes merely a means to alleviate withdrawal symptoms. Therefore, once these disorders are overcome, persistent spontaneous remissions are possible, whereupon the patients' lives acquire a new meaning: concern for their deteriorated health, medical examinations, a fascination with various longevity recipes, and so on. Even when intellectual decline in patients with alcoholism reaches the degree of alcoholic dementia, its reversal can be observed with sufficiently prolonged abstinence from alcohol. In this case, the first clinical signs of improvement begin to appear within 3 to 6 months to 1 year of continuous sobriety. The reversibility of alcoholic dementia is of tremendous importance in shaping our understanding of the prognosis and treatment of patients with Stage 3 alcoholism.

As for the weakening of the pathological craving for alcohol alongside the deepening of the alcoholic mental deficit, this confirms a general psychiatric regularity according to which reproductive psychopathology at a certain stage is inversely proportional to the degree of negative mental changes.

Metalcoholic (Alcoholic) Psychoses

Metalcoholic (alcoholic) psychoses are psychotic states—diverse in their clinical picture (exogenous, organic, or endomorphic) and course (acute, protracted, or chronic)—that arise during the dynamics of the second and third stages of alcoholism.

Psychotic states typically develop not against the background of heavy intoxication, but several days after the patient has stopped consuming alcohol, meaning when alcohol is absent from the blood or its concentration is sharply reduced.

The primary cause for the development of psychoses is considered to be not so much the direct effect of alcohol on the brain, but rather Metabolic Disorders and the onset of intercurrent diseases. It is precisely in this regard that the use of the term "metalcoholic psychosis" is more justified. The development of metalcoholic psychoses is frequently preceded by additional somatic and psychological injuries.

The incidence of metalcoholic psychoses correlates most clearly with the level of alcohol consumption. It is believed that the higher the consumption, the higher the morbidity rates for alcoholic psychoses. On average, the frequency of metalcoholic psychoses accounts for about 10% of the total number of individuals suffering from alcoholism.

Pathogenesis of Metalcoholic Psychoses

Most studies on the pathogenesis of metalcoholic psychoses pertain to alcoholic deliria and encephalopathies. Meanwhile, the pathogenesis of other metalcoholic psychoses remains largely unknown. A major role is attributed to additional organic noxious factors and constitutional factors.

The leading pathogenetic factor in delirium tremens is the disruption of metabolic and neurovegetative processes. Liver damage leads to the impairment of its antitoxic and metabolic (protein, fat) functions. As a consequence, toxic damage to the central nervous system develops, primarily affecting its diencephalic regions, which in turn leads to a breakdown of neurohumoral compensatory mechanisms. The impairment of the liver's antitoxic function causes a disruption and slowing of alcohol oxidation processes. As a result of this vicious cycle, more toxic, under-oxidized transformation products are formed. Furthermore, because alcoholism is accompanied by hypovitaminosis (especially B Vitamins), disruptions arise in the metabolism of A number of Amino acids, notably glutamic acid, ultimately leading to increased excitability of The Nervous System. Another important factor drawing attention in the development of delirium is electrolyte metabolism disturbance, specifically the redistribution of potassium between cells and extracellular fluid. The triggering mechanism in the development of delirium is considered to be a sharp shift in internal Homeostasis—the development of withdrawal syndrome, compounded by somatic illnesses, possibly local Circulatory Disorders, and increased vascular permeability to toxic substances.

In the pathogenesis of alcoholic encephalopathies, alongside the disorders characteristic of delirium, an important place belongs to disturbances in vitamin metabolism, particularly a deficiency of vitamins B1, B6, and PP.

Among exogenous-organic injuries, The most significant are the consequences of TRAUMATIC BRAIN INJURIES and chronic somatic diseases. One cannot also deny a certain role of the hereditary factor, with which imperfections in homeostatic mechanisms may be associated.

Classification of Metalcoholic Psychoses

The classification of metalcoholic psychoses is based on their syndromological division, as this helps to correctly qualify the features of a specific pathological condition and apply appropriate therapeutic methods.

The main forms of psychoses include: 1) alcoholic delirium; 2) alcoholic hallucinosis; 3) delusional psychoses; 4) alcoholic encephalopathies; 5) alcoholic depression; 6) alcoholic Epilepsy; 7) dipsomania.

Alcoholic Delirium

Delirium (commonly known as delirium tremens) is a syndrome of altered consciousness characterized by arrays of pareidolias, stage-like visual hallucinations, and figurative delusions against a background of severe psychomotor agitation. The course of delirium unfolds against a backdrop of pronounced Affective Disorders, typically accompanied by an acute sense of fear.

The delirium symptom complex in alcoholism is conventionally used as a clinical model for exogenous psychoses.

Delirium is characterized by specific somatoneurological disorders: profuse sweating with a sharp, highly specific odor, hyperemia of the skin (especially on the face and neck), tachycardia, blood pressure fluctuations, ataxia, muscular hypotonia, hyperreflexia, and tremor (fine-amplitude and generalized). Autonomic and neurological disturbances appear before the onset of consciousness disorders and persist for quite a long time after their resolution. Characteristic Water-electrolyte balance disorders are also observed (dehydration, hyperazotemia, acidosis, decreased blood sodium and magnesium levels, etc.); blood test alterations (leukocytosis, a left shift in the leukocyte formula, accelerated ESR, elevated bilirubin levels, etc.); and low-grade (subfebrile) body fever.

Delirium is the most frequent psychotic form, accounting for half or more of all metaholcoholic psychoses. The first episode of delirium is usually preceded by a prolonged binge or continuous daily alcohol abuse lasting for months; subsequently, psychoses may occur even after brief periods of heavy drinking. The onset of alcoholic delirium often coincides with the development of acute somatic illnesses, injuries, or surgical interventions. Somatic distress almost invariably accompanies the development of psychosis. P. B. Gannushkin identified "somatogenic asthenia" as one of the most frequent preconditions for the emergence of delirium in general.

As noted by many researchers, the frequency of delirium cases increases with age. It is known that the later alcoholism begins to form, the sooner a patient develops delirium under otherwise identical conditions. Deliriums are classified According to the depth of altered consciousness accompanying the psychopathological disorders, the severity of somatoneurological disturbances, and their combinations; duration serves as an additional criterion for the psychosis.

"Classical Delirium"

Alcoholic delirium undergoes a series of successive stages in its development. As epidemiological studies show, the first episode of delirium most frequently develops no earlier than 7–10 years after the onset of the advanced stage of alcoholism.

Prodromal Period

In the prodromal period, which lasts from several days to several weeks, sleep disorders, nightmarish and frightening dreams, and fears predominate; a fluctuating affect in the form of timidity and anxiety is characteristic. Asthenic Complaints are constant. In 1/5 of the cases, the development of delirium is preceded by major and, less frequently, abortive epileptic seizures, which usually occur on the first or second day of the alcohol withdrawal syndrome (AWS). They are rarely seen on the 3rd or 4th day from the onset of AWS. Occasionally, delirium may develop following an episode of verbal hallucinations or an outbreak of acute sensory delusions. When diagnosing this condition, one should not forget that the prodromal period may be absent.

Stage 1

The mood changes present in the prodrome become increasingly noticeable, with a rapid shift of opposing affects: depression or anxiety and timidity easily give way to euphoria and causeless merriment. Patients are excessively talkative and restless (akathisia). Speech is rapid, inconsistent, and somewhat disjointed, and attention is easily distracted. Facial expressions and movements are lively, rapid, and sharply variable. Disorientation or incomplete orientation in place and time is not uncommon. Orientation to one's own personality is usually preserved even in the advanced stages of delirium. Patients exhibit psychic hyperesthesia—a sharp increase in receptivity to various stimuli, sometimes even indifferent ones. There are rushes of vivid memories, figurative representations, and visual illusions; episodes of auditory hallucinations in the form of akoasmas and phonemes occur, along with various elements of figurative delusion. Toward evening, all symptoms sharply intensify. Night sleep is disturbed, with frequent awakenings in a state of anxiety.

Stage 2

Pareidolias—visual illusions of a fantastic nature—join the symptoms of the first stage. They can be black-and-white or colored, static or dynamic. Hypnagogic hallucinations of varying intensity are characteristic. Sleep remains brief, accompanied by frightening dreams. A patient awakened on time cannot immediately distinguish a dream from reality. Hyperesthesia intensifies, and photophobia appears. Lucid intervals are possible, but they are short-lived. Oneiroid (dream-like) experiences alternate with states of relative agitation or torpor.

Stage 3

In the 3rd stage, complete insomnia is observed, and true visual hallucinations appear. Microscopic, mobile, multiple hallucinations—such as insects or small animals—predominate. Hallucinations in the form of large animals or fantastic monsters are significantly rarer. The affect of fear and anxiety prevails.

During delirium, the patient acts as an engaged spectator. Hallucinations are stage-like or reflect specific situations, can be singular or multiple, and are most often colorless. As the delirium deepens, auditory, olfactory, thermal, tactile, and general somatic hallucinations join in. The perception of time also changes; for the patient, it may seem to shorten or lengthen. Behavior, affect, and delusional statements correspond to the content of the hallucinations. Patients are restless and can barely stay in one place. Driven by the dominant affect of fear, patients try to run away, drive away, hide, shake something off themselves, swat or pick at things, and address imaginary interlocutors. Speech in this case is fragmented, consisting of short phrases or individual words. Attention is excessively distracted, the mood is extremely volatile, and facial expressions are expressive. Surprise, complacency, astonishment, and despair rapidly replace one another, but fear is the most frequent and constant presence. In delirium, delusions are fragmented and reflect hallucinatory disorders; their content is dominated by delusions of persecution, physical destruction, and, more rarely, jealousy or marital infidelity. Delusional disorders in delirium are not generalized; they are affectively charged, concrete, unstable, and entirely dependent on hallucinatory experiences.

Patients are highly suggestible. For instance, if a patient is given a blank sheet of white paper and asked to read what is written, they see text on the sheet and try to recite it (Reichardt's symptom); the patient engages in a long conversation with an interlocutor if handed a disconnected telephone receiver or any other object referred to as a receiver (Aschaffenburg's symptom). When pressure is applied to closed eyes and specific questions are asked, the patient experiences corresponding visual hallucinations (Lippmann's symptom). Signs of heightened suggestibility arise not only at the height of the psychosis but also at its very onset and after its resolution, when acute symptoms are no longer present. Thus, for example, persistent visual hallucinations can be induced in a patient even after the end of delirium by having them gaze at shiny objects (V. M. Bekhterev's symptom).

Another interesting point is that psychotic symptoms can diminish under the Influence of External factors, such as distracting moments or conversations with the doctor or medical staff. The awakening symptom is quite typical. Lucid intervals may also be observed in the dynamics of the 3rd stage, during which patients exhibit significant asthenic symptoms. Toward evening and at night, a sharp increase in the severity of hallucinatory and delusional disorders occurs, psychomotor agitation mounts, and anxiety may reach the level of raptus. By morning, this described state is replaced by a soporific sleep.

At this point, the development of delirium ends in the majority of cases. Recovery from the psychosis is typically critical—following a deep, prolonged sleep—though a gradual (lytic) recovery also occurs. Symptoms may resolve in a wave-like manner, alternating between the attenuation and resurgence of psychopathological symptoms, but now at a less intense level.

The patient's memories of the experienced mental disorder are fragmentary. They may remember (often in great detail) the content of the morbid experiences and hallucinations, but they do not remember and cannot reconstruct what was happening around them in reality or their own behavior. Partial or complete amnesia is observed.

The termination of delirium is accompanied by intensely expressed emotional-hyperesthetic weakness. Mood is volatile—tearfulness, depression, and elements of lability alternate with a causeless sentimental mood; asthenic reactions are mandatory. Following the resolution of the clinical picture of delirium, transitional syndromes are sometimes observed. These include residual delusions—an uncritical attitude toward the experience or isolated delusional ideas—as well as mild hypomanic (more frequently in men), depressive, subdepressive, or asthenodepressive states (more frequently in women).

The dynamic and structural-dynamic characteristics of the thought process are partially altered, but pronounced incoherence or thought disintegration is not observed. After emerging from the psychotic state, thinking is slowed and shows low productivity, but it remains fairly consistent and coherent. Manifestations of peculiar alcoholic over-inclusion (resonerstvo) and alcoholic humor are possible.

The course of delirium is generally continuous (in 90% of cases), but it can also be intermittent, featuring 2–3 attacks separated by "lucid intervals" lasting up to 24 hours.

The duration of alcoholic delirium typically ranges from 2 to 8 days, though quite rarely (in up to 5% of cases) it may persist for 7–10 days.

Alcoholic Hallucinosis

Alcoholic hallucinosis (hallucinatory insanity of drinkers, alcoholic hallucinatory delusion) is a meta-alcoholic psychosis characterized by the predominance of auditory verbal hallucinations and hallucinatory delusions occurring against the background of a clear, unclouded consciousness. According to many authors, it is the second most frequent meta-alcoholic psychosis. Hallucinosis develops no earlier than 10–14 years after the onset of full-blown alcoholism and is more commonly observed in women.

Hallucinosis is also classified according to its primary Clinical Features—the course and specific characteristics of psychopathological manifestations. Similar to delirium, the Clinical presentation of hallucinosis is divided into the following forms: "classic" (acute), abbreviated, mixed, and atypical. Based on its clinical course, it is categorized as acute, protracted (subacute), or chronic. The duration of acute hallucinosis is up to 4 weeks; subacute hallucinosis lasts from 1 month to six months; and chronic hallucinosis persists for more than six months.

Acute Hallucinosis ("Classic")

Acute alcoholic hallucinosis almost invariably begins following an alcoholic binge, against the backdrop of hangover-related disorders accompanied by anxiety symptoms, paranoid attitudes, autonomic dysfunction, and, in women, depressive disturbances. It is extremely rare for hallucinosis to develop directly during an ongoing drinking bout.

The symptomatology of acute alcoholic hallucinosis comprises genuine auditory hallucinations, their delusional interpretation, and an affect of fear.

The onset of the disease is typically acute. Prodromal symptoms such as restlessness, anxiety, depressed mood, and dizziness may persist for several weeks. The psychosis generally develops in the evening or at night. Patients are seized by intense restlessness; they either find it completely impossible to fall asleep or wake up terrified, drenched in sweat, after a brief and fitful sleep. Initially, auditory hallucinations are elementary: noise, clinking, crackling, rustling, whispering, shouting, or isolated simple words. Soon, they rapidly evolve into monologues, dialogues, and, in The final stage, polyvocal verbal hallucinosis consisting of a sequence of shifting scenes unified by a common theme. As a rule, the voices refer to the patient in the third person, though occasionally they address them directly. There are numerous voices, varying from quiet to a deafening roar. They speak simultaneously, intertwining, arguing, and swearing. The content of the hallucinations is distressing to the patient, consisting of various threats, accusations, and reprimands for past deeds, particularly excessive drinking and its consequences. The voices offer advice, argue, and discuss what to do with the patient and how to punish them. They may not only accuse but also defend the patient. Naturally, the patient is a witness to these disputes and sometimes becomes a participant. The topics discussed are always related to real events from the patient's current or past life. A rush of hallucinatory experiences can trigger brief periods of motor inhibition and detachment, which may be classified as phenomena of hallucinatory substupor or stupor.

Delusional ideas are closely linked in content to the hallucinations, making them fragmented, disjointed, and unsystematized. In full-blown hallucinosis, the prevailing affects are fear, anxiety, and despair. The patient is always an active participant in the unfolding events, and their behavior corresponds to the content of the hallucinations and delusions. In the first days of the illness, driven by delusions, the patient may feel "there is no way out of the current situation" or, when imperative voices dominate, may attempt suicide. Later, as anxiety becomes the primary affect, the patient attempts to flee, leading to severe motor agitation. In such states, patients frequently resort to desperate self-defense: they barricade doors, nail windows shut, disconnect communication lines, and set up private alarm systems, creating what is known as a "siege mentality." Often, patients begin to defend themselves by turning into aggressors, anticipating invisible enemies while arming themselves with sharp objects, cold steel, or firearms. At the next stage, the persecuted patient transforms into the persecutor. This can lead to unpredictable consequences, such as attacking random people "in self-defense," because everything in this state is interpreted as a threat. The frequency of maladaptive behaviors increases when delirium symptoms supervene, typically during the nighttime hours. However, over time, the patients' behavior may become sufficiently organized to mask their capacity for socially dangerous actions.

Unlike delirium, suggestibility is absent in alcoholic hallucinosis: it is impossible to convince the patient of the falsity of their delusional interpretations or situation, or to implant alternative hallucinations.

Alcoholic hallucinosis occurs against the background of an unclouded consciousness, as evidenced by intact orientation regarding their own personality—a crucial distinction from delirium tremens. Only upon thorough clinical and psychopathological examination can a certain degree of mental torpor be detected.

Patients recount the content of their morbid experiences quite accurately and in detail; external events are not erased from their memory either, and patients recall them almost flawlessly and sequentially. Memory is unimpaired in alcoholic hallucinosis, and confabulations are virtually absent.

The psychosis typically terminates critically, following a prolonged, deep sleep. When hallucinosis ends by lysis, the intensity of verbal hallucinations first decreases, then the affective charge subsides, and finally the delusional constructions fade. A critical attitude toward the experience does not emerge immediately; residual delusions may persist (more commonly in men), whereas women are more prone to subsequent depressive disorders. The duration of acute hallucinosis ranges from several days to 4 weeks.

Delusional Psychoses

The clinical manifestations of alcoholic delusional psychoses are polymorphic, characterized by extreme lability, fluidity, and dynamism of psychopathological symptoms, alongside a heightened vulnerability to endogenous and exogenous influences. The most common variants of delusional psychoses are alcoholic paranoid psychosis and jealousy-induced delusions.

Alcoholic persecutory delusion (alcoholic paranoid psychosis) is a meta-alcoholic psychosis characterized by the predominance of imaginative delusions, an affect of fear, motor agitation, and focal sensory disturbances, occurring as an attack of varying duration.

Prodromal symptoms last for 3–5 days, developing during the withdrawal phase, and are characterized by a depressed mood, malaise, an anxious-fearful affect, and disturbances in sleep and appetite. Autonomic symptoms (tremor, sweating, palpitations, etc.), which are also characteristic, intensify in the evening and at night. The psychosis itself develops against the backdrop of abstinence syndrome, typically following complete insomnia in the evening or at night. A state of bewilderment in patients gives way to acute terror and motor restlessness. Concurrently, ideas of reference emerge alongside elementary sensory deceptions such as tapping, rustling, coughing, footsteps, and the like, which are quite rapidly joined by fragmentary verbal hallucinations accompanied by persecutory delusions. The elaboration of the delusional plot depends on illusory-hallucinatory disorders: these serve as the foundation for delusions of poisoning, physical influence, and jealousy. Within the structure of the paranoid syndrome, alongside delusions of physical influence, isolated phenomena of psychic automatism appear, which are single-themed, fragmentary, and exceptionally unstable. Auditory pseudohallucinations that are simple and concrete in content are frequently observed.

In all cases of acute alcoholic paranoid psychosis, brief impulsive actions are noted: patients suddenly dash off, jump out of moving vehicles, plead for help, and so on. However, aggressive acts directed at imagined persecutors are rare. In the evening and at night, patients experience elementary visual illusions and hallucinations, while the full-blown clinical picture of psychosis, rich in psychopathological symptoms, persists for an average of 10 to 24 days. The resolution of the psychosis proceeds much more slowly, and the regression of psychopathological symptoms sometimes drags on for 1–1.5 months. Initially, the affect of fear diminishes, followed by the disappearance of psychic automatisms and auditory deceptions, and finally, the delusional ideas fade. These clinical variants of psychotic states are also united by the fact that alcoholic paranoid psychosis most frequently develops in a "travel Setting." A critical perspective on the past psychosis is not restored immediately and is accompanied by prolonged residual phenomena, post-intoxication asthenia, and symptoms of a psycho-organic personality defect.

Abortive alcoholic paranoid psychosis most commonly develops during drinking bouts while the patient is intoxicated. The clinical presentation resembles acute alcoholic paranoid psychosis, but the duration of such a psychosis is limited to just a few hours.

Protracted alcoholic paranoid psychosis. The transition to a protracted course is indicated by a transformation of affect and delusions. The affect of fear becomes less intense, and an anxious-depressed mood begins to dominate. The sensory-illusory component of the delusions also regresses, showing a degree of systematization: for instance, the patient begins to suspect specific individuals rather than everyone indiscriminately. The motives for persecution likewise become more concrete and defined. Outwardly, behavior appears normal, yet suspiciousness, mistrust, and poor rapport with the patient persist. It is sometimes difficult to distinguish residual delusions from prolonged paranoid psychosis—the presence of altered affect speaks in favor of the latter. Repeated drinking binges exacerbate the course of the paranoid state, and in such cases, the psychosis may become recurrent. The duration of the psychosis spans several months.

Alcoholic jealousy delusion (alcoholic marital infidelity delusion, alcoholic paranoia) is a chronic form of alcoholic delusional psychosis dominated by primary paranoid delusions. It occurs exclusively in males. It should be noted that acute forms of delirium and hallucinosis, in which erotic pathological experiences—including ideas of marital infidelity—occupy a leading role, are not classified as alcoholic paranoia. Nor does this form of psychosis encompass residual jealousy delusions of varying duration following resolved psychoses of another etiology.

The psychopathological assessment of paranoid disorders in alcoholism is complicated not only because thoughts of marital infidelity may stem from a real-life situation, but also due to the presence of specific premorbid traits and alcohol-induced personality changes in these patients. Individuals with certain character traits—predominantly hysterical and excitable, as well as those prone to forming overvalued ideas—are predisposed to developing paranoid delusions. These character traits become more pronounced during periods of alcoholic binges. The development of alcoholic paranoia may be preceded by acute alcoholic psychoses in the form of delirium and hallucinosis.

The Formation of the psychosis is gradual and step-like. At the initial stage, psychopathy-like disturbances escalate in the form of emotional tension and suspiciousness, against which ideas of reference and jealousy develop. General somatic and neurological disorders intensify; sexual dysfunction, a very characteristic symptom of long-standing alcoholism, also worsens. Heightened irritability and suspiciousness are further fueled by these factors. Subsequently, emotional disorders intensify in the form of anxiety and increased excitability; against this background of affective disturbance, ideas of reference and jealousy take ROOT. Patients are constantly gloomy, depressed, and tormented by painful doubts, sinking ever deeper into an imaginary world of distrust toward their wives and others. At this stage, if alcohol consumption ceases, ideas of reference and jealousy may smooth out, and relationships within the family and workplace can be restored. In the event of a relapse into alcoholism, these psychopathy-like disorders transform into paranoid delusions. The transition of these disorders into frank delusions is accompanied by a profusion of visual and auditory illusions, unfolding against an anxious-fearful affect and mounting emotional tension, followed by a loss of insight into the morbid symptoms. From this point on, the range of delusional ideas expands: ideas of persecution or poisoning (aimed at getting rid of the patient) join the delusions of jealousy and reference. The delusional experiences may also take on a retrospective character: patients claim that their wives have been unfaithful to them for many years, that the children were fathered by lovers, and so forth. Delusional experiences markedly impact patient behavior, manifesting as sophisticated forms of surveillance over the spouse, potential refusal to eat food prepared by the wife, and similar actions.

A defining feature of fully established paranoid delusions is the patient's absolute conviction in their wife's infidelity, her intentionally hostile attitude toward them, and a constant fear for their own life. Delusional ideas are concrete, marked by extreme absurdity, focused on domestic themes, and tend to expand the circle of imaginary lovers, accomplices, and persecutors. Patients do not exhibit withdrawal, detachment, or emotional coldness. Within the family, they are rude, egotistical, and display brutal persistence in their sexual demands toward the object of their jealousy; severe violence—primarily directed at the wife—is also possible. Occupational and social adaptation deteriorates, reflected in a narrowing of interests, a decline in work capacity, the inability to acquire new job skills, and a restricted circle of acquaintances.

The illness fluctuates in intensity and persists for years. The outcome of the disease is twofold: in some cases, organic-type personality changes progress (associated with co-occurring cerebral atherosclerosis), causing the delusional system to disintegrate; in others, under the influence of treatment, the delusional ideas merely lose their urgency, leaving behind intellectual-mnestic impairments.

Alcoholic encephalopathies

Alcoholic encephalopathies are a broad definition encompassing a group of non-alcoholic psychoses that typically develop during the course of stage 3 alcoholism. In encephalopathies, psychiatric disorders are invariably combined with systemic somatic and neurological disturbances, which play a leading role in the clinical picture. Men are affected more frequently.

Alcoholic encephalopathies are conventionally divided into acute and chronic forms. Although transitional variants may occur between them, they are of no decisive clinical significance. The set of baseline factors contributing to the development of alcoholic encephalopathies is as follows. The duration ranges from 7-10 to 20 years or more. Alcoholic encephalopathies most frequently develop in stage 2-3 or stage 3 alcoholism accompanied by prolonged binge drinking lasting for months, or by continuous alcohol consumption against the background of lowered tolerance. The poor quality of alcoholic beverages plays a major role in the development of encephalopathy. According to clinical observations, such patients frequently consume surrogates, fortified wines, and alcohol-containing liquids characterized by quite high toxicity.

The alcohol withdrawal syndrome is typically severe; psychopathological and, in particular, somatovegetative neurological disorders are pronounced to a significant degree, and the course of the hangover syndrome is prolonged. In half of the cases, epileptic seizures occur in the course of AWS in these patients. As a rule, alcoholic encephalopathy is not the first non-alcoholic psychosis experienced by the patient. In 50-65% of cases, the Anamnesis of this patient category reveals deliria of various structures. Naturally, as with other non-alcoholic psychoses, concomitant somatic diseases are present here. Most frequently, these include toxic hepatitis, gastritis, colitis, and PEPTIC ULCER DISEASE.

Alcoholic depression

Alcoholic depression (alcoholic melancholia) is a group of conditions that integrates depressive disorders varying in clinical picture and duration among patients with chronic alcoholism.

Depressive disorders typically emerge during the development of the alcohol withdrawal syndrome and may persist even after its cessation; slightly less frequently, they are observed following a prior delirium or hallucinosis. In the latter case, alcoholic depression can be attributed to Wernicke's transitional syndromes, representing the next stage of psychosis development accompanied by productive symptoms.

Today, a clear distinction is made between the development variants of affective pathology in patients with alcoholism: 1) the deepening of premorbid features with a tendency to form various affective disorders at the level of cyclothymia or affective psychosis; 2) secondary, "acquired" affective disorders, which serve as a sign of toxic brain damage and the formation of encephalopathy. In the first case, patients exhibit deeper and more intense affective disorders; vital components account for a fairly large specific weight; ideas of self-destruction and elements of depressive depersonalization are frequent. Suicide attempts may occur. In the second variant, shallow anxious depressions with hypochondriacal inclusions, tearfulness, and emotional lability predominate. Dysphoric depressions are also quite common in clinical practice. Patients complain of depressed mood and feelings of hopelessness, are tearful, but a short time later can be seen conversingly lively with ward neighbors. Psychogenic formations, hysterical and dysphoric manifestations, and exhaustion predominate in the structure of "alcoholic depression". The duration of these disorders ranges from 1-2 weeks to 1 month or more.

Alcoholic epilepsy

Alcoholic epilepsy (epileptiform syndrome in alcoholism, alcohol-epilepsy) is a type of symptomatic epilepsy that occurs in alcoholism and its complications.

To designate these disorders, the majority of authors use the term "alcoholic epilepsy", proposed by V. Magnan in 1859.

The most complete definition of alcoholic epilepsy was provided by S. G. Zhylin (1938; 1965): "Alcoholic epilepsy should be understood as one of the varieties of symptomatic and, specifically, toxic epilepsies, i.e., those forms in which it can be proven that every single seizure without exception is the result of intoxication, and in which the elimination of the intoxication factor leads to the disappearance of these seizures and other epileptic phenomena."

Dipsomania (true binge drinking)

Dipsomania (true binge drinking) is very rare. It is observed in individuals who do not suffer from chronic alcoholism. It was first described in 1817 in Moscow by the physician Salvatori. Hufeland in 1819 suggested calling this form of drinking dipsomania. It develops predominantly in psychopathic personalities, primarily of the epileptoid circle, in individuals suffering from manic-depressive psychosis, Schizophrenia, and also against the background of endocrine psychosyndrome.

The clinical picture consists of the following mandatory features. True binge drinking is preceded by a depressive-anxious mood background, a significantly pronounced dysphoric component; increased fatigability, poor sleep, restlessness, and a sense of fear may be noted. In other words, affective tension and charge are invariably present. An ardent, irresistible desire to consume alcohol arises. The components of alcohol craving (ideational, sensory, affective, behavioral, and vegetative) are expressed to a high degree. The craving for alcohol is so intense that the patient, despite any obstacles, starts drinking and continues until a severe degree of intoxication. Alcohol is ingested in A wide variety of forms and in enormous quantities—ranging from 1 to 2-4 liters. However, symptoms of intoxication are negligible or absent. During such a binge, the patient abandons work, all their affairs, and family. If away from home, they may drink away all their money and clothing. Appetite is absent, and the patient practically eats nothing. Many researchers note that dromomania may be observed during binges. The duration of this state ranges from several days to 2-3 weeks. The Termination of the binge is usually sudden, with a persistent disappearance of the craving for alcohol, most often accompanied by an aversion to it. A gradual reduction in alcohol doses, as occurs in pseudobinge, is not observed. Following the excess, mood often improves, accompanied by tireless activity. This fact, according to many authors, indicates a connection between binges and altered affect. The binge may end in prolonged sleep; partial amnesia of the binge period is sometimes noted. During "lucid intervals", patients adhere to a sober lifestyle and do not consume alcoholic beverages.

Course, pathomorphosis, and prognosis of non-alcoholic psychoses

Psychoses in alcoholism can occur either once or repeatedly. The recurrent development of psychoses is caused by only one reason—continued abuse of alcoholic beverages. However, a reverse relationship is not traced: a suffered psychosis may be the sole occurrence even if alcohol consumption continues.

In the same patient, alcoholic psychosis may run its course now as delirium, now as auditory hallucinosis, or as paranoid state. Such clinical observations undoubtedly indicate the close affinity of the "independent" forms of alcoholic psychoses.

The type of course of alcoholic psychosis and the subsequent prognosis are largely determined by the following factors: the severity of alcoholic encephalopathy, the Features of the constitutional background, and additional exogenous damaging factors.

The occurrence of single alcoholic psychoses depends entirely on chronic alcohol intoxication, in particular on the duration of "binge" periods. Single psychoses are more characteristic of stage 2 alcoholism, with a lesser severity of alcoholic encephalopathy. As a rule, in this case, deliria are observed with a fairly deep clouding of consciousness, auditory hallucinosis with symptoms of delirium tremens, on the one hand, and the transitoriness of clinical symptoms, on the other. The clinical picture of experienced single psychoses (deliria and hallucinoses) virtually lacks mental automatisms, elements of Kandinsky-Kram bộ syndrome, as well as deceptions of perception of erotic content, jealousy delusions, and imperative hallucinations. The above-mentioned features of the psychopathological structure of past psychoses are regarded as prognostically favorable. Thus, given compliance with the aforementioned clinical features, the probability that the alcoholic psychosis will be single, without a tendency toward further relapse, is very high.

Alcoholic psychoses with an unfavorable protracted course develop, as a rule, in stages 2-3 and 3 of alcoholism, during intermittent or continuous forms of alcohol abuse, against the background of significant personality degradation of the alcoholic type. Constitutional factors—premorbid personality Anomalies of the paranoid and schizoid circle—also play a considerable role. Prognostically unfavorable signs include: the inclusion of complex hallucinatory-paranoid phenomena and systematized delusions in the clinical picture of psychosis; the presence of jealousy ideas in the psychopathological structure of delirium or hallucinosis; and the appearance of deceptions of perception of erotic content.

In the dynamics of alcoholic psychoses, a firm regularity is revealed: with the progression of alcoholism and the increasing severity of alcoholic encephalopathy, the clinical picture transforms in the direction from deliria to hallucinoses and delusional states. The "endogenization" of the clinical picture and the increasing dominance of schiziform psychopathological disorders are accompanied by a decrease or even disappearance of the "obligate" syndrome of exogenous psychoses—clouding of consciousness. In these cases, Differential diagnosis with schizophrenia can be very difficult.

When psychoses are added, the subsequent course of alcoholism becomes more severe: the progredience of the disease increases, remissions become shorter, and relapses become longer and more severe.

Past alcoholic psychoses undeniably intensify the manifestations of alcoholic encephalopathy. First and foremost, this is evidenced by a decline in professional qualifications, as well as the commission of antisocial acts and unlawful deeds.

Clinic of substance use disorders and addictions

DEFINITIONS. TERMINOLOGY. GENERAL CLINICAL MANIFESTATIONS

Drug addiction (substance abuse) is a collective group of chronic disorders characterized by a pathological craving for various psychoactive substances (PAS), altered tolerance, the development of dependence on them, and profound medical and social consequences.

The high significance attached to the detection, treatment, and prevention of drug addiction (substance abuse) is determined by the following factors:

1. High mortality rates among individuals suffering from drug addiction (substance abuse), caused by PAS overdoses, accidents while in a state of drug (toxic) intoxication, various somatic diseases resulting from drug use, and frequent suicides.

2. Severe medical consequences of abusing narcotic drugs or other PAS: somatic and neurological complications, as well as personality changes.

3. The social «contagiousness» of drug addictions, which can spread like epidemics and affect wide segments of the population.

4. High criminogenicity among drug-dependent patients, primarily associated with personality changes and moral-ethical deterioration. Alongside criminal acts committed to acquire drugs, drug users frequently commit socially dangerous acts due to psychotic states resulting from substance use.

In domestic narcology, it is customary to distinguish between drug addiction (narkomaniya) and substance abuse (toksikomaniya). Narcotics refer to psychoactive substances that, firstly, exert a specific effect on the central nervous system (sedative, stimulating, hallucinogenic, etc.), which prompts their repeated non-medical use; secondly, the non-medical use of these substances reaches socially significant proportions; and thirdly, they are included in a special legally regulated list of narcotics, meaning they are recognized as narcotics by law. Thus, the term «narcotic drug» encompasses three criteria: medical, social, and legal. The absence of any of these criteria does not provide grounds to classify a given PAS as a narcotic drug, even if the substance can become an object of abuse and induce dependence. The diagnosis of «drug addiction» is applied exclusively to the abuse of specific PAS that are officially recognized as narcotics. This necessitated the Introduction of the term «substance abuse» (toksikomaniya) into the terminology of narcological disorders. Substance abuse is a condition caused by the abuse of a psychoactive substance not included in the list of narcotics, i.e., not recognized as a narcotic by the state. From a legal standpoint, patients with Drug Addiction and substance abuse constitute different cohorts. From a clinical and medical perspective, the approach to both groups is identical, and their treatment principles are the same.

In narcological practice, diagnostic concepts may undergo transformation. If a substance not included in the list of narcotic drugs is abused and diagnosed as substance abuse, and this substance is subsequently added to the list of narcotic drugs, the diagnosis transforms accordingly: a diagnosis of «drug addiction» is established, while the clinical picture remains unchanged.

When classifying the population according to their attitude toward narcotic drugs, the following groups can be distinguished (E. A. Babayan, 1988):

1. The main body of the population, comprising individuals who do not use narcotic drugs.

2. Legitimate drug consumers — individuals who use them for medical indications.

3. Individuals who abuse narcotic drugs. Any use of narcotic drugs, regardless of quantity, without a physician's prescription constitutes abuse.

Individuals who abuse PAS are categorized as follows:

a) «experimental» individuals who, for various motives, consider it acceptable to try the effects of a particular narcotic drug;

b) occasional consumers who episodically use narcotic drugs to achieve a known effect — occasional users;

c) regular consumers, from whom a certain proportion of individuals eventually develops drug addiction (substance abuse).

The diagnosis of «drug addiction» or, accordingly, «substance abuse» is established only when clinical signs of the disease are present. If the illness has not yet fully developed and only single or irregular use of narcotics or other psychoactive substances is observed, the case is classified as abuse without a dependence syndrome.

When formulating a diagnosis, it is necessary to specify the exact narcotic (or non-narcotic) substance abused by the patient. If an abuser transitions from one psychoactive substance to another, the diagnosis must be modified to correspond to the substance last used.

When two or more narcotic drugs are used simultaneously or in a specific sequence, and dependence has formed toward each of them, the diagnosis of «polydrug addiction» is established. In cases where dependence has developed toward a narcotic drug simultaneously with another substance not recognized as a narcotic (i.e., not included in the drug list), the condition should be diagnosed as «complicated drug addiction».

The International Classification of Diseases, 10th Revision, does not make a distinction between drug addiction (narkomaniya) and substance abuse (toksikomaniya). All substances subject to abuse are designated as «psychoactive substances». Ten groups of psychoactive substances causing «mental and behavioral disorders» are identified: alcohol; opioids; cannabinoids; sedatives and hypnotics; cocaine; other stimulants, including caffeine; hallucinogens; tobacco; volatile Solvents; and the concurrent use of drugs and other psychoactive substances. Each type of abuse features additional characteristics reflecting the patients' condition. Thus, this classification relies solely on the specific effects of various psychoactive substances, i.e., medical and clinical criteria. The legal criterion is not taken into account here.

Disorders resulting from the concurrent use of drugs and other psychoactive substances (polydrug addiction or complicated drug addiction in our understanding) include «only those cases where the pattern of drug use is chaotic and indeterminate, or where the effects of various drugs are inextricably mixed».

When coding a diagnosis according to ICD-10, in addition to the primary code, the letters «T» (substance abuse) or «N» (drug addiction) must be added.

The foundation of drug addiction and substance abuse development is euphoria — the subjective positive effect resulting from the action of the consumed substance. The term « euphoria», as used in narcology, is not entirely appropriate and does not correspond to the psychopathological concept of euphoria, which is defined as «an elevated, good-natured mood combined with lightheartedness and an insufficient critical assessment of one's condition». Euphoria associated with the use of narcotic and other intoxicating substances is characterized not only by an uplifted emotional background, lightheartedness, and a benevolent mood, but also by specific psychic and somatic sensations, and in some cases, alterations in thinking, perceptual disturbances, and varying degrees of impaired consciousness. It is more accurate to speak of intoxication with a specific intoxicating agent or, alternatively, of drug-induced intoxication. However, since the term «euphoria» is well-established in domestic narcological literature, we deem it appropriate to retain it. Each narcotic exhibits its own unique profile of euphoria, which will be described in greater detail in the sections dedicated to specific types of drug addiction.

During initial drug intakes, protective reactions may occur in the form of unpleasant sensations such as itching, nausea, vomiting, dizziness, and profuse sweating. With subsequent drug administrations, these reactions disappear.

During the process of drug addiction, the quality and intensity of euphoria change. At a certain stage, even increasing the dose of the drug no longer produces the desired effect, and euphoria as such disappears. The drug is used solely to restore work capacity and vitality, and to prevent the development of withdrawal syndrome.

Researchers distinguish between "positive" and "negative" euphoria (I. N. Pyatnitskaya, 1994). Positive euphoria is the state observed during the initial stages of drug use. Negative euphoria, seen in chronic drug users, is a state of intoxication where drugs merely alleviate subjectively severe sensations and discomfort, without producing any pleasant feelings.

The quality of euphoria depends on the route of administration, being most pronounced with intravenous injection. The nature of euphoria can be altered by external interventions and depends on the physical and psychological state of the individual who has taken the drug, including their emotional background and somatic condition. For certain forms of substance use disorders, the psychological set or expectation regarding the expected effect is crucial (e.g., in cannabis and barbiturate use disorders).

The clinical presentation of substance use disorders (addictions) is characterized by three main syndromes:

1. Psychological dependence.

2. Physical dependence.

3. Tolerance.

Psychological Dependence

Psychological dependence is a compulsive urge to continuously or periodically take a drug or other psychoactive substance in order to experience certain desired sensations or to relieve symptoms of psychological discomfort.

Psychological dependence occurs in all cases of systematic drug use, but it can also develop after a single intake. It is a powerful psychological factor that promotes the regular use of drugs or other psychoactive substances, hinders the cessation of drug use, and causes relapses of the disease.

Psychopathologically, psychological dependence is manifested by a pathological craving to alter one's state through drug use. A distinction is made between psychic (psychological, obsessive) and compulsive craving.

Psychic craving is characterized by persistent thoughts about the drug, often having the character of a monoidea, accompanied by elevated mood, excitement in anticipation of taking it, as well as depression and dissatisfaction in the absence of the drug. Since thoughts about the drug often have an obsessive nature, this has given some authors reason to define psychic craving as obsessive. Psychic craving may be accompanied by a conflict of motives and partial critical insight, but it can also be unconscious, manifesting as changes in the patient's mood and behavior depending on the abused substance. Psychic craving can be constant, periodic, or cyclical, and may be triggered by situational or psychogenic factors.

Compulsive craving is characterized by an irresistible urge for drug use, totally consuming the patient's drive to obtain the drug; it may be accompanied by narrowed consciousness, a complete lack of critical insight, and dictates the behavior, actions, and motivation of the patients. At its peak, compulsive craving may be characterized by psychomotor agitation. The specificity of symptoms is lost in this type of craving, and the clinical picture becomes common to all types of substance use disorders. The patient's individual personality traits disappear, and The behavior of drug users becomes similar regardless of individual premorbid personality features and social attitudes. Compulsive craving is characterized not only by psychopathologic disorders, but also by somatoneurological ones: mydriasis, hyperhidrosis, dry mouth, hyperreflexia, and tremor.

Compulsive craving can manifest in the following ways:

1. Outside of intoxication, specifically: a) within the structure of withdrawal syndrome; b) in remission, when it inevitably leads to relapse.

2. During intoxication, when at the peak of intoxication patients experience an irresistible desire to "top up" with the drug (known as "chasing the high" in drug slang). This type of compulsive craving is observed in certain forms of addiction, such as barbiturate and ephedrine dependence. Compulsive craving during intoxication is frequently accompanied by a loss of control and can lead to overdose.

Physical Dependence

Physical dependence is a state of restructuring of all the body's functional activity in response to the chronic use of drugs or other psychoactive substances. It is manifested by pronounced physical and psychological disturbances when drug use is stopped or when its effect is neutralized by specific antagonists. These disturbances are referred to as "withdrawal syndrome", "deprivation syndrome", or abstinence syndrome. They are alleviated or completely relieved by a new administration of the given drug or a substance with a similar pharmacological action. Physical dependence is a potent factor in reinforcing the impact of psychological dependence on the continuous use of drugs or in returning to use after cessation.

The clinical manifestations of withdrawal syndrome vary across Different types of substance use disorders. The timelines for the development of physical dependence (withdrawal syndrome), as well as its duration, also differ depending on the type of addiction, the rate of drug use, the doses used, and the route of administration. Withdrawal syndrome does not develop all at once, but over a certain period of time, accompanied by a sequence of symptom appearance characteristic of the specific type of addiction.

Sometimes, outside of drug intake—several weeks or even months after cessation—patients with opioid addiction may exhibit symptoms characteristic of acute withdrawal syndrome, a state known as pseudo-abstinence ("dry" withdrawal). Pseudo-abstinence typically leads to the activation of pathological drug craving and contributes to relapses.

Physical dependence (withdrawal syndrome) does not develop during the chronic use of all narcotic substances.

Tolerance. Altered Tolerance

Altered tolerance refers to a state of adaptation to narcotic or other intoxicating substances, characterized by a reduced response to the administration of the same amount of the drug. A higher dose of the substance is required to achieve the previous effect.

Some time after the onset of regular drug use, the initial dose ceases to produce the desired effect, and the patient is forced to increase the dose. Subsequently, this dose also becomes insufficient, and the need for its increase arises, leading to a rise in tolerance. At this point, the drug user's body can tolerate doses that significantly exceed therapeutic levels and, in some cases, are lethal to a healthy, drug-naive person. In opioid users, for example, tolerance may exceed the physiological level by 100–200 times. Increasing tolerance is accompanied by the suppression of protective reflexes (disappearance of vomiting, coughing, etc.). Increased tolerance may manifest as an increase in single doses and a higher frequency of drug intake, with drugs being used at shorter intervals.

Tolerance Plateau. At a certain stage, tolerance reaches its maximum and remains constant for a long period. During this period, the patient takes the highest doses of the drug for them. Further increases in dosage no longer induce euphoria, but may lead to overdoses.

Decreased tolerance. In patients with a long History of the disease, a period arrives when they can no longer tolerate their previously high doses of the drug and are forced to reduce the dose. Euphoria is no longer achieved, and increasing the dose leads to overdose. Sometimes patients artificially lower their dose to cope more easily with withdrawal symptoms if they decide to interrupt their drug use. Moreover, after a period of abstinence, lower doses of psychoactive substances can once again induce euphoria (known in drug user slang as "rejuvenating").

Cross-tolerance is a phenomenon where tolerance developed to one substance extends to other drugs that the patient has not previously used. This occurs with the concurrent use of two or more psychoactive substances. The most striking example of cross-tolerance is seen when individuals with chronic alcoholism begin abusing sedatives, particularly barbiturates or tranquilizers. They initially exhibit an extremely rapid increase in tolerance to sedatives. Sometimes, individuals with a history of chronic alcoholism can initially tolerate higher doses of barbiturates and tranquilizers than drug-naive individuals who do not suffer from alcoholism.

The development of drug addiction is determined by four factors:

1) the patient's personality characteristics;

2) the individual sensations derived from consuming the intoxicating substance;

3) socio-cultural characteristics;

4) the pharmacodynamic properties of the substances consumed.

The course of substance use disorders (addictions) exhibits certain general patterns. The formation of dependence is preceded by a stage of episodic, occasional use of psychoactive substances. During this period, there is no fixed rhythm of drug use, nor is there an increase in tolerance. As for psychological dependence, it generally develops some time after the onset of episodic use, though in some cases it appears after just the first few attempts, facilitating continued drug use.

Subsequently, a distinct rhythm of drug use is established; drugs are taken regularly, and tolerance begins to rise, although physical dependence has not yet formed. This period corresponds to the initial (first) stage of addiction.

As drug use continues, tolerance increases and physical dependence develops. By this point, tolerance reaches its maximum, marking a plateau phase. In this phase, the quality of euphoria changes. This is the onset of the fully developed (second) stage of the disease. With prolonged drug use, patients can no longer tolerate the high doses they used to take. Tolerance decreases. Euphoria as such no longer occurs. Administration of the drug merely maintains the organism in a more or less comfortable state. The nature of the withdrawal syndrome changes, with somatoneurological disorders becoming most prominent. This represents the final (third) stage of addiction.

Abuse of Different Types of Drugs

Opiates

This group of drugs includes morphine, heroin, codeine, synthetic analgesics such as pethidine, methadone, as well as homemade opium preparations derived from the opium poppy, which are most commonly used in Ukraine. These drugs produce the desired effect of euphoria, but they also cause analgesia, respiratory depression, constipation, decreased appetite, and low libido. They can be administered orally, intravenously, or via inhalation (smoking). Heroin is the most widely used among these drugs, possessing a particularly potent euphoric effect. Although some individuals use heroin periodically without developing dependence, systematic use, especially intravenous administration, rapidly leads to the development of dependence.

Tolerance develops rapidly, accompanied by a swift escalation in doses. Upon cessation of drug use, tolerance decreases again. This drop in tolerance can be dangerous and sometimes fatal—for instance, as a result of respiratory depression if, after a prolonged break, drug use is resumed at the same dose that was taken when use was interrupted during a hospital stay or imprisonment.

Withdrawal symptoms include intense drug craving, sleep disturbances and insomnia, muscle and joint pain, lacrimation and rhinorrhea, hyperhidrosis, abdominal cramps, nausea, diarrhea, piloerection, dilated pupils, increased heart rate, and impaired thermoregulation. For individuals abusing heroin, withdrawal symptoms typically appear approximately 6 hours after the last dose, peak at 36–48 hours, and then subside. Although withdrawal symptoms are subjectively distressing and drive the patient to intensely seek the drug, they are rarely life-threatening unless the patient has underlying serious psychiatric disorders.

The Course of Opiate Dependence

After 7 years of abuse, only about 1/4 of opiate-dependent individuals have ceased opiate use, while approximately 10–20% have died from causes related to drug use. Fatalities most frequently resulted from accidental overdose—often linked to lowered tolerance following a period of abstinence—as well as from HIV infection.

Pregnancy and Opiate Dependence

Children born to opiate-dependent mothers are significantly more likely than other children to be premature and have low birth weight. They may also display signs of neonatal abstinence syndrome, including irritability, restlessness, tremors, and persistent crying. These symptoms appear within a few days of birth if the mother used heroin, but are delayed if she used methadone, which has a longer half-life.

Subsequently, these children tend to be hyperactive and emotionally unstable. It remains unclear whether this is a consequence of the unfavorable home environment created by such mothers or the prolonged prenatal exposure to the drug.

Treatment of Opiate Dependence

Management of Crisis States

Heroin-dependent individuals may seek medical help during a crisis under three sets of circumstances.

First, when their drug supply is exhausted, patients may request prescriptions for narcotic drugs, demanding them outright or directly simulating some medical disorder. Although withdrawal symptoms are extremely unpleasant, they are generally not dangerous for an individual without pronounced somatic disorders. Therefore, it is preferable not to prescribe the drug unless it is the first step in a coordinated treatment program (in Ukraine, physicians are legally not authorized to prescribe heroin or certain other narcotics as a therapeutic agent for drug addicts).

The second type of crisis situation is a drug overdose, which requires treatment specifically aimed at preventing respiratory depression, a characteristic effect of the drug.

The third form of the crisis involves complications from intravenous drug use, such as acute local infection, injection-site necrosis, or distant organ infections, most commonly affecting the heart or liver.

Scheduled Opioid Cessation (“Detoxification”)

The General principles of drug cessation were outlined above. Following heroin cessation, psychological support is particularly crucial. In Western countries, pharmacological management typically involves substitution therapy with methadone (a longer-acting drug).

Treatment Outcomes

Despite intensive treatment, the peak incidence of relapse occurs within the first year. Clinicians must be prepared for these setbacks, continue helping patients mitigate the harms associated with intravenous drug use, and stand ready to offer renewed support whenever patients express a desire to overcome their addiction.

Tranquilizers and Sedatives

The most severe medical complications stem from barbiturate abuse; although rarely prescribed for medical purposes anymore, barbiturates remain widely available as "street drugs." Currently, benzodiazepines are the most frequently abused psychoactive substances.

Barbiturates

Barbiturates are administered both orally and intravenously. Some patients, particularly middle-aged and older adults, become dependent on barbiturates originally prescribed as sleeping aids many years prior. Younger individuals often use barbiturates illicitly; some engage in the dangerous practice of injecting the contents of oral capsules, which carries a high risk of local complications such as phlebitis, ulcers, abscesses, and gangrene.

Symptoms of intoxication resemble those of Alcohol poisoning, characterized by slurred, incoherent speech, drowsiness, and depressed mood. Younger intravenous users are often unkempt and disheveled. A valuable diagnostic sign, nystagmus, can frequently be detected.

Laboratory evaluation should include urine toxicology screens to rule out the simultaneous use of other psychoactive substances. Blood barbiturate concentration testing is useful primarily in cases of acute overdose. Tolerance to barbiturates develops, albeit not as rapidly as to opioids.

Over time, the margin between the intoxicating and toxic doses narrows significantly, increasing the risk of accidental, fatal overdose.

Abrupt cessation of barbiturates can trigger a withdrawal syndrome whose symptomatology closely mirrors alcohol withdrawal, carrying a high risk of seizures. In chronic users of long-acting barbiturates, withdrawal symptoms may be delayed for several days following the last dose; consequently, monitoring must be prolonged to ensure no dangerous complications arise. Barbiturate withdrawal begins with restlessness, agitation, disturbed sleep, anorexia, and nausea, and may progress to disorientation, tremors, hallucinations, vomiting, hypotension, and—most critically—seizures. Without treatment, this condition can be fatal.

Patients who have stopped using barbiturates should be immediately referred to an inpatient facility, unless their dosage was minimal.

Benzodiazepines

Intoxication symptoms are similar to those seen in barbiturate poisoning. Tolerance and dependence develop with prolonged, continuous use. While the exact timeframe for dependence development remains unknown, a 6–8 week period is widely accepted as the threshold for safe use without dependency risks.

The withdrawal syndrome associated with benzodiazepine abuse is analogous to that of barbiturism, marked by irritability, restlessness, anxiety, nausea, heightened sensitivity, and somatic symptoms such as tremors, hyperhidrosis, headaches, and myalgia. Seizures are less common, though they may occur with high-dose benzodiazepine use. During medically supervised tapering, the dosage is reduced gradually. Withdrawal symptoms are generally less pronounced with long-acting agents compared to short-acting ones.

For this reason, some clinicians switch patients from a short-acting drug to an equivalent dose of a long-acting agent prior to initiating withdrawal. The dosage is then tapered gradually, typically by 0.5–2.5 mg per week for diazepam or equivalent amounts of another benzodiazepine. If withdrawal symptoms emerge during the taper, the dose may be temporarily increased and then reduced again, but by smaller increments than before. Some practitioners utilize liquid formulations (such as diazepam elixir or nitrazepam syrup) to facilitate cessation. Clonidine is occasionally prescribed to mitigate withdrawal severity, though most patients do not require these additional measures. Anxiety management techniques help alleviate the stress caused by withdrawal symptoms.

Psychostimulants

Amphetamines and cocaine are the most frequently abused psychostimulants: amphetamine sulfate is taken orally and intravenously, while cocaine hydrochloride is typically insufflated (snorted).

These drugs induce euphoria, hyperactivity, logorrhea, insomnia, anorexia, and dryness of the oral and nasal mucosa. Physical signs include mydriasis, tachycardia, and elevated blood pressure; high doses may precipitate Cardiac Arrhythmias and vascular complications. Patients occasionally report abnormal tactile hallucinations, such as the sensation of insects crawling beneath the skin.

Chronic high-dose use of these substances can precipitate a psychosis characterized by delusions resembling paranoid schizophrenia, persecutory delusions, auditory and visual hallucinations, and, at times, aggressive behavior. This state typically subsides within 1–2 weeks of drug cessation, though it occasionally persists for several months.

Tolerance is not a characteristic feature of psychostimulants. The withdrawal syndrome is mild, consisting primarily of depressed mood and fatigue; consequently, physical dependence is questionable, although psychological dependence undoubtedly develops.

Overdose management requires sedation along with the correction of hyperthermia and cardiac arrhythmias. Psychotic symptoms can be managed with neuroleptics.

Hallucinogens

This group of drugs includes synthetic compounds such as lysergic acid diethylamide (LSD) and dimethyltryptamine, as well as naturally occurring substances found in certain species of mushrooms. Both synthetic and natural anticholinergic drugs are also used to induce hallucinogenic effects.

Drugs cause distortion or intensification of sensory perception, sometimes with a "cross-over" between sensory modalities so that, for example, sounds are perceived as visual sensations. Objects may blur or move rhythmically, time seems to pass slowly, and ordinary sensations appear to carry profound significance. Body schema may seem distorted, or individuals may feel as though they are outside their bodies. These experiences can be euphoric, but at times they are deeply disturbing and lead to unpredictable and dangerous behavior. The somatic effects of hallucinogens are variable; LSD can lead to an increased heart rate and dilated pupils.

Phobias experienced by patients are typically managed with anxiolytics such as diazepam. Neuroleptics are also effective, but medications with pronounced anticholinergic effects (such as chlorpromazine) are not recommended if the patient has ingested an anticholinergic drug like benzhexol or phencyclidine.

Memories of the sensations experienced during intoxication persist for weeks and months. Because these experiences can be terrifying, some patients require anxiolytic therapy.

Methylenedioxymethamphetamine (MDMA) is an amphetamine derivative known as "ecstasy" and classified as a hallucinogen; it is used to reduce social anxiety and enhance aesthetic pleasure.

Phencyclidine (PCP) ("angel dust") is a synthetic hallucinogen with particularly dangerous consequences. Intoxication can be prolonged and hazardous, accompanied by agitation, aggressive behavior, hallucinations, nystagmus, and elevated blood pressure. High doses may cause ataxia, muscle hypertonia, convulsions, and, in severe cases, an adrenergic crisis resulting in cardiac arrest, vascular complications, or malignant hyperthermia. Chlorpromazine should be avoided during treatment as it can exacerbate anticholinergic effects. Haloperidol or diazepam is recommended instead.

Cannabis

Cannabis, derived from the plant Cannabis sativa, is consumed in two forms. Dried vegetative plant parts form marijuana ("weed"), while the resinous secretions of the female plant's inflorescences serve as the basis for hashish resin. In some countries, cannabis is used as widely as alcohol in the West. In developed Western countries, cannabis use is illegal yet quite widespread.

The effects of cannabis depend on the dose, user expectations (suggestibility), and social setting. Much like alcohol, cannabis elevates mood or induces euphoria or dysphoria. It fosters a sense of enhanced appreciation for aesthetic experiences and distorts the perception of time and space. Somatic effects of cannabis include conjunctival injection, dry mouth, and tachycardia.

Cannabis does not lead to a withdrawal syndrome and, although psychological dependence may develop, physical dependence does not occur. There is still no consensus regarding the potential onset of psychoses against the background of cannabis abuse. Some patients develop acute psychosis upon consuming large quantities of cannabis, yet recovery is rapid after discontinuation of the drug. In such cases, it remains unclear whether cannabis was the direct cause of the psychosis or if it merely triggered psychotic symptoms of a different etiology. Fortunately, this ambiguity is of little practical significance, because regardless of the genesis of the psychosis, the therapeutic strategy remains unchanged: drug use must be halted; if psychotic signs do not resolve within a week, chlorpromazine or another antipsychotic is prescribed.

Volatile Solvent Abuse

Organic solvents are abused primarily by adolescents, usually as an occasional experiment. Serious problems arise in the minority who abuse solvents regularly. Any user can cause accidental overdose, leading to asphyxiation during administration.

Cleaning fluids, glues, aerosols, and occasionally gasoline and other substances are most frequently used for abuse.

The substance is inhaled from a partially closed container—where concentration can build up—by evaporating it from a soaked fabric or a plastic bag. Solvent intoxication resembles alcohol intoxication: slurred speech, disorientation, uncoordinated movements, nausea, and vomiting occur. Some users develop hallucinations, typically visual and often terrifying. The effects of solvents begin and end similarly to those of alcohol. Psychological dependence develops rather quickly, but the development of physical dependence is questionable. Individuals engaged in long-term, intensive solvent use commonly develop psychotic states.

A number of solvents exert neurotoxic effects, resulting in peripheral neuropathy and cerebellar disorders. Overdose can be fatal, resulting directly from the effects of the substance: asphyxiation or aspiration of vomitus.

Medical and Social Consequences of Substance Dependence

Personality and Behavioral Disorders

Among the medical consequences of chronic intoxication with drugs or other psychoactive substances, the characteristic personality changes in patients immediately draw attention. In the mechanisms underlying personality pathology in substance-dependent patients—as in personality development in general, which is an integrative characteristic of an individual's psychological and behavioral traits—a significant role is played by their upbringing and socialization processes, as well as the motivational system driving their activity. This system forms on the basis of a complex of needs, including those arising from the dynamics of the illness.

In the most general terms, the development of an addictive personality type is conditioned by the patient's entry into a new social environment, accompanied by profound personality transformations resulting not only from this process but also from pathological central nervous system alterations caused by chronic intoxication.

According to L. S. Vygotsky (1958; 1960), whose views are widely reflected in psychological literature, The entry of individuals (patients) into a dysfunctional social niche leads to characteristic personality changes. This process goes through phases of adaptation, individualization, and integration. Adaptation occurs first—the assimilation of norms and values active within the group, the mastery of appropriate (in this case, for the addict) means and forms of activity and specific skills, and thereby, to some extent, the individual's assimilation with other members of the same community (the drug-using environment), meaning addicts come to resemble one another in their behavior. Next comes the phase of individualization, characterized by the search for means and methods to define one's individuality under new circumstances: combined or concurrent use of various psychoactive substances, individual increases in doses, boasting to the group about one's "adventures" and proficiency in acquiring drugs, Special Methods of distributing them, The ability to vividly describe the state of a "high" and thus attract heightened attention from others. The integration phase is determined by the contradiction between the patient's desire to be ideally represented by their specific traits and differences in a normal environment (family, school, university, work, physicians), on the one hand, and the need of the drug-subculture community to accept, approve, and cultivate only those addictive traits that genuinely contribute to the patient's degradation.

In the process of chronic drug use, a gradual mental desolation occurs, accompanied by a decline in interests and an impoverishment of emotions. Even in the early stages, patients exhibit a drop in activity, which primarily affects socially positive directions of activity. When it comes to acquiring drugs or obtaining the means to purchase them, however, patients become extraordinarily active and resourceful.

Moral and ethical decline within the structure of the "addictive" personality is characterized as follows. Patients are intensely egotistical. Their own interests take precedence (concern solely for themselves), alongside an urge to avoid discomfort. A characteristic trait is dishonesty. Virtually all addicts use deception as a means to obtain what they want. They deceive their parents, begging for money for drugs while demonstrating incredible agility and a certain kind of artistry. They deceive medical staff, attempting to conceal attempts to smuggle prohibited medications, narcotic substances, or alcohol into the hospital setting. They seek to leave the ward during exacerbations of drug craving; if successful, they carefully attempt to cover this up by inventing elaborate stories: "I need to go to a funeral, a close friend's memorial, my mother's hospital, my lawyer," etc. During outpatient visits, they meticulously mask a relapse of drug use by employing various medications: instilling atropine into their eyes, taking tranquilizers, or consuming light alcoholic beverages (beer). They evade urine drug screening by failing to bring samples to the laboratory while offering deliberate falsehoods ("I accidentally broke the vial"), asking healthy individuals to provide urine samples on their behalf, or diluting them with water. They deceive not only relatives, doctors, and nurses, but also their fellow "comrades in misfortune." Above all, they deceive themselves, refusing to dwell on the consequences of the disease and constantly swearing by everything imaginable that "this time is the last."

When interacting with others, patients strive to make a good impression and often display ostentatious self-confidence. They exaggerate their financial and sometimes physical capabilities, and may behave defiantly or familiarly, lacking appropriate personal boundaries. In terms of appearance, untidiness and neglect, or conversely, bizarre clothing, hairstyles, and behavior, frequently attract attention. Conflicts frequently arise with relatives and medical personnel. In such instances, patients may behave rudely, sometimes even obscenely, expressing outrage in harsh terms without emotional control, resorting to slang, profanity, and occasionally physical violence. In personal life and family relations, sexual promiscuity, indifference toward children, lack of care for them, and absence of responsibility for their future are frequently observed. Patients show no drive to provide financial stability for the family; instead, they evade the need to work by all means possible, occasionally resort to theft, most often live off relatives, and lead a parasitic lifestyle. Quite often, they commit reckless acts, take important decisions lightly, or prove entirely incapable of independently resolving even minor problems.

A volatility of interests is traceable: patients frequently change their hobbies, workplaces, or fields of study over short periods. They drop out of their studies, citing a loss of interest in their previously chosen major. Their professional level gradually declines. Many patients show little interest in their own future destiny. In all their failures, they tend to blame others—parents and other close relatives, work colleagues, educators—while making no effort themselves to rectify the situation. When committing socially unacceptable acts, patients frequently feel no remorse, and insight into their own condition is sometimes entirely absent.

Thus, in all patients, regardless of the type of drug consumed, a moral and ethical decline develops in the course of chronic drug use. Its characteristic features include egoism, dishonesty, posturing, parasitic tendencies, frivolity, indifference to one's own fate, brutality, volatility, inconsistency, arbitrariness, ostentatious self-confidence, instability of intentions, poor emotional control, attempts to evade responsibility, blaming others for one's failures, a propensity for parasitism and a dissolute lifestyle, cynicism, cruelty toward loved ones, obscene and rude antics, impudence, lack of boundaries, blunting of parental feelings—including the loss of the maternal instinct—blunting of professional duty, and sexual promiscuity. An inflated self-esteem is noted alongside an inability to cope with difficulties, challenges in adapting to the environment, and heightened dependence on adults or relatives. At the same time, There is a total lack of insight regarding drug use.

The severity of moral and ethical personality deterioration is significantly influenced by premorbid factors, as well as the type of drug used and the duration of its abuse. During periods of remission, the prominence of personality degradation symptoms may regress, but they resurge following a "slip" or relapse.

Personality changes develop gradually, beginning with the accentuation of premorbid character traits. Subsequently, as drug abuse continues, distinct psychopath-like disorders emerge, characterized by the aforementioned profound moral and ethical decline, emotional and judgmental impoverishment, decreased activity, intensified affective disturbances, diminished and lost working capacity, social maladaptation, and the formation of character defects. Concurrently, cognitive and mnestic impairments (varying in form and severity) become increasingly noticeable.

The development of psychoorganic syndrome in patients with substance use disorders combines impairments associated with transient or permanent brain dysfunctions. Brain dysfunction can be primary—stemming directly from cerebral pathology caused by the Direct impact of a pathogenic agent on brain tissue—or secondary, resulting from a disease of any other organ or organ system that consequently impairs cerebral functions.

The rate of onset, severity, and psychopathological presentation of psychoorganic syndrome depend on the type of psychoactive substance, duration of drug use, premorbid background, and other factors.

Psychoorganic syndrome develops most rapidly in patients who inhale organic solvent vapors; next are those who abuse preparations made from ephedrine and ephedrine-containing mixtures. In cannabis abusers and individuals with opioid dependence, it develops over a more protracted timeframe. The syndrome forms more quickly in patients with an earlier onset of drug use across all forms of dependency, as well as in those whose premorbid state reveals congenital or residual symptoms of central nervous system organic insufficiency. The most pronounced cognitive and mnestic impairments are observed in patients abusing barbiturates and other sedatives: in the terminal stages of these forms of substance dependence, a state of organic dementia is observed.

Characteristic manifestations of cognitive and mnestic impairments in patients with substance use disorders include: mental torpidity, poverty of imagination, impairments in immediate and mediated memory, the motivational component of memory, and the dynamics of mnestic activity, and less frequently, weakened fixation and reproductive memory. Patients exhibit primitive judgment and an inability to analyze, synthesize, and extract the main points. During conversation, they tire quickly, struggle to concentrate, and fail to follow the flow of discussion attentively; sometimes they cannot recall specific moments of their lives, forget the current topic of discussion, and repeatedly ask for clarification; they are also prone to distraction and shifting to other topics. Complex situations frequently leave patients at a loss, causing bewilderment as they attempt by all means to shield themselves from the newly arisen problem.

It should be noted that cognitive and mnestic impairments are transient in nature. As follow-up (catamnestic) studies show, prolonged cessation of drug use leads to a significant improvement in cognitive and mnestic functions, although their complete recovery is not observed.

Peculiar affective disorders also arise during periods of remission: the dysphoric symptom complex gradually shifts to a depressive state, and subsequently (after 2-4 months or more) to an apatico-abulic state. The less time that has elapsed since the abatement of withdrawal symptoms, the more pronounced the dysphoria and explosiveness; conversely, the further removed the patient is from withdrawal, the lower the explosiveness, accompanied by a more prominent sense of gloom, apathy, abulia, and incapacity for work. Patients become completely idle, carefree, frivolous, uninhibited, at times unruly, with fickle intentions. It is noteworthy that against the backdrop of a constant desire for independence and a pursuit of material goods, patients do nothing to earn a living. As previously mentioned, they clearly exhibit a propensity for an idle lifestyle and parasitism.

Thus, in all patients, regardless of the type of drug used, as drug addiction progresses, individual personality traits become blunted, patients increasingly resemble one another, and a distinct addict personality defect is formed. The latter is characterized by escalating affective disorders in the form of dysphoric or apatico-abulic depressions, affective lability, a predominance of hystero-excitable reaction patterns, psychosocial dysfunction manifested by a gradual fading of interests, various anomalies of the emotional-volitional sphere, drive disorders—including sexual disinhibition—along with existing moral-ethical decline and cognitive-mnestic disorders that may be transient in nature. Overall, all these factors unite patients in terms of personality changes into a single group that can be classified as an "addict personality." The presence of cognitive-mnestic decline, characteristic affective disturbances, exhaustion, fatigue, asthenia, and inactivity can be assessed as an organic lowering of the personality level accompanied by desocialization, or as a distinct psychoorganic syndrome that developed as a result of the illness and varies in severity among patients with different forms of substance dependence.

Social consequences of substance use disorders

For the most part, patients neither work nor study. A large proportion of them are involved in criminal structures or engaged in various forms of commerce. As the disease progresses, almost all patients with opioid, heroin addiction, and polydrug addiction experience a decline in their professional level, and their labor activity becomes substandard. Among employed patients, repeated violations of labor discipline are observed, along with difficulties in fulfilling professional duties and an attitude of indifference or negativity toward the work performed.

Typical negative social consequences of drug abuse include the deformation, distortion, and destruction of family ties. Addicts marry significantly less often than healthy individuals of the same age, and their families quickly disintegrate unless the spouse is also a drug addict. Frequently, patients form a so-called addict "family." The purpose of such a "family" is drug use in the safest possible environment and facilitated access to drugs. The "family" has its own "home," which may be an empty apartment, a basement, an attic, or some isolated building. Such a "family" has its own means and methods of procuring drugs and the money to pay for them. Sexual relations, ordinary promiscuity, and not infrequently homosexuality are possible within the "family." For instance, pairs of heroin addicts often use the drug together to enhance sexual activity. Over time, drug use—rather than sexual drive or other joint interests unrelated to drugs—becomes the primary factor determining relationships in such "families."

In most families of patients who remain married, disruptions in family relations are noted—frequent conflicts, quarrels, sexual debauchery, indifference toward children and family, lack of care for loved ones, and a consumerist attitude toward them. Most often, family conflicts arise on the grounds of drug use. Children in such families are predominantly raised apart from their parents.

Female drug addicts frequently exhibit promiscuous Sexual Behavior; among them, the percentage of sex workers is extremely high, despite the suppressive effect of heroin on sex hormone synthesis and the weakening of libido. Female drug addicts have a greater number of sexual partners compared to men, are more frequently drawn into prostitution, and continue street-level work solely to sustain their drug supply.

Women suffering from drug addiction are affected more profoundly on a personal and social level because their role as a mother or potential mother is incompatible with the lifestyle of a drug addict.

Antisocial behavior is characteristic of patients with drug addiction. Their actions frequently contradict legal or moral norms. They are prone to criminally unpunishable yet immoral actions (drunkenness, venality, sexual debauchery, conflicts within the family and immediate environment). They often cultivate immoral habits, thereby creating adverse situations for themselves and their loved ones, and inadequately assess their capabilities, which negatively impacts interpersonal relationships.

Drug-dependent patients frequently commit aggressive acts, often in violation of the law, displaying hostility or malice ranging from verbal insults to the use of crude physical force to demonstrate superiority over another person or group of individuals. Most often, their affective outbursts arise psychogenically and are characterized by turbulent emotional and autonomic manifestations—anger, elation, anguish, fear, or anxiety.

Criminogenicity among patients with drug addiction is extremely high. Sooner or later, every consumer turns to increasingly criminal methods of acquiring the financial funds necessary to purchase drugs. This circumstance explains the high level of crime and other social anomalies among drug addicts.

Except for cases of conviction under Criminal Code articles concerning the manufacture, possession, and sale of drugs, crime among drug addicts is dominated by fraud and theft of personal (rather than state or public) property. This is because such crimes require fairly organized actions of which drug addicts are largely incapable.

The criminogenicity of patients with substance use disorders is determined by a range of factors: the need for money, as drugs are extremely expensive; forced association with drug dealers, which is also an unlawful act; and the aforementioned personality changes resulting from drug use, manifested in pronounced moral and ethical decline. Furthermore, drug addicts may commit unlawful acts while under the influence of drugs or in a psychotic state caused by the use of a particular intoxicating substance. Most offenses are committed while intoxicated, most frequently during withdrawal, as well as during periods of economically or socially induced remissions.

A wide range of various offenses committed by patients has been described. These include professional offenses: drug addicts fail to fulfill employment contracts and repeatedly commit various violations within their profession. These include criminal offenses that pose a danger and inflict harm on society and individuals (inflicting harm on health and life, property theft, etc.). These include administrative offenses (misdemeanors) manifested in encroachments on established public order and the rights and freedoms of citizens. Patients violate traffic regulations and customs control, and encroach upon the activities and property of private or legal entities, and so on. Finally, these include economic offenses—such as illegal entrepreneurial and banking activities, tax evasion, knowingly false advertising, smuggling, and counterfeiting money and documents. It should be noted that offenses are most frequently committed by patients with opioid (heroin) and cocaine addictions, and less frequently by those with hashish and Other forms of drug addiction.

Such, in brief, are the general medical and social consequences of chronic consumption of narcotic or other psychoactive substances.