Acute endogenous psychosis. Part 5

Italian psychiatrists are experiencing great uncertainty regarding acute atypical psychosis. Although they recognize the classification of Kraepelin’s psychosis, with regard to acute psychoses with confusion, Italian psychiatrists are closer to the French. As a result, some of the acute atypical psychosis is included in the framework of mental confusion (episodic twilight states of Kleist, Meduna one-point fermentation, periodic amentia, delirium acutum). With respect to other atypical schizoform psychosis, the authors’ efforts are directed at resolving the issue of their belonging to schizophrenia or manic-depressive psychosis.

Nobile and Sciorta (1953) divided “autonomous” and “mixed” psychoses into three groups:

1) cases in which there is a schizophrenic picture with elements of manic-depressive psychosis. Options: episodes of manic arousal and depression with schizophrenic elements; cyclical forms of schizophrenia; delusional forms with a rich affect (for example, fantastic parafrenia);

2) atypical pictures that can not be attributed either to schizophrenia or to manic-depressive. psychosis (states of inhibition, some manic and depressive states, polymorphic delusional episodes);

3) atypical pictures of manic-depressive psychosis (pictures mostly manic-depressive with schizophrenic elements).

Giannini (1959) divides the “mixed” psychosis into 4 groups: circular attacks with an outcome to dementia; alternation of episodes of clearly schizophrenic and more typical circular; combination of schizophrenic and circular symptoms in one attack; circular schizophrenia without outcome in dementia.

Gregoretti and Gasparone (1961) believe that acute delusional psychosis can be divided into a form with a delusion of interpretation and into a psycho-sensory-interpretative form. Deep anxiety and a narrowing of the field of consciousness are characteristic of all forms. Nosologically, these psychoses are unclear.

Fiume and d’Avossa (1959) described a similar psychosis called “oneiric syndromes”. In their opinion, these psychoses are characterized by the fact that hereditary readiness and psychogenic provocation play a decisive role in their occurrence. Psychopathologically, there is hyper-acidity of consciousness and its affective narrowing, arousal, quickly turning into a stupor, “pendulum transfer from the real world to the world of hallucinations”, fluctuation of affect, loss of temporal-spatial connections of experienced events. This “presence and non-presence in the world” gives rise to disorientation and secondarily delusional mood. The prognosis of the disease is very favorable. The authors attribute these “syndromes” to atypical schizophrenia. In another work – Giannini and Del Carlo Giannini (1959), on the contrary, believe that they should be attributed to atypical manic-depressive psychosis.

A great interest in these psychosis has been shown for many years. Scandinavian psychiatrists. The works of Langfeld (1939, 1961) and his collaborators on the division of “schizophrenia” into procedural and combined groups of “schizoform” psychoses are known. For these works, the desire is primarily with the help of the follow-up check to separate schizophrenia from schizoform psychosis.

Welner and Stromgren (1958) call these psychosis benign schizophrenia and attach great importance to the effects of nonspecific factors, and especially psychogenias. In addition to reactive (paranoid, depressive, confused) psychoses, it is assumed that “schizoform psychosis” sometimes includes true schizophrenia, atypical manic-depressive psychosis, and some organic psychoses (Stromgren, 1965).

In the works of Astrup, Possum and Stolmboe (1963), Astrup and Noreik (1966), “functional psychosis” was subjected to clinical and catamnestic, clinical and genetic studies, the study of prognostic factors, etc. Acute atypical psychosis is located between schizophrenia and manic-depressive psychosis. They are grouped around two diagnostic concepts – “schizoform” and “reactive” psychoses of depressive, paranoid, hysterical and confused types.

For the designation of individual types of attacks, either the terms of the Kleist – Leonhard school (various cycloid psychosis, unsystematic schizophrenia, etc.), or more general concepts: depression, agitation (mania), confusion, paranoid, hebephrenic, catatonic, were used.

The concepts of “schizoform” and “reactive psychosis” used by Scandinavian psychiatrists, as shown by their own tests, do not have a clear content. In a large number of cases [in 37% ‘of Astrup, Dalgard, Itolmboe (1967)] reactive psychosis, a follow-up revealed schizophrenia. The study of the frequency of diagnostic errors revealed some of their decline (Holm-boe, Noreik, Astrup, 1968).

The famous Dutch psychiatrist Rumke (1958) paid attention to the clinical division of pseudochemophrenia. Separating pseudo-schizophrenia from true schizophrenia, the author divides them into atypical circular psychosis, degenerative psychosis, paranoid psychosis, “acute outbreaks in schizoids, and occasional delusions of degenerants” (he refers to pseudoshizophrenia as organic psychoses).

In US psychiatry, the clinical side of these psychoses has been little studied. Some studies recognize the separation of schizophrenia into classical early dementia and reactive schizophrenia (Bellak, 1958). In the manual on psychiatry edited by Arieti (1959), these psychosis are mentioned when describing catatonic and schizoaffective forms of “schizophrenic reaction”, manic-depressive psychosis (acute parafrenia, delirium acutum), paranoid reactions (acute delusional psychosis). Polatin (1964) among atypical forms of schizophrenia describes: 1) acute states of confusion, characterized by sudden onset disorder of orientation and confusion. When they are observed “dreaming experiences and the similarity of the clinical picture with delirium.”

The author considers the clinical type of such psychosis to be transient, so-called “three-day schizophrenic reactions”, observed in the military during the war, some postpartum psychosis. In these attacks, psychomotor disorders (stupor or agitation), hallucinations and illusions also occur. These psychosis can be provoked; 2) “micro-catatonia”, which is “a periodic or cyclic form of schizophrenia with unreal experiences, special behavior and a sudden exit with almost no personality change”; 3) schizoaffective psychosis. Depressive psychosis in a broad sense. At the beginning of attacks to 30 years can not make a prediction.

A group of authors (Wada, Tanaka, Ogasavara and Sacu-rada, 1963), who agree with the concept, divides atypical psychosis into 3 groups: the first group is characterized by a pronounced disorder of consciousness, acute hallucinatory-delusional disorders, a one-way nervosa, delirium or stupor. The attack lasts 1-2 months, the prognosis is good. The second group is characterized by manic-depressive colouration, emotional instability, psychomotor symptoms, delusions and hallucinations. For phase, the duration of attacks 2-3 months., The prognosis is favorable. Patients of the third group have a pronounced “schizophrenic nuance”, catatonic symptoms, and a large variability of affect. The attacks last 4-5 months, the course of the type “continua”, the prognosis is relatively favorable.

Hatotani et al. (1962) believe that atypical psychosis is borderline between epilepsy, manic-depressive psychosis, and the schizophrenia group. According to the clinical picture, they distinguish between acute hallucinatory-delusional, oneiric, and confused-delirious states. The clinical picture is dominated by affective disorders, disorders of consciousness and psychomotor disorders.

Thus, in Japanese psychiatry, we find the same diversity of opinions on the clinical evaluation of these psychoses. In terms of the syndromological designation of seizures, the opinion of Kleist and Leonhard is quite common. In terms of the psychopathological structure, many Japanese psychiatrists accept the concept.

In modern Soviet psychiatry, the clinical assessment of acute atypical psychosis also gives rise to controversy. These disagreements concern not only the issues of nosological assessment, classification, typology, but also the definition of the psychopathological structure of the attacks, their designations, and systematics.

Mental and behavioral disorders due to cocaine use

Epidemiology. Cocaine is a derivative of the coca plant (Egthroxylon coca, birthplace – Central America), the leaves of which the Indians have long used to chew in order to obtain a stimulating effect and reduce hunger. Cocaine was part of the original formula of coca-cola drink and, until now, has medical use as a local anesthetic. In connection with the cheaper manufacturing process, cocaine use has been steadily increasing since the late 1970s. Psychological mechanisms predisposing to cocaine use, are the desire to improve their self-affirmation, social status and escape from depression.

Clinic. The main pharmacodynamic effect of cocaine is blockade of dopamine, serotonin and epinephrine receptors. The nature of its specific activation of mesocortical dopaminergic structures is unclear. Cocaine powder is more often inhaled through the nose, or when smoking (“crack”) its alkaloid form is inhaled. Subcutaneous and intravenous administration is also used. The drug gives an intense feeling of euphoria, lasting 15-30 minutes. after intravenous or intranasal administration.

In addition to the main ones (see below), signs of acute intoxication can be impulsive sexual and psychomotor agitation, often reminiscent of a hypomanic condition, decreased concentration, insomnia. Signs of intoxication are spontaneously stopped within 48 hours, however, the state of dysphoria and increased fatigue accompanying the reversal is easily removed by cocaine, alcohol or sedatives, which stimulates repeated abuse. A characteristic behavioral trait is the desire, being in a social environment, often retire to take the drug.

Many of the users of cocaine, while controlling its use, have long avoided physical dependence, but the opinion that cocaine does not cause it, which was widespread in the 1970s, turned out to be erroneous. The period of dependence formation is 4 years in adults and 1.5 years in adolescents. Psychological dependence develops very quickly and may appear after a single dose. Under experimental conditions, monkeys, which are given the opportunity to introduce themselves to cocaine, do this all the time, until death occurs against the background of suppression of the activity of the centers of the medulla oblongata. People often have a “drunken” stereotype of use – from several hours to several days with weight loss, dehydration, high risk of psychosis and death. Death, however, is more likely when cocaine is used to potentiate the effects of opiates.

Cocaine psychosis is clinically similar to amphetamine. Perhaps dangerous to others aggressive behavior. Tactile hallucinations are often accompanied by a feeling of insects crawling under the skin. This phenomenon is referred to as “crawling”, “cocaine insect” or Magnan symptom, which was first described in 1889. It is usually associated with the parenteral administration of cocaine.

With prolonged intranasal admission develops chronic rhinitis, ulceration of the nasal mucosa, up to necrosis of the nasal septum due to vascular spasm. Reducing serotonin levels contributes to the appearance of depression and suicidal tendencies on the background of withdrawal syndrome. The peak of the withdrawal syndrome occurs at 2-4 days after discontinuation, although some symptoms (depression, irritability) can persist for up to several weeks.

Cocaine has a generalized sympathomimetic effect on the vascular system, which can lead to cardiac arrhythmias and a high rise in blood pressure with hemorrhage in the brain as a possible complication. Other complications can be myocardial infarction and status epilepticus.

The diagnosis of acute intoxication is made on the basis of common for Fix. On the criteria, as well as: 1) the presence of at least one of the following mental symptoms: a) euphoria with a sense of energy surge, b) a feeling of increased vigor, c) a tendency to reassess one’s own personality, grandiosity of plans, d) conflict, aggressive behavior, e a) affective instability, e) repeatability, stereotyped behavior, g) auditory, visual or tactile illusions, h) hallucinations with intact orientation, and) paranoid ideas, j) reduced mental productivity and productivity; 2) the presence of at least two of the following somatic symptoms: a) tachycardia (sometimes bradycardia), b) cardiac arrhythmia, c) hypertension (sometimes hypotension), d) alternation of profuse sweat with a feeling of cold, e) nausea, vomiting, e) loss weight, g) pupil dilation, h) psychomotor anxiety (sometimes adynamia), and) muscle weakness, j) chest pain, l) convulsive seizures.

The diagnosis of withdrawal syndrome is made on the basis of common criteria for Flx.3, the presence of affective disorders (for example, depression or anhedonia), as well as at least two of the following symptoms: a) feeling of increased fatigue, b) psychomotor retardation or anxiety, c) craving for cocaine, d) increased appetite, e) insomnia or increased sleepiness, f) freakish or unpleasant dreams.

Treatment. In case of acute cocaine intoxication, oxygenation of the lungs (if necessary under pressure) in the Trendelenburg pose is prescribed. In the presence of seizures, intravenous diazepam (5-10 mg). The latter is also indicated in the presence of anxiety with hypertension and tachycardia. It is also possible to introduce an antagonist of the sympathomimetic effect of cocaine – propranolol (every minute / 1 mg to 8 minutes), although it is not a defense against lethal doses or a treatment for severe overdose.

Emerging psychotic symptoms is an indication for the appointment of neuroleptics. A stationary stay when taken out of a state of intoxication has, inter alia, The goal is to prevent access to the drug and control suicidal tendencies. Sleep therapy (lorazepam) aims to better subjectively tolerate withdrawal symptoms. In some cases, tricyclic antidepressants, MAO inhibitors, and lithium (with an affect cycle) are effective for maintaining abstinence.

Psychotherapy and rehabilitation is carried out as in alcoholism. Significantly contributing to the substitution of the illusory psychological effect of cocaine more realistic self-affirmation of the patient in social life. Interpersonal therapy focuses on the analysis of communicative behavior, specific situations that are the starting points for anesthesia. In a state of cocaine abstinence, substitution alcoholism is fraught with a relapse of cocaine.

Mental and behavioral disorders resulting from the use of other stimulants, including caffeine

Clinic. The most well-known nervous system stimulants are amphetamine dextroamphetamine (dexedrine), methamphetamine (methedrine), methylphenidate (Ritalin). The pharmacodynamic effect is ensured by interfering with the metabolism of serotonin, norepinephrine and (more so than cocaine) dopamine. Stimulants are usually taken by mouth, although intravenous administration is also used. Small doses cause a rapid improvement in health, an increase in mental productivity, a decrease in feelings of fatigue and hunger, and a reduction in the pain threshold. This justifies the medical use of drugs for concentration disorders in children and adults, obesity and potentiation of the action of antidepressants.

High-risk groups of abuse: patients undergoing obesity treatment, professional athletes, drivers on long-haul flights. With an increase in tolerance, the daily dose can reach 1 g; conditionally lethal dose is 120 mg. The symptoms of acute intoxication and withdrawal are generally identical to those of cocaine use (see F14). In addition to the main somatic symptoms, in a state of intoxication can be observed: the game of vasomotors, cyanosis, minor hemorrhages, subfebrile, bruxism (gnashing of teeth), difficulty breathing, tremor, ataxia; in severe cases, coma. Here are often observed t. amphetamine stereotypes are essentially purposeless repetitive actions, such as the constant cleaning of shoes or the assembly and disassembly of electrical appliances. Mental manifestations may include anxiety, dysphoria, irritability, internal stress, logorei, insomnia, disturbances of the body, anxiety, confusion.

A characteristic sign of caffeine withdrawal may be a persistent or throbbing headache that develops 15–18 hours after the last dose. Death from overdose occurs on the background of hyperthermia, seizures, and cardiovascular insufficiency. The most dangerous and characteristic symptom of withdrawal is depression with suicidal tendencies. In contrast to schizophrenia, psychotic intoxication episodes characterize hyperactivity, hypersexuality, the prevalence of visual hallucinations over the auditory, less pronounced disorders of thinking.

Treatment. With overdose therapy, the oxidation of urine (ammonium chloride) contributes to the acceleration of the drug from the body. When treating withdrawal syndrome, hospitalization may be necessary to control suicidal and socially dangerous behavior. The high degree of dependence on the drug makes psychotherapy especially difficult here.

Mental and behavioral disorders due to the use of hallucinogens

Clinic. Hallucinogens (psychedelics, psychotomimetics) are not a very successful designation for a team of over 100 natural and synthetic drugs. The most well-known of the natural ones are psilocybin, derived from mushrooms, and mescaline, produced from a certain type of cactus; Lysergic acid diethylamide (LSD), dipropyltryptamine (DPT) and 3,4-methylenedioxymethamphetamine (MDMA, also known as Extasy) are synthetic. Hallucinogens interfere with the metabolism of catecholamines, dopamine, acetylcholine, serotonin and GABA, causing the disinhibition of the activity of the occipital regions of the brain and limbic structures. For some drugs, there may be zones of specifically sensitive receptors in the brain.

Psilocybin has long been used in religious rituals of American Indians. The use of hallucinogens is largely susceptible to sociocultural influences. Their greatest popularity in the United States and Europe falls on the 60-70-ies, when they were considered one of the symbols of the youth subculture.

The quality and duration of subjective sensations when taking depends on the type of drug. Thus, affective changes are more characteristic of the action of MDMA; the widest range of perceptual disorders is characteristic of LSD. The effect occurs within an hour after oral administration and lasts 8-12 hours; with other drugs, the effect lasts from several hours to several days.

Psychological manifestations are largely determined by the personal characteristics of the user, his expectations and micro-social factors, but LSD almost always gives deep violations of perception, affect and thinking. In some cases, the effect of the drug is subjectively perceived as a manifestation of mental illness, accompanied by panic reactions. The intensity of perception of smells and tastes increases, the colors are perceived as richer, the texture and outlines of objects are more distinct, the emotional perception of music deepens. Marked so-called. synesthesia: colors may be perceived as sounding, sounds may be perceived as visible. Observed disorders of the body scheme, violations of the perception of space and time. Own Self is perceived dissolved in the surrounding world, separated from the body, floating in mystical ecstasy. Visual hallucinations predominate, often in the form of geometric shapes and figures. The intensity and changeability of emotions increases, various variants of affect can be felt simultaneously. Non-verbal perception becomes more significant, suggestibility increases sharply. A general increase in the severity of perception can cause a subjective feeling of internal organs, the emergence of long-forgotten memories. Usually there is a deepening of introspection, philosophical ideas, religious feelings, after which there remains a false idea of ​​increasing the creative potential of one’s own personality, of its cardinal changes.

The most typical complication is the so-called. “Bad trip” (bad trip), similar to a panic reaction with intoxication with cannabinoids, usually accompanied by psychotic symptoms lasting up to several weeks or longer. It occurs in approximately 25% of users. It is also possible flashback (return to the past), lasting from a few seconds to several hours, occurring outside the drug intake and provoked by a stressful state, the use of cannabinoids. Sometimes they can be called arbitrarily. In some cases, hallucinogens provoke endogenous psychosis. Anxiety-depressive syndromes with suicidal behavior are also a complication. The most susceptible are persons with anxious, unstable, schizoid personality traits and in a prepsychotic state.

Prolonged addiction rarely occurs due to the lack of reliable euphoria and the unpredictability of each episode of intoxication. There is no physical dependence, withdrawal syndrome. Tolerance develops quickly, disappearing just as quickly, within 2-3 days.

The diagnosis of acute intoxication is made on the basis of common criteria for F1x.0, as well as: 1) the presence in the clinical picture of at least one of the following signs: a) fear, anxiety, b) visual, auditory or tactile illusions and hallucinations with an increase in the perception acuteness and concentration, c) depersonalization, derealization, d) paranoid ideas, relationship ideas, e) affective instability, e) increased activity, g) impulsive behavior, h) concentration disturbances, and) a decrease in mental productivity; 2) at least two of the following symptoms: a) increased frequency, as well as increased heartbeat, b) alternation of profuse sweat and cold feeling, c) tremor, d) blurred vision, e) pupillary dilation, e) coordination disorder.

Treatment. In acute intoxication, emotional support and encouragement are usually sufficient, although in case of severe anxiety, the appointment of anxiolytics may be necessary, and sometimes – butyrophenones (phenothiazines should be avoided, since they can potentiate the anticholinergic effect).

F17 Mental and behavioral disorders due to tobacco use

Clinic. The average cigarette contains 0.5 mg of the active substance of tobacco – nicotine. A conditionally lethal dose is 60 mg. Physiological effects include narrowing of peripheral vessels, increased peristalsis, increased release of catecholamine, norepinephrine and epinephrine, a general decrease in metabolism, and tremor. In smokers, women have a low birth weight.

Social factors influence consumption: in adolescents, this may be a manifestation of reactions of protest, emancipation, the desire to appear as adults, conformity to the subculture of their peers. In adults, reinforcement is provided by pleasant associations with situations of feasts, sex; trade advertising plays a significant role.

Smokers are distinguished by a certain set of personality traits: greater impulsive behavior, a lower level of education, a higher frequency of divorces, greater extroversion, anxiety, ill will, and a tendency to alcohol abuse. Nicotine stimulates the hypothalamic pleasure center, which may explain the appearance of addiction. The euphoric effect is somewhat similar to the action of cocaine and opiates. The calming effect is proportional to the duration of the pause between smoking.

In addition to the main signs, the state of acute intoxication may include increased salivation, abdominal pain, diarrhea, headaches, dizziness. Smoking can complicate psychiatric medication, increasing liver metabolism and reducing the level of antipsychotics and antidepressants in the blood. Dependency, primarily psychological, develops quickly, about 85% of people continue to smoke after the first cigarette. To nicotine produced tolerance.

The withdrawal syndrome develops within 1.5-2 hours after the last use, reaches a peak during the first days and lasts for several weeks or longer. The core symptom of withdrawal — craving for smoking — can persist for many years of abstinence in the absence of other signs of withdrawal. Drowsiness during the day is combined with the difficulty of falling asleep. There is a slowing of the heartbeat, a decrease in blood pressure and motor activity. The temporal stereotype and mechanisms of recurrence are similar to those in the use of alcohol and opiates. Relapse is observed in 80% of smokers in the first 2 years of abstinence. Recurrence is promoted by a high level of social stress, social maladjustment, low self-esteem.

The diagnosis of acute intoxication is made on the basis of the criteria common to Flx.0, as well as: 1) the presence of at least one of the following symptoms: a) insomnia, b) fancy dreams, c) affective instability, d) derealization, e) reduced mental productivity; 2) at least one of the following symptoms: a) nausea, vomiting, b) profuse sweating, c) tachycardia, d) cardiac arrhythmia.

The diagnosis of withdrawal syndrome is made on the basis of common criteria for Flx.3, as well as the presence of at least two of the following symptoms: a) craving for tobacco use, b) malaise, weakness, c) anxiety, d) dysphoria, e) irritability or anxiety, e) insomnia, g) increased appetite, h) cough, and) ulceration of the oral mucosa, k) decreased concentration.

Treatment. Many therapeutic approaches are used, none of which have demonstrated advantages over the other. The most commonly used are various forms of suggestion (the so-called “coding”, acupuncture), aversive behavioral therapy, replacement therapy (chewing gum with nicotine to alleviate the withdrawal syndrome, or lobeline, giving a nicotine-related effect). In the period of cancellation, anxiolytic therapy is advisable. Success is promoted by the presence of support from relatives and a group of abstinent smokers, fear of the somatic consequences of smoking (lung cancer, CHD).

Smokers seeking help are the most therapeutically resistant, treatment programs yield not more than 20% of successful cases; at the same time, 95% of abstinents did not receive medical care, leaving it unclear how or why they stopped smoking. Prognostically unfavorable factors are unsatisfactory social adaptation, female gender, a high level of use before therapy.

F18 Mental and behavioral disorders due to the use of volatile solvents

Clinic. For narcotic purposes, the following volatile solvents are used: gasoline, lacquer solvents, various types of glue, cleaning liquids, aerosols (especially paints), amyl and butyl nitrates. Nitric oxide, ester, is specifically used by health professionals who have access to these substances and are a contingent that is fundamentally different from the main users. The overwhelming majority of users are children and adolescents from 6 to 16 years of age from low-income strata of society.

Inhalation is carried out directly from the packaging or with a cloth moistened with a substance or a plastic bag that is pulled over the head. Intoxication occurs in 5 minutes and lasts 15-30 minutes. During intoxication, the euphorizing effect is replaced by inhibition.

In addition to the main, signs of acute intoxication can be an overestimation of one’s own personality, a feeling of invulnerability, superior strength, a feeling of soaring, dizziness, disturbances in spatial perception, and certain psychotic symptoms. Possible amnesia period of intoxication. Rod aggressive behavior leads to frequent offenses; decrease in mental productivity is accompanied by difficulties in learning.

Among the somatic effects may be nausea, loss of appetite, decrease in tendon reflexes. Death may occur as a result of central respiratory arrest, cardiac arrhythmias and accidents. Somatic effects affect the bone marrow, kidneys, liver, peripheral neuritis. There is an increase in tolerance, although there is no convincing evidence of the presence of withdrawal syndrome. The use of volatile substances, being, as a rule, a transient disorder, often ends with a transition to other forms of drug addiction or alcoholism.

Diagnosis. Traces of volatile solvents (as well as hallucinogens) are not detected in the urine by laboratory methods. Tangible signs of use can be hyperemia of the skin in the nasal area, conjunctivitis, inflammation of the mucous membranes of the upper respiratory tract, peculiar smell from the mouth, traces of the substance on the face, hands and clothes. The diagnosis of acute intoxication is made on the basis of the criteria common to F1x.0 and: 1) the presence of at least one of the following mental symptoms: a) apathy, indifference, b) conflict, aggressive behavior, c) affective instability, d) reduced focus of thinking, d ) impaired concentration and memory, e) psychomotor inhibition, g) decreased mental productivity; 2) as well as at least one of the following neurological signs: a) unsteadiness of gait, b) Romberg’s negative test, c) blurred speech, d) nystagmus, d) impairment of consciousness (eg, stupor, coma), e) muscular weakness, g) blurred vision, diplopia.

Mental and behavioral disorders due to use of sedatives or hypnotics

Epidemiology. All hypnotics and sedatives potentiate the action of each other and alcohol. Abuse has different stereotypes. One of them is for persons of predominantly middle-aged persons to receive constant access to drugs through doctors as part of anxiety and insomnia therapy. They can prescribe medications from several doctors at the same time, drug dependence often remains unnoticed by others until the appearance of physical signs of abuse. Drugs can be used occasionally by adolescents to obtain a sedative or euphoric effect. They are used by experienced drug addicts for intravenous administration due to their greater cheapness compared to heroin or to potentiate the effect of weak opiates. Alcoholics use them to increase intoxication or alleviate the syndrome. Abusive stimulants use them to relieve excessive arousal. Diazepam is used by cocaine addicts to alleviate the withdrawal syndrome.

Clinic. Intoxication is subjectively perceived as a feeling of pleasant, warm drowsiness, its small degrees resemble alcohol intoxication. In addition to the main ones (see below), symptoms include a decrease in the focus of thinking and memory, a slowdown in speech and understanding, episodes of sexual disinhibition, and an accentuation of the main personality traits. General inhibition disappears in a few hours, but violations of fine motor skills, thinking and affect can last 10-20 hours. Against the background of dysphoria, transient paranoid perceptions and suicidal tendencies can occur.

Physical signs, besides the main ones (see below), may include diplopia, strabismus, decrease in blood pressure and height of tendon reflexes. Death can occur as a result of suicide, an accident, or an unintentional overdose (the lethal dose for an experienced drug addict can be, under certain conditions, not higher than for a novice). These drugs are most often used in the implementation of suicidal tendencies. Death comes on the background of deep coma, respiratory arrest and cardiac activity.

With regular admission, increased tolerance is produced. The dose of an experienced drug addict is 1.5-2 g per day. Physical dependence develops as a result of taking low doses (10-40 mg per day) for several years or high doses in just a few weeks or months. Receiving doses higher than therapeutic for several weeks or more becomes a prerequisite for the onset of withdrawal syndrome, characterized, in addition to the main symptoms (see below), anxiety, sweating, loss of appetite, fever, up to delirium (clinically indistinguishable from alcohol), amnestic syndrome and coma. The syndrome reaches its highest intensity on day 2–3 of abstinence. Convulsive manifestations always precede delirious. Symptoms last 2–3 days, rarely up to 2 weeks.

Unlike barbiturates, benzodiazepines have a higher safety threshold. They suppress the respiratory center to a lesser extent, the lethal dose correlates with the narcotic effective as 200: 1. High doses (more than 2 g) taken with a suicidal purpose cause drowsiness, ataxia, and sometimes confusion, leaving no residual marks. In individuals with low frustration tolerance, benzodiazepines can have a disinhibitive effect with aggressive behavior. Due to the lower level of euphoria attained, the risk of addiction is relatively lower, which does not exclude the possibility of increasing tolerance and the appearance of withdrawal syndrome.

The daily dose of an experienced drug addict can be 1–1.5 g of diazepam. Withdrawal syndrome develops on the background of a daily dose of about 40 mg, but can also be observed at therapeutic doses (10-20 mg) if the drug has been taken for more than a month. Longer-acting drugs (diazepam) give a more delayed withdrawal (5-7 days). Convulsive manifestations may be the first sign of not expected benzodiazepine withdrawal syndrome. Symptoms of withdrawal include anxiety, numbness of the limbs, dysphoria, increased sensitivity to light and sound, nausea, sweating, muscle twitching. Withdrawal syndrome is not necessarily accompanied by a desire to resume taking the drug. Due to the slow release of benzodiazepines from the body, signs of withdrawal can last up to several weeks.

The diagnosis of acute intoxication is made on the basis of common for measure:

1) the presence of at least one of the following mental symptoms:

a) euphoria and disinhibition,

b) apathy, sedation,

c) conflict, aggressive behavior,

d) affective instability,

e) decrease in concentration,

f) anterograde amnesia,

g) psychomotor disturbances, and a decrease in mental productivity;

2) at least one of the following somatoneurological signs:

a) uncertainty of gait,

b) Romberg negative test,

c) blurred speech,

d) nystagmus, and impairment of consciousness (stupor, coma),

e) skin erythema, pustules.

The diagnosis of withdrawal syndrome is made on the basis of common criteria for as well as the presence of at least three of the following symptoms:

1) tremor of the fingers of the outstretched hands, the tip of the tongue or eyelids,

2) nausea, vomiting,

3) tachycardia,

4) orthostatic hypotension,

5) psychomotor anxiety,

6) headaches,

7) insomnia,

8) weakness, malaise,

9) transient visual, tactile or auditory hallucinations or illusions,

10) paranoid perceptions,

11) large convulsive seizure.

The diagnosis is further confirmed by specific laboratory methods.

Treatment. It is more expedient to start the removal from the cancellation state in stationary conditions. In a state of coma or with marked signs of intoxication, the appointment of barbiturates is not recommended. When removing the moderate withdrawal syndrome method of sampling is selected dose of the drug, allowing to achieve a mild sedation. After keeping it for 1-2 days, the dose gradually decreases (not less than 10% per day, the last 10% is brought to zero within 3-4 days). When signs of withdrawal are resumed, dose reduction should be even more gradual. Short-term barbiturates should be replaced with drugs with a longer-term effect (phenobarbital). Replacing barbiturates with benzodiazepines is not advisable due to the risk of replacing one dependency with another.

With a psychological deficit of problem-solving behavior, a drug certainly helps to cope with internal stress, anxiety, a sense of its own low value. Therefore, at the exit to the full abstinence of the patient must be accompanied by appropriate psychosocial activities, otherwise he will be doomed to again turn to the use of the drug. Prevention of abuse requires the orientation of the doctor on the appointment of drugs in a short time in the presence of a specific therapeutic target. The doctor should be wary of such indirect signs of abuse as visits to other doctors, requests for higher doses, for issuing new prescriptions to replace lost ones.

Mental and behavioral disorders due to the use of opiates

Epidemiology, etiology.

Opium – the basic substance contained in the juice of opium poppy (Papaver somniferum). About 20 alkaloids are obtained from opium, the most famous of which is morphine. It is possible to get t, n. semisynthetic alkaloids based on naturally found in opium (heroin, codeine, hydromorphine), as well as fully synthetic (meperidine, methadone, propoxyphene). The most widely used opiate is heroin, the main supplier of which to the world market are the regions of the Middle and Far East. It is mainly used among the urban population, more often by men than by women (3: 1), at the age of 18-25 years. More than 50% of them come from incomplete or divorced families in which parents often abused psychoactive drugs. About 90% of them have any mental disorder, most often – depression, then – alcoholism, various forms of psychopathy.

In the overwhelming number of cases, the identity of patients is characterized by self-doubt, low self-esteem, asocial inclinations, dominant dysphoric affect, low frustration tolerance. Morbidity is also determined by the subcultural influence of certain groups of the population and by facilitated access to drugs, as a result of which the incidence is higher among doctors than in the population.

Clinic. Parenteral administration of the drug causes analgesia, indifference to pain, drowsiness, misting of consciousness, a feeling of warmth, heaviness in the limbs and dry mouth. As a rule, there is euphoria (“onset”) that occurs shortly after intravenous administration and lasts 10–30 minutes, then sedation (“dragging”) dominates. The first dose may be accompanied by a dysphoric affect tinge, nausea and vomiting.

The analgesic effect reaches a maximum after 20 minutes after intravenous administration, approximately one hour after subcutaneous administration and lasts 4-6 hours, depending on the type of drug, dose and length of anesthesia. Hyperemia and itching of the skin of the face, especially the nose, may occur. There is a narrowing of the pupil, a spasm of smooth muscles (including the ureter and biliary tract), constipation. Idiosyncrasy to the drug occurs in the form of allergic reactions, anaphylactic shock, pulmonary edema.

Overdose is accompanied by slowing of breathing, bradycardia, a decrease in response to external stimuli, a decrease in temperature and blood pressure. Opioids suppress the function of the respiratory center in the brainstem (this effect is potentiated by phenothiazines and MAO inhibitors, and tolerance to it is not developed). Death in overdose is usually associated with respiratory arrest. The classic triad of opiate overdose: coma, “pin head” type pupils and respiratory depression. Conditionally lethal dose with initial tolerance – 60 mg of morphine; a gradual increase in tolerance makes it possible to receive several thousand mg.

The withdrawal syndrome (“breaking”) of morphine and heroin begins 6-8 hours after the last dose, with a background of at least 1-2 weeks of constant intoxication. The highest intensity of the syndrome is observed on days 2–3, decreasing over the next 7–10 days, although some manifestations (insomnia, bradycardia) may persist for up to several months. The more active the opiate is, the faster, shorter and more intense the withdrawal syndrome is. The clinical picture in mild cases is a lot like the state of the flu. In addition to the main symptoms (see below), dysphoria, hot flashes, weight loss, temperature dysregulation can occur. Death against the background of cancellation is rare, mainly due to concomitant pathology of cardiac activity.

The desire to resume taking opiates rarely accompanies withdrawal syndrome when prescribing them as analgesics, for example, during surgical intervention. Side effects of opiate abuse: endocarditis, septicemia, pulmonary embolism, infection with hepatitis viruses and HIV.

Diagnosis. To make a diagnosis of acute intoxication, in addition to manifestations common to F1x.0, the condition must meet the following criteria: 1) at least one of the following symptoms: a) apathy, sedation, b) psychomotor inhibition or disinhibition, c) decreased concentration and memory , restriction of higher mental functions, reduced mental productivity; 2) the presence of at least one of the following signs: a) drowsiness, b) blurred speech, c) constriction of the pupil (or expansion due to anoxia in severe overdose), d) impairment of consciousness (stupor, coma).

For the diagnosis of withdrawal syndrome, in addition to manifestations common to F1x.3, the condition should be characterized by at least three of the following symptoms: a) desire to resume taking the drug, b) a runny nose or sneezing, c) sweating, d) nausea, vomiting, g ) tachycardia or hypertension, e) psychomotor restlessness, g) headaches, h) insomnia, and) general malaise, weakness, j) transient visual, tactile or auditory hallucinations or illusions, l) a large convulsive fit.

Treatment. With an overdose, an opiate antagonist is injected (naloxone, nalorphine – 0.4 mg IV, again 4-5 times during the first 30-45 minutes). Owing to the short duration of the operation of nalok-son, the appearance of a pre-comatose state is possible in the first 4-5 hours, which requires careful monitoring of the condition.

When suppressing withdrawal, synthetic opiate methadone is used to replace heroin (20–80 mg orally). It should be canceled after the withdrawal of withdrawal syndrome, since it itself has a narcotic effect. To relieve methadone withdrawal (much weaker than with heroin), clonidine is used, 0.1-0.3 mg 3-4 times a day for the period of detoxification. The advantages of methadone are oral intake, the possibility of its legal production and productive activities during the reception; disadvantage – the preservation of drug addiction. Its use is particularly indicated in the treatment of female drug addicts in the state of pregnancy to prevent withdrawal syndrome in the newborn.

Similar to methadone opiate L-alpha-acetylmethadol provides for the suppression of withdrawal within 72-96 hours, making it possible for more rare reception. The use of opiate antagonists (naloxone, naltrexone) interrupts the euphoric effect of the drug, but by itself does not provide the patient with motivation to stop the abuse.

Due to the fact that pharmacological intervention does not provide a definitive solution to all psychosocial problems of the patient, the treatment complex should always include rehabilitation measures. For this purpose, individual and group psychotherapy, self-help groups (the program “Anonymous Addict”) are used,

Psychotherapy increases the overall effectiveness of treatment programs, especially if there is a concomitant psychiatric pathology. The optimal framework for rehabilitation is a therapeutic community that tears the patient out of their usual habitat, where most of the staff consists of former drug addicts who have the skills to carefully control the patient’s motivation to withdraw, without which patients are not allowed to be treated. Patients are in groups of the therapeutic community for 12–18 months until they can return to their place of residence. The goal is not only to achieve abstinence, but also the acquisition of useful social skills, the correction of antisocial attitudes. 90% of applicants leave therapy during the first year; for those remaining, a rather high effect is achieved.

Mental and behavioral disorders due to cannabinoids

Indian cannabis plant-based drugs (Cannabis sativa) have different narcotic activity depending on the content of the most psychoactive of 60 cannabioids delta-9-tetrahydrocannabiol (THC), the percentage of which determines the quality of the narcotic products circulating in the market.

Marijuana (“plan”, “weed”) is a diverse mix of leaves, seeds, stems, and hemp flower heads. According to the degree of activity, the narcotic products made from it are divided into 3 categories, denoted by Indian names. The least active bhang product is made from the heads of uncultivated plants. A greater amount of hemp resin is found in ganja, obtained from flowering heads and leaves of carefully selected cultivated plants. The most active is charas, which is the actual resin obtained from the tops of mature hemp; he is designated as hashish.

Cannabinoids can be consumed with food and drink, but are usually inhaled during smoking. Marijuana is called the gateway to the world of drugs. The first experiments with it in adolescents are often not accompanied by dangerous consequences characteristic of other psychoactive substances, which reduces the fear of transition to them. With relevant experience, the combined use of alcohol gives here a significant additive narcotic effect. Usage usually begins in high school. Risk factors are pedagogical neglect, contacts with asocial subcultures, depressive symptoms, low skills of problem-solving behavior.

Clinic. Intoxication develops immediately after smoking, reaches a maximum in 10-30 minutes. and lasts 2-4 hours, although psychomotor disorders may persist for several hours. The effect of oral administration lasts from 5 to 12 hours. Introspection, suggestibility, sensitivity to external stimuli, sharpness of apperception, intensity of perception of color, taste and music increase. There is a feeling of greater saturation of time with events, self-confidence, at the same time a feeling of relaxation and soaring, an increase in sexual urges. A smoker can often perceive himself as if from the outside, laughing at the symptoms he has. Perhaps the emergence of anxiety, aggressive impulses occur rarely. The ability to maintain contact with reality may allow an experienced smoker to hide the state of intoxication from others.

In high doses, marijuana, like hallucinogens, can cause disorders of the body pattern, perception of space and time. In addition to the main somatic symptoms (see below), dilated pupils and cough may be noted. With long-term intake of high doses, some signs of increased tolerance and mild withdrawal reactions (sleep disturbance, anxiety, irritability, vomiting, tremor, sweating, muscle pain) are detected, which, however, do not present major problems for experienced smokers.

Observations on chronic smokers of the Caribbean islands and eastern cultures (Jamaica, Egypt, India, Jamaica) allow us to distinguish as the main so-called. amotivational syndrome (passivity, reduction of impulses, purposeful activity and higher mental functions, apathy, weight gain, sloppiness). The significantly lower severity of the syndrome in North American smokers suggests its etiology, participation of socio-cultural and personal factors.

Oral administration can be a triggering factor for the appearance of delirium, transient delusional syndromes. Delayed episodes of intoxication that occur outside of smoking usually follow the preceding use of hallucinogens. Long-term use may be accompanied by obstruction of the pulmonary tract, emphysema, an increased risk of lung cancer. It also marks the so-called. amotivational syndrome characterized by passivity, lack of interests and motivations, “fallout” in the process of conversation, and difficulty concentrating. Sometimes this term is also used to refer to deficiency symptoms in schizophrenia.

The diagnosis of acute intoxication is made on the basis of the condition, in addition to the general for Flx.0, the following criteria: 1) the presence of at least one of the following symptoms: a) euphoria and disinhibition, b) anxiety, anxiety, c) suspicion or paranoid views, d) a sense of slowing down the course of time, e) a decrease in the focus of thinking, e) a decrease in concentration, g) a decrease in the speed of reactions, h) auditory, visual or tactile illusions, and) hallucinations with intact orientation, j) depersonalization or deres lizatsiya, l) reduced mental productivity; 2) the presence of at least one of the following symptoms: a) increased appetite, thirst, b) dry mouth, c) conjunctivitis symptoms, d) tachycardia.

Treatment. There is no specific therapy for the abuse of can-nabioids. When using the drug as a means of relieving anxiety, depression, attention should be paid to the accompanying mental pathology. The correction of social life, family relations is decisive. The abstinence control includes the periodic determination of the relevant metabolites in the urine.

Acute endogenous psychosis. Part 4

It is interesting to try to qualify acute psychosis not by using atomized, randomly intertwining symptoms, but by recognizing a regular shift of more holistic states. At the same time, impaired consciousness ceases to be a symptom only of mental confusion, and it is given a large place during “crazy flashes” and even with purely affective ones. As for the general assessment (from a clinical point of view) of the concept of acute psychoses of Ey, its weakest place is excessive schematization and psychologisation of mental diseases, an attempt to “break the deadlock” with the help of exclusively psychological and philosophical concepts. General pathological, biological basis of psychosis is bracketed, actually turning into a group of causes divorced from the nature of the phenomena they cause.

Ey is almost not concerned with the relationship of catatonic disorders with oneiric, individual acute psychosis or syndromes, where fear affect and nonsense prevail. The place of delirium, which seems to be dissolved in the concept of “amentia” (mental confusion), remains unclear. Having noted the weak points of the old approaches to the description of many acute psychosis, and in part using the new achievements of clinical psychiatry, Ey still bases his psychopathological synthesis on the materials of the clinical analysis of the past and only proposes his own scheme for them. Regarding the course of these acute psychoses, EU also allows a transition to schizophrenia or other chronic delusional states, although in most cases he considers the course of the disease favorable.

In German psychiatry, three main approaches to acute atypical psychosis were defined. Unlike French psychiatry, the answer to the question about the relationship of these psychosis to schizophrenia and manic-depressive psychosis often constitutes the main task. For one group of psychoses, although the atypical nature of their clinic is beyond doubt, it is still considered possible to classify them as either schizophrenia or manic-depressive psychosis. Loyalty to the dichotomous division of endogenous psychosis according to Krepelin and at the same time some deviation from it towards their typological understanding is expressed by these authors in that they admit the existence of mixed, or intermediate, psychosis.

Schneider (1957, 1967) divides the intermediate psychosis into 3 groups: in the first picture of the disease contains both schizophrenic and cyclothymic symptoms, in the second attacks of manic-depressive psychosis and schizophrenia alternate. The third group includes psychosis, the clinical picture of which is mainly schizophrenic, but at the “height” has a “manic-depressive tone” and vice versa. Schneider’s cycloid psychosis (see below) is atypical autochthonous psychosis related to manic-depressive psychosis.

Another major representative of classical German psychiatry — Mayer-Gross (1960) also attributed atypical psychosis mainly to schizophrenia and manic-depressive psychosis. Thus, in the manic-depressive psychosis, the author included a form with catatonic manifestations, a hereditary and familial form sui generis, and true mixed psychosis (with two pathological heredities). True, the author acknowledged the existence of forms that can not be attributed either to schizophrenia or to circular psychosis.

Questions of clinical description, classification of acute endogenous psychosis for many years have been the subject of a large German psychiatric school, the leading representatives of which are Kleist and Leonhard.

In Leonhard’s classification (1957), acute atypical psychosis is included in phase psychoses, in cycloid psychosis, in unsystematic schizophrenia. In phase psychoses described:

a) pure depression (suspicious depression, or depressive psychosis of a Kleist relationship);

b) pure euphoria (confabulatory euphoria, or acute expansive confabulous disease according to Kleist);

c) dreamy euphoria. Non-systematic schizophrenia includes affectively saturated paraphrenia, schizophasia, and periodic catatonia.

Of greatest interest is the group of cycloid psychoses, which, according to Leonhard, are bipolar positively flowing psychosis. This group includes the psychosis of fear — happiness, agitated-inhibited confusion, and hyperkinetic-akinetic psychosis. The psychosis of fear — happiness is characterized at one extreme by the presence of fear with distrust and ideas of relationship. The other pole (happiness) is determined by the experience of bliss with delusions of grandeur. There may also be pseudo-hallucinations, ecstatic stupor, delusions of physical influence, confabulation, incoherence of thoughts, etc.

In the case of another cycloid psychosis – “agitated inhibited confusion”, thinking disorder is a determining disorder according to Leonhard. When excited confusion there is incoherence of thoughts, which leads to the formation of abnormal ideas (false recognition, ideas of relationship). Auditory illusions are observed, and less often visual ones. With inhibited confusion

thinking is “still”, and this gives rise to ideas of attitudes, meanings, pronounced confusion, etc.

Finally, hyperkinetic-akinetic psychosis is characterized by the presence of “pure psychomotor arousal” or “inhibition”, independent of thinking disorder or affective disorders. In the hyperkinetic pole, expressive and reactive movements are observed. In the pole of akinesia, posture and facial expressions are noted, patients do not perform the simplest proposed movements, they offer resistance. Akinesis is often accompanied by confusion, and sometimes incoherent arousal with a frozen posture and facial expressions.

Ecstasy, ideas of the relationship can be observed, and sometimes the picture resembles mania or melancholy (most often this is observed when the motor psychosis increases or decreases).

Leonhard distinguishes clinical forms on the basis of a grouping of disorders around one core disorder: in one case of affective, in the other – thinking disorders, in the third – psychomotor. The remaining symptoms are more or less optional and most often “secondary”. It is interesting to note that neither the semiotics nor the role of the disturbance of consciousness is discussed in detail by the author. It is only mentioned that at the height of cycloid psychosis, disorders of consciousness can easily arise, and they can determine the scenic nature of false recognition. When describing periodic catatonia (in the group of non-systematic schizophrenia), the author does not include oneiroid disorders in its clinical manifestations.

In the literature, the nosological assessment of cycloid psychosis, proposed by Leonhard, meets many objections. Separate from psychoses, isolated from Kleist and Leonhard, are recognized by many psychiatrists as forms of acute “attacks” (motor psychosis, expansive confabulous disease).

The works of Kleist, Leonhard, and their numerous students allowed them to describe clinical contours in a new way and to describe in part the content of many acute psychoses. The work of this school, however, shows how important methodological principles are for the successful clinical description.

After identifying a definitive core disorder in these complex psychoses, the rest of the symptoms turned out to be very weakly associated with it. As a result of this approach, the oneyroid series of symptoms and other signs of disorder of consciousness fall out. Another weak point in the classification of these psychoses (reaching the level of nosological synthesis) is the recognition of phase as the defining and obligatory feature. How risky it can be seen from the results of the follow-up check 10 and more years after the first attack, 29 patients diagnosed with expansive confabulese (Giebner, 1961). Benign phasic course of the disease took only 14 patients. In 13 patients, a follow-up check established schizophrenia (paranoid or hebephrenic form), in 2 patients — organic psychosis (progressive paralysis, arteriosclerosis).

In German psychiatry, more and more supporters are finding a more extreme, purely typological assessment of acute anti-acute psychosis within a single psychosis.

So, Janzarik (1962), believing that with the current level of knowledge in psychiatry it is impossible to strive for the nosological distinction between endogenous psychosis, proposes to distinguish only psychopathological types. Within a single psychosis, he distinguishes between 4 types of dynamic psychopathological disorders that correspond to the clinical concepts of depression (“dynamic reduction”), mania (“dynamic expansion”), acute schizophrenic psychosis (“instability”), and schizophrenic defect (“emptying”). Conrad (1958), also a supporter of a single endogenous psychosis, divided it into 4 types depending on the severity:

1) the type of pure cyclothymic psychosis;

2) type of phase psychosis with delirium, a sense of change (schizoaffective psychosis, catatonia with “release of fantasy”, etc.);

3) the type that proceeds with seizures, but with residual effects in the states of remission, which makes it possible to speak of a fur coat, and not a phase;

4) the type of schizophrenic process in understanding Kraepelin early dementia.

The existence of typologically intermediate phase psychosis (between manic-depressive psychosis and schizophrenia), their interpretation from the standpoint of a single endogenous psychosis we find in recent years in the works of a number of leading German psychiatrists: Kranz (1969), Pauleikhoff (1969), Weitbrecht (1969), Petrilowitsch 1969, 1972). These authors did not specifically engage in the clinical study of individual forms of the psychoses in question, but even with a summary of the division of endogenous psychoses, they recognize a special clinic of acute atypical psychosis.

Portuguese psychiatrists have shown great interest in acute atypical psychosis for many years. Polonio (1954) called “cycloid psychosis and reactions” described acute psychosis, which divides into two groups: paranoid and incoherent. For both groups, the author considers as characteristic the occurrence on the background of “super clear” (“hyperlucidic”) or dimmed consciousness, an increase or decrease in mood and psychomotor activity. The beginning is usually sudden. The prognosis is favorable, personality changes do not occur. The author believes that these types of reaction are more likely than nosological units. According to the features of the clinical picture, Polonio distinguishes between: confabulous, hallucinosis, neurotrophy, paranoid expansive psychosis, paranoid attitudes towards oneself, paranoids of suggestion and influence, incoherent hyperkinetic and akinetic psychosis.

In addition to these “reactions,” Polonio described occasional schizophrenia. He referred those cases at which it was observed not less than three attacks divided by remissions to the last. He distinguishes paranoid, hebephrenic and catatonic forms (the latter is the most frequent). With all these forms, the pyknic constitution was more common, exogenous hazards before attacks. The most frequently observed were catatonic states of excitement and stupor, manic-disjointed, expansive delusions or delusions of persecution and hallucinosis. Often there is confusion, change of mood. The remaining symptoms are the same as for other (nuclear) forms of schizophrenia. Personality changes are not very pronounced and consist in the superficial nature of emotions and the absence of a clear sense of reality. The average duration of attacks in the absence of treatment – 7 months.

Barahona Fernandes (1959) identified a group of holodisfrenia, which includes several clinical types of psychosis: paranoid, hallucinatory, incoherent, motor, as well as twilight states and delirium. The author considers the main disorders of the global disorder of consciousness, attention and incoherence of thinking. There are disorders of sleep, instincts and affect, feelings of time, orientation. In the occurrence of these psychoses, constitutional, exogenous and psychogenic factors play a role. The course of the disease is acute, complete remission, without defect. Holodisfrenia differs from schizophrenia, according to the author, by the absence of a real discrepancy between behavior and frustrated functions. Nosologically, these psychoses are unclear, located between schizophrenia and manic-depressive psychosis.

As you can see, Polonio and Fernandes, adhering in terms of the clinical division of these psychoses of similar views with the Kleist and Leonhard schools, emphasize the special role of the disorder of consciousness. This brought them closer to the concept of Ey, which was reflected in the work of Goncalves (1961), an employee of their clinic.

When studying 45 patients (at the onset of the disease and at remote stages of the course), Goncalves came to the conclusion that the clinical picture of holodisphrenia is not always clear (as in the case of Leonhard’s cycloid psychosis), and he draws on the concept of disruption of Ey consciousness to explain this phenomenon. The author believes that with these psychosis, consciousness is almost always disturbed. The clinical picture may vary from attack to attack. Noting that the development of an attack goes through a regular change of syndromes, and recovery through a reverse change of states, Goncalves tries to concretize this situation. Acute delirium (delirium acutum), in his opinion, may be the final stage of these psychoses. In terms of nosology, Goncalves believes that a global disorder of mental functions distinguishes these psychoses from schizophrenia.

Acute endogenous psychosis. Part 3

In the clinical evaluation of acute atypical psychosis, French psychiatrists do not raise the question of their relationship to schizophrenia. This is explained by the fact that schizophrenia is regarded by them only as a purely psychopathological concept. This is “chronic discordant psychosis”, the essence of which lies in a peculiar personality change, “total modification of human existence”, etc. (Follin, 1958; Ey, 1958). Discordance and autism are considered to be determining disorders (Ey adds nonsense). Clinically, schizophrenia includes 4 nuclear forms according to Kraepelin’s classification and some cases with a sluggish course (Eue et al., 1967).

Understanding schizophrenia as a purely psychopathological phenomenon, the content of which is personality change, it is assumed that a variety of illnesses can cause schizophrenia, including acute delusions and confusion. Acute psychoses (“syndromes”) are considered nosologically free, mobile. So Laboucarie and Barres (1959) with the clinical and follow-up study of 400 patients with acute psychosis (follow-up period 5–20 years) obtained the following results: in 100 patients, mental confusion or manic-depressive psychosis was determined after analysis of the first attack. The remaining 300 patients were divided into two groups according to the characteristics of the clinical picture of the first attack: a) with the state of the polymorphic structure (170 patients) and b) with acute depersonalization syndromes (130 patients).

For the states of the polymorphic structure, the authors consider the characteristic: a sudden onset without prodrome (as a rule, after psychogeny); global disorder of consciousness of the type of true oneiroid with fluctuations of its degree; affective disorders (most often of the type of purely manic or with elements of disturbing melancholia); polymorphic nonsense without systematization.

The first attack ended in complete remission after a few weeks or (less) months. The further course of the disease according to the follow-up was estimated as follows: in 30% of cases, remission after the first attack was stable, and there was no recurrence of the disease; 50% of patients had relapses, either with the same picture of the attack, or in the form of phases of manic-depressive psychosis. In 15% of patients, the disease took the form of chronically current schizophrenia.In conditions of acute depersonalization, the first attack was almost always preceded by a prodromal period, such as neurotic changes with elements of autism.

Psychosis often began spontaneously, and, if psychogeny occurred, it was rather a prolonged conflict situation in the family. The attack itself was characterized by ambivalence, an abundance of senesthopathic and catatonic symptoms against the background of unexpressed consciousness disorder (such as a reduced one-neuroid). The attack lasted from 3 months to 1 year, regardless of treatment.

The follow-up history of this group of patients revealed the following course options: “recovery” after the first attack in 20% of patients; rapid transition to classical schizophrenia in 30% – (the disease has taken a particularly malignant course); 50% of patients had relapses. In some of these patients, recovery from the defect sometimes occurred after many attacks. In other patients, after many years of almost complete recovery, there were bouts of melancholia, which are easily treatable. In other cases, relapses retained a schizophrenic nature, including the type of periodic catatonia.

The schizophrenic or affective structure of seizures depends, according to the authors, most of all on age. It is assumed that, despite the apparent schizophrenic structure of the first attacks (at a young age), the course of the disease in later periods proceeds very often in the manner of manic-depressive psychosis.Lacassin (1959), on the basis of a study of 180 patients with acute schizophrenia (the disease was at least 5 years old), concluded that the clinical picture of the initial period does not have the characteristic features that allow one to predict the course and even make a diagnosis. Regarding the psychopathological structure of these psychoses, Lacassin joins Ey’s point of view, considering them to be a manifestation of a particular level of consciousness destructuring, namely the oneiric level (see below).

Of the post-war works of French authors, the most significant in volume, depth of analysis and original views are the works of Ey. Most fully the views of this author are set forth in a large monograph on the structure of acute psychosis (1954). In this work, Eu expresses a special point of view on the question of the psychopathological structure and pathogenesis of all acute psychoses (manic-depressive psychosis, symptomatic affective psychoses, acute toxico-infectious, organic, epileptic psychoses, delusional outbreaks).Staying in terms of the clinical division of the true traditions of French psychiatry, Ey tries to explain the existence of many clinical options from the perspective of a special understanding of the whole of psychopathology.

In terms of psychopathology, in which, according to the author, the classification of psychosis is only possible, all psychotic states are divided into two groups: acute psychosis, which is caused by a pathology of consciousness (especially understood by him), and psychosis associated with personality pathology. The author refers to the first group:

1) manic and depressive seizures (endogenous or symptomatic, mono- or bipolar),

2) acute delusional and hallucinatory outbreaks and one-iroic states (also regardless of their etiology)

3) confused-onyric psychosis (delirious and amental structure).

Three groups of acute psychosis represent, in Ey’s view, the clinical expression of the three levels of consciousness destructuring. In the first degree of consciousness destruc- tion, a manic and depressive state arises; with a deeper disturbance of consciousness, acute delusional and hallucinatory flashes and oneiric states arise, and finally, the third, deepest degree of consciousness destruc- tion corresponds to psychosis, designated as exogenous delirium, exogenous confusion, amentia, etc. This understanding and classification of acute psychosis follows from general theoretical positions of the author, defending the need for an application to the psychiatry of the Jackson concept.

Ey understands consciousness as a form (“layer”) of psychic life, which “organizes in the field of the presenting present” sensually experienced at the moment (including data of perception, part of past experience and ideas about the future). In the “field of consciousness” at each moment the subjective and objective are presented, which are ordered by consciousness. The main content of consciousness is ordered sensory experiences. Hence the concepts of “phenomenal field”, “scene”. This field has a dynamic structure and organization. Consciousness has its own structure, reflecting the stages of evolution during life. The first, least profound degree of impairment of consciousness is “temporarily ethical destruction”.

Clinically, this is expressed in manic and depressive syndrome.In the manic state, only the direction of the stream of consciousness, its “ethical-temporal” orientation, changes. The consciousness of a maniacal patient is a “propulsion movement”, thanks to which the subject “breaks away from the forms of the present and eliminates them as rules of behavior”. Subjectively, this disorder is experienced by the patients as “endless striving forward”, as “celebration”, in which “all impulses of mastering the world are satisfied”, and clinically it is ecstasy, enchantment, etc. With melancholy, the negative structure consists, on the contrary, “to stop and retreat in the face of the requirements of the present. ” The positive structure of melancholia is expressed in tragedy or anxiety, in which all sorts of fears are actualized.

Both the manic and the depressive patient are characterized by “impossibility to balance with the present” and to keep in it. This ability, according to the author, is part of the functions of consciousness and is upset in the first place.With the next, deeper level of consciousness destruc- tion, except for a temporary ethical disorder, that is, a violation of the direction and purpose of consciousness, the sensory representation in the field of consciousness of reality itself is also disturbed.

This level of destructiveness corresponds to “delusional flashes”, epileptic twilight states, intoxication hallucinatory-delusional psychosis without confusion, oneiric syndrome, etc. With such a disorder of consciousness, there is a destruc- tion of the perception itself, which leads to a change in the temporal-spatial structure of the relationship between “I” and “peace”.

With a mild degree of disturbance of the temporal-spatial “layer” of consciousness, a disorder in the perception of the body arises, that is, the “bodily space” is upset (depersonalization, violations of the body pattern and senestopathy). If the violation is more profound, depersonalization reaches the depth of the “thinking person” and this is experienced by the patient as penetration, seizure, parasitism in thinking (mental automatisms and hallucinations, “experiencing hallucinatory splitting or acute states of mental automatism”).

With a somewhat deeper destruc- tion, the “fantastic encompasses the whole consciousness”, a “complete overturn of the space” sets in and a one-way state arises.Thus, Ey divides this second level of consciousness destruction into several degrees, with each of which connects groups of symptoms.When, finally, the destruction of consciousness encompasses “the ability to create a field,” the ability to “present,” there is a syndrome of mental confusion (amentia), in which clinically there is the impossibility of differentiating mental processes, deep obscuration, disorientation in space and space, and the world almost completely ceases. ” introduce myself. ”

According to Ey, each subsequent level of consciousness destruc- tion includes the violations of the previous level and therefore the clinic has affective disorders, for example, in the oneiric state, and affective disorders and symptoms inherent in the oneiric state in the amential state.In terms of clinical classification, Ey does not deviate from the traditional clinical division characteristic of French psychiatry, and proposes only with regard to psychoses of the “second level of destruction”, i.e. hallucinatory-oneiric, to distinguish two thematic modalities: the theme of happiness (ecstasy) and the theme of unhappiness (disaster, torment).

The concept of Ey represents, therefore, an attempt to more modernized the rationale for the traditional division of acute psychosis into large syndromes.Интересной является попытка квалифицировать

Mental and behavioral disorders due to alcohol use. Part 1

Alcohol is the most widely used psychoactive substance in the population. Due to the fact that not all cases of abuse are in the field of medical observation, epidemiological data on the alcoholization of the population, in addition to the number of patients with relevant diagnoses undergoing treatment, are obtained in a variety of ways: per capita consumption, life expectancy, suicide rate, germinal alcoholic the syndrome, the prevalence of cirrhosis of the liver, the cost of treatment for somatic diseases caused by alcoholism, the cost of lost as a result of alcoholism What time is it?

Morbidity varies greatly depending on geographical and socio-cultural conditions. In some countries, alcohol consumption is considered high (Russia, France, Scandinavia, Ireland, Korea), in some – low (China, countries of the Islamic world and the Mediterranean basin).

Mostly alcohol problems are typical for men; there are also significant transcultural differences. In women, pathological alcoholism begins later, spontaneous remissions are less likely. Pathology is most common at a young age (15-30 years), in individuals divorced or single, with lower levels of education and antisocial tendencies in adolescence. There is no systematic data on the role of the profession in the occurrence of the disease, however, there was a significant predominance of cases of liver cirrhosis in the service sector and literary circles.

Alcoholization is associated with 50% of road accidents, 50% of homicides, 25% of suicides. As a result of cirrhosis of the liver and a number of generalized somatic diseases provoked by alcoholism, the average life expectancy of patients is shortened by 10 years compared with the healthy population. Patients with alcoholism have the same risk of suicide as depressive patients – 15% of them complete their lives in this way.

Etiology. The disease is apparently the end result of a complex interaction of the biological vulnerability of the body and the influence of environmental factors. Hereditary burden plays an absolute role, although the mechanism of genetic transmission is still unknown. Children of alcoholics are 4 times more likely to get sick than non-alcoholic children, even if they were not brought up by their biological parents. In the presence of hereditary burden, the clinical picture is characterized by a more severe course.

The concordance of alcoholism among identical twins is twice as high as that of opposing people of the same sex. Neuropsychiatric pathology in childhood contributes to the development of the disease, for example, behavioral disorders (F91) or tic disorders (F95). A number of metabolic products when exposed to alcohol causes a change in the neurochemical adaptation of the brain at the cellular level. Perhaps this makes the body dependent on alcohol to maintain established pathological homeostasis. Alcohol can also lead to increased activity of endorphins or morphine-like substances.

The theory of learning was also used to explain the emergence of dependence. Temporary relieving of internal tension, fear, and the concomitant feeling of success in one’s social behavior during the first episodes of alcohol abuse can play the role of positive reinforcement, fixing a behavioral pattern dependent on alcohol.From the point of view of psychoanalytic theory, alcohol addiction predisposes excessively expressed, learned in the course of upbringing, excessive demands on moral attitudes and social behavior (“Super-I”). Stress arising from the inconsistency of the patient with these standards, decreases with alcoholism (“Super-I dissolve in alcohol”). Psychological features formed in early childhood that are generally typical for the personality of an alcoholic are described. It is characterized by timidity, difficulty in establishing contacts, insufficient self-assertion, impatience, irritability, anxiety, hypersensitivity and taboo in the course of education sexuality. An increased level of aspirations is combined with insufficient opportunities to achieve goals. Alcohol can give an illusory feeling of inner strength and success.

F10.0 Acute alcohol intoxication

Clinic, The state develops soon after taking an excessive (different depending on individual tolerance, rate of absorption and metabolism) amount of alcohol. A variety of clinical manifestations include disorders of social behavior, intellectual functions, motility, affect, vegetatics. In some cases, there is an increased talkativeness and sociability, in others – the desire for solitude and dysphorically suppressed background mood. Affective lability can reach the level of intermittent episodes of laughter and crying.

Symptoms increase as the level of alcohol in the blood increases, but they can also decrease with a sufficiently high tolerance, despite continued administration.

Depending on the dosage, the clinical picture changes, ranging from a state of mild euphoria (0.3 mg% in blood with normal tolerance) to impaired coordination, ataxia (1 mg%), confusion, constriction of consciousness (2 mg%), coma, suppression respiration and, occasionally, death (at a level in excess of 4 mg%).


In addition to signs common for acute intoxication, the condition should meet the following criteria: 1) the presence of at least one of the following behavioral and cognitive impairments: a) disinhibition, b) conflict, c) aggressiveness, d) affective lability, e) concentration disorders, f) narrowing of mental abilities, g) decrease in mental and productive productivity; 2) the presence of at least one of the following neurological disorders: a) unsteadiness of gait, b) negative Romberg test, c) signs of dysarthria, d) nystagmus, d) impairment of consciousness (for example, somnolence, coma).Differential diagnosis is carried out with soporous comatose states of a different etiology: injuries of the skull and spine, diabetic and hepatic coma, cardiac arrhythmia, myasthenia, overdose with a combination of use with other psychoactive substances.

F10.07 Pathological intoxicationThe etiology is unknown.

Predisposing factors are organic brain damage (especially in connection with encephalitis and injuries), old age, general fatigue, and alcoholism while taking sedatives and hypnotics. Since this rare violation is more common in people with an increased level of anxiety, for whom aggressive behavior is generally not characteristic, it is assumed that alcohol, causing disorganization of mental processes and loss of self-control, may contribute to the release of aggressive impulses.


The condition is characterized by behavioral disorders that suddenly appear shortly after drinking small amounts of alcohol (the level in the blood is usually below 1.5 mg%). Behavior is characterized by impulsive aggressiveness with tendencies that are dangerous for others or, more rarely, for oneself against the background of confusion, disturbances of orientation and perception (illusions, transient visual hallucinations and delusions). The condition lasts up to several hours, ending with a long sleep, followed by amnesia of the episode.


In addition to the fact that pathological intoxication occurs after taking a dose that does not cause a state of intoxication in most people and the signs common to Flx.0 are observed, the following criteria must be met: 1) the presence of verbal and / or non-verbal aggression towards others, which is atypical for a person sober condition, 2) the condition develops very quickly, usually within a few minutes after taking alcohol, 3) there is no data on the presence of any other cerebral or mental disorders.The differential diagnosis is carried out with episodes of sudden behavioral changes in temporal epilepsy.


The focus is on preventing the consequences of allo- and auto-aggressive behavior. Motor restriction may be necessary, but difficult because of the suddenness of development of the state. Plegiruyuschiy effect (if possible) is achieved by injection of antipsychotic (haloperidol).

F10.1 Harmful use of alcoholClinic.

Massive use of alcohol causes reversible fatty infiltration of the liver – the center of alcohol catabolism. It is not yet known exactly how this infiltration contributes to the occurrence of cirrhosis of the liver. Inflammation and, then, destruction of liver cells in cirrhosis is fatal in 10–30% of carriers of this disease.

Alcohol dissolves the gastrointestinal mucosa, causing irritation and bleeding, and contributes to achlorhydria, gastritis, and stomach ulcers. Diseases of the small intestine, pancreatic insufficiency and pancreatitis are also associated with alcoholism (75% of patients with pancreatitis are alcoholics). Alcohol interferes with the normal processes of digestion and absorption of food, reducing the intestinal absorption of a number of important nutrients, including vitamins and amino acids.

Chronic alcohol consumption violates the performance and rhythm of the heart, myocardial oxygenation, causing cardiomyopathy after 10 years or more of alcohol abuse. Chronic alcoholism due to a decrease in the number of leukocytes reduces the body’s resistance to infectious and oncological diseases, adversely affecting the body’s immunity.

As a result of direct effects on testosterone levels and testicular atrophy, alcohol reduces sexual and reproductive functions in men. Increasing the level of female hormones leads to female type of hair growth and an increase in the mammary glands in 50% of alcoholics. The indirect toxic effect of alcohol in the zone of limbic structures and the hypothalamus, as well as the neuropathy of the peripheral parasympathetic nerves involved in erection, also plays a role in impaired sexual function. In alcoholic women, there are dysfunctions of the sex glands, accompanied by insufficient production of female hormones, changes in secondary sexual characteristics, extinction of the menstrual cycle, infertility.

Alcohol use during pregnancy is fraught with the emergence of the so-called fetus in the fetus. fetal alcohol syndrome (slow growth before or after childbirth, abnormal configuration of the face and skull with a decrease in head circumference and flattening of facial features, signs of mental retardation and behavioral disturbances).

F10.2 Alcohol addiction syndrome


In addition to common for F1x. 2 manifestations of the syndrome of addiction should be mentioned that the specificity of chronic alcoholism includes various stereotypes of alcoholism. Drinking significant amounts of alcohol can be daily or limited to weekends. Alcohol abuse for several days / weeks / months (binges) can be interrupted by long periods of abstinence (dipsomanic stereotype). Daily alcoholism during off-hours can be accompanied for a long time by relatively safe professional status and lack of awareness of uncontrollable abuse.Binges can also be of a different nature, ending either spontaneously or involuntarily as a result of the corresponding complications of the social situation or physical condition (the latter is called “gamma-alcoholism” in the USA).

Characteristic signs are also episodes of complete or partial amnesia (the so-called palimpsests) of the period of intoxication, during which the patient could make the impression of a person with a safe mind on others.Amnestic manifestations generally correlate with the severity and duration of the disease.

The tendency to the use of non-food alcohol (technical alcohol, polish, brake fluid, etc.) is quite typical, increasing with the social degradation.Diagnosis. Diagnosis of addiction syndrome, especially in its initial stages, as a rule, complicates the tendency of patients to reject alcohol abuse. Sometimes the family of the patient takes the same position. The clinician should pay attention to such signs of early problems associated with alcoholism, such as difficulties in communicating with the spouse partner, loss of contact with children, loss of interest in family problems, frequent outbreaks of irritability.

Alcohol can be used both to relieve sexual lethargy and to avoid sexual contact. Late arrivals, inability to properly organize work, and meet the deadlines become typical for professional activities. Morning vomiting, diarrhea, gastritis, liver enlargement, cigarette burns on the fingers can be early somatic stigmas.


Central is the problem of abstinence from alcohol. Due to the fact that the so-called. controlled use still represents a high risk of relapse, the patient should be offered complete and lifelong abstinence, on the assumption that there is no condition: “recovered alcoholic”.The formation of motivation for total abstinence determines the overall success of treatment and depends on the proper use of intrapsychic and social factors that are important for motivation. Here, a proper assessment is needed in each case of an individual complex system of hereditary factors, conditions for early development, personal structure, socio-cultural and family influences, and concomitant psychiatric pathology.

The pessimistic conclusion about the lack of motivation for treatment too often hides the inability of the doctor to find an individual approach to the patient, to establish a therapeutically productive relationship with him.

At the initial stages, individual psychotherapy sets the tasks of emotional support for the patient with a gradual analysis of the mechanisms of dependence on others, lack of self-esteem, aggressive impulses, and such maladaptive psychological defenses as lies and denial. The most successful is a combined psychotherapeutic approach, which includes both identifying the internal causes of alcoholism (lack of resistance to social stress, low self-affirmation, etc.) with the development of more effective strategies for resolving behavior, and connecting with emotionally stimulating social influences that are important for the patient ( family relations, goal-setting behavior in the professional sphere).

Here, various group and matrimonial therapy programs are very effective, carried out both in inpatient conditions and for the purpose of long-term supportive psychotherapy in outpatient settings, including self-help groups (the most famous of them is the Alcoholic Anonymous program).

f it is impossible to correct the pathogenic influence of the family and close social environment, it is advisable to temporarily place the patient after the inpatient treatment in specially structured conditions of out-of-hospital residence.

The latter have not yet received practical distribution in Russia.Of the drugs, the most widely used is antabuse (disulfiram), the metabolism of which is accompanied by the accumulation of acetaldehyde in the blood when even small amounts of alcohol are consumed. The toxic reaction caused by a daily dose of 250 mg of antabus includes facial flushing, feeling of heat in the sclera, upper limbs and chest, nausea, dizziness, marked malaise, blurred vision, tachycardia, feeling of suffocation, numbness of the extremities.

The most serious consequence is a pronounced decrease in blood pressure. The reaction usually lasts 30-60 minutes. At higher doses of antabus, impaired consciousness and memory disorders may develop. The success of therapy depends on the motivation of the patient to regularly receive antabus.

At the initial stages of withdrawal symptoms of anxiety, anxiety, sleep disturbances dominate, which are controlled by anxiolytics; the clinical severity of depression during this period necessitates the use of antidepressants, lithium.

To relieve anxiety, behavioral therapy techniques can be successfully used (relaxation programs, self-control, self-affirmation enhancement). Chemical observational conditioning (apomorphine, against the background of which alcohol intake causes vomiting), as well as various suggestive methods (acupuncture, shock psychotherapy, coding, therapeutic vows, etc.) have a long-term effect only in a narrow category of highly motivated to treatment. patients, by virtue of which they are not funded by the insurance system, and they find much more limited use in world narcology than in Russia.

F10.3 Cancellation status due to alcohol use

Clinic. The condition is characterized primarily by a variety of vegetative symptoms, gross rapid-frequency generalized tremor, aggravated by movement or excitement. Due to the reduction in alcohol by the convulsive threshold, often within the first day, large convulsive seizures may develop, especially if they are in history. Usually disturbed sleep, accompanied by vivid nightmare dreams. Symptoms are enhanced by prolonged use of significant doses, dipsomanic alcoholism stereotype, general weakening of the body as a result of overwork, malnutrition, concomitant physical illness or depressive state.

The syndrome develops in 24–48 hours after stopping the intake and does reverse development within 5–7 days (including without treatment), although irritability and sleep disturbances can last even longer. In some cases, the development of symptoms leads to the resumption of alcohol intake for its removal.


In order to make a diagnosis, in addition to meeting the general criteria for withdrawal syndrome (Flx.3), at least 3 of the following symptoms should be observed: a) tremor of the fingers of the hands extended in front, the tip of the tongue or the eyelids, b) sweating, c) foul condition, nausea, vomiting, d) tachycardia or hypertension, e) psychomotor agitation, e) headaches, g) insomnia, h) malaise, weakness, and) transient visual, tactile or auditory hallucinations or illusions, j) large convulsive seizures.

Symptomatic treatment with bed rest, rehydration with severe fluid loss (sweating, vomiting, low-grade fever), elimination of vitamin B12 deficiency and folic acid. With reduced nutrition, thiamine is injected parenterally (before glucose, since the latter can impede the absorption of thiamine). If there is information about convulsive seizures in the history, magnesia sulphate is prescribed (2.0 50% w / m 4 times a day for two days). In general, anticonvulsants are less effective in preventing and treating convulsive manifestations with withdrawal syndrome.

In this regard, as well as to relieve hyperactivity of the sympathetic nervous system, benzodiazepines (diazepam, chlordiazepoxide) are more effective.

F10.4 Cancellation status with delirium due to alcohol use


The condition is also known as delirium tremens (delirium tremens). This is the most severe manifestation of withdrawal syndrome; it develops within a week after stopping or reducing doses, most often at the age of 30–40 years after 5–15 years of consuming significant doses. It develops in about 5% of alcoholics who are on a permanent basis, often being the first sign of alcoholism not previously diagnosed. Dipsomanic stereotype of alcoholism and concomitant somatic pathology contributes to the emergence.

Vegetative disturbances (tachycardia, sweating, hypertension), low-grade fever, wakefulness of perception (often visual and tactile, in the form of insects, small animals) and rudimentary delusional ideas defining the patient’s behavior, often dangerous, join signs common for delirium (F05). for myself and others. Large convulsive seizures are common, usually anticipating the onset of delirium in a third of patients with convulsive syndrome, most likely due to the deficiency of pyri-doxin (vitamin B6). Increases the pressure of the liquor and the level of globulin in it. In half of the cases transient albuminuria is noted.

The syndrome differs from delirium of non-alcoholic genesis by more severe impairments of consciousness and behavior, deeper amnesia of the episode at the exit from it, and greater vestige-related concomitant delusions.In the absence of complications, death is relatively rare (3-4%). The presence of auditory hallucinations is a prognostic sign of a more protracted course. In the absence of recovery, the state progresses to the formation of Korsakov syndrome in 15% of cases. If untreated, as a result of concomitant somatic pathology (pneumonia, fat embolism, renal, hepatic or heart failure as a result of hypohydration and hyperkalemia) delirium can be fatal in 20% of cases.


The most reliable way of dealing with delyriya is its prevention. 25-50 ‘mg of Elenium (chlordiazepoxide) every 2-4 hours during the most dangerous period of the withdrawal syndrome usually prove to be sufficient. If delirium could not be prevented, the dose is increased to 50-100 mg every 4 hours. The use of phenothiazine preparations should be avoided due to the fact that they lower the threshold of convulsive readiness, and may also contribute to a further reduction in liver function.Important is a high-calorie diet rich in carbohydrates and vitamins, if necessary – measures for rehydration.

The physical limitation of agitated patients is impractical, since they usually do not stop their attempts to free themselves, continuing to complete exhaustion. Skillful sedative psychotherapy may be important.

F10.5 Psychotic disorders as a result of alcohol

Manifestations of alcoholic hallucinosis (usually auditory) usually begin within 48 hours after the cessation of alcoholism and persist after the withdrawal of withdrawal syndrome, while not being a component of possibly accompanying delirious symptoms. The content of votes is usually unpleasant for the patient, causing reactions of fear and anxiety, sometimes defining behavior and making it dangerous. This is usually a critical, threatening or offensive comment, where the patient is mentioned in the third person. Auditory deceptions can take on the character of elementary sounds (for example, calls).

The disorder is relatively rare, more common in men; the syndrome appears at any age, but against the background of an already formed dependence on alcohol. Its duration is varied – from several weeks to several months.Psychotic disorders can take on the character of paranoiac symptoms or systematized delusions, the most famous of which is the alcoholic delirium of jealousy.

The diagnosis of the latter can be complicated by the existence of real justifications for jealousy due to the sometimes existing decline in sexual function and the loss of the patient’s interest in family matters.

From schizophrenia and affective disorders, these conditions are distinguished by the lack of relevant data in history, a temporary connection with the abolition of alcohol, the relative short duration of the course, the characteristic content of votes. The syndrome differs from alcoholic delirium by preservation of consciousness, the preferred appearance of hallucinations not at night.Treatment includes primarily activities carried out with withdrawal syndrome. In the absence of effect, small doses of high-potency neuroleptics can be used with discontinuation after the symptoms have been eliminated.

F10.6 Alcohol-based Amnesia Syndrome

Wernicke’s encephalopathy (delirium, ataxia, nystagmus, ophthalmoplegia), acutely developing amid perennial alcohol abuse with concomitant tiamin deficiency due to nutritional deficiencies and vitamin B1 absorption, in 85% of cases without treatment ends with amnestic syndrome (psychosis) of Korsakov, nature a feature of which is a violation of short-term memory (but not direct memorization) against the background of an unbroken consciousness with the impossibility of transition of short-term memory into long-term yu Both disorders sometimes designate Wernicke-Korsakov syndrome.

The syndrome in recent years has become increasingly rare due to the routine use of thiamine during detoxification. The common amnesia disorder can be accompanied by the usual somatic and neurological consequences of alcohol abuse. With daily use of 50-100 mg of thiamine chloride, it is possible to achieve different degrees of recovery, but in most cases, Korsakov’s syndrome remains irreversible, despite withdrawal and continued administration of thiamine. Structural deficiency of the trunk and diencephalic brain regions is determined pathologically.

Acute endogenous psychosis. Part 2

As an in-depth psychopathological study of early dementia, the concept of “schizophrenia” appeared and was recognized. However, the solution to the problem of acute atypical psychosis has not progressed significantly. The clarification of the clinical forms of schizophrenia, made somewhat later by Kraepelin (1913), did not lead to the final solution of the question. As you know, Kraepelin recognized the existence of circular schizophrenia, schizophrenia with a depressive-delusional clinical picture, the possibility of recovery from schizophrenia, its periodic course. For all these reasons, by the end of the 10s and especially in the 20s of our century, the controversy surrounding atypical psychosis intensified.

There were again points of view about the impossibility of reducing many forms of psychosis to one of two endogenous diseases according to Kraepelin’s classification. In France, many psychiatrists again put forward, with minor amendments, the teaching of Magnan on acute polymorphic attacks.

In Germany, by this time, even more attention began to attract direction, whose supporters viewed acute atypical psychosis as a group of endogenous diseases (along with manic-depressive psychosis and schizophrenia). Representatives of the Kleist school in the 1920s proposed a new clinical classification of acute atypical psychosis. This direction has many supporters. Other psychiatrists (Kretchmer, Mautz) have suggested the genetic or constitutional conditionality of the mixed clinical picture of acute atypical psychosis.

A point of view emerged that many of the schizophrenic manifestations of psychosis are “schizophrenic reactions” and their occurrence is associated with the presence of a special form of degenerative background (Popper, 1920), with a schizoid predisposition (Kahn, 1921).

Thus, in the 1920s, the following clinical guidelines for assessing acute atypical psychosis were already determined:

  1. The classical dichotomous direction, which has many supporters at the present time, according to which all atypical psychosis, including acute, can be attributed either to manic-depressive psychosis or to schizophrenia. It may be noted that for supporters of this point of view it was still a controversial question as to which of these two psychoses one should nevertheless refer certain variants of acute atypical psychoses.
  2. The direction according to which acute atypical psychosis should be considered as a special group of endogenous psychosis (Kleist and his school).
  3. The direction that treats atypical psychosis as mixed as a result of combining different constitutional radicals or as reactions when they are especially ready.

In the following decades, up to the 1940s, the central issue regarding acute atypical psychosis remained the issue of their nosological affiliation in numerous discussions on schizophrenia. True, the view was increasingly expressed that it was necessary to consider the possibility of their exogenous conditionality in their nosological assessment. A similar point of view arose after psychiatrists considered “endoform pictures” and began to allow for exogenous mental diseases. Many psychiatrists, supporters of the nosological direction, began to describe various types of acute psychosis, the clinical picture similar to manic-depressive psychosis and schizophrenia. In particular, psychogenic delusional psychosis (acute paranoids, prison psychosis), various catatonic and delusional psychosis in infectious, somatic diseases, etc. were described.

A broader understanding of somatogenic and reactive psychoses led to the “dissolution” of a large number of acute atypical psychoses in them. Nevertheless, the study of acute psychosis from the standpoint of “exogenesis” made it possible to find out a number of important aspects of acute atypical psychosis, in particular, to establish a close connection between the onset of seizures and certain harmful factors.

The literature data on the development of views on acute endogenous psychosis show how difficult they have been for clinical analysis for many decades. As is known, up to the present, these psychoses remain one of the most difficult problems of clinical psychiatry. The extensive literature is devoted to them, in which questions of clinic, psychopathology, systematics, nosological assessment are considered. There are numerous disagreements about these issues. This fact determined the direction of our analysis of the main modern works devoted to the psychoses under consideration. It seems to us important to identify the main sources of still existing difficulties and disagreements regarding the most important clinical aspects of acute endogenous psychosis. Such an analysis of modern literature, together with the historical data, should, in our opinion, facilitate the development of approaches to overcome the difficulties of the clinical evaluation of acute endogenous psychoses.

In determining the scope of the literature to be analyzed, the following provisions were taken into account, arising from the state of clinical psychiatry.

  1. The most clinically clear and generally accepted acute endogenous psychosis are typical manic-depressive psychosis and seizure-like remitting schizophrenia with a fairly pronounced schizophrenic seizure pattern and characteristic schizophrenic personality changes (dissociative defect type). For these two psychoses, the classic differences between manic-depressive psychosis and schizophrenia remain true.
  2. Difficult for clinical evaluation are those acute endogenous psychosis, which are referred to as atypical circular psychosis, schizoaffective psychosis, acute atypical psychosis, recurrent schizophrenia.

In French psychiatry, acute atypical psychosis is currently included in manic-depressive psychosis, in the syndrome of mental confusion (confusion mentale) and in the group of delusional flashes (bouffees delirantes) singled out by Magnan.

In the understanding of French psychiatrists, mental confusion, or “states of confusion,” is a psychopathological syndrome characterized by stupefaction, irregular thinking, disorientation, false recognition (not always), oniric (dreaming) nonsense. Considering the main, determining disorder of confusion (simple or with hallucinatory-delusional phenomena), the syndrome of mental confusion can be understood very broadly.

Along with delirious states (such as delirium tremens), with Korsakov’s psychosis, with various acute infectious and intoxication psychosis, the concept of mental confusion also includes acute delirium (delirium acutum, febrile catatonia), and acute catatonic psychoses (non-febrile) and even psychoses with frustrated mind. leading to organic dementia.

All acute psychoses with catatonic symptoms and disorders of consciousness (including delirium acutum) are practically included in mental confusion as a syndrome of toxic-infectious genesis. Other acute, schizophrenia-like hallucinatory-delusional psychoses are combined by Magnan, the common term “delusional outbreaks”. True, at present (unlike Magnan), this group does not include catatonic psychoses. The delusional outbursts themselves are considered as a syndrome of different etiology, which is not only found in “degenerants”. Clinical and psychopathological description of such psychosis, made by Magnan. remains classical and almost generally accepted. Thus, the main clinical features of these psychoses are: the suddenness of the appearance of delirium (“instant illumination”), polymorphism and instability of delusional stories, massive affect (elevation or decline of mood), clarity of consciousness (at least apparent), and most often a sudden end of an attack. Although relapses are allowed and considered frequent, there is usually no personality change after an attack. The classic clinical forms of these delusional outbreaks are as follows:

  1. Acute fantastic psychoses described by Dupre (1925). We are talking about acute psychosis, the clinical picture of which is determined by the acute fantasy that has arisen, more often such as delusions of grandeur and less often self-incrimination with the nature of immensity.
  2. Acute interpretative psychoses (described by Serieux, Capgras, 1909) and later designated as “acute interpretative states” . These psychoses are delusional syndromes such as acute paranoid with fear and anxiety.
  3. Acute hallucinatory outbreaks and acute hallucinatory psychoses with a predominance of auditory, verbal hallucinations, pseudohallucinations, and impact ideas;
  4. True polymorphic forms, under which the systematization of delusional ideas does not occur.

Many of the acute transient psychoses are considered by French psychiatrists as atypical attacks or equivalents of manic-depressive psychosis. A catatonic equivalent (replacement of one or more affective attacks with catatonic attacks), episodic delusions of exposure, a senestopathic equivalent (an acute senestopathic attack), intermittent hebephrenia, acute paranoids, pseudo-paired melancholia are described; schizoform melancholia, pseudoshizophrenic postpartum psychosis of catatonic structure.

Recently, new terms have appeared and continue to appear to denote individual acute psychosis or whole groups. Baruk distinguishes postpartum hallucinatory delusions and postpartum delusions of persecution. Courchet et al. described acute psychosis in men and called it “transient mania” (according to Krafft-Ebing). According to the authors, this psychosis is a suddenly beginning state of motor excitation or confusion with disorientation, deep anxiety, mutism, without delusions and hallucinations. The psychotic state lasts 2–3 days, followed by a short phase of asthenia, and then recovery occurs. The acute period is completely amnesized. Attacks are not associated with any exogenous factors.

Acute endogenous psychosis. Part 1

In the first period of development of clinical psychiatry, when psychosis was a very poorly differentiated mass, acute endogenous psychosis, naturally, did not stand out.

The clinical picture of the psychoses discussed here can be found in the descriptions of the concepts “idiocy” (Pinel), “acute dementia”, “mania”, “lipemania” (Esquirol).

As clinical psychiatry developed, mental illness began to be treated more differentially. Boismont in 1845 described in detail the clinical picture of acute delusions and differentiated it from both acute mania and meningitis. Calmeil (1851) clarified the clinical features of delirium acutum to an even greater degree, and since that time the controversy over this acute psychosis began to concern mainly its nosological evaluation. Thus, by the middle of the 19th century, one of the types of acute atypical psychosis was already identified, its clinical-psychopathological features were described quite accurately.

At about the same time, a second clinical type of acute psychosis has been noted in the literature, currently referred to as “periodic catatonia” (or oneiric catatonia). Within the framework of melancholy and acute dementia, Georget (1820) described stupidite, which he identified as a new disease. Ferrus (1838) joined Georget, emphasizing the non-febrile nature of psychosis. This author noted a favorable outcome of the attack. Ferrus described the condition of the patients as “the elimination or rather the delay of all brain processes, rapidly advancing, without temperature,“ curable ”. Soon Baillarger (1843), Griesinger (1845), and then many other psychiatrists recognized the existence of a special form of melancholy — melancholy with a stupor and described it in detail.

By this time, individual forms of mania began to be distinguished, some of which were actually described as independent types of seizures (hyperacute mania, frenzy, madness). Judging by the cited case histories, under this name, the authors described the attacks of the oneiric-catatonic, manic-delusional, paraphrenic structure. Within the framework of a single Grizipger psychosis, the psychoses considered by us were included as options in melancholia, mania and “madness”. Phase affective, affective-delusional and affective-oneiric (according to modern estimates) psychosis related to melancholia and mania. “Madness” is more consistent with modern paroxysmal progredient schizophrenia.

The process of differentiation of mania and melancholia was further intensified after the isolation of various types of circular insanity by French psychiatrists Baillarger (1854) and Falret (1851) in the middle of the 19th century. These studies confirmed the possibility of alternating mania and melancholia, which was noted long ago by doctors, and made it possible to single out a circular insanity with characteristic psychopathological picture and course.

Thus, the clinical-psychopathological contours of certain types of acute psychosis, characterized by seizures in the form of attacks, were described. In subsequent years, a group of acute psychosis began to grow in quantitative terms and be refined in its clinical and psychopathological content. A classification of acute forms of insanity began to appear. It was soon noted that circular insanity, delirium acutum, melancholy with stupor, hyperacute mania, etc., do not exhaust the whole group of acute psychoses. The concept of acute paranoia appeared (Westphal, 1876), which for a long time was the center of numerous discussions. The isolated psychosis soon turned out to be much more complicated than the simply acutely occurring delusional state.

Already in 1879, Merklin noted that acute paranoia is characterized by a darkening of consciousness or confusion, similar to those that occur in dreams or febrile delusions. Dreams, confusion of experiences of patients with acute paranoia have become more and more emphasized by psychiatrists. As a result, acute paranoia was divided into two large groups: psychosis with a predominance of delusional symptoms (without gross disturbance of consciousness) and psychosis, which were characterized not only acutely emerging delusions, but also hallucinatory, affective disorders and blackout. These two main forms of acute insanity remained at the center of controversy over the next two decades. Soon, to overcome the differences that arose, the concept of “amentia” Meinert (1893) was proposed, which included cases of acute paranoia with severe disorders of consciousness and many other acute psychoses. As it is known, the concept of amentia, which is extremely broad in the understanding of Meinert, soon began to narrow, and at present it has limited application.

In the last decades of the XIX century a large number of works appeared in which it was proposed to divide the acute forms of insanity into separate types. V.P. Serbian (1892, 1906) besides mania, melancholia, and acute dementia distinguished acute amentia and acute paranoia. Contrary to the opinion of Meinert, that with amentia there are no cardinal symptoms, V.P. Serbsky singled out as characteristic signs of amentia a disorder of consciousness (according to the dream type), affect lability and disturbance of associative activity. Typical for acute paranoia, V.P. Serbsky believed: acute or subacute occurrence of unstable and unsystematized delusions, the presence of a pronounced affective state (depressive or expansive), a relatively clear consciousness. V. P. Serbsky referred to mixed forms (luck) as paroxysmal psychosis, in the clinical picture of which affective and delusional symptoms are combined with elements of confusion.

S. S. Korsakov (1901) further deepened the clinical analysis of “acute forms of insanity”. He described in detail the varieties of dysnoi (acute psychosis with a disorder of consciousness) and acute paranoia. S. Korsakov considered relative clarity of consciousness to be a characteristic sign of acute paranoia.

A similar point of view was Seglas (1895), who believed that it was necessary to distinguish between acute psychosis and confusion, that is, confusion (confusion mentale), and acute psychosis without stupefaction (acute paranoia). Within the framework of acute paranoia (simple and hallucinatory), he described depressive-paranoid oneiric attacks.

In Germany, by this time we also find a similar division of acute psychosis into psychosis without a sharp disturbance of consciousness (Wahnsinn) into psychosis with confusion (Verwirrtheit) (Kirchof, Zienn, Kraepelin).
Kraepelin himself in 1895 distinguished several forms of acute treatable psychoses: mania, melancholy, delirium, exhaustion psychosis, acute dementia, hallucinatory and depressive forms of acute delirium.

Thus, on the eve of the emergence of Kraepelin’s nosological classification with respect to acute forms of insanity, there were undoubted successes, which concerned mainly the issues of clinical differentiation of these psychoses. Most of the acute forms of psychosis were by this time grouped around affective, psychomotor, delusional disorders, and confusion syndrome.

At the end of the 19th century, principles that did not allow for a fairly complete clinical and psychopathological characterization of these complex psychoses were based on the isolation of individual forms of acute psychosis. Affective disorders (for circular insanity), febrile, catatonia, death (for delirium acutum), catatopic stupor with depressive delusions (for melancholy with stupor) were insufficient to characterize many of these psychoses. The concepts of acute paranoia, mental confusion were also unsatisfactory. As you know, for the psychoses designated by these concepts, a very different course was allowed: an exceptionally benign (one attack followed by recovery), a remitting or recurring course without gross changes (recurrent amentia, paranoia) and an unfavorable course, as a transition to a chronically current psychosis or in a state of dementia.

Particularly difficult to describe and designate were those of the acute forms of insanity, in which there was a complex clinical picture and a large variability of symptoms (affective, psychomotor, hallucinatory-delusional, impaired consciousness, etc.). These psychosis did not fit even in such broad concepts as amentia, acute paranoia, catatonia.

All this indicates that at the time of the emergence of the classifications of Krapelin’s mental diseases, many forms of acute psychosis were not yet sufficiently studied, even in their psychopathological structure. Other forms of acute mental illness were clinically quite clearly outlined, although the principles of their psychopathological description in many respects suffered from the shortcomings inherent in all static psychopathology.

Classification of mental illness Krepelin did not solve the issue of acute atypical psychosis in their essential clinical and psychopathological aspects. Moreover, against the background of a more definite situation in which other acute psychosis (typical manic-depressive psychosis, various forms of early dementia, many febrile, somatogenic and infectious psychosis) found themselves, the clinical “disorder” of acute atypical psychosis immediately appeared before psychiatrists as one of complex clinical problems.

As is known, in the initial nosological classification of Kraepelin, as well as in the classifications of his supporters, at first there was a desire to abstract from many psychopathological, clinical aspects of these psychoses, to a significant simplification of their structure, thanks to which it was possible to attribute them to one of the two main endogenous diseases . Thus, acute delusional psychosis (acute paranoia) was treated by many psychiatrists to manic-depressive psychosis; acute catatonic psychosis without an outcome in dementia was more readily regarded as a catatonic form of early dementia. Such a hasty nosological formulation of insufficiently studied forms of acute psychosis immediately led to difficulties in attempting to classify psychoses that do not fit into the concepts of manic-depressive psychosis and early dementia. This soon led psychiatrists to amend and supplement the original scheme. Such a need was due to the fact that the clinical picture of many endogenous psychosis was closer to early dementia, while their paroxysmal course and the appearance of affective attacks more resembled manic-depressive psychosis. Rehm (1919) described a catatonic form of remitting insanity with a clearly circular course, despite the fact that many attacks were in the nature of a catatonic stupor. Tamburini described catatonic manic-depressive psychosis, etc. Urstein (1912) came to the conclusion that early dementia can occur circularly and that it is legitimate to include manic-depressive psychosis in catatonia. Other psychiatrists described cases of early dementia with a depressive onset (Pascal, 1911).

Thus, almost simultaneously with the spread of the nosological concept of Kraepelin, the disadvantages of the dichotomous division of endogenous psychoses began to be revealed. It is important to note that among the psychoses that do not fit into the scheme, acute psychosis with severe affective disorders and catatonia with remitting course, ie, psychoses, considered up to the present time as acute atypical psychosis, occupied a large place.