Psychiatry - G.T. Sonnyk 2003

Psychogenic disorders (psychogenias) and neuroses

Neuroses represent a group of functional psychogenically conditioned mental disorders characterized by a tendency toward a transitory, protracted course. Clinically, they manifest as asthenic, obsessive, and hysterical disorders, while reality testing and insight into one's condition remain intact.

Neurotic-range mental disorders that frequently accompany somatic and neurological diseases and bear the independent designation of neurotic reactions are not classified as neuroses. Neurotic reactions, neuroses, and psychopathies fall within the purview of so-called borderline, or minor, psychiatry. Neurosis-like disorders must also be distinguished from true neuroses; clinically, they typically present as asthenic, obsessive-phobic, or hysterical disorders of non-psychogenic origin, forming part of the clinical picture of other prolonged psychiatric conditions (such as Schizophrenia) or somatic diseases (such as Hypertension or PEPTIC ULCER DISEASE).

Historical Background.

METABOLISM/2.html">THE CONCEPT OF "neurosis" was first introduced into medical literature by the Scottish physician W. Cullen in 1776. He used the term to denote a nervous disorder unassociated with fever, unrelated to a local lesion of any single organ, and caused by "a general affection, upon which motions and thoughts depend." He viewed tension and relaxation of The Nervous system as The basis of The regulation of vital processes, and attributed the onset of deviations in mental activity, which he termed neuroses, to their disruption.

By the beginning of the 19th century, A wide variety of diseases, conditions, and symptoms were categorized under neuroses. However, in the mid-19th century, driven by major advancements in pathomorphology, The Scope of the concept underwent significant revision and clarification.

With the refinement of pathomorphological research and the identification of morphological organ abnormalities, many conditions and disorders were reclassified from neuroses into other nosological categories. In the second half of the 19th century, the definition of neurosis presupposed the absence of organic Changes in the disease. Nevertheless, this view was not universally shared at the time; in 1907, F. Raymond hypothesized that neuroses lack only those anatomical alterations that could not be detected by the Research Methods available at that point.

Concurrently, the Etiology of neuroses was further refined, giving rise to the understanding of them as Psychogenic Disorders. Significant contributions to this field were made by G. Beard (1868), L. Strümpell (1878), J. Charcot (1888), and P. Janet (1903).

Decisive in this direction were the studies of P. Dubois (1912), who considered the primary feature of neuroses to be the involvement of the psyche—the "mental representation"—in all their symptoms. Based on this, he suggested replacing the term "neurosis" with "psychoneurosis."

The Study of the Clinical presentation of neuroses and the differentiation of their forms underwent a complex evolution. Specifically, hysteria as a disease was recognized even before the Common Era; the Kahun Papyrus mentions it as a pathological condition rooted in the Displacement of the Uterus within the body.

Nearly a century after the Introduction of the term "neurosis," the American physician G. Beard (1869) detailed a condition of irritable weakness among American industrial workers. Initially, he termed this phenomenon "American neurosis" and later neurasthenia. In 1880, C. Westphal formulated the definition of obsessive-compulsive states, which allowed them to be differentiated from neurasthenia.

Thus, by the beginning of the 20th century, the principal forms of neuroses had been described, but their differentiation continued. This process was influenced by such scientific movements as Sigmund Freud's psychoanalysis, behaviorism, and existentialism, alongside the pivotal teachings of I.P. Pavlov on Higher Nervous Activity.

Major studies on this issue were conducted by S.N. Davidenkov (1963), O.V. Kerbikov (1962), A.M. Svyadoshch (1974), B.D. Karvasarsky (1980), and others.

PREVALENCE.

Neuroses have always been a widespread pathology, but recently the number of such patients has begun to grow rapidly. This trend is attributed to social transformations driven by the relentless advancement of scientific and technological progress. Alongside its obvious benefits, progress demands the mobilization of an individual's adaptive resources, for which not everyone is prepared. The high prevalence of neuroses among the population is evidenced by their substantial share within The Structure of mental illnesses, which, according to various authors, accounts for 15–30%. In the USSR, the prevalence of neuroses was 21.1–21.8 per 1,000 population (O.R. Chitava, 1981) and showed a steady upward trend.

ETIOLOGY.

Today, there is no doubt that the onset of neuroses is triggered by informational factors (psychic trauma). This was first demonstrated by I.P. Pavlov in animal experiments.

Psychogenic factors may include:

✵ external conflicts;

✵ intrapsychic conflicts;

✵ prolonged (psychotraumatic situations) or excessively intense emotional or intellectual mental overstrain.

The potency of a psychotraumatic effect is determined primarily not by the physical intensity of the signal or the volume of information it carries, but by its personal significance to the individual. Therefore, neurosis cannot be viewed through the lens of a simple stimulus-response framework. A person's upbringing, life experience, attitudes, ideology, and other factors shape the significance—and consequently the pathogenicity—of any given piece of information.

A major role in The Development of the disease can be played by innate typological Features of the nervous system, as well as its current state. Individuals with asthenic, hysterical, and psychasthenic personality traits prove most vulnerable in this regard, especially if these traits reach a psychopathic level. Thus, P.B. Gannushkin emphasized that no fundamental difference exists between a phase, as a dynamic form of psychopathy, and a neurosis. It is widely accepted that the probability of developing a particular form of neurosis is determined by premorbid character accentuation features.

Specifically:

✵ individuals with asthenic accentuation are prone to developing neurasthenia;

✵ those with anxious accentuation are prone to obsessive-compulsive neurosis;

✵ characterized by a histrionic accentuation, leading to hysterical neurosis.

The onset of neuroses can also be facilitated by long-standing, affectively charged groups of ideas that reflect profound psychotraumatic experiences. E. Bleuler suggested calling them complexes.

Pathogenesis.

According to I.P. Pavlov, the pathogenetic basis of neuroses is a Breakdown of Higher nervous activity involving the overstrain of neural processes or their excessive mobility under The Influence of overly strong stimuli.

Specifically, neurasthenia is characterized by a pathological predominance of excitation over internal conditioned inhibition due to the failure of the latter under the influence of pathogenic factors. This occurs in individuals who, in their premorbid state, exhibited a choleric or, in severe cases, a sanguine temperament. With the continued impact of psychotraumatic circumstances, the process develops toward the stable dominance of supraliminal protective inhibition and the capitulation of excitation. In individuals with a weak type of higher nervous activity, inhibition begins to dominate over excitation immediately, owing to the initial weakness of cortical Cells.

Hysterical neurosis, according to I.P. Pavlov, occurs in patients with a weak artistic type of higher nervous activity. The main factors are the dominance of the subcortex over the cortex due to the functional weakness of the latter, the dominance of the first signaling system over the second in the Cerebral Cortex, and the pathological prominence of negative induction. Under the influence of powerful affective impulses from subcortical ("instinctive") structures, as well as verbal stimuli—whether external or self-generated—a focus of intense excitation flares up in the cortex. It is immediately enveloped by a zone of powerful negative induction, isolating it from other cortical areas. This explains THE ORIGIN OF extraordinary hysterical suggestibility, as the pathological process is isolated from past life experience. When foci of excitation localize in the motor areas of the cortex, various tics and hyperkinesias arise, whereas in the opposite case, paresis, paralysis, and astasia-abasia develop.

The core pathophysiological mechanisms of obsessive-compulsive states were established by I.P. Pavlov in 1933. According to the doctrine he formulated, they are based on a breakdown of higher nervous activity resulting in The formation of persistent (unlike in hysteria) pathological foci in the cortex of individuals with a weak analytical type of higher nervous activity. Alongside the unconditional recognition of the Pavlovian school's merits in studying this problem, it should be noted that as early as 1913, the prominent domestic psychiatrist M.M. Asatiani published research on phobias as conditioned Reflexes, viewing them as "pathological inert stagnant excitation in foci."

Summarizing previously obtained data and the results of his own research, A.G. Ivanov-Smolensky (1952, 1974) concluded that a definitive role in the mechanism underlying obsessive states belongs to phenomena of pathologically positive and pathologically negative induction, accompanied by impairments in the inhibitory processes formed during ontogeny.

Sometimes it is necessary to take into account The Significance of phase states. For instance, The Mechanism of the ultraparadoxical phase underlies The Emergence of contrast thoughts and drives. A significant portion of obsessive states is associated with the second signaling system. The temporary relief experienced by patients after performing obsessive ritualistic actions can most likely be explained by the emergence of a new focus of excitation in the motor analyzer, accompanied by the development of negative induction and the suppression of the primary focus of inert excitation.

According to alternative views on the pathogenesis of neuroses, the central factor is a malfunction of the cerebral systems that regulate adaptation processes. The greater the discrepancy between the actual situation and the anticipated one, the higher the likelihood of pathological consequences for the Organism. This gives rise to nervous tension accompanied by a sense of dissatisfaction—frustration—along with stress and its corresponding endocrine and autonomic manifestations.

Predictive processes influence the emergence of emotions in response to informational input. According to electroencephalographic studies, prediction is carried out through the interaction of the reticular formation, the limbic system, and the cingulate gyrus. A particularly prominent role belongs to the limbic system ("the visceral brain"), which regulates emotional arousal.

A deviation of events from the predicted course triggers the mobilization of the organism for high-energy actions, primarily at the endocrine level (increased adrenaline secretion, etc.). Emotional tension—and with it, the potential psychotraumatic impact of a conflicting situation—can be neutralized only if a clear behavioral strategy is developed that facilitates emotional discharge.

Classification.

In domestic literature, it is traditional to distinguish three classical forms of neurosis:

✵ hysterical neurosis,

✵ neurasthenia,

✵ obsessive-compulsive neurosis (obsessional neurosis).

In the past, the terms "organ neuroses" (referring to The Heart, Lungs, or Stomach) and "systemic neuroses" (referring to the cardiovascular, respiratory, or urogenital systems) denoted a form of neurosis characterized predominantly by the patient's fixation on functional disorders of a specific organ or system—in other words, a clinical variant of generalized neurosis. Such autonomic disorders without an organic basis were previously termed autonomic neuroses. However, it is more accurate to refer to them as the autonomic (initial) stage of neurosis development.

According to ICD-10, the term "neurotic disorders" is adopted as a synonym for "neurosis"; "obsessive-compulsive disorder" replaces "obsessive-compulsive neurosis"; "dissociative (conversion) disorders" replaces "hysteria"; while the term "neurasthenia" has been retained.

Separately, the new classification singles out anxiety neurosis, as well as hypochondriacal and depressive neuroses.

This classification is intended to foster greater mutual understanding among physicians worldwide, though certain inconsistencies should be noted, as it places individual Clinical forms of neuroses alongside specific syndromes and even symptoms.

Over time, under the persistence of a psychotraumatic situation, neuroses can become chronic—meaning chronic neurosis develops—which leads to a pathological transformation of the patient's personality structure. In such cases, we speak of neurotic personality development, characterized by a predominance of asthenic, obsessive-phobic, and hysterical disorders within the clinical picture, leading to the patient's social maladjustment.

NEURASTHENIA.

Neurasthenia (from Greek *neuron* — nerve + *asthenia* — feebleness, weakness) is a psychogenic disorder belonging to the group of neuroses, the primary manifestation of which is a state of irritable weakness, characterized by heightened fatigability and delayed recovery of mental processes. Synonyms: nervous exhaustion, nervous overstrain, asthenic syndrome. It predominantly occurs between the ages of 20 and 40, slightly more often in men than in women. Neurasthenia was first described in 1869 by the American physician G. Beard, who linked its onset to prolonged emotional and physical overstrain of the nervous system, leading to its exhaustion.

Clinical presentation.

The disease develops subacutely and gradually. In the early stages, physical or emotional stress triggers autonomic disorders (tachycardia, hyperhidrosis, cold extremities, dyssomnia) that are disproportionate in intensity to the trigger and resolve quickly. At the next stage, sensoromotor disorders emerge (hypersensitivity, meteorsensitivity), which induce hypochondriacal traits and sharply reduce work capacity. Subsequently, Affective Disorders join in (excessive emotional lability, affective incontinence, inadequate reactions of offense or irritation over minor matters). If the patient nevertheless continues trying to fulfill their routine duties, ideational disorders come to the forefront, characterized by difficulty concentrating, memory decline, and a propensity for relentless self-analysis.

In domestic psychiatry, it is customary to distinguish a series of successive phases in the development of neurasthenia, corresponding to its specific clinical forms.

1. The hypersthenic form, with which the disease debuts, primarily manifests as irritability and a tendency toward rapid exhaustion. Stimuli that are insignificant or indifferent to a healthy person begin to provoke an intensified reaction (hyperesthesia). Patients become irritable, easily provoked by the smallest trifles, and intolerant of loud noise, bright light, or crowded gatherings. The emergence of hypersensitivity regarding intero- and proprioceptors also explains the numerous Complaints of unpleasant sensations in various PARTS OF THE body (headaches, toothaches, tinnitus, paresthesias, etc.).

The decline in work capacity at this stage stems not so much from overwork, but rather from the mental disorganization and confusion of such patients, caused by the primary weakness of active attention. Upon starting a task, they cannot sustain the necessary mental effort for long and, distracted by extraneous stimuli, abandon it. Attempts to overcome the "difficult start" and resume work may be numerous, but due to massive time losses, work efficiency remains very low.

These disorders are unstable and quickly disappear with Treatment and rest.

2. The second form (or stage of the disease)—irritable weakness—is essentially transitional, characterized by elaborated manifestations and greater persistence of irritable weakness. Alongside increased emotional excitability, hyperesthesia, lack of restraint, and low frustration tolerance, feelings of mental exhaustion intensify sharply, and active attention is further impaired. Irritability remains pronounced, but affective reactions involving agitation and shouting quickly fade, giving way to mental exhaustion accompanied by a sense of injury, total emotional capitulation, and tears. Characteristically, such polar manifestations arise from trivial triggers, demonstrating the emotional frailty inherent in these patients.

Upon undertaking a task, the patient tires quickly, begins to experience headaches, loses The ability to concentrate, and stops working in a state of complete exhaustion. Continually increasing the intervals between work "paroxysms" does not help, as strength is not restored.

A decrease in Muscle tone and tremors of the fingers and Tongue, which worsen during emotional distress, are frequently observed. An important place in this stage of neurasthenia is occupied by Sleep disturbances, manifesting as difficulty falling asleep, anxious anticipation of insomnia, and occasionally hypnagogic hallucinations. Sleep is shallow and accompanied by anxious dreams, leaving patients feeling unrefreshed and battered upon waking. Insomnia may be combined with increased daytime sleepiness.

An obligatory component of neurasthenia is polymorphic somatoautonomic disorders associated with diencephalic-autonomic dysfunction. The most characteristic functional cardiovascular disorders include transient arterial hypotension and hypertension, sensations of vascular pulsation, and headaches often accompanied by a feeling of tightness in the HEAD (the so-called "neurasthenic helmet"). General or localized hyperhidrosis and functional digestive disorders (anorexia, hyposalivation with a dry Mouth sensation, nausea, flatulence, and constipation sometimes alternating with diarrhea) are also common. Sexual disorders are occasionally noted: decreased libido, weakened erection, and premature ejaculation. These disorders typically occur against a backdrop of unstable, predominantly subdepressive mood.

The third (hyposthenic) form of neurasthenia arises either primarily in asthenic and anxious-suspicious personalities, or as a developmental phase (Third Stage) of the disease in individuals with a strong type of higher nervous activity.

This form is dominated by persistent asthenia against a backdrop of lowered mood. The emotional background is somewhat anxious, tinged with sadness and apathy. Tearfulness and excessive emotional lability are observed. Hypochondriacal complaints and a fixation on internal sensations are frequent.

HYSTERICAL NEUROSIS.

Hysteria (hysteria, Greek *hystera* - uterus) is a type of psychogeny that arises in connection with a psychotraumatic environment in individuals with a specific character structure (hysterical personality).

In the pathogenesis of this disorder, a crucial role is played by the mechanism of "flight into illness" and the "conditional pleasantness/desirability" of the pathological symptom. I.P. Pavlov demonstrated that temporary impairments of bodily Functions, when they afford a person certain life benefits—such as escaping a threatening situation or fleeing grim reality—can become consolidated through the mechanism of a conditioned reflex due to their "conditional pleasantness." This forms the basis for the hysterical fixation of a pathological symptom.

Hysteria occurs predominantly in young women, although men are also affected. Outwardly, it mimics a wide variety of diseases, earning it such monikers as "a chameleon that constantly changes its colors," "a great malingerer, an actress," and so forth. The hallmarks of patients with hysteria include demonstrativeness, a striving to attract attention by any means, high suggestibility and autosuggestibility, and infantile psychological defense mechanisms in conflict situations.

Clinical picture.

Given the highly diverse symptomatology of hysteria, its disorders are conventionally divided into motor, sensory, vegetative-visceral, and mental.

1. Motor disorders may manifest as hysterical paroxysms, functional paralyses, pareses, aphonia, muscle contractures, hyperkinesia, astasia-abasia phenomena, various gait disturbances, stuttering, etc.

A hysterical paroxysm usually occurs in the presence of an audience and manifests as a fall—typically safe, in the form of a slow descent—after which, in E. Kretschmer's phrasing, "a fire of diverse expressive reflex movements ignites, one after another." Patients tremble, roll on the floor, arch their backs while resting on the floor with their occiput and heels (the "hysterical bow"), scream, groan, shout out phrases or quotes, sing or whisper, bite their hands, scratch their faces and bodies, tear their clothing, pull out their Hair, wring their hands, and assume so-called "passionate poses" with characteristic facial expressions and facial hyperemia (very rarely cyanosis or pallor).

A hysterical attack lasts from several minutes to several hours. It can be interrupted by external influences, such as a loud sound, a sharp command, splashing with cold Water, etc.

Frequently, the attack transitions into crying, a state of fatigue, exhaustion, powerlessness, or less commonly, sleep. Partial memories of the hysterical attack period are retained.

Hysterical paralyses (as well as pareses) occur in the form of monoplegias (monopareses), paraplegias (parapareses), tetraplegias (tetrapareses), etc. At the same time, the zone of paralysis (paresis) may be limited to the size of a finger, hand, FOOT, arm, or leg ("bird claw"). As a rule, unlike organic ones, they are not accompanied by pathological reflexes or pyramidal signs and do not topographically correspond to the course of nerve trunks.

Hysterical aphonia is based on paralysis of the vocal cords.

Hysterical contractures involve both individual muscle groups—such as hysterical blepharospasm or hysterical Torticollis—and complex chains, causing a patient suffering from hysteria to freeze in an "affected pose" for prolonged periods.

Hysterical hyperkinesia predominantly manifests as tic-like and tremulous movements of either individual body parts (chin, eyelids, hands, legs, head) or the entire body. Its onset depends on the patient's affective state and carries many elements of imitation, which distinguishes it from organic hyperkinesia.

Astasia-abasia is a hysterical disorder characterized by the inability to stand or walk independently in the absence of any organic lesions of The Musculoskeletal System. When in bed, patients can move their legs freely, but they fall to the floor the moment they try to walk.

2. Sensory disturbances may manifest as decreased sensitivity, complete anesthesia to tactile, thermal, or painful stimuli, or hyperesthesia to the exact same influences.

Areas of anesthesia or hyperesthesia often do not correspond to anatomical zones of innervation: they may appear as jackets, half-jackets, shorts, half-shorts, stockings, socks, gloves, etc. Frequently, phenomena such as hysterical blindness, deafness and mutism (surdomutism), loss of Smell and Taste, and the absence of the pharyngeal reflex occur. Hysterical pain, varying in duration and intensity, can be observed in any part of the body (head, back, joints, abdomen). Cases have been described where the abdomen of a patient with hysteria takes on a "checkerboard" appearance due to scarring deformities from numerous laparotomies. Such patients migrate from one clinic to another solely to obtain conservative or even Surgical treatment. Sometimes, pain in the region of the heart simulates angina pectoris or myocardial infarction.

3. Vegetative-visceral disorders in hysteria are the most frequent and diverse. Due to smooth muscle spasms, patients may experience a sensation of constriction in the throat (globus hystericus), a feeling of air hunger resembling Bronchial Asthma, a sensation of esophageal obstruction (dysphagia), urinary retention, and constipation. Hysterical anorexia (sometimes accompanied by an aversion to specific types of food), hiccups, regurgitation, salivary disorders, diarrhea, and nausea are also possible. Vomiting can be either sporadic or very frequent, almost constant, resembling hyperemesis gravidarum. It is not associated with gastrointestinal pathology and is caused by psychogenic pyloric spasms. Disorders mimicking intestinal obstruction or the clinical picture of chronic appendicitis may occur. Various cardiovascular disturbances (pulse lability, dystonia) are common, along with thermoregulation disorders manifesting as low-grade, irregular Temperature spikes.

Among sexual disorders, Menstrual cycle abnormalities are the most characteristic: Amenorrhea, dysmenorrhea, menorrhagia, and vaginismus.

Sometimes women develop hysterical pseudocyesis, which is mimicked by a complex of symptoms (amenorrhea, abdominal enlargement due to flatulence, breast enlargement, nausea, vomiting, etc.).

Occasionally, so-called vicar bleedings occur, where localized changes in vascular permeability lead to bleeding from undamaged areas of the Skin.

In some cases, such changes in vascular permeability also cause so-called hysterical dermatoses, where autosuggestion allows patients to induce local lesions such as areas of skin redness, hemorrhagic rashes, blisters, etc. Hysterical dermatoses also include various skin lesions artificially inflicted by patients to draw attention to themselves. In subsequent instances, amnesia regarding their own actions is often observed.

4. Mental disorders primarily manifest as heightened affectivity; patients fly into a rage over the slightest provocation, stamping their feet, breaking dishes, and throwing tantrums like children. Their mood is labile, with frequent sharp swings from feigned enthusiasm to sullen grumbling. Hysteria can mimic specific symptoms of any mental illness about which patients have even a vague notion.

Psychogenic amnesias (total or partial) frequently occur.

Fixed fears and hysterical depressions are generally superficial and accompanied by striking external displays such as theatrical poses, groaning, pathetic declarations, etc.

Hysterical hallucinations are figurative, brightly colored, usually reflect the psychogenic situation in a way desired by the patients, tend to be short-lived and episodic, and may be staged in character. Delusional fantasies are also possible.

Hysterical losses of consciousness (fainting) differ from true syncopes by a lesser degree of clouding of consciousness, less weakening of Respiration and Blood Circulation, and typically the absence of sudden facial pallor.

Hysterical twilight states last from a few minutes to several days. Consciousness is narrowed, the surrounding reality is not fully perceived, and patients are completely absorbed by their painful experiences. At this time, brightly colored hallucinations and delusion-like fantasies dominate consciousness, reflecting the experienced psychotraumatic situation in a real or (more frequently) much more favorable light for the patient.

Hysterical twilight states of consciousness can manifest as somnambulism, hysterical fugues, trances, and dromomania.

During a period of typically unresolved psychogenic situations, patients may exhibit the syndrome of puerilism, pseudodementia, or Ganser syndrome.

Psychogenic (hysterical) stupor may occur (usually accompanied by a distinct posture), combined with phenomena of mutism (refusal to communicate with others). Hysterical mutism can also occur in isolation as an independent disorder.

OBSESSIVE-COMPULSIVE DISORDER.

This is a form of neurosis whose primary manifestations are psychogenically induced obsessive states—images, thoughts, feelings, or actions that spontaneously arise in consciousness; patients understand their groundlessness, fight against them, but are unable to overcome them.

The core clinical content of this neurosis comprises:

1. Phobias – obsessive fears.

2. Obsessions – various intrusive thoughts, ideas, and representations.

3. Compulsions – obsessive urges and actions.

Previously, this form of illness was subsumed under the broad concept of psychasthenia, but as early as the 1920s, E. Kraepelin proposed classifying it as an independent nosology—"obsessive neurosis." Today, psychasthenia is understood as a form of psychopathy, while obsessive-compulsive disorder refers to a neurosis that can arise both on the basis of a psychasthenic constitution and in healthy subjects.

Sometimes, obsessive-compulsive neurosis is triggered by psychotraumatic situations that generate a coexistence of conflicting intrapsychic tendencies. Examples include: whether to live with one's mother or separately; sexual desire coupled with the conviction of the impermissibility of satisfying it; feelings of hatred toward a loved one, a desire for their death, and the recognition of the unacceptable nature of such desires.

Obsessive-compulsive neurosis can develop in individuals with diverse typological character traits. It is particularly prone to occur in anxious, fearful, and excessively conscientious people.

Typically, the initial stage involves the development of a neurotic background (irritability, emotional lability, dyssomnia), followed by phobias, then obsessive-compulsive disorders (such as contrasting impulses), and subsequently, obsessions.

Clinical Picture.

Obsessive fears, or phobias, are extremely common and present in a wide variety of forms. The most prevalent include: agoraphobia (fear of open spaces), claustrophobia (fear of enclosed or confined spaces), acrophobia/hypsophobia (fear of heights), pantophobia (fear of everything), erythrophobia (fear of blushing in public), dysmorphophobia (fear of a physical defect), mysophobia (fear of contamination), thanatophobia (fear of death), and taphephobia (fear of being buried alive). Various Forms of nosophobia—the fear of contracting a serious illness—are also frequent, such as acarophobia (fear of Scabies), bacteriophobia, helminthophobia, cancerophobia, lyssophobia (fear of rabies), syphilophobia, AIDS phobia, and others.

Special cases include obsessive anxiety regarding the potential inability to perform a routine daily or professional activity, such as a lecture for a teacher, a performance for a singer, and so on.

All of these forms tend to accumulate vegetative-hypochondriacal overlays, which significantly complicate treatment.

Obsessive fears are usually accompanied by various protective actions, or rituals. As a rule, these serve as direct protection, are concrete rather than symbolic in nature, and may expand and become more complex over time.

Obsessive thoughts represent futile and morbid overthinking, which Griesinger referred to as "mental rumination." Examples include: Why does a table have 4 legs? Why is chalk white?

Obsessive memories are vivid recollections of an unpleasant event. Contrasting ideas and thoughts involving profanity run counter to the patient's worldview and ethical guidelines.

Obsessive doubts involve uncertainty regarding the correctness and completion of one's actions, such as wondering whether the door was locked, whether the iron was unplugged, and so forth.

Obsessive impulses are a distinct urge to commit a pointless, dangerous, or inappropriate act, for example: hydromania (the urge to throw oneself into water), homicidomania (the urge to kill someone), or pyromania (the urge to set something on fire).

It must be emphasized that, unlike violent or impulsive actions, obsessive impulses are not acted upon.

Primitive compulsive actions include tics—characteristic stereotyped movements where the patient needlessly runs a hand through their hair (adjusting their hairstyle), throws their head back, blinks, etc. These occur predominantly in childhood and adolescence and have a favorable prognosis. In contrast, complex compulsive actions (rituals) are closely linked to obsessive doubts and phobias.

Obsessive-compulsive neurosis may be accompanied by various general neurotic disorders, such as irritability, hyperesthesia, sleep disturbances, and autonomic dysfunctions.

The course of obsessive states is characterized by fluctuations ranging from near-complete remission to significant exacerbation, even after long intervals.

Neurotic disorders in dental practice.

Patients with congenital and acquired facial defects exhibit a very high incidence of various neurotic reactions. Because such patients frequently consult dentists for corrective Procedures, an awareness of the Clinical Features of their condition is unquestionably essential for successful treatment. It is worth noting that neurotic reactions in individuals with congenital anomalies differ from those in patients who acquire a cosmetic defect in adulthood. This is because in the former group, psychogeny has existed since childhood, and the pathoplasticity of psychological reactions changes depending on the duration and frequency of psychogenic decompensations. In the latter group, a disfiguring facial injury is an unexpected trauma that triggers a distinct and specific neurotic reaction, which should be regarded as primarily psychogenic. Long-standing defects that do not respond to cosmetic surgery can lead to profound qualitative personality changes.

In congenital defects, neurotic reactions typically emerge during early school age (7–11 years) or Puberty (12–14 years). These reactions are usually triggered by mockery, remarks, and offensive comments regarding the physical defect. As a rule, they are unstable and arise directly in response to the triggering situation.

In the clinical picture of neurosis associated with either congenital or acquired facial defects, dysmorphophobia syndrome occupies a central place. Unlike in schizophrenia, these cases have an objective basis and a psychogenic mechanism of origin.

The clinical manifestations of dysmorphophobia syndrome depend on the duration and severity of the defect, as well as microsocial conditions. Three variants of neurotic syndromes are distinguished: asthenic, astheno-depressive, and astheno-phobic.

In early school age, asthenic and affective reactions are frequently combined with passive-defensive or aggressive forms of behavior. Older and mature age groups are characterized by astheno-depressive and sensitive-phobic reactions.

In acquired cosmetic defects that alter facial appearance, neurotic reactions emerge after the acute post-traumatic period. It is important to note that these reactions appear once patients come to the realization that their facial appearance has permanently changed. This reaction should be viewed as distress resulting from social and personal decompensation.

Clinically, this manifests as depressive or astheno-depressive symptomatology. Patients experience heightened emotional vulnerability and a fear of interacting with people. Autonomic symptoms frequently develop, such as palpitations, blood pressure fluctuations, and hyperhidrosis. Patients become tearful, and sleep disturbances are common. The Nature and severity of the prior trauma, baseline mental health, and premorbid personality traits play a major role in the onset of these reactions.

Neurotic reactions are unstable, and their recurrence is linked to additional psychogenic factors, such as reminders of disfigurement or encounters with relatives and close acquaintances.

In many cases, pathological symptoms disappear 1.5–2 months after comprehensive treatment or successful plastic surgery. However, upon exposure to additional psychosocial stressors, acute neurotic reactions may evolve into a persistent neurotic state characterized by frequent decompensations and worsening emotional disturbances. Patients spend most of their time in a depressed mood, experience a profound sense of hopelessness, and develop obsessive thoughts about "losing their face." This condition may be accompanied by suicidal tendencies. The "mirror sign" appears—the compulsive habit of constantly examining one's face in the mirror. Patients seek solitude and lose social contacts and friends. At this stage of the illness, the leading syndromes emerge: depressive, astheno-depressive, and depresso-phobic. Against the background of depression, ideas of self-blame or reference arise (the belief that others are intentionally staring at their face or hinting at their deformity). Asthenic phenomena increase (increased fatigue, low work productivity), alongside various phobias: fear of one's own deformity (dysmorphophobia), fear of speech (lalophobia), fear of being mocked (scoptophobia), and fear of people (anthropophobia), among others.

TREATMENT.

Treatment should necessarily combine pharmacotherapy with psychotherapeutic interventions; in particular, family therapy is highly effective for children. Physiotherapy and remedial gymnastics are also recommended. In severe cases of neurosis, patients should be isolated from the psychotraumatogenic environment, preferably through hospitalization, to help distract them from the conflict situation.

For neurasthenia, patients require adequate rest and general strengthening therapy (multivitamins, adaptogens, glucose, low doses of Insulin), while prolonged sleep therapy proves quite effective. In cases of acute psychological agitation and lack of self-control, alongside tranquilizers (phenazepam 1-2 mg three times daily, meprobamate 0.2 - 0.4 daily), it is advisable to prescribe low doses of phenothiazine antipsychotics (chlorpromazine, tizercin). To combat insomnia (hypersthenic neurasthenia), physicians use radedorm 5-20 mg per dose, melleril 10-75 mg per dose, and phenazepam 2-3 mg daily with the main dose administered at bedtime.

For hysterical neurosis, antipsychotics such as sonapax and melleril are effective in dosages of 40-60 mg per day.

In cases of asthenic conditions accompanied by somnolence and lethargy, therapy should begin with sedatives, bromine preparations (a 2% solution, one tablespoon 3-4 times a day), and low doses of hypnotics for a month. Only thereafter can tonic remedies and stimulants be prescribed. Biological options are preferred—such as tinctures of ginseng or Schisandra chinensis—though transition to synthetic stimulants (centedrin, sydnocarb, etc.) and nootropics (piracetam, aminalon) may follow later.

For obsessive-compulsive neurosis characterized by pronounced phobias and anxiety, the most effective approach involves administering tranquilizers such as phenazepam, lorazepam, and elenium (librium), as well as intravenous drip infusions of antipsychotics like trifluoperazine and azaleptin in moderate doses.

While all modalities of psychotherapy are utilized in treating neuroses, rational psychotherapy is mandatory. At the initial stage, it should be predominantly sedative, aiming to relieve the patient's internal tension. Once this goal is achieved, the therapist can proceed to review and adjust the patient's system of personal and social relations, followed by a stage of personally oriented reconstructive therapy. This process typically concludes with so-called activating therapy, which prepares the patient to resume work and successfully reintegrate into society.

EXPERT ASSESSMENT.

Medical and Labor Expertise. The vast majority of patients with neuroses recover and return to full employment. Grounds for disability status may include prolonged and unfavorable courses of obsessive-compulsive neurosis accompanied by cardiophobia, photophobia, or obsessive fear of mental illness, as well as severely pronounced hysterical paresis, paralysis, or astasia-abasia.

Military Medical Expertise. Patients suffering from neuroses remain on active military duty while receiving standard outpatient or inpatient treatment.

Forensic Psychiatric Expertise. Committing an offense while in a neurotic state does not constitute grounds for exemption from criminal responsibility, as such patients are fully aware of their actions and capable of controlling them.

CONTROL QUESTIONS.

1. Define the concept of "neuroses".

2. Historical Milestones in the study of neuroses.

3. What factors contributing to the development of neuroses do you know?

4. What pathogenetic mechanisms underlie neuroses?

5. What are short-term neurotic reactions?

6. Classification of neuroses, features according to ICD-10.

7. Clinical presentation of neurasthenia.

8. Clinical presentation of hysteria.

9. Clinical presentation of obsessive-compulsive neurosis.

10. Cytology/practical/136.html">Differential Diagnosis OF hysterical and epileptic seizures.

11. Principles of treatment for neuroses.

12. Labor, military, and forensic psychiatric expertise in neuroses.

REACTIVE PSYCHOSES

Reactive psychoses (reactive states) are temporary disorders of mental activity that occur As a result of psychological trauma. The Latin prefix "re-" denotes repetition or restoration, while "activus" means active or acting.

They differ from neuroses in the severity and intensity of the psychological trauma, which results in profound psychotic-level mental disorders. Furthermore, patients with reactive psychoses lack critical insight into the presence of productive symptoms. The term "reactive psychoses" is used predominantly in domestic psychiatric literature, whereas foreign literature often employs terms such as "abnormal reactions," "psychogenic reactions," and others.

HISTORICAL BACKGROUND.

In 1897, S. Ganser first described a case of psychogenically induced clouding of consciousness accompanied by hysterical sensory disturbances. It subsequently entered psychiatric classifications as Ganser syndrome (Ganser twilight state), which he defined as a hysterical twilight state of consciousness. Prior to this, in 1888, The phenomenon of "approximate Answers" (Ganser symptom) in prisoners was observed by C. Moeli, who, however, interpreted it as malingering. The opinion was expressed (Nissl, 1902) that Ganser syndrome can be interpreted as hysterical only when it arises on the basis of constitutional hysteria; in all other cases, it is a manifestation of catatonic negativism triggered by psychological trauma, typically in incarcerated individuals. Final clarity on this issue was brought by I.N. Vvedensky (1905), who pointed out that "approximate answers" of a psychogenic origin remain relevant to the question asked, whereas in catatonic syndrome, the responses bear no relation whatsoever to the content of the question.

In 1898, N.M. Popov described infantilism as a reactive state, and this issue was subsequently further developed by K. Raecke (1901) and E. Dupre (1903). The works of K. Birnbaum (1908) already contained data reflecting The impact of psychological trauma on the symptoms of the illness.

The clinical understanding of psychogenic delusional formations has undergone a complex evolution. Cases of acute reactive paranoia were first highlighted by P.B. Gannushkin (1904), and in 1910, E. Kretschmer and R. Gaupp provided a more detailed description of reactively induced delusional states. Defining the diagnostic boundaries of reactive depressions and separating them from endogenous ones is primarily the merit of E. Reiss (1911), M. Reichard (1922), and J. Lange (1925).

An important milestone in the study of reactive psychoses, resulting from the synthesis of previous research, was the formulation of the core diagnostic principles by K. Jaspers (1923), known as Jaspers' triad:

1) reactive states arise under the influence of psychological trauma,

2) the content of the psychotrauma is reflected in the symptoms of the illness,

3) upon deactivation of the psychotrauma, reactive states subside.

Subsequent research demonstrated the relativity of the second principle and the clear

conventionality of the third. This is evidently due to the Specific features of K. Jaspers' existential approach, which fails to account for cerebral-pathogenetic mechanisms.

A major contribution to the study of reactive states was made by A.N. Buneyev, N.I. Felinskaya, and F.I. Ivanov.

PREVALENCE.

There are no exact data on the prevalence of reactive psychoses in the general population. Certain statistical challenges stem from the fact that some authors use the concept of hysterical psychoses as a synonym for reactive ones, although they possess nosological independence. Information is available only regarding reactive depression, which accounts for 59% of all reactive psychoses.

It is believed that reactive states occur twice as frequently in women as in men.

ETIOPATHOGENESIS.

In the onset of reactive psychoses, a decisive role is played by the combination of The Nature of the psychological trauma (its intensity, onset rate, and pattern), the constitutional personality traits (particularly in the presence of a sensitive or hysterical accentuation), and the current functional state of the Central nervous system.

Factors predisposing to this pathology include alterations caused by past TRAUMATIC BRAIN INJURIES, chronic infections, intoxications, atherosclerosis, and age-related crises.

The impact of psychotraumatic factors can be acute or protracted. Despite their diversity, the resulting psychogenic disorders are largely determined by the individual's personal value system.

While the duration of the psychotraumatic situation matters, of greater significance are the personality's coping mechanisms regarding this situation, namely adaptation or sensitization. Equally important is the hierarchical position of the psychotraumatic circumstances within the person's system of personal values.

For affective-Shock reactions, premorbid personality traits are not decisive; the primary importance lies in the strength and Significance of the psychological trauma. In hysterical psychoses, the disorder develops via suggestion and autosuggestion as a mechanism to protect the personality from an unbearable situation. Conversely, in subjectively significant situations, a substantial role belongs to the premorbid personality traits and the level of psychological maturity.

CLASSIFICATION.

Based on their onset and clinical course, reactive states are categorized into:

I. Acute (affective-shock) states.

✵ hypokinetic variant (acute reactive stupor);

✵ hyperkinetic variant:

- acute twilight state;

- acute reactive confusion;

- acute reactive paranoid state.

II. Subacute (hysterical).

✵ hysterical twilight state;

✵ pseudodementia:

- agitated variant;

- depressive variant;

✵ regression ("primal forest" syndrome).

✵ puerilism;

✵ Ganser syndrome;

✵ delusional-like states;

✵ hysterical stupor.

III. Protracted (subjectively significant).

✵ reactive depression:

- paranoid;

- asthenic;

- hysteroid.

✵ reactive paranoid state:

- paranoid;

- hypochondriacal;

- related to external circumstances (wartime, "railway", prison).

CLINICAL FEATURES.

I. Acute reactive psychoses.

Affective-shock reactions are short-lived psychotic states that predominantly occur in situations of sudden, overwhelming threat to an individual's very existence, such as an earthquake, fire, flood, or similar disasters. They are invariably accompanied by a twilight state of consciousness, a profound sense of despair, along with motor and autonomic disturbances (tachycardia, severe pallor or flushing of the skin, and profuse sweating).

Hypokinetic and hyperkinetic variants of affective-shock reactions are distinguished.

Acute reactive stupor corresponds to the hypokinetic variant of acute reactive psychoses. This condition was described by E. Kretschmer (1924) as the reaction of "supposed death." It is characterized by the sudden onset of complete immobility coupled with mutism in a traumatic situation. In this state, patients are unresponsive to their surroundings; an expression of horror freezes on their faces, their eyes are wide open, cold sweats appear, and involuntary urination and defecation are frequently observed.

Acute twilight state begins very acutely and is characterized by disorientation, the inability to establish verbal contact with the patient, psychomotor agitation, and erratic attempts to flee (sometimes running straight into danger).

The resolution of pathological disorders often occurs suddenly, with the patient seemingly waking up from a nightmare. However, the complete restoration of clear consciousness typically happens gradually and may pass through a stuporous phase—namely, a transient, sharp depletion of intellectual activity that makes patients appear somewhat demented.

The simple form of twilight clouding of consciousness usually lasts for several minutes or hours and is followed by amnesia, sometimes mediated through sleep.

Patients experiencing a twilight clouding of consciousness, even in cases of partial amnesia, typically view their actions (such as committing a crime or murder) as something alien, performed by someone else.

Acute reactive confusion develops abruptly as a twilight clouding of consciousness accompanied by a panic affect and psychomotor agitation, against the background of which continuous speech "production" resembling a "word salad" is observed.

Acute reactive paranoid state is frequently encountered in forensic practice; it is defined by a combination of persecutory and referential delusions accompanied by verbal hallucinations and distinct phenomena of psychic automatism. The content of a reactive hallucinatory-paranoid psychosis is closely linked to the psychotraumatic situation.

A characteristic feature is a state of bewilderment accompanied by an affect of fear and anxiety. The delusions are affectively charged, and their plot reflects the psychotraumatic situation. At the peak of the paranoid state, consciousness may be impaired—ranging from affective narrowing to twilight states. Hallucinations (both true and pseudo-hallucinations) and other elements of the Kandinsky-Clérambault syndrome may emerge.

Mentism occurs during the initial period, accompanied by the surfacing of memories regarding long-forgotten episodes. Alongside this, patients experience a sensation of having their thoughts "extracted" or "read," a feeling of "internal exposure," which combines with situational auditory pseudo-hallucinations (most commonly related to investigative proceedings). Patients report Hearing internal voices that interfere with the flow of their thoughts, reenacting the investigation and echoing inside their head. Isolated components of cenestopathic automatism also appear, such as unpleasant bodily sensations—feelings of coldness or burning.

At the height of psychosis, against the backdrop of intense affective fear, true verbal hallucinations emerge whose content is tied to the traumatic situation. The voices may be multiple in nature (polyvocal hallucinosis) or take the form of a dialogue (discussing the patient's behavior, issuing threats, or prophesying death). Occasionally, isolated visual hallucinations appear that likewise reflect the situation.

Delusions of reference, significance, and persecution, as well as ideas of external influence and constant surveillance carried out through hypnosis, special devices, or similar means, play a prominent role in the clinical picture.

A shift in the clinical presentation occurs immediately upon admission to the inpatient unit. Hallucinations are the first to disappear; the tense affect of fear gives way to depression, and the delusions assume a residual character. Insight into the past pathological disorders gradually develops. For a month or more following recovery from the psychosis, patients exhibit asthenia and irritable weakness that intensify in the latter half of the day and evening, alongside affective lability characterized by a predominant low mood, captiousness, discontent, and tearfulness.

II. Subacute reactive psychoses.

Hysterical reactive psychoses feature a polymorphic clinical picture driven by the combination and transformation of various hysterical disorders.

Unlike acute hysterical twilight states, subacute ones are characterized by an affective narrowing of consciousness, which leads to a peculiar, fragmented perception of the environment. The clinical picture is notable for its dynamism and polymorphism. The patient's behavior is demonstrative, and short-lived agitation tinged with anxiety and fear gives way to a substupor. Manic-like states, hysterical convulsive paroxysms, and illusory-eidetic visual phenomena may also occur.

Figurative delusions can be accompanied by illusions of false recognition (Capgras and Fregoli syndromes). Affective disturbances during twilight clouding of consciousness are highly intense and marked by extreme tension—most frequently fear, horror, dull malice, anger, or ecstasy. Motor disorders manifest as agitation, often taking the form of senseless destructive actions directed at surrounding objects and people.

The course of twilight clouding of consciousness with productive symptoms can be continuous or alternating, meaning that many or even all symptoms temporarily disappear spontaneously only to reappear later.

The duration of this form of twilight state ranges from a few hours to 1–2 weeks. Amnesia following the episode may be partial (when the content of predominantly visual hallucinations and their accompanying affect remains in consciousness for varying periods), retarded (delayed), or complete.

Pseudodementia (from Greek *pseudos* – false and Latin *dementia* – madness) is a psychopathological state of transient mental regression that mimics dementia. It is observed more frequently in men and was first described by C. Wernicke (1906).

The clinical picture is characterized by a sudden decline in mental activity, manifested through erroneous responses (paraphasias) and actions (parapraxias). Patients are disoriented regarding their surroundings: they do not know where they are and cannot correctly state the current month or year. They give incorrect answers to elementary questions and perform simple tasks with gross errors: when asked to show their eyes, they point to their Nose; instead of a hand, they show a foot; they try to put boots on their hands, push their legs into the sleeves of a robe, or attempt to light a match from the wrong end, and so on. At the same time, their answers are always given within the framework of the question asked. For example, white is called black, summer is called winter, and a window is called a door. When asked how many fingers they have on their hands or how many eyes they possess, the patient might reply that they have 4 fingers and 5 eyes.

Disturbances in reading and writing are observed (agrammatisms, omitted letters, uneven handwriting). The patients' outward appearance is characteristic—they look bewildered, stare wide-eyed, and smile inappropriately.

Agitated and depressive Variants of the pseudodementic syndrome are distinguished.

Agitated pseudodemented syndrome develops acutely, with psychomotor agitation emerging against the background of hysterical narrowing of consciousness. Patients are restless, unable to sit still, and quite difficult to engage. They perform numerous unnecessary movements, needlessly Touch surrounding objects, fidget with their clothing, and pull grimaces. Euphoria predominates, easily giving way to tension mixed with anxiety and fear. Speech is accelerated, and patients answer questions without delay.

Depressive pseudodemented syndrome develops against the backdrop of psychomotor retardation. Patients' moods are anxiously depressed; they sit with a mournful expression, wide-open eyes, and silent tears, looking bewildered and fearfully glancing around. Thinking is slowed in pace, and questions are answered only after repeated prompting, with responses taking the form of denials ("I don't know," "I don't remember," "I've forgotten") or perseverations. The symptom of incorrect actions has a mild, rudimentary character. For example, when asked to extend their left hand, the patient examines both hands for a long time, then lifts first one and then the other, and finally extends one of them. Pseudodemented syndrome can entirely dictate the clinical picture of a reactive psychosis. As the condition deepens, the agitated variant of pseudodemented syndrome frequently transitions into puerilism, while the depressive variant transitions into psychogenic stupor.

The duration of pseudodementia typically ranges from 2 weeks to 3 months, occasionally presenting a protracted course. Throughout this period, the clinical picture remains monotonous and uniform against a backdrop of substupor. Memories of the morbid state are either entirely absent (particularly in the agitated variant) or fragmentary.

The "syndrome of wildness" (feral syndrome) is quite rare, manifesting as hysterical twilight states accompanied by specific psychomotor agitation, in which the regression of mental activity reaches an extreme degree: patients crawl on all fours, eat directly from plates with their mouths, growl, bark, bite, etc. Sometimes such behavior is accompanied by delusions of transformation (attempts to move and behave like animals).

Puerilism (from Latin puer – boy) is a state of regression in mental activity characterized by the appearance of childlike traits in the speech and behavior of an adult. The term "puerilism" itself was proposed by Dupré in 1903.

In puerilism, patients speak with childlike intonations, lisp, use baby talk, address everyone informally, and refer to people as "uncles" and "aunts." They display joy upon seeing shiny, bright objects, reach out for them, gladly participate in children's games (building little houses, assembling picture puzzles, playing with dolls), throw tantrums, pout discontentedly, and cry with a sense of being wronged. Overall, however, their behavior is not identical to normal childhood behavior. It is marked by dissociation—alongside childlike traits, the patient retains certain habits and skills of an adult, such as the correct manner of striking matches or lighting a cigarette.

Sometimes the reactive state maintains a cohesive, uniform form of puerilism throughout the entire illness, but more often puerilism serves as one of the forms or Developmental Stages of hysterical reactive psychosis. In such cases, puerilism arises following psychogenic depression or pseudodementia and, as the reactive state deepens further, may be succeeded by the

"syndrome of wildness." In isolated instances, puerilism is replaced by psychogenic stupor.

Ganser syndrome is a symptom complex of profound hysterical twilight disorder of consciousness dominated in the clinical picture by the phenomenon of "Vorbeireden" (approximate answers / talking past the point).

The polymorphic clinical picture of Ganser syndrome is defined by vague orientation in the environment, impaired perception of reality, disrupted connection with the outside world, and phenomena of puerilism. The patient is focused on a narrow, isolated circle of ideas that retains some internal coherence and sequence. Their mood fluctuates between elevated and anxiously fearful. Hallucinations occasionally occur—predominantly visual, scenic, and threatening in content (situationally conditioned courtroom scenes featuring witness testimonies, sentencing, etc.). The phenomena of approximate answers manifest as hyperbolically absurd responses to everyday questions. These are sometimes joined by "Vorbeihandeln" (approximate actions)—the patient incorrectly performs actions requested of them. Instances of unresponsiveness to pinpricks and insensitivity to cold and heat are also observed.

Ganser syndrome lasts from several days to a week. Everything that happens to the patient during the twilight state is subsequently amnesized.

The syndrome of delusional-like fantasies, first described by K. Birnbaum (1918), is manifested by labile, fantastic ideas that do not fit into a coherent system.

In some cases, delusional-like fantasies develop acutely against the background of a hysterically narrowed state of consciousness. Here, unstable ideas of grandeur and wealth predominate, hyperbolically reflecting a desire to escape an unbearable situation. Thus, patients recount travels to Mars, the untold riches they possess, and major discoveries of state importance. The content of these statements contradicts the general anxious mood backdrop, which shifts depending on external circumstances and the physician's questions. The fabula of these thoughts usually bears an inverse relationship to the psychotraumatic situation, meaning that the patients' own misdeeds are portrayed as heroic feats or acts of charity.

In other instances, delusional-like fantasies are more complex and persistent, exhibiting a tendency toward systematization.

During the period of reduction in reactive symptomatology, situationally conditioned depression comes to the fore; fantastic utterances pale, reviving only briefly when patients experience anxiety related to the impact of additional psychotraumatic experiences.

Hysterical stupor occasionally arises acutely, immediately following psychological trauma as an independent form of reactive psychosis. In most cases, however, it develops gradually as The final stage in the dynamics of hysterical syndromes: hysterical depression, pseudodementia, and puerilism.

Despite immobility and mutism, the facial expressions of such patients reflect the dominant affect. Facial expressions may appear gloomy, malignant, or occasionally reflective of suffering and despair. Against the backdrop of psychomotor retardation, a series of symptoms typical of pseudodementia and puerilism are revealed.

Consciousness in such patients is altered, approaching an affectively narrowed state. Their physical status, despite prolonged refusal of food, is generally satisfactory. The resolution of stuporous disorders may occur abruptly or gradually.

III. Protracted reactive psychoses.

Protracted reactive psychoses last for 6 months or longer.

Reactive depression is characterized by a gradual onset and a protracted course. The fabula of depressive experiences reflects the content of psychotraumatic circumstances, while vital manifestations are less pronounced than in endogenous depression. Critical insight into one's condition is preserved, albeit somewhat diminished, and primary blame is typically attributed to others rather than oneself. It most frequently occurs in the following clinical variants:

- Astheno-depressive syndrome manifests as a melancholic mood, psychomotor retardation, listlessness, rapid fatiguability, and difficulty concentrating. Hyperesthesia is characteristic (intolerance of bright light, loud sounds, and sharp odors). This syndrome presents with headaches, sleep disorders in the form of hypersomnia or insomnia, and autonomic dysfunctions. Depending on barometric pressure fluctuations, patients with asthenic syndrome may experience increased fatigue, exacerbated irritable weakness, and hyperesthesia (Schröter's symptom);

- Hystero-depressive syndrome is characterized by extreme expressiveness of external manifestations. Affective disorders present as a combination of despondency, anxiety, irritability, and tearfulness; they are labile and situation-dependent. Ideas of self-blame are absent—patients blame everyone else for everything. Alongside this, exaggerated concerns regarding their own health are expressed, along with the conviction that their condition is extremely severe, which precludes any possibility of demands being placed upon them. Facial expressions, motor activity, and utterances are marked by theatricality and a striving to draw attention and elicit sympathy; psychomotor retardation is absent. Melancholy is sometimes combined with irritability, and depression takes on an agitated character. Such patients frequently inflict self-injury and make demonstrative suicide attempts. This form is often combined with hysterical manifestations such as pseudodementia, puerilism, and delusional-like fantasies. The course of hysterical depression is favorable. Reduction of morbid disorders may occur immediately following a positive shift in circumstances or administered treatment. Upon recovery, partial amnesia is noted as a result of hysterical narrowing of consciousness during the psychosis;

- Paranoid-depressive syndrome develops gradually. Melancholy and motor retardation appear initially, in the absence of ideational retardation. Patients experience an influx of thoughts whose content is linked to the psychotraumatic situation. Consciousness concentrates on dominant experiences, allowing it to be defined as affectively narrowed. The surrounding environment is perceived as unreal, in "gray tones," as if "through a fog" or a "body of water." With the deepening of depression, delusional interpretation of surroundings is noted (patients perceive hints of future punishment in the words and gestures of others, etc.), along with elements of Kandinsky-Kladko syndrome, and bradypsychia appears. Depressive stupor may subsequently develop.

Depressive stupor develops gradually as the terminal stage of psychogenic depression accompanied by psychomotor retardation. Its clinical picture retains the affect of melancholy, manifested in the patients' facial expressions and motor activity. They almost never get out of bed, and when they do, they sit in a uniform, sorrowful posture, hunched over with their heads bowed low. Patients neglect their personal hygiene and appearance, frequently refuse food—resulting in sharp weight loss—and cease maintaining contact with those around them. Their facial expression is depressed and suffering, their gaze fixed, the corners of the mouth dropped, and their Lips trembling.

Psychomotor retardation typically reaches a substuporous level. Patients find it difficult to comprehend the meaning of questions asked. They either do not respond at all or give monosyllabic answers after the questions have been repeated multiple times. Their speech is slow, with prolonged pauses, and their voice is quiet and poorly modulated; their statements reflect self-blaming ideation and suicidal tendencies.

Emergence from the stuporous state occurs through a period of depression, followed by partial amnesia. Depressive stupor usually lasts 2-3 months, during which patients lose weight and exhibit pronounced autonomic disturbances (tachycardia, blood pressure fluctuations, feelings of constriction, pain, and heaviness in the cardiac region).

When the situation changes or upon treatment, the depressive stupor resolves first, followed by the delusional interpretation of the surroundings, and, lastly, the affect normalizes. Concurrently with mood improvement, insight into the past pathological condition emerges. Asthenia persists for about a month thereafter.

Reactive paranoid psychosis is a reactive psychosis characterized by imaginative persecutory delusions accompanied by fear and anxiety. It occurs in individuals placed in an unusual situation (relative isolation). Insomnia plays a major role in this condition.

In the initial phase, patients develop an inexplicable, agonizing anxiety. This is subsequently joined by delusions that reflect a specific psychotraumatic situation. Patients defend themselves against imaginary pursuers, which occasionally results in instances of hetero- and autoaggression. This state lasts from 2 weeks to 2 months. Gradually, passing through a stage of doubt, insight into the pathological condition is restored, and the delusions disappear.

The following forms of reactive paranoid psychosis are distinguished:

Paranoid - delusions are unstable, devoid of hallucinations, and reflect the psychotraumatic situation.

Hypochondriacal - develops in connection with a specific somatic pathology. It is characterized by patients' conviction in their own incurability, ideas of reference and influence, and dysmorphophobia.

Reactive paranoid psychosis of external circumstances has several varieties:

a) wartime paranoid psychosis - the delusional theme correlates with the situation. Patients are terrified, perceive those around them as enemies, and make impulsive attempts to escape.

b) "railway" paranoid psychosis - develops during prolonged, challenging journeys in an unfamiliar environment against a background of exhaustion. The delusional theme involves ideas of persecution and reference.

c) prison paranoid psychosis - the patient experiences predominantly verbal hallucinations of a blaming, threatening, or commenting nature. Their main theme revolves around the situation related to arrest and imprisonment.

TREATMENT.

In reactive psychoses, antidepressants are used in combination with neuroleptics and tranquilizers, depending on the clinical features and the stage of the reactive psychosis.

To manage acute psychogenic motor agitation, psychogenic twilight states, and the agitated form of pseudodementia, intramuscular injections of neuroleptics are administered: aminazine (150 mg), triftazine (10 mg), haloperidol (5-10 mg) three times daily. Among tranquilizers, seduxen 15-45 mg/day intramuscularly is effective in such cases. These medications are also indicated for oral administration in patients with acute and subacute delusions.

In psychogenic stupors, single amytal-caffeine unblocking procedures or even ether rouse anesthesia are indicated, which are sometimes quite effective. Prolonged apathetica states, sluggish stupors, and asthenia are indications for the prescription of nootropics and general strengthening therapy (especially in reactive psychosis presenting with sluggish stupor). During the recovery phase, the administration of psychopharmacological agents should be combined with well-designed, phased rational psychotherapy.

EXPERT ASSESSMENT.

Occupational. Patients with reactive psychoses receive inpatient treatment while on sick leave and generally do not require disability status. In cases of protracted psychoses, the Medical and Social Expert Commission (MSEC) typically limits the extension of the sick leave certificate to no more than four months. Exceptions include patients with progressive protracted reactive psychoses who are assigned disability group III, and occasionally even group II. In psychogenic paranoid delusions, due to the preservation of intelligence and work skills, assigning a disability group is in most cases inappropriate; however, overall, the issues of medical and social expert assessment in this disorder must be resolved on a strictly individual basis.

Military Medical. In subacute and most cases of protracted reactive psychoses, patients are not exempt from military service. Exceptions to this principle include patients with progressive protracted reactive psychoses and those with psychogenic paranoid delusions, who are deemed unfit for military service and removed from military registration.

Forensic Psychiatric. Individuals who commit an offense while in a state of reactive psychosis, which is quite rare, are recognized as not guilty by reason of insanity (incapable) and are subject to compulsory treatment. In the event that the defendant develops reactive psychosis after committing a crime but before sentencing (during the investigation), the court merely suspends the criminal proceedings for the duration of the illness, and the examinee stands trial after recovery. Only in cases where a protracted progressive psychosis develops are the proceedings finally terminated, and the patient is referred for compulsory treatment.

CONTROL QUESTIONS.

1. Definition of psychogenias and reactive psychoses.

2. Main historical trends in the study of reactive psychoses.

3. Etiopathogenesis of reactive psychoses.

4. Classification of reactive psychoses.

5. Clinical manifestations of acute reactive psychoses.

6. CHARACTERISTICS OF THE reactive twilight state of consciousness.

7. Clinical manifestations of subacute reactive psychoses.

8. Characteristics of reactive stupor and reactive depression.

9. Characteristics of reactive paranoid states.

10. Characteristics of pseudodementia and Ganser syndrome.

11. Clinical manifestations of protracted reactive psychoses.

12. Treatment and expert evaluation of reactive psychoses.