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

Mental disorders in various diseases and poisoning. Fundamentals of gerontology

Mental disorders resulting from syphilitic Brain damage

In recent years, syphilitic brain damage has emerged as one of the leading factors contributing to psychoses among all infectious diseases. This is despite the fact that in the 1970s and 1980s, progressive paralysis and cerebral Syphilis were virtually non-existent in Ukraine and the former USSR. A well-established system for the early detection and Treatment of syphilis ensured the complete absence of late-stage complications. Why then, despite medical advancements, are we facing this pathology once again? One of the reasons lies in social prerequisites, namely The breakdown of previously established social networks and The system of control over the treatment of socially dangerous diseases, which includes syphilis. When anarchy swept across the country in the mid-1980s, medical profiteers emerged whose primary motivation was financial gain. They treated syphilitic infections without proper training, leading to the chronicity of the condition. The spread of prostitution became the second reason why statistics show an increase in cerebral syphilis and progressive paralysis.

Cerebral syphilis and progressive paralysis are classified as intracranial infections, meaning the pathogen (in this case, Treponema pallidum) crosses the Blood-brain barrier. In cerebral syphilis, this penetration is confined to the Meninges and Blood Vessels, whereas in progressive paralysis, the pathogen invades the Neurons directly. This determines the Clinical presentation and Specific features of the course of both pathologies.

Progressive Paralysis

Progressive paralysis is the first nosological entity in psychiatry, described by the French psychiatrist Bayle as early as 1822. Nearly a century passed before the Japanese researcher Noguchi isolated the causative agent, proving that the brain Cells of individuals who died of progressive paralysis contain Treponema pallidum. Clinically, progressive paralysis is a syphilitic meningoencephalitis. If left untreated, it leads to marasmus and death within 2 to 5 years. Men are affected more frequently. It remains unclear why Tertiary and Quaternary syphilis manifest as progressive paralysis predominantly in Caucasians, whereas individuals of color typically exhibit Skin and bone lesions.

The incubation period for progressive paralysis is 10–15 years. The onset of the disease is slow and inconspicuous, presenting with pseudoneurasthenic features, yet it is invariably accompanied by personality changes leaning toward brutalization (coarsening). Patients in the early stage of progressive paralysis (PP) exhibit mild torpor and appear somewhat intoxicated. They experience impaired concentration, making it difficult for them to comprehend surrounding events, and their responses sometimes seem thoughtless. Forgetfulness, untidiness, and frivolity are also characteristic. Critical insight diminishes early on, and intellectual inadequacy becomes apparent when solving novel creative tasks. As a rule, psychoses are absent in the initial stage. According to the old Classification, this stage is referred to as neurasthenic, reflecting the predominance of asthenic manifestations.

The Second Stage—the fully developed or expansive stage—is characterized by distinct Changes in the patient's behavior and The Development of paralytic dementia. The leading symptoms of this stage are expansive (megalomaniacal) paralytic delusions, along with disturbances in emotions, drives, and critical insight. The former is manifested by patients' absolute conviction in their omnipotence. They believe they possess immense wealth, wield incredible influence across various spheres of life, and are sexually peerless. They offer their services, gifts, and unsolicited sexual advances to those around them, promising to bestow boundless riches. Sexual disinhibition is the primary disorder in the realm of drives, while a euphoric mood tone is the predominant emotional disturbance. Attempts to somehow correct The behavior of patients with PP are completely ineffective due to their lack of critical insight. As is well known, The ability to critically self-evaluate in relation to the social environment is a core characteristic of human intellect. Consequently, in cases of PP, the patient's condition is appropriately classified as demented, with the aforementioned dementia termed paralytic dementia (paralytic dementia can occur not only in PP but also in various intoxications, particularly alcoholism, in which case it is designated as pseudoparalytic to emphasize the lack of connection with a syphilitic infection). Depending on which mental function's impairment predominates in the patient, progressive paralysis is divided into simple, euphoric, paranoid, and depressed forms.

The Third Stage of PP is known as the marantic stage. As the name implies, it is marked by profound marasmus. Such patients are severely untidily neglected, are no longer capable of even the simplest routine intellectual activities, yet remain sexually disinhibited and voracious. Death most commonly results from intercurrent diseases.

Several specific forms of PP should be noted:

1. Taboparesis—a combination of the simple demented form of PP and tabes dorsalis syndrome (locomotor ataxia, loss of tendon Reflexes, sensory disturbances, optic atrophy, Argyll Robertson sign).

2. Stationary paralysis—a form lasting 8 years or more in untreated patients, which may feature spontaneous normalization of the CEREBROSPINAL FLUID.

3. Lissauer's (focal) form—a variant in which dementia is accompanied by persistent spastic, aphasic, and apractic disorders.

4. Galloping form—a form of PP characterized by apoplectiform and epileptiform seizures that may occur in series. It is also marked by autonomic and trophic disorders.

5. Agitated form—a malignant form of PP characterized by a very rapid course, unrelenting psychomotor agitation, incoherent speech, panic fear, hallucinatory experiences, and signs of cerebral irritation, such as picking at clothing or bed linen and Teeth-grinding.

It is useful to recall the neurological symptoms that are obligate for the Diagnosis of progressive paralysis. The Argyll Robertson sign is observed in 80% of patients. It consists of pupil deformation, anisocoria, absence of pupillary light reflex, and miosis. Symptoms of dysarthria and scanned speech are characteristic. The faces of such patients appear puffy and mask-like. Fibrillary twitching of the Tongue and perioral Muscles is noted. Tremor and changes in handwriting are also typical.

It is appropriate to recall from the neurology curriculum the laboratory data: the Wassermann reaction is positive at a dilution of 0.2; TPI (Ribt) and FTA-ABS (RIF) tests are positive. The cerebrospinal fluid exhibits pleocytosis, globulin reactions (Pandy's test, etc.), and the so-called paralytic curve in the Lange colloidal gold test.

Cerebral Syphilis

Cerebral syphilis (CS) involves damage to the blood vessels and meninges, as well as The formation of gummas. Unlike PP, it develops more rapidly—within 5–6 years after primary infection. The First stage of CS is often referred to as syphilitic neurasthenia, but for the reasons mentioned above, it is more accurately termed syphilitic asthenia. It is characterized by frequent psychogenic reactions in the form of mild depression with anxiety and overvalued hypochondria. This stage typically unfolds against a backdrop of elevated body Temperature. Irritability, touchiness, excitability, unpleasant sensations in various PARTS OF THE body, pronounced hyperesthesia, and a persistent lowering of mood with anxiety and dejection are observed. Headaches are very intense and worsen at night. Memory deteriorates, and patients fatigue easily. Neurological examination reveals anisocoria, sluggish pupillary light reflexes, hyperreflexia with Asymmetry on both sides, word-finding difficulties, and transient speech disorders. The Wassermann reaction is positive in both blood and cerebrospinal fluid. The Lange curve yields a syphilitic or paralytic curve. Among somatic symptoms, hepatomegaly, Splenomegaly, jaundice, and albuminuria are noteworthy.

The following forms of cerebral syphilis are distinguished:

1. Syphilitic Meningitis and meningoencephalitis. Its clinical presentation differs little from the psychiatric syndromes seen in other infectious meningoencephalitides. It most frequently has an acute onset. Consciousness is marked by torpor or twilight states. If delirium is present, a multitude of somatic hallucinations is characteristic. As a rule, epileptiform seizures and dysfunctions of the III, VI, and VII cranial nerve pairs are observed. Anisocoria, pupil deformation, sluggish pupillary reflexes, ptosis, strabismus, aphasia, and apraxia are also typical. Nuchal rigidity and Kernig's sign are present. The disease invariably runs its course with hyperthermia. Patients complain of headaches, syncopal states, nausea, and vomiting. The cerebrospinal fluid reveals an exceptionally high count of protein and formed elements (15–20 cells/mL), a typically positive Wassermann reaction, and a syphilitic notch or meningeal-type Lange curve. Meanwhile, the blood Wassermann reaction may be inconclusive. The course of syphilitic meningoencephalitis is generally relatively mild, yet prone to relapses.

2. Syphilitic endarteritis of cerebral vessels. This pathology inevitably leads to dementia. Initially, patients complain of headaches, syncopal episodes, and general malaise. They experience frequent strokes accompanied by paresis. Passivity is noted in such patients, alongside a significant decline in memory for recent events. Subsequently, intellectual-mnestic impairments become so severe that they resemble progressive paralysis. Patients are euphoric, complacent, thoughtless, and occasionally express unstable delusions of grandeur. However, euphoria easily gives way to tearful-hypochondriacal depression, accompanied by groundless persecutory or jealous delusions. Unlike progressive paralysis, these patients exhibit a dissociation of symptoms; for instance, awareness of the illness is preserved for a long time despite a profound mnestic deficit, and spontaneous remissions are possible. Furthermore, speech and handwriting alterations are absent.

3. Gummatous form of cerebral syphilis. The neurological symptoms of this form depend on the size and localization of the gummas. The clinical picture resembles that of a brain tumor (elevated intracranial pressure, vomiting, headaches, adynamia, papilledema, torpor).

4. Epileptiform cerebral syphilis. This variant of cerebral syphilis resembles Epilepsy, characterized by convulsive seizures, twilight states of consciousness, dysphoria, absences, and personality changes.

5. Hallucinatory-paranoid form of cerebral syphilis. This condition develops against a Background of moderately severe dementia. Auditory hallucinations and delusions of persecution, grandeur, and hypochondriasis predominate. The mood is unstable, with irritability alternating with anxiety or depression. Anger is occasionally observed, and euphoria more rarely. In the later stages, epileptiform seizures and disturbances of consciousness join the clinical picture.

6. Congenital syphilis. This condition presents with numerous developmental defects, such as microcephaly, tower Skull, saddle Nose, Hutchinson's triad, and oligophrenia, which are further complicated by other psychiatric and neurological disorders, including epileptic seizures, disturbances of consciousness, and strokes. Less frequently, congenital syphilis may give rise to psychopathy-like states without significant intellectual decline. In unfavorable cases, juvenile progressive paralysis develops between the ages of 10 and 15, marked by skeletal defects, Adiposogenital Dystrophy, Hypogenitalism, and specific lesions of the Liver, Lungs, and skin.

Treatment of PP and CS involves the administration of Antibiotics for an adequate duration, along with medications targeted at managing exacerbations and increasing the permeability of the blood-brain barrier to antibiotics (e.g., pyrogenal).

Having examined the pathological processes caused by the pale spirochete, let us focus on another spirochetal infection that has become widespread in recent decades.

Mental disorders in the Clinical Picture of Lyme Disease

Borreliosis, or Lyme disease, is caused by the spirochete B. burgdorferi, which is transmitted by ticks, most commonly Ixodes ricinus. The initial stage of the disease is associated with the body's reaction to the local spread of the spirochete in the skin. A pathogenic manifestation is erythema migrans, occurring in 40-80% of patients. In 60-80% of patients who do not receive treatment in the early stage, joint inflammation develops, which becomes chronic in 10% of cases. Approximately 15-20% of infected individuals develop signs of Central Nervous system involvement within a few weeks or months. This particular presentation is commonly defined as neuroborreliosis.

Lyme disease attracts the attention of specialists across various medical fields, including psychiatry. Its course can be atypical, and the clinical picture varies significantly depending on the time elapsed since infection and the localization of the pathogen within the body. High incidence rates have been observed globally since the 1990s. A serious diagnostic challenge arises when mental disorders—most commonly depression—appear in the clinical course of the disease. Alongside encephalopathy and Sleep disturbances, depression is characteristic of Lyme disease. Prompt administration of antibiotics provides a favorable therapeutic effect, halting the progression of the disease and preventing various complications, including psychiatric disorders. Depressive mental disorders are observed across all forms of Lyme disease during its chronic course, as well as in acute neuroborreliosis and the cutaneous form (erythema migrans). In the articular form of Lyme borreliosis, mental disorders appear in the vast majority of patients prior to antibiotic therapy. Ranked in decreasing order of frequency, these manifestations include: mild cognitive disorder, episodes of depression, organic mood disorders, mild intellectual decline, asthenoneurotic symptoms, and anxiety-phobic disorders. While antibiotic therapy reduces the frequency of these manifestations, organic mood disorders remain highly treatment-resistant. Neuroborreliosis is characterized by the obligate presence of mental disorders. Their most common forms include mild cognitive disorder, organic mood disorder, mild intellectual decline, episodes of depression, and anxiety-phobic disorders. In the cutaneous form of Lyme disease, mental disorders occur in a significantly smaller number of individuals, most frequently manifesting as asthenoneurotic symptomatology and depressive episodes. The resolution of psychiatric symptoms following antibiotic therapy indicates that they are part of the infectious process (specifically, the body's reaction to it) caused by B. burgdorferi spirochetes. Ongoing collaboration between psychiatrists and infectious disease specialists in the management of Lyme disease patients, alongside the timely use of antibiotics and symptomatic psychotropic medications, helps prevent the development of complications.

Mental Disorders Associated with HUMAN IMMUNODEFICIENCY VIRUS Infection

Human immunodeficiency virus (HIV)-associated dementia is typically characterized by Complaints of forgetfulness, psychomotor retardation, and difficulties in concentration, problem-solving, and reading. Apathy, reduced spontaneous activity, and social withdrawal are frequent. In some cases, the condition may manifest as atypical Affective Disorders, psychoses, and seizures. Somatic examination may reveal tremor, impairment of rapid alternating movements, coordination deficits, ataxia, hypertonia, generalized hyperreflexia, frontal release signs, and oculomotor abnormalities.

HIV-associated impairment can also occur in children, characterized by developmental delay, hypertonia, microcephaly, and Basal Ganglia calcification.

HIV-associated dementia most commonly progresses rapidly (over the course of weeks and months) to global dementia, mutism, and death. Treatment is generally symptomatic. Patients require nursing care and are classified as having a primary disability group.

Features of Mental Disorders in Certain Other Somatic Infectious and Non-Infectious Diseases

Rheumatic Fever

The active phase of rheumatic fever is accompanied by asthenic states of varying depth and severity: ranging from increased physical fatigue and exhaustion to states characterized by profound and rapid depletion of mental processes, hyperesthesia, irritable weakness, and massive autonomic disturbances; in some cases, these states are accompanied by phobias and hypochondriasis. Emotional disorders manifest as depressed mood and motiveless mood swings. Hysteriform disorders in the form of vegetomotor attacks with adynamia, expiratory difficulty, or astasia-abasia develop less frequently. Delirious states, oneiric disturbances of consciousness, stupor, psychosensory disorders, and spells of anguish accompanied by anxiety and fear may also occur.

The development of cardiac decompensation frequently leads to depressive-delusional states accompanied by anxiety and marked Variability in the clinical picture.

In rheumatic chorea, alongside asthenic manifestations and pronounced emotional lability, behavioral disinhibition with enhanced drives and euphoria may be observed. Protracted psychoses in the form of manic states and depressions are frequent.

Rheumatic involvement of cerebral blood vessels presents with depressive-Delusional syndromes accompanied by agitation and anxiety, apathetic stupor, epileptiform seizures, various psychic equivalents, and pseudoparalytic disorders.

A prolonged course of rheumatic fever may lead to the development of a psycho-organic syndrome of varying severity.

Subacute Bacterial Endocarditis

Asthenic disorders in subacute bacterial endocarditis are typically accompanied by depressed mood and adynamia. Manic disorders with a marked lack of insight occur less frequently. The Emergence of asthenic disorders and euphoric states indicates an exacerbation of the disease.

Psychoses in subacute bacterial endocarditis may present with disturbances of consciousness in the form of delirium, ammentia, or epileptiform excitement, as well as depressive-agitated states resembling involutional melancholia and hallucinatory-delusional psychoses.

Malignant Tumors

Mental disorders associated with malignant tumors (MT) are characterized by asthenic symptoms with pronounced affective lability. Reactive states with severe depression are common, particularly upon the patient learning of their diagnosis.

Psychoses in malignant tumors develop during the progression of cachexia and occasionally following surgical intervention.

Acute symptomatic psychoses typically manifest as delirium accompanied by mild agitation, sparse hallucinations, illusions, and oneiric states at the peak of the psychosis. In severe cases, often in pre-terminal situations, murmuring delirium or ammentia may be observed. Protracted symptomatic psychoses in the form of depressive or delusional states occur less frequently. Depressions are accompanied by anxiety; their depth and severity fluctuate, and episodes of delirium are possible.

Delusional states present with suspiciousness, limited social engagement, specific content-bound delusional ideas, anxiety, and asthenic disorders.

The development of apathetic stupor indicates a critical deterioration in the patient's somatic condition.

Influenza

Mental disorders in influenza emerge at the peak of the infection, during the febrile or postfebrile period. The prodromal stage of psychoses is marked by asthenic disorders, adynamia, sleep disturbances (nighttime insomnia and daytime somnolence), as well as phenomena of derealization and fears accompanied by unpleasant sensations in the cardiac region.

Acute psychotic states manifest as pictures of acute delirium, epileptiform agitation, and anxious-dysphoric agitation with delusions of self-blame and sinfulness, and less commonly, with ideas of persecution. Characteristic features include asthenic disorders, primarily heightened exhaustion and autonomic dysfunctions. Occasionally, hypomanic states occur, marked by animation and a drive toward action. Psychoses are more frequent during epidemics and very rare in sporadic cases of the disease. In those who are severely and chronically ill, changes in intellectual activity predominate: attention and concentration capacity are impaired. These disorders may also persist during the convalescence period, where post-influenza depression is an important symptom.

Tuberculosis

Patients with tuberculosis generally exhibit various asthenic disorders: pronounced irritable weakness, tearfulness, and helplessness. Patients with destructive forms of Pulmonary Tuberculosis (fibrocavernous) are characterized by an elevated mood with an euphoric undertone, carelessness, superficial judgment, and increased sexual activity (vividly described in the novels of E. M. Remarque), or sometimes conversely, by a fixation on the manifestations of the disease. Psychoses are rare, with manic conditions being more common, and hallucinatory-paranoid states less so. The onset of epileptiform seizures provides grounds to suspect the development of cerebral tuberculomas. There is also a view that psychoses in tuberculosis are linked not to the disease itself, but to The Use of antituberculosis drugs. Indeed, we owe the discovery of antidepressants precisely to phthisiatric practice, where iproniazid began to be used and induced states of elevated mood in patients (its side effect on the monoamine oxidase enzyme).

Postpartum Psychoses

Delirium, verbal hallucinosis, anxiety-laden depressions, and confusional manias are most frequently observed; previously, ammental states were considered characteristic, though they are virtually never seen in the era of widespread antibiotic use. Postpartum psychoses can be symptomatic (associated with postpartum septic processes) and endogenous (Schizophrenia, manic-depressive psychosis), the latter being triggered by Pregnancy and Childbirth. Differential diagnosis presents significant difficulties because psychoses of diverse genesis share a similar clinical picture. However, delirious episodes and the development of catatonic disorders exclusively at the height of an ammental state point toward a symptomatic psychosis, whereas the development of ammentia following catatonic agitation is more characteristic of schizophrenia. If psychosis occurs in an uncomplicated postpartum period, the diagnosis of symptomatic psychosis is doubtful.

Mental Disorders in Endocrine Diseases

Mental disorders in endocrine diseases are polymorphic; however, their development follows certain patterns that are crucial for diagnosis. These patterns consist of the emergence, in the early stages and during a relatively benign course of the illness, of the so-called psychoendocrine or psychopathlike syndrome (the "endocrine psychosyndrome"). As the disease progresses, this syndrome gradually transitions into a psycho-organic (amnestic-organic) one. Against the background of these syndromes, predominantly (though not exclusively) in connection with complications of the endocrine disorder, acute or protracted psychoses may develop. These regularities are characteristic of all endocrine diseases, regardless of the dysfunction of a particular gland. Similar mental alterations can accompany both hyperfunction and hypofunction of individual glands.

Psychopathlike Syndrome (Endocrine Psychosyndrome)

The psychopathlike syndrome is characterized by a decrease in mental activity, along with altered drives, instincts, and mood.

The decrease in mental activity can vary in degree—ranging from heightened exhaustion and passivity within asthenic states to complete aphasia/aspontaneity with a significant narrowing of interests and a primitivization of social contacts, approaching an apatico-abulic state.

Unlike schizophrenic apathetic states marked by an "energetic potential drop," patients with endocrine diseases retain their response to emotionally significant stimuli, even in states of pronounced decline in mental activity.

Alterations in drives and instincts manifest as a decrease or increase in sexual drive, appetite, and thirst; patients may develop a tendency toward wandering or, conversely, remain confined to their usual surroundings, and alterations in their need for sleep, warmth, etc., occur. Endocrinopathies are characterized by both quantitative and qualitative changes in drives. Such patients frequently exhibit perversions. Dissociation with an increase in certain drives and a decrease in others is also possible.

Mood disturbances are varied and differ in severity. Characteristic features include mixed states—depression with dysphoria, manic and depressive states accompanied by malice and feelings of hatred, depressive-apathetic states, asthenic depressions, and the like. Mood lability is also typical. Alterations in thinking and motor activity characteristic of classical affective syndromes (retardation in depression and hyperactivity in mania) are atypical in endocrine states. Conversely, dissociated states are frequently encountered, such as an elevated mood combined with complete inactivity and motor retardation. Affective disorders in the endocrine-type psychopathlike syndrome are sometimes protracted (occasionally constituting one facet of personality changes), and sometimes episodic, resembling the affective paroxysms of epilepsy and atypical periodic psychoses.

Reactive depressions may also develop in endocrine diseases (for example, a reaction to changes in appearance in Cushing's Disease).

Simmonds' pituitary cachexia, Sheehan's syndrome, Addison's disease, and certain other endocrinopathies are characterized by a decrease in mental activity. In cases of sufficiently pronounced acromegaly, these impairments manifest as apathy and aspontaneity. Combined with a carefree, euphoric mood and a sense of passive self-satisfaction, they form the specific Features of the psychosyndrome in this condition. In hyperthyroidism, heightened affective excitability, mood lability, and vivid emotional expressions come to the forefront. Mood alterations occupy a significant place in the clinical picture of Cushing's disease and adiposogenital syndrome. In these instances, astheno-hypochondriacal, hypochondriaco-cenestopathic states, and reactive depressions are frequently observed.

Amnestic-Organic Syndrome

With a protracted and particularly severe course of endocrine diseases, an amnestic-organic syndrome develops. This is a more general, global impairment of mental Functions that affects all aspects of the personality and significantly blunts its individual traits. The organic-amnestic syndrome is characterized by memory disorders (amnesia, dysmnesia, Korsakoff-like syndromes, etc.), intellectual decline with a marked impairment of awareness and critical insight into one's condition; previously acquired skills are lost, thinking becomes sluggish and more superficial; and features of emotional inertia and blunting begin to dominate the affective sphere. In the most severe cases, a syndrome of organic dementia develops.

Acute Psychoses

Acute psychoses develop against the background of the aforementioned syndromes and can occur at any stage of the disease. Frequently, they are driven by the increasing severity of the underlying condition with an intensification of metabolic, vascular, and other disorders (during Addisonian crises, hypertensive crises in patients with Cushing's disease, hypertoxic crises, etc.). Typically, psychoses in such cases develop following an exogenous reaction type with its characteristic syndromes (delirium, ammentia, twilight state of consciousness). Epileptiform agitation or epileptiform seizures are possible. The correlation between the onset of acute psychoses and the appearance and severity of somatic complications is not absolute. Sometimes such psychoses arise without apparent causes. Primarily, this concerns psychoses with a predominance of affective disorders (depressive, depressive-paranoid syndromes) and psychoses of a schizophreniform Structure. These psychoses frequently become protracted and recur. Atypical or periodic psychoses are rather challenging from a differential diagnostic standpoint.

Practically all syndromes known in psychopathology have been described in psychoses among patients with endocrine disorders. Concurrently, however, typical hallucinatory, paranoid, and especially catatonic syndromes occur relatively rarely.

Features of Certain Poisonings by Household and Industrial Poisons

Asthmatol Poisoning

In individuals forced to systematically use asthmatol, attention should be paid to the early signs of intoxication—asthennia, severe somnolence, and visual disturbances.

Facial hyperemia, mydriasis, slurred and indistinct speech, and speech incoherence are characteristic. Chaotic, motiveless agitation resembles that seen in Sydenham's chorea.

Typically, delirium with microzoopsia or acute verbal hallucinosis develops, followed by fragmented, unsystematized hallucinatory delusions.

Atropine Poisoning

It is characterized by delirium with agitation and a fluctuating affective state, which (in severe cases) progresses to obtundation, leading into stupor and coma. Diagnostic signs include tachycardia, dry Mouth, mydriasis, cycloplegia, tremor, and twitching in certain Muscle groups. As a rule, atropine delirium resolves spontaneously after a critical sleep, but one must also keep in mind the possibility of hypertoxic forms that can be fatal. Treatment of atropine delirium may involve medications with cholinomimetic action (such as neostigmine, physostigmine, etc.).

Aniline Poisoning

A pathognomonic sign is that the skin and mucous membranes acquire a gray or grayish-black hue.

In mild cases, symptoms include headache, nausea, vomiting, clouding of consciousness, and isolated convulsive twitches.

In severe cases, delirium with pronounced psychomotor agitation progresses to muttering delirium, stupor, and coma.

Acetone Poisoning

Asthenia with dizziness, unsteady gait, eructation, nausea, and vomiting.

Delirium states are protracted, being most pronounced in the evening.

Depressive states accompanied by anxiety, anguish, and ideas of self-blame are possible.

Acetone use rapidly leads to the development of an psychoorganic syndrome. Since acetone (or Solvents containing it) is used in the manufacture of illicit homemade drugs, this syndrome is observed in many patients with substance use disorders.

One might recall the lyrics of a song by the band Nautilus Pompilius: "...Your girlfriends sniff glue, getting a bit more foolish with every passing day."

Gasoline Poisoning

Euphoria or asthenia accompanied by headache, nausea, and vomiting.

Psychotic disorders follow a delirium or oneiroid pattern.

Further clinical deterioration leads to stupor and coma accompanied by seizures and paralysis.

Benzene (Nitrobenzene) Poisoning

The clinical picture is similar to that of aniline poisoning. Additional diagnostic criteria include leukocytosis and the smell of bitter almonds in the air.

Mercury Poisoning (Chronic)

Obligate signs of this poisoning include dysarthria, ataxic gait, and tremor.

Organic-type psychopath-like symptoms with affective lability, emotional incontinence (less commonly, euphoria), and reduced insight.

In the most severe cases, lethargy and aspontaneity are observed.

Arsenic Poisoning

The first symptoms of poisoning include vomiting with blood, digestive disorders, and hepatosplenomegaly (recall the grim finale of Gustave Flaubert's novel Madame Bovary).

Clouding of consciousness rapidly progresses to sopor and coma.

Chronic poisoning with low doses leads to the development of psycho-organic syndrome and even dementia.

Manganese poisoning (chronic)

Typically, there are pronounced asthenic conditions and algia (in the lower back and lower extremities), sensory-perceptual disorders, anxiety, fears, depression with suicidal ideation, unstable ideas of reference, parkinsonian symptoms, leg edema, and impotence.

Pronounced psychopath-like personality changes and psycho-organic syndrome may develop. These are frequently observed in individuals suffering from drug addiction caused by the use of pervitin, an illicitly homemade psychostimulant (the so-called "shirka"). This exemplifies a dual (or even triple, considering that the drug production technology involves the use of crystalline iodine) toxic impact of potent neurotoxins on the brain, as psychostimulants themselves also lead to neuronal destruction.

Carbon monoxide poisoning

The acute period is typically characterized by stupor, which can progress to a deep comatose state.

Delirium with olfactory hallucinations is frequent (unless the poisoning immediately results in a coma).

Several days after severe poisoning, against the backdrop of apparent initial recovery, psychopath-like disorders, Korsakoff's syndrome, aphasia with agnosia, or parkinsonism may develop.

Lead poisoning

The initial signs include headache, dizziness, and asthenic disorders dominated by irritable weakness.

In severe cases, delirium and epileptiform agitation are possible.

Chronic poisoning leads to psycho-organic syndrome accompanied by epileptiform seizures and severe memory impairment.

Tetraethyllead poisoning

Initially, there are asthenic disorders, bradycardia, hypotension, hypothermia, headache, nausea, vomiting, hypersalivation, diarrhea, severe abdominal pain, sweating, and hyperkinesia accompanied by muscle hypotonia and ataxic gait.

Delirium, characterized by the "foreign body in the mouth" symptom. In severe cases, stupor and epileptic seizures typically develop.

Chronic intoxication presents with pseudoparalytic and Korsakoff's syndromes.

Organophosphate poisoning

The most Characteristic Features of this poisoning include asthenia, emotional lability, photophobia, photopsia, anxiety, restlessness, convulsive phenomena, bradycardia, hyperhidrosis, nausea, dysarthria, and nystagmus.

Uncontrollable vomiting is very characteristic, with the vomitus smelling of garlic and glowing in the dark.

Severe poisoning presents with amnesia or various degrees of impaired consciousness, giving way to prolonged sleep.

Chronic poisoning most frequently manifests as hallucinatory-paranoid states or catatonic stupor.

Fundamentals of Gerontopsychiatry

Late-onset dementias

Dementia is a syndrome caused by a brain disorder—typically of a chronic or progressive nature—characterized by the impairment of several higher cortical functions, including memory, thinking, orientation, comprehension, calculation, learning capacity, language, and judgment. Consciousness in dementia is formally unimpaired.

Thus, dementia represents a marked decline in intellectual functioning that most commonly leads to impairments in activities of daily living, such as dressing, bathing, eating, personal hygiene, and independent physiological self-care.

Dementias caused by degenerative-atrophic brain disorders, which belong to the so-called "primary dementias," can be conditionally divided into 4 groups based on the Topography of the lesion:

1) cortical (Alzheimer's disease, frontotemporal lobar degenerations, including Pick's disease);

2) subcortical (progressive supranuclear palsy, Huntington's disease, Parkinson's disease, and some cases of multi-infarct dementia);

3) cortico-vascular (dementia associated with Lewy bodies, corticobasal degeneration, and some cases of vascular dementia);

4) multifocal disorders (so-called "prion diseases": Creutzfeldt-Jakob disease, Gerstmann-Sträussler syndrome, fatal familial insomnia, and atypical prion dementias).

Dementia in Alzheimer's Disease

Today, alongside vascular pathology, Alzheimer's disease (AD) is one of the most frequent causes of dementia. Among hospitalized dementia patients in the USA, those suffering from AD account for 50% to 65%.

This is predominantly a cortical disorder characterized by primary impairment of functions in the medial and posterior Regions of the cortex. Characteristic brain changes include a significant reduction in the neuronal population, especially in the hippocampal region; alterations in the temporoparietal area and frontal cortex; the appearance of neurofibrillary tangles composed of paired helical filaments; neuritic (argyrophilic) plaques, predominantly amyloid, with a certain tendency toward progressive development; and granulovascular bodies. Neurochemical changes have also been found, which include a marked decrease in the enzyme Choline acetyltransferase, acetylcholine itself, and other Neurotransmitters and neuromodulators.

Memory disorders are the earliest symptoms. Impairments in acquiring new information and forgetting everyday events are observed, although memory for remote past events may remain intact. Amnestic symptoms may be the sole sign for many years before the development of other cognitive impairments that reflect a relatively limited spread of the pathological process to the mediotemporal regions of the cortex. Visuospatial disturbances associated with Atrophy of the parietal cortex are characteristic and precede the development of amnestic symptoms in some patients. Patients find it difficult to navigate their surroundings (e.g., getting lost even in familiar settings like their own home, or struggling with table Setting arrangements). At later stages, impairments in recognizing faces—including one's own reflection in a mirror—as well as the misidentification of objects are noted. Language impairments appear when the pathological process spreads to the perisylvian regions. Speech is halting, reflecting difficulties in word-finding and maintaining a single train of thought. Difficulties in sentence construction, impairments in complex limb movements, and the loss of independent dressing skills due to spatial disorientation are observed. Overall, this refers to "cortical" symptomatology described by terms such as apraxia, acalculia, alexia, agnosia, etc. (in various forms and combinations). The affective background in these patients may be depressive or euphoric, flat or labile.

The presence of depressive symptoms sometimes causes differential diagnostic challenges. When conducting differential diagnosis, one should bear in mind that the "depression–true dementia" combination is most often caused by a primary dementing process that frequently manifests with depression as well, especially if the dementia has "subcortical" features. In this case, depression may respond to antidepressants, but extremely rarely (and only in the initial stages when emotional disorders dominate the clinical picture) is it accompanied by a significant improvement in cognitive functions.

It is believed that awareness of one's intellectual deficit is characteristic of many, if not all, patients, at least in the Cytology/cytology/16.html">Early stages of the disease. In later stages, personality changes and intellectual decline become obvious. An incidental somatic illness can trigger delirious confusion, leading to a sharp deterioration in cognitive functions. In the terminal stages, urinary and fecal incontinence, myoclonus, parkinsonian symptoms, rigidity, seizures, and increasing cachexia, decortication, mutism, and a tendency toward contracture development are observed. Death typically ensues As a result of septic complications.

Traditionally, two forms of AD are distinguished according to the age at onset. AD with early onset debuts before 65 years of age, and late onset after 65, as reflected in the ICD-10 classification. The former form is likely more closely related to genetic predisposition and is characteristic of family members with hereditary AD.

While the prevalence of AD is 2.3–10.3% in individuals under 65 and 13–48% after the age of 65, it is practically nonexistent in certain ethnic groups, such as the populations of Nigeria and some Native American tribes—a fact sometimes explained not solely by genetic factors, but also by environmental influences and the difficulty of detecting this pathology in the respective regions.

Risk factors for AD include advanced age, a family history of AD in close relatives, Down syndrome, HEAD trauma, low educational attainment, and genetic factors—namely, the presence of specific alleles on Chromosomes 21, 19, 14, and 1. Individuals with one first-degree relative with AD have a 4-fold higher risk of developing the disease than the general population, and those with two or more relatives have a 40-fold higher risk. However, monozygotic twins are not always concordant for this trait. Smoking and a high level of education act as protective factors.

Vascular Dementia

Dementia may result from cerebral infarction, atherosclerosis, Hypertension, or other vascular pathology, thus having either an acute onset following a single ischemic event or a gradual onset during a stroke-free course of the vascular process. A single stroke can cause dementia, as well as other cortical function impairments such as aphaso-apractic disorders, which can determine patient disability; typical personality and emotional-affective changes are well described. The term "multi-infarct dementia" has largely replaced the previously accepted term "arteriosclerotic dementia." The initial psychopathological manifestations of vascular lesions may be emotional and personality disorders, followed by intellectual-mnestic impairments with characteristic fluctuations in severity. Episodes of mental confusion are frequent, especially at night. In some cases, episodes of cerebral ischemia are noted, though they are sometimes absent in the Anamnesis, which can complicate diagnosis. An uneven disease course with signs of lacunar deficits in mental functions is characteristic. Somatic examination reveals arterial hypertension and signs of peripheral and retinal arteriosclerosis; neurological disorders such as pseudobulbar palsy and other focal neurological deficits are also possible.

Multi-infarct dementia typically features an uneven course with periods of deterioration sometimes followed by partial recovery lasting several months. About half of patients die from coronary artery disease, while the rest succumb to cerebral infarctions or renal complications. Life expectancy from the time of diagnosis averages 4–5 years, though it varies widely.

Regarding morphological changes, multi-infarct dementia is defined by prominent organic pathology in the form of local or generalized brain atrophy, ventricular enlargement with areas of cerebral infarction, and atherosclerosis of large vessels. The histological picture is determined by multiple foci of infarction and ischemia. It has been established that the total volume of functionally inactive brain tissue correlates with the severity of dementia, wherein what matters is not the actual volume of the affected tissue, but the volume of cortical areas functionally inactivated due to disconnection from the basal ganglia and thalamus.

A distinct entity is so-called "subcortical vascular dementia," which corresponds to Binswanger's encephalopathy resulting from hypertension and is morphologically defined by diffuse demyelination of the White matter, sometimes involving the Cerebral Cortex with the development of "Alzheimer-like" states.

Dementia in Pick's Disease

Pick's disease (PiD) is a disorder described by the Prague psychiatrist Arnold Pick in 1892 and viewed by him as an atypical variant of senile dementia. Today, PiD is classified among the degenerative-atrophic brain disorders, characterized by atrophic involvement of the frontotemporal regions of the cortex and the presence of specific inclusions in the brain tissue—Pick bodies. Microvacuolation and FLD-type astrocytic gliosis, with or without the formation of ballooned cells, are frequently found.

Based on the topography of the lesion and the lateralization features of the degenerative-atrophic process in the patient's brain, three clinical variants of frontotemporal atrophy are distinguished, which sometimes succeed one another and may represent stages of a single process.

1. Frontotemporal dementia, characterized by bilateral atrophy of the frontal and anterior temporal cortex, accompanied by progressively worsening emotional-volitional disorders leading to the complete disintegration of the core personality in the form of social decline, apathico-abulic or euphoric-erethetic symptom complexes—depending on the predominance of damage to the orbital or convexity regions of the cortex—impaired insight, stereotypies, perseverations, and echolalia, in the absence of the visuospatial impairments characteristic of Alzheimer's dementias.

2. Progressive non-fluent aphasia. This condition is typically observed in cases of predominant left-sided lesions in the anterior regions of the brain. It is characterized by a loss of speech fluency and the impaired ability to repeat words. Other features include paraphasia, impaired spelling in both oral and written speech, while the comprehension of word meanings remains preserved. Behavioral disturbances may emerge later, reflecting the spread of the pathological process to both temporal lobes. In some patients, language deficits remain the sole manifestation of the disease for many years, a condition referred to as primary progressive aphasia.

3. Semantic dementia, characterized by the predominant involvement of the frontal regions in both hemispheres, manifests as multimodal impairments affecting word comprehension, face recognition, and object recognition. Spontaneous speech remains preserved—it appears effortless to the patient and grammatically correct, yet it is rich in semantic paraphasias involving phonetically similar words. Phonemic disturbances characteristic of the previous form are virtually absent. Marked impairments are evident in naming, as well as in the comprehension of spoken and written words during repetition and reading aloud. Agnosic phenomena are observed despite the preserved ability to copy and compare objects and words. The balance between semantic impairments in the verbal and visual domains reflects the degree of involvement of the left and right temporal lobes. Mnesic impairments are typically absent. Symptoms of spinal motor neuron involvement may also develop, resembling an AMYOTROPHIC LATERAL SCLEROSIS-like syndrome, followed by respiratory complications that dictate a rapid fatal outcome.

Psychiatric Disorders in Epilepsy

Epilepsy is a multi-etiological disorder; it is studied in detail within the neurology curriculum, and such patients are predominantly managed by neurologists. The reasons for which epilepsy patients are referred to a psychiatrist can be categorized into the following groups:

1) aggressive behavior resulting from specific personality changes;

2) an unfavorable disease course refractory to antiepileptic treatment, leading to the development of a psychological deficit (most commonly seen in epilepsy starting in childhood or adolescence);

3) seizures presenting as psychiatric disorders with positive symptoms (most frequently when the focus is localized in the frontal lobe) and/or interictal schizophrenia-like psychoses.

At the beginning of the 20th century, the prevailing view was that epilepsy and its characteristic personality profile—marked by egocentrism, irritability, captiousness, stubbornness, envy, religiosity, vindictiveness, viscosity of thought, a tendency to idealize authoritative figures in society (such as a physician), frequent use of diminutive words and terms of address, an inability to understand humor, and a propensity for brutal sexual aggression—were the consequences of some underlying deep-seated pathology. This viewpoint is now considered erroneous, as it stemmed primarily from observations of institutionalized clinical patients. Patients who maintain their social status through adequate antiepileptic treatment do not suffer from such personality alterations. It is also worth recalling that history offers numerous Examples of prominent political and artistic figures who, according to contemporaries, experienced epileptic seizures (such as Julius Caesar, Alexander the Great, Peter the Great, Napoleon, and F. M. Dostoevsky). Yet, they either lacked the aforementioned pathological personality traits or these traits did not define their standing in society. Today, it is more widely accepted that personality disorders in epilepsy patients are the consequence of temporal lobe involvement, essentially representing organic personality changes. Another factor contributing to these changes was the widespread use of barbiturate therapy (phenobarbital and benzonal), which was common until recently for patients suffering from convulsive seizures.

If dementia develops in an epilepsy patient, it most typically progresses as so-called concentric dementia: interest in social life, the surrounding environment, hobbies, and work gradually fades, until the patient becomes entirely consumed by concerns related solely to their illness and its treatment. In children suffering from severe forms of epilepsy, a significant decline in cognitive functions is observed—manifested by slowed thinking, the inability to distinguish the essential from the trivial, and ultimately an inability to Abstract from concrete facts, leading to profound developmental delays.

Among the psychotic manifestations of epilepsy, a distinction should be made between seizure "equivalents" presenting as delirious states (one hypothesis regarding Vincent van Gogh suggests he suffered from epilepsy complicated by psychoses with impaired consciousness due to alcohol and absinthe abuse), twilight states of consciousness, pronounced dysphoria, and interictal disorders resembling schizophrenia. The latter are again most commonly observed in temporal lobe epilepsy and present as chronic hallucinatory-parandoid psychoses. The differential diagnostic criteria for such psychoses include the absence of a premorbid profile characteristic of schizophrenia and the preservation of appropriate emotional responses. The Importance of differentiating between epilepsy and schizophrenia in these cases is primarily determined by the choice of therapeutic strategy: certain neuroleptics and antidepressants prescribed for schizophrenia (chlorpromazine, imipramine, amitriptyline, clozapine) can provoke a seizure, whereas the timely administration of antiepileptic drugs, conversely, helps resolve psychotic symptoms.

Currently, the most common medications for treating epilepsy are sodium valproate (depakote) and carbamazepine. Ethosuximide has proven effective for absence seizures. Occasionally, in severe cases, it is necessary to use hydantoins (phenytoin), introduced into clinical practice back in 1938, and barbiturates, known to physicians since 1912. However, these drugs possess numerous side effects, which limits clinicians' interest in them. In status epilepticus, the primary feature of which is persistent unconsciousness even during the interictal interval, the drug of choice is diazepam (seduxen, sibazon, relanium). If diazepam proves ineffective, rectal chloral hydrate is administered. Finally, in life-threatening cases to reduce cerebral edema, therapeutic lumbar puncture is used. Most physicians, however, lean toward general anesthesia and mechanical ventilation as soon as diazepam is found ineffective. Also crucial are the correction of plasma electrolyte composition (most frequently hypokalemia) and the maintenance of adequate blood alkali reserve (taking into account seizure-induced Hypoxia).