Psychiatry - O. K. Napreyenko 2001

Clinical Psychiatry
Late-life mental disorders. Vascular mental disorders

The increase in the average life expectancy has led to a growing elderly population and, consequently, a rise in late-life mental disorders.

The prevalence rates of Mental disorders in individuals over 60 range from 10 to 25%. Overall, Mental Disorders Associated with cerebrovascular diseases develop in approximately 23% of older adults.

Etiology, Pathogenesis, Classification

Mental disorders in the elderly are etiologically heterogeneous. Traditionally, they are divided into two groups.

The first group comprises patients whose mental disorders always develop in late life. These include functional mental disorders, presenile and senile dementias, as well as psychiatric disturbances caused by cerebrovascular pathology.

The second group consists of elderly patients with mental disorders that began at an earlier age and recur with the onset of Aging, as well as psychiatric disturbances that first appear in late life but are not specific to it. These encompass various clinical-nosological forms: Schizophrenia, Epilepsy, manic-depressive psychosis, psychogenias; psychopathies, and psychoses caused by somatic illnesses, infections, TRAUMATIC Brain INJURIES, alcoholism, drug addiction, and substance abuse. Among the factors associated with aging, notable ones include Climacteric neuroendocrine changes, age- and somatic disease-related changes in Internal Organs, involutional personality changes, and psychotraumatic socio-psychological situations.

In domestic literature, late-life mental disorders are traditionally classified as follows:

Presenile

Functional:

✵ climacteric neurosis-like states;

✵ involutional depression (presenile melancholia);

✵ involutional delusional psychoses (paranoid, paranoiac, hallucinatory, and hallucinatory-paranoid forms);

✵ late catatonia.

Atrophic (dementias):

✵ Alzheimer's disease;

✵ Pick's disease;

✵ Creutzfeldt-Jakob disease;

✵ Huntington's chorea;

✵ Parkinson's paralysis agitans.

Senile

Functional:

✵ senile delirium;

✵ Wernicke's presbyophrenia;

✵ hallucinoses (optical, verbal, tactile, olfactory);

✵ acute confusional state.

Atrophic (dementias):

✵ senile dementia: simple form; psychotic form.

Mental disorders in cerebrovascular diseases predominantly occur in patients with: cerebral atherosclerosis; Essential Hypertension; hypotension; cerebral obliterating thromboangiitis.

According to ICD-10, these disorders are coded under the following categories:

F 0 Organic, including symptomatic, mental disorders

F 00 Dementia in Alzheimer's disease

F 00.0 Dementia in Alzheimer's disease with early onset

F 00.1 Dementia in Alzheimer's disease with late onset

F 00.2 Dementia in Alzheimer's disease, atypical or mixed type

F 00.9 Dementia in Alzheimer's disease, unspecified

F 01 Vascular dementia

F 01 Vascular dementia with acute onset

F 01.1 Multi-infarct dementia

F 01.2 Subcortical vascular dementia

F 01.3 Mixed cortical and subcortical vascular dementia

F 01.8 Other vascular dementia

F 01.9 Vascular dementia, unspecified

F 02 Dementia in diseases classified elsewhere

F 02.0 Dementia in Pick's disease

F 02.1 Dementia in Creutzfeldt-Jakob disease

F 02.2 Dementia in Huntington's disease

F 02.3 Dementia in Parkinson's disease

F 02.8 Dementia in other specified diseases classified elsewhere

F 03 Unspecified dementia

F 04 Organic amnesic syndrome, not induced by alcohol or other psychoactive substances

F05 Delirium not induced by alcohol or other psychoactive substances

F06 Other mental disorders due to brain damage or dysfunction, or to physical disease

F09 Unspecified organic or symptomatic mental disorders

F34.8 Other persistent mood disorders

According to DSM-IV:

290.XX Dementia of the Alzheimer's type, early onset

.10 Uncomplicated

.11 With delirium

.12 With delusions

.13 With depressed mood

— with behavioral disturbance

290.XX Dementia of the Alzheimer's type, late onset

.0 Uncomplicated

.3 With delirium

.20 With delusions

.21 With depressed mood

— with behavioral disturbance

290.XX Vascular dementia

.40 Uncomplicated

.41 With delirium

.42 With delusions

.43 With depressed mood

— with behavioral disturbance

294.1 Dementia due to Parkinson's disease

294.1 Dementia due to Huntington's disease

290.10 Dementia due to Pick's disease

290.10 Dementia due to Creutzfeldt-Jakob disease

294.0 Amnestic disorder due to... chronic

311 Depressive disorder, unspecified

300.4 Dysthymic disorder with late onset. Neurosis-like states resemble neuroses and neuropsychiatric disorders traditionally referred to as "climacteric neurosis." Most frequently, such disturbances are part of the climacteric syndrome with its somatoendocrine changes. Neurosis-like disorders, characterized by their inherent polymorphism, are classified among the manifestations of pathological age-related crises.

In the clinical picture of non-psychotic disorders, asthenia forms the primary Background. Characteristic Complaints include loss of drive and working capacity, mental and physical fatigue, nervousness, and frequent unpleasant sensations in various PARTS OF THE body, particularly burning, numbness, coldness, and hot flushes. Mood changes are accompanied by anxiety, vulnerability, and irritability. Hypochondriacal concerns regarding internal organ diseases that may be recognized by physicians are common. Phobic manifestations are triggered by intrusive memories of unpleasant events, fear of death, inability to move about without accompaniment, etc. Typical symptom complexes also include depressive, hypochondriacal, and hysteriform types, which manifest as episodes with significant fluctuations in intensity.

The prognosis for neurosis-like disorders is favorable. In the majority of patients, these disorders last from several months to several years, followed by recovery. In some patients, prolonged disorders lead to character changes and The Development of pathological personality traits. Progression into an involutional psychosis is possible.

Neurosis-like disorders are most commonly observed in women (20–30%), occurring half as frequently in men. Pathogenic roles are played by neuroendocrine changes, diencephalic dysfunction, and general involutional processes.

Treatment of neurosis-like disorders involves tranquilizers, psychostimulants, hormonal agents (estrogens, androgens), physiotherapeutic Procedures, and psychotherapy.

Late-life psychoses. Psychotic disorders first developing after the age of 45 are conventionally divided into involutional (45–60 years) and senile (after 60 years).

Presenile psychoses. The syndromal manifestations of affective and delusional late-life psychoses were described by Krafft-Ebing (1878), Cotard (1882), Schüle (1886), and others. However, involutional melancholia was first distinguished as an independent nosological entity by E. Kraepelin (1896). The Description of the psychosis reflects the anxiety-depression states of late life. Delusional presenile psychoses were characterized by many psychiatrists (Kleist, 1913; Albrecht, 1914; Serko, 1919). Today, however, the validity of dividing them into two age subgroups is questioned; consequently, data on the prevalence of involutional psychoses remain scarce.

Involutional melancholia develops between the ages of 45 and 55, with an insidious onset. The involutional period lasts from several weeks to a year and is characterized by depression accompanied by lethargy, dysphoria, and hypochondriacal disorders. Anxiety progressively increases, accompanied by apprehension and tense anticipation of misfortune. Over time, anxious depression intensifies with agitation and psychomotor excitation. The manifestation of psychosis with a similar clinical picture may begin acutely when preceded by psychic trauma or an acute somatic illness. The combination of depression with anxiety and the monophasic Nature of the disorder are considered essential Clinical Features of involutional melancholia. The anxiety lacks a specific object, saturated instead with ominous premonitions that worsen toward evening and at night. Changes in familiar surroundings intensify the anxiety. Agitation is regarded as a hallmark clinical sign; motor restlessness may reach the point of frenzy, and speech becomes incoherent, consisting of a nonsensical string of phonetically similar words. Recently, agitation has been observed less frequently. In many patients, anxious-depressive sadness is accompanied by lethargy, hypokinesia, and inarticulate speech. The anxiety-depression affect is accompanied by depressive delusions (ideas of self-blame, condemnation, ruin, and hypochondriasis). Ideas of persecution, poisoning, loss, and jealousy also occur. Sometimes, particularly in older age, Cotard's syndrome develops. This nihilistic delusion is fantastic in nature: patients claim they have no internal organs, and that food "falls straight into the Abdominal cavity AND is not digested." Patients may express ideas of malignant omnipotence (predicting suffering and the doom of the world; "people are suffering, suffocating in the toxic fumes emitted by the patient"). Ideas of painful immortality—resembling sinners in hell—are frequent. Morbid ideas may assume a megalomanic character, encompassing an entire country, the planet, or the universe. Cotard's syndrome indicates deep and severe depression. Verbal illusions correspond to the depressive experiences. Following The formation of the anxiety-delusional depression syndrome, the patient's condition typically stabilizes and becomes monotonous, presenting a "frozen" picture of affective, delusional, and motor disorders. Patients repeat the same complaints expressing fears and anxiety; they frequently wring their hands, become restless, and sometimes offer resistance. Following stabilization, a gradual reduction of mental disorders may be observed. Agitation phenomena lose their affective charge, anxiety and fear subside, giving way to depression, indifference, and apathy. Complete recovery in complex and protracted depression-delusional psychoses is rare. The psychotic state transforms into mental weakness characterized by a persistently depressed mood, decreased mental activity, and diminished emotional responsiveness. As a result of presenile psychoses, mental life seems to "freeze on a greatly narrowed basis," although this basis may vary in the degree of personality leveling. Alongside severe forms of involutional depression, relatively benign monophasic anxious depressions ending in recovery are observed. These represent involutional melancholias with clear reactive-situationally colored depressive symptomatology.

Rare but highly malignant presenile depressions manifest as frenzied anxious agitation with incoherent speech, bewilderment, an oneiroid state of consciousness, and progressive cachexia. The prognosis for these depressions is unfavorable.

Involutional delusional psychoses (paranoid, paranoia, late hallucinatory-paranoid, and hallucinatory forms).

In involutional paranoid states, the core of the clinical picture consists of petty delusions of persecution (poisoning, Various Forms of sabotage, jealousy) and reference. The delusion is directed at a specific person and is frequently interpretive (i.e., paranoid), explaining numerous facts and events. Delusional ideas develop slowly, and the delusional system is usually simple and concrete. Past facts are also interpreted, rendering the delusion retrospective. The "persecutors" allegedly steal and substitute the patients' belongings, break into their rooms, and do everything to get rid of them. A frequent occurrence is the delusional conviction of being poisoned, accompanied by sensory deceptions (olfactory and gustatory illusions). Poison is "introduced" through the ventilation duct or keyhole. The persecutors attempt to deprive them of their living space. The delusions incorporate concrete notions of loss combined with ideas of inadequate motivation. Exposé ideas appear alongside passive defense mechanisms (moving to a new place, installing additional locks, filing police reports, etc.). The background mood is predominantly optimistic yet irritable, though anxiety and depression are noticeable. Despite their delusional sphere, patients maintain social connections and care for themselves. A distinctive feature of late paranoid states is the absence of marked organic mental changes. The psychosis follows a chronic or fluctuating course. Some authors include late catatonia syndrome among involutional psychoses, manifesting as the onset of catatonic stupor at the age of 45–50. Other researchers consider it a manifestation of late-onset schizophrenia.

Functional psychoses of old age. Psychosis resulting from the biological and socio-psychological consequences of aging, without organic mental impairment or dementia, may develop after the age of 60–65. The clinical manifestations of senile psychoses closely resemble those of involutional depressions or paranoid states. Some psychiatrists classify them as late manifestations of presenile psychoses, while others view them as functional psychoses of old age. During the senile period, functional psychotic disorders of various structures may occur. These include senile delirium (confabulatory form), optic, verbal, tactile, and olfactory hallucinoses, as well as acute confusional states with disorientation in the environment, fragmentary hallucinations and delusions, motor restlessness, and amnesia for the psychotic period.

The delirious form (senile delirium) is characterized by a delirious disorder of consciousness; however, this delirium is impoverished in terms of illusions, hallucinations, and fantastic ideas. Occasionally, senile delirium with vague illusory perception of the environment assumes a professional character, or a muttering character in severe cases. Impairments in object orientation intensify toward evening and, particularly, at night. Nighttime restlessness with disorientation, temporal displacement into the past, packing for a journey, and corresponding purposeful activities are characteristic of senile delirium, or pseudodelirium. Syndromal manifestations in old age are reduced, rudimentary, or dissociated in nature; consequently, fear and motor agitation are typically absent in senile delirium.

The confabulatory form, or Wernicke's presbyophrenia, is accompanied by euphoria, bustling activity, and gross confabulations. Patients exhibit liveliness and cheerful agitation resembling a hypomanic state, along with an inability to comprehend their surroundings. For instance, a patient returning from the dining hall who cannot find their bed in the ward may fluently quote entire pages of classical works or impress others with knowledge of chronological dates of obscure political events. Amnestic disorientation is characteristic of patients with profound memory impairments.

Hallucinoses are classified among functional psychoses of old age based on criteria shared with senile psychoses. Foremost among these is their primary onset in late life and their dissimilarity to endogenous hallucinoses. Common features uniting senile hallucinoses include chronic hallucinating against a background of clear consciousness and an association with petty delusions of persecution. The transformation of one form of hallucinosis into another is observed exclusively within the group of senile psychoses. Senile hallucinoses account for 1.2% of all psychoses developing after the age of 60, comprising auditory (0.5%), olfactory (0.5%), tactile (0.09%), and visual (0.1%) forms.

Visual hallucinosis arises suddenly and is characterized by imagery and vividness. Patients frequently "see" panoramic scenes involving multiple individuals. Their attitude toward the hallucinations is ambivalent: patients understand that this is a sign of illness, yet simultaneously behave as though they perceive the "visions" as reality. During exacerbations of the hallucinosis, petty delusions of persecution take shape.

Tactile hallucinosis is accompanied by the "appearance" of insects or foreign bodies on or beneath the Skin. Critical insight is lost, and the hallucinations are accompanied by everyday ideas of persecution.

Olfactory hallucinosis appears abruptly and is persistent. Patients frequently complain of unpleasant odors from which they must seek protection. This form of hallucinosis arises in a specific situation and disappears once the situation changes.

Auditory hallucinosis reflects everyday situations and generates petty delusions. Ideas of psychic automatism are absent.

When one type of hallucination transforms into another, The Structure of the delusion remains unchanged, indicating an underlying predisposition to hallucinate. Peripheral receptor analyzers also play a role; specifically, Hearing loss in auditory hallucinations and Vision impairment in visual hallucinations are observed in all patients. Confusion accompanied by hallucinations and delusions typically occurs in patients with a somatogenic radical (3.4% of all patients over 60 years of age). Somatogenesis plays a special role here, yet such "confusion" may manifest as a functional rather than an organic psychosis.

An acute onset is preceded by episodes of vague orientation, subsequently evolving into a picture of amentia marked by clear disorientation and motor restlessness. Incoherence of thought and speech dictates The Nature of contact with patients. At times, orientation is dual in character: patients recognize relatives while confusing the present with the distant past. They perceive their surroundings as threatening and plead for help. This condition typically lasts 15–20 days. Excessive excitability frequently leads to additional fatal complications (up to 50%). However, "confusion" may lack a direct link to somatic factors, in which case psychogenic reactions, sensory isolation, or vascular disorders are implicated.

The ETIOLOGY AND PATHOGENESIS of presenile and senile psychoses remain unclear, with various hypotheses proposed. Attempts are made to explain involutional psychoses by age-related changes in endocrine gland function and other somatic abnormalities. Clinical observations indicate that in late life, mental illnesses lose their endogenous character.

These psychoses occupy a unique position between exogenous and endogenous disorders, as they combine numerous constitutional, situational, psycho-, and somatopathogenetic factors.

The primary diagnostic criteria are as follows: a) the Development of the illness during a specific age period (presenile or senile); b) distinctive psychopathology (a protracted, single episode of anxious-agitated or anxious-delusional depression, interpretation of delusions with impoverished content, protracted hallucinosis); c) the absence of pronounced organic decline in personality level and dementia, as well as productive disorders such as pseudohallucinations, psychic automatism, and delusions of control.

Treatment and Prevention of functional mental disorders in late life must be comprehensive and individualized. Old age is not a pathological process; it is continuous, beginning at the moment of birth—or more precisely, in utero—and ending with death. Physiological aging represents a steady progressive restriction of environmental adaptation. Premature aging, observed in senile and presenile disorders, indicates a partial or generalized acceleration of the human aging rate. This aging is polyetiological, occurring when an individual's biological age outpaces their chronological age.

Preventing premature aging is linked to numerous socio-hygienic factors. The social factor is primarily connected to environmental health, The Nature and regimen of work, rest, and Nutrition. Addressing these issues positively is the key to preventing premature aging. According to the adaptation-regulatory theory, aging processes are explained by uneven changes across various links of self-regulation. At THE CELLULAR LEVEL, the Organism loses its capacity for reproduction and renewal, accompanied by the accumulation of plasma debris within The Cell.

Immunodeficiency is a major group of disorders rooted in the impaired functioning of The Immune System to protect the organism from microbes, Viruses, allergens, and tumor Cells. Immunity is weakened by A wide variety of factors, including Protein deficiency, starvation, vitamin shortages, overwork, trauma, bad habits, chemical exposures, ionizing radiation, and overdosing on certain medications. Disorders in the presenium, as a manifestation of premature aging, also represent secondary immunodeficiency. Therefore, geriatric preparations containing Vitamins, Amino Acids, and macro- and microelements serve as means of preventing premature aging. At the age of 40–50, they should be taken in courses lasting 3–4 weeks (2–3 courses per year), particularly during the autumn-winter period, as well as during periods of physical and mental exhaustion or following illnesses. Polyhypovitaminosis and a deficiency of essential microelements (copper, cobalt, magnesium, manganese) negatively impact numerous metabolic processes and hormone synthesis. Consequently, twice a year, patients are prescribed "Decamevit", "Unifit", "Unicap M", or "Unicap T" (1–2 tablets daily for 20–30 days). Vitamins, macro- and microelements help improve neural Functions, myocardial contractility, and the secretory and motor Functions of the digestive organs. They activate The excretion of ethereal sulfates, strengthen Connective Tissue, and enhance Blood regeneration and repair processes.

A nonspecific stimulant of defense mechanisms is purple coneflower (Echinacea purpurea). Its preparations are prescribed at 20 drops three times daily for 8 weeks, which increases the count of granulocytes and T-lymphocytes. Thymostimulin, decaris, and other agents may also be recommended.

An effective geriatric remedy is apilac (royal jelly). It contains 18 protein substances, a complex of vitamins, amino acids, and minerals. Apilac is prescribed at 1 tablet twice daily (sublingually) for 20 days and stimulates all bodily functions.

Among geriatric remedies, adaptogens, anabolic substances, antireticular cytotoxic serum, Placenta preparations, vitreous body preparations, and aloe are also recommended. Oxygenation is likewise effective (300–500 cm³ of oxygen subcutaneously; No. 20).

Patients with involutional melancholia are prescribed antidepressants (amitriptyline up to 0.2 mg; cipramil up to 40 mg; prozac up to 60 mg daily; zoloft up to 150 mg daily) and neuroleptic agents (teralene, pyrazidol, eglonyl, fluanxol). For agitated depression, sedative neuroleptics are indicated (clopixol, risperidone, zyprexa, solian, thioridazine, azaleptin, sonapax). Patients with delusions, in the absence of contraindications, undergo electroconvulsive therapy (6–10 sessions).

For involutional paranoid states, neuroleptic agents are used (trifluoperazine, clopixol, fluanisone, perphenazine, risperidone, haloperidol, zyprexa, solian in low doses).

For functional psychoses of old age, antidepressants and neuroleptics are indicated.

PRESENILE AND SENILE DEMENTIAS

The classification of these disorders is based on two principles: age and nosology. This group of late-life mental illnesses shares A number of common Clinical and Biological features.

The primary clinical sign is total progressive dementia developing in early and late life on The basis of a cerebroatrophic process.

Presenile dementias. This group comprises nosologically heterogeneous diseases that begin between the ages of 40 and 60, are accompanied by progressive total dementia, psychopathological symptoms, and an atrophic process of the Cerebral Cortex AND subcortical structures, and carry an unfavorable prognosis.

The presenile dementia group includes Alzheimer's disease, Pick's disease, Creutzfeldt-Jakob disease, Huntington's chorea, and Parkinson's paralysis agitans.

Alzheimer's disease is characterized by progressive dementia, psychotic disorders, and an atrophic process predominantly localized in the temporal and parietal lobes of the cerebral cortex.

Alzheimer described the disease in 1906 based on the post-mortem examination of a female patient's brain. He discovered cortical atrophy, senile plaques, and specific neurofibrillar changes later named Alzheimer's changes.

The initial manifestations of the disease involve deepening memory impairments. This period lasts from several months to 4 years. Patients are aware of these changes and experience significant distress regarding their cognitive decline. Fluctuations may occur regarding the manifestation of amnestic syndrome and memory revitalization through the recollection of past events. Gradually, object orientation is disrupted, and accumulated knowledge is lost (judlogical level declines), leading to complete intellectual helplessness. In the Cytology/cytology/16.html">Early stages of the disease, productive psychotic disorders may emerge in the form of micro-scale delusions of loss, poisoning, jealousy, hallucinosis, and confusion (under somatic burdening). The fully developed stage of the disease begins when intellectual-mnestic insufficiency is combined with disorders of speech, reading, writing, calculation, gnoseology, and praxis. The appearance of aphato-agnosopractic syndrome (the three A's) provides the basis for diagnosing Alzheimer's disease. Aphasia pertains to sensory-type impairments and is characterized by a failure to understand speech. Sometimes logorrhea is observed with dysarthric and logoclonic disturbances. Speech becomes increasingly incomprehensible. Affective Disorders are accompanied by anxiety, irritability, and occasionally euphoria or psychomotor agitation. Convulsive and non-convulsive epileptiform seizures occur in 30% of patients. Slowness of movement gradually transitions into an inability to perform automated actions; patients forget how to stand, sit, and walk, and often remain lying down without changing posture. The average life expectancy for such a patient is 8 years (ranging from 1 to 20 years), with death typically resulting from secondary infections.

Pick's disease debuts at ages 45–50 and is characterized by total dementia developing on the basis of an atrophic process of the cerebral cortex localized in the frontal and temporal lobes. The onset of the disease can be slow and progressive. Intellectual functions decline, accompanied by bizarre actions and inappropriate affective reactions. The degree of personality alteration depends on the localization of the pathological process. Atrophy of the convexital surface of the frontal lobes leads to lethargy, apathy, and a general impoverishment of mental activity. In cases of atrophy in the orbital cortex of the frontal lobes, a pseudoparalytic syndrome develops with puerile euphoria, sexual disinhibition, and a loss of insight. Memory and orientation remain intact. Temporal lobe atrophy is accompanied by automatisms, stereotyped actions and movements, and an impoverishment of intellectual processes. Memory and spatial orientation are preserved for a long time, but gradually become noticeably impaired during the fully developed stage of the disease. Speech disorders manifest as perseverations and the loss of spontaneous speech production. It is believed that impairments in speech, writing, and reading (agraphia, alexia) occur earlier, being detected in 60% of cases in Pick's disease and 30% in Alzheimer's disease. Profound cognitive decline leads to increased suggestibility and stereotypy of gestures and facial expressions. The terminal stage of the disease is characterized by four symptoms: polylalia, echomimia, mutism, and amimia.

The duration of the disease is 5–10 years, and death results from infection.

Creutzfeldt-Jakob disease (see also Chapter 17) is characterized by progressive dementia resulting from neuronal dystrophy in the deep Regions of the cortex, the striatum, and the thalamus. It is rare, occurring in 1 case per 1 million population. It develops between the ages of 50 and 60, though onsets between 21 and 79 years have been described. It progresses acutely over 4–5 months. Sleep is disrupted, patients lose weight, and extrapyramidal changes and dysarthria appear. Amyotrophic, thalamic, occipital, and amaurotic forms are distinguished. At one time, the disease was considered hereditary-degenerative, but cases of transmission from one person to another (via corneal transplantation, stereotactic surgeries) have been observed. In recent years, some authors have linked this disorder to the slow development of a transmissible virus. General neuronal degeneration occurs in the brain with the destruction of Gray matter in the frontal and temporal lobes. Death occurs within an average of 2 years.

Huntington's chorea begins between the ages of 30 and 45 and can last up to 15–25 years. It starts with choreic hyperkinesias. Intellect is impaired with a loss of capacity for creative work, irritability, and affective lability coupled with a tendency toward depression. The condition progresses slowly and is accompanied by apathy. Degenerative Changes in the Basal Ganglia manifest as chronic chorea syndrome. Unlike Creutzfeldt-Jakob disease, the characteristic extrapyramidal disorders are absent, and patients frequently resort to suicide.

Parkinson's paralysis agitans develops between the ages of 45 and 70. It presents with extrapyramidal disorders and, in 50% of cases, psychiatric disturbances. During the debut period of the disease, even before the appearance of neurological disorders (tremor, Muscle rigidity, hypokinesia), characterological disorders are detected: irritability, egocentrism, and suspiciousness. In 70% of patients, depressive manifestations occur, most often mild and psychogenically colored. A portion of patients exhibit delusional experiences with small-scale ideas of persecution and loss. In 40–80% of patients in the late stages, memory and judgment decline are revealed alongside a persistent intellectual-mnestic defect against the backdrop of mild euphoria.

In the later stages, psychotic disorders may occur, including delirium, confusional states accompanied by agitation, and hallucinosis with tactile and visceral hyperpathic features.

The disease belongs to the degenerative-atrophic spectrum and is inherited in an autosomal dominant manner. There are families in which, alongside Parkinson's disease, Pick's disease and Huntington's chorea have been observed.

Senile dementia typically develops between the ages of 65 and 85. Its onset is gradual and subtle, initially resembling characteristic aging processes but progressing at a faster rate. In the early stages, individual personality traits become accentuated before eventually smoothing out. Pathological personality changes characteristic of senile dementia then accumulate, often referred to as senile psychopathization of the personality. Consequently, patients begin to resemble one another. Callousness, caricatured egocentrism, miserliness, and hoarding of old, useless items replace former interests and hobbies. Elemental instincts become disinhibited, and appetite increases disproportionately. Patients may exhibit a heightened interest in younger individuals of the opposite sex, a propensity for erotic conversations, and occasionally, libertine behavior. The mood becomes gloomy and irritable, with a narrowed range of emotional shading dominated by a single affect. Some patients become quarrelsome, petty, or fault-finding, while others are carefree, good-natured, self-satisfied, and prone to monotonous jokes. Initially, mechanical memory impairments are masked by psychopathic behavior, a phenomenon typical of a slowly progressing atrophic process. Over time, progressive amnesia sets in, and the pattern of intellectual decline is reflected in memory loss. Differentiated concepts are the first to suffer. With the onset of fixation amnesia, amnestic disorientation emerges—initially regarding public events, and later concerning personal life. Eventually, spatial and environmental orientation is disrupted. Patients fail to recognize close family members, addressing them by other names. As total dementia deepens, patients fail to recognize themselves in the mirror, manifesting the amnestic variant of the mirror sign. Over time, they regress to events of the distant past, believing themselves to be young or even children. When recounting life events, they mix actual occurrences with clearly fabricated facts. Initially, There is a clear dissociation between the profound mental deterioration and the physical condition; however, physical marasmus eventually develops. Focal disorders may also be observed, including grammatical speech impairments, stereotyped linguistic turns, verbigeration, and echolalia. The physiological process of falling asleep and waking up is disturbed. Sleep is often deep, lasting anywhere from 2–4 to as long as 20 hours, though prolonged wakefulness can also occur. In the terminal stage, cachexia develops, leaving patients curled in an "embryonic" posture, in a state of slumber, and muttering incoherently.

The etiology and pathogenesis of presenile and senile dementias remain largely unclear. Genetic studies have established that The Role of hereditary factors is undeniable, yet certain contradictions persist. This particularly concerns The impact of genetic factors on the course of presenile and senile dementias. Both familial and sporadic forms of Alzheimer's and Pick's diseases have been described without any apparent hereditary burden. Even in Huntington's chorea, which is associated with an Autosomal dominant inheritance pattern approaching 100% penetrance of the pathological Gene, non-hereditary cases do occur. Genetic factors also contribute to pathological aging. Senile dementia is 4.3 times more common in families with a history of such disorders compared to the general population. For monozygotic twins, the risk of developing senile dementia reaches 42.8%.

Pathogenetic mechanisms are closely linked to biochemical alterations. In Alzheimer's disease, The activity of acetylcholinesterase and Choline acetyltransferase decreases in the frontal cortex and hippocampus, accompanied by impaired acetylcholine synthesis and reduced levels of norepinephrine and dopamine. The accumulation of Trace Elements in the brain is of undeniable significance: aluminum in Alzheimer's disease and zinc in Pick's disease. These alterations are believed to affect the interaction of various neurotransmitter systems and receptors. Furthermore, the immune theory of aging examines The rate of this process across different populations of immunocompetent cells. Disruption of immunoregulatory mechanisms leads to autoimmune processes, wherein autoantibodies exert damaging effects on brain Cells and Tissues. The CEREBROSPINAL FLUID contains immunocompetent cells of all major types, which normally perform a protective function. However, their functional properties can be impaired and altered by shifts in subpopulation ratios, sometimes triggering pathological changes within the Central Nervous system. A diffuse atrophic process affects the gray matter of the cerebral hemispheres, particularly the convexity, whereas the Base of the brain is affected to a lesser degree. The morphological substrate of senile dementia is considered to be senile plaques (senile drusen), the number of which under a Microscope ranges from 20–30 to 60 or more. Nevertheless, a strict parallelism between the severity of mental disorders and dementia and the extent of pathomorphological changes is not always observed.

Pick's disease is regarded as an organic localized psychosyndrome characterized by the atrophy of cerebral convolutions, giving the frontotemporal regions the appearance of a "shrivelled walnut kernel." Spherical intracellular inclusions known as "Pick bodies" or "argyrophilic bodies" appear in the Cytoplasm. The degeneration of Neurons in the cortex of the frontotemporal lobes, the caudate Nucleus, the amygdala, and Ammon's horn is accompanied by intense gliosis in these areas.

Alzheimer's disease is associated with neurofibrillary degeneration within the cytoplasm, containing vacuoles centered around an argyrophilic granule, ultimately leading to the destruction of the neuron. Neurofibrillary degeneration has been experimentally reproduced through aluminum poisoning.

Treatment

There are currently no effective treatments for presenile and senile dementias. Unfortunately, management of the atrophic process remains purely symptomatic, aimed at normalizing sleep disturbances, affective disorders, hallucinatory-delusional episodes, and preventing seizure activity. Special attention should be paid to treating comorbid conditions and boosting the body's immune defenses. Due to decreased bodily reactivity, many illnesses follow a latent course. Somatic pathology often manifests merely as a loss of appetite, and a general malaise may be indicated simply by the patient's desire to lie down, even if they were previously active and lively. Patients with atrophic processes benefit from agents that enhance neuronal neurotransmitter METABOLISM (nootropics). Nootropic therapy should be initiated at low doses and increased gradually over several weeks. For sleep disturbances, medications such as nitrazepam, thioridazine, or promazine may be prescribed (at one-third of the adult dosage). In Alzheimer's disease, 20–25% of patients show clinical improvement with cholinesterase inhibitors such as tacrine, as well as memantine, donepezil, and selegiline.

In recent years, information has accumulated regarding the treatment of various late-life mental disorders using embryonic neural tissue transplantation and other neurosurgical interventions (V. I. Tsymbalyuk et al., 1997).

Prognosis

While functional psychiatric disorders of late life do not lead to dementia, the overall prognosis for recovery is unfavorable. States of acute confusion frequently precede a fatal outcome. In presenile atrophic mental disorders, the prognosis is extremely grave: a personality defect forms rapidly, and the patient typically dies within a few years. Senile dementia culminates in profound mental and physical marasmus and death.

Expert Evaluation

Medical and social evaluation: Late-life psychotic disorders significantly diminish daily functioning, rendering the individual unable to work, and in cases of atrophic processes, incapable of independent mobility.

Military fitness evaluation: Patients with persistent psychiatric disorders are unfit for military service and are permanently discharged from the military registry. In cases of moderate functional mental disorders, the fitness of officers, warrant officers, midshipmen, and female military personnel for active service is determined on an individual basis.

Forensic psychiatric evaluation: Patients suffering from atrophic psychosis are deemed legally incompetent. In the event of a criminal offense, they are recognized as not responsible for their actions (insane).

VASCULAR MENTAL DISORDERS

Vascular mental disorders, which are more frequently observed in advanced age, are caused by cerebral atherosclerosis, hypertension, hypotension, and occasionally, obliterating

thromangiitis. Nearly a quarter of elderly individuals registered in psychiatric facilities suffer from vascular mental disorders. Vascular-origin mental impairments are found in 17.4% of the population over the age of 60 (S. I. Gavrilova, 1977). These disorders are categorized into three groups: 1) non-psychotic; 2) psychotic; and 3) vascular dementia.

Non-psychotic disorders: At the onset of the disease, neurosis-like states most commonly arise, presenting as pseudo-asthenic, neurasthenic, astheno-hypochondriacal, astheno-depressive, astheno-phobic, or dysphoric symptoms. These disorders either progress continuously or follow a fluctuating, wave-like course.

Psychotic disorders: These manifest as acute exogenous-type reactions. Variants of clouded consciousness develop acutely or subacutely, followed by so-called transitional syndromes—either asthenic (prognostically favorable) or psycho-organic (unfavorable). Among endoform Psychopathological Syndromes of organic origin, hallucinatory (usually verbal), paranoid, and hallucinatory-paranoid syndromes are observed. These are frequently accompanied by, or independently develop into, a depressive state characterized by the asthenia, hypochondria, emotional lability, and dysphoria typical of vascular disorders (without speech or motor retardation), accompanied by The Emergence of personality traits such as egocentrism, hypersensitivity, grumpiness, and a narrowed range of interests. These psychopathological manifestations may occur episodically or take a protracted course.

Vascular dementia accounts for 15–30% of all dementia cases, most frequently occurring in men aged 60 to 70 years. It results from multiple cerebral infarctions, strokes, transient (hypertensive) crises, and acute or chronic vascular insufficiency secondary to extracardiac cardiovascular diseases. In its initial stages, vascular dementia is conventionally termed uncomplicated. It is characterized as lacunar and presents with neurosis- and psychopath-like symptoms, an accentuation of premorbid personality traits, and the preservation of the moral and ethical core of the personality. At this stage, Memory and Attention are impaired, and patients exhibit excessive emotional lability and cognitive inflexibility, often unable to control their emotions. Following the restoration of cerebral Circulation, such impairments are partially reversible.

If the underlying vascular disease takes an unfavorable course—particularly against the backdrop of acute cerebrovascular accidents or concurrent somatic illnesses—the dementia assumes a diffuse character. This leads to a profound intellectual-mnestic personality defect. Conditions such as Korsakoff's Amnestic Syndrome, anosognosia (pseudoparalytic variant of dementia), delirium and other disturbances of consciousness, delusional states, depressive states, and deficits in gnosia, speech, and praxis (amnestic dementia) may develop. Focal neurological signs (limb weakness, gait abnormalities, hyperreflexia, positive Babinski sign, pseudobulbar palsy, etc.) are characteristic of vascular dementia.

Asthenic dementia resembles Alzheimer's and Pick's dementias in its clinical course. According to post-mortem studies, in 50% of patients with vascular dementia, the condition coexists with Alzheimer's disease.

The Diagnosis of vascular mental disorders, particularly in the early stages, relies on identifying an asthenic syndrome, affective disturbances, an accentuation of premorbid personality traits into a "caricatured distortion" (K. Schneider), and dysmnestic disorders. The latter are manifested by marked fluctuations in the severity of memory impairment and a disproportion among the components of memory function (fixation, retention, recall, and recognition of information). In later stages, these disorders are characterized by disorganized thinking processes, focal dementia, and ultimately, in terminal stages, diffuse dementia accompanied by complete mental marasmus.

Differential diagnosis involves identifying the aforementioned mental disorders and comparing the features of their onset and dynamics with the somatoneurological signs of atherosclerosis, hypertension, hypotension, and cerebral obliterans thromboangiitis.

Thus, atherosclerotic cerebral disorders are typically characterized by a combination of such clinical manifestations as increased fatigue, affective disorders, and other symptoms of asthenic syndrome, memory impairments, and the aggravation of personality traits.

Hypertension is typically characterized by headaches, pseudo-neurotic states, a melancholic-depressed mood or anxiety and restlessness, and occasionally paroxysms of fear, delusions of reference, persecution, jealousy, or self-blame with hypochondriacal content. Episodes of altered consciousness (ranging from obnubilation to coma in stroke, as well as twilight states, oneirism, delirium, and amnesia), various degrees of memory impairment, and psycho-organic syndrome are also common. Cerebral vascular aneurysm may present with a pseudotumor clinical picture (headache, euphoria or moria, irritability, sometimes wrathfulness, and bradyphrenia—a slowing of thought, speech, and emotional responses). Occasionally, the disease leads to post-stroke (post-apoplectic) dementia.

Neuropsychiatric disorders in hypotension manifest as general lethargy, dizziness (especially when changing body position from horizontal to vertical), headaches, and tinnitus. Subdepressive and anxiety states, periods of morbid fastidiousness, hypochondria, and phobias sometimes occur. These disorders worsen during hypotensive crises accompanied by vasomotor disturbances and, occasionally, fainting.

Cerebral obliterans thromboangiitis is characterized by generalized weakness, drowsiness, headaches, episodes of schizophrenia-like states and twilight states of consciousness, epileptiform seizures, and potential pseudotumorous disorders. The latter most frequently occur in aneurysms of the intracranial segment of the Internal Carotid Artery and are accompanied by pain in the corresponding part of the forehead and eye, as well as visual disturbances (amaurosis, scotoma, hemianopsia), along with symptoms of oculomotor, abducens, and Trigeminal nerve damage. The disease frequently leads to marked dementia. Vascular pseudotumorous disorders lack the changes in the optic fundus, ECG, echo-EG, and cerebrospinal fluid that are characteristic of Brain Tumors.

Neuropsychiatric disorders of vascular origin differ from late-life atrophic brain lesions. For instance, Vascular Diseases do not present with the symptoms observed in Alzheimer's and Pick's diseases, speech disorder syndromes, or focal neurological symptoms. Unlike senile dementia, vascular diseases have an acute onset and a non-uniform (wave-like) course. Psychotic episodes typically occur at night.

Neurosis-like states of vascular origin are differentiated from neurotic disorders (which are also frequently observed in elderly individuals).

Vascular endomorphic psychoses should be distinguished from endogenous ones—manic-depressive psychosis, schizophrenia, and functional involutional psychosis. Distinctive features of vascular disorders include: mental instability; deepening of intellectual and mnestic mental defects; and the attenuation of psychotic symptoms depending on the degree of dementia.

Treatment

General conditions for the treatment of vascular mental disorders include: prolonged duration; abstinence from alcohol and smoking; prevention of mental overexertion; systematic (metered) Physical Exercise; a balanced regimen of work, rest, and sleep; systematic treatment of somatic and endocrine diseases (such as Diabetes Mellitus); and adherence to specific dietary recommendations. For instance, in cerebral atherosclerosis, Cholesterol-rich foods are restricted in the diet, whereas in hypertension, spices, spicy foods, and coffee are not recommended.

In atherosclerosis, treatment aims to normalize Lipid Metabolism and cerebral hemodynamics, and to activate the metabolism of the vascular wall and neural tissue. To this end, the following are prescribed: vitamins (especially ascorbic acid and nicotinic acid); iodine preparations (calcium iodide, potassium iodide, kelp, and other iodine-containing products); nootropics (nootropil, aminalon, piracetam, etc.); and medications that improve cerebral circulation (cinnarizine, stugeron, cavinton, trental, etc.). For hypotension, effective treatments include: B-group vitamins; biogenic stimulants (preparations of ginseng, Schisandra chinensis, eleutherococcus, pantocrine, etc.); balneotherapy (wet rubbing, showers, carbon dioxide baths, etc.); therapeutic exercise; and anticoagulants as indicated. Patients with cerebral obliterans thromboangiitis are prescribed: B-group vitamins, ascorbic acid, iodine preparations, magnesium sulfate, antispasmodics, vasodilators, and anticoagulants.

In vascular psychoses, psychotropic drugs are administered cautiously, starting with minimal doses, as the bodies of such patients are extremely sensitive to these agents. Preference is given to tranquilizers (sibazon, tazepam, seduxen, relanium, rudotel, elenium, radedorm, etc.). When necessary, drugs with relatively low neuroleptic activity (such as melleril) are prescribed. At the same time, the possibility of a sharp drop in blood pressure, potentially leading to collapse, must be taken into account. For vascular depression, the following are prescribed: tranquilizers with antidepressant effects (alprazolam, kasadan); antidepressants (amitriptyline, cipramil, zoloft, prozac, etc.); and neuroleptic agents with stimulating and thymoleptic effects (flupenthixol, eglonyl, sulpiride). In the post-stroke period, a course of treatment with cerebrolysin is prescribed.

Prognosis

The prognosis depends on the severity and localization of cerebral vascular lesions, as well as on the presence of acute cerebrovascular accidents. The prognosis is relatively favorable when the clinical picture is limited to prolonged neurosis-like symptoms. It worsens when psychotic disorders appear and, even more so, when they progress; it becomes unfavorable in vascular dementia against the backdrop of cerebral infarctions, strokes, hypertensive crises, vascular insufficiency, and concomitant intercurrent diseases, which lead to mental marasmus. Patients become helpless in daily life, organs and tissues atrophy, all vital processes fade, and death ensues.

Expertise

Medical and social expertise. In the early stages of vascular diseases, the level of life functioning decreases moderately. Despite increased fatigue, patients can continue working in their specialty (albeit with noticeable effort), but their working conditions are alleviated. Occasionally, they are offered lighter work. In cases of protracted psychotic states or marked dementia, disability group II is established, and group III/I if care is required [Note: translating directly as second or first disability group depending on standard terminology].

Military expertise. For individuals subject to military expertise due to their age, the assessment is conducted analogously to that outlined in the chapter "Late-Life Mental Disorders".

Forensic psychiatric expertise. During an exacerbation of a psychotic disorder or in cases of pronounced dementia, the patient is considered of unsound mind and legally incompetent.

CONTROL QUESTIONS

1. Classification of late-life mental disorders.

2. Forms, etiopathogenesis, Clinical presentation, and treatment of involutional (functional) psychoses.

3. Mental disorders in atrophic brain diseases. Types, Epidemiology, and etiopathogenesis.

4. Clinical manifestations of senile dementia.

5. Clinical manifestations of Alzheimer's disease.

6. Clinical manifestations of Pick's disease and Huntington's chorea.

7. Types, epidemiology, etiopathogenesis, and classification of mental disorders in cerebrovascular diseases.

8. Clinical presentation of early manifestations of cerebrovascular pathology.

9. Acute vascular psychoses and endomorphic psychoses.

10. Dementia syndromes in cerebrovascular pathology.

11. Treatment and prevention of vascular mental disorders.