Psychiatry - H.T. Sonnyk 2003

Disorders of Mental Activity in Presenile and Senile Age

The mental activity of the elderly acquires A number of distinct features. They frequently develop suspiciousness, hypersensitivity, touchiness, and other psychological traits. Occasionally, severe psychiatric disorders, such as delusional psychoses, may occur in late life. Thus, the psychiatric perspective in studying old age is entirely relevant.

Despite this, the scientific community's attitude toward late-life mental disorders is far from unanimous. For instance, some researchers view late-life functional psychoses merely as atypical variants of Schizophrenia, bipolar affective disorder, and reactive or somatogenic psychoses modified by Aging, although the majority of specialists still recognize them as nosologically independent entities.

Historical Background.

The initial syndromal descriptions of late-life affective and delusional psychoses were provided by Schüle (1868), Krafft-Ebing (1878), and Kotseard (1882). However, involutional melancholia was first identified as an independent nosological entity by E. Kraepelin in 1896. Later, the problems of late-life psychoses were studied by Kleist (1913), Albrecht (1914), and Serko (1919).

This topic has also been addressed in numerous studies by S.G. Zhylin, A.V. Snezhnevsky, E.Ya. Shternberg, V.M. Banshchikov, and others.

PREVALENCE.

The prevalence rates of Mental disorders in individuals over 60 years of age range from 10% to 25%. Meanwhile, patients with functional psychoses account for 11% to 48% of all psychiatric cases in late life; the risk of presenile dementia (ages 45–60) is 0.1%, while senile dementia (after age 60) affects 5–10%. Climacteric neurosis-like disorders occur in 20–30% of women.

Recently, due to the increase in average human life expectancy, there has been a growth in the elderly population, and consequently, an increase in the number of patients suffering from late-life mental disorders.

Etiology AND Pathogenesis.

Climacteric neurose-like states. Neurosis-like disorders are among the most typical manifestations of pathological menopause. They result from neuroendocrine shifts occurring during the climacteric period, primarily the impairment and subsequent cessation of ovarian function. Diencephalic disorders, thyroid hyperactivity, and general aging also play a certain role.

Late-life functional psychoses. Data regarding their etiopathogenesis remain largely hypothetical.

The most widely accepted concept suggests that these psychoses arise from the combined effect of a group of evolution-related factors. Alongside biological and psychological aging, somatic factors are considered among the most critical. A certain role in their genesis is also attributed to the adverse socio-psychological consequences of aging, such as retirement, social isolation, and financial or living hardships.

In the United States, a concept has gained popularity which views late-life functional psychoses (particularly involutional paraphrenias/paranoids) as an unconscious defense mechanism of the personality against the situation of aging.

A predisposition to late-life functional psychoses has been established in individuals of specific psychological makeups. Premorbidly, patients with involutional depression are typically characterized by anxious suspiciousness and hypothymia, whereas patients with involutional paranoia in their youth are often noted for their uncompromising nature, straightforwardness, inflexibility, and mental rigidity.

Consequently, it can be stated that presenile and senile psychoses occupy an intermediate position between exogenous and endogenous disorders. Their onset involves a complex interplay of constitutional and situational, psychogenic and somatogenic factors.

Senile and presenile dementias. Many psychiatrists consider senile dementia an endogenous-organic mental pathology and view it as a manifestation of pathological general aging of the Organism. A certain role in its development is played by a burdened heredity, somatic illnesses, and autoimmune disorders leading to destructive Changes in the Central Nervous system (diffuse atrophy and The formation of senile plaques in the Cerebral Cortex).

In The Development of Huntington's chorea, the hereditary factor plays an undisputed role. A well-known case documented the dominant transmission of hereditary chorea within a single family across twelve generations.

The existence of familial forms of Pick's disease leaves no doubt about The Role of heredity in its origin. A dominant inheritance pattern is assumed, similar to Alzheimer's disease. However, isolated, sporadic cases of the disease remain predominant.

Classification.

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

I. 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.

II. Senile.

Functional:

• senile delirium;

• Wernicke's presbyophrenia;

• hallucinoses (optic, verbal, tactile, olfactory);

• acute confusional state.

Atrophic (dementias):

• senile dementia:

• simple form;

• psychotic form.

Clinical Features.

I. Presenile (pre-senile or involutional) mental disorders. Functional presenile mental disorders.

Presenile mental disorders typically occur in individuals aged 45–60 years, with a slightly higher prevalence in women.

Neurosis-like states predominantly develop in women (twice as frequently as in men) as a component of menopausal syndrome. The core feature of their clinical picture is asthenia. Characteristic Complaints include loss of energy, decreased working capacity, irritability, and abnormal bodily sensations across various regions. Affective Disorders manifest as anxiety, hypersensitivity, irritability, hypochondriacal tendencies, and phobias. These phenomena may combine into distinct symptom complexes: depressive, hypochondriacal, or hysteriform.

The prognosis for neurosis-like disorders is favorable; they generally last from several months to a few years and culminate in recovery. However, in severe cases, pathological personality changes or progression into involutional psychosis may occur.

Involutional melancholia is the most common form, developing insidiously and characterized in its initial stages by profound depression accompanied by lethargy, dysphoria, and hypochondriacal symptoms. Delusional ideas of guilt gradually emerge, accompanied by mounting free-floating anxiety, agitation, and verbal hallucinations. All of these symptoms become particularly pronounced in the evening and at night. The patients' thoughts and utterances center on grandiose delusions of guilt and damnation. The most minor past transgression is magnified into an atrocious crime, leaving the patient trembling in fear and despair, awaiting severe retribution. Delusions concerning physical bodily transformation are nihilistic in nature and indicate a particularly severe course of the disease. Such patients complain that their entire body "has degenerated," "the Esophagus and Stomach are blocked," "the body is rotting," "the Brain is disappearing," and so forth (Cotard's syndrome). Delusions of jealousy are also characteristic of involutional melancholia.

Despite their depressed mood, such patients exhibit almost no psychomotor retardation; instead, they are restless and agitated. The combination of depression with anxiety and the monophasic Nature of the disorder serve as important differential diagnostic signs of involutional melancholia. The somatic status of these patients is also striking. They appear older than their chronological age (premature graying, wrinkling). Nutritional disturbances are noted, with weight loss occurring even when food intake is regular.

Presenile melancholia lasts for several months, occasionally years, and in most cases concludes with recovery, leaving some residual deficit.

Involutional paranoid state is manifested by so-called minor-scale delusional ideas without profound personality changes. The clinical picture is dominated by delusions of persecution and damage: the female patient believes, for instance, that neighbors or acquaintances are plotting against her to evict her from her apartment or separate her from her husband; they file false complaints with the police, her employer, and other institutions, or slip poison into her food; her husband constantly deceives and betrays her with mistresses. Patients frequently hear the voices of their enemies through walls, presenting as verbal hallucinations. They actively combat their "enemies," file complaints with various authorities, install extra security locks, and take other similar measures.

In involutional paranoia, olfactory ("poisoning by gas") or gustatory ("poison is added to food") hallucinations are often noted, which is largely characteristic precisely of this pathological condition. Patients become withdrawn, reclusive, and sometimes exhibit a tendency toward aggression.

The course of involutional paranoia is typically slowly progressive.

Late catatonia occurs at the age of 45–50, is relatively rare, and is characterized by prolonged motor inhibition up to the point of stupor, refusal to eat, and phenomena of mutism. The leading features in the clinical picture of the illness are negativism, stereotypies, food refusal, inaccessibility to contact, the presence of affective fear, and persecutory and reference delusions.

Delusional ideas more frequently arise as fleeting episodes against the background of pronounced catatonic manifestations. The disease has a protracted course and leads to dementia.

Presenile dementias.

This group comprises nosologically heterogeneous disorders that begin at the age of 45–60 and are accompanied by total progressive dementia. These diseases are based on a slowly progressive, irreversible brain atrophy process that entails a poor prognosis with an inevitable fatal outcome.

The fact of their development at a presenile age gave rise to the term "presenile dementia," which was introduced into Clinical Psychiatry by Binswanger in 1898.

Alzheimer's disease was first described by the German psychiatrist Alzheimer in 1906 based on a thorough examination of the brains of patients who had died against a background of total dementia. The author noted that, alongside ordinary senile plaques, this condition features characteristic changes in neurofibrils. As later transpired, the pathomorphological picture of the brain in Alzheimer's disease is very similar to that of ordinary senile dementia (see below). However, despite this morphological similarity, the Clinical presentation of Alzheimer's disease possesses a number of specific features that justified its classification as a separate nosological entity.

The earliest manifestations of the disease are memory impairments; this period may last several months but frequently drags on for years. Amnestic disorders lead to early, progressive loss of elementary skills and an inability to perform routine household chores. Subsequently, this results in apraxia—the inability to use objects according to their intended purpose. Despite profound mental disintegration, patients retain a sense of alteration and personal inadequacy for a relatively long time, which becomes a source of severe emotional distress for them.

Gradually, profound dementia develops, accompanied by complete intellectual helplessness. The very nature of dementia in Alzheimer's disease exhibits several differences compared to senile dementia. Phenomena of "living in the past" are pale and fragmented, there is no "pseudia" associated with projecting oneself into the past, and confabulatory delusions are sparse, monotonous, and rudimentary.

Highly characteristic of this pathology is the progressive disintegration of speech, which becomes indistinct and consists of irregular sequences of individual syllables. Syllabloklonia—the repetition of the same syllables preceding complete motor aphasia—is particularly characteristic. Speech disorders are combined with writing impairments, which precede oral language disturbances. Simultaneously, a loss of The ability to read (alexia) and impairments in oral calculation (acalculia) are observed.

Disorders of Visual Perception manifest as optical agnosia: the loss of the ability to recognize objects at a distance, perceive perspective, and comprehend the Spatial Structure of the room the patient is in (patients fail to find doors or windows and bump into objects). The Emergence of the aphaso-agnoso-apraxic syndrome (loss of the capacities for speech, recognition, and purposeful action) serves as a clear diagnostic criterion for Alzheimer's disease.

Personality changes are characterized by gloomy alienation, growing distrust, suspiciousness, and stinginess. Ideas of damage, jealousy, poisoning, persecution, and robbery predominate. The following neurological symptoms are frequently observed: epileptiform seizures, parkinsonian-like symptoms, and hyperkinesia.

At the end stage of the disease, markedly pronounced cachexia and flexion contractures develop. The exhausted patient lies in bed in an immobile embryonic posture. The average life expectancy of such patients is 8 years. They predominantly die from infectious diseases.

Pick's disease is a distinct form of psychosis in presenile age, first described by the German psychiatrist Pick in 1892 (note: historical date kept/adapted contextually). The nosological independence of this disorder is nowadays beyond doubt. Pathomorphological studies have revealed a characteristic morphological substrate of the disease, consisting in the predominant localization of the atrophy process in certain areas of the frontal and temporal lobes, mostly in the upper cortical layers, in the absence of senile plaques, Alzheimer's neurofibrillary changes, and vascular alterations.

Pick's disease arises at the age of 45–50. Its clinical feature is intellectual impairment expressed as a loss of the capacity for judgment, comprehension, and criticism. Primitive mental Functions are preserved for a relatively long time, allowing patients to properly orient themselves in their surrounding environment.

At the onset of the disease, there is typically a decline in intellect and "odd" actions with inadequate affective reactions. The Nature of personality changes depends on the localization of the pathological process. Atrophy of the convexital surface of the frontal hemispheres leads to sluggishness, apathy, and general impoverishment of mental activity. In cases of atrophy in the orbital cortex of the frontal lobes, a pseudoparalytic syndrome develops, characterized by puerile euphoria, sexual disinhibition, and lack of criticism toward one's actions while memory and orientation remain intact. If atrophy occurs in the temporal regions, the main manifestations will be automatisms, stereotyped actions, and an impoverishment of intellectual processes. A profound decline in intellect leads to increased suggestiveness, as well as stereotypes of gestures and facial expressions.

Characteristic speech impairments appear in the form of stereotypies and disorders of receptive speech, up to the complete loss of the ability to understand others. Among neurological symptoms, syncopal states and seizure episodes without loss of consciousness during which the patient typically falls should be noted. Mention should also be made of possible extrapyramidal disorders (hyperkinesia, parkinsonian symptoms) as well as spastic pyramidal signs.

The terminal stage of the disease resembles that of Alzheimer's disease: progressive dementia up to the complete disintegration of the psyche, progressive cachexia, and the patient's embryonic posture. It is characterized by four main symptoms: polylalia, echomimia, mutism, and amimia. The total duration of the illness is 5–10 years, and death usually ensues from infection.

Huntington's chorea begins at the age of 30–45, can last 15–25 years, and does not always lead to dementia, sometimes exhibiting a benign character. The morphological substrate in this disease consists of atrophy of Nerve Cells and glial proliferation in the striatal system, caudate Nucleus, lentiform nucleus, and subthalamic region.

The disease debuts with choreic hyperkinesia, accompanied by irritability and affective lability with a tendency toward depression. Intellectual impairments progressively increase. Dementia in this condition is not total in nature and is sometimes expressed as a reduced capacity for memorization, mental rigidity, and extreme distractibility, which may simulate a greater depth of intellectual decline than actually exists.

Among personality changes in this disorder, attention should be drawn to excessive importunity, lack of self-restraint, indifference, and nonchalance. Delusional ideas and hallucinations are also characteristic of these patients. Delusional and hallucinatory-paranoid syndromes can be pronounced and bear some resemblance to schizophrenia. Delusions of jealousy develop with particular frequency.

Severe forms of the disease culminate in profound dementia and transition into a marasmic stage.

Parkinson's paralysis agitans is a degenerative-atrophic pathology inherited in an autosomal dominant manner and developing at the age of 45–70. In addition to the extrapyramidal disorders characteristic of this disease, mental disorders are observed in 50% of patients. Even before the appearance of neurological symptoms (tremor, Muscle rigidity, hypokinesia), characterological changes are detected: egocentrism, suspiciousness, and irritability. Later, in 70% of patients, mild psychogenically colored depressive manifestations arise, and in 40–80% of cases at late stages, memory declines and a persistent intellectual-mnestic defect emerges against a background of euphoria. In advanced stages, psychotic disorders are possible: delirium-like confusional states with agitation, and hallucinosis with a tactile and visceral hyperpathic coloring.

II. Mental disorders of old (senile) age.

Functional psychoses of old age.

Psychoses caused by the biological and socio-psychological consequences of aging, occurring without organic mental impairment or dementia, typically manifesting after 60-65 years of age.

Senile delirium is a disorder of consciousness which, unlike classic delirium syndrome, is poor in illusions, hallucinations, and fantastic ideas. Fear and motor agitation are usually absent. Characteristic of senile delirium is nocturnal fussiness accompanied by disorientation and a shift of the situation into the past, rummaging through belongings, and corresponding goal-directed activities. In severe cases, senile delirium may acquire an occupational or even a murmuring (mussitant) character.

Wernicke's presbyophrenia is a confabulatory form of senile psychosis, accompanied by euphoria, restlessness, and massive confabulations. This condition resembles hypomania with elements of disorientation.

Hallucinoses — their diagnostic criteria include primary onset at a late age and dissimilarity to endogenous hallucinoses. Characteristic features are chronic hallucinating against a clear background of consciousness, association with small-scale persecutory delusions, and the potential for one form of hallucinosis to transform into another.

Acute confusional state occurs predominantly in patients with a somatic background (burdened by internal organ diseases). The acute onset is preceded by episodes of blurred orientation, subsequently developing into a picture of amrementia with disorientation and agitation. Sometimes orientation may be dual in nature — patients recognize relatives but confuse the present with the past. Communication is problematic due to incoherence of thinking and speech. Such a state lasts 15-20 days, but in severe cases may end fatally As a result of somatic complications.

Senile dementia.

It can develop at the age of 65-85 and is characterized by a slow, progressive course, in which several stages can be distinguished: initial, the stage of pronounced dementia progression, and the final (terminal) stage.

In the initial stage, a gross accentuation of premorbid personality traits draws attention. Principles turn into petty stubbornness, sociability into intrusiveness, and thriftiness into stinginess. Patients become intolerant, losing self-control and the ability to critically evaluate themselves and others. Over time, a reverse process occurs — individual personality traits become smoothed out.

The main symptom of the disease is a progressive memory impairment. Patients lose the ability to memorize current events (fixation amnesia), names, Abstract concepts, and names of objects; recognition of familiar things and surrounding people is impaired.

Characteristically, while memory for current events is impaired, memory for the distant past is preserved (Ribot's law). Remote memories acquire "vividness" in the patients' consciousness, and they are transported back to a situation that occurred many years ago. Thus, a female patient may believe she is 20 years old, living in the city where she lived at that age, that she has just gotten married, and perceives surrounding people as relatives who actually died long ago. This profound disorientation, "living in the past," represents an amnesic syndrome characteristic of senile dementia.

A specific disorder in senile dementia is confabulatory delusion. It is characterized by simplicity and content limitations, which are generally typical of organic destructive processes (senile and atherosclerotic dementia), and lacks a tendency toward further progression. The patient, as a rule, repeats the same fabrication over and over. In contrast, confabulatory delusion in middle-age paraphrenic psychoses is characterized by greater vividness, unbridled fantasy, and constant metamorphoses.

Memory impairments and intellectual decline lead to a loss of insight into one's actions, complacency, euphoria, a decrease in moral and ethical standards, and sexual uninhibitedness. Gradually, callousness, egoism, and general coarsening of the psyche increase. The patient's circle of interests narrows down to purely physiological ones. In the final period of the illness, the patient remains almost constantly in a drowsy state. Noteworthy is the relative somatic preservation, which contrasts sharply with the profound disintegration of the psyche.

In The final stage, characterized by mental and physical marasmus, patients cease to understand even simple environmental phenomena and are completely unable to care for themselves. They lose the ability to distinguish between edible and inedible items, and to use household objects and the toilet. Most of the time they spend in bed, doing nothing, and incontinent.

Such patients require constant and meticulous care. The disease runs a slow course lasting 5-10 years. Death usually ensues from concomitant somatic diseases: Pneumonia, stroke, or cerebral thrombosis.

Treatment.

All patients with late-life mental disorders primarily require general strengthening therapy, i.e., a complex of non-specific agents that tone up the body and increase its reactivity and resistance.

These include so-called biostimulants — FIBS, vitreous body, aloe. A milder stimulating effect is exerted by preparations of Echinacea, ginseng, Eleutherococcus, and Schisandra chinensis. Vitamin therapy is indicated, predominantly with B-group Vitamins and nicotinic acid.

Due to Mineral METABOLISM disturbances in old age, salts of potassium, magnesium, and phosphorus are prescribed; their content decreases with age, yet they are essential for the normal activity of brain cells and the entire body. Since the levels of sodium, chlorine, and calcium increase in elderly individuals, a restriction of foods containing them is necessary. All types of Oxygen therapy are indicated due to Tissue and organ Hypoxia.

A certain therapeutic effect is observed with course treatment using novocaine and procaine, which act as non-specific activating agents whose MECHANISM OF ACTION remains not fully understood (capillary dilation, direct action on the diencephalic region and reticular formation, etc.).

Due to the reduced functional activity of the Liver, detoxifying agents, glutamic acid, and unithiol are indicated to enhance its detoxification capacity. Glutamic acid is prescribed orally in powder form at a rate of 0.1-0.2 g per 1 kg of body weight for several months. Unithiol is administered intramuscularly daily at 2.5 ml of a 5% solution for 15-20 days. The administration of hepatoprotectors and sedatives is also indicated.

It is recommended to reduce caloric intake to 1800-2500 kcal per day (depending on the body's Energy Expenditure).

Protein intake is estimated at 1.5 g per 1 kg of the patient's body weight per day, while CARBOHYDRATES are restricted. Fats are indicated in amounts of 70-75 g/day, with 2/3 of them being of plant origin. Four meals a day in small portions are advisable. Food should be rich in VITAMINS AND MINERALS. Physical exercises, massage, and Water Procedures are of great importance in the treatment.

In the therapy of neurosis-like climacteric states, alongside tranquilizers and sedating antidepressants, The Use of hormonal preparations (climacterium, climonorm) plays a certain role.

Psychotherapy is a key component of treatment, focusing on reassuring patients that their lives have been meaningful and that they remain valued and useful members of society. This approach incorporates individual and group therapy, as well as occupational therapy.

When prescribing psychotropic medications, it is essential to account for the heightened pharmacological sensitivity of elderly patients compared to younger adults. Consequently, the prescribed dosages of psychotropic drugs are typically set at 1/2 to 2/3 of the standard recommended doses.

Neuroleptics (such as chlorpromazine, trifluoperazine, thioridazine, haloperidol, risperidone, and olanzapine) are utilized to alleviate fear, anxiety, and psychomotor agitation, while tranquilizers (such as meprobamate, clorazepate, oxazepam, chlordiazepoxide, and diazepam) are primarily employed to treat neurotic symptoms. Stimulants and antidepressants are also widely prescribed. Stimulants enhance nervous system tone and promote alertness, including compounds such as amphetamine, methylphenidate, and sydnocarb. Antidepressants relieve despondency, elevate mood, and resolve depression and motor retardation. This category includes imipramine, amitriptyline, and monoamine oxidase inhibitors (such as nialamide, tranylcypromine, moclobemide, sertraline, and citalopram).

Mild mental health disturbances that do not reach psychotic proportions are managed with herbal sedatives (such as valerian and motherwort).

For patients presenting with lethargy and depressed mood, mild psychotonic agents may be recommended, including low doses of methylphenidate or Choline chloride. In cases where irritability and restlessness predominate, herbal preparations of valerian and peppermint (such as Novo-Passit or Persen) or low doses of tranquilizers (such as meprobamate or amizyl) are advised.

Electroconvulsive therapy (ECT) is occasionally utilized. The primary indications for its use are treatment-resistant depression and contraindications to antidepressant pharmacotherapy. ECT effectively reduces fear, restlessness, anxiety, depression, as well as delusional and catatonic states.

Unfortunately, radical curative treatments for senile dementia have not yet been developed; therefore, such patients primarily require attentive monitoring, dedicated nursing care, and symptomatic management.

EXPERT ASSESSMENT.

Medical and Occupational Expertise. Patients diagnosed with depressive and catatonic forms of involutional psychosis are generally classified as having a Group II or even Group I disability. In cases of profound and sustained remission, reclassification to a Group III disability may be possible. The vast majority of patients with involutional paranoid psychosis do not require disability status; many can continue practicing their profession for years without a decline in professional qualification. However, should their mental state deteriorate, questions of disability assessment are evaluated on a strictly individual basis.

Military Medical Expertise. All individuals diagnosed with involutional psychoses are deemed unfit for military service.

Forensic Psychiatric Expertise. If they commit an offense, individuals suffering from involutional psychoses are deemed legally insane (non compos mentis) and are remanded for compulsory medical treatment.

Review Questions.

1. Definition of mental disorders in senile and presenile age.

2. Etiological factors of involutional psychoses.

3. Pathogenetic mechanisms of involutional psychoses.

4. Classification of mental disorders in presenile and senile age.

5. Clinical manifestations of presenile depression.

6. Climacteric mental disorders.

7. Clinical manifestations of presenile paranoid psychosis.

8. Clinical manifestations of Kraepelin's disease.

9. Typical forms of senile psychoses.

10. Atypical forms of senile psychoses.

11. Treatment of involutional psychoses.

12. Expert assessment issues in involutional psychoses.