Psychiatry - O. K. Napryeyenko 2001

Clinical Psychiatry
Mental disorders in infectious diseases. Neurosyphilis

MENTAL DISORDERS IN GENERAL INFECTIOUS DISEASES

Psychological disorders associated with infectious diseases have been known since antiquity. The works of ancient physicians already made reference to psychotic disorders in patients with febrile conditions.

Etiology AND Pathogenesis

The scientific approach to studying mental disorders in infectious diseases was pioneered by the German scientist E. Kraepelin. In 1881, he proposed dividing them into febrile—manifesting at the onset of the disease and during the peak of body Temperature—and post-febrile or asthenic. He attributed febrile psychiatric disorders to the direct action of the infectious agent, and post-febrile ones to underlying asthenia. Influenced by scientific breakthroughs* in microbiology (L. Pasteur, R. Koch), E. Kraepelin believed that the clinical manifestations of infectious psychoses depended solely on the infectious factor.

An alternative view was put forward by K. Bonhoeffer. Guided by A. Hoche's concept that the Brain possesses specific mechanisms for reacting to internal and external harmful factors, Bonhoeffer introduced the notion of exogenous reaction types. He argued that The Development of infectious psychoses was driven not by the infectious pathogen itself, but by the brain's reaction. In doing so, he denied any direct link between infectious diseases and a specific clinical picture of infectious psychoses.

Observations of the course of infectious diseases during epidemics have demonstrated that infectious psychoses feature both general disturbances caused by the brain's generalized reaction and specific symptoms characteristic of a particular infectious disease.

G. Stertz (1927) suggested that the symptoms and syndromes observed in exogenous psychoses, including infectious ones, could be divided into obligatory (constant Features of the clinical picture) and facultative (inconstant, periodically appearing). Stertz regarded states of impaired consciousness and dementia—as a potential consequence of severe forms of illness—as obligatory. The facultative manifestations of infectious psychoses were characterized by Affective Disorders, schizophreniform symptoms, and seizure states. H. Wieck (1961) categorized exogenous psychoses into functional (or reversible) disorders and those contributing to the development of psycho-organic changes, i.e., deficit syndrome. According to Wieck, between acute exogenous reactions manifested by altered states of consciousness and an organic deficit syndrome lies a group of transitional syndromes, or registers. He included among these conditions marked by alterations in drive, affective and schizophreniform disorders, as well as amnestic and Korsakoff syndromes. Wieck maintained that the presence of a particular transitional syndrome allows for a prognostic Assessment of the disease. Affective states were considered the most favorable, whereas organic register syndromes were deemed unfavorable, with The Emergence of the latter signaling the onset of dementia.

In addition to psychotic disorders of infectious origin, non-psychotic mental disorders may also develop. Chief among these are asthenic states, which manifest both during the prodromal period and at The final stage of the disease. Asthenic states are accompanied by mood changes, most commonly depression with hypochondriacal features. Hypochondriasis points to Autonomic Nervous system dysfunction preceding the specific manifestations of the infectious illness. Hypochondriacal symptoms may also mark the Conclusion of an infection when recovery is, for various reasons, "advantageous" to the patient. During this period, patients complain about their physical condition despite the absence of objective signs of somatic pathology. Occasionally, infectious diseases trigger (serving as a release reaction, according to A. Kępiński, 1975) the development of neurotic-type non-psychotic manifestations.

It remains unclear what drives the development of infectious psychoses and why their clinical picture and course often show no significant differences despite being caused by entirely different infectious diseases.

At the same time, specific symptomatology can be observed in various neuroinfections.

It is believed that febrile states and organic brain changes induced by the infectious process make The Nervous System particularly prone to reacting in a specific manner to the infectious agent.

The development, clinical picture, and course of infectious psychoses depend on the interplay between the macro- and microorganism and the body's reactivity on the one hand, and the virulence of the infectious agent on the other.

I. F. Sluchevsky (1957) identified four types of clinical courses for infectious psychoses.

Type One. The infectious psychosis develops against the backdrop of adequate bodily reactivity. In this case, the illness begins acutely and tumultuously, most often with symptoms of delirium or amentia.

Type Two. The infectious agent affects an Organism with diminished reactivity, which fails to mobilize protective mechanisms, causing the psychosis to take on a protracted character. The disease lasts for several months.

Type Three. The immunoreactive forces gradually weaken, and degenerative changes occur within the Nerve Cells, fostering the development of a persistent organic deficit.

Type Four. This course of infectious psychosis is associated with an inflammatory process in the brain—the development of encephalitis. In such cases, the patient either recovers or develops persistent, residual psychopathological and neurological symptoms.

Thus, K. Bonhoeffer's Concept of the exogenous reaction type, along with related notions regarding the lack of specific features in psychoses caused by infectious diseases, remains fundamental to our understanding of this psychiatric pathology. Most authors apply an etiological principle to the Classification of infectious psychoses, as it highlights The connection between the infectious process and psychotic disorders. This approach AIDS in accurate Diagnosis and facilitates comprehensive, adequate Treatment.

Infectious psychoses are preceded by various states: compromised immune defenses, overwork, negative emotional stress, hypothermia, intoxications, non-infectious somatic diseases, and others.

Infectious psychoses are characterized by general features that do not depend on the etiological factor, namely:

1) acute onset of psychosis;

2) manifestations of the underlying infectious disease that caused the psychopathological disorders;

3) somatic signs of the infectious illness;

4) presence of amentia (clouded comprehension) within the clinical Structure OF THE psychopathological syndrome;

5) manifestations of physical and mental asthenia in the clinical picture of the infectious psychosis (persisting even after the psychotic symptoms have resolved).

Classification of mental disorders caused by infectious diseases:

According to DSM-IV

293.0 Delirium due to...

294.9 Dementia due to HIV disease

294.1 Dementia due to...

310.1 Personality change due to...

293.9 Unspecified mental disorder due to...

According to ICD-10

F02.4 Dementia in diseases classified elsewhere caused by HIV

F02.4 Dementia in other specified diseases classified elsewhere

F05 Delirium not induced by alcohol or other psychoactive substances

F06.0 Organic hallucinosis

F06.6 Organic emotionally labile (asthenic) disorder

F06.8 Other specified mental disorders due to brain damage and dysfunction and physical illness

F07.1 Postconcussional syndrome

F07.8 Other organic personality and behavioural disorders due to brain disease, damage and dysfunction.

The development of infectious psychosis is preceded by prodromal phenomena, namely: fatigue, emotional instability, sensitivity, Sleep disorders, inner restlessness, headache, a sense of impending doom, etc. This state lasts for several days. Against the Background of this discomfort, infectious psychosis develops, most commonly manifesting as delirious, oneiric, amuretic, and choreatic (acute delirium type) syndromes.

Clinical presentation

Delirious syndrome develops at the peak of the febrile state in the evening and at night. The patient becomes agitated, experiencing pareidolic illusions, visual and tactile hallucinations, and metamorphopsias. Allopsychic orientation is impaired. Sensorial-figurative delusions of persecution, reference, and physical influence emerge. Perceptual disturbances cause fear and motor restlessness. Patients are unable to stay in bed, try to escape from imaginary danger, and fail to comprehend their current situation (amentia). Aimless anxiety appears. Facial expressions constantly change; the gaze alternates between wandering and fixed. After emerging from the delirium, memories of the painful experiences are partially retained. Physical and mental asthenia persists.

Oneiric syndrome. Following the prodromal period, vivid, large-scale, panoramic visual hallucinations appear, and orientation in the environment—and sometimes in one's own person—is impaired. A characteristic feature is double orientation in one's own person, where the patient seems to observe themselves from the outside as a detached participant in hallucinatory events. If the hallucinatory images pose no threat, the patient observes the unusual, fantastic surroundings with interest, failing to understand what is happening around them. Facial expressions reflect their emotional state. In the oneiric form of infectious psychosis, somatic signs of infection are mild or unnoticeable. After recovering from the psychosis, patients can describe what they experienced, but they have amnesia for real surrounding events. An asthenic state persists for a long time.

Amentive syndrome. Following prodromal phenomena and against the background of exhaustion, an amentive state emerges. Patients are disoriented in their environment and their own person. Due to impaired thinking (synthesis), they exhibit confusion and a failure to fully comprehend ongoing events. Facial expressions convey astonishment combined with anxiety and fear. Patients understand nothing, looking around and peering at various objects and people's faces. They constantly ask questions such as: "Where am I?" "Who are they?" "What is happening?". A characteristic feature is amentive speech incoherence—the patients' utterances are disjointed and fragmentary. Occasionally, a random string of words is interrupted by subdued laughter or sobbing. Perceptual disorders, unlike in delirium, do not take center stage. Episodic auditory, olfactory, and gustatory hallucinations may occur, less frequently visual and tactile. Patients express isolated, fragmented delusional ideas of reference, persecution, and physical influence. Motor agitation is uncoordinated. As mental disorders recede, physical and mental asthenia becomes apparent, accompanied by depressed mood and bewilderment.

Choreatic syndrome ("acute delirium syndrome") is the most severe manifestation of infectious psychosis. It is observed in septic conditions of various origins and combines features of delirious, oneiric, and amentive states. The association of "acute delirium" with an unfavorable course of infection was described by S. S. Korsakov (1893), V. P. Serbsky (1906), V. P. Osipov (1923), A. S. Chistovich (1954), and B. Ya. Pervomaysky (1977). However, some psychiatrists (V. A. Romasenko, 1967; O. S. Tiganov, 1982) classify conditions manifesting as "acute delirium" as febrile Schizophrenia provoked by infection.

Choreatic syndrome occurs acutely in the evening or at night. Psychomotor agitation with profound clouding of consciousness develops against the background of a high body temperature. The patient's somatic condition is severe. The Skin is dry, pale with an earthy tint. The face is flushed, sclerae injected, Lips dry with fissures and herpetic eruptions. The Tongue is dry, coated with gray-brown plaque. Petechiae and bruises are present on the body. Pronounced hyperhidrosis and physical exhaustion are observed. Body weight drops catastrophically. The patient refuses to eat independently, holding food in the Mouth for a long time. Body temperature reaches 40–41 °C, Heart rate 120–130 bpm. Blood pressure decreases. Heart sounds are muffled. Respiration rate is accelerated. Blood tests show leukocytosis with a left shift, absence of eosinophils, accelerated ESR, and elevated residual nitrogen. Urine tests show increased protein levels and specific gravity.

Psychomotor agitation in bed (jactitation): patients throw off bed linen and blankets, twist them up, toss and turn, wave their arms, and let their legs hang down. Movements are uncoordinated, speech is poorly modulated, exhibiting choreatic incoherence (shouting isolated words or sentence fragments devoid of semantic meaning).

If left untreated, the condition worsens and the body becomes dehydrated. Intoxication and pressure ulcers may develop, and the patient may die.

In recent decades, the Clinical Presentation and course of infectious psychoses have changed significantly. This is driven by multiple factors, most notably clinical pathomorphosis. Infectious psychoses tend to have a protracted course, known as protracted psychoses (N. Ya. Dvorkina, 1975; B. Ya. Pervomaysky, 1977; O. S. Tiganov, 1978). Clinically, they resemble endogenous psychoses. They develop insidiously in patients with a torpid infectious process and follow a progredient course, accompanied by the onset and escalation of both positive (productive) and negative symptoms.

The structure of psychopathological symptoms, particularly in relapsing infectious psychoses, is complex. Beyond the states described above, the illness may manifest with auditory verbal hallucinations, Kandinsky–Klerambault syndrome, cenestopathic-hypochondriacal, paranoid, paraphrenic, and paranoid-hallucinatory syndromes. Affective disturbances are also common, including hypomanic states and depression accompanied by anxiety and fear. Protracted infectious psychoses may lead to organic personality changes (O. S. Tiganov, 1978) featuring an endomorphic clinical picture reminiscent of schizophrenia. However, these symptoms manifest against an asthenic background in the absence of emotional flattening. The pathomorphological basis of protracted infectious psychoses is encephalopathy occurring without an active inflammatory process. The onset and progression of these psychoses are triggered by additional detrimental factors (infection, intoxication, psychological trauma, etc.). Deficit-organic states in infectious psychoses are accompanied by an organic psychosyndrome characterized by impaired insight, lacunar or total dementia, as well as epileptiform and Korsakoff syndromes.

MENTAL DISORDERS IN ENCEPHALITIS

Epidemic encephalitis. In the acute stage of the disease, against the backdrop of a febrile state, somnolence (lethargy) transitioning into insomnia is most frequently observed. Delirious and oneiric states occur, characterized by threatening visual, tactile, and auditory hallucinations. Cases of occupational and muttering delirium have been described. Episodes of psychomotor agitation alternating with adynamia are also documented.

The chronic stage (associated with postencephalitic parkinsonism) is characterized by the retardation of all mental processes, primarily thinking and drives. Depressive states with suicidal tendencies may occur, and occasionally euphoria is observed. Patients retain insight into their altered mental state. Dementia is relatively rare.

Mosquito-borne (summer-autumn) Japanese encephalitis. The acute period of Japanese encephalitis is marked by various manifestations of altered consciousness—delirious episodes, amentive confusional states, and twilight states—which develop both during the febrile phase and after body temperature drops. Sopor and coma are possible. Acute psychoses featuring hallucinatory-paranoid and depressive syndromes develop considerably less frequently. Following the resolution of acute psychotic episodes, patients exhibit amnestic disorders covering the duration of the illness. The sequelae of Japanese encephalitis are quite diverse. Alongside neurological symptoms (paresis, paralysis, speech disorders, Parkinson's syndrome), organic mental disorders are observed, including amnestic, Korsakoff, and dementive syndromes.

Tick-borne (spring-summer) encephalitis. The psychotic Disorders of the acute period in tick-borne encephalitis are virtually indistinguishable from those seen in epidemic and Japanese encephalitis. Syndromes of altered consciousness are observed (obtundation, delirious and amentive disorders accompanied by psychomotor agitation). These mental disorders develop against the background of prominent neurological symptoms. The chronic stage is characterized by Kozhevnikov's Epilepsy, as well as psychosensory disturbances and twilight states. Schizophrenia-like disorders occasionally occur.

FEATURES OF MENTAL DISORDERS IN SPECIFIC INFECTIOUS DISEASES

AIDS. Mental Disorders Associated with Acquired Immunodeficiency Syndrome are quite diverse, spanning virtually the entire spectrum of psychopathological responses, with a clear predominance of organic psychosyndrome and dementia.

In AIDS patients, apathy, feelings of loneliness, and somnolence may be observed several months or even years before the manifestation of the disease. As the illness progresses, fever, night sweats, diarrhea, lymphadenopathy, Pneumonia, and other symptoms appear. A crucial factor contributing to mental disorders is the patient's psychological reaction to the diagnosis, which manifests as affective disturbances and psychological personality disorganization.

The Cytology/cytology/16.html">Early stages of the disease feature functional mental disturbances—anxiety, depression with suicidal ideation, cenestopathic-hypochondriacal disorders, and a loss of future Prospects. Anxiety is often combined with agitation, panic, insomnia, anorexia, and feelings of anger.

When the disease manifests fully, a diverse range of psychopathological symptoms emerges, similar to those seen in endogenous psychosis: hallucinations, suspiciousness, grandiose overvalued ideas, delusions, and antisocial behavior. These symptoms precede organic brain damage and dementia. AIDS is also characterized by obsessive-compulsive disorders: patients meticulously search their bodies for specific rashes or spots; intrusive thoughts about death arise, along with memories of sexual partners who might have been the source of infection, and fears of transmitting the disease to family members through casual contact.

In nearly half of AIDS cases, symptoms of organic brain damage develop, manifesting as diffuse encephalopathy or subacute encephalitis. Over time, patients become incapable of sustaining attention, lose memory for recent and past events, lose self-awareness (insight), and develop an organic psychosyndrome and dementia. Within a few months, these symptoms intensify; consciousness becomes impaired, and epileptiform seizures, urinary and fecal incontinence occur. Coma eventually develops, leading to the patient's death.

Influenza. The prevalence of influenza-related psychosis depends on the epidemiological situation. Psychoses in influenza are categorized into acute and protracted forms. Acute psychosis manifests as states of altered consciousness of the amentive and delirious types. Amentive syndrome may develop at the peak of the fever as well as after temperature normalization. Amentia can be combined with delirious, hallucinatory-paranoid, or catatonic symptoms. Delirious syndrome without amentia is significantly less common. The duration of acute influenzal psychoses ranges from a few hours to 3–5 days.

Recovery is accompanied by severe physical and mental asthenia, which persists for quite some time after the psychotic disorders have resolved.

The clinical picture of protracted influenzal psychoses is dominated by affective disorders manifested as anxiety-depressive and depressive-hypochondriacal states, accompanied by fragmented delusions of persecution, self-blame, and harm. Manic states with elements of clouded consciousness and psychomotor agitation are rarely observed.

These affective disorders are reversible in nature. They are characterized by emotional-hyperesthetic weakness, manifested as excessive excitation, irritability, emotional lability, headaches, attention deficits, and a sense of bewilderment.

Protracted psychosis may also present as prolonged hallucinatory-paranoid states, featuring both true hallucinations and pseudohallucinations, as well as delusions of persecution, physical influence, and mind control. Patients are convinced they are being manipulated by specialized machinery, devices, or individuals with supernatural abilities. The duration of protracted psychosis ranges from several weeks to several months.

Recovery is gradual. Alongside prolonged asthenia, mood fluctuations may occur, ranging from depression with heightened irritability and tearfulness to hypomanic episodes. In severe cases of influenza complicated by organic brain changes, influenzal psychosis can lead to an organic psychosyndrome—either thymopathic or demented—as well as psychopath-like personality changes.

Pneumonia. Psychotic disorders in pneumonia are caused by intoxication, Hypoxia, and neuro-reflex influences on the brain. The onset of the disease is marked by an asthenic symptom complex: generalized lethargy, excessive irritability, hyperesthesia, emotional lability, headaches, sleep disturbances, alterations in tendon and periosteal Reflexes, hyperhidrosis, acrocyanosis, red dermographism, and finger tremor.

During the manifest period, delirious syndrome ("febrile delirium") frequently occurs, accompanied by vivid visual hallucinations and psychomotor agitation. In severe cases, amentive syndrome may develop, characterized by disorientation, impaired comprehension of the surroundings, amentive speech incoherence, delusions of persecution, fear, and psychomotor agitation. The reduction of psychopathological symptoms does not always coincide with the drop in body temperature. A prolonged asthenic syndrome typically follows the psychotic episode.

Rheumatism. Psychopathological manifestations depend on the stage of the rheumatic process. Non-psychotic disorders present as an asthenic syndrome, neurosis-like and psychopath-like states combined with depressive and hypochondriacal reactions.

In neuro-rheumatism, patients exhibit pronounced physical and mental asthenia, irritability, tearfulness, fear, and an anxious-dysphoric mood. Psychosensory disorders are also observed: metamorphopsia; micro- and macropsia; the appearance of colored bands and spots before the eyes; body schema disorders; impaired perception of spatial object layouts; and retardation of thought and movement.

During the active phase of rheumatism, acute psychosis may occur, manifesting as delirious, oneiric, or amentive syndromes, or as a twilight state of consciousness. A distinctive feature of acute rheumatic psychosis is the Abundance of psychosensory disorders and marked hyperesthesia. Recovery from this state coincides with the subsiding of the inflammatory process, though astheno-depressive and astheno-hypochondriacal manifestations persist for a long time afterward.

Protracted and chronic psychoses develop in patients suffering from rheumatic meningoencephalitis and cerebral rheumavasculitis. They manifest as hallucinatory-paranoid, depressive-paranoid, cenestopathic-hypochondriacal, epileptiform, and catatonic syndromes, alongside neurological symptoms. In rheumatic chorea, uninhibited drives and euphoria are observed.

Tuberculosis. Literature data regarding mental disorders associated with tuberculosis are rather contradictory. Some authors believe that mental disturbances in tuberculosis are linked to schizophrenia, arguing that schizophrenia patients exhibit a predisposition to tuberculosis, alongside a constitutional commonality between these two conditions. There is also a view that mental disorders in tuberculosis are caused not by the tuberculosis infection itself, but by the medications administered for its treatment.

Tuberculous psychosis refers to psychotic disorders occurring during the preterminal period, manifested by syndromes of impaired consciousness (delirium,

amhenia, twilight state). Tuberculosis patients often experience euphoria, which was previously considered a pathognomonic sign of fibrocavernous forms. Epileptiform seizures indicate the presence of tuberculomas in the brain.

Psychotic disorders in acute Tuberculous meningitis manifest as syndromes of impaired consciousness. Prolonged psychotic disorders (lasting from several weeks to several months) in tuberculous meningitis present as a state of stupor, against which brief delirious and amhenic episodes occur. Once the symptoms of impaired consciousness resolve, patients remain lethargic, apathetic, and difficult to engage in verbal communication. Transitional syndromes in tuberculosis include affective disorders and mnemonic impairments (amnestic and Korsakoff syndromes).

Malaria frequently leads to severe mental disorders due to brain damage. Disturbances of consciousness can occur when body temperatures are high, presenting as stupor, delirium, amhenia, twilight states, or coma. Coma may develop following delirium, a twilight state, or epileptiform convulsive seizures. Convulsive syndrome is a hallmark of cerebral (encephalitic) manifestations of malaria. The diagnosis of organic brain lesions is based on the detection of nuchal rigidity, cranial nerve palsies (particularly ocular Muscle paralysis), monoplegia, hemiplegia, impaired motor coordination, and hyperkinesia. The duration of malarial psychosis ranges from several days to several weeks.

Rabies is accompanied by organic lesions of the nervous system. Several days before the onset of the disease, pain, hyperesthesia, and paresthesias appear at the site of the bite. The disease progresses through three stages: prodromal, excitation, and paralysis.

The First stage is characterized by restlessness, anxiety, angst, depressed mood, and low spirits. Within one to two days, the Second Stage of the disease develops, manifested by spasms of the Respiratory Muscles and convulsions of the pharyngeal, laryngeal, and esophageal muscles. Hydrophobia is characteristic (sight of running Water or even glassware triggers spasms of the pharyngeal and respiratory muscles). Spasms may also be triggered by a draft of air (aerophobia). Any Touch induces tonic convulsions in the patient. The face flushes and becomes covered in sweat droplets. The patient is unable to swallow, drooling occurs, and pupils are dilated. As the disease progresses, fear, restlessness, and aggressiveness emerge. Convulsive episodes alternate with complete prostration. After 2–3 days, the Third Stage sets in. Patients become calm. Paralysis of the facial muscles, limbs, and trunk develops, and the pupillary light reflex disappears. Death results from respiratory center paralysis and cardiac arrest. Consciousness in rabies patients remains intact until the final hours of life. Occasionally, brief visual hallucinations occur.

Tularemia. Mental disorders are characteristic of severe forms of tularemia when meningoencephalitis develops and syndromes of impaired consciousness (delirium, amhenia) appear.

Erysipelas is rarely accompanied by mental disorders. In the acute course of the disease against a background of asthenia, abortive delirium may develop. A sluggish or protracted course sometimes triggers an amhenic syndrome, which develops following a brief hypomanic state. Among the intermediate or transitional syndromes in erysipelas, astheno-depressive, astheno-hypochondriacal, and hypomanic states stand out. The prognosis for transient and prolonged psychoses is favorable.

Intestinal infections can cause mental disorders manifested by astheno-depressive states combined with anxiety, angst, and tearfulness. Hyperthermia and intoxication may lead to impaired consciousness (delirium, amhenia).

Typhoid fever. At the onset of the disease, an asthenic symptom complex arises, accompanied by depressed mood and psychomotor retardation. As the disease progresses, a delirious syndrome may develop, characterized by visual hallucinations, fear, anxiety, and motor excitation. In severe cases, delirium progresses to sopor. In exhausted patients, an amhenic syndrome is observed, featuring disorientation, auditory and visual illusions and hallucinations, impaired environmental comprehension, persecutory delusions, and motor excitation.

Infectious hepatitis is accompanied by mental disorders characterized by depression with irritability and adynamia, hypersensitivity to external stimuli, emotional lability, and malice. Psychopath-like states with hysterical elements may develop. In acute yellow Liver atrophy, stupor, sopor, convulsive seizures, and epileptiform excitation are observed.

Salmonellosis in the initial stage is accompanied by lethargy, somnolence, and periodic restlessness. In the acute period, stupor joins in, which over time may progress to sopor and coma. Occasionally, brief delirious disorders develop, and convulsions appear. In the post-infectious period, pronounced asthenia with adynamia is revealed.

Brucellosis. Alongside asthenic and astheno-hypochondriacal disorders, acute psychoses manifested by delirious, amhenic, and twilight states have been described (N. Ya. Dvorkina, 1975).

Protracted psychoses are characterized by hallucinatory-paranoid, cenestopathic, and depressivo-hypochondriacal syndromes. Chronic psychoses most frequently manifest as hallucinosis with a depressive coloring and a relapsing course. Causes of chronic psychosis may include meningoencephalitis and encephalitis, accompanied by neurological symptoms and epileptiform seizures. The duration of brucellar psychoses ranges from several days to several months. The disease leads to psychopath-like personality changes and organic psychosyndrome.

Measles. The prodromal period reveals irritability, restlessness, a sense of dissatisfaction, depressed mood, lethargy, decreased appetite, headache, and episodes of psychomotor excitation.

During the rash and hyperthermia phase, with manifestations of meningoencephalitis, delirious, oneiric, and amhenic syndromes occur, alongside twilight clouding of consciousness and stupor with neurological symptoms (nuchal rigidity; Kernig's and Brudzinski's signs; Asymmetry of tendon and periosteal reflexes; pyramidal signs). During convalescence, an asthenic symptom complex is detected.

Measles in adults is accompanied by asthenic, dysthymic, delirious, oneiric, and amhenic syndromes.

Scarlet fever. The Nature of mental disorders in scarlet fever depends on the form and clinical course of the disease. In mild cases, an asthenic symptom complex develops early on, following a brief period of excitation. In moderate and severe forms, asthenia combines with a sensation of stupor. In severe clinical courses, psychotic states may develop, specifically delirious and oneiric states with fantastical hallucinations. The course of these psychotic states is undulating in character.

Asthenic manifestations following scarlet fever can serve as a foundation for the development of neurotic states. Toxic and septic forms of scarlet fever may be complicated by organic brain damage (meningitis, encephalitis). An organic psychosyndrome develops, characterized by epileptiform seizures, memory and intellectual decline, and psychopath-like personality changes.

Mumps, chickenpox, and rubella are rarely complicated by encephalitis and meningoencephalitis. Psychopathological disorders in these diseases manifest as psychotic episodes (delirium, amhenia, twilight state). In later stages, various manifestations of organic psychosyndrome are observed. Rubella can contribute to the development of embryopathies if contracted by a woman during Pregnancy, particularly in the first trimester. Clinical manifestations of embryopathies include fetal brain Dysplasia, leading to profound impairments in the child's mental development (idiocy, imbecility).

Diagnosis

The diagnosis of an infectious mental disorder is established following a thorough comprehensive clinical and laboratory evaluation, the results of which confirm The Link Between the existing psychopathology and a specific infectious disease.

During Differential diagnosis, these disorders must be distinguished from the onset or exacerbation of endogenous psychoses. Evidence pointing toward infectious psychotic deviations includes episodes of impaired consciousness, pronounced asthenization, and a characteristic dynamic progression of the mental disorder throughout the infectious process (initial, febrile, and residual periods).

Treatment

Patients with acute and protracted infectious psychoses should be admitted to psychosomatic units of a general hospital or infectious disease wards of a psychiatric hospital. There, they must remain under the constant supervision of not only a psychiatrist, but also a general practitioner and an infectious disease specialist. If a patient stays in the infectious disease ward of a general hospital, a separate room must be allocated and round-the-clock monitoring ensured, especially if the patient is experiencing psychomotor agitation or depression (suicide risk). Patients with pronounced organic personality changes must without fail be hospitalized in the infectious ward of a psychiatric hospital.

The treatment of patients with infectious psychosis must be comprehensive. First and foremost, its underlying causes (the primary disease) must be eliminated. The main method of treatment is etiopathogenetic therapy.

Active anti-inflammatory therapy is administered during the acute period of the illness. Immunostimulants are used. Convalescent serum, homologous γ-globulin, and hyperimmune animal serum are administered (in epidemic, tick-borne, and mosquito-borne encephalitis). For measles, measles antisera; for influenza, anti-influenza serum, anti-influenza γ-globulin or serum polyglobulin, interferon, and the like are used. Broad-spectrum Antibiotics are prescribed (tetracycline, oleandomycin, rondomycin, ristomycin, lincomycin, ceporin, gentamicin, etc.), as well as antibiotics targeting specific pathogens (penicillin group drugs, erythromycin, chloramphenicol, etc.). Antibiotics are prescribed in high therapeutic doses until the inflammatory process is resolved. To prevent the development of candidomycosis, nystatin and levorin are prescribed. Sulfonamide drugs (norsulfazole, sulfadimethoxine, etazole) are recommended.

Along with the administration of antibiotics and sulfonamides, the following are carried out: detoxification therapy (isotonic glucose and sodium chloride solutions, hemodez, rheopolyglucukin, sodium thiosulfate, etc.); dehydration therapy (lasix, magnesium sulfate, hydrocortisone); desensitizing therapy (calcium chloride, diphenhydramine, seduxen, tavegil); vitamin therapy (thiamine chloride, pyridoxine chloride, cyanocobalamin, ascorbic and nicotinic acids); general strengthening therapy (phosphorus and iron preparations, etc.).

Psychotropic drugs are prescribed taking into account the leading psychopathological syndrome. For asthenic and neurosis- or psychopath-like states, tranquilizers (diazepam, phenazepam, rudotel, radedorm) and low-dose antipsychotics (chlorpromazine, risperidone, zyprexa, clopixol, fluanxol, thioridazine, sonapax) are recommended. For anxiety-depressive syndrome, sedating antidepressants (amitriptyline, cipramil, triptizol, zoloft) are used; for agitation, diazepam, thioridazine; for retarded depression, imipramine, prozac; for lethargy and adynamia, sydnocarb, sydnofen.

For acute, protracted, and chronic psychoses with hallucinatory and delusional symptoms, neuroleptic drugs (chlorpromazine, thioridazine, haloperidol, trifluoperazine, clopixol, fluanxol, risperidone, zyprexa, frenolone, etc.) are recommended. For patients with organic defect states, in addition to neuroleptics, resorption agents (bioquinol, lidase), biogenic stimulants, and Vitamins are indicated. For mnestic disorders, nootropil (piracetam), aminalon (gammalon), encephalabol (pyriditol), and cerebrolysin are prescribed. Anticonvulsants are given according to indications.

Along with drug therapy, psychotherapeutic Methods should be employed, and measures for socio-occupational rehabilitation implemented.

NEUROSYPHILIS

Mental disorders of syphilitic origin belong to severe conditions. Considering the nature of brain damage, the time of their onset, and the characteristics of mental disorders, two forms of neurosyphilis are distinguished: cerebral Syphilis and progressive paralysis. In cerebral syphilis, Tissues of mesodermal origin (Blood Vessels, Meninges) are affected—mesodermal neurosyphilis; in progressive paralysis, the ectoderm (brain parenchyma) suffers—parenchymatous neurosyphilis.

Cerebral syphilis develops 4–7 years after syphilis infection, and progressive paralysis develops after 10–12 years or more. Therefore, cerebral syphilis is called early neurosyphilis, and progressive paralysis is called late neurosyphilis.

Psychoses in cerebral syphilis (syphilitic psychoses)

In psychiatric practice, syphilitic psychoses are often equated with cerebral syphilis. However, METABOLISM/2.html">THE CONCEPT OF "cerebral syphilis" is much broader than the concept of "syphilitic psychoses." Syphilitic psychoses represent a distinct form of cerebral syphilis. Sometimes, psychotic disorders are not detected in cerebral syphilis, and therefore this term should not be used as a synonym for syphilitic psychosis.

Post-mortem examinations in cerebral syphilis reveal meningitis and meningoencephalitis, syphilitic endarteritis, proliferation of granulation tissue around blood vessels, within the brain substance and its membranes (syphilitic gummata). Consequently, the symptomatology of cerebral syphilis is quite polymorphous.

Syphilitic psychoses encompass a variety of forms that defy classification because transitional and mixed variants are frequently observed.

The Diversity of clinical manifestations is explained by the Specifics of the pathological process, its localization, and the presence of toxic effects associated with the syphilitic infection. Their course also depends on the time elapsed since infection, premorbid personality traits, previous treatment, etc.

Different authors provide varying classifications of mental disorders. Dividing syphilitic psychoses into acute, subacute, and chronic is impossible because it is difficult to draw a clear line between them. The forms of syphilitic psychoses are not separate diseases; they should be viewed merely as clinical variants of cerebral syphilis.

Most authors believe that the following forms of syphilitic psychoses may develop in cerebral syphilis: neurosis-like (syphilitic neurasthenia); delirious; psychosis in Syphilitic Meningitis; psychosis in cerebral gummata; hallucinatory (syphilitic hallucinosis); depressive; manic; hallucinatory-paranoid; paroxysmal (epileptiform); catatonic; Korsakoff's; pseudoparalytic (syphilitic pseudoparalysis); demented.

The neurosis-like (syphilitic neurasthenia) form is characterized by symptoms typical of neuroses and, above all, neurasthenia. Patients complain of headache, irritability, increased fatigue, reduced working capacity, insomnia, memory impairment, and depressed mood. They may exhibit minor meningeal signs, anisocoria with sluggish pupillary light reaction, facial muscle innervation asymmetry, and hyperactive or uneven tendon and periosteal reflexes. The Wassermann reaction (in CEREBROSPINAL FLUID analysis) is positive. The cerebrospinal fluid contains a high amount of protein and cellular elements. If this symptomatology is not the onset of more severe manifestations of cerebral syphilis, it disappears under The Influence of specific therapy.

The delirious form is characterized by sudden clouding of consciousness with disorientation, numerous visual and auditory hallucinations, fragmentary persecutory delusions, fear, and psychomotor agitation. The neurological symptomatology is the same as in the neurosis-like form.

Syphilitic meningitis. Acute syphilitic meningitis is accompanied by persistent fever. Patients complain of intense headache, dizziness, nausea, and vomiting. Typical meningeal signs are observed (nuchal rigidity, Kernig's and Brudzinski's signs, etc.). Consciousness may be impaired in the manner of obtundation, delirium, or amremia; convulsive seizures and epileptiform agitation occur.

More frequently, a chronic inflammatory process develops in the meninges, spreading to the brain and causing chronic meningoencephalitis. It is characterized by impaired consciousness resembling a mild delirious syndrome or twilight state, and occasionally convulsive seizures. In syphilitic meningitis (meningoencephalitis), delirium symptoms subside quickly but tend to recur.

The following neurological disorders are crucial for diagnosing syphilitic meningoencephalitis: meningeal signs, ptosis, strabismus, anisocoria, sluggish pupillary light reaction, accommodation and convergence impairment (typical Argyll Robertson syndrome; not always present); nystagmus, Hearing loss, cranial nerve involvement (facial and trigeminal), aphasia, and apraxia.

Cerebral gummata. This form of syphilis is observed infrequently. Gummata are localized both in the meninges and within the brain parenchyma. Intracranial pressure increases. Syphilitic gummata can cause mental disorders, which are driven not only by cerebrospinal fluid Hypertension but also by the localization of the gummata. The clinical picture of the gummatous form of syphilis reveals individual symptoms depending on the Location and size of the gumma. Sluggishness, apathy, indifference to everything, progressively worsening consciousness disturbances (delirium, hallucinosis), headache, papilledema, paresis, paralysis, hyperkinesia, and convulsive seizures are observed.

The hallucinatory form (syphilitic hallucinosis) manifests as unpleasant auditory hallucinations (threats, swearing, condemnation of the patient's actions). They are quite persistent. In addition to true hallucinations and pseudohallucinations, there may be symptoms of psychic automatism (thought broadcasting, thought echo, thought insertion). The mood is depressed. Neurological symptoms are constant but not sharply defined.

The depressive form is characterized by a melancholic syndrome, though the depressed mood lacks a vivid affective background. Hypochondriacal delusions are present. The illness lasts for several months, sometimes up to a year. Toward the end, all mental processes weaken. Neurological symptoms are constant. There is a tendency toward relapse.

The manic form manifests as a manic syndrome featuring absurd delusions of grandeur, though the absurdity does not reach the extent characteristic of the expansive form of general paresis. Occasionally, the disease course fluctuates between depressive and manic states.

The hallucinatory-paranoid form begins with the onset of true auditory hallucinations and pseudohallucinations. Somatic, olfactory, and gustatory hallucinations may also occur. Persecutory delusions develop, tending toward systematization. Patients claim that an Organization is persecuting them, and so forth. Subsequently, delusions of grandeur emerge. Psychomotor agitation is observed episodically. As the disease progresses, signs of dementia dominate, and the delusional system disintegrates. The delusions become fragmented and absurd. The illness lasts for many years.

The paroxysmal (epileptiform) form clinically resembles epilepsy. Periodically, patients experience epileptiform seizures accompanied by loss of consciousness, as well as twilight states and phenomena of ambulatory automatism. Dementia develops quite rapidly. Neurological symptoms are distinct: anisocoria with sluggish pupillary light reaction; strabismus, ptosis, monoparesis, anisoreflexia, and pyramidal signs.

The catatonic form is more frequent at a young age. It is characterized by negativism, mutism, stereotypies, and stupor. Catatonic symptoms may manifest alongside paranoid features. Patients express non-systematized, fragmented delusions of persecution and physical influence. Frequently, delusions are associated with hallucinations. Hebephrenic symptoms are sometimes observed, such as childish behavior, silliness, and mannerisms. The course of the catatonic form is prolonged, with occasional remissions. Over the years, dementia sets in. Clear focal neurological symptoms are detected in patients. The prognosis depends on the quality of treatment.

Korsakoff's form manifests as progressive memory loss. At the onset of the disease, The ability to encode new information is impaired, followed by the retrieval of past events. Patients are unable to name the dates of prominent events in their lives. Some patients exhibit retrograde and anterograde amnesia accompanied by pseudoreminiscences, confabulations, and phantasms. Intellect and attention are significantly impaired. Patients become indifferent to their surroundings and apathetic. Neurological symptoms are quite pronounced. Several months after specific treatment, the condition improves, though a deficit in the intellectual and emotional-volitional spheres remains.

The pseudoparalytic form (syphilitic pseudoparalysis)

clinically resembles general paresis. All forms of mental activity gradually weaken. Memory, intellect, and attention are significantly impaired. Patients become complacent and euphoric. They are unable to perform daily duties and eventually lose interest in them. Focal neurological symptoms are quite pronounced in such patients. Following specific therapy, the condition improves somewhat. In the absence of treatment, profound dementia ensues.

The demented form is characterized by progressive dementia associated with focal brain lesions (strokes), resulting in transient mono- and hemiplegia, aphasia, apraxia, and agnosia. Apoplectic seizures tend to recur. With each seizure, the manifestations of dementia deepen further. Death occurs following one of the strokes.

General Paresis

General paresis was first described as an independent disease by the French psychiatrist A. Bayle in 1822. Following the discovery of Treponema pallidum in the brains of patients by the Japanese scientist Noguchi in 1911, the syphilitic Nature of the disorder was proven.

The incubation period lasts approximately 10 years, though the development of general paresis 3 or even 20 years after syphilis infection is possible.

General paresis develops gradually. Four stages are distinguished in the course of the disease: the initial stage; the stage of clear disease manifestation; the stage of profound paralytic dementia; and paralytic marasmus.

The initial stage lasts from 4–6 months to a year and is characterized by the development of neurosis-like symptoms. Patients complain of headaches, increased fatigue, irritability, sleep disturbances, and decreased work capacity. At the same time, uncharacteristic character traits emerge. Patients become inattentive and irritable, prone to outbursts of anger over minor matters. They neglect their official duties, fail to care for their families, and squander money on satisfying base needs. They lose ethical standards, becoming rude, crude, cynical, talkative, and frivolous. A tendency toward alcohol and sexual excesses appears. Patients fail to notice their own mistakes and are incapable of understanding the reasons for their occurrence.

Already in the initial stage, neurological symptoms typical of general paresis are detected: unequal pupils (anisocoria), weakened or absent pupillary light reaction with preserved accommodation and convergence (Argyll Robertson syndrome), and speech articulation disorders (dysarthria). Patients' movements become unsteady, coordination is impaired, and handwriting changes. The face becomes mask-like and asymmetrical. Tongue deviation is observed. A characteristic symptom is tremor of the tongue, eyelids, and fingers. Tendon and periosteal reflexes are exaggerated and asymmetrical.

The stage of clear disease manifestation has three forms: expansive (manic), depressive, and demented.

The expansive (manic) form manifests as a manic syndrome. Patients exhibit elevated mood, accelerated thought processes, and psychomotor agitation. Patients are cheerful, constantly laughing and joking, though their jokes are crude. Delusions of grandeur, wealth, inventiveness, and great physical strength arise. Patients claim they are billionaires, possess vast amounts of jewels (tons), are the smartest and most beautiful, and can lift thousands of centners with one hand. They assert they hold the highest awards (pinning various slips of paper with depictions of orders to their clothing). Such delusions are termed megalomaniacal. In the expansive form, memory declines, and absurd paralytic phantasms appear.

The depressive form is characterized by the presence of a melancholic syndrome. Against a background of a depressed, sorrowful mood, patients express delusions of self-blame, self-abasement, sinfulness, hypochondriacal, and nihilistic delusions. They claim their Internal Organs have rotted, their intestines do not function, food remains in their abdomen and rots, their heart has stopped, and they are already dead. Micromaniacal delusions occasionally occur: patients report that they have become as small as a match or a pin.

The demented form. Delusions are absent. Patients display complacency. They are satisfied with everything, yet incapable of comprehending simple matters and forget current events. All interests are focused on biological needs.

Regardless of the form the disease takes during its progression, the symptoms of mounting dementia come to the fore. Patients are incapable of productive thinking. Self-criticism is lost. Memory (total amnesia) and active attention are severely impaired. While reading and writing, patients skip letters and individual syllables, leave words unfinished, and substitute one word for another. Previous knowledge and skills are lost. Higher feelings (social-ethical, aesthetic, intellectual, religious) suffer, while lower ones become exacerbated (hypersexuality, gluttony). In this stage of the disease, irritability and affect lability emerge, arising over minor triggers and rapidly giving way to complacency.

At the end of the second stage, delusions fade, lose their affective coloring, and eventually disappear. All initiative vanishes; patients lie in bed for long periods or sit apart. In general paresis, patients are easily suggestible. Neurological symptoms are more distinct during the second stage of the disease.

Occasionally, the disease follows an atypical course. For instance, the so-called agitated form is accompanied by psychomotor agitation. Patients are constantly moving, running, shouting, and becoming aggressive. Speech is incoherent. The prognosis is unfavorable—stroke and death.

Galloping paresis also carries an unfavorable prognosis. The patient dies within a few weeks.

Taboparesis manifests with symptoms of tabes dorsalis (absence of tendon reflexes in upper and lower extremities, sensory disturbances, ataxia) and the demented form of general paresis.

Lissauer's form of general paresis arises from atypical brain involvement (occipital and parietal lobes) and is characterized by focal symptoms. Epileptiform seizures, hemianopia, aphasia, agnosia, and apraxia are observed. Patients frequently die from a stroke.

Congenital syphilis or syphilis acquired in the first years of life (household transmission) can cause general paresis in childhood and adolescence. In its course, juvenile paresis resembles the demented form. Significant somatic pathology is observed: skeletal defects, Hutchinson's triad (interstitial diffuse keratitis, deafness, and Hutchinson's Teeth), Adiposogenital Dystrophy, Hypogenitalism, hyperkinesis, etc. Epileptiform seizures are possible.

The stage of profound paralytic dementia lasts for nearly a year and is characterized by the loss of all mental Functions (total dementia). The patient is unable to assess the situation. At this stage, the thought process is severely impaired. The patient cannot even comprehend a question. Speech becomes incomprehensible and loses its function. The unfortunate individual utters only isolated words, syllables, or sounds. They cannot remember current or past events and fail to recognize relatives (total amnesia). Emotional reactions are reduced to the primitive instincts of satisfying or dissatisfying the appetite. Patients eat greedily and in large quantities.

During the stage of paralytic marasmus, patients either do not speak at all or produce only isolated sounds. Only unconditioned reflexes remain intact. For instance, if an object is brought close to the patient's lips, they begin to suck on it. They are unable to care for themselves. Pronounced physical weakness is evident, accompanied by a complete loss of the ability to perform purposeful actions. At this stage, spastic paralysis of the limbs occurs, and flexion contractures develop. Tissue trophism is disrupted—Osteoporosis causes bones to become brittle, Hair falls out, edema appears, and trophic ulcers form on the skin of the lower extremities, most commonly on the soles. Osteomas develop in the Cartilage of the auricle, leading to its deformation. Cachexia sets in. Patients die from stroke or other intercurrent diseases.

Diagnostics

The diagnosis of syphilitic psychoses and progressive paralysis is established based on the results of a comprehensive patient evaluation, a detailed life and medical history, the presence of psychopathological symptoms, and neurological signs (anisocoria, pupil deformation, miosis, Argyll Robertson syndrome, ptosis, strabismus, nasal speech, dysarthria, amimia, loss of sensation, etc.), as well as somatic pathology (trophic disorders, non-healing bedsores, hair loss, pathological bone fragility, myocardial dystrophy, aortic deformation, etc.).

Specific Laboratory Diagnostic Methods are of great importance in diagnosing neurosyphilis. The basis for its confirmation includes: positive Wassermann reactions in the blood and cerebrospinal fluid, alongside Pandy, Nonne-Appelt, and Weichbrodt protein tests; elevated Levels of Protein and cellular elements in the cerebrospinal fluid; a positive fluorescent treponemal antibody absorption test (FTA-ABS); and a positive Treponema pallidum immobilization (TPI) test in the cerebrospinal fluid.

The DIFFERENTIAL DIAGNOSIS OF cerebral syphilis and progressive paralysis is aided by Lange's colloidal gold test, which reveals the "syphilitic zone" characteristic of syphilitic psychoses (decolorization of the fluid in the middle tubes), and the "paralytic curve" characteristic of progressive paralysis (decolorization in the first tubes).

Treatment

Treatment for cerebral syphilis and progressive paralysis should be initiated as early as possible. Specific antisyphilitic drugs are prescribed according to traditional regimens. Antibiotics are used (penicillin group drugs, erythromycin, etc.). A course of treatment requires 12,000,000–20,000,000 units of benzylpenicillin sodium salt (averaging 14,000,000 units). Six to eight courses are administered at intervals of 0.5–2 months. Concurrently, bismuth and iodine preparations are prescribed: bioquinol and bismoverol, 40–50 ml per course (2–3 ml intramuscularly every 2–3 days), potassium iodide and sodium iodide (3% solution, 3–4 tablespoons daily), as well as pyrogenal or sulfazin—10–15 injections.

In addition to specific treatment, vitamin therapy and general strengthening agents are employed. Specific therapy must be carried out under the supervision of internal organ function. Throughout the course of treatment, blood, urine, and cerebrospinal fluid parameters should be monitored.

Psychotropic drugs are prescribed taking into account the leading psychopathological syndrome.

Prognosis

The prognosis depends on the specific clinical manifestations and the course of the infectious psychoses. Most often, with timely and effective treatment, patients with acute psychoses recover. This also applies to neurosyphilis. In cases of protracted mental disorders, the prognosis depends on the nature of the psychopathological symptoms. Affective disorders usually have a favorable course. In organic brain damage (amnestic Korsakoff syndrome), the condition may result in an organic psychosyndrome and dementia. A severe course of delirium can lead to marked agitation and a mussitant delirious state, frequently resulting in a fatal outcome. In primary infectious encephalitis and meningitis, or when complicated by them, the prognosis is most often unfavorable.

Medical Certification

Medicosocial. The level of social functioning, including working capacity, declines in cases of irreversible mental disorders, primarily the psycho-organic syndrome.

Military. All examinees with sharply pronounced mental disorders are deemed unfit for military service and are removed from the military register. Individuals with moderately pronounced, prolonged asthenic states or pathological personality changes are also considered unfit. The fitness of officers, warrant officers, michmans, and female military personnel is determined on an individual basis. In cases of moderately pronounced, short-term asthenic states, soldiers, sailors, sergeants, and foremen are temporarily fit for military service (granted leave or vacation), whereas submarine personnel are unfit. In cases of mild, short-term asthenic states, submarine personnel, officers, warrant officers, michmans, female military personnel, and individuals serving in airmobile forces, flying crews, marine infantry, and special structures are unfit. All others are fit for military service.

Forensic psychiatric. Patients are declared legally insane during acute and protracted states. In cases of residual mental disorders, sanity or insanity is determined by the severity of the mental disorder, depending on the patient's ability to understand and control their actions.

Review Questions

1. Definition of the concept of "infectious psychoses." Etiology, pathogenesis, classification. Bonhoeffer's concept of exogenous reaction types.

2. Mental disorders in systemic infections.

3. Transitory psychoses.

4. Protracted psychoses.

5. Persistent mental disorders — Korsakoff and psycho-organic syndromes.

6. Nature of mental disorders in specific infections.

7. Mental disorders in cerebral infections (neuroinfections).

8. Treatment, rehabilitation, prognosis. Medical certification in severe psychoses.

9. Mental disorders in AIDS.

10. Neurosyphilis. MAIN CLINICAL MANIFESTATIONS and diagnosis of cerebral syphilis and general paresis.