The diagnostic group as a whole is characterized by a combination of disorders of thinking, perception and emotional-volitional disorders that last at least a month, but a more accurate diagnosis can only be made for 6 months. observations. Typically, the first step is a diagnosis of acute transient psychotic disorder with symptoms of schizophrenia or schizophrenia-like disorder.
Disease stages: initial, manifest, remission, repeated psychosis, deficiency. In 10% of cases, spontaneous exit and prolonged (up to 10 years remission) are possible. The reasons for the differences in the prognosis are predominantly endogenous. In particular, the prognosis is better for women, with a picnic physique, high intelligence, life in a complete family, as well as with a short (less than 1 month) initial period, a short manifest period (less than 2 weeks), no abnormal premorbid background, no dysplasias, low resistance to psychotropic drugs.
According to E. Bleiler, axial disorders of schizophrenia include disorders of thinking (tearing, resonance, paralogy, autism, symbolic thinking, narrowing of concepts and mantism, perseveration and poverty of thoughts) and specific emotional-volitional disorders (dulling of affect, coldness, paratimia, hypertrophy of emotions, ambivalence and ambivalence, apathy and abulia). M. Bleiler believed that axial disturbances should be outlined by the presence of manifest manifestations, the absence of exogenous type of reaction syndromes (amentia, delirium, quantitative changes in consciousness, seizures, amnesia), the presence of torn thinking, splitting in the sphere of emotions, facial expressions, motor skills, depersonalization, mental automatisms, catatonia and hallucinations. V. Meyer-Gross attributed the primary symptoms to mental disorders, passivity with a sense of influence, primary delirium with ideas of attitude, emotional flattening, sounding of thoughts and catatonic behavior.
Symptoms of the first rank according to K. Schneider found the greatest recognition in diagnosis, which include: the sound of one’s own thoughts, auditory contradictory and mutually exclusive hallucinations, auditory commentary hallucinations, somatic hallucinations, effects on thoughts, effects on feelings, effects on motives, effects on actions, a symptom of open thoughts, sperrung and delusional perception, close to acute sensory delirium. Symptoms of the second rank include catatonia, pathological expression in speech, emotions, and feelings. Most of these symptoms are also taken into account in the current classification thanks to the International Schizophrenia Study in 9 countries.
According to ICD 10, at least one of the following symptoms should be noted:
- “Echo of thoughts” (sounding of one’s own thoughts), insertion or withdrawal of thoughts, openness of thoughts.
- Delusions of exposure, motor, sensory, ideator automatism, delusional perception. Such a combination in domestic psychiatry is referred to as Kandinsky-Clerambo syndrome.
- Auditory commenting on true and pseudo-hallucinations and somatic hallucinations.
- Delusions that are culturally inadequate, ridiculous and grandiose in content.
Or at least two of the following symptoms:
- Chronic (more than a month) hallucinations with delusions, but without pronounced affect.
- Neologisms, sperprings, fragmentation of speech.
- Catatonic behavior.
- Negative symptoms, including apathy, abulia, impoverishment of speech, emotional inadequacy, including coldness.
- Qualitative changes in behavior with loss of interest, lack of focus, autism.
The course of schizophrenia can be established already in the period of the manifesto, but more precisely – after the third attack. With a tendency to remissions of good quality, seizures are usually polymorphic, include the affect of anxiety, fear. A continuous course is distinguished, which means the absence of remission for more than a year, episodic with an increasing defect, when negative symptoms progressively (continuously) increase between psychotic episodes, episodic with a stable defect, when persistent negative symptoms are noted between psychotic episodes. The episodic course corresponds to the symptoms of a paroxysmal course accepted in domestic psychiatry. Episodic remitting when complete remissions between episodes are noted. This variant of the course corresponds to the symptoms of a periodic course accepted in domestic psychiatry. After the attack, incomplete remission is also possible. Earlier in Russian psychiatry, this concept corresponded to remissions “B” and “C” according to M. Ya. Sereysky, in which behavioral disorders, impaired disorders, an encapsulated psychosis clinic, or neurotic symptoms are found in a remission clinic. Complete remission corresponds to remission “A” according to M.Ya. Sereysky.
Persistent negative symptoms during remissions (defect) include in your clinic the erased symptoms of productive symptoms (encapsulation), behavior disorders, decreased mood against the background of apathic-abulic syndrome, loss of communication, decreased energy potential, autism and fencing, loss of understanding, instinctive regression.
In childhood, this diagnosis can be made quite accurately only after 2 years, from 2 to 10 years, nuclear forms predominate, which manifest in a slightly different form. Paranoid forms are described from the age of 9 years. Characteristic symptoms of childhood schizophrenia are regression, in particular, regression of speech, behavior (symptom of manege, ballet walking, choice of non-game items, neophobia), emotional-volitional disorders and developmental delay. The equivalents of delirium are overvalued fears, delusional fantasies.
The premorbid background is often without features. The initial period is short – from several days to several months. In the clinic of this period – symptoms of anxiety, confusion, individual hallucinatory inclusions (hail), impaired concentration. The onset can also be a type of reactive paranoid or acute sensory delirium, which is initially regarded as an acute transient psychotic disorder with schizophrenia symptoms or schizophrenia-like. The manifest period is from 16 to 45 years old.
Options for paranoid schizophrenia are: paraphrenic with symptoms of predominantly systematic paraphrenia; hypochondria, in which the delirium of infection is clearly associated with the content of auditory, olfactory, somatic hallucinations; hallucinatory-paranoid variant, proceeding with Kandinsky-Clerambo syndrome. Particular variants of paranoid schizophrenia are affective-delusional variants characteristic of the remitting course. These include depressive-paranoid and expansive-paranoid variants. The depressive-paranoid variant usually begins as hypochondriacal delirium, which grows to a degree of enormity, depressive affect is secondary. The expansive-paranoid variant proceeds with the clinic of expansive paraphrenia, however, the expansion continues less than the ideas of greatness. Classical paranoid schizophrenia is accompanied by polythematic delirium, in which it is difficult to separate the ideas of persecution, attitudes, meanings.
With paranoid schizophrenia, all course options are possible (continuous, episodic, and remitting), and negative disorders during the period of remission include sharpening of character traits, fixation of apathetic-abulic symptoms, “encapsulation”, in which certain symptoms of hallucinations and delusions are found in the remission clinic.
In the manifest period and the further course of the disease are characteristic:
- Delusions of persecution, attitudes, values, high descent, special purpose or ridiculous delusions of jealousy, delusions of influence.
- Auditory true and pseudo-hallucinations of a commenting, contradictory, judgmental and imperative nature.
- Olfactory, gustatory and somatic, including sexual, hallucinations.
The classical logic of the development of delirium described by V. Magnan corresponds to the sequence: paranoid (monotemic delirium without hallucinations) – paranoid (polythematic delirium with the addition of auditory hallucinations) – paraphrenic. However, this logic is not always noted, the development of acute paraphrenia and the absence of a paranoid stage are possible.
At the first stages, it is necessary to differentiate with acute transient psychotic disorders, and then with chronic delusional and schizoaffective disorders, as well as organic delusional disorders.
Acute transient psychotic disorders can occur with productive and negative symptoms of schizophrenia, however, these conditions are short-term and limited for about two weeks with a high probability of spontaneous release and good sensitivity to antipsychotics. This section, meanwhile, can be considered as “cosmetic” at the stage of manifest psychosis in paranoid schizophrenia.
Chronic delusional disorders include monothematic delusions, if auditory hallucinations occur, they are often true. This group includes those delusions that were commonly called paranoid (love delirium, delirium of reformism, invention, and persecution).
In schizoaffective disorders, delusional disorders are secondary to affect, and affect (manic, expansive, depressive) lasts longer than delirium.
With organic delusional disorders, exogenous symptoms are often present, and neurologically, neuropsychologically and using objective research methods, it is possible to identify the main organic brain disease. In addition, personality changes in such disorders have a specific organic color.
Until now, it is believed that treatment of acute manifest psychosis in paranoid schizophrenia is best to start with detoxification therapy, as well as antipsychotics. The presence of depressive affect in the structure of psychosis forces the use of antidepressants, but expansive affect can be stopped not only with tisercin, but also with carbamazepine and beta-blockers (propranolol, inderal). The onset of paranoid schizophrenia in adolescence is usually accompanied by an unfavorable course, so the increase in negative disorders can be prevented by insulinocomatous therapy, small doses of rispolept (up to 2 mg) and other antipsychotic drugs. In acute psychosis, rispolept doses increase to 8 mg. Antipsychotics – prolongs are used as maintenance therapy, and if there is an affect in the structure of psychosis, lithium carbonate. Therapy is based either on the principle of influencing the leading syndrome, which is chosen as the “target” of therapy, or on the principle of a complex effect on the amount of symptoms. Initiation of therapy should be careful to avoid dyskinetic complications. With resistance to antipsychotic therapy, monolateral ECT is used, while the application of electrodes depends on the structure of the leading syndrome. Maintenance therapy is carried out depending on the characteristics of the seizure clinic with either antipsychotic prolongs (haloperidol-depot, lioradin-depot), or antipsychotics in combination with lithium carbonate.
Behavioral disorders are common in premorbid: antidisciplinary, antisocial, and criminal behavior. Dissociative personality traits, early puberty and homosexual excesses are frequent. This is often perceived as a distortion of the puberty crisis. The onset most often covers the age of 14-18 years, although the manifestation of later hebephrenia is also possible. Further, in the manifest period, a triad is characteristic, which includes the phenomenon of inaction of thoughts, unproductive euphoria and grimacing, reminiscent of uncontrolled tics. The style of behavior is characterized by regression in speech (obscene speech), sexuality (random and abnormal sexual intercourse) and in other instinctive forms of behavior (eating inedible, aimless dromomania, sloppy).
In the structure of hebefren syndrome, the following are detected:
- Motor-volitional changes in the form of grimacing, foolishness, regression of instincts, unmotivated euphoria, aimlessness and lack of focus.
- Emotional inadequacy.
- Formal paralogical disorders of thinking – resonance and fragmentation.
- Unfolded delirium and hallucinations that do not come to the fore and are of the nature of inclusions.
The course is often continuous or episodic with an increasing defect. In the structure of the defect is the formation of disocial and schizoid personality traits.
Hebephrenic schizophrenia should be differentiated with tumors of the frontal lobes and dementia in Peak and Huntington’s disease. With tumors, cerebral symptoms, changes in the fundus, EEG and CT can be detected. Peak’s disease is noted at a much later age, and with Huntington’s disease, hyperkinesis of thinking, facial expressions, gesture, and posture is specific. On CT, in patients with schizophrenia who have been taking antipsychotics for a long time, there may be changes similar to Huntington’s disease.
Treatment includes the use of insulin therapy, hypervitamin therapy, tranquilizers and large antipsychotics (chlorpromazine, majeptil, trisedil, haloperidol, zeprex, rispolepta in doses of about 4 mg per day). Maintenance therapy is carried out by combinations of antipsychotic prolongs and lithium carbonate, which allow you to control impulses, in particular aggression.
Premorbid background is characterized by schizoid personality disorder, although it is possible to develop against a premorbid unchanged background. In the initial period, depressive episodes, simplex syndrome with fencing, loss of initiative and interests. The manifestation is likely as an acute reactive stupor, after traumatic brain injury, flu, although more often psychosis develops for no apparent reason.
Classical catatonic schizophrenia occurs in the form of lucid catatonia, catatonic-paranoid states and oneiric catatonia, as well as febrile catatonia. The motor component in catatonia is expressed in the form of stupor and arousal. At present, classical catatonia has been replaced by microcatatonic states.
Catatonic stupor includes mutism, negativism, catalepsy, rigidity, solidification, automatic subordination. Usually, Pavlov’s symptom is noted in the stupor (the patient responds to whispering speech, but does not respond to normal speech), gear symptom (jerking resistance is observed when the arm is bent and extended), a symptom of an air cushion (the head remains raised after the pillow is removed), a symptom of a hood ( the patient seeks to hide with his head or covers his head with clothing).
Catatonic arousal proceeds with the phenomena of randomness, unfocusedness, perseveration and fragmentation of thinking. The entire clinic can be expressed either in a change of excitement and stupor, or in the form of repeated stupors (excitations).
With lucid catatonia, purely motor psychosis is noted, and behind the facade of motor disorders, no productive disturbances are noted. The catatonic-paranoid variant suggests that delirium lies behind the catatonia. Often, such productive irregularities can be indirectly detected as a result of observing the patient’s facial expressions: he looks, the facial expression changes, regardless of the context of the doctor’s questions. With oneiric catatonia, behind the catatonia facade, an influx of fantastic visual images of a cosmic, apocalyptic nature is noted. The patient visits other worlds, heaven and hell. Amnesia after exiting this condition is absent. Febrile catatonia as a variant of catatonic schizophrenia is recognized only by some psychiatrists, most believe that the adherence of temperature to the stupor is due to either additional somatic pathology, or unrecognized stem encephalitis, or malignant antipsychotic syndrome. In the clinic, there are discrepancies in the pulse rate and the temperature, a petechial rash appears on the lower extremities, a gray film appears on the mucous membrane of the lips, and muscle tone gradually increases.
Signs of microcatatonia include increased tone of the muscles of the shoulder girdle, increased activity of the oral zone, stereotyping of facial expressions, postures, gestures, gait, speech stereotypes, mutism, stereotyped playing with fingers, hypokinesia of the posture, decreased mobility of the hands with increased activity of the fingers, and the absence of blinking. Sometimes a catatonic stupor appears only in the form of mutism.
All flow options are possible. The defect is usually expressed in apathetic-abulic states.
The diagnosis is based on the identification of:
- chaotic, non-targeted excitation;
- catalepsy and negativism;
- subordination and stereotypy (perseveration).
Catatonic schizophrenia should be distinguished from organic catatonic disorders resulting from epilepsy, systemic diseases, tumors, encephalitis, and from depressive stupor.
With organic catatonia, atypicality of motor disorders is noticeable. For example, against the background of catalepsy – tremor of the fingers, choreoathetoid movements, the difference in the symptoms of rigidity and catalepsy on the upper and lower extremities, muscle hypotension. CT, EEG and neurological examination data help to clarify the diagnosis.
Depressive stupor is accompanied by a characteristic facial expression of depression with a fold of Veragut. Depression is revealed in the anamnesis.
Symptoms of microcatatonia resemble both signs of neuroleptic intoxication and behavioral signs of a defect in schizophrenia, such as apathetic-abulic. In the latter case, they speak of secondary catatonia. For a differential diagnosis, detoxification therapy, tremblex, parkopan, cyclodol, or akineton is useful. The use of this course usually reduces the signs of antipsychotic intoxication.
Catatonic mutism should be distinguished from selective (selective) mutism in children and adults with schizoid personality disorders.
Medium and large doses of antipsychotic drugs for catatonia can lead to the fixation of symptoms and their translation into a chronic course. Therefore, with stupor, therapy should be prescribed with the intravenous administration of tranquilizers in increasing doses, sodium oxybutyrate, droperidol, nootropics, with careful monitoring of the patient’s somatic condition. A good effect is given by 5-6 ECT sessions with bilateral application of electrodes. The occurrence of a febrile state in the absence of contraindications forces an ECT or transfer to the intensive care unit. Catatonic excitation is stopped by chlorpromazine, haloperidol, tisercin.
The clinic includes signs of paranoid, catatonic and hebephrenic schizophrenia in a state of psychosis. Such a high polymorphism within the framework of one psychosis usually involves an episodic remitting course. However, with the development of symptoms from one typology to another in a sequential chain of psychoses, the course can be continuous, for example, when a transition from paranoid to nuclear syndromes is noted in dynamics. The lack of differentiation of symptoms is sometimes associated with the fact that the disease proceeds against the background of dependence on drugs or alcohol, against the background of the immediate and long-term consequences of a traumatic brain injury.
The diagnosis is based on the identification of symptoms of paranoid, catatonic and hebephrenic schizophrenia.
A high polymorphism of psychosis is also characteristic of schizoaffective disorders, but with them affective disorders last longer than those characteristic of schizophrenia.
The complexity of therapy lies in the choice of a “target” of exposure and a complex of maintenance therapy. For this purpose, the selection of axial symptoms is important, which is almost always visible in the dynamics of the disease.
Post schizophrenic depression (F20.4).
After a typical episode previously experienced with productive and negative symptoms of schizophrenia, a protracted depressive episode develops, which can be considered as a consequence of schizophrenic psychosis. Usually this episode is atypical. That is, there is no typical diurnal dynamics of mood disorders, for example, mood worsens by the evening as asthenic depression. Complex senestopathies, apathy, reduction of energy potential, aggressiveness may be present. Some patients interpret their condition as the result of a psychosis. If the level of depression corresponds to a mild to moderate depressive episode, it can be considered as a special remission clinic, and with the prevalence of negative disorders, as the dynamics of the defect.
The diagnosis is based on the identification of:
- a history of schizophrenic psychosis;
- depressive symptoms, combined with negative symptoms of schizophrenia.
At the onset of the disease after 50 years, it is necessary to differentiate these disorders with the initial period of Alzheimer’s disease, more precisely, with its variant, the disease with Levy bodies. In this case, additional neuropsychological and neurophysiological studies are needed to differentiate.
Treatment includes a combination of tricyclic antidepressants and antipsychotics. It is possible to apply braking with nitrous oxide, as well as ECT with application of electrodes to the non-dominant hemisphere.
This diagnosis can be considered as a delayed (for more than a year after psychosis) diagnosis of a typical defect in the emotional-volitional sphere after a psychotic episode that meets the criteria for schizophrenia.
Diagnostic criteria are as follows:
- Negative symptoms of schizophrenia in the emotional-volitional sphere (decreased activity, emotional smoothness, passivity, poor speech and non-verbal communication, decreased self-care and social communication skills).
- In the past, at least one psychotic episode corresponding to schizophrenia.
- A year has passed, during which productive symptoms have been reduced.
The need for a differential diagnosis arises when there is no objective information about the past psychosis or the patient hides his past. In this case, the specified disorder can be considered schizotypic.
In therapy, small, stimulating doses of antipsychotics, fluoxetine, nootropics in combination with long-term group psychotherapy and rehabilitation are used.
This type of schizophrenia is not included in the American classification, since it is difficult to differentiate from the dynamics of schizoid personality disorder. However, if the personality was relatively harmonious in premorbid, its transformation and the appearance of regression traits in combination with emotional-volitional disorders suggest the specified diagnosis.
The onset of the disease is from 14 to 20 years. In the initial period – obsessive-phobic, neurotic or affective episodes. In the manifest period, formal disorders of thinking (autistic, symbolic, resonant, paralogical), dysmorphopsia and senestopathy can be noted. Negative symptoms of schizophrenia are detected in the emotional-volitional sphere, activity decreases, emotional coldness occurs. Goal setting is disturbed, as a result of ambivalence passivity arises. Poverty of thinking is accompanied by complaints of emptiness in the head, speech is poor. Hypomimia, sometimes paramimia. Lost previous acquaintances and friends. The range of interests that may become fanciful is narrowed or stereotyped. Autistic thinking can be actively manifested and presented to others (autism inside out), but more often it is hidden from others by external self-absorption, staying in a fantasy world that has no points of contact with the world. Relatives often consider the patient lazy, stupid.