Carlos R. Hojaij: Schizophrenia, the Psychiatric Sacred Illness*
"Dementia Praecox consists of series of states, the common characteristic of which is a peculiar destruction of the internal connections of the psychic life."
“I consider it an open question whether the same morbid process is not after all the cause of the divergent forms, though differing in the point of attack and taking a varying course."
One century investigating schizophrenia still is not enough to elucidate all of the complex issues related to the essential symptomatology, clinical boundaries, aetiology, pathogenesis, outcome, treatment and prevention. Despite the extraordinary progress in the neuroscience field, no definitive data is available for schizophrenia. After the initial successful activity of the psychopharmacological era introducing the major tranquillisers (or neuroleptics or anti-psychotics), nothing new happened to treatment of schizophrenia. On the other hand, the clinical phenomenological psychopathological investigations were reduced and almost replaced by the mechanistic operational diagnosis. This latter devaluation of phenomenological psychopathology has caused an impoverishment in psychiatry.
Tracing some historical aspects of schizophrenia since the Kraepelinian Dementia Praecox, this article intends to demonstrate the failure of the current model of diagnosis and the current neuroscience’s limitation and advocates the reinforcement of Clinical Psychopathology as the foundation for the appropriate first step in the investigation of schizophrenia. The splitting disease remains the greatest challenge to psychiatry.
After more than a century of modern investigation of schizophrenia, psychiatrists are not able to accurately certify its cause(s), properly identify the pathophysiological process, clearly circumscribe its clinical pictures, precisely distinguish its boundaries from other psychopathological syndromes, successfully provide efficient and definite treatment, and not able to instruct on its prevention.
Under a clinical perspective, this paper refers to an article intended to celebrate 100 years of the most important milestones in the history of psychiatric nosology. In just a few pages, it reviews some aspects (leaving aside many others) of the 100-year history of Dementia Praecox, and discusses and explores some diagnostic, treatment and research dilemmas. Besides revising the origins of schizophrenia, it considers how much psychiatry has evolved in this subject, where it stands and where it is heading.
It is valid to ask how much more now is known than at the time of Kraepelin. Are current schizophrenic patients comparatively better and more precisely diagnosed than those of one century ago? Has psychiatry been able to really draw the boundaries of Dementia Praecox, or schizophrenia, as a nosological entity? Or, it is a syndrome with heterogeneous causes acting upon the same cerebral mechanisms? One way or another, it remains as an ideal nosological entity, according to Jaspers' concept (1997), or its diagnosis is made only by exclusion, according to Schneider’s criterion (1959). Should the term itself - schizophrenia - which intends to reveal all the dramatic ruptures experimented by the schizophrenic be maintained? If so, why not value the extravagant symptomatology and correlated phenomena of split personality that gave origin to naming the illness schizophrenia? Why does the investigation of schizophrenia not advance, in the sharp detail, the psychopathological examination and description, and prefers the adoption of a sterilising semiological pragmatism? Does the elementary division and value of all the enormous symptomatological wealth of schizophrenia in groups of positive-negative and disorganised symptoms (Andreasen and Olsen, 1982; Andreasen, 1983, 1984) really take into consideration the true semiology of this psychosis (Mojtabai, 1999)?
Attempts of definition
The history of psychiatrists who have described and theorised about schizophrenia parallels the history of psychiatry itself. Kraepelin was the first to develop a comprehensive definition of schizophrenia that gained widespread acceptance. In 1886 he used the term Dementia Praecox (taken from Morel) to identify a syndrome that tended to begin early in life (praecox) and produced a pervasive and persistent impairment in many different aspects of the psychic life, "a more or less well-marked mental enfeeblement (dementia): Dementia Praecox consists of a series of states, the common characteristic of which is a peculiar destruction of the internal connections of the psychic personality" (Kraepelin, 1919).
Among the symptoms that compose the whole picture of Dementia Praecox, one may find: unsteadiness of attention, hearing of voices giving commands, influences on thought, constraint of thought, morbid tactile sensations, morbid sexual sensations, loss of mental activity, derailments in linguistic expression, neologism, stereotypes of all sorts, evasions, delusions, ideas of reference, exalted ideas, emotional dullness, “no human feelings," sudden oscillations of emotional equilibrium, loss of sympathy, sudden outburst of laughter, less sensitivity to bodily discomfort, weakening of volitional impulses, automatic obedience, all sort of catatonic symptoms, autism and scission in personality (Kraepelin, 1919). While acknowledging that 13% of his patients had significant remissions for some period of time, Kraepelin found a chronic course and a poor outcome to be important features of the illness: “According to my former grouping into hebephrenic, catatonic and paranoid forms, I had come to the conclusion that in about 8 per cent of the first group and in about 13 per cent of the second group, recovery appeared to take place, while paranoid forms probably never issue in complete recovery" (Kraepelin, 1919).
In this respect, it is important to mention that Kraepelin made a distinction between its "Dementia Praecox" and "other forms of dementia such as are known ... as a result of paralysis, senility or epilepsy." At that point he was not talking about dementia as a result of a pathological process, but just about the appearance of the clinical picture.
“Dementia Praecox” (1886) is a very large work comprising many issues in a methodological presentation, from psychic symptoms, body signs (including pupillary disorders, tendon reflexes, vasomotor disorders, blood pressure, perspiration, secretion of saliva, temperature, menses, metabolism, nourishment, weight, etc.), clinical forms, course and remissions, to causes, anatomy, differential diagnoses and treatment. At some point Kraepelin tried to establish a relationship between the "morbid anatomy and the clinical picture: ...the disease attacks by preference the frontal areas of the brain, the central convolutions and the temporal lobes..." (Kraepelin, 1919).
In a comparative study of Dementia Praecox involving 100 Javanese patients plus 25 Chinese patients and 100 European patients, Kraepelin (also a pioneer in cultural psychiatry) reached conclusions concerning the universality of schizophrenia and the importance of culture as a pathoplastic factor (Dalgalarrondo, 1996).
According to Minkowiski (1966), it is possible to conclude from Kraepelin's Dementia Praecox:
1. the inter-changeable characteristic of the symptoms
2. the principle of hereditary similarity
3. the specificity of terminal states
4. the confrontations with the manic-depressive psychosis.
With further descriptions, in 1911 Bleuler recommended that "the group of schizophrenias” supersede the term Dementia Praecox. It is worthwhile quoting from Bleuler's definition of schizophrenia: "We designate 'dementia praecox' or 'schizophrenia' a group of psychosis determined by an evolution sometimes chronic, sometimes defined by intermittent attacks, that can be interrupted or retrocede at any time, but that do not permit a complete restitutio ad integrum. (...) we are facing more or less a clear breakdown of the psychic functions. If the disease is severe, there is a loss in the personality unity; in different moments different psychic complexes seem to represent the previous personality. The integration of the different complexes and impulses is not enough, or even does not exist. (...) It is not possible to demonstrate primary disturbances in perception, orientation and memory. In serious cases it seems to be a complete lack of emotion and affective expressions" (Bleuler, 1950). His meticulous descriptions gave rise to the famous "four As" that characterise schizophrenia: association (disturbances), affect (disturbances), ambivalence, and autism. Bleuler (1960) also distinguished the symptomatology of inpatients from that of outpatients, "in most of the inpatients ...hallucinations, delusional ideas, confusion, stupor, mania, melancholic fluctuations and catatonic symptoms" (accessory symptoms). (...) Outside the hospital there are schizophrenic patients in whom the accessory symptoms are less evident or even do not exist."
Like Bleuler, Schneider (1959) attempted to identify fundamental symptoms that might be helpful in making a psychopathological diagnosis of schizophrenia. In some way distinct from Kraepelin's importance given to the course of the illness, Schneider (1959) states,“For me, the psychiatric diagnosis is fundamentally based on the clinical picture, and not on the course." Schneider was influenced by the work of Jaspers (1997) that introduced the Phenomenology and the Comprehensive Psychology in Psychiatry, and the important notions of “understanding" (or comprehension) and “non-understanding" (or non-comprehension) to the psychopathological phenomena. Schneider concluded that one critical component of schizophrenia was the inability to find the boundaries between self and non-self and a loss of the sense of personal autonomy. This conclusion led him to discuss “first-rank symptoms,” which he identified as audible thoughts; voices arguing, discussing, commenting; somatic experiences of passiveness; thought withdrawal; thought broadcasting; and delusional perceptions. He also identified second-rank symptoms, such as other disorders of perception, depressive and euphoric mood, and feelings of emotional impoverishment (Schneider 1959). An unrecognised aspect of the Schneiderian first-rank symptoms should be emphasised: they are very much based on the Jaspers (1997) studies of disturbances of self-consciousness (activity of the self, unity of the self, identity of the self and awareness of self as distinct from the outside world) and Jaspers' (1997) distinction between primary (non-comprehensible) and secondary (comprehensible) delusions.
Schneider's ideas became the conceptual framework for diagnostic classifications. Schneiderian symptoms were incorporated into several standard diagnostic instruments, such as the Schedule for Affective Disorders and Schizophrenia (Endicott and Spitzer, 1978), Research Diagnostic Criteria (Feighner et al., 1972), Diagnostic and Statistical Manuals (American Psychiatric Association) and the International Classification of Mental Disorders (World Health Organisation). Unfortunately, the utilisation of Schneider criteria was not followed by some very important lessons given by this author: first, sometimes - in the absence of at least visible first-rank symptoms - the diagnosis is based on the second-rank symptoms considering the connections of the whole clinical picture; second, in exceptional situations the diagnosis may be based just in behavioural features (physiognomy and mimic); third, sometimes the presence of first-rank symptoms does not necessarily mean this is schizophrenia, since those symptoms could also be present in symptomatic psychosis; and fourth, the psychopathological diagnosis is made by an assemble of significant symptoms (the total clinical picture), not by a schematic addition of symptoms.
In line with a clinical (existential) approach, Binswanger (1972) offers a profound vision of the schizophrenic way of being, the eccentricity, an important clue for the apprehension of schizophrenia. A patient of Bumke (1948) serves as an example: a father places a coffin near a Christmas tree as a gift for his cancerous daughter. In this case of eccentricity, the father is missing the capability that would give him condition to-see-abroad and then consider not only what he was offering to his daughter, but also consider his daughter in her circumstance. The father gave a logical destination to the coffin (for what a coffin should be used), not considering, however, the daughter’s situation (the other’s situation). His reference is solely the gift (a useful gift) to a person in agony who will soon need a coffin; he is not able to live a reciprocal experience, taking into account the feelings and reaction of his daughter. (Of course, this isolated description of eccentric behaviour is not enough to affirm the most probable father's blunting schizophrenic affect.) In other words, he is unable to comprehend; he does not participate in the other's life. He is dissociated from the others and from the circumstances: he is out of the common axis; he is an eccentric (Hojaij, 1978, 1987).
Looking for some fundamental and permanent feature in the schizophrenic patient, Hojaij (1987), in a long-term study, investigated the possibility of a structural disturbance in the capability of comprehension in the schizophrenic patient. The study is related not to the comprehension that the psychiatrist may or not may have about the schizophrenic phenomena, but how the process of comprehension presents itself in the schizophrenic, how the patient manages this process of intuitive knowledge. Comprehension is considered as a natural capability to - through intuition - immediately apprehend the whole situation, considering the total sequence of the events (from the past to the future) and to sit in the other' situation through empathy (transposition capability). After some point in life, the schizophrenic loses the capacity to discern the essential from the non-essential according to the general, and then is no longer moved by relations of common sense. The teleological sense is lost and the intuitive enfolding apprehension fails. The chain of events in life does not follow the comprehensive spiral (progressive and broader knowledge), but causal laws. The transposition capability is damaged; in other words, the patient is not able to be in the place of the other person and then feel, think, live as if he was the other; the capacity for loving is lost. The schizophrenic is moved by some part of the reality, not by the totality of reality; he is attained at the moment, not taking into consideration the continuous process of existence (past, present, future); he is here, but not living here; he is apart, may be delirious (out of the route). He is split (dissociated) from the reality, as well as split (dissociated) from his own vital history. There is a both complex rupture in the structure of the personality and in the vital history.
The notion of rupture described by Jaspers (1977, 1997) is essential to distinguish the schizophrenic process from other similar psychopathological syndromes. Jaspers calls attention to the "something new" that happens in the psychic life of a schizophrenic. This unspecific “something new” mentioned by Jaspers was developed by Hojaij (1985, 1987): at some point in time something new and heterogeneous appears in relation to the previous personality; it is as if something strange has been inserted in the personality or, more precisely, something strange replaces, to more or less a degree, the original personality; from now on, the “strange” becomes the one. The psychic life follows a different process, a schizophrenic process. The identification of this point of rupture - a radical transformation in the personality - is a very important element for the clinical diagnosis of schizophrenia.
The same essential notion captured by the German authors about the split personality in schizophrenia is found in the French school: Chaslin in “Les folies discordantes” 1912 (cited by Minkowiski, 1966); de Clerambault in “Automatisme Mental et Scission du Moi” (1920); Minkowiski (1927,1966): “la perde de contact vital avec la réalité." In "Le temp vécu," Minkowiski (1973) explains how in the schizophrenic there is a breach in the chain of the existential process with appearance of "acts without tomorrow" - "frozen acts"; the things (all things) are disconnected, the things are more embodied than tasted.
After Kraepelin had assembled the forms hebephrenia described by Hecker in 1871 (Jaspers, 1963) and, catatonia described by Kahlbaum in 1874 (Barnes et al., 1986) with paranoia to compose Dementia Praecox, he described 11 more sub-types: simples (from Bleuler), silly (hebephrenia), simple depressive (stupor), delusional depressive, circular, agitated, periodic, catatonia (excitement, stupor, melancholia atonita), paranoid gravis, paranoid mitis and confusional speech (schizophasia).
Bleuler (1950) added the form simple to the first group described by Kraepelin. On the other hand, Schneider (1959) just accepted the traditional simple, paranoid and catatonic; hebephrenia - he thinks - should be included in the simple, considering that if schizophrenia begins in adolescence, it presents the appearance of such age (pathoplastic significance).
An advancement in discriminating new clinical forms in the group of schizophrenia, and at the same time discriminating groups other than schizophrenia and manic depressive psychosis, is attributed to Leonhard. Kleist largely influenced Leonhard during his years at the Frankfurt Mental Hospital. Leonhard (1999) personally examined approximately 1,450 schizophrenic patients. It is from this magnificent clinical experience that he developed the differentiation between the two groups and sub-groups of schizophrenia, "If independent sub-forms are differentiated, many ambiguities can be cleared..." and discrepancies solved (1999). He separated schizophrenia in two groups: a) systematic schizophrenia (catatonia, paranoid and hebephrenia); and b) asystematic schizophrenia (periodic catatonia, affective paraphrenia and schizophasia). The latter group has a high genetic loading and a relatively good outcome. On the other hand, the systematic schizophrenias have a very low genetic loading (rare family history of psychosis) and a poor outcome.
A further schizophrenic syndrome was added by Kasanin (1933). He described a series of nine patients who had all been assigned diagnoses of Dementia Praecox. They had all demonstrated an acute onset of the disease that was followed by a relative rapid recovery. "Noting that the patients' symptoms represented a combination of schizophrenic and affective components, Kasanin suggested the term schizoaffective psychosis to describe these patients' disease. This category subsequently became part of the American concept of schizophrenia" (Neale and Oltmanns, 1980). It should be discussed whether this group identified by Kasanin is composed of schizophrenic patients with intense mood symptomatology and relatively good outcome, or bi-polar patients with intense productive symptomatology, or even, if they are not part of the same group identified by Leonhard as having cycloid psychosis, or a group of patients having a temporal lobe epilepsy.
Huber (1971), a Schneider's disciple, based on the study of 50 patients (pre-pharmacological era), describes a new sub-type: cenestesic schizophrenia. Usually, the cenestesic phenomena are mentioned as prodromal phase or accompanying other symptoms that dominate the clinical picture. Under the designation of cenestesic schizophrenia there are syndromes characterised by abnormal experiences in bodily sensations, many autonomic, motor and sensorial symptoms that follow during all the course of the disease. The cenestesic symptoms have a peculiar feature of continuous movement, changing in the presentation, in the course (phasic, paroxistic) and in a spectrum that goes from a hypochondriac configuration to body hallucinations with passivity experiences (Bacci and Hojaij, 1984). A few authors make reference to this form described by Huber, perhaps due to the fact that they do not present the so well-known first-rank symptoms. The almost complete absence of the classical symptoms makes the cenestesic schizophrenia misidentified as a hypochondriac (neurotic or depressive) syndrome, psychopathic personality, epilepsy, etc. (Bacci and Hojaij, 1984).
Crow and Carpenter carried out another attempt in the exploration of subtypes. In 1980 Crow pointed out what he described as the “paradox" of schizophrenia. Computerised tomography studies revealed structural brain changes in some patients with schizophrenia. Yet, there was evidence also of a neurochemical disturbance, since schizophrenic symptoms often responded to antipsychotic medications. To resolve the paradox, Crow (1980, 1982) proposed that two syndromes could be distinguished in schizophrenia and that these syndromes are related to different underlying pathological processes. The concept is not that there are two separate diseases, but two separate components to the disease process; in a particular patient at one point in time, one or other processes predominate or both may be present (Crow, 1986). He proposed that positive symptoms (abnormal psychological features such delusions, hallucinations and thought disorder) be labeled the Type I Syndrome, while the negative symptoms (diminished or absent normal functions such as flattening of affect, poverty of speech and loss of volition) be labeled the Type II Syndrome. “The importance of this distinction is that the two syndromes predict different things. Specifically, the presence of the Type I Syndrome predicts response to neuroleptic drugs, while the presence of the Type II Syndrome predicts poor long-term outcome, irrespective of drug treatment. Because they appear to represent separate dimensions, I suggest the two syndromes be related to distinct pathological processes: disturbance of dopaminergic transmission being related to the drug responsive (the Type I Syndrome) and a quite separate and perhaps encephalitis-like process being associated with the Type II Syndrome" (Crow 1980).
Further defining the typology, Crow and colleagues (1980, 1982, 1985) characterised Type I as having acute onset, usually normal intellectual function, normal brain structure, good response to antipsychotic drugs, possible increase of D2 dopamine receptors and the absence of negative symptoms. In contrast, Type II schizophrenia is characterised by insidious onset, intellectual deterioration, enlarged cerebral ventricles, poor response to antipsychotic drugs and prominent negative symptoms (Crow, 1989).
It should be considered that these schematic ideas regarding the two subtypes of schizophrenia (Type I and Type 11) do not exist in clinical practice. Many times, in the same patient, there is an overlap between the two kinds of symptomatology referred to the subtypes, and up to now there is no cerebral evidence of pathology in patients with deteriorate symptomatology. Other very important observations to contest Crow's theory are: the so-called new antipsychotics (such as clozapine, olanzapine, etc.) do promote a significant reduction of negative symptoms and a significant improvement of all personality aspects, some sort of a partial psychopathological recovery.
Carpenter and colleagues (1988) refined the typology of negative symptoms by providing a rationale for distinguishing the primary, enduring negative symptoms of schizophrenia (termed deficit symptoms) from the more transient negative symptoms secondary to other factors. For instance, social withdrawal is not always a direct measure of negative symptoms. Additionally, behaviours and inner experiences that are postulated to be negative symptoms may be either primary or derivative. "The clinician, when encountering putative negative symptoms, such as apathy, avolition, anhedonia and anergia should attempt to discern whether factors such as drug effects, dysphoric mood, self-protective reduction of stimulation are causative. It is important to differentiate derivative or secondary negative symptoms from those that are primary or direct expressions of a pathologic dimension of schizophrenia. The treatment and course of secondary negative symptoms are expected to be responsive to temporal changes in the factors with which they are associated," they added.
Under a different perspective, Carpenter and colleagues are replaying the old and useful German concepts of "pathogenia and pathoplastia.” The concepts "pathogenia and pathoplastia" were developed by Birbaum in his "structural analysis" to differentiate what was directly related to the psychosis from others not directly related and non-essential for its determination: "The psychosis is a complex with specific structure. The symptomatological arrangement is recognised by pathogenic factors (specific aetiology) and pathoplastic factors (disease's configuration, special design of the presented psychosis)” (Birbaum cited in Leme Lopes, 1980). The personal characteristics and circumstances (pathoplastic elements) have a significant contribution in the presentation, giving the "colour" of the psychosis, many times the more attractive and appealing phenomena.
Beyond consideration of positive and negative symptoms in schizophrenia, both Huber (1990, 1995, 1996) and Gross (1996) emphasised basic symptoms (defective symptoms). Basic symptoms are defined as self-experienced, affective-cognitive deficiencies reported by the patients. Basic symptoms appear as prodromal phase, lasting up to three years. Through a personal investigation composed of 1,800 schizophrenic patients, Huber emphasised the importance of diagnosing schizophrenia in its early stages, before the first clear psychotic episode. Founded in Prodromes and Outpost Syndromes, determined by basic symptoms, Huber and Gross et al. (1987) developed a standardised survey of basic symptoms in the Frankfurt Questionnaire and the Bonn Schedule for the Assessment of Basic Symptoms. The richness of the Bonn Scale and its effectiveness in terms of a diagnostic tool are still awaiting international recognition.
A similar approach, looking for "minor" symptoms (such as anhedonia) in schizophrenia, was developed by Chapman and Chapman (1980).
There is no doubt as to the long evolution of schizophrenia and as to its definition as an illness that touches the whole personality. What has not been well determined yet are its clinical forms and types of outcome. The developments proposed by the authors who followed Kraepelin did not come to a consensus and many of the sub-types described do not appear to be completely delimited. Although it is possible to differentiate many types of clinical arrangements and evolutions, it is not possible, until now, to predict the outcome of a specific patient (Schmid et al., 1991). On the other hand, the different types of evolution very often confuse even the most experienced psychiatrists and do not allow an appeasing acceptance of a nosological unit.
Part of the disagreement over core symptoms, boundaries and course emanates from a reduced emphasis on the natural history of schizophrenia. In terms of Dementia Praecox, the knowledge of the natural course was given by studies which began systematically in the last century in the French and German schools. Jaspers' (1977, 1997) studies characterising schizophrenia as a Psychic Process, a basic difference between the primary delusion and the secondary delusion beginning with the study of the structure and content of the delusion, the distinction of Schneider's first and secondary rank symptoms, the distinction of Leonhard's several clinical forms, the phenomenological studies by Conrad (1958), Huber's (1995, 1996) prodromic symptoms, etc., were all established from a natural vision of the illness.
The concept of a bad prognosis of schizophrenia, its incurability, was determined by longitudinal studies with almost no therapeutic intervention. This natural vision of the illness is either captured directly as the disease progresses, or in a retrospective vision by means of anamnesis. Being a chronic illness, the understanding of schizophrenia can only be achieved through a historical personal perspective. How does schizophrenia begin? What are its evolutionary forms? Is it possible to establish a schedule for its clinical forms? Do they follow any criterion, or do they present themselves at random in each patient? Is it possible to establish a prognosis according to the type of beginning, as it is usually said: acute beginning, good prognosis; insidious beginning, bad prognosis? Or establish a prognosis according to the clinical type?
In the schizophrenic syndromic universe there are significant differences in terms of beginning, course and outcome. What leads to a stabilisation of the disease, a not so intense personality disintegration such as we find in some paranoid psychosis, or to a good outcome through hypomanic, manic or depressive episodes such as in some hebephrenia? Is it possible to compare an akinetic catatonia to a paranoid-hallucinatory schizophrenia? What can be said about the patient's having a certain clinical presentation at the beginning, and then another one, then returning to the previous form, etc? The symptomatological arrangements (syndromes) identified as hebephrenic, paranoid, catatonic, etc., seem to be not really types or forms of schizophrenia, but states (clinical states), transient states of just one psychopathological unity.
Is there really an acute beginning in schizophrenia, or only a progressive acuteness (explosion of pseudo-hallucinations and primary delusional experiences, or catatonic states, or a highly stressing delusional mood) of a process which is being brewed for some time? Authors such as Weitbrecht (1970) and Huber (1995) observe a gradual beginning of the psychosis, which could extend for months or years, with a relative social adaptation. In many cases, over many years delusions and hallucinatory experiences are encapsulated; in these cases, psychopathological signs would only be identified at the personality level. As it is known, these signs are often only considered as personal extravagances. Other symptoms, such as Huber's (1995) prodromic symptoms, can extend for years without interfering significantly in the life of the patient, or leading to medical identification. Hafner identified a gap of more than four years between the onset of schizophrenia and first-time hospitalisation.
Often the beginning of some gradual process is very rich in experiences of strangeness in relation to the self (depersonalisation) and the world (derealisation). Sometimes it can be a particular mood (delusional mood of Grühle) with vague feelings, no clear suspicions, or obsessive-compulsive phenomena with experiences of strangeness, perplexity, delusional ideas of influence and end of world. Some patients live a strange gradual dissolution of the personality, a progressive feeling of uselessness and powerlessness. In some other cases of a more rapid explosion of the schizophrenic process, the patients notice themselves submerged and possessed by a gigantic complex of delusions and hallucinations developed in an atmosphere of intense agitation or beatific serenity (Hojaij, 1985).
Conrad (1958) gives a very impressive description of the beginning of the schizophrenic process in his book “Incipient Schizophrenia.” Studying 117 male soldiers (1941-1942) with recent first episodes, Conrad defines a detailed structure and process for the schizophrenic experience: 1. trema (prodromal phase: anxiety, threatening, fears, feelings of guilt, sinfulness, hopelessness, thought blocking, feeling of dissolution, suspicions, self-absorbed); 2. apophenia (consciousness of abnormal meaning to everything: delusions); 3. anastrophe (consciousness that everything is related to the patient); 4. apocalipse (catatonic behaviour); 5. consolidation (gradual reduction of the level of symptoms and some adaptation to them) 6. residual (loosening of will and impulse to life).
In relation to the diagnosis of schizophrenia there are still all kinds of conflicts. All the extraordinary technological advances of cerebral investigation have, to date, not been able to get close to the truth of schizophrenia. Sometimes the studies give an impression of "shooting at random," trying to come across fortuitous cerebral findings which then might be related to the schizophrenic symptomatology. The fact is that, as the laboratory investigation is not forestalled by a correct clinical investigation, by rigorous psychiatric propaedeutics, any and all findings will be the object of mere speculation without underlying principles (Hojaij, 1995). It is evident that this scission between the clinical reality and the basic investigation contributes to many frustrated attempts at understanding schizophrenia. The same call has been recently made by Andreasen (1998): "Therefore, we need to make a serious investment in training a new generation of real experts in the science and art of psychopathology. Otherwise, we high-tech scientists may wake up in ten years and discover that we face a silent spring. Applying technology without the companionship of wise clinicians with specific expertise in psychopathology will be a lonely, sterile, and perhaps fruitless enterprise."
Following Schneider (1959), it is not possible to say "this is schizophrenia" (at his time and until now there has been no clear somatic data), but just "this is currently designated schizophrenia." There is not a positive and conclusive statement on the clinical diagnosis of schizophrenia as a disease. The classical medical diagnosis (encompassing aetiology, pathogenesis, clinical picture, treatment, etc.) cannot be currently reached for schizophrenia. The diagnosis is just under the psychopathological level, and sometimes a fluid and vague impression to be further confirmed by means of a detailed phenomenological investigation. All the tentative steps to reach a consensus in terms of diagnosis for schizophrenia crashes into the absence of definite somatic base and into the kaleidoscopic richness of this intricate phenomenon. At the end, there is always a diagnosis for close estimation.
Which is the best consideration for the diagnosis: the clinical form, that is, a set of symptoms, or types of outcome? From a strict clinical point of view, it is necessary to combine the cross-sectional examination of the symptomatology with the long-term observation (via anamnesis and/or via direct follow-up). As a process, schizophrenia must be grasped in longitudinal perspective, and as an illness suffered by someone must be apprehended immediately through the mental state examination.
It should be mentioned that an epidemiological analysis of Conrad's work has been performed by Hambrecht and Hafner, partially validating his findings (Hafner, 1995). The Iowa 500 Study (Winokur and Tsuang, 1996) is a modern and controversial naturalistic longitudinal approach to schizophrenia (and depression and mania) touching many of the important aspects pointed out in this paper.
Undoubtedly, the restoration of anamnesis is essential. Anamnesis is a joint journey allowing revelation of the nearly entire peculiarity of each patient, and cannot, by no means, be substituted by structural interviews. The dilemma is how to find a way of returning to the peculiar anamnesis and develop a reliable objectivity to the descriptions.
Schizophrenia is considered a splitting illness, a splitting process, a splitting structure, a splitting person, a person split from his own original vital history, a person split from the common world. If this particular aspect is taken into account, a descriptive phenomenological criterion from classical authors (despite some personal differences) is still necessary to give some certainty in terms of diagnosis. Thus, there will be comparison not just of clusters of symptoms, but with the complete clinical picture in its whole sense, as well.
It is not the intention of this paper to go into a discussion about the structured interviews and the operational diagnosis. For the diagnosis of schizophrenia, in the absence of biological markers, the importance relies, most of the time, on symptoms of a qualitative and subjective nature. On the other hand, the measurement (it does not matter how well-constructed a structured interview is in terms of reliability and validity, and how excellent are the operational definitions) will always be executed by a person, and subject to the level of knowledge and expertise of this person.
There is a direct proportionality between the number of “somatic symptoms" and reliability in a way that organic and psychotic disorders have higher reliability than neuroses and personality disorders (Kendell, 1992). Thus, if the assessment is not made by an experienced researcher, able to detect sometimes a sophisticated psychopathology, the result will be restricted not by the rating scale but by the clinician. Kendell (1992) advocates the use of the structured interviews by "skilled hands," and alerts that “clinical judgments, whether they concern depersonalisation or bronchial breathing, are inevitably imprecise and imperfect, and the best we can do is to understand what the problems are and do our best to minimise them."
The so-called operational diagnosis has not been able to offer a solution, and what happens is almost a neglect of the patient. There are diagnoses of questionable validity based on questionnaires tested in origin by non-psychiatrists (DSM-III 1980) trying to accommodate the patient within some diagnostic box. These sorts of diagnostic tools are often simplistic (although including some classical concepts), made by a descriptive behaviourist and are of a statistical nature, leading to classifications (ICD-10 1992 and DSM-IV 1994) composed by a strange and incompatible mixture of symptomatological, syndromal and etiological structures (Hojaij,1994). One cannot leave aside the fact that some researchers who are tied to modern classifying systems (DSM and CID types) may be determining limitations and distortions in clinical research.
To surpass this impasse in the area of diagnosis, psychopathology must be reintegrated in psychiatric research and practice. There is a need to rehabilitate the phenomenological description which admits the wealth of special inner experiences, the same phenomenological description that originated the definition of Bleuler's (1950) fundamental symptoms and allowed this author to create the term schizophrenia, or Schneider's (1959) first-rank symptoms, or the phenomenological psychopathology which allowed Jaspers (1977) to elaborate the idea of Psychic Process, or Binswanger (1972) penetration into the intimate living of the schizophrenic. From the psychiatrist side, Weitbrecht (1970) uses the expression "schizophrenic atmosphere" to be apprehended by the experienced clinician. Should the “precocious feeling” by Rümke (1942) be put aside when facing a lack of spontaneous, non-reflexive, naive happiness? Or a cold, indifferent, self-engrossed, non-spontaneous, affected, formalistic, rigid, pompous (paranoid) person? The great challenge for a psychopathologist is to transform all the subjective data elicited from the patient and others into objective and shared data. This is a task for many psychiatrists, for many years.
The investigation of schizophrenia cannot be developed without the observation, intuition, knowledge and experience of the psychiatrist. Therefore, as in the rest of Medicine (and life in general), the aptitude for diagnosis develops along with the clinical practice and the identification of complex entities is sometimes - one most admit - reserved for the most experienced.
Apropos, it is worth to bring back this quote by Schneider (1959): “Experience shows us that it is often difficult to establish a psychiatric diagnosis from a psychopathological finding. In this case, it does not mean from the beginning, to add and combine symptoms perceived and demonstrate objectively, as in a somatic diagnosis, but of a judgment of manifested life experiences, of an evaluation of behaviour and of attitudes of the patient and the consideration of the impressions of the examiner." Leme Lopes (1980), commenting on the great challenge that is the diagnosis of schizophrenia, said: "To work with such a vast keyboard one has to be a good player. And this is an ability which can only be progressively attained while one practices this difficult science which is Psychiatry."
A great responsibility in the diagnosis process lies on genetic studies, not only of family lineage, but mainly those related to the study of gene anomalies. Interestingly, epidemiological conclusions (Hafner, 1991; Jablenski et al., 1992) are concordant in relation to the worldwide distribution of schizophrenia, pointing out the relevant genetic factors that should show up in genetic research. Hopefully, accurate genetic findings will be able to provide an explanation for the cause of schizophrenia and help in the prevention and treatment; but genetics maybe will not provide an understanding of the symptomatology and the whole and absolute transformation of the personality. As Wyrsch (1957) said: "Everything indicates that the disorder occurs where a person is contained as a single unit, where the psyche arises, and where the spiritual person is possible. In this sense, schizophrenia is, among all the psychiatric illnesses, the one that can best be designated a disease of spirit (Geisteskrankheit).
Are the methodologies used in the study of schizophrenia appropriate, or are we still living the precarious body-soul dichotomy, and therefore looking for motivations of all kinds (meaningful connections), or strictly matter alterations for the explanation (causal methodology) of an illness which comprises the totality of the personality? It should be reinforced that the two fundamental psychopathological methods introduced by Jaspers (1997) do not exclude each other and should be used in a complementary way. In the current epistemological situation, a dialectic use of both methods brings the opportunity to progress further into the neuroscience investigation related to and anticipated by correct phenomenological psychopathology. Since there is no unitary method for approaching the mentally disturbed human being, the two methods should be used appropriately to compose the best approximate picture.
Concerning the genesis of schizophrenia, should one speculate, dare and experience an area of research that would consider not only the neurotransmitter systems (Sokoloff et a1., 1995; Iqbal and Van Praag, 1995) or specific cerebral areas (Taylor, 1995), or certain enzymes such as, for instance, glutamate (Ebert et a1., 1995), or neuropeptides (Verhoeven, 1995), but an area of research - considering the illness as having reached the totality of the person - such as the irradiating energy in the brain? (Popper and Eccles, 1977). Should one look for more than an alteration of matter, try more than to relate motivational situations, distinguish, locate and measure energetic systems, or even further, consider an energetic meta-structure (Hojaij 1996a)?
Through the effective introduction of modern therapeutic techniques, the observation of schizophrenia in natural evolution has been practically suppressed. The schizophrenics are all found (or almost all) maculated by therapeutics; symptoms are weakened or disappear (delusions and hallucinatory experiences), others appear directly promoted by drugs (neuroleptic apathy) and others as a consequence of neuropathological alterations (tardive dyskinesia). On the other hand, during the symptomatological course after an acute outbreak, symptoms of a depressive nature may occur which, for a long time, had been considered not to be related to schizophrenia.
Delay (1961) already commented about the transformation of symptomatology and the evolution of psychosis as a result of antipsychotics: "This transformation possibly represents the deepest and true 'revolution' due to the new therapeutic method." Therefore, this pharmacological effect has increased the cases of the so-called incipient schizophrenia and residual schizophrenia. Delay, so long ago alerted: "It is necessary to have great patience and a solid clinical experience to distinguish banal symptoms of asthenia from lack of concentration, instability or professional maladjustment from those due to a psychosis or neurosis, or even a problem of medication. The classical 'macroscopic' symptomatology tends to be substituted by a finer symptomatology…"
However, in the last five decades a certain therapeutic enthusiasm has been observed. The so-called antipsychotics present an ample spectrum of clinical action and are handled relatively easily, thus giving chance to a ready therapeutic intervention. This intervention may end up erasing the clinical picture of the psychosis before the diagnosis is completed. If the use of antipsychotics is used in larger doses than those suitable for that patient in particular, the pharmacological blot reaches a dimension that surpasses the symptomatology of the psychosis: the totality of the psychic life ends up by deteriorating. Consequently, this untimely therapeutic intervention may be one of the factors responsible because the exact knowledge of schizophrenia has progressively been lost in the last decades. There is no doubt that a quick therapy is necessary, especially knowing that a precocious beginning in the treatment of schizophrenia, in general, allows a more favourable prognosis. However, the dramatics of the clinical picture must not correspond to a violent intervention.
It may be said that the traditional antipsychotics and the “novel antipsychotics” do not touch the essence of schizophrenia: 1. they act as a temporary delusion's and hallucination' solvents; 2. they gradually erode (not completely) the psychosis, allowing certain return of the natural life categories (Hojaij 1987); 3. they permit some return of the personality modulation, but not to a completely recovery; 4. they promote a change in the schizophrenic psychopathology, the main evident symptoms are abolished and the fundamental psychotic structures like pure defect (Huber 1972) and comprehension disturbance (Hojaij 1987) start to appear more clearly.
Treatment resistance of endogenous psychosis derives from the lack of knowledge of aetiology, as well as from the restricted efficacy of current therapeutics. Despite the great progress made since 1952, and particularly the introduction of the so-called atypical antipsychotics, the schizophrenic reality resists treatment, or is revealed in a greater or lesser degree of an affective-volitional dullness, or in personality disorders.
Some interesting questions should be considered: In which way do the antipsychotics modify the psychopathology of schizophrenia? Which symptoms remit or simply have reduced their intensity and remain during the entire course of the psychosis, and which of them resist current therapeutics? Which are the most favoured clinical forms? Can new determined pharmacological clinical subtypes be defined? Which are the long-term therapeutics effects observed? As regards the current drugs, is it possible to suppress the antipsychotics after a certain period of use? (Johnstone, 1991). Does the delusional nucleus disappear completely? Are new types of “defects" coming up with current therapies? The investigation should be open to look for new symptoms that could come up during the treatment, besides those caused by the anti-psychotics.
Since there is no complete psychopathological resolution due to psychopharmacotherapy, the symptomatological cleaning by means of antipsychotics should lead to a more profound investigation of the most original (or resistant) schizophrenic symptomatology. Perhaps, from this perspective, the psychopathological research could progress and direct itself to the core and essence of psychosis (Hojaij, 1987).
The social-cultural influence
Forms of social organisation in the last decades, with life predominately in big cities which favours anonymity, offer a favourable field for the easy mimetic of schizophrenics in marginal groups, or the acceptance of their extravagances due to the loosening of social values. In one way or another, this may influence the diagnosis, and thus the indices of incidence and prevalence can be underestimated. On the other hand, it is important to verify up to which point the intense social factors, with current characteristics of rapid transformation and great pressure on individuals, only remain as pathoplastic factors with no direct interference in the form, course and evolution of schizophrenia.
Considering the advances of modern biology and evolutionary theory it is valid to hypothesise that some genetic mutation is forced by significant and persistent social and cultural factors. Apart from vulnerability issues (Hafner, 1991), researchers should be prepared for a structural change in schizophrenia reflecting its symptomatology, evolution and results to treatment.
It is necessary to take into consideration "ambulatory schizophrenia" in opposition to an "asylum schizophrenia" (or "hospital schizophrenia"). The deteriorating pictures of bygone days have given place to pseudo-psychopathic forms, with significant relief of the productive symptoms. Today, the patient is always under demanding situations, social life is much more intense, professional life is very diversified in big cities, which permits a relative adaptation of schizophrenics, and accentuated non-deterioration (just a psychological character of dullness). A great number of them are capable of social readjustment and to re-establish - to a greater or lesser degree - a work productivity. The acknowledgment of "ambulatory schizophrenia" compels the question: Is schizophrenia today studied in an outpatient service, identical in its clinical forms and evolution to schizophrenia classically attended and studied in hospital?
To go beyond
For 100 years the history of psychiatry has evolved around schizophrenia. How is it possible that a certain psychopathological syndrome, so fundamental to the human being, has not been completely disclosed yet? How many thousands of studies of all kinds have been looked up in all the libraries of the world without ever having reached the necessary precision in conclusions? How the researchers have treated Dementia Praecox over these 100 years? What should be done from now on? (Hojaij 1996b).
Schizophrenia still needs a solid theory. It is an excellent field to conceive from the perspective of an evolutionary (Crow, 1995), neurodevelopmental (Weinberger, 1995), neurophysiological (Pantelis et a1., 1996; Pantelis and Brewer, 1996) disease. In methodology, the object of study, schizophrenia is completely different from all other psychiatric syndromes such as Major Depression, Organic Psychosis and Personality Disorder, in the sense that it is innovative and absolutely transforms the whole personality. It is a special condition of the human being. From an evolutionary and integrative conception (Popper and Eccles, 1977; Eccles, 1979; Eccles, 1992), the schizophrenic could be considered a being (human being) with a disturbance of consciousness, a disturbance of self-consciousness (Hojaij, 1987).
Considering that all organisms have a purpose (intentionality) in their actions (von Uexkull cited in Hoff, 1955), the person considered schizophrenic is making use (for some unknown reason) of non-common associations of neuronal systems. Perhaps the problem would not strictly be in the central-neuronal-system, or in the brain specifically, but in the way self-consciousness makes use of these neuronal systems. The music is no longer good - not because the music itself is not good or because the musicians are bad now - but because the conductor (the self-consciousness) is not all right. A deeper study of the self-consciousness, in conjunction with new methods and techniques looking for the energy in the brain, would be an interesting and challenging proposition. However, no matter the method, the original apprehension will come from the psychopathological approach.
Improvements to the studies of the predictors (Parnas and Mednick, 1991) and early recognition of schizophrenia (Gross et al., 1992; Huber, 1995; McGorry et al., 1996) are still needed, under the idea that precocious diagnosis means early treatment and better outcome. But there is also a need for long-term studies, since the disease has, until now and despite the many good social outcomes, an irreversible character. This perspective will help in the search for a real anti-schizophrenic drug (not an “antipsychotic" that acts only symptomatologically), a drug that goes into the disease initiating a specific electromagnetic cascade, or more appropriately a reorganisation of brain’s electromagnetic activity.
A pattern of mental illness, or a radical transformation of the human way of being, schizophrenia remains an enigma from the medical point of view. A hundred years of clinical investigation and cerebral explorations have not been enough to elucidate the real sacred illness. Only the united efforts of experienced clinicians and basic researchers with a clinical vision may bring the answers related to the origin and essence of schizophrenia.
However, when that time comes true, psychiatry will lose plenty of its charm.
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