Schizophrenia/Dementia Praecox: Emergence of the Concept

   (See also Psychosis: Emergence; Schizophrenia: Recent Concepts; Unitary Psychosis; Wernicke–Kleist–Leonhard Pathway.)

   Schizophrenia remains among the most puzzling of all diseases in psychiatry because there is no single symptom characteristic of it. Nor is there a common course for all patients, for some do well, although the majority do not. Nor is there a common outcome of treatment, for some patients respond nicely to antipsychotic drugs, others not at all. (Nor a characteristic family history, for some have family trees laden with illness; for others, the illness comes, sometimes as late as mid-life, as a complete surprise.) It is tempting, of course, to see in "schizophrenia" a collecting basin for a number of different illnesses. Yet to date, despite decades of intense research, distinctive subtypes have not been teased out.

   The concept of schizophrenia emerged as an amalgam of earlier diagnoses. It became conceived as an outcome rather than a typical symptom picture at any moment in time. Many diverse clinical presentations could end up having the same outcome, namely, in the language of the day, "dementia."

   Dementia praecox (démence précoce) (1860). In his Textbook of Mental Illnesses (Traité des maladies mentales), Bénédict-Augustin Morel characterized a distinctive kind of adolescent insanity (folie) that he considered hereditary and degenerative in the sense of worsening from one generation to the next. Striking in the teenage years, dementia praecox ultimately eventuated in premature "dementia" (in the nineteenthcentury meaning of incoherence rather than low intelligence). Although Morel had used the term in passing in 1853, only here did he characterize it more fully, describing for example a youth of 14 years of age who "progressively forgot all he had learned at school; his brilliant intellectual faculties underwent a very disquieting interruption. A kind of torpor close to hebetude took over from his earlier activities and when I saw him again [later in adolescence], I felt that the fatal transition to the state of premature dementia [démence précoce] was underway. This desperate prognosis is ordinarily far from the minds of parents and even of the physicians who care for these children" (p. 566).

   Morel was the first psychiatric writer to use the label "premature dementia" for what was later called schizophrenia. But, he also was the first psychiatrist to classify psychotic illnesses on the basis of outcome rather than clinical presentation at a given moment in time. He drew up an entire class of insanity, of varying causes and symptoms, that had in common the termination in dementia: "The special state designated by the term dementia will be the terminal form of various mental afflictions, and will represent the most numerous class of patients accommodated in our asylums" (p. vi.) Kahlbaum’s Vesania typica (typical insanity) (1863). Part of the nosology of the Prussian psychiatrist Karl Ludwig Kahlbaum was based on outcome rather than momentary clinical picture. In his Classification of Mental Disorders (Die Gruppirung der psychischen Krankheiten, 1863), Kahlbaum was struck that there seemed to be two classes of illness than ran downhill irreversibly ("progressively") into dementia. One was what Bayle described (understood only in hindsight) as the syphilitic infiltration of the central nervous system, later called neurosyphilis (at the time progressive paralysis). The other Kahlbaum simply labeled Vesania typica, "typical insanity of the brain that includes all functions . . . until finally the onset of dementia occurs and mental life sinks away" (pp. 84–85). There is no doubt that many cases of what later was called schizophrenia were included in this set of outcomes.

   Hebephrenia (1871). After Kahlbaum left the Allenberg asylum in 1867, he acquired a post at a private nervous clinic in the East Prussian town of Görlitz, and took his assistant Ewald Hecker (1843–1909) with him. At Görlitz, in the youth division of the clinic, the two men saw a number of young male patients with premature dementia. In 1871, in an article in the Archive of Pathological Anatomy and Physiology for Clinical Medicine (Archiv für pathologische Anatomie und Physiologie für klinische Medizin), Hecker offered a portrait of these patients, who presented a constantly changing series of clinical pictures before ending in dementia, suffering from what Kahlbaum had called in his lectures "hebephrenia."

   Of the perhaps 500 adolescent patients whom Kahlbaum and Hecker had seen in Allenberg and Görlitz, 14 had the characteristic course of "hebephrenic dementia": Hecker emphasized the disorganized nature of their late-adolescent behavior (hence the Greek "hebe" for youth plus "phrenia" for mind): "First of all they show a distinctive deviation from logical sentence building . . . a characteristic indifference in the stringing together of sentences and the inability to conclude a thought in a precise way" (p. 404). Hecker continued, "There is also a very pronounced tendency . . . to mix up the language and to speak and write in a strange jargon." The young patients then progress, via mixed episodes of mania and melancholia, to a dulled form of dementia, interrupted by momentary bursts of agitation and periodic bouts of hallucinations, especially of the auditory variety. The dementia is terminal. No other psychiatric illnesses are characterized by onset at the time of puberty and an inevitable progression to early dementia. This description served Emil Kraepelin as a model for dementia praecox (see below).

   Catatonia (1874). Catatonia means motor (muscle or movement) abnormalities— in the context of psychiatric illness—and today one distinguishes conventionally between catatonic excitement (an increase in spontaneous and purposeless movements) and catatonic stupor (the opposite); motor stereotypies, waxy flexibility, proskinesis, parakinesis and numerous mannerisms constitute additional motor symptoms. Yet catatonia figures in the schizophrenia narrative mainly because Kraepelin considered certain aspects of it as hallmarks of dementia praecox. (Catatonia may be found as well in delirium, depression, and in manic-depressive illness, but certain symptoms such as posturing [remaining in a fixed position], echolalia [repeating a doctor’s question], and echopraxia [doing as the examiner is doing] are virtually pathognomic for schizophrenia.)

   The term "catatonia" was coined by Karl Ludwig Kahlbaum in an 1874 monograph (Die Katatonie, oder das Spannungsirresein), but he had used it in public lectures since 1868. The phenomenon had, however, been long familiar in psychiatry and was recognized as part of the immobile apathy traditionally called melancholia attonita (attonita_thunderstruck). Schizophrenic symptoms were part of the clinical course that Kahlbaum depicted: "Catatonia is a brain disease with a cyclically variable course, in which melancholia, mania, stupor, confusion and finally dementia succeed one another" (p. 87). As for a cause, Kahlbaum attributed it to some kind of neurological convulsion. In fact, as German Berrios has shown in a reanalysis of Kahlbaum’s 31 cases, most of Kahlbaum’s patients probably had some kind of organic delirium or psychotic depression rather than schizophrenia (History of Mental Symptoms, pp. 382–383).

   Schizophrenia and Emil Kraepelin’s dementia praecox (from 1893). Emil Kraepelin, who characterized the illness dementia praecox, emerges as arguably the central figure in the history of modern psychiatry. His achievements were (1) to differentiate schizophrenia as an independent illness and not just a late-stage consequence of some other primary disorder; (2) to establish diseases on the basis of outcome (course) rather than clinical picture at a given moment; and (3) to erect "dementia praecox" (later called schizophrenia) and manic-depressive illness as the chief disease entities of psychiatry. Even today these traditions, for better or worse, are much alive in psychiatry.

   It was only in the fourth edition of his textbook, in 1893, a year after arriving in Heidelberg, that Kraepelin used the term "dementia praecox." Kraepelin cited Karl Kahlbaum and Hecker as intellectual forbears rather than Bénédict-Augustin Morel. In the time since Morel had written, numerous European psychiatrists had described the same clinical picture of premature "dementia." It was Kraepelin’s accomplishment to bring together under a single roof these various partial descriptions of démence précoce, Vesania typica, hebephrenia, catatonia, and the like: making of them a single well-defined disease—distinct from depression and manic-depressive illness—having a familiar set of symptoms and a predictable, indeed, inevitable course, the convergent path of deterioration. In this fourth edition, he assigned dementia praecox (DP) to the "psychic degenerative processes," alongside catatonia and "dementia paranoides" (a form of illness that Kraepelin had separated from Kahlbaum’s "paranoia," by which Kraepelin meant sudden-onset psychosis that progresses to "feeble-minded confusion" (p. 456). The prognosis of DP was gloomy: "The further course of these cases diverges to the extent that sometimes dementia sets in quickly, sometimes more slowly, and may cease to advance at often highly variable stages" (p. 438).

   In this and several subsequent editions, Kraepelin left psychoses that were con-fined mainly to delusional disorders without deterioration as a separate category: "Madness (paranoia)" (die Verrücktheit [Paranoia]); they were not part of any larger disease class. (See Paranoia.)

   In the fifth edition of his text in 1896, Kraepelin made DP part of the "metabolic disorders leading to dementia," again alongside catatonia and dementia paranoides. In the sixth edition in 1899, Kraepelin distinguished between the two great psychiatric diseases that would imprint psychiatry for the next 100 years: dementia praecox and manic-depressive illness, today called "bipolar disorder." (See Manic-Depressive Illness [1899].) DP now included dementia paranoides and catatonia, expressing itself in three forms: the hebephrenic, the catatonic, and the paranoid. These subdivisions as well would survive for decades.

   In the seventh edition in 1904, Kraepelin changed little, merely adding a tiny ray of hope in the discussion of outcomes: "In a small number of cases of dementia praecox, a complete recovery does seem to take place." The point was grudgingly made. Yet, he added a second category that, in view of discussions of outcome in previous editions, also sounded rather optimistic: "In any event, much more frequent is recovery with a deficit" (Heilung mit Defekt). After all symptoms had fled, the patient remained rather enfeebled (Psychiatrie, 7th ed., II, pp. 261–262).

   In the eighth edition, which started appearing in 1909, the last he was to complete himself, in volume III(2) (1913), Kraepelin took DP from the independent causal status it had occupied in the several previous editions (meaning not part of any larger illness) and attached it to "the endogenous dementias" (die endogenen Verblödungen). In the discussion of prognosis he now admitted that 26% of these patients experienced some form of remission, if even only of a few months (vol. III[2], pp. 862–863). In this volume, Kraepelin shifted some periodic forms of psychosis from the manic-depressive group to dementia praecox. (See Psychosis: Emergence: periodic catatonia [1932 and after].) The periodically repeating episodes appear to come out of the blue, with recovery just as quickly. Many patients, after a series of attacks stay well; others deteriorate.

   Kraepelin had hoped that the resemblance of dementia praecox to neurosyphilis ("progressive paralysis") would ultimately vindicate his assertion that DP was a unitary disease with a common clinical course and outcome. The clinical picture of neurosyphilis at any given moment was quite varied, just as that of DP: "What turns out in the end to be Paralysis," he wrote in 1909, "is a disease process with a unitary cause, a definite clinical course and a clear anatomical basis. On the other hand, the momentary clinical pictures show such a confusing variegation that on the basis of symptom picture alone it never would have been possible to recognize their common identity. . . . It is to be expected that the clarification of our other tentative large clinical entities [such as DP] will be achieved in a similar manner" (eighth edition, 1909, pp. 526–527).

   On balance, some contemporaries were enthusiastic about Kraepelin’s great concept of the two different diseases because they thought it made possible the prediction of prognosis. As Tübingen psychiatry professor Robert Gaupp (1870–1953) pointed out in 1926, "Every clinical concept is obliged to demonstrate its merit in its ability to tell, for an individual patient, what happens next. The prognosis is the measure of all of our scientific accomplishment" (Archiv für Psychiatrie und Nervenkrankheiten, pp. 77–78). One notes that predicting treatment response was still far from anyone’s mind in the uses of diagnosis, because there were no treatments.

   Stransky’s intrapsychic ataxia (1903). Vienna psychiatrist Erwin Stransky (1877–1962) was uneasy about Kraepelin’s notion of "dementia," because in fact the patients seemed more to suffer from a loosening of associations than from dementia as such. He referred to this "functional disharmony" among various parts of the psyche as "intrapsychic ataxia," and emphasized such symptoms as language confusion, paralogia (perverted logic), and the "derailment of volition" (or Entgleisung). In brief, a dementia-psychosis had turned into a derailment-psychosis. Stransky’s first contribution appeared in 1903 in the Yearbook of Psychiatry and Neurology (Jahrbuch für Psychiatrie und Neurologie). Stransky had formulated the concept of intrapsychic "schism" and was disappointed when in 1908 Bleuler coined it as schizophrenia. Stransky later said that his idea had been overwhelmed by the psychoanalytic express train coming out of Vienna and running through Bleuler’s Zurich (Swiss Archive of Neurology and Psychiatry [Schweizer Archiv für Neurologie und Psychiatrie], 1954, p. 323). Kraepelin acknowledged Stransky’s work in the eighth edition (1913) of his textbook (p. 747).

   Bleuler’s schizophrenia (1908, 1911). Bleuler rebaptized Kraepelin’s dementia praecox as "schizophrenia" at the annual meeting of the German Psychiatric Association in Berlin in 1908, saying he preferred "schizophrenia" because dementia praecox lent itself so poorly to use as an adjective and because he considered that there was some kind of "split" in psychic function. Up to that point, 647 patients with the diagnosis schizophrenia had been admitted to the Burghölzli in Zurich, and Bleuler had a good overview. The disease Bleuler described was much milder and broader than Kraepelin’s, fully 73% of the acute cases going on to have relatively normal lives (though none fully recovered). The paranoid variety had a better prognosis than the catatonic, although Bleuler despaired at isolating truly distinctive subgroups within the illness. So upbeat was Bleuler about the general course of the illness (in contrast to the substantial gloom of Kraepelin) that Bleuler preferred to speak of illness episodes (Schübe) from a presumably normal state rather than of relapses (Rezidiven) from an abnormal underlying state.

   Most at variance from Kraepelin were Bleuler’s notions of the "primary," or core, symptoms—meaning part of the basic illness process—and "secondary" reactions of the patient to the environment or to the illness. By secondary, Bleuler understood virtually all the symptoms that Kraepelin had considered usually present in dementia praecox: hallucinations, delusions, social isolation, even deterioration ("dementia"). Bleuler considered even such symptoms as negativism and mutism secondary because they were subject to "psychic influences." To the ranks of primary symptoms, Bleuler assigned the neurological changes, such as differences in the pupils of the eye, a certain intellectual slowing and dazedness, and most importantly, "changes in associations" (meaning logical thought): "In schizophrenia, it is as though the physiological controls and channels [of thought] go amiss; the familiar normal pathways are not so sought out and the train of thought is easily lost in unfamiliar, false pathways. Thus the train of associations is given over to incidental influences, above all, emotional in nature, which leads to a partial or a complete loss of logical function." It was this loss of logic in schizophrenia, rather than "dementia" (which Bleuler considered easily reversible) that characterized the illness (General Journal of Psychiatry [Allgemeine Zeitschrift für Psychiatrie], 1908, p. 457). (Kraepelin found distinctions between primary and secondary symptoms "artificial.")

   By the time of his 1911 book, Dementia Praecox, or The Group of Schizophrenias (Dementia Praecox oder Gruppe der Schizophrenien), Bleuler was calling primary symptoms "basic symptoms" (Grundsymptome) and secondary symptoms "accessory." Later usage would deem the basic symptoms to be "negative," meaning social withdrawal and the blocking of affect, the accessory symptoms "positive," meaning hallucinations and delusions. (See Positive vs. Negative Symptoms.) By 1911, Bleuler had provisionally settled on four subtypes of the disease: paranoid, catatonic, hebephrenic and "simple" (only a few specific basic symptoms) (p. 7). Among the basic symptoms he had added "relationship to reality: autism."* "The sickest patients . . . live in a world of their own; they have cocooned into themselves [verpuppen] with their wishes, which they see as fulfilled, or with the misery of their persecution, and they restrict contact with the outside world as much as possible. This dereism [Loslösung von der Wirklichkeit] together with the relative and absolute predominance of their interior life we refer to as autism" (p. 52).

   The passage from dementia praecox to schizophrenia was a transition from clinical course to the structure of thought. The difference between Kraepelinian and Bleulerian concepts of schizophrenia would continue to resonate. Said Hans Walther Gruhle (1880–1958) at Heidelberg in 1931: "Physicians who see every eccentric personality, every lonely person, as an undiagnosed schizophrenic, will naturally have different views about the arrest of the illness, or its practical cure, than those who make a demonstrable acute psychotic phase a precondition of the diagnosis" (p. 25). Bleuler’s schizophrenia greatly expanded the circumference of the diagnosis, as opposed to Kraepelin’s more austere version. With Bleuler’s definition, a number of rather vague symptoms could qualify as evidence of the disease. As psychopharmacologist Paul Janssen (1926–2003) observed later, "The etiology of schizophrenia is Dr. Bleuler" (Healy, Psychopharmacologists, II, p. 60).

   First finding of large anatomical changes in brains of patients with schizophrenia (1914). In 1910, Elmer Ernest Southard (1876–1920), director of the psychopathic department of the Boston State Hospital and professor of neuropathology at Harvard, began the systematic microscopic and macroscopic examination of randomly selected brains of deceased schizophrenic patients, concentrating especially on structural abnormalities visible to the naked eye. Of the 50 brains he examined, he noted, in an article in the American Journal of Insanity in October 1914, that 45 showed "gross anomalies or other lesions" (p. 387). In particular, in the original group of 28 brains he had studied in 1910, nine had what he called "internal hydrocephalus," or dilatation of the ventricles (noted in the January 1915 issue, p. 639). This finding, * In fact, Bleuler first describes "autism" ("der Autismus") in his 1910 article on "Schizophrenic Negativism" in the Psychiatrisch-Neurologische Wochenschrift (p. 185f ). which went widely unheralded, represents the first linking of schizophrenia to gross (meaning macroscopically visible) anatomical brain changes. Southard did not have a control group of brains of non-ill persons.

   Kraepelin backpedals on the "disease" concept (1920)

   In 1920, toward the end of his life, Kraepelin grew increasingly pessimistic about the possibility of separating dementia praecox from manic-depressive illness on the basis of symptoms alone, so much did the symptoms overlap. Kraepelin now reflected upon Berlin psychiatrist Karl Birnbaum’s (1878–1950) distinction in 1919, in the General Journal of Psychiatry (Allgemeine Zeitschrift für Psychiatrie), between the "pathogenetic" contributions to the clinical illness (meaning the underlying brain forms) and the "pathoplastic" contributions (meaning how the patient responded to illness and environment).

   Kraepelin thought that many symptoms belonged more in the pathoplastic than the pathogenetic group, and were not specifically distinctive, or pathognomonic, in revealing the underlying disease. He thus stepped back somewhat from the "nosological" concept that psychiatry consisted of disease entities and edged toward the notion of illness as nonspecific symptom groups generated by endogenous underlying patterns of brain activity, a viewpoint for which Alfred Hoche had argued. "Every day it becomes clearer that it is impossible to demarcate satisfactorily both illnesses [schizophrenia and MDI]. . . . Yet I believe it remains clear that the notion of basically diffferent illness processes must be retained." His article on "The Manifestations of Insanity" appeared in the Journal of Combined Neurology and Psychiatry (Zeitschrift für die gesamte Neurologie und Psychiatrie) (p. 27). Kurt Schneider said later of this important article, "In this contribution Kraepelin did nothing more and nothing less that give up the basic idea of his life’s work" (Problems of Clinical Psychiatry [Probleme der klinischen Psychiatrie], 1932, p. 21). "Athymhormie" (lack of vital impulse) (1922). Maurice Dide (1873–1944), chief of the Braqueville mental hospital, and Paul Guiraud (1882–1974), one of his staff psychiatrists, proposed in their 1922 textbook, Psychiatry for the Medical Practitioner (La psychiatrie du médecin practicien) a pathogenic mechanism for dementia praecox: disregulation of the suboptic centers of the midbrain—especially the locus niger—as a key factor in the lack of vital force in the illness (dementia praecox they called "a hereditary illness characterized by the fragility and elective involution of groups of neurons that regulate the cenesthetic synthesis and instinctive vital activity" [p. 209]). They proposed rebaptizing dementia praecox as "juvenile athymhormie," suggesting as its central quality "the loss of the élan of the cenesthetic [sense of the body] and affective capacity" (p. 178).

   The choice of this neologism Guiraud explained in his General Psychiatry (Psychiatrie générale) in 1950 as follows: "We wanted to suggest that the essential element in hebephrenia is . . . a lack of vital dynamism . . . From athymhormie all the essential symptoms are derived: uninterest, inertia, lack of affectivity . . . A lack of physiological dynamism could thus be the result of a lack of cellular dynamism" (pp. 493–494). Henri Ey defined the condition in his 1960 textbook as "a change in affective life: the patient becomes withdrawn into himself, seems indifferent and inattentive to the pleasures and pains of life. This behavior ends up in sulkiness, moroseness, frequently interrupted with paradoxal acts, ideas or sentiments, such as a sudden interest in philosophy or the theater" (Manuel de psychiatrie, p. 479). Today in France, "athymhormie" counts as a deficit or autistic symptom in schizophrenia. Dide, who was active in the Resistance during the war, was arrested by the Gestapo and died in Buchenwald. (The notion of Hormé, or Greek for "I put into motion," enjoyed a certain psychiatric currency in the interwar years, and Zurich neurologist Constantin von Monakow [1853–1930] and psychiatrist Raoul Mourgue in their 1928 book, Biological Introduction to the Study of Neurology and Psychopathology [Introduction biologique à l’étude de la neurologie et de la psychopathologie], speak of the "vital activity" of the brain as part of the "matrix of instincts or Hormé" that differentiate the body and its capacity of self-regeneration from a machine that has been damaged [p. x].) Schizoaffective psychosis (1933). The question of "combined psychoses"— meaning generally a combination of schizophrenia and manic-depressive illness— had long been discussed in clinical circles. In 1903 Tübingen psychiatry professor Robert Gaupp (1870–1953) had examined the "combined psychoses" in the Zentralblatt für Nervenheilkunde, and the phrase "mixed psychoses" (Mischpsychosen) was familiar to German psychopathologists. Identifying such combinations as a homogeneous clinical subgroup was the work of Jacob S. Kasanin (1897–1946), research director of the state hospital in Howard, Rhode Island, who proposed as a separate category of "the acute schizoaffective psychoses" a group of young men and women, "quite well integrated socially, who suddenly blow up in a dramatic psychosis and present a clinical picture which may be called either schizophrenic or affective." There was, Kasanin pointed out, a research tradition of finding so-called schizophrenic features such as catatonia in manic-depressive illness. Yet unlike the cases in the literature, the nine patients whom Kasanin presented did not deteriorate. "Stress" had typically precipitated the illness, which might then recurr over time. Premorbidly, they had healthy personalities. "The fact that there is comparatively little of the extremely bizarre, unusual and mysterious, is what perhaps gives these cases a fairly good chance of recovery" (p. 101).

   In the discussion following Kasanin’s paper at the American Psychiatric Association’s annual meeting in 1932, one participant said, "We have been in the habit of labeling these cases as psychopathic personalities with schizoid make-up or personalities with schizoid substrata. I think the name of schizoaffective is more appropriate" (I. L. Polozker of Detroit, American Journal of Psychiatry, pp. 123).

   Kurt Schneider’s first-rank and second-rank symptoms of schizophrenia (1939). Although Schneider did not believe in the existence of schizophrenia as a separate disease, he nonetheless accepted it as a type of illness. In this type, he distinguished between symptoms that were distinctive to schizophrenia but not seen in normal people or in other types of psychiatric illnesses ("qualitatively abnormal"), and symptoms that represented an exaggeration of otherwise normal types of experiences ("quantitatively [gradmässig] abnormal"). The former he called "first-rank symptoms," the latter "second-rank." Among the first-rank symptoms were delusions (Wahnwahrnehmungen), audible thoughts (Gedankenlautwerden), voices arguing (Stimmen in der Form von Rede und Gegenrede), voices commenting on one’s actions (Begleitung des eigenen Tuns mit halluzinierten Bemerkungen), the belief that one’s bodily organs, especially the sexual organs, are driving one’s behavior (körperliche, insbesondere sexuelle Beeinflussungen), thought withdrawal and influencing by others (Gedankenentzug und Gedankenbeeinflussung), everything "made" by others (alles "Gemachte") in the area of feelings, drives, and the will. (In the 1946 edition of his classification, Contributions to Psychiatry [Beiträge zur Psychiatrie], Schneider added thought-broadcasting (Gedankenausbreitung) to the list of first-rank symptoms [p. 54].) Among the "second-rank symptoms" were hallucinations (Sinnestäuschungen), the experience of thought-slowing (Denkhemmung), the flight of ideas (Ideenflucht), distractedness and perplexity (Zerfahrenheit und Ratlosigkeit), compulsive behavior (der Zwang), sudden delusional notions (der Wahneinfall), out-of-body experiences (die Entfremdungserlebnisse), "most disgruntlements" (die meisten Verstimmungen), and emotional blunting (die erlebte Gefühlsverarmung) (Psychiatric Findings and Psychiatric Diagnosis [Psychischer Befund und Psychiatrische Diagnose], 1939, p. 25). Schneider prided himself on having derived these characteristic features from a careful study of psychopathology based on the work of Karl Jaspers. Schneider later said, "When first-rank symptoms are present, that always means schizophrenia to us, but first-rank symptoms are not always present" (in the journal Progress in Neurology, Psychiatry [Fortschritte der Neurologie, Psychiatrie], 1957, p. 490). (Clive Sidney Mellor [1932–], a psychiatrist at Manchester University, later found that each of the first-rank symptoms occurs in only a minority of schizophrenic patients, the commonest being thought-broadcasting [in 21.4% of a sample of 173 schizophrenics], the least common, impulses "made" by others [2.9%]. See his article in the British Journal of Psychiatry, 1970.)

   Yet Schneider’s most reliable guide to the diagnosis of schizophrenia did not make it into the "first-rank" symptoms but was articulated, almost in passing, in his psychiatric lectures to family doctors (Psychiatrische Vorlesungen für Ärzte) in 1933: "Making the diagnosis from the doctor—patient relationship. [Erfassung aus der Beziehung]: This is in workaday psychiatry usually the method of diagnosis. It concerns what is referred to as rapport or contact. Here the relevant fact is that most schizophrenics simply seem to occupy another, alien space, that one cannot simply relate to them as to a healthy individual or to a psychopath or to a cyclothymic depressive. It is diffi-cult to express it other than in images [elsewhere Schneider spoke of a "glass wall" between the doctor and patient], and it is impossible to articulate this method as a concept " (p. 182 from the second edition in 1936).

   Schizophreniform psychosis (1939). In contrast to the deteriorating form of schizophrenia, there were patients with previously more or less normal personalities who became acutely ill, often in response to stress. It was this kind of reactive schizophrenia that Gabriel Langfeldt (1895–1983), a staff psychiatrist at the university psychiatric clinic in Vinderen, near Oslo, called "schizophreniform." "Schizophrenia-like cases and particularly those revealing manic-depressive features, a strong hereditary taint and reactive . . . precipitation . . . give the best results [with insulin or cardiazol shock treatment], while the typical endogenic process psychoses characterized by depersonalization do not react to the treatment" (pp. 10–11). Langfeldt singled out the "schizophreniform psychoses" as a distinct group after the "typical schizophrenias" have been removed. The former had high rates of spontaneous remission and did well on shock therapy. The diagnosis of "schizophreniform psychosis" became popular because it suggested the existence of a treatment-responsive subpopulation and because clinicians liked its milder prognosis. Langfeldt’s book The Schizophreniform States appeared in 1939 (in Copenhagen, in English). (See also Convulsive Therapy: Chemical.)