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Emil Kraepelin 

Emil Kraepelin
Chapter:
Emil Kraepelin
Author(s):

Edward Shorter

and Max Fink

DOI:
10.1093/med/9780190881191.003.0004
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Kraepelin founded an epoch as no other German had done, indeed as no one else at all.1

Kurt Schneider, 1956

Psychiatry took Kahlbaum’s diagnosis of catatonia, which corresponded to a real clinical entity, and almost discarded it. Kraepelin (pronounced Krep-LEEN), however, picked up catatonia and eternalized it as a subform of dementia praecox; until recently, that is exactly how most clinicians knew catatonia.

The story develops in two lines.2 One line is anatomical localization, seeking the roots of catatonia in specific areas of the brain and treating the clinical symptoms as neurological phenomena. Further chapters will introduce Carl Wernicke and Karl Kleist, who, with such concepts as “disordered motility,” pursued this organic biological agenda.

In a second line, Kahlbaum saw catatonia as a mixture of neurology and psychiatry. Symptoms such as negativism were “phenomena of the disordered action of the will,” meaning the mind. Thus, catatonia depended on psychological sources, on the mind and its derangements. Emil Kraepelin, who makes an appearance in this chapter, continued this psychological analysis and placed great emphasis upon “disorders of the will.” By contrast, Kraepelin’s interest in localizing catatonia in the brain or in neurophysiological fancies was close to zero.

Dementia Praecox Before Kraepelin

Although Kraepelin turned adolescent insanity into a disease of its own—one that represented 50 percent of all admissions to the Heidelberg University Psychiatric Hospital by 1901—he was not the first to come across the concept. It is possible that the incidence of schizophrenia had been rising steadily throughout the nineteenth century.3 In this case, a number of clinicians would have appreciated that here was something new. Among the first to use the term “dementia praecox,” or “la démence précoce,” was French clinician Bénédict-Augustin Morel at the Maréville asylum in eastern France in 1852. “When the manic excitement is not terminated, as frequently happens, by une démence précoce or by death, it invariably results . . . in establishing a kind of order within this extreme disorder.”4 Here, he used the term not as a disease sui generis but as a condition.5 In 1890, René Charpentier, a staff psychiatrist at the Bicêtre Hospice, dilated upon “les démences précoces,”6 and, in 1891, Arnold Pick, at the medical school in Prague charted the “primary chronic dementia (so-called dementia praecox) of youth.”7

When, in 1893, Kraepelin, described “dementia praecox” he could scarcely claim priority for the label. Yet what he recounted was a clear disease entity: “As dementia praecox we designate the subacute development of a distinctive, simple condition of mental weakness in the youthful years.”8 He devoted an extensive section to it, followed by another on catatonia. Catatonia and dementia praecox were, at this point, both distinctive and well-defined disease entities.

Kraepelin Changes His Mind

Between 1893 and the First World War, Emil Kraepelin gave us the disease structure of modern psychiatry. He originated three changes: first, proposing manic-depressive illness and dementia praecox as the basic diseases of psychiatry; second, creating a firewall between them so that, forever after, mood disorders would be quite distinct from “schizophrenia”; and third, creating schizophrenia subtypes, of which catatonia was one. There was no place for anxiety in Kraepelin’s nosology, and, as anxiety later gained prominence, it was owing to the influence of Sigmund Freud. But otherwise the psychiatry of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) series is heavily indebted to the psychiatry of Heidelberg and Munich.

It may seem curious to dwell at such length on the various editions of a textbook—given that journal articles today are the fundamental vehicle for conveying new knowledge. Yet Kraepelin’s textbooks did report new knowledge, and every fresh edition was eagerly awaited. The textbook offered the unity of a “clinical” system of diagnoses—not a system based on pathological anatomy or genetics—that pulled together the sprawl of previous classifications into two master diagnoses: dementia praecox and manic-depressive insanity. And such was the intellectual power of this division that, rightly or wrongly, it has remained with us to this day. In 1926, Swiss-born Adolph Meyer, professor of psychiatry at Johns Hopkins University, called the Kraepelin textbook “the most comprehensive presentation of psychiatry ever written by any one writer.”9

Kraepelin was born in 1856—the same year as Freud—in the North German town of Neustrelitz, then in the Grand Duchy of Mecklenburg-Strelitz; this was before the German unification of 1871. His father was a musician and opera singer, much given to alcohol. Kraepelin was, say his biographers, “a child of the Founding Years of the German Empire. He grew up during the euphoria of the Unification that Bismarck had directed politically and pushed through militarily.” Kraepelin, his biographers continue, “experienced his academic socialization in the medical schools of Würzburg, Munich and Leipzig in the late 1870s and early 80s, those halcyon years of scientific optimism and national self-assertion.”10 He graduated with an MD from Würzburg in 1878, after clerking in Franz von Rinecker’s university psychiatric hospital, then trained in psychiatry for four years in Munich under Bernhard von Gudden (who notably was dragged to his death at the bottom of Lake Starnberg in 1886 by his crazed patient, King Ludwig II).

In the 1880s, a powerful surge began among German psychiatrists away from brain anatomy and toward psychology, and, as historian Eric Engstrom points out, Kraepelin was part of this trend.11 Kraepelin’s psychological interests began with a two-year stint with Wilhelm Wundt, the founder of measurement in experimental psychology, in his laboratory in Leipzig. Simultaneously in Leipzig, Kraepelin worked with neurologist Wilhelm Erb in the outpatient department of the psychiatric hospital. It was apparently on Wundt’s advice that, in 1883, Kraepelin penned the first edition of his psychiatric textbook12, which heavily emphasized the “psychological standpoint of psychiatry . . . as opposed to Berlin-style slicing up the spinal cord,” as Kraepelin told Zurich psychiatrist August Forel.13 The volume went on to become in its subsequent editions the standard world guide to the discipline, comparable to the status of the DSM today.

This first edition gave full measure to motor disorders in psychiatry but under the label of “catalepsy.” Kraepelin, who by this time had accumulated in Würzburg, Munich, and Leipzig about seven years of clinical practice, described “stupor” as “a psychopathic condition in which the perception of the outside world is distorted with hallucinations and delusions, thought is slowed, while the mood is dominated by severe depressive feelings, and the transformation into actions is almost completely blocked.” This was a conventional description of catalepsy, with its waxy flexibility and stupor. Kraepelin considered the prognosis of catalepsy guarded: “Not infrequently does it pass into incurability, and even to death. Seldom does a recovery occur quickly, within a few days, but rather as a rule slowly and with time.” Death, he pointed out, might eventuate through suicide “or through exhaustion as a result of food refusal and the profound depression of all bodily functions.” There was indeed a role for psychotherapy, “but only after the anxious tension begins to subside.”14 It is curious that Kraepelin should have used this phrase without mentioning Kahlbaum’s catatonia. After Kraepelin’s little Compendium appeared, a friend wrote to him in 1885 to ask, “Did you leave out the stupor of the insane . . . catatonia, on purpose, just because of Kahlbaum?”15 Kraepelin’s reply is unknown.

In this first edition, there surfaced a theme that would stay with Kraepelin for the rest of his days and that hallmarked much of the epoch’s psychiatry as well: psychiatric pathology as disorders of the “will.” It was assumed that weak people did insane things because they were lacking in willpower. As Kraepelin explained in 1883, “In fully developed normal people the capability exists, up to a certain extent, of dominating natural drives through a superior will, and of satisfying these drives only when no other rational considerations demand their suppression.”16

In 1886, at 30, Kraepelin was called to the chair of psychiatry at the University of Dorpat (now Tartu), the capital of Estonia. There, at least the middle classes spoke German. In 1887, the second edition appeared, by now entitled Psychiatry: A Short Textbook. Kraepelin acknowledged the existence of Kahlbaum’s catatonia, though only to pour cold water on it. Kraepelin called it “catatonic delusional disorder” (die katatonische Verrücktheit). He said that Kahlbaum had united the various disease pictures in which catatonic symptoms might appear into the single disease entity. “Because this effort appears to me to have had unsatisfactory results, in my own account I have treated separately these highly diverse forms of illness—melancholia attonita, ecstatic insanity—clinically different in course and prognosis.” Kraepelin accepted catatonia as the main stupor diagnosis and left catalepsy behind.17

A third edition in 1889, written at Dorpat, moved even more explicitly to link “catatonic insanity” (“katatonischer Wahnsinn”) to motor disorders. “We are dealing essentially with the acute appearance of confused psychotic ideation and hallucinations having episodic depressive or expansive episodes of agitation, combined with the appearance of a singular psychomotor blocking that manifests itself as catalepsy and tonic cramping.”18 This is tantamount to announcing catatonic insanity as a distinctive psychomotor disease of its own, and the importance of this third edition in 1889 has often been overlooked. (In this edition, Kraepelin said the prognosis was “grim”: “A large number of cases pass into incurable feeble-mindedness.”19 And some of the cases on which he based this judgment were truly grim: a medical student in Dorpat investigated two of the catatonic patients Kraepelin had seen to learn that they had serious brain lesions and had died.20)

In June 1890, with Kahlbaum present in the audience, Kraepelin read a report to the Society of East German Alienists on what he persisted in calling “catalepsy.” Yet the influence of the Wundt years was evident in Kraepelin’s emphasis on “will” and “suggestion”: “The phenomena of experimental catalepsy under hypnosis shine a light on [clinical catalepsy]. [Under hypnosis] catalepsy is obviously only an epiphenomenon of general suggestibility, a particular form of automatic obedience that manifests itself in the involuntary execution of all suggestions coming from outside.”21

It was in these Dorpat years that the importance of clinical course started to dawn on Kraepelin. “[I began to realize] from these continual cases of more or less quickly dementing outcomes that this was hebephrenia as Hecker had conceived it.”22 Kraepelin’s assistant at the time, Leon Daraszkiewicz, became especially interested in this question and wrote his 1891 doctoral dissertation on forms of catatonia that ended in dementia.23 Once again, the theme of disorders that begin in youth and reach a grim end reared its head.

By this time, Kraepelin’s textbook was arousing such interest that he was ready for one of the big psychiatry chairs and simultaneously the direction of a university psychiatric hospital in a main German center. In 1891, he accepted the chair at Heidelberg. He assembled about him residents and associates who would form a tight circle defending his thoughts. For better or worse, Kraepelin now concentrated on the major psychotic illnesses because lesser disorders at Heidelberg fell into the province of neurologist Wilhelm Erb. Aided by his ability to present patients to the students in lectures and get their feedback (which he could not do in Dorpat because he didn’t speak Estonian), Kraepelin now began sorting out the principal disorders requiring institutional care.24

In the fourth edition of the textbook in 1893, Kraepelin changed his mind in two ways. First, he announced that catatonia was a definite disease of its own, adding the phrase “a distinct disease” (eine eigenartige Krankheitsform) to a discussion not otherwise much unchanged from 1889 except to ascribe it to “processes of psychic degeneration.” (The word “degeneration” suggested a genetic express train that gathered speed over the generations in its downhill race.)

Second, in this 1893 edition, Kraepelin added the concept of dementia praecox to his nosology, which also counted as a form of psychic degeneration. Dementia praecox was an insanity occurring expressly in adolescence and young adulthood. The distinctive feature from other forms of youthful insanity was the trend to “feeble-mindedness [Verblödung], progressing sometimes quickly, sometimes more slowly, that may stop at various stages.” He acknowledged Hecker’s 1871 description of hebephrenia as an account of mild cases but noted that the dementia praecox diagnosis also included much more severe cases, described by other workers.25 Why call it “dementia praecox”? Kraepelin later said he had selected the term because the French were using it and it was familiar.26

In 1893, to whittle paranoia down, Kraepelin introduced into the fourth edition “dementia paranoides” as a separate disease—delusions of rapid onset that quickly eventuate in dementia.

Now firmly ensconced in Heidelberg, with the entire Klinik reoriented toward research, Kraepelin was rapidly spinning off ideas. In 1894, he told a meeting of the Southwest German Psychiatrists that such huge concepts as “paranoia” were scientifically pointless. Said the stenographer, “He demanded the dissolution of this clinical population into small groups of truly homogenous cases that could be described monographically, under the most exact observation, not only of individual symptoms but of the entire illness picture, on the basis of etiology, course, duration and outcome.”27 This was Kraepelin’s operational principle for originating new disease entities. (And even though we today have inherited Kraepelin’s dementia praecox as “schizophrenia,” it is precisely this principle that we do not follow in our own use of the term.)

By this time, Kraepelin had inserted into his schema all the concepts that would later constitute the dementia praecox subtypes—catatonia, dementia paranoides, and hebephrenia (which in this edition he described as core dementia praecox28).

The fifth edition, in 1896, stands as a landmark, ending the concern with momentary symptom pictures and shifting attention to underlying diseases, as defined by course and outcome. Kraepelin is thought to have changed his mind: going from symptoms to diseases. A kind of conventional wisdom, initially laid down by Kraepelin’s colleague in Heidelberg, the neurohistologist and psychiatrist Franz Nissl, insisted that with the fifth edition of his textbook Kraepelin initiated a historic change, shifting the focus from current clinical pictures to underlying diseases.

Nissl claimed that “Kraepelin’s views in the first four editions of his textbook corresponded to the conventional concepts of the day. In the fifth edition he abandoned the symptom viewpoint and, adopting Kahlbaum’s research methods, went over to the clinical viewpoint. In delineating various diseases, he relegated symptoms to second place, and then took up concepts that arose from the course and outcome of individual disorders. Quite specifically, Kraepelin noted the practical significance of prognosis, a factor to which Hecker twenty years previously had called attention. Kraepelin emphasized the certainty with which one could forecast the future course of events if one used Kahlbaum’s method of circumscribing the individual diseases.” The impact of this change was enormous.

Nissl continued: “This was a new departure, a fresh wind for clinical psychiatry in its previous sterility. People started once again to think more of purely clinical problems. Therewith the period of brain-anatomical research came to an end.”29 Thus, as in neurosyphilis, the presentation of an illness at any particular moment was not meaningful. At a given point, a neurosyphilitic might exhibit symptoms of mania, depression, paralysis, or insanity. Thus it was in the mainline psychiatric diagnoses: what counted was the underlying disease, and determining its prognosis and outcome.

This interpretation of events, while not false, is incomplete. The problem with this “epochal” interpretation of Kraepelin’s years at Heidelberg is that it doesn’t work very well for dementia praecox and catatonia, which Kraepelin now considered as “metabolic diseases” rather than diseases of degeneration. He had already designated dementia praecox and catatonia as independent diseases, and his analysis of both in 1896 differs little from the previous edition. The “epochal” reading of Kraepelin’s system may well be based on the insertion in 1896 of a new section on “constitutional predisposition,” which attempted to take the long view on “paranoia,” the “periodic insanities,” epilepsy, hysteria, and the traumatic neuroses. Kraepelin did, however, announce with confidence that his diagnostic scheme permitted the future to be forecast: “What convinces me of the superiority of the clinical procedure I recommend here is the certainty with which we are in a position to forecast the future course of things.”30 Kraepelin had previously uttered similar sentiments, but never before with such confidence.

The issue of clinical course in catatonia is crucial, given that Kahlbaum in 1874 had adjudged the prognosis as “not bad.” In addressing the Southwest German Psychiatric Association in November 1895, Kraepelin tried to pin down the prognosis of catatonia. Does it progress to dementia or not? He presented data on 63 patients from Heidelberg, of whom 39 were still symptomatic years later. Of interest are the 24 who experienced remissions. Fourteen of them later relapsed, most within five years. Even in remission, the relatives continued to view them as ill; the patients themselves lacked insight, and each new relapse carried the patients closer to dementia. Kraepelin concluded: “In catatonia we are dealing with an organic brain disease, which leads to a more or less deep dementia.”31 Kraepelin repeated this judgment, though not the data, in the fifth edition, in 1896: “Catatonia ends most commonly . . . in deep dementia.”32

It was in this fifth edition in 1896 that Kraepelin laid down his first detailed description of dementia praecox, which, together with dementia paranoides—mentioned earlier as well—now replaced the “insanity” (Wahnsinn) of earlier editions. Here, we encounter such classic descriptions of dementia praecox as the supposed “silliness” of the patients, which has survived as a core trait: “Very conspicuous is the frequent humorless laughter, which lacks the slightest pretext and occurs uncounted times in every interview; entirely absent is any kind of euphoric mood. To the contrary, one learns from the patients that it comes over them automatically, even against their will.” Kraepelin also described in these dementia praecox patients numerous catatonic symptoms, such as grimacing and stereotypies, though he makes no mention of catatonia. Onset is in youth, with a long prodrome involving fluctuating mood, followed by psychotic episodes, followed finally by dementia: “The common outcome of all severe forms of dementia praecox is dementia.” As the cause, Kraepelin indicted not heredity but an as yet unidentified organic brain change, or “autotoxicity.”33

In a talk in November 1898, at the Southwest German Psychiatric Society, Kraepelin summarized what he understood by “dementia praecox”: Emotional blunting and the lack of interest and of intellectual activity, delusional systems in the absence of affect or agitation, mannerisms and stereotypies, and changes in mood or agitation in the absence of changes in affect.34

Much of Kahlbaum’s ideas on the importance of course and outcome are embodied in these ideas of Kraepelin. Clemens Neisser later noted that Kahlbaum’s original emphasis in 1874 on course had been on the verge of becoming lost, submerged in contemporary musing about “paranoia,” until Kraepelin came along: “[It was Kahlbaum’s idea] that the entirety of the symptoms, their existence alongside, before, and after one another, the course and the outcome—should all form the basis of the clinical diagnosis. In the meantime, this clinical viewpoint has become generally accepted, thanks not least to Kraepelin’s own work, and it is from him that the towering doctrine of dementia praecox was conceived and executed.”35 Here, Hecker and Kahlbaum shine through clearly. Yet “dementia praecox” was ripe for a change.

Big Changes

In 1899, in the sixth edition, Kraepelin created two new illness entities that are with us today: “manic-depressive insanity” that included mood disorders of whatever polarity, and an enlarged “dementia praecox” that included as subtypes several diseases previously held separate: catatonia, hebephrenia, and dementia paranoides. Thus, Kraepelin changed his mind again, but this time, the consequences for catatonia as an independent disease were catastrophic. By making catatonia a subtype of dementia praecox, he ensured that whenever clinicians encountered catatonia in obviously nonschizophrenic patients, they would either overlook the symptoms or make some other diagnosis. Catatonia, a previously well-recognized disease of its own, was to become clinically invisible save as a form of schizophrenia.

How did this dramatic fusing together of what had been three separate disease entities come about? For one thing, several members of the tight Heidelberg circle around Kraepelin had been urging him to consider hebephrenia and catatonia the same disease. In November 1897, Gustav Aschaffenburg, then a staffer at the Heidelberg Klinik, reported his study of 227 catatonic patients admitted from 1891 to 1897 who had since been discharged. Comparing this cohort with a group of hebephrenic patients, Aschaffenburg said that both diseases began in adolescence, that hebephrenia had many catatonic features, and that both ended in dementia. “Under these circumstances, we may reach no other conclusion than that the diseases of hebephrenia and catatonia form a unitary disease process. The name ‘Dementia praecox’ seems to me most suitable for it.”36 Thus, Aschaffenburg may deserve part of the credit for the subtypes that Kraepelin proposed in the sixth edition of his textbook in 1899.

At the above-mentioned meeting of the Southwest German Psychiatry Society in November 1898, Kraepelin himself presented data on almost 300 dementia praecox patients observed over four years: Of those with “pronounced catatonic signs,” 59 percent ended in severe dementia, 27 percent in milder dementia, 13 percent in recovery. Of those with hebephrenic tendencies, 75 percent ended in severe dementia, 17 percent in milder dementia, 8 percent in recovery.37 The differences were not great.

In this sixth edition in 1899, the subtypes were characterized as follows. First came hebephrenia, defined as “a mental disturbance that begins subacutely entailing a simple state of more or less severe weak-mindedness.” This was close to Hecker’s 1871 concept, and, in the future, hebephrenia would be regarded as “core schizophrenia.”

Second, catatonia. Kraepelin invoked Kahlbaum as the originator of this form of dementia praecox with its initial mood disorder, followed by stupor, confusion, and dementia, and accompanied by motor symptoms of all kinds. “The end stage of catatonia in 59 percent of my cases is a distinctive, constitutionally predisposed [erblicher] dementia.” Here, Kraepelin parted from the Kahlbaum model of catatonia as a mostly recoverable illness. Kraepelin attached great importance to negativism and automatic obedience as symptoms, and it is here that the notion of “negative symptoms” of schizophrenia was reinforced, although Kraepelin meant by the term patients’ resistance to clinical care, mutism, food refusal, and misbehavior around toileting rather than flatness of affect.

Third, Kraepelin distinguished a “dementia paranoides” form, which, in contrast to the main diagnosis of paranoia (found elsewhere in the volume as Verrücktheit), ended in dementia. The main feature was delusions and hallucinations in the presence of otherwise preserved presence of mind (Besonnenheit).38

The Achilles heel of the entire dementia praecox construct is at once apparent: if one doesn’t accept the notion that all three end almost inevitably in “dementia,” they have little to do with one another. Hebephrenia is adolescent insanity, denoted by age at onset; catatonia had been well characterized by Kahlbaum, and, even though Kahlbaum thought all kinds of other mental symptoms accompanied it, motor symptoms nonetheless clinched the diagnosis, and the mental changes were accessory. Dementia paranoides seemed really a variant on “paranoia,” on what became delusional disorder, and delusional disorder did not usually end in dementia.

Did all these disorders truly end in dementia? It is quite possible that Kraepelin and his acolytes confused episodes with end-stage conditions. Patients who relapsed in the Heidelberg University Psychiatric Hospital often recovered later. As well, it was difficult to follow many patients who’d been transferred from the overcrowded Heidelberg Klinik to other mental hospitals in Baden because the hospital superintendents were begrudging about cooperating with Kraepelin, who represented for them the threat of university academic psychiatry.39 Then, too, patients discharged to the community as recovered were often lost completely from view.

The seventh edition in 1904, composed while Kraepelin was still in Heidelberg, changed little. It showed, perhaps inadvertently, how “catatonic” features easily come and go. Kraepelin pointed to the confused, nonsensical writings of catatonics as examples of “catatonic incoherence” (katatonische Zerfahrenheit).40 In the eighth edition in 1913, he said that incoherence better characterized dementia praecox as a whole than catatonia in particular.41 Such was Kraepelin’s prestige by this time that, we may be sure, had he decided to maintain “catatonic incoherence,” it would appear today in the symptom lists.

In the seventh edition, Kraepelin refined the markers of catatonic motor disturbances to include “eccentricity” (Verschrobenheit) and “the loss of graceful movement” (der Verlust der Grazie). Both terms addressed the idea that the movements of catatonic patients were often stiff, awkward, and ungainly. There isn’t really a good English translation of the German term “Verschrobenheit,” but by it Kraepelin meant movements that were clumsy and involved the loss of efficiency and purposefulness inherent in normal human movement. The term survived in German analyses for years but was not really accepted abroad. By “loss of graceful movement” Kraepelin again approached the same concept: “Graceful movement attains its goal with the least possible but sufficient expenditure of energy and movement. In contrast, catatonic movements are either stiff and wooden with excessive contraction of antagonistic muscles, or flaccid and slow as a result of an insufficient expenditure of energy. . . . The simple naturalness, which aspires directly to a goal, is lost through bizarre movements and derailments [Verschnörkelungen und Entgleisungen].”42 Kraepelin singled out a marker of motor pathology that should have survived—the “awkwardness” marker—but somehow hasn’t.

Where to situate catatonia in the diagnostic classification had a big influence on the apparent prevalence of “dementia praecox” or “manic-depressive insanity.” At the Heidelberg University Psychiatric Hospital, the number of dementia praecox cases soared from zero to more than half of all admissions between 1893 and 1901. Kraepelin said, “This development is explained by the fact that, as people got accustomed to applying the diagnosis of dementia praecox, at first the pathognomonic significance of individual symptoms was overestimated. In particular, many cases of manic-depressive insanity with catatonic phenomena were incorrectly assigned to dementia praecox.” This error was then realized and corrected, so that, at Heidelberg after 1901, the frequency of dementia praecox fell appreciably and that of manic-depressive insanity rose sharply.43 Given such erratic shifts in diagnostic judgment at the very home of dementia praecox and manic-depressive illness themselves, it is difficult to take seriously the argument that these are two sharply delineated disease conditions. Such dramatic shifts, moreover, were reported from other venues. In 1959, Paul Hoch, at the New York State Psychiatric Institute, mentioned an (unnamed) US state where, “In the beginning they admitted about 45 to 50 percent manic depressives. In five years they admitted the same number of schizophrenics, and the manic depressives dropped down to only 5 percent, where before the schizophrenics represented about 5 percent.”44

In 1903, Kraepelin assumed the professorship of psychiatry in Munich and held the position until his retirement in 1922; he died in 1926. He had begun to tower over the field. His Viennese colleague neurologist Constantin von Economo called him “[a] North German schoolteacher in giant format.”45 Kraepelin himself cut a formidable figure, as Edinburgh psychiatrist David Henderson, who trained for a year at the Munich Klinik, recalls. “He was thick-set, bullet-headed, intensely serious, a total abstainer from alcohol and tobacco, and very determined in his views. His appearance was more of a prosperous industrialist than that of a world-renowned professional man.”46

The Last Edition

The last edition of Kraepelin’s work, the dementia-praecox volume which was published in 1913, bears the stamp of the Munich years, with its large and highly variegated patient population, as opposed to the Heidelberg period. By the time of the five-volume eighth edition in 1909–1915 (the last edition that Kraepelin himself completed), Kraepelin had become a little less absolute about whether dementia praecox always ended in dementia; he also conceded that catatonia could be found in other illnesses. “The supposition has been often expressed, that apparently recovered cases [of dementia praecox] probably belong to some other disease process than the dementing process. I am not going to dispute this possibility. Partly, some of these will be simple missed diagnoses, usually cases of manic-depressive insanity. But there may be other, recoverable diseases with catatonic phenomena, that we at present are not capable of differentiating from dementia praecox.”47

Kraepelin went on to make a distinction, already adumbrated in 190l by Schüle, between catatonic symptoms that could be found in various illnesses and “Kahlbaum’s catatonia,” a disease of its own, which is to say a subtype of the disease dementia praecox. . . . We may consider Kahlbaum’s catatonia mainly as a distinctive kind of dementia praecox. And ‘catatonic phenomena’ are undoubtedly observed in many other disease processes . . . so that their occurrence alone does not permit the conclusion that catatonia in the narrow sense is present.”48

The characteristic symptom of Kahlbaums’ catatonia, for Kraepelin, was the alternation of agitation and stupor: “I think we may consider as the catatonic form of dementia praecox those cases in which the co-occurrence of characteristic agitation with catatonic stupor dominates the clinical picture.”49

Kraepelin considered patients with the catatonic type of dementia praecox to be psychotic from their early depressive phases. At the same time as the patients demonstrate depression, “They express highly bizarre delusional notions; ‘battles’ and ‘premonitions’ are coming . . .; they feel strange, as though someone were pursuing them; their life is no longer of value; everything has failed; no-one can help them. They are mocked by wanton sluts, belittled, spat upon, cursed; they are supposed to go to jail, to be sentenced to death, slaughtered, tied to the railway track, their house blown to bits . . . the daughter will be murdered, the children executed.” Then hallucinations crept in. Catatonia, for Kraepelin, was essentially a psychotic experience.50

This eighth edition made a distinction between flaccid stupor and rigid stupor (schlaffer Stupor v starrer Stupor). In flaccid stupor, the main symptom is catalepsy, with automatic obedience and stereotypies. Echopraxia, or imitating the movement of others, is included, and the patients talk so much that the actual stupor must be rather abbreviated. Kraepelin does not say that their eyes are wide open and follow movements in the environment, but others do. Set against this is “rigid stupor,” the main characteristic of which, aside from stupor itself, is negativism. The patients are entirely unresponsive, and their eyes are either tightly shut or “wide open, staring with widened pupils into the distance, not fixating.”51

Kraepelin’s interest in the psychology of dementia praecox, in the “will,” was by this last edition stronger than ever. “All disorders that influence psychic life find their ultimate and most important expression in the will and the actions of the patients,” he wrote in 1909,52 and proceeded to divagate on factors that increased and decreased the action of the will. It is interesting that in other medical specialties by this time the medical model was in full sway, permitting the delineation of distinctive diseases, with tests and verifications, as in cardiology and infectious diseases. Yet Kraepelin never evidenced interest in medical-model thinking—isolating distinctive diseases on the basis of biochemical, histological, and anatomical parameters—even though rapid progress was being made in these years in finding the organic bases of such diseases as pellagra and myxedema that had once belonged to psychiatry. Kraepelin’s influence ensured that the field would remain true to psychology and Freudian psychoanalysis, of course, completed this divergence of psychiatry from the rest of medicine.

This eighth edition greatly widened the scope of dementia praecox. In a mania classificatoria, Kraepelin increased the subtypes from three to nine, one of which remained catatonia. The “simple demented form” of dementia praecox, for example, was Hecker’s hebephrenia. It was perhaps a sign that Kraepelin was losing confidence in the unity of his concept, and, a few years later, in 1920, he conceded that it was not always possible to differentiate between dementia praecox and manic-depressive insanity on the basis of symptoms.53 The nine different subtypes in this edition represented a large expansion of the concept of dementia praecox, slicing off big chunks of mood disorder, for example, and attaching them to “dementia praecox.” Gone were all the former “degeneration” diagnoses. This expansion left a toxic legacy to psychiatry, making everything that could not be considered a “psychoneurosis” into “dementia praecox” or “schizophrenia.”

In this edition, Kraepelin raised a question that has bedeviled catatonia researchers ever since: How many catatonias are there? In the seventh edition in 1904, he had adumbrated a “late catatonia,” identical to those surfacing earlier in life and characterized by a remote prehistory of depression. In the eighth edition, he retracted this thought and suggested that catatonia beginning late in life might be a different illness entirely: “After much experience, this [earlier] concept now seems to me increasingly untenable. It seems particularly striking that the anatomical investigation of many of these late-catatonias reveals a completely different disease process than we encounter in similar forms during youth. And at the clinical level it seems more and more the case, that at least the majority of the late catatonias show only superficial resemblance to the corresponding illnesses of the earlier periods. . . . At present, the assumption having the most to be said for it seems to be that at least a considerable part of the late catatonias are an expression of very different disease processes.”54

The idea is an intriguing one, yet Kraepelin himself doomed it to marginality by making catatonia a subtype of schizophrenia.

Indeed, Kraepelin was so convinced of catatonia as a subtype of dementia praecox that he misdiagnosed it when he encountered it in other contexts, for example, in the context of manic-depressive illness. In manic-depression, Kraepelin identified a kind of special stage between mania and depression of “manic stupor.” Alternation was among its symptoms: “Quite suddenly [the stuporous patient] becomes lively, curses loudly, and amidst boisterous laughter makes animated observations. They leap out of bed, throw their food around the room, suddenly undress, storm about through several of the wards, tear up their clothing, or mishandle without obvious reason other patients, and then immediately sink back into their earlier stupor. . . . Some patients wander in measured steps about the ward, speak almost not at all except for the occasional joke.” Later, said Kraepelin, the patients remember quite precisely these episodes, but are not able to account for their strange behavior. “I didn’t want to have any will, one patient told me. He refused food but . . . felt obliged by hunger to take in large quantities of milk through his nose.” Kraepelin appended a photo of a patient with “manic stupor,” “with her rigid facial expression staring always at the same spot; she shows clearly the inhibition that dominated her for months and made her mute.”55 In retrospect, “manic stupor” was probably the alternation of agitation and stupor of garden-variety catatonia.

Yet these nuances and reservations were quickly forgotten. For the next hundred years, catatonia would be a type of schizophrenia.

Notes:

1. Schneider K., Kraepelin und die gegenwärtige Psychiatrie/ Fortschritte der Neurologie und Psychiatrie. 1956;24:1–7, 1.

2. This analysis borrows from Schröder P. Ueber katatone Symptome. Zeitschrift für die gesamte Neurologie und Psychiatrie. 1922;29:75–76.

3. Edward Hare raised this possibility in Schizophrenia as a recent disease. BJP. 1988;153:521–531.

4. Morel B-A. Études Cliniques: Traité Théorique et Pratique des Maladies Mentales. Nancy: Grimblot; 1852, I, 361.

5. On evolving concepts of adolescent insanity in the nineteenth century, see Shorter E. What Psychiatry Left Out of the DSM-5: Historical Mental Disorders Today. New York: Routledge; 2015, 101–107.

6. Charpentier R. Les Démences Précoces. Paris: Leve; 1890.

7. Pick A. Ueber primäre chronische Demenz (sog. Dementia praecox) im jugendlichen Alter. Prager Medizinische Wochenschrift. 1891;16:312–315; here Pick also offers a comprehensive overview of the previous literature.

8. Kraepelin E. Psychiatrie: Ein kurzes Lehrbuch für Studirende und Aerzte, 4th ed. Leipzig: Abel; 1893, 435–445, 435.

9. Meyer M. Emil Kraepelin, M.D., 1856–1926. In FG Ebaugh, ed., The Collected Papers of Adolf Meyer. Baltimore: Johns Hopkins University Press; 1951, III, 526.

10. Burgmair W et al. eds., Emil Kraepelin vol. I: Persönliches Selbstzeugnisse. Munich: Belleville; 2000, 77–78.

11. Engstrom EJ. Clinical Psychiatry in Imperial Germany: A History of Psychiatric Practice. Ithaca: Cornell University Press; 2003, 124–125.

12. Wirth W. Emil Kraepelin zum Gedächtnis! Archiv für die gesamte Psychologie. 1927;58:III.

13. Walser HH ed. August Forel: Briefe, Correspondance, 1864–1927. Berne: Huber; 1968, 166–167.

14. Kraepelin E. Compendium der Psychiatrie zum Gebrauche für Studirende und Aerzte, 1st ed. Leipzig: Abel; 1883, 222–227.

15. Burgmair W et al. eds., Emil Kraepelin, Briefe I, 1868–1886. Munich: Belleville; 2002, 333.

16. Kraepelin, Psychiatrie, 1st ed. (1883), 121

17. Kraepelin E. Psychiatrie: Ein kurzes Lehrbuch für Studirende und Aerzte, 2nd ed. Leipzig: Abel; 1887, 337–339.

18. Kraepelin E. Psychiatrie: Ein kurzes Lehrbuch für Studirende und Aerzte, 3rd ed. Leipzig: Abel; 1889, 332–336.

19. Kraepelin, Psychiatrie, 3rd ed. (1889), 335.

20. Behr A. Die Frage der ‘Katatonie’ oder des Irreseins mit Spannung. Dorpat: Medical dissertation; 1891, 56–58.

21. Kraepelin E. Ueber Katalepsie. AZP. 1892;48:170–172, 171.

22. Kraepelin E. Lebenserinnerungen. Berlin: Springer; 1919/1983, 49.

23. Daraszkiewicz L. Ueber Hebephrenie, insbesondere deren schwere Form. Dorpat: Medical dissertation; 1892.

24. Kraepelin, Lebenserinnerungen (1919/1983), 70–74.

25. Kraepelin, Psychiatrie, 4th ed. (1893), 438, 442.

26. Kraepelin E. Fragestellungen der klinischen Psychiatrie. Zentralblatt für Nervenheilkunde. 1905;28:573–590 (also quoted in Pauleikhoff, Die Katatonie (1969), 463.

27. Kraepelin E. Die Abgrenzung der Paranoia. AZP. 1894;50:1081–1082.

28. Kraepelin, Psychiatrie, 4th ed. (1893), 442.

29. Nissl F. Ueber die Entwicklung der Psychiatrie in den letzten 50 Jahren. Verhandlungen des naturhistorischen-medizinischen Vereins, NF. 1908;8:510–524, 521.

30. Kraepelin E. Psychiatrie: Ein Lehrbuch für Studirende und Aerzte, 5th ed. Leipzig: Barth; 1896, v. In 1897, in a talk to the German Psychiatric Society, Kraepelin gave an exact description of his research techniques, explaining how each patient received a one-pager (Zählkarte), which permitted the patient to be followed and gave an overview for the purposes of sorting patients into categories. Of course, this raised, in a collegial setting, the issue of course as opposed to a momentary clinical snapshot. And from this overview emerged, in particular, the importance of the underlying disease process of dementia (Verblödungsprocesse). Kraepelin did not overclaim discoveries of psychopathology at this point and was content to say: The more we can differentiate in the clinical pictures the essential phenomena from the incidental, the more we come closer to the goal of constructing etiologically similar groups. Kraepelin E. Ziele und Wege der klinischen Psychiatrie. AZP. 1897;53:840–848, 843, 847.

31. Kraepelin E. Ueber Remissionen bei Katatonie. AZP. 1896;52:1126–1127. The meeting, as noted, occurred in 1895.

32. Kraepelin, Psychiatrie, 5th ed. (1896), 458.

33. Kraepelin, Psychiatrie, 5th ed. (1896), 429, 436, 439.

34. Kraepelin E. Zur Diagnose und Prognose der Dementia praecox. AZP. 1899;56:254–263, 258–259.

35. Neisser C. Discussion. AZP. 1908;65:474.

36. Aschaffenburg G. Die Katatoniefrage. AZP. 1898;54:1004–1026, 1017.

37. Kraepelin, Zur Diagnose und Prognose (1899), 254–263, 257.

38. Kraepelin E. Psychiatrie: Ein Lehrbuch für Studirende und Aerzte, 6th ed. Leipzig: Barth; 1899, II, 149, 159–160, 163–164, 175, 182–183.

39. See Engstrom’s informative discussion, Psychiatry in Imperial Germany (2003), 135–145.

40. Kraepelin E. Psychiatrie: Ein Lehrbuch für Studierende und Aerzte, 7th ed. Leipzig: Barth; 1904, II, 224. Note that in this edition the spelling of Studierende became modernized.

41. Kraepelin E. Psychiatrie: Ein Lehrbuch für Studierende und Aerzte, 8th ed. Leipzig: Barth; 5 vols. 1909–1915; III (2) (1913), 687. Kraepelin distinguished Zerfahrenheit from oral Entgleisungen (derailments), III, 738.

42. Kraepelin, Psychiatrie, 7th ed. (1902), I, 279, 301. Note that volume I appeared in 1903, volume II in 1904.

43. Kraepelin, Psychiatrie 8th ed. (1909–1915), vol. I, 528; see fig. 22 on 527.

44. Hoch P. Discussion. In J Zubin, ed., Field Studies in Mental Disorders. New York: Grune & Stratton; 1961, 119; the conference was in February 1959.

45. Stransky E. Ms Autobiography, p. 272, archived in Institut für Geschichte der Medizin in Vienna, HS 2.065.

46. Henderson DK. The Evolution of Psychiatry in Scotland. Edinburgh: Livingstone; 1964, 173.

47. Kraepelin, Psychiatrie, 8th ed. (1913), vol. III, 944.

48. Kraepelin, Psychiatrie, 8th ed. (1913), 809.

49. Kraepelin, Psychiatrie, 8th ed. (1913), 810.

50. Kraepelin, Psychiatrie, 8th ed. (1913), 810

51. Kraepelin, Psychiatrie, 8th ed. (1913), 819–820, 825. On dilated pupils in catatonia and their restoration to normal following ECT, see Arias LM et al. Catatonic pupil in the setting of electroconvulsive therapy. J ECT. December 7 2016(Epub ahead of print).

52. Kraepelin, Psychiatrie, 8th ed., vol. I (1909), 366.

53. Kraepelin E. Die Erscheinungsformen des Irreseins. Zeitschrift für die gesamte Neurologie und Psychiatrie. 1920;62:1–29, 28.

54. Kraepelin, Psychiatrie, 8th ed., vol. II (1910), 537–538.

55. Kraepelin, Psychiatrie, 8th ed., vol. III (1913), 1292–1293.