Jornal of the History of the Behavioral Sciences IS SCHIZOPHRENIA WHAT IT WAS? A RE-ANALYSIS OF KRAEPELIN’S AND BLEULER’S POPULATION MARY BOYLE It has been noted that the term “schizophrenia” is now applied to group in many ways dissimilar to Emil Kraepelin’s cases of dementia praecox and Eugen Bleuler's of schizophrenia. No detailed explanation has been offered for the difference, This article offers evidence that Kraepelin’s and Bleuler’s concepts were derived from a Population largely suffering from organic disorders including the Parkinsonian se- quelae of encephalitis leshargica; it describes the conceptual confusion which followed the introduction of the concept of post-encephalitic Parkinsonism and discusses some implications for the modern concept of schizophrenia. It is suggested that the differences between earlier and later groups of schizophrenics may be accounted for by the decline in prevalence of post-encephalitic Parkinsonism and of the neurological and behavioral sequelae of other diseases, and by the parallel unsystematic develop ment of the concept of schizophrenia. Although there has often been disagreement about who should or should not be included in the population called schizophrenic, there is one aspect of this population on which many writers appear to be in agreement: it is that the kind of deteriorated cases seen by Emil Kraepelin and Eugen Bleuler are rarely seen today.' No detailed at- tempt appears to have been made to account for this, although some of those who have noted the difference have made tentative suggestions that the illness may have become less severe over time, that its progress has been halted by modern drugs, or simply, that the reasons for the difference are unknown.’ This paper will suggest another possible explanation for the difference in the populations and one which, if accepted, would have important implications for the modern concept of schizophrenia and for the evaluation of research said to support it, In 1917, a few years after Kraepelin and Bleuler had completed their major writings, the Austrian alienist and neurologist Constantin von Economo presented his observa- tions on a “new, hitherto unknown epidemic infectious disease” which he called encephalitis lethargica.* A much more detailed description of the disorder was published in English in 1931.* Von Economo seems to have intended “new” to mean “apparently new,” as he himself concluded from his historical survey that the disorder had probably been (unknowingly) described in the sixteenth century and possibly much earlier. His contribution, however, was to link a set of phenomena, in which somnolence and various neurological signs were often prominent, with later Parkinsonian features, to demonstrate the infectious nature of the disorder and its association with a “remarkably constant” picture of brain damage.* Although the sequelae of the initial infection became known as post-encephalitic Parkinsonism, the phenomena observed in these patients was far more severe, wide-ranging, and dramatic than had ever been observed in idiopathic paralysis agitans. It is now generally assumed that new cases of post-encephalitic Parkin- sonism are relatively rare and that the large majority of the present population of sufferers are survivors of the early twentieth-century pandemic.® Many Bovis is senior lecturer in Psychology and Head of the Masters Programme in Clinical Psychology at North East London Polytechnic, London E1S 4LZ, England, She has recently completed a detailed study of the origins and use of the concept of schizophrenia, published by Routledge 323324 MARY BOYLE Tape 1 Descriptions of Dementia Praecox, Schizophrenia, Encephalitis Lethargica/ Post-Encephalitic Parkinsonism The spasmodic phenomena in the musculature of the face and speech, which often appear, are extremely peculiar.’ Fibrillary contractions are particularly noticeable in the facial muscles and “sheet lightning” has long been known as a sign of a chronically developing (schizophrenic) illness.? ‘Asa rule, other spontaneous movements are associated with the choreic movements of Encephalitis Lethargica, the myclonic and fasciscular twitches of the disease: an important point with regard to differential diagnosis. These myclonic movements are more or less rhythmical and symmetrical flash-like short twitches of separate muscles or groups of muscles.” Dufour has described disorders of equilibrium, staggering, adiadochokinesia, and tremor, which he regards as the expression of a “cerebellar’ form of dementia praecox.* Constraint is also noticeable in the gait of the patients. Often indeed it is quite impossible to succeed in ex- periments with walking. The patients simply let themselves fall down stiffly, as soon as one tries to place them on their feet.* In some cases the ataxia attains such a degree that the instability of gait, the deviation towards one side, the tendency to fall backwards on standing, the tremor, the giddiness, and the nystagmus can only be ascribed to an involvement of the cerebellum in the inflammatory process.® (Ermes) found that a fall of the leg held horizontally only began after 205 seconds (in cases of dementia praecox), while in healthy persons it made its appearance on an average after 38 seconds, at latest after 80 seconds, There followed then (in dementia praecox) either a repeated jerky falling off with tremor or a gradual sinking.” if... one lifts up the forearm of a patient (suffering from the amyostatic-akinetie form of encephalitis lethargica) the arm remains raised for quite a time after having been released, and is only gradually brought back in jerks and with tremors." During acute thrust (of schizophrenia), though rarely in the chronic conditions, we often encounter som- nolence, Patients are asleep all night and most of the day. Indeed, they often fall asleep at their work. Fre- quently, this somnolence is the only sign of a new thrust of the malady.” In the now increasing somnolence (of the acute phase of the somnolent opthalmoplegic form of encephalitis lethargica) one often observes that the patients, left to themselves, fall asleep in the act of sitting or standing ‘or even while walking . . . (somnolence) is repeatedly found in quite slight cases as the only well marked symptom."° Hoche also mentions the markedly increased secretion of the sebaceous glands (in schizophrenic patients)."' A hypersecretion of the sebaceous glands (probably centrally caused) causes the peculiar shining of the faces of these patients.'* “The tendency to edema (si) is usually ascribed to poor circulation, but it may have other causes, In.a physically strong female patient with a beginning mild schizophrenia, edemas were noted in the thigh area. . . . At times ‘more severe edemas may make movement painful."? - oedema of hands and feet... are... more frequent in the amyostatic than in the other forms of encephalitis lethargica." In the most varied (schizophrenic) conditions, (the pupils) are often found to be unequal without having lost their ability to react ... this pupillary inequality is rarely persistent; it often varies within a few hours, becoming equal or reversed." (The) behavior of the pupils is of great significance. They are frequently in the earlier stages (of dementia praccox) and in conditions of excitement conspicuously wide . . . here and there one observes a distinct difference in the pupils, The light reaction of the pupils often appears sluggish or slight."* (continued)KRAEPELIN AND BLEULER POPULATION 325, Table 1 (Continued) pupillary disturbances are very common. In patients (with the hyperkinetic form of encephalitis lethargica), one generally finds unequal and myopic pupils with a diminished and sluggish reaction but sometimes also one-sided or double or complete absence of reaction or an absence of light reaction only. These pupillary disturbances often vary considerably (in the same patient)."” A differential diagnosis between (encephalitis lethargica and chorea) must necessarily be very difficult except where thee exist for our guidance pupillary disturbances or other objective signs of encephalitis lethargica."* 1, Emil Kraepelin, Dementia Praecox and Paraphrenia (Edinburgh: Livingstone, 1919); translated from Psychiatrie, 8th ed., 1913, p. 166. 2. Eugen Bleuler, Dementia Praecox or The Group of Schizophrenias (New York: International Univer: sities Press, 1950); translated from the original published in 1911, p. 170. 3. Constantin von Economo, Encephalitis Lethargica: Its Sequelae and Treatment (Oxford: Oxford University Press, 1931), p. 39. 4. Kraepelin, Dementia Praecox, p. 83 Kraepelin, Dementia Praecox, p. 148, emphasis in original Von Economo, Encephalitis Lethargica, p. 32. Kraepelin, Dementia Praecox. p. 79. Von Economo, Encephalitis Lethargica, p. 44 9. Bleuler, Dementia Praecox, p. 169. 10. Yon Economo, Encephalitis Lethargica, p. 27 11. Bleuler, Dementia Praecox, p. 167 12. Von Economo, Encephalitis Lethargica. p. 46, parenthesis in original. 13, Bleuler, Dementia Praecox, p. 166. 14. Von Economo, Encephalitis Lethargica, p. 46 15. Bleuler, Dementia Praecox, p. 173. 16. Kraepelin, Dementia Praecox, p. 77. 17. Von Economo, Encephalitis Lethargica, p. 38 18, Von Economo, Encephalitis Lethargica, p. 39 Von Economo’s claims, though later widely accepted, were originally greeted with some scepticism, as he himself describes in the preface to his 1931 text. Perhaps one reason for this was that the phenomena which he grouped together resembled in part many other known or assumed disorders: Ives Hendrick, for example, noted an account of twenty-six different diagnoses which had been given to patients before a final diagnosis of post-encephalitic Parkinsonism.” One disorder which bore a striking resemblance to the “new” disease was dementia praecox or schizophrenia. C. Farran-Ridge declared that: Among all the psychoses whose symptoms may thus be simulated by epidemic encephalitis, dementia praecox occupies the foremost place; in fact the semiological resemblance between the two diseases is in some cases so striking as to give rise to real difficulty in differential diagnosis.” He was able to list major areas of identity in the symptoms of the “two diseases” and suggested that damage to the basal ganglia was most likely responsible for the striking similarity. Some idea of the extent of the resemblance can be gained from the descriptions in Table 1. As well as the phenomena listed there, Kraepelin, Bleuler, and von Economo provided descriptions of marked peculiarities of gait;! excess production of saliva and urine; dramatic weight fluctuations; cyanosis of hands and feet; constraint of move-326 MARY BOYLE ment and the inability, in spite of effort, to complete “willed” acts. All three described delusions and hallucinations involving various sensory modalities. The striking resemblance between what were assumed to be two different disorders gave rise to much discussion about the criteria which might be used to distinguish demen- tia praecox and post-encephalitic Parkinsonism. But the discussants failed to consider a crucial assumption on which their discussion was based: that Kraepelin’s and Bleuler’s concepts were valid, that they had demonstrated that a group of phenomena were related or co-occurred above chance level—the necessary condition for the introduction of new hypothetical constructs.'’ As has been argued in detail elsewhere, however, this demonstration had never been made: neither Kraepelin nor Bleuler had provided any empirical evidence in support of their concepts. '? Kraepelin was well aware of the fact that, to justify his concept, he was required to demonstrate empirically that certain phenomena “went together” but he latterly admitted that his concept of dementia praecox was based entirely on his subjective impressions. Bleuler, whose concept was equally subjective, made no reference to the problem." Given this state of affairs, it is not surprising to find that the criteria suggested for distinguishing dementia praecox and post-encephalitic Parkinsonism were often highly subjective. Hendrick, for example, suggested that: when the patient’s confidence can be attained (the encephalitis lethargica patient), . . . can be shown much more easily than the schizophrenic to be highly sensitive and his withdrawal from contact with others is a motivated defence rather than a product of preoccupation and dulling of external interest. . ."* and that _. « there was an exaggeration of the dramatic, artificial character of these postures (in post-encephalitic Parkinsonism) which, in a person making good contact, is quite different from the frequent haughty aloofness and more natural attitudes of prayer and abhorrence found commonly in the schizophrenic.!? while yon Economo claimed that: Stransky in 1903 established the fundamental thesis that in the schizophrenic iseases an intra-psychic ataxia (that is, a dissociation of the “nod and the thymo- psyche”) exists as a basic sympton. In this division he meant “nod-psyche” to be the representative of the purely intellectual functions while “thymo-psyche” embraced the urges, emotions and volition. . . . In encephalitis lethargica, though no genuine dissociation as in dementia praecox occurs, an isolated disturbance of the thymo- psyche takes place, leaving the noo-psyche intact."® In addition, many of the symptoms suggested by one writer or another as indicative only of dementia praecox were apparently suggested by others as symptoms of post- encephalitic Parkinsonism.” Von Economo, for example, appeared to claim that in- tellectual functions remained intact in post-encephalitic patients, in contrast with schizo- phrenics.'* Hendrick, however, claimed that “impairment of general intelligence” was common in adults and childen with post-encephalitic Parkinsonism with psychotic features." Similarly, P. K. McCowan and L. C, Cook claimed that close observation would show “some degree of mental degeneration in nearly every case (of post-en- cephalitic Parkinsonism).""” McCowan and Cook claimed also that muteness with catatonia, in the face of attempts to rouse patients, was characteristic only of dementia praecox.”! Oliver Sacks, however, has claimed that some of the most severe cases of encephalitis lethargica were mute until the advent of L-dopa in the late 1960s when they were, for the first time, able to give accounts of their “catatonic entrancement.””*KRAEPELIN AND BLEULER POPULATION 327 McCowan and Cook devoted considerable attention to the problems of distinguishing dementia praecox and post-encephalitic Parkinsonism. It is interesting to note some of the means by which they accommodated contradictions in their argu- ment, where features they had claimed to be specific to dementia praecox were elsewhere said to be observed in patients to whom they had given a definite diagnosis of encephalitis lethargica. They claimed, for example, that “The main criteria (for differentiating demen- tia praecox from post-encephalitic Parkinsonsim) lie in the constant absence of inac- cessibility and indifference in the typical emotional reactions of the encephalitic.”” Several of the cases they described, however, and to whom they had given a definite diagnosis of Parkinsonism, were said to show such indifference. This was then described as “schizophrenic indifference,” so great as to “mask successfully the customary interest of the encephalitic in his illness.”* A similar argument was put forward for stupor.?*By contrast, a woman of twenty was described thus: “She was rather irrational and showed incipient dementia. She was definitely apathetic, and when roused her manner was in- different and uninterested. The diagnosis of dementia praecox has been abundantly con- firmed.” The woman, however, also showed a “Parkinsonian gait” but this was claimed to be simulated.”* There is, of course, no objection in principle to the idea of different patterns of phenomena, which give rise to different diagnoses, nevertheless having large areas of overlap. This is so, for example, in the patterns on which diagnoses of tuberculosis of the lungs and cancer of the lungs are based, or in heart failure and asthma or jaundice due to gallstones or pancreatic tumor. But the reason why it makes sense to discuss the differential diagnosis of these conditions is that the diagnostic terms are based on empirically supported claims to have observed patterns which, though superficially similar, also show reliable and well-described differences in their correlates or antecedents. But in the absence of evidence that the concepts of dementia praecox or schizophrenia were derived from the observation of patterns, discussion of differential diagnosis made no sense, Farran-Ridge merely asserted that dementia praecox and post-encephalitic Parkinsonism were “aetiologically unrelated,””” but neither he nor anyone else provided evidence to support this idea; indeed he did not even suggest what the different antecedents of dementia praecox might be. These attempts at differential diagnosis were thus rather like attempts to distinguish, say, acute delerious mania from meningitis or amentia from Huntingdon’s chorea. We must, however, be careful of assuming that the similarity of Kraepelin’s, Bleuler’s, and von Economo’s descriptions means that Kraepelin and Bleuler can be credited with unknowingly having discovered post-encephalitic Parkinsonism, There are three main reasons for caution. First, von Economo’s descriptions overlapped with other known or assumed disorders—as witness Hendrick’s reference to twenty-six different diagnoses applied to one patient —and what von Economo had called a remarkably con- stant picture of brain damage was, of course, visible only at post-mortem. Thus, although there is no serious doubt now that von Economo described a reliable pattern of phenomena, diagnosis at the time of the great epidemic was not straightforward, and relied on the observation of signs and symptoms together with possibly inaccurate reports of previous infection. Some of the similarity between Kraepelin’s, Bleuler’s, and von Economo’s descriptions might therefore come from all three sets overlapping with other organic disorders. The second reason for caution is that Kraepelin himself claimed that some “signs of dementia praecox” which he attributed to the “failure of healthy voli- tional impulses,” were observed in “many forms of idiocy” and there is no good reason to suppose that all of these were, in fact, post-encephalitic Parkinsonism.”*328 MARY BOYLE Finally, there must be doubt as to whether the prevalence of encephalitis lethargica and post-encephalitic Parkinsonism prior to the 1916 epidemic would have been sufficient to account for the numbers said to be suffering from dementia praecox. It is interesting to note, however, Oliver Sacks’s claim that the prevalence of post-encephalitic Parkin- sonism before this epidemic may have been seriously underestimated, and that variously named European epidemics during the sixteenth, seventeenth, eighteenth, and nineteenth centuries were probably related to the later “great” epidemic.”? Clearly, such issues cannot be settled in the absence of reliable epidemiological data. What can be argued with some confidence is that Kraepelin and Bleuler derived their concepts from a population many of whom were suffering from neurological and other organic, possibly post-infection, disorders, including post-encephalitic Parkinsonism. The evidence for this view comes from several sources. The first is the population descrip- tions themselves. Not only do these overlap considerably with von Economo’s, but Kraepelin and Bleuler referred not infrequently to signs of infection and clouding of consciousness in their patients as well as to phenomena such as cessation of menstruation and dramatic weight changes, which may have had a primary or secondary endocrino- logical basis. Kraepelin also provided detailed descriptions of the severe brain damage he observed microscopically at post-mortems on many cases of dementia praecox; he referred particularly to severe damage to nerve tissue and to the proliferation and in- filtration of abnormal glia cells.” The second source is the considerable diagnostic con- fusion which followed the introduction of von Economo’s concept. While this does not demonstrate that post-encephalitic Parkinsonism and dementia praecox were synony- mous, it does emphasize the extent to which Kraepelin’s and Bleuler’s concepts overlapped with neurological and other organic concepts. And, third, it is notable that the type of patient said in the early decades of this century to be suffering from dementia praecox or schizophrenia, that is, the inaccessible, the stuporous catatonic, the intellectually deteriorated,”" is, apparently, the type now said to be very rare in the modern popula- tion of schizophrenics.” In addition, many symptoms said—also in the early decades of this century—to be shared by Parkinsonian and schizophrenic patients” or to con- stitute the organic symptoms of schizophrenia™ (including pupillary disorders, dramatic weight loss and gain, oedema, severe constipation, cyanosis of the extremities, polyuria, and blepharoclonus and facial seborrhoea) are not now mentioned as possible symp- toms of schizophrenia.** It is surely stretching credulity to suggest that, as post-en- cephalitic Parkinsonism and the neurological sequelae of other infectious diseases have become rarer, there has also been a coincidental decline in certain types of schizophrenia which closely resembled them, as well as in many organic symptoms of schizophrenia which happened to be identical to those described by von Economo. IMPLICATIONS FOR THE MODERN CONCEPT OF SCHIZOPHRENIA It might be argued that the relationship between Kraepelin’s and Bleuler’s concepts and that of post-encephalitic Parkinsonism is of little relevance to the modern concept of schizophrenia, for two reasons. First, it could be said that Kraepelin and Bleuler, from understandable ignorance, simply misdiagnosed some of their patients and that the remainder could properly be said to be suffering from dementia praecox or schizophrenia. This argument, however, overlooks the fact that Kraepelin and Bleuler were engaged in concept development, and were required to provide an empirical base for their concepts before discussion of the observation of new exemplars of a pattern — diagnosis—or discussion of possible misdiagnosis could have any meaning. If some ofKRAEPELIN AND BLEULER POPULATION 329 their population were suffering the sequelae of encephalitic infection, or from other organic disorders, then Kraepelin and Bleuler were required to demonstrate after this group had been removed that the remaining patients showed a pattern of phenomena which justified the introduction of their concepts of dementia praecox or schizophrenia. It is obvious from their writings, and from the diagnostic confusion which followed von Economo’s discovery, that this demonstration was never attempted, far less made. A second argument might be made that the modern concept of schizophrenia is not dependent on Kraepelin or Bleuler, but has developed its own empirical base. This argument, however, is difficult to reconcile with the fact that modern writers credit Kraepelin and Bleuler with having first described or discovered schizophrenia and it is also based on the assumption that the modern concept is valid.** It has been argued, however, that the present concept has developed in an idiosyncratic way’” and that recent attempts to provide it with a valid set of referents are misguided and have, predictably, failed.** It has been argued also that the concept has generated a research literature both contradictory and equivocal” —a fact not denied by supporters of the concept.*° But this disarray is exactly what would be expected from the concept’s history, and from the failure to take account of the possible significance of the nature of Kraepelin’s and Bleuler’s population, What appears to have happened is that, as infectious diseases and their sequelae have become rarer, and as diagnosis and treatment of other disorders which may have had neurological or behavioral sequelae have become more sophisticated, then some of the phenomena observed by Kraepelin and Bleuler in their patients, notably delusions and hallucinations, and deterioration in personal functioning, have become “detached” from Kraepelin’s and Bleuler’s original conception of schizophrenia and now form the core of the modern concept. But because itis likely that hallucinations, culturally unacceptable beliefs, and social behavior are not necessarily related, and that each has multiple causes, then the present population would be expected to be heterogeneous and to yield inconsistent data. It is rather as if, say tuberculosis had declined in prevalence but that some of its symptoms such as coughing and losing weight—each with multiple causes and not necessarily related—came to form the core of another “disorder.” The populations in which the disorder was diagnosed would, of course, yield unreliable data.*t There are some indications of this transformation in the writings of Kurt Schneider, which have been extremely influential in European psychiatry, although the paucity of his descriptions makes it difficult to know what kind of population he may have been working with.*? Schneider, however, in contrast to Kraepelin and Bleuler, made vir- tually no reference to the physical and neurological features of his patients.*® He claimed also that insight into the illness was “rare,” where Bleuler had claimed it to be “typical.”* ‘One part of the research literature surrounding the modern concept of schizophrenia is of particular interest here. Some studies of family resemblance in diagnoses of schizophrenia are claimed to have “proved” or “provided incontrovertible evidence” that schizophrenia has a genetic base,** The literature is of three main kinds: the study of the concordance for diagnoses of schizophrenia in identical and same-sexed fraternal twins; the study of “adopted-away” children of mothers with diagnoses of schizophrenia; and the study of the biological parents of adopted children diagnosed as schizophrenic.** The claims made for these studies have been strongly challenged on methodological and statistical grounds, and these criticisms stand regardless of the nature of the subject population.*” It is, however, notable that the majority of twin studies used subjects who were born before or during the great epidemic of encephalitis lethargica; many of them were originally diagnosed as schizophrenic at the time of diagnostic confusion described330 MARY BOYLE earlier.** It is therefore not surprising to find that the case descriptions which some of the twin researchers provided contain frequent reference to phenomena which overlap with those described by von Economo and are not claimed now to be symptoms of schizophrenia. These include cyanosis of the extremities, dramatic weight fluctuations, greasy skin, profuse sweating, chronic constipation, convulsions, difficulty in swallow- ing, and tics and facial wwitches.*° It is interesting to note that Eliot Slater appears to have used the virtually identical motor and other phenomena shown by some twin pairs, including in one pair, cyanosis of the extremities, to support some of his more uncertain judgments of monozygosity.*° CONCLUSIONS There is no doubt that the descriptions of Kraepelin’s precocious dements, Bleuler’s schizophrenics, and von Economo's Parkinsonian patients are st rikingly similar and that all three descriptions overlap with those of a variety of other organic disorders. Taken together with Kraepelin’s and Bleuler’s failure to provide data in support of their con- cepts, this suggests that their inferences were mistaken. It suggests also a likely explana- tion for the differences between Kraepelin’s and Bleuler’s patients and today’s schizo- phrenics: that as the incidence of post-encephalitic Parkinsonism and other infectious diseases with neurological sequelae declined, then so too, obviously, would the incidence of Kraepelinian and Bleulerian schizophrenics. The modern behavioral and experien- tial concept of schizophrenia has developed in parallel with this decline, so that it may now refer to a heterogeneous group who bear only a superficial resemblance to Kraepelin’s and Bleuler’s population. Kraepelin’s and Bleuler’s apparently mistaken inferences and the subsequent unsystematic development of the concept of schizophrenia may well pro- vide a more plausible explanation of the failure to produce reliable data than does the past lack of noninvasive methods of studying brain function.*! Notes 1, John S, Strauss and William T, Carpenter, Schizophrenia (New York: Plenum Medical, 1981); M. V. Seeman, S.K, Littmann, E, Plummer, J. F. Thornton, and J. J. Jeffries, Living and Working with Schizophrenia (Milton Keynes, England: The Open University Press, 1982); John Cutting, The Psychology of Schizophrenia (Edinburgh; Churchill Livingstone, 1985); and Edward H. Hare, “Schizophrenia as an Infectious Disease,” in Contemporary Issues in Schizophrenia, eds. Andrew Kerr and Peter Snaith (London: Royal College of Paychiatrists/Gaskell, 1986), pp. 231-234 2. The issue of the difference between Kracpelin’s and Bleuler’s populations and present-day “schizophreni is mentioned only very briefly and in passing by these authors with no suggestion that the phenomenon may be significant or any attempt to evaluate the tentative explanations mentioned. 3. Emil Kraepelin, Dementia Praecox and Paraphrenia (Edinburgh: Livingstone, 1919), translated from Psychiatrie, 8th ed., 1913; and Eugen Bleuler, Dementia Praecox or The Group of Schizophrenias (New York International Universities Press, 1950), translated from the original published in 1911 4, Constantin von Economo, Encephalitis Lethargica: Its Sequelae and Treatment (Oxford: Oxford University Press, 1931) 5. _Indiscussing how he had “seen” a pattern that had apparently been overlooked by others, von Economo, in Encephalitis Lethargica, mentions his debt to his mother, whose recollection of the mysterious Italian epidemic, the great “Nona,” “perhaps turned my researches into the right path.” He was, presumably, also helped by advances in the study of infectious diseases and by the sheer number of cases with which he and his colleagues were presented during the European epidemic of 1916-1927 6. C. A. Pallis, “Parkinsonism: Natural History and Clinical Features,” British Medical Journal 3 (1971): '683-690. There is a stronger point of view, which this author discusses, that, when all survivors of the great epidemic have died, post-encephalitic Parkinsonism will disappear altogether (cf. note 41) 7. Ives Hendrick, “Encephalitis Lethargica and the Interpretation of Mental Disease,” American Journal ‘of Psychiatry 7 (1928): 989-1014.KRAEPELIN AND BLEULER POPULATION 331 8, The use of either of these terms seems 10 have been determined by personal preference, possibly influenced by the extent of adherence to Kraepelin’s original belief in an unfavorable outcome. For economy of style, the terms are therefore used here as if they referred to one disorder. 9. _C, Farran-Ridge, “Some Sympioms Referable to the Basal Ganglia and Occurring in Dementia Praccox and Epidemic Encephalitis,” Journal of Mental Science 72 (1926): 513. Hendrick, in Encephalitis Lethargica, also gives an account of the difficulties he and various colleagues experienced in attempting to distinguish encephalitis lethargica and dementia praecox. 10. Bleuler, Dementia Praecox, described his schizophrenic patients as having a “will-o'-the-wisp” gait and claimed that he could distinguish them from other patients by watching them walk in the garden when his view of their heads was obscured 11, Lewis White Beck, “Constructions and Inferred Entities,” in Readings in the Philosophy of Science, eds. H. Feigh and M. Brodbeck (New York: Appleton Century Crofts, 1953), pp. 368-381 12. Mary Boyle, Schizophrenia—A Scientific Delusion? (London: Routledge, 1990), 13. Kraepelin, Psyehiatre, Sth and 6th eds, used a criterion — similarities in onset, course, and outcome which can be shown to be inappropriate for identifying relationships amongst phenomena. He also, however, provided no evidence that the group said to be suffering from dementia praecox actually showed similarities in onset, course, and outcome. He later (Dementia Praecox) abandoned this criterion for the idea of “Disorders Which Characterise the Malady,” but without ever providing the necessary independent criteria for identify ing “the malady.” Toward the end of this text (pp. 261 and 275), he also appeared to reinstate the problemat criterion of “similarities in onset, course, and outcome.” Bleuler did not suggest any criterion for identifying relationships amongst the phenomena in which he was interested and itis not clear from his writings which hhe used. Bleuler also appeared to be unaware of the inconsistency in his acceptance of Kraepelin’s concept and his rejection of an inevitably poor outcome for patients suffering from dementia praecox: if “similarity ff outcome” had been used by Kraepelin as part of his criterion for identifying a pattern of phenomena, then it was logically impossible to find some patients suffering from dementia praecox who showed a good ‘outcome. In order to justify his concept of schizophrenia, Bleuler was therefore required to demonstrate, independently of Kraepelin, that he had observed a pattern of phenomena that would justify the introduction of a new hypothetical concept 14. Hendrick, Encephalitis Lethargica, p. 1087. 15. Ibid., p. 1008. 16. Von Economo, Encephalitis Lethargica, p. 163, parenthesis in original 17. Because the descriptions are often nonspecific, it can only be assumed that similar phenomena are being discussed. 18. Von Economo, Encephalitis lethargica, p. 163 19, Hendrick, Encephalitis Lethargica, p. 1011 20. P. K. McCowan and L.. C. Cook, “The Mental Aspect of Chronic Epidemic Encephalitis, 30 June 1928): 1316. 21. Ibid., p. 1318 22. Oliver Sacks, Awakenings (London: Picador, 1982), p. 16. 23, MeCowan and Cook, Mental Aspects, p- 1318. * The Lancet 24. Ibid. 25. Ibid., p. 1319, 26. Ibid. 27. Farran-Ridge, Some Symptoms Referable 10 the Basal Ganglia, p. $14. 28. Kraepelin, Dementia Praecox, p. 4. 29, Oliver Sacks, “Parkinsonism —A So-Called New Disease,” British Medical Journal (9 October 1971): 111 30, These descriptions may be indicative of severe infection, and they contrast with the failure of modern research reliably to demonstrate clear signs of brain pathology that could be related to present-day “schizophrenic” behavior; see Richard Bentall, Howard Jackson, and David Pilgrim, “Abandoning the Con- ‘cept of Schizophrenia; Some Implications of Validity Arguments for Psychological Research into Psychotic Phenomena,” British Journal of Clinical Psychology 27 (1988): 303-324, for a brief review and discussion of some recent findings. 31. McCowan and Cook, Mental Aspects, and see also Hendrick, Encephalitis Lethargica. 32. Cutting, The Psychology of Schizophrenia, and see also Seeman et al., Living and Working with Schizophrenia, and Strauss and Carpenter, Schizophrenia. 33. Farran-Ridge, Some Symproms Referable to the Basal Ganglia. 34. R.G. Hoskins and F. H. Sleeper, “Organic Functions in Schizophrenia," Archives of Neurology and Psychiatry 30 (1933): 123-140.332 MARY BOYLE 35, American Psychiatric Association, Diagnostic and Statistical Manual of Mental Diseases, 3rd rev. ed. (Washington, D.C.: American Psychiatric Association, 1987), 36. Irving Gottesman and James Shields, in Schizophrenia: The Epigenic Puzzle (Cambridge: Cambridge University Press, 1982), p. 39, talk of schizophrenia as the disorder which *[Kraepelin and Bleuler] both described so thoroughly and sensitively”; Seeman et al., in Living and Working with Schizophrenia, p. 3, ask “How was schizophrenia discovered?” and claim that “Kraepelin . . . christened the illness dementia praecox”; Robert Kendell, in The Role of Diagnosis in Psychiatry (Oxford: Blackwell Scientific Publications, 1975), p. 62, credits Kraepelin with having delineated syndromes, including dementia praecox, “from the midst of chaos.” 37. W.S. Fenton, L. R. Mosher, and S. M. Matthews, in “Diagnosis of Schizophrenia: A Critical Review ‘of Current Diagnostic Systems,” Schizophrenia Bulletin 7 (1981): 452-476, suggest that the various sets of diagnostic criteria put forward for “schizophrenia” are all to some extent arbitrary. 38. Boyle, Schizophrenia, in Chapters 4 and 5, provides a detailed critical review of the historical background to and the development of the DSM-111 and DSM-I11R diagnostic criteria. 39. See Bentall, Jackson, and Pilgrim, “Abandoning the Concept of Schizophrenia,” for a review and discus- sion of some implications of the lack of reliable research data. 40, See John Wing, “Abandoning What?" British Journal of Clinical Psychology 27 (1988): 325-328, for a detailed example of an attempt to retain the concept of schizophrenia in the face of inconsistent research data; most academic texts on the topic also mention the lack of consistent findings. 41. There is another possibility: Oliver Sacks, in a letter to The British Medical Journal, 9 October 1971, p. 111, has emphasized the dangers of “forgetting” about viral infections, or assuming them to be extinct, between epidemics. This, he suggests, happened before von Economo’s observations on encephalitis lethargica and appears to be happening again. Although Sacks is not apparently suggesting that encephalitis lethargica and its sequelae are very prevalent now, it is perhaps not unreasonable to suppose that the virus, in a more benign or in a related form, may be implicated in some cases of what is now called schizophrenia, The idea that “schizophrenia is an infectious disease” has recently become popular amongst a few researchers (see Timothy Crow, “A Re-Evaluation of the Viral Hypothesis: Is Psychosis the Result of Retroviral Integration at a Site ‘Close’ to the Cerebral Dominant Gene,” British Journal of Psychiatry 145 (1984): 243-253, and Hare, Js Schizophrenia an Infectious Disease?), although no convincing direct evidence has been offered in support Of this thesis. These authors, however, do not discuss the possibility that Kraepelin and Bleuler were partly describing the same type of population as von Economo and appear to take for granted the validity of the modern concept of schizophrenia. Their questions are therefore framed less constructively than they might be. The two possibilities are not, of course, mutually exclusive, 42. Kurt Schneider, Clinical Psychopathology, Sth ed. (New York: Grune and Stratton, 1959). 43. The physical and neurological features described by Kraepelin and Bleuler were apparently striking, for example, problems of voluntary movement, somnolence, and incontinence. So too were many of the behavioral descriptions which are similar to those of von Economo: patients rousing themselves from stuporous states and indulging in “maniacal excitement,” smashing crockery, beating other patients, grunting and how!- ing, turning somersaults. It seems unlikely that, if Schneider’s patients—whether medicated or not—had behaved in these ways, he would have overlooked them as possibly important features of his “schizophrenia.” 44.__Kraepelin, Dementia Praecox, Bleuler, Dementia Praecox, and von Economo, Encephalitis Lethargica, provide similar descriptions of some patients’ attempts to describe and to understand their bewildering ex- periences, which they apparently recognized as alien to them. 45. Diagnostic and Statistical Manual, p. 186, and Kendell, The Role of Diagnosis, p. 185. 46. Gottesman and Shields, Schizophrenia; Seymour Kety, David Rosenthal, Paul Wender, Fini Schulsinger, and Bjarn Jacobson, “Mental Iiness in the Biological and Adoptive Families of Adopted Individuals Who have Become Schizophrenic: A Preliminary Report Based on Psychiatric Interviews,” in Genetic Research in Psychiatry, eds. Robin Fieve, David Rosenthal, and Henry Brill (Baltimore: John Hopkins University Press, 1978), pp. 147-165; and David Rosenthal, Paul Wender, Seymour Kety, Fini Schulsinger, Joseph Welner, and Lise Ostergaard, “Schizophrenics’ Offspring Reared in Adoptive Homes,” in The Transmission of ‘Schizophrenia, eds. David Rosenthal and Seymour Kety (Oxford: Pergamon, 1968), pp. 377-391 47. Steven Rose, Leon Kamin, and Richard Lewontin, Not In Our Genes (Harmondsworth, England: Penguin, 1984), Chapter 8; Boyle, Schizophrenia, Chapter 6; Theodore Lidz, Sydney Blatt, and Barry Cook, “Critique of the Danish-American Studies of the Adopted-Away Offspring of Schizophrenic Parents,” American Journal of Psychiatry 138 (1981): 1063-1068; and Theodore Lidz and Sydney Blatt, “Critique of the Danish- ‘American Studies of the Biological and Adoptive Relatives of Adoptees Who Became Schizophrenic,” American Journal of Pyschiatry 140 (1983): 426-435. 48. It is usual to divide twin studies into “earlier” and “later” according to the date of publication (see Gottesman and Shields, Schizophrenia). This practice, however, can mask the fact that many of the subjects in some later studies, notably that of Margit Fischer (“Genetic and Environmental Factors in Schizophrenia,” Acta Psychiatrica Scandinavica Supplement 238 [1973)), were born in the mid to late nineteenth and early ‘twentieth centuriesKRAEPELIN AND BLEULER POPULATION 333 49, Eliot Slater, Psychotic and Neurotic Minesses in Twins (London: Her Majesty’ Stationery Ofice, 195 Irving Gottesman and James Shields, Schizophrenia and Genetics: A Twin Study Vantage Point (London: Academic Press, 1972); and Fischer, “Genetic and Environmental Factors in Schizophrenia.” $0. Slater, Psychotic and Neurotic Hinesses, p. 149. Si. Wing, in Abandoning What?, p. 327, suggests that the lack of noninvasive methods of studying brain function “has been chiefly responsible” for siow progress in relating schizophrenic symptoms to possible causes ‘or pathologiesCopyright of Journal of the History of the Behavioral Sciences is the property of John Wiley & Sons Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. Hewever, users may print, download, or email articles for individual use.