Error Kraepelin
Error Kraepelin
Error Kraepelin
314–320, 2010
doi:10.1093/schbul/sbp059
Advance Access publication on July 8, 2009
Max Fink1,2, Edward Shorter3, and Michael A. Taylor4 In the 19th century, many authors sought to extract
distinctive in their course. Kahlbaum made the clinical ‘‘Special importance in the establishing of dementia prae-
course a principal feature of nosological classification. cox has, not without justification, been attributed to
His student, Ewald Hecker, used Kahlbaum’s approach the demonstration of the so-called ‘catatonic’ morbid
to delineate hebephrenia as another distinct disease.2 symptoms.’’8(p257)
Clemens Neisser, a young staff psychiatrist in a provin- Kraepelin, professor of psychiatry in Heidelberg and
cial German asylum considered Kahlbaum to be ‘‘one of then after 1903 in Munich, is a founding parent of mod-
those quite unusual investigators in science who come to ern psychiatric nosology. His influence is manifest in the
conclusions on the basis of their thorough clinical expe- popularity of successive editions of his textbooks, the first
rience, and few break with the old Pseudo-system as bril- of which appeared in 1883.10 Catatonia was not men-
liantly as Kahlbaum does in catatonia.’’3 tioned in this first edition, and a friend wrote him to
Within 3 years, catatonia was recognized in 4 patients ask why he had not included it.11
distinctive clinical course of Dementia praecox.’’ And, with 200 patients meeting Kraepelin’s constructs for
‘‘We must limit the designation [catatonia] to those cases manic-depressive illness and dementia praecox in
alone in which the pathological process of Dementia follow-up studies covering more than 10 years of illness.
praecox is at work.’’15 He found catatonia to be more common among the
In 1920, Kraepelin’s position turned once again, manic-depressive patients than among those with demen-
expressing doubts as to the meaningfulness of separating tia praecox.
dementia praecox and manic-depressive illness because It was Eugen Bleuler, professor of psychiatry in Zurich,
the 2 presentations and clinical courses intermingled.16 who brought Kraepelin’s view that catatonia equaled
This renunciation of much of his life’s work reinforces schizophrenia to North America. In his 1916 textbook,
the view that Kraepelin’s entire system was impression- Bleuler24 assimilated catatonia within schizophrenia. He
istic, including the rather arbitrary shifts about catatonia. had a milder view of schizophrenia, anticipating many
the identification of the NMS.59 The patients were mute, a type of schizophrenia, and that view is supported by
rigid, posturing, and in stupor, accompanied by fever, the data collected over the 20th century. Nevertheless,
tachycardia, hypertension, and tachypnea. The early some modern clinicians who adhere to Kraepelin’s writ-
authors saw a similarity to malignant hyperthermia and ings and the supporting opinions of Bleuler, Meyer, Kleist,
suggested treatment with dantrolene. They also accepted and Leonhard continue to accept Kraepelin’s image of
dopamine blockade as the central action of these com- catatonia as schizophrenia, however else they differ in
pounds and recommended treatment with dopamine ago- their formulations.
nists. Neither approach was useful. In time, NMS was In 1981, a writer asked where the catatonics had gone,
appreciated as a form of MC with a specific precipi- suggesting that the widespread use of antipsychotic drugs
tant.19,60 Successful treatment trials with benzodiazepines may be responsible.70 A better explanation comes from
and electroconvulsive therapy (ECT), the known effective the early 20th century shift in psychiatric practice from
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