Thomas A. Ban’s response to Victor Peralta’s answer

Thomas A. Ban: Peralta, Cuesta and their associates finding on the highest familiality of Leonhard’s classification in polynosologic study


            Thank you for answering my question whether time has come to implement Leonhard’s diagnostic system in psychiatric research. I understand your pessimistic appraisal of the situation and agree with you about the problems with Leonhard’s classification, even if I would not attribute its lack of success to those problems, but to other factors and especially to the format in which Leonhard presented his classification in his text (Leonhard 1957).

            We certainly agree also about the powerful influence that DSM-III and its successors has had on psychiatric practice, education and research. Yet, by the end of the 20th century it was evident for all those actively involved that consensus-based diagnoses were inadequate for biological and molecular genetic research. Further, in the new millennium DSM-5 has become vulnerable to the extent that Thomas Insel, as Director of the US National Institute of Mental Health, made it a prerequisite to use the Research Domain Criteria (RDoC) he developed with Bruce Cuthbert in studies supported by the Institute. In the RDoC, DSM diagnoses are replaced by five “domains” of “neurobiological circuits” with the idea that identification of the “sites (domains) of dysregulation” will provide information on the structural underpinning of psychoses (Insel and Cuthbert 2009; Insel, Cuthbert, Garvey, et al. 2010).

            RDoC was discussed on INHN’s website and to open the exchange Samue Gershon (2015) pointed out that “NIMH ‘jettisoned’ a long tradition of diagnosis-driven research and mandated that all research must begin from a matrix of neuro-scientific structures, such as genes, cells, circuits that cut across behavioral, etc., domains.” He also raised the questions, “How can one do this? What are the benchmarks?”  as “the diagnostic system is in fact very defective, and the data in the genetic realm are undefined?” In his reply to Gershon’s questions, Bernard Carroll (2015) argued that RDoC is “a contrived matrix of metaphysical constructs” and its authors “don’t seem to understand the need to advance nosology by incorporating biomarkers along with clinical symptoms in diagnostic definitions, as happened in general medicine.” In support of his argument, Carroll pointed out how meaningless it would be to “lump together Cushing disease with juvenile onset diabetes mellitus, Type II diabetes mellitus, severe psychological or physiological stress, metabolic syndrome, anorexia nervosa, and pregnancy on the basis of an abnormal glucose tolerance test, which these all can display.”

            Gershon’s questions and Carroll’s reply are in line with the recognition that “In a historical perspective, the RDoC is a tabula rasa, in which 200 years of development in psychiatry is dismissed” (Ban 2015). As presented, it is floating in the air, without any clinical anchors. Nevertheless,  if the population of “circuit-based units”   would be defined  in terms of “nosological homotypes,” by using a matrix in which the rows consist of psychopathological symptoms and the columns, nosological organizing principles (such as form of onset, course, polarity and outcome), the RDoC  could  provide a bridge between psychiatry in the mid-20th century, based on psychopathology and psychiatric nosology, and a psychiatry in development in the 21st century with the capability to integrate into its body of knowledge findings generated by rapid advances in the neurosciences (Ban 2002). Considering that Karl Leonhard’s classification of “endogenous psychoses” is the one, among all the different classifications, that would provide diagnoses closest to the diagnoses that nosological homotyping could offer, one would have expected that introduction of the RDoC would generate interest in using Leonhard’s classification in psychiatric research in the “endogenous psychoses.” 

            This was not to be the case as Leonhard’s classification was considered to be complex and difficult to use.

            It is a common contention that Leonhard’s classification is complex and difficult to use. Yes, it is for those without an education in psychopathology and psychiatric nosology, but not for those with a background in these disciplines.  In fact, for those educated in psychopathology and psychiatric nosology, the disciplines which provided a foundation for modern psychiatry by the mid-20th century, the use of Leonhard’s classification is rather simple. It also spares its users from the burden of having to memorize again and again with every new edition, the artificially derived criteria of consensus-based classifications in which form and content of psychopathology is mixed with behavioral deviations and impairment of social adaptation.

            Leonhard’s classification with its forms and subforms of disease is the culmination of the Wernicke-Kleist-Leonhard (WKL) tradition in psychiatry. It has its roots in: (1) Carl Wernicke’s (1881) adoption of Wilhelm Griesingers’ (1843) notion that mental activity is “reflex” activity; (2) Wernicke’s (1899) classification of psychoses as “hypo (deficit)-functioning,” “hyper (excess)-functioning,” or “para (distorted)-functioning” of one or another component (paths, phases) of the “psychic reflex”; and Wernicke’s identification of subpopulations within the different psychoses with the employment of his “elementary symptoms” approach. An “elementary symptom” within Wernicke’s (1990) frame of reference is a symptom from which, assumedly, all other symptoms of a disease are derived.

            Kraepelin’s (1899) division (“dichotomy”) of the “endogenous psychoses towards the end of the 19th century, in the 6th edition of his textbook,” on the basis of “temporal characteristics,” i.e., “course” and “outcome, into “manic depressive insanity,” a disease that follows an episodic course with full remission between episodes, and “dementia praecox,” a disease that follows a continuous deteriorating course, distracted attention from Wernicke’s contributions. Nevertheless, in the 1920s, and ‘30s Kraepelin’s dichotomy of “endogenous psychoses” was re-evaluated by Karl Kleist, a disciple of Wernicke and subsequently, in the 1940s and ‘50s, by Karl Leonhard, a disciple of Kleist.  

            In his re-evaluation, Leonhard employed Edna Neele’s (1948) concept of “polarity” and Wernicke’s concepts of “mental structure” and “elementary symptoms” in classifying patients. With the employment of “polarity,” he divided the population already separated by Kraepelin on the basis of “course” and “outcome,” into “bipolar” and “unipolar diseases,” and separated within both subpopulations (forms) on the basis of the site of the dominant psychopathology, i.e., in the afferent-cognitive (“psychosensory”), central-affective (“intrapsychic”), or efferent-motor (“psychomotor”) component of Wernicke’s “mental structure.” Furthermore, with the employment of Wernicke’s “elementary symptom” approach, he detected within each subpopulation several distinct psychopathology–based subforms.

            In Leonhard’s classification, “bipolar diseases” are characterized by a continuously changing, “polymorph” (multiform), disease picture with a potential to display both extremes in mood, thinking, emotions and/or motility, whereas “unipolar (monopolar) diseases” are characterized by a consistent, unchanging, “monomorph” (simple, also referred to as pure) disease picture with no variation of mood, thinking, emotions and/or motility.

            On the basis of “polarity,” Leonhard splits Kraepelin’s “dementia praecox” into two classes of disease: “(bipolar) unsystematic (non-systematic)  schizophrenias” and “(unipolar) systematic schizophrenias”; and on the basis of Wernicke’s “mental structure,” he divides the  “unsystematic schizophrenias” into three forms of disease, i.e., “cataphasia,” “affect-laden paraphrenia” and “periodic catatonia,” and the “systematic schizophrenias” into paraphrenias (with six elementary symptom-based sub-forms: hypochondriacal, phonemic, incoherent, fantastic, confabulatory and expansive), “hebephrenias” (with four elementary symptom-based sub-forms: silly, eccentric, insipid or shallow and autistic) and “catatonias” (with six sub-forms: parakinetic, affected or manneristic, proskinetic, negativistic, voluble or speech prompt, and sluggish or speech inactive).

            Similarly, on the basis of “polarity,” Leonhard also splits Kraepelin’s “manic depressive insanity” into “(bipolar) manic depressive disease” and “(unipolar) phasic psychoses” and, with consideration of Wernicke’s “mental structure,” he separates from “manic depressive disease” the “cycloid psychoses” and divides the “cycloid psychoses” into “excited-inhibited confusion psychosis,” “anxiety-happiness psychosis” and “hyperkinetic-akinetic motility psychosis.” Furthermore, on the basis of “totality,” the nosological organizing principle introduced by William Cullen (1769, 1776), he separates “pure mania” and “pure melancholia,” “universal” diseases, from the “pure euphorias” (unproductive, hypochondriacal, enthusiastic, confabulatory and non-participatory) and “pure depressions” (harried, hypochondriacal, self-torturing, suspicious and non-participatory), “partial” diseases, each displayed in five distinct elementary symptom-based subforms.

            Within the “bipolar-polymorph” diseases, the signal difference between “manic depressive disease” and the “cycloid psychoses” is that in “manic depressive disease” the “polarity” primarily is in mood, whereas in the “cycloid psychoses” the “polarity” primarily is in thinking (“excited-inhibited confusion psychosis”), emotions (“anxiety-happiness psychosis”) or  psychomotility (“hyperkinetic-akinetic motility psychosis”); and within the “unipolar-monomorph” diseases, the signal difference between “pure mania/melancholia” and the “pure euphorias/depressions” is that in “pure mania” and in “pure melancholia” the entire “mental structure” is affected, whereas in the “pure euphorias” and “pure depressions” only parts of the mental structure is involved.         Leonhard’s classification of “endogenous psychoses” was first published in 1957, just about the time when neuropsychopharmacology was born. Yet, in spite of early findings which indicated that therapeutic responsiveness to the same psychotropic drug widely differs in the different subpopulations in Leonhard’s classification, Leonhard’s nosology has remained isolated from the main stream of neuropsychopharmacological and molecular genetic research (Astrup 1959; Fish 1964). In fact, in so far as I know, it was your study, the first and probably still the only one, in which Leonhard’s classification of endogenous psychoses was employed in molecular genetic research (Peralta et al 2016).



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November 23, 2017