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Tuesday, 26.05.2020

Edward Shorter’s comment on Jack R. Foucher et al.’s paper on  Wernicke-Kleist-Leonhard phenotypes of endogenous psychoses: A review of their validity


        The DSM nosology has proven so unsatisfactory that efforts to recast it – and to  free it from the dominance of the American psychiatric establishment – are long overdue.  This is the first serious attempt to propose an alternative to DSM, and it is entirely the work of European and Latin American scholars.  This is with the exception of Tom Ban, who leads INHN and  is of Hungarian origin (and now lives in Toronto).  Otherwise,  the investigators are entirely continental European and Latin American.  There are no North Americans nor British present.  Finally it happens that nosology is being rescued from the American Psychiatric Association.  And the system being proposed is not at all novel but the classification offered by East German psychiatrist Karl Leonhard in 1957.

        Among the locations of the 22 co-authors, Würzburg and Strasbourg are the centers of gravity.  Würzburg had long been a center of enthusiasm for Karl Leonhard since the late Helmut Beckmann served there as professor of psychiatry and more recently the prematurely departed Gerald Stöber.  Ernst Franzek also carried on that work and a number of other authors as well have as home base the University of Würzburg.  Strasbourg is equallty a focus and clearly Leonhard’s work has caused excitement there.  Carlos Morra, also an INHN editor, is based in Córdoba and there are two staffers at the famous private psychiatric hospital in Prangins in Switzerland;  the Netherlands is represented, and also other centers.

        It is a measure of the grasp of the dead hand of DSM that the world’s major psychiatric research centers – in Paris, London, New York, Los Angeles, Berlin (with the exceptioon of co-author Barbara Bollmann), Munich and Vienna – are entirely unrepresented!  Just as psychopharmacology originated in the 1950s in the “red brick” universities of the UK (and not in Oxbridge) and in the research centers of the Mississippi Valley in the US (and not on the coasts), this dramatic challenge to the primacy of DSM arises in the periphery of Europe and in Latin America and not in places where Pharma – with its fondness for the lucrative diagnoses of DSM – has felt very much at home.

        The authors are members of the Wernicke-Kleist-Leonhard Society, a group with an almost cult-like attachment to the nosology of Karl Leonhard.  Carl Wernicke was a the professor of psychiatry in Breslau, (then in Gerrmany now in Poland), and Halle, Germany, whose own diagnostic ideas rivaled those of Kraepelin.  Karl Kleist, a student of Wernicke, was professor of psychiatry in Frankfurt (and remained in office during the Nazi years, not entirely free of contamination from National Socialist ideas); and Karl Leonhard was Kleist’s pupil, ending up in Erfurt and in East Berlin as the professor of psychiatry at the Charité during the Communist years.  Leonhard’s teachers had laid out some of the elements of “WKL” thinking, but it was in 1957, in a great book that is one of the fundaments of modern nosological thinking, that Leonhard laid out his own classification in all of its complexity  (Leonhard 1957).  There is an English translation, but almost that everything Leonhard ever wrote was in German, a recipe for oblivion  in the modern world of the mental sciences.  (It is a sad commentary that one of the main expositions of the development of Wernicke-Kleist-Leonhard thinking is my own little discussion (Shorter 2015).

        The authors distinguish between consensus-based diagnoses, as found in DSM – the product of the kind of horse-trading that goes on in a commnittee – and phenotypic diagnoses, as they exist in Nature and are the product of scientific research. 

        Here’s where the going gets tough.  The WKL school identifies 35 major forms of phenotypic diagnoses in the psychoses (which are not just confined to delusions and hallucinations but really encompass all serious psychiatric illnesses).  Combinations of these major diagnoses produce in turn some 36 minor forms, each supposedly a separate disease.  Each of these diseases has  “construct validity,”  evidence showing that it really exists.  That evidence is not presented in this paper, which is content merely to lay out the system – with the promise that the evidence will follow later.  So, here is the first note of doubt:  Does this evidence really exist and if so why has no one presented it to date with the exception of responsiveness to phenothiazines of the diagnosis “afffect-laden paraphrenia”  (Fish 1964) and a few other papers listed in an extensive bibliography?

        The authors explain, “Phenotypes are grouped into five families according to their course, mono- or  bipolarity, and . . . [the] domains: affect, thought, and psychomotricity.” 

        In the monopolarity group we get the various “pure” depressions, mania and melancholia.  Thus, some mood disorders may be monopolar.   Here the authors make an important distinction between “pure depression” and “pure melancholia” which, in the current revival of thinking about melancholia, may provide grist for the mill.

        In the bipolar group we find: manic-depressive illness, and such cycloid psychoses as anxiety-happiness psychosis – a big diagnosis in the WKL stream of thinking:  the patients alternate between anxiety and happiness.  Many clinicians will have seen this and ask, why should it not be a separate disease?  (Sure, but is it differentially responsive to anything?  Does it have its own genetics?)  Here as well is “affect-laden paraphrenia,” the diagnosis that mathematician John Nash evidently  had in the movie A Beautiful Mind (Nasar 2001).  Affect-laden paraphrenia is said to be a “progressive relapsing” disorder.  Leonhard ranked it among the “non-systematic schizophrenias,” meaning not necessarily a horrible outcome.  Again, there are many of today’s patients with “schizophrenia” who do not go progressively downhill, but who do not remit to baseline either.  We don’t have a separate term for them but the WKL group does.

        Finally, in the “monomorphic” polarity group we get the “systematic schizophrenias,” the bad news diagnoses.  These do go progressively downhill and do not respond well to medication. 

        Thus far, we have sorted the patients on the basis of course and polarity.  This seems quite straightforward.  The authors present data on the frequency of the individual diagnoses within the entire stystem and a bit of information on pharmacological responsiveness.  Of particular interest is the authors’ separation of manic-dperessive illness from the unipolar depressions:  “On average, MDI episodes are of shorter duration than monopolar ones, i.e., 6 months on average for depressive episodes.  Acute onset, sudden cessation; or rapid switches are common.”  Relapses are said to be commoner than in the monopolar variety; MDI has a greater hereditary loading.  Could  there  be differential responsiveness to medication?  This crucial dimension has apparently not yet been studied.

        Then there are the “cycloid psychoses,” such as “hyperkinetic-akinetic motility psychosis” (which is almost certainly a form of catatonia, though the authors do not call it that).  One of these psychoses is episodes of “BDA,”  bouffées délirantes aiguës des dégénérés.  This was a diagnosis initiated by Parisian psychiatrist Valentin Magnan late in the 19th century, when the psychiatric world was gripped by the concept of “degeneration” (Shorter 2005). It is mildly disconcerting to see this come back to life as a “real” disease.  Possibly the authors are unfamiliar with the arc of the BDA diagnosis.  I can think of no other reason for incorporating it.

        The “schizophrenias” come in for an extended discussion as “phenotypes with build-up of residual symptoms,” in other words, mild or steep downhill courses.  “Cataphasia,” for example, is one of the phenotypes, characterized by thought disorder and derailment.  This dismantling of the global concept of a single “schizophrenia” is very much to be applauded, and here the authors are reaching into the “schizophrenia” basin and pulling out distinct disorders, comparable to the recent separation, in mainline psychiatry, of catatonia from “schizophrenia.”  The flood of neologisms on the page here is offputting, but the impulse is sound, and long overdue.

        I was dismayed to see “periodic catatonia” described as another of the “non-system schizophrenias.”  It has been with so much trouble that psychiatry has recently detached catatonia from schizophrenia and made it a disease of its own.  Now, for the authors to reinsert catatonia in schizophrenia, and to claim that it is response to antipsychotics, is to weep.  Antipsychotics are counter-indicated in catatonia; the remedies of choice are the benzodiazepines and convulsive therapy  (Shorter and Fink 2018).

        When we get to the “system schizophrenias” we have crossed the line into irreversible, downhill madness.  The authors say, “They have an insidiously progressive course resembling that of slow encephalitis.” Here the classification threatens to trudge into the swamp.  There are four “phenotypes of hebephrenia,” six of ”system paraphrenia” and six varieties of “system catationia.”  One starts to realize why it is that the Leonhard diagnoses have not received wide international acceptance.  But that does not mean they are wrong.  The germ theory of disease did not at first win wide international acceptance either.

        What is at stake here?  A few obscure diagnoses by even more obscure German psychiatrists?  No.  There have been no innovative new drug classes in psychiatry for the past 40 years.  The field is badly in need of effective medications for the many patients who are unresponsive to the current offering.  There will be no progress in drug discovery until we can isolate homogeneous clinical populations who may share the same underlying pathophysiology – and respond to the same remedies.  Such current diagnoses as “major depression” and “schizophrenia” are anything but homogeneous.  Once we have accurate phenotypes, we can move ahead with clinical chemistry.  This is important.

        The WKL system should not be seen as cast in stone.  The authors have made some modifications to Leonhard’s original schema.  As well, all of the operational ceriteria that the authors use to characterize each of the 35 disorders may not hold up under further scrutiny.  Some of the categories may be collapsed as others spring into place.  That is beside the point.  The main point is that this pioneering piece of scholarship opens up the whole nosology debate.  It consigns DSM to the trash heap and suggests there are really very different ways of looking at defining disease in psychiatry, once we put our minds to it.



Fish F. The Influence of the Tranquiilizers on the Leonhard Schizophrenic Syndromes.  L’Encéphale, 1964; 53(suppl.):245-9.

Foucher JR, Gawlik M, Roth JN, Clément deCdeB, Jeanjean LC, Obrecht A, Mainberger O, Clauss JME, Elowe J, Weibel S, Schorr B, Cetkovich M, Morra C, Rebok F, Ban TA, Bollmann B, Roser MM, Hanke MS, Jabs BE, Franzek EJ, Berna F, Pfuhlmann B. Wernicke-Kleist-Leonhard phenotypes of endogenous psychoses: a review of their validity. Dialogues in Clinical Neuroscience, 2020; 22(1):37-49.

Leonhard K. Die Aufteilung der endogenen Psychosen. East-Berlin: Akademie-Verlag, 1957.

Nasar S. A Beautiful Mind : the Life of Mathematical Genius and Nobel Laureate John Nash. New York, NY: Simon & Schuster, 2001.

Shorter E. A historical dictionary of psychiatry. New York : Oxford University Press, 2005.

Shorter E. What Psychiatry left Out of the DSM-5: Historical Mental Disorders Today. New York, Routledge, 2015, pp. 79-81.

Shorter E, Fink M. The Madness of Fear: A History of Catatonia.  New York, Oxford University Press, 2018.


May 7, 2020