Edward Shorter`s comment on Jack R. Foucher et al. Wernicke-Kleist-Leonhard phenotypes of endogenous psychoses : a review of their validity
Foucher JR, Gawlik M, Roth JN, de Billy CdeC, 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. reply
Metatheses of the Wernicke-Kleist-Leonhard research program
We feel honored and thankful to Dr. Shorter for his comment on our recent review of WKL achievements (Foucher, Gawlik, Roth et al. 2020). We particuliarly appreciated the kindness and constructiveness of his critiques. We are also very thankful to INHN for giving us the opportunity to clarify some points as it is clear from some of Shorter’s remarks that we missed some of our goals in the writing of the paper.
As there are many points to discuss, we propose to post our responses not all at once, but one after the other. Let us start from a very basic philosophy of science answer to the remark about us:
“The authors are members of the Wernicke-Kleist-Leonhard Society, a group with an almost cult-like attachment to the nosology of Karl Leonhard.”
Dr. Shorter is perfectly right in stating that we are all members of the Wernicke-Kleist-Leonhard International Society which might cast doubts on our goals and our impartiality. This is an identity question: is our Wernicke-Kleist-Leonhard society stuck in the past or is it pointing towards the future? The answer is not a simple yes or no.
Preserving traditional clinical skills
Members of our society embrace three commitments. The first two are: “to preserve the tradition of clinical excellence in differentiated psychopathology”; and “to promote, teach and diffuse knowledge and clinical skills in differentiated psychopathology.” Importantly, despite the name of our society our ambition is to embrace more largely any refinements in psychopathology and phenotypical proposals, in line with Prof. Helmut Beckmann’s vision (Beckman 2000).
Though considering its precision and near-comprehensiveness, Karl Leonhard’s classification remains our leading differentiated psychopathological framework (Leonhard 1999). But the preservation of Leonhard’s “tradition” should be viewed less as a “cult-like attachment” than a way to maintain the understanding of old texts and the departure of rephrased concepts from the originals.
This applies also to other reference frames. There is a need to be multi-lingual in order to understand the differences between these reading grids. The importance of being multi-lingual is perhaps better appreciated by those of us who were first trained in the ICD-DSM framework before being interested in WKL and other traditions. We could measure how deep these grids biased and limited our perception of patients’ manifestations; the power of this imprint being even stronger than when the same labels are used to mean two very different things - the “periodic catatonia” point will be a perfect illustration of this.
Yet this article has been written in the perspective of our last commitment as members: “to encourage, support and take part in scientific studies based on differentiated psychopathology.”
From a philosophy of science perspective, the society embraces most metatheses of dialectic critical realism (DCR) (Sousa 2010). While DCR postulates the existence of a mind independent reality, it also acknowledges that our access to it is indirect and that our representations will remain incomplete and fallible, but hopefully also perfectible. Hence, we fully agree with Dr. Shorter when he states that the aim should be to develop a revisable, rather than a “cast in stone,” representation of psychiatric disorders. Our ontological realism and epistemological fallibilism are incompatible with any parochialism. Hence, we are fully in line with DRC’s advocacy for the method of “multiple working hypotheses” (Chamberlin 1965).
In the field of psychoses, the decline of the DSM’s categorical paradigm left room for a surge of alternatives proposals: DSM-5’s dimensions (Sousa 2010), Hierarchical Taxonomy of Psychopathology (HiTOP) (Chamberlin 1965), Research Domain Criteria (RDoC) (Kuhn 1996), Systems Neuroscience of Psychosis (SyNoPsis) (Kahneman 2003), biotypes (Brain Research through Advancing Innovative Neurotechnologies). The purpose of our review article was a reminder that there still is room for classical biomedical approaches of which the WKL classification seems to us as the best illustration in our field.
The problem is that even the deepest understanding of these different reading grids will not allow us to order their respective adequacy with reality. Because the most exclusive gathering of evidence is according to a single framework, in post-positivistic terms they will remain incommensurables (Kuhn 1996). The only way to break this vicious circle would be to confront the verisimilitude of each proposal in the same adversarial collaborative (Kahneman 2003) crucial experimental series (Marcum 2007). Our first attempt only challenged DSM’s schizophrenia and was tuned out to the advantage of the periodic catatonia and cataphasia distinction, but this was a proof of feasibility (Foucher, Zhang, Roser M et al. 2018). Moreover, the idea is not to kill the less adequate models or paradigms, but rather to help them find their weaknesses, give their supporters the opportunity to improve and perhaps to pick up ideas from the other models before the next experimental run. We take the opportunity of this response to encourage researchers interested in this approach to contact the first author. Indeed, we need dialectic argumentation with adversarial collaborators to help us be critical with our models.
Our core belief is that most of the psychoses are diseases, i.e., “natural morbid entities,” that take their categorical nature from their specific etiology or pathophysiology. We also view these diseases as affecting one or several brain systems, hence anchoring our approach in systems neuroscience, systems biology and, more widely, in the emerging field of complex adaptive systems. We feel that this should not betray Wernicke’s thoughts about brain functioning according to “psychic circuits” (Wernicke 2015) following “diagram-kinds” of brain networks (Rutten 2017).
We believe that neither disorders nor dimensions could accurately capture the real nature of psychotic entities. If psychotic symptoms result from the disfunction of one or several brain systems, they are expected to have power law distributions and to aggregate in definite clusters (Foucher, Clauss, Obrecht et al. 2020).
Why not dimensions?
This would be incompatible with current dimensional accounts which are based on normal distributions, i.e., implicitly assuming dimensions to result from the mere addition of many causes of very small effects. This is at odds with the misfunctioning of a system. Systems’ dynamics depend on the evolving pattern of asymmetrical interactions (Holland 2006). Even a single cause can have multiplicative effects resulting in the abnormally frequent emergence of rare events, e.g., positive symptoms and/or destructive effects resulting in the abnormally frequent loss of others, e.g., negative symptoms. Normal distributions cannot account for these normally exceptional occurrences; Fat-tail distributions do (Thurner, Klimek and Hanel 2018).
Why not disorders?
Such rare symptoms are not supposed to occur in various combinations of equally meaningful symptoms in a list for ICD-DSM disorders. Rather, specific symptoms’ clusters are expected to occur depending on the system(s) or the disordered domain(s). Yet their probability of occurrence is also conditioned by the context. The most regular should be the ones that directly result from the malfunctioning system(s), i.e., be primary symptoms (or “elementary”) according to Wernicke (Krahl, Schifferdecker and Beveridge 1998). Secondary manifestations depend on the context given by the macro-systems in which the disordered one(s) is(are) embedded, e.g., the whole central nervous systems and/or the physical or social environment of the patient.
But symptoms-complexes and phenotypes
This is why we keep on with the traditional biomedical paradigm: isolating and optimizing the description of symptoms-complexes and phenotypes and try to see if they can be the manifestations of syndromes or diseases (either simple or complex). It is clear to us that the strategy might fail. Our biggest fear would be that there would not be only 71, not even a 100, but thousands of different very rare diseases in what we consider today as a schizoaffective spectrum. But our hope is that as in the field of mental retardation, beside the thousands of very rare diseases, there remain more frequent entities, like the fragile-X syndrome. In our mind, phenotypes like periodic catatonia or cataphasia are among the most credible candidate. But this is a bet, by no way a definitive statement.
As a matter of conclusion
“Yes,” the identity of the Wernicke-Kleist-Leonhard International Society is rooted in the achievements of our forefathers. And, “Yes,” we want to follow up their ambition in contributing to deciphering the code of psychotic illnesses, even if it happens that we will have to refute some of their proposals and embrace those of others. There is no definite Truth, just temporary adequate representations; the most important is that some of them could translate into efficient therapies for our patients.
Beckmann H. Foreword. In: Franzek EJ, Ungvari GS, Rüther E, Beckmann H, editors. Progress in Differentiated Psychopathology. Würzburg, Germany: International Wernicke-Kleist- Leonhard Society; 2000 p. xv.
Chamberlin TC. The Method of Multiple Working Hypotheses: With this method the dangers of parental affection for a favorite theory can be circumvented. Science. 1965; 148(3671):754-9.
Foucher JR, Zhang YF, Roser M, Lamy J, De Sousa PL, Weibel S, Vidailhet P, Mainberger O, Berna F. A double dissociation between two psychotic phenotypes: Periodic catatonia and cataphasia. Prog Neuropsychopharmacol Biol Psychiatry. 2018; 86:363-9.
Foucher JR, Gawlik M, Roth JN, de Billy CdeC, 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 Clin Neurosci. 2020; 22(1):37-49.
Foucher JR, Clauss J, Obrecht A, de Billy C, Mainberger O, Schorr d B, Berna F, Bonah C. Bases épistémologiques de la recherche sur les psychoses. Quelle solution pour le choc des cadres paradigmatiques ? Ann Médico-psychologiques, Rev Psychiatr. 2020.
Holland JH. Studying complex adaptive systems. J Syst Sci Complex. 2006; 19(1):1-8.
Kahneman D. Experiences of Collaborative Research. Am Psychol. 2003; 58(9):723-30.
Krahl A, Schifferdecker M, Beveridge A. Carl Wernicke and the concept of “elementary symptom.” Hist Psychiatry. 1998; 9(36):503-8.
Kuhn TS. The Structure of Scientific Revolution. Vol 29.; 1996.
Leonhard K. In: Beckmann H, editor. Classification of Endogenous Psychoses and Their Differentiated Etiology. Vienna: Springer Vienna; 1999.
Marcum JA. Experimental Series and the Justification of Temin’s DNA Provirus Hypothesis. Synthese. 2007; 154(2):259-92.
Rutten G-J. In: The Broca-Wernicke Doctrine. The Diagram Makers and Their Critics. Cham: Springer International Publishing; 2017, pp. 57-75.
Sousa FJ. In: Advances in Business Marketing and Purchasing. Metatheories in research: Positivism, postmodernism, and critical realism. Emerald Group Publishing Limited; Vol 16. 2010, pp. 455-503.
Thurner S, Klimek P, Hanel R. Introduction to the Theory of Complex Systems. Oxford, OUK: Oxford University Press; 2018.
Wernicke C. In: Miller R, Dennison J, editors. An Outline of Psychiatry in Clinical Lectures: The Lectures of Carl Wernicke. Cham: Springer; 2015.
October 15, 2020