Tuesday, 18.05.2021

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

 

Hector Warnes’ comment on Foucher et al’s reply to Edward Shorter’s comments

 

        Prof. Foucher metathesis is indeed an excellent paper on the philosophy of science, at least in clinical psychiatry. Because of its highly theoretical nature I would like to address some questions.

        What does Prof. Foucher mean by a "differentiated psychopathology"?  As far as I am aware the same semiotic trait may apply to different psychopathological syndromes of different etiologies (a common observation in our field) unless they cluster with other traits repeatedly in time and kindle similar physiopathological brain circuits along with a similar biochemical marker. 

        The complexity of the genetic-phenotypes number of interactions and sequences creates a diversity rather than a singularity. Edward Shorter's comments on revisable rather than "cast in stone" or Foucher's concept of fallibilism and realism raises Popper's (1959) falsifiability principle in the scientific methodology.

        I wonder why we are at odds with well-defined morbid entities that over time are still being questioned or dismissed? I agree with Prof. Foucher about limiting our categorical nosology rather than opening it up to an endless number of disorders or dimensional spectrum states without clear-cut boundaries and increasing diverse etiological factors.

        Would Prof. Foucher explain what he means when he writes, "If psychotic symptoms result from the dysfunction of one or several brain systems, they are expected to have power low distribution and to aggregate in definite clusters"? Or when he writes, "Even a single cause can have multiplicative effects resulting in the abnormality frequent emergence of rare events"? 

        I would tend to disagree with Prof. Foucher by stating that neither positive nor negative symptoms in schizophrenia are rare events (unless I misunderstood his point). Further, we are aware that comorbidities are the rule rather than the exception and that the pre-morbid personality is an important epigenetic variable. What is also unclear to me is his statement that "…isolating and optimizing the description of symptoms-complexes and phenotypes… to see if they can be the manifestations of syndromes or diseases (simple or complex) of a thousand different very rare diseases in what we consider today as a schizoaffective disorder."

        In a 2015 paper written by Orgogozo, Morizot and Martin the authors dissect the interaction between genes with multiple environmental and biological variables (cellular environment, mechanical forces, symbionts, external molecules, temperature, epigenetic imprinting and individual experience). Even when the most important variables are accounted for, repeated experimental results, the evolution of the disease or the new discoveries may prove us to be on the wrong path. The repetition of hundreds of research studies over the decades indicate many disease entities are showing new perspectives or new findings or new correlations with other diseases which are likely to alter treatment.  Scientists have to replicate and reconfirm their findings (ad nauseam) until the classification of facts (is tenable?) and their interconnectivity is beyond reasonable doubt.

 

Reference:

Orgogozo V, Morizot B, Martin A. The differential view of genotype-phenotype relationships. Front. Genet. 2015; 6:179. 

Popper KR. The logic of scientific discovery. University Press. 1959.

 

November 19, 2020