Carlos Morra´s comment on Donald F. Klein’s final comment

Thomas A. Ban: The Wernicke – Kleist - Leonhard Tradition with Special Reference to Mania, Melancholia and Manic-Depressive Psychosis
Collated by Olaf Fjetland

I see the point that Donald Klein raised in his final comment and I may say that it maintains the point of view of many of the psychiatrist and psychologists of the Western world, shared by many, but possibly contradicted by many, too. The basic objective of nosology is to identify the natural categories of diseases; we have not completed this task, specially in the field of psychosis. Natural categories are still a mystery to us. Although we have for many years followed the psychopathology of Kraepelin and Bleuler, doing so has lead to a divorce between clinical practice and research; continuing to do so will condemn us to failure and/or isolation.

Regarding genetics, there are several reports of families studied based on Leonhard´s classification which showed better correlation than Kraepelin´s subtypes of schizophrenia (Ungvári 1985; Franzek et al. 1995; Beckmann et al. 1996; Franzek and Beckmann 1996, 1998; Ban 2004; Schanze et al. 2012; Peralta et al. 2016), but still the findings are not sufficiently strong to change the modern paradigm of several genes that are not directly responsible for the disease, but for the predisposition to generate the disease (DiLalla et al. 2017).

There have been certain groups that adopted Leonhard´s Classifications and found a significant difference in electrophysiological and brain perfusion studies between the three main groups of schizophrenic patients: Hebephrenic, Catatonic, and Paraphrenic.  In a conference at the World Psychiatric Association (WPA) meeting in Buenos Aires, Strik (2008) presented the analysis of his data separated in three groups: patients who had predominant affective Symptoms/signs, patients who had predominant thought symptoms/signs and patients who had predominant motor symptoms/signs. This year the WPA published a study with similar results on cerebral perfusion patterns in schizophrenic patients (Stegmayer 2017). The three groups where significantly discriminated.     

Despite of the complexity of the clinical subtypes within each category, the main groups are still there to be studied and validated. We cannot say that the categories are not valid because there isn´t enough evidence to eliminate this hypothesis.

The power of prediction is pretty much the same between the different categories. Unsystematic schizophrenias have a better prognosis than systematic schizophrenias and they both have a worse prognosis than cycloid psychosis. Within the group of systematic schizophrenias, hebephrenia has the worst prognosis while catatonia has a better prognosis than hebephrenia, but still worse than paraphrenia (Leonhard 1995).

In my everyday practice, I use Leonhard´s classification to stablish a prognosis, an evaluation of possible dangers and also a better selection of the treatment because there wasn´t a valid prognosis and treatment use for the DSM-IV, and we have introduced some of Leonhard´s categories camouflaged in RDoC´s dominions (i.e., affect, delusions/hallucinations, etc.).

I also may say that we know that the brain´s complexity is likely to have several different manifestations of each single nosological entity. We have only a few types of cells in the pancreas, yet we can have several diseases (Cancer, pancreatitis, diabetes, etc.).  Having several types of cells, circuits and structures, we shouldn´t wait to have only a few diseases in the brain. Leonhard´s classification is difficult to teach and also difficult to learn, but the difficult road, which often leads to the right finding, is the one less used.  Everyone choses the simple road that, in the best of the cases, leads to partially true, but incomplete findings.

References:

Ban TA. Neuropsychopharmacology and the genetics of schizophrenia: a history of the diagnosis of schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry. 2004; 28: 753-62.

Beckmann H, Franzek E, Stöber G. Genetic heterogeneity in catatonic schizophrenia: a family study. Am J Med Genet. 1996; 67: 289-300.

DiLalla LF, McCrary M, Diaz E.  A review of endophenotypes in schizophrenia and autism: The next phase for understanding genetic etiologies. Am J Med Genet C Semin Med Genet. 2017 Jun 29. doi: 10.1002/ajmg.c.31566. [Epub ahead of print].

Franzek E, Beckmann H. Different genetic background of schizophrenia spectrum psychoses: a twin study. Am J Psychiatry. 1998; 155: 76-83.

Franzek E, Beckmann H. Genetic heterogeneity of schizophrenia. Results of a systematic twin study. Nervenarzt. 1996; 67: 583-9.

Franzek E, Schmidtke A, Beckmann H, Stöber G. Evidence against unusual sex concordance and pseudoautosomal inheritance in the catatonic subtype of schizophrenia. Psychiatry Res. 1995; 59: 17-24.

Leonhard K. Aufteilund der endogenen psychoses und ihre differenzierte atiologie, 7ª Stuttgart: George Thieme;1995..

Peralta V, Goldberg X, Ribeiro M, Sanchez-Torres AM, Fañanás L, Cuesta MJ. Familiality of Psychotic Disorders: A Polynosologic Study in Multiplex Families. Schizophr Bull. 2016; 42: 975-83.

Schanze D, Ekici AB, Pfuhlmann B, Reis A, Stöber G. Evaluation of conserved and ultra-conserved non-genic sequences in chromosome 15q15-linked periodic catatonia. Am J Med Genet B Neuropsychiatr Genet. 2012; 159B : 77-86.

Stegmayer K, Strik W, Federspiel A, Wiest R, Bohlhalter S, Walther S. Specific cerebral perfusion patterns in three schizophrenia symptom dimensions. Schizophr Res. 2017 Mar 17. pii: S0920-9964(17)30131-7.

Strik W, Dierks T. Neurophysiological mechanisms of psychotic symptoms. Eur Arch Psychiatry Clin Neurosci. 2008; 258 Suppl 5: 66-70.

Ungvári G. Clinicogenetic studies within the scope of Leonhard taxonomy. Psychiatr Neurol Med Psychol (Leipz). 1985; 37: 309-17.

December 14, 2017