104 Years Later

In 1911 Eugen Bleuler wrote Dementia Praecox or the Group of Schizophrenias and for a BLEULERcentury we’ve used his construct of this mysterious condition. Bleuler realized how limited was his knowledge in writing:

“At the present time, we cannot solve the problem of dissecting schizophrenia into its natural subdivisions. Nonetheless, we do have the practical need for characterizing the various clinical pictures that present themselves to us in this disease by terms corresponding, at least, rather broad and crude subdivisions. This much is possible, but not much more.

Even then, however, it is not a question of defining and delimiting different disease entities, but of grouping symptoms… A case which begins as hebephrenic may be a paranoid several years later.”

I doubt Bleuler would object to DSM 5 now having done away with the four subtypes. The APA wrote that “The DSM-IV subtypes of schizophrenia (i.e., paranoid, disorganized, catatonic, undifferentiated, and residual types) are eliminated due to their limited diagnostic stability, low reliability, and poor validity.”

The focus now is on deciphering the genetics behind what’s going on. It seems clear that whatever the genetic underpinnings there isn’t going to be a single gene responsible.

In a recent paper with a mouthful of a title Uncovering the hidden risk architecture of the schizophrenias: confirmation in three independent genome-wide association studies (Am J Psychiatry 2015 Feb) the authors conclude that

“Schizophrenia is a group of heritable disorders caused by a moderate number of separate genotypic networks associated with several distinct clinical syndromes. “

Even when the genetics becomes clearer, there will still be much to sort out: How do any genetic changes  result in manifestations of illness? Why is the concordance in identical twins only 40-50%?

Back to Blueler:

“… even in the event that all of our hypotheses should eventually prove correct, we would still be acquainted with only a very small part of all the mechanisms which are probably involved in the symptomatology of this disease. Conversely, it is obvious that at this time no one can claim to explain all or even the greater part of the symptoms.

The pathology of schizophrenia gives us no indications as to where we should look for the causes of the disease. Direct investigation for specific causal factors has also left us stranded. Certainly we know that “mental diseases” are more common in the families of schizophrenics than in those of the healthy.”

 We know more than we did in 1911 but there’s so much more to learn. In the meantime those of us working in the field will need to continue to use the tools that we know work – client-centred recovery work, PSR and MI.

To be continued…

Shalom Coodin


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