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Max Fink: Reconceptualization of catatonia


Edward Shorter’s comment


       Amid the chaos of DSM-III, Max Fink points to two solid achievements, meaning diagnoses that we can be sure exist in nature.  We are sure of this because they are identified with the medical model (as opposed to the biopsychosocial model).

       One diagnosis is melancholia, which is not just a severe form of depression but a disorder so unremittingly dreadful that it constitutes a disease of its own.  The medical model permits us the identification of melancholia (with the Hamilton Depression Rating Scale); the verification of melancholia (with the Dexamethasone Suppression Test); and the validation of melancholia (with its response to tricyclic antidepressants and to ECT).  The medical model, which is used throughout medicine, identifies diseases that exist in nature, as opposed to disorders limned about the DSM horse-trading table.

       The other solid diagnosis is catatonia, which the medical model helped us extract from the unsavoury “schizophrenia” brew and establish it as a disease of its own.  Catatonia is identified with the Bush-Francis Catatonia Rating Scale; verified by a rapid response to a single injection of lorazepam; and validated with an enduring response to lorazepam or ECT.

       These are actually the two main solid diagnoses in psychiatry.  The rest of them - schizophrenia, major depression and anxiety - constitute diagnoses that have staggered down across the path of history, propped up only by billions of pharmaceutical profits; or they represent diagnoses that nobody has been able to “disprove” - because it is so hard to disprove anything in psychiatry.  Proving is more difficult, and that brings us back to the medical model.

       (Interestingly, melancholia and hebephrenia are not in DSM at all; and catatonia made it into DSM-5 only after an intense science-based campaign.)   

       Now, three points:

—    First, how can we further extend the medical model?  What else in that toxic slurry of “schizophrenia” constitutes a real disease entity, just waiting, like catatonia, to be pulled out and dragged into the light of science?  Some observers talk about Ewald Hecker’s “hebephrenia,” which Emil Kraepelin turned into a dementia praecox subtype.  Hebephrenia does seem to constitute a disease of its own: social withdrawal in late adolescence, devastating psychotic illness, no restitutio ad integrum.  Here, two of the three criteria of the medical model are met:  identification and validation by response to treatment.  But biological verification is lacking.  No one has yet discovered a  biomarker for hebephrenia and that is because research has been diverted into the amorphous entity of “schizophrenia,” for which no biological marker has ever been discovered - nor ever will be.  (This would be comparable to finding a biological marker for “hysteria" or “ovarian insanity.”)  So, we should keep charging down the hebephrenia trail and the medical model will keep us focused.

—    Second:  a serious academic exchange about catatonia is long overdue, as Max Fink’s post suggests, and the INHN website would be a perfect forum for it.  The work of Max Fink and Mickey Taylor in 2003 and 2006 has posted trail markers for this, but there  is a lot about catatonia that we don’t know.  What is the prognosis?  Does it keep relapsing or is an ECT-aided recovery a definitive remission?  What is the epidemiology?  Young vs old, men vs women?  And is the DST  a biological marker for it as well as for melancholia?

—    Last:  why is it that all three of these diagnoses, which are discoverable with the medical model, respond to ECT?  Clinically, melancholia, catatonia and hebephrenia are quite different.  Yet the first two respond beautifully to convulsive therapy and scattered data suggest that aspects of hebephrenia are ECT-responsive as well.  


       These are huge questions.  They will not be resolved in an animated INHN exchange,  but it can help steer the discussion within the field:  here is grist for the NIMH mill.  The Institute has frittered away billions of dollars of government funding on useless SSRI trials.  Under its new director this phase seems to be over, but now the vast Institute lies dead in the water.  What is the next big agenda?  Melancholia, catatonia, hebephrenia:  kind of catchy, isn’t it?



Fink M,  Taylor MA.  Catatonia: A Clinician’s Guide to Diagnosis and Treatment.  New York: Cambridge University Press; 2003. 

Taylor MA, Fink M.  Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness.  New York: Cambridge University Press; 2006.


April 1, 2021