Improving the Mental Health System by Addressing Core Problems

Psychiatric TimesVol 32 No 3
Volume 32
Issue 3

What psychiatry needs is a new approach to “psychiatric theory.” Here are a few practical suggestions.


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Change the model

Use the medical model, not the “biopsychosocial model,” to delineate diseases in psychiatry. This means a careful psychopathological clinical description of disease entities, separating them from other disorders; their verification with biological tests; and their validation with a specific response to treatment.

Robins and Guze1 at Washington University in St Louis first proposed this in 1970 as a way forward for psychiatry. The field has now made a stab at this by delimiting the symptoms of melancholia; verifying the distinctiveness of the disease with a biomarker in the dexamethasone suppression test; and validating its treatment with electroconvulsive therapy (ECT).2 One hopes for further progress in this direction.


Break the “Kraepelinian grip” on diagnosis by abolishing the firewall Kraepelin erected in 1899 between mood disorders and chronic psychosis. Parts of Kraepelin’s great synthesis remain standing (or should do so), such as delineating “adolescent insanity” (dementia praecox) as a separate form of psychosis and calling attention to manic-depressive insanity as a disease basin of its own, including all forms of serious depression and mania.3 But Kraepelin erred in erecting a firewall between the two, for there is a huge overlap. Ignoring the overlap persuades us that adolescent insanity must be treated with antipsychotics and manic-depressive symptoms must be treated with antidepressants, a guarantee of polypharmacy.

On the other hand, restore the Kraepelinian unity of mood disorders by lumping major depression, bipolar disorder, and the manias into the same pot, which, following Bernard Carroll’s4 suggestion, we will now call “Kraepelin disease.” (There will be much psychosis in this pot, since we have abolished the firewall.)

Fink disease

Complete the liberation of catatonia as an independent disease entity by calling it “Fink disease” after Max Fink, who fought against great odds to have catatonia removed as a “subtype” of schizophrenia and be given a home of its own. This exemplifies the medical model in action: delimiting the exact symptoms of catatonia, as DSM-5 has recently done; verifying it as a stand-alone disease state with a benzodiazepine challenge; and validating its response to treatment with lorazepam and ECT.5


Take the classification of disease away from the American Psychiatric Association (APA) and DSM, and give it to an independent agency, such as the Karolinska Institute or the NIMH, for a completely new beginning. (The World Health Organization would not be a candidate for this mission, since its ICD has now been largely corrupted by DSM.) DSM has been a rolling disaster. DSM-III in 1980, under the leadership of Robert Spitzer, was a step forward in releasing the clench of psychoanalysis upon the field.

But later editions have preserved many of the errors-eg, mechanically reproducing such artifacts as “major depression,” which lumps together the two very distinct depressions that psychiatry has always had: melancholia and nonmelancholia, also called neurasthenia, reactive depression, and so forth. Gordon Parker6 resurrected melancholia in 1996 as a distinctive disease entity. Yet the gates of DSM have remained firmly shut to this venerable wanderer. (In DSM-5, it is dismissed as a “specifier,” and it is not even mentioned in the index.)

Drop psychoanalysis

Abolish psychoanalysis from the psychotherapy training of residents. (It is like making a course in astrology requisite for the training of astronomers.) DSM-III in 1980 represented the historic Waterloo of psychoanalysis. Thereafter, general psychiatry quickly lost confidence in Freud’s wisdom, although the field’s current absolute trust in neurotransmitters seems equally misplaced. Yet even today, at the field’s commanding heights, a few demoralized analysts continued to hold forth and to impose a knowledge of depth psychiatry, familiarity with the “unconscious,” and so forth as requirements for training. This atavism is as absurd as the persistence of witchcraft, and it must be brought to an end.


Vastly increase the psychopathology content of residents’ training. Although the study of psychopathology is still alive and well in Scandinavia and Germany, it seems to have largely come to an end in North America, replaced with the “operative criteria” of DSM. Yet only a fine understanding of signs and symptoms gives clinicians the wherewithal to break down these huge, heterogeneous basins of DSM (eg, major depression, schizophrenia) into distinctive disease entities that might have differential responses to treatment and prognoses.

There is no pharma conspiracy to rivet these vast DSM constructs in place-although they do make convenient pharmaceutical markets. What retains them is mainly the determination of the APA not to further introduce large changes in the field’s classification of disorders. Yet it is as though medicine, “to avoid confusion,” had insisted on retaining Galen’s classification of chest diseases. It would be wonderful if genetics were to point the way to a truly scientific classification in the future. But genetics will not be able to do that in the absence of scientifically based phenotypes, and that is what we now need.


Firm up cross-training between psychiatry and neurology, so that “clinical neuroscience” ceases to be dominated by neurology, and psychiatry gets another shot at being scientific. At the moment, there is little dialogue between the two disciplines: If one mentions to a neurologist that there might be a role for convulsive therapy in the management of parkinsonism, the response is an incredulous stare.7

Neurologists simply have not been exposed to this considerable advance. And neurologists express surprise at psychiatry’s studied indifference to the EEG in the diagnosis of anything except epilepsy (not a psychiatric disease in any event).8 There have, in other words, been big doings on both sides of the fence, but it is as though the fence were 9 feet tall and painted black.

Pharmaceutical influence

End the hysteria about not accepting ballpoint pens and the like from industry on the grounds that such tokens will bias clinical judgment. Psychiatry is subject to fads, and of the fads none is more exasperating than this sissy sanctimony about not being corrupted by “Big Pharma.” Guess what? Big Pharma has already hopelessly corrupted the field by promoting these unscientific DSM diagnoses!

“Major depression” and “general anxiety disorder” have made billions of dollars in profit for the pharmaceutical industry. Industry is not interested in corrupting the field by giving out pens or neat little desk clocks. It’s too late for that! And what is so irritating is not just the belief that free penknives will sway us, but the belief that in barring them we have safeguarded ourselves from pharmaceutical influencing. You have to be living on cloud 9 to believe this.

History as a cornerstone of psychiatry

Restore the history of psychiatry to a prominent place in the postgraduate curriculum (and in the leisure reading of practitioners), because it is historical wisdom that tells us how fragile are our diagnoses today, how inadequate our treatments. Psychiatry goes back 2 centuries, and over that span a lot of knowledge has accumulated about diagnosis and, even in the early days of psychopharmaceuticals (the 1920s to the 1940s), about treatment. Delirious mania as a diagnosis, amphetamine as a treatment for anything other than rest-less male adolescents: all forgotten. Yet there’s gold in them thar hills. When the field’s main diagnoses are major depression and schizophrenia, its main treatments Prozac and the “SGAs” (second-generation antipsychotics), it is time to bring in the historians!


1. Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia. Am J Psychiatry. 1970;126:983-987.

2. Shorter E, Fink M. Endocrine Psychiatry: Solving the Riddle of Melancholia. New York: Oxford University Press; 2010.

3. Shorter E. What Psychiatry Left Out of the DSM-5: Historical Mental Disorders Today. New York: Routledge; 2015.

4. The Neurocritic. Carroll’s comment of August 5, 2013. Accessed January 29, 2015.

5. Fink M. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl. 2013;(441):1-47.

6. Parker G, Hadzi-Pavlovic D, eds. Melancholia: A Disorder of Movement and Mood. Cambridge, UK: Cambridge University Press; 1996.

7. Pintor LP, Valldeoriola F, Fernández-Egea E, et al. Use of electroconvulsive therapy in Parkinson disease with residual axial symptoms partially unresponsive to L-dopa: a pilot study. J ECT. 2012;28: 87-91.

8. McLoughlin G, Makeig S, Tsuang MT. In search of biomarkers in psychiatry: EEG-based measures of brain function. Am J Med Genet B Neuropsychiatr Genet. 2014;165B:111-121.

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