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What the DSM-II Got Right

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The DSM-II, or Diagnostic and Statistical Manual of Mental Disorders, Second Revision, was the diagnostic guide specifying the criteria for psychiatric disorders between 1968 and 1980.

In general, the DSM-II is very suspect. Until 1974, the DSM-II famously listed homosexuality as a mental disorder – specifically, it was listed under Personality Disorders and Certain Other Non-Psychotic Mental Disorders, Sexual Deviations, as DSM-II 302.0, Homosexuality. (Certain wacky Christian fringe groups and many Catholics still think the removal of homosexuality from the DSM was a real shame.) The DSM-II uses quaint terms like “neurosis” and includes controversial diagnoses like “Psychosis with childbirth,” “Involutional melancholia,” and “Depersonalization syndrome.”

More recent revisions of the DSM (DSM-III, DSM-IV, and DSM-IV-TR) are generally considered to contain diagnoses that map more scientifically onto observable real-world phenomena.

Partially due to a realization of ignorance of the etiology of many diseases, revisions beginning with the DSM-III tended to erase etiology from the names and diagnostic criteria of many conditions (except conditions where the etiology is obviously central, such as 292.1, “Psychosis with other syphilis of central nervous system” (psychosis caused by syphilis).

Unfortunately, the refusal to link mental diseases with etiology resulted in a step backwards in the diagnosis and treatment of depression, according to Professor Gordon Parker (“Is depression overdiagnosed? Yes,” British Medical Journal 2007:328).

“Fifty years ago [under DSM-II criteria],” says Professor Parker, “clinical depression was either endogenous (melancholic) or reactive (neurotic). Endogenous depression was a categorical biological condition with a low lifetime prevalence (1-2%). By contrast, reactive depression was exogenous – induced by stressful events affecting a vulnerable personality.” In other words, the DSM-II recognized a type of biologically-determined depression, with a population frequency similar to other major, debilitating psychiatric disorders such as schizophrenia. (In fact, for various reasons including the severity and similar lifetime prevalence as schizophrenia, my reading of this is that endogenous “melancholic” depression, if studied in more detail, would be found to be specifically genetically linked, just like schizophrenia.) Another type of depression, much less severe and much more common, resulted from people “becoming depressed” secondary to negative life events.

Then, in 1980, the DSM-III revisions changed all that. They created a new taxonomy of depression, and rather than exogenous and endogenous, began to classify depression as “major” or “minor,” with no reference to etiology. Only the diagnostic modifier “melancholic features,” which I’ve previously discussed in my essay “Depression, Cognition, and Value,” was left of the endogenous depression distinction.

Unfortunately, the major/minor classification has never been borne out by scientific studies (though the “melancholic features” modifier is scientifically robust). As Professor Parker points out,

Meta-analyses show striking gradients favouring antidepressant drugs over placebo for melancholic depression. Yet trials in major depression show minimal differences between antidepressant drugs, evidence based psychotherapies, and placebo. . . . Extrapolating management of the more severe biological conditions to minor symptom states reflects marketing prowess rather than evidence. Depression will remain a non-specific “catch-all” diagnosis until common sense prevails. [Emphasis mine; citations omitted.]

Scientific studies do not back up diagnoses of “major” and “minor” depressive disorders as true disorders. The DSM-III criteria for major depression has “failed to demonstrate any coherent pattern of neurobiological changes or any specific pattern of treatment response outside in-patient treatment settings,” says Professor Parker. In other words, while the quaint diagnosis of “melancholic depression” under the DSM-II retains some scientific validity, the diagnosis of Major Depressive Disorder under the DSM-IV is not scientifically valid in any of the normal senses.

The implications for suicide rights are several. First, to the extent that everyone who is suicidal is assumed to be suffering from “Major Depressive Disorder,” we are being diagnosed with a disease whose scientific validity is extremely questionable. The laughable overdiagnosis of “Major Depressive Disorder,” coupled with the diagnosis’ failure to “demonstrate any coherent pattern of neurobiological changes or any specific pattern of treatment response,” must shake our confidence in the fashionable hypothesis that all suicide is secondary to a genuine mental disorder. Second, to the extent that our psychiatric establishment chooses to use these diagnostic criteria (Major Depressive Disorder), and since meta-studies generally show little significant difference between antidepressant medications, “evidence-based psychotherapies,” and placebo, if we have depression, we must be said to have an incurable disease. Both citizens in general the those in medical professions should be much more circumspect about their willingness to force people with “Major Depressive Disorder” to remain alive against their will, and especially to forcibly medicate or “treat” this “disease.”

While I think endogenous depression is a “real” disease, unlike DSM-IV Major Depressive Disorder, I do not think that all suicides have endogenous depression – not even close – nor do I think that endogenous depression is always treatable. At best, it is marginally more treatable than DSM-IV Major Depressive Disorder – that is to say, not very. The famous study that found that SSRIs work no better than a placebo found a slightly significant difference between drug and placebo for the most severely depressed people, which could be tracking endogenous depression, but this was primarily due to that group’s much lower response to placebo. From the study:

Drug–placebo differences increased as a function of initial severity, rising from virtually no difference at moderate levels of initial depression to a relatively small difference for patients with very severe depression, reaching conventional criteria for clinical significance only for patients at the upper end of the very severely depressed category. . . . Drug–placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.

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Written by Sister Y

August 1, 2008 at 10:31 pm

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