Overdiagnosis of bipolar disorder is an increasing concern, particularly since the widely cited study by Zimmerman and colleagues.1 Findings from that study indicate that there is a problem with overdiagnosis (positive predictive value of only 43%) as well as with the much less publicized parallel finding of 30% underdiagnosis (sensitivity of 70%).
A recent review noted a much lower underdiagnosis rate of 4.8%, which is an inaccurate interpretation of the original data.2 Zimmerman and colleagues themselves allude to the higher figure.3
Will the new criteria in DSM-5 address these varying claims of overdiagnosis and underdiagnosis? After all, concern about overdiagnosis is one of the driving forces behind these debated changes.4 I’ll take up that question in the next essay in this series, suggesting that the new criteria will not significantly improve positive predictive value—the most debated aspect of diagnostic accuracy. But an important step should precede that review of predictive value and specificity, namely, a careful examination of the very concept of overdiagnosis.
Consider the implicit assumptions.
Bipolar disorder is like bacterial sepsis or mononucleosis: a patient either has it or he does not. One of the origins of dichotomous diagnosis in psychiatry is bacterial. The discovery that many debilitating illnesses were caused by invasive bacteria was a tremendous medical advance. An illness was present if the offending agent was present and absent if it was not—the first of Koch’s 4 postulates. But this perspective has been carried forward into the realm of mental health, where emerging understanding of phenomenology is not consistent with this black-and-white, yes or no way of thinking.5,6
The DSM’s dichotomous system—mental illnesses are either present or absent—is an accurate model for bipolar disorders. Consider the sheer number of genes and consider the role of environmental variation in modifying gene impact, as seen in the short/long variation of the serotonin transporter gene and depression vulnerability, where an otherwise substantial gene effect is completely overridden by benign up-bringing.7 Imagine the number of combinations of genes and environments possible and imagine the array of phenotypes that would emerge from them?
A DSM-5 committee considered all of these factors in their 2006 discussion of whether to introduce a spectrum approach to diagnosis in the upcoming edition. Virtually everyone involved was in favor of incorporating a “dimensional” approach (as opposed to the current “categorical” approach). Michael First8 wrote a masterful summary of those proceedings. Ironically, at this meeting, the mood disorders subgroup chose to work on the spectrum of depression severity, not the unipolar-bipolar spectrum. That side step leaves the entire “overdiagnosis” debate open, in spite of a new DSM.
The Structured Clinical interview for Diagnosis (SCID) is a valid gold standard. Even if one presumes that bipolar disorder can be regarded as present or absent and that a diagnostic system should operate accordingly, another major assumption remains: the SCID is a realistic gold standard against which to judge clinicians’ diagnoses. Obviously, the only way to judge diagnostic accuracy is to have some means of recognizing whether the illness is truly present. The SCID is accepted in this role, because psychiatry lamentably has little else to replace it. Is it adequate?