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In Reply

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Drs. Lynch and Seth raise several issues in their letter to which we wish to respond. We agree that psychiatric diagnosis, particularly of depressive disorders, is complex and requires a review of the patient's history, an examination of both physical and mental status, and a review of laboratory studies. Longitudinal information is particularly valuable. The process of differential diagnosis uses this information first to develop an accurate description of the mental phenomena that the patient is exhibiting. It is at this step that we decide whether a recognizable mental syndrome is present. Laboratory studies are not needed at this step. The second step involves a classification of the mental syndrome as to its cause. This involves review of laboratory studies that might explain the syndrome, since mental syndromes might be secondary ("organic," caused by) to a specific general medical or neurological condition, or to a substance, or they might be primary (idiopathic). Both primary and secondary syndromes are of interest to psychiatrists, as we are the experts in their evaluation, diagnosis, and treatment. Our editorial¹ sought to address the issue of how to assign causes to depressive syndromes by proposing specific operational criteria.

With regard to depressive syndromes in the context of HIV infection, the articles by Bialer et al.² and Seth et al.³ give different estimates of the prevalence of depressive syndromes in patients referred for psychiatric consultation. They also give widely differing estimates of the prevalence of major depressive disorder, one of the causes of depressive syndromes. These discrepancies, in part, are caused by the use of differing criteria for attributing a depressive syndrome to a medical condition (regardless of whether the information used is cross-sectional or longitudinal). Bialer et al.² may have overattributed depressive symptoms to HIV infection and thus underestimated the prevalence of depressive syndromes and of major depressive disorder.

Both Bialer et al.² and Lynch et al. (in their letter) seem to suggest that a brain-imaging study is always a critical part of deciding if a depressive syndrome is present and of deciding its cause. We disagree with this position. A depressive syndrome is best defined on its phenomenology, and it is best to be inclusive in defining the syndrome.⁴ Also, the causal attribution of a depressive syndrome requires biological coherence. Thus, it is not appropriate to attribute a depressive syndrome to marijuana use given that marijuana use per se is not associated with the development of depressive syndromes. Similarly, it is not appropriate to attribute a depressive syndrome to any lesion that might be seen on a brain-imaging study, particularly if the lesion is in a brain region that is not clearly associated with mood disorder, such as the right occiput, or the pons. It is critical to take into account the patient's history as well in deciding the causal attribution of a depressive syndrome to a general medical condition. We believe that many of these issues can be addressed by the use of operational criteria for causal attribution, such as the ones we proposed.¹

REFERENCES

1. Lyketsos CG, Treisman GT: Depressive syndromes and causal associations. Psychosomatics 1996; 37:407–412[Free Full Text]
2. Bialer PA, Wallack JJ, Prenzlauer SL, et al: Psychiatric comorbidity among hospitalized AIDS patients vs. non-AIDS patients referred for psychiatric evaluation. Psychosomatics 1996; 37:469–475[Abstract/Free Full Text]
3. Seth R, Granville-Grossman K, Goldmeier D, et al: Psychiatric illnesses in patients with HIV infection referred to the liaison psychiatrist. Br J Psychiatry 1991; 159:347–350[Abstract/Free Full Text]
4. Cohen-Cole SA, Stoudemire A: Major depression and physical illness. Psychiatr Clin North Am 1987; 10:1–17

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