A Pragmatic Consideration of the Relation Between Depression and Melancholia

THE MELANCHOLIA OF THE PAST and the major depression of the present are extraordinarily complex notions that represent different things to different people. With her compelling article "Is This Dame Melancholy? Equating Today's Depression and Past Melancholia," Jennifer Radden makes an important contribution to the debate on whether these concepts are identical, overlapping, or distinct. Exploring both conditions from descriptive and causal points of view, Radden appropriately concludes that fully equating the two of them would constitute a "troubling oversimplification." Her line of reasoning runs as follows. Because past descriptions of melancholia and current descriptions of major depression are marked by dissimilarities (such as the genius and creativity associated with the former and the self-loathing and emphasis on loss associated with the latter), only an underlying causal base common to both conditions would justify our equating them. But the cause (or causes) of melancholia and depression remain mysterious. Thus, although Radden acknowledges that a causal explanation might yield substantial benefits ("research possibilities, further hypotheses, and even hope of prevention, or cure"), she suggests that we remain in a descriptive mode when comparing the two conditions and conclude that they are not one and the same.

Radden's argument that past melancholia and contemporary depression are descriptively distinct is convincing and, I think, indisputable. But I would like to challenge and expand upon some of her ideas about considerations of causality and about the role of pragmatic reasoning in working out the relation between melancholia and depression. First of all, although Radden is correct that the cause of many (or perhaps most) depressive states is unknown, she underrates the extent of the empirical knowledge that we have acquired about the causation of depression and, in so doing, undervalues the relevance of causal reasoning to making the melancholia/depression distinction. Recent empirical research has revealed that major depressive episodes can result from brain lesions such as left-sided strokes or metabolic disorders such as hypothyroidism (Yudofsky and Hales 2002). Psychosocial research, moreover, has suggested that stressful life events also can be understood as causes of depression (Kendler, Karkowski, and Prescott 1999). These findings provide some hope that the identification of causes of various clinical states is a real possibility. Identification of such causes, I believe, could empower us to make some plausible claims about the similarities or differences between past melancholia and current depression. A melancholic individual like van Gogh, for example, had a different illness than a contemporary stroke patient with major depression in a present-day hospital, not only on the basis of descriptive distinctions between their conditions, but also on the basis of the causes of their respective states. Although of course we cannot know the cause of van Gogh's melancholia, we can reasonably assume that it was not the result of a left-sided stroke due to the absence in his case of other clinical deficits that usually result from such a stroke (such as language and motor deficits). Plausible assertions about the causes of melancholic and depressive states would add to the robustness of any claims regarding the distinctness of the conditions.

Conversely, careful consideration of the etiology of various clinical presentations might prompt us to hypothesize a shared pathophysiology and thereby lead us to believe that they are essentially identical conditions. It is difficult or impossible to discover a cause of melancholia in individuals who lived in past eras. But we might achieve our goal by comparing well-defined major depression to various forms of what Radden calls "masked depression," such as those seen in cross-cultural settings, where the subjective symptoms of sad mood are absent but numerous somatic signs of depression are observed. If it turned out that major depression and masked depression had the same cause, then differences in their clinical phenomenology would become merely surface differences that belie a shared etiological process. How might one discover the existence of such a process...