Functional Neuroimaging Studies of Depression: The Anatomy of Melancholia, by Wayne Drevets
In 1998, Wayne C. Drevets, who later became senior investigator at the Neuroimaging Section of the NIMH Mood and Anxiety Disorders Program in Washington, D.C., reviewed the contributions of functional neuroimaging to knowledge of the pathophysiology and “anatomical correlates” of major depression (Drevets 1998, 341).
He hoped that such neurocorrelational studies would “ultimately localize specific brain regions for histopathological assessment, elucidate anti-depressant treatment mechanisms, and guide pathophysiology-based classification of depression” (342). At the time, Drevets noted that the capabilities of neuroimaging to determine diagnosis or guide treatment had not yet been established. Functional imaging seemed nonetheless a promising approach: The fact that some depressive symptoms could be experimentally induced in nondepressed subjects opened the way for depressed-control comparisons of the changes in cerebral blood oxygenation and glucose metabolism “associated with” depression.
However, the exact nature of the association remained nebulous. For example, nondepressive conditions sometimes present in depressed patients can affect functional brain imaging measures; regional blood oxygenation or metabolic differences between depressives and control subjects “may thus reflect either the physiological correlates” of depression “or pathophysiological changes that predispose subjects to or result from affective disease” (Drevets 1998, 342).
Functional brain imaging techniques, which permit noninvasive measures of neurophysiology and neuroreceptor binding, are powerful and sensitive tools for research aimed at elucidating the pathophysiology of major depression. The application of these technologies in depression research has produced several studies of resting cerebral blood flow (BF) and glucose metabolism in subjects imaged during various phases of illness and treatment. This review examines these data and the principles relevant to their interpretation and discusses the insights they provide into the anatomical correlates of depression. Within the anatomical networks implicated in emotional processing by other types of evidence, these BF and metabolic data demonstrate that major depression is associated with reversible, mood state–dependent, neurophysiological abnormalities in some structures and irreversible, trait-like abnormalities in other structures. In some of the regions in which trait-like abnormalities appear, abnormal metabolic activity appears at least partly related to the anatomical abnormalities identified in magnetic resonance imaging (MRI) studies of depression.
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