In other words, functional imaging data alone cannot adjudicate whether the abnormal activity profiles observed in dlPFC and vmPFC are a cause or consequence of the disorder. However, the correlative nature of functional imaging data precludes any causal inference. These imaging data hint that an imbalance in vmPFC/dlPFC activity may contribute to depression. vmPFC is hyperactive at rest and decreases in activity during remission of symptoms, whereas the dlPFC is hypoactive at rest and increases in activity during remission of symptoms. In sum, the functional imaging studies converge to suggest that depression is associated with seemingly opposite activity profiles in vmPFC and dlPFC. In light of the resting state data indicating dlPFC hypoactivity in depression, these results suggest dysfunction (or at least inefficiency) in the dlPFC of depressed patients. Data from these studies demonstrate that depressed patients exhibit greater task-related activation in dlPFC during tests of working memory and cognitive control when performance is matched to non-depressed subjects. Ī third, more recent, type of functional imaging study compares task-related brain activations (blood flow) of depressed patients to that of non-depressed comparison subjects. In these studies, recovery from depression is associated with increased activity in dlPFC, but decreased activity in vmPFC. Ī second type of functional imaging study identifies areas of the brain where changes in activity are associated with recovery from depression, as in response to psychotherapy or antidepressant medication. Results from these studies associate depression with abnormally high levels of vmPFC activity, but abnormally low levels of dlPFC activity. This type of study identifies regional abnormalities in resting brain activity associated with depression. blood flow or glucose metabolism) of depressed patients to that of non-depressed comparison subjects. The earliest functional imaging studies of depression compared the resting state brain activity (e.g.
Several types of functional imaging studies have been employed to identify brain areas involved in depression. We conclude with speculation on how the function of each area may be related to depression. In the following sections, we describe human neuroscientific data that implicates each area in the pathophysiology of depression. Indeed, dlPFC has primarily been associated with “cognitive” or “executive” functions, whereas vmPFC is largely ascribed “emotional” or “affective” functions. The distinct patterns of connectivity in these two regions of PFC suggest disparate functionality. By contrast, the dlPFC, which includes portions of the middle and superior frontal gyri on the lateral surface of the frontal lobes ( Fig 1B), receives input from specific sensory cortices, and has dense interconnections with premotor areas, the frontal eye fields, and lateral parietal cortex. In addition, vmPFC has dense reciprocal connections with the amygdala, which is involved in threat detection and fear conditioning. Targets of vmPFC projections include the hypothalamus and periaqueductal gray, which mediate the visceral autonomic activity associated with emotion, and the ventral striatum, which signals reward and motivational value. The vmPFC includes the ventral portion of the medial prefrontal cortex (below the level of the genu of the corpus callosum) and medial portion of the orbital surface (approximately the medial one-third of the orbitofrontal cortex in each hemisphere) ( Fig 1A).
Perhaps the most widely accepted division of prefrontal cortex, based on anatomical connectivity and functional specialization, is between the dorsolateral and ventromedial sectors. Neuroanatomy of PFC: dorsolateral and ventromedial sectors
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