Abstract
BackgroundDespite advances in neurobiological research on Major Depressive Disorder and Social Anxiety Disorder, little is known about the neural functioning of individuals with comorbid depression/social anxiety. We examined the timing of neural responses to social stress in individuals with major depression and/or social anxiety. We hypothesized that having social anxiety would be associated with earlier responses to stress, having major depression would be associated with sustained responses to stress, and that comorbid participants would exhibit both of these response patterns.MethodsParticipants were females diagnosed with pure depression (n = 12), pure social anxiety (n = 16), comorbid depression/social anxiety (n = 17), or as never having had any Axis-I disorder (control; n = 17). Blood oxygenation-level dependent activity (BOLD) was assessed with functional magnetic resonance imaging (fMRI). To induce social stress, participants prepared a speech that was ostensibly to be evaluated by a third party.ResultsWhereas being diagnosed with depression was associated with a resurgence of activation in the medial frontal cortex late in the stressor, having social anxiety was associated with a vigilance-avoidance activation pattern in the occipital cortex and insula. Comorbid participants exhibited activation patterns that generally overlapped with the non-comorbid groups, with the exception of an intermediate level of activation, between the level of activation of the pure depression and social anxiety groups, in the middle and posterior cingulate cortex.ConclusionsThese findings advance our understanding of the neural underpinnings of major depression and social anxiety, and of their comorbidity. Future research should elucidate more precisely the behavioral correlates of these patterns of brain activation.
Highlights
Despite advances in neurobiological research on Major Depressive Disorder and Social Anxiety Disorder, little is known about the neural functioning of individuals with comorbid depression/social anxiety
We know much less about the neural functioning of individuals with comorbid depression/social anxiety – whether comorbid individuals exhibit neural responses that are more similar to the responses of people with one disorder or the other, an additive combination of the disorder-specific responses, or an intermediate blend of the disorder-specific responses
We examined the magnitude and timing of neural responses to social stress in participants diagnosed as having pure depression, pure social anxiety, comorbid depression/social anxiety, or as never having had any Axis-I disorder
Summary
Despite advances in neurobiological research on Major Depressive Disorder and Social Anxiety Disorder, little is known about the neural functioning of individuals with comorbid depression/social anxiety. Investigators have examined the psychological and neurobiological mechanisms that underlie Major Depressive Disorder (MDD) and Social Anxiety Disorder (SAD), most researchers have assessed these disorders separately. In response to emotional stimuli, participants with social anxiety exhibit hyperactivity in the amygdala (similar to depressed participants), [6] as well as hyperactivity in the rostral anterior cingulate cortex [10] and insula [11]. These neural models, are based on findings of studies conducted with pure, non-comorbid forms of these disorders. We know much less about the neural functioning of individuals with comorbid depression/social anxiety – whether comorbid individuals exhibit neural responses that are more similar to the responses of people with one disorder or the other, an additive combination of the disorder-specific responses, or an intermediate blend of the disorder-specific responses
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