Common Neural Engagement during Cognitive Reappraisal across Internalizing Psychopathology
thesisposted on 01.11.2017, 00:00 by Jacklynn Fitzgerald
Individuals who suffer from excessive anxiety often also have excessive depression. A parsimonious model would suggest that both anxiety and depression reflect a core deficit in emotion regulation, demonstrated by a inefficient or ineffective down-regulation of negative affect using cognitive strategies such as reappraisal. Prior neuroimaging work in discrete samples of patients with anxiety and depressive disorders (e.g., generalized anxiety disorder [GAD], social anxiety disorder [SAD], major depressive disorder [MDD]) has commonly implicated under-engagement of the prefrontal cortex (PFC) during emotion regulation; however, findings have been mixed in regard to magnitude, locality and extent of the dysfunction across the PFC. Differences between disorders (anxiety vs. depression) and across individuals (extent of anxiety and/or depression symptoms severity) could contribute to this heterogeneity. To address this question, I examined PFC engagement/activation and its functional connectivity to the amygdala - a region instrumental for negative affect - using functional magnetic resonance imaging (fMRI) in a large sample of N=238 individuals with a wide range of anxiety and depression symptomatology (n=64 without psychiatric illness, n=47 GAD, n=78 SAD, n=49 MDD) during a reappraisal-based emotion regulation task. Across the sample, results showed that: 1) greater anxiety symptom severity, as measured by the Hamilton Anxiety Rating Scale, was related to less engagement of the dorsolateral prefrontal cortex (DLFPC), ventrolateral prefrontal cortex (VLPFC), dorsomedial prefrontal cortex (DMPFC) and dorsal anterior cingulate (dACC); and 2) greater depression symptom severity, as measured by the Hamilton Depression Rating Scale, was also related to less engagement in the DLPFC and VLPFC. Both anxiety and depression symptom severity were related to less functional connectivity between the amygdala and VLPFC. Focal results held when accounting for depression severity, but not when accounting for anxiety severity. These findings demonstrate that individual differences in anxiety and depression severity can help explain extent of PFC dysfunction observed across anxiety and depressive disorders, and that much of this dysfunction is driven by anxiety but not depression.