Neurocognitive mechanisms of body dysmorphic disorder

Abstract

Body dysmorphic disorder (BDD) is a severe psychiatric condition characterized by intrusive preoccupation with perceived appearance flaws, compulsive checking behaviors, and profound functional impairment. Despite its prevalence and clinical burden, the neurocognitive mechanisms that generate and sustain this disorder remain incompletely understood. This dissertation aims to advance the neurobiological model of BDD across three empirical chapters, each targeting a distinct but interrelated level of analysis: neuromodulation of attentional bias, effective connectivity within visual-affective circuits, and early-stage spatial frequency processing. The first chapter utilizes computational modeling methods to discern latent cognitive parameters of decision making during a Modified Posner task. Using drift diffusion modeling, we show distinction between individuals with BDD and healthy controls in measures of attentional bias toward threat. The second chapter highlights a study in which we employed dynamic causal modeling (DCM) of fMRI data acquired during a fearful face viewing paradigm to characterize effective connectivity within BDD’s fear-processing network. We identify distinct aberrant connectivities underlying passive-threat viewing in BDD: heightened feedforward connectivity between the amygdala-mOFC, reduced feedback connectivity between the amygdala-pulvinar, and heightened within-FFA connectivity in individuals with BDD compared to healthy controls. These findings implicate amplified secondary affective appraisal of threatening social stimuli, impaired attentional modulation via thalamic feedback, and over-engagement of the ventral visual steam as circuit-level features of BDD’s heightened threat sensitivity that underlies symptoms. The third and final chapter attempted to characterize mechanisms underlying the perceptual distortion that characterizes BDD. We employed a multimodal paradigm spanning both behavioral and neural measures of spatial frequency processing. We found that individuals with BDD showed significantly reduced behavioral contrast sensitivity to low-spatial frequency stimuli and correspondingly reduced activation in bilateral middle temporal (MT) area, relative to healthy controls. These findings provide the first evidence of a bottom-up sensory deficit in magnocellular stream processing in BDD, extending prior accounts of a local-over-global perceptual imbalance beyond top-down attentional mechanisms. Taken together, these findings converge on an integrated neurocognitive model of BDD in which a bottom-up spatial frequency processing deficit, dysregulation of amygdala-centered threat circuit connectivity, and heightened selective attention to threat may be mutually reinforcing to generate and sustain symptoms in BDD.