Body dysmorphic disorder (BDD) is an often severe and disabling condition, affecting up to 2% of the population. Despite its prevalence and clinical significance, very little is known about the pathophysiology of BDD. However, clues to its possible neurobiological substrates and abnormalities in information processing are starting to emerge. This article reviews findings from genetic, brain lesion, neuroimaging, neuropsychological, and psychopharmacological studies that have allowed us to develop a tentative model of the functional neuroanatomy of BDD. There is likely a complex interplay of dysfunctions in several brain networks underlying the pathophysiology of BDD. A combination of dysfunctions in frontal-subcortical circuits, temporal, parietal, and limbic structures, and possibly involving hemispheric imbalances in information processing, may produce both the characteristic symptoms and neurocognitive deficits seen in BDD. An improved understanding of the pathophysiology of BDD will be crucial to guide the development of better treatments.
Body dysmorphic disorder (BDD) is defined by the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV-TR) ( American Psychiatric Association, 2000) as a preoccupation with an imagined defect in physical appearance or excessive concern about a slight physical anomaly that causes significant impairment or distress. It is believed to affect close to 2% of the general population ( Rief, Buhlmann, Wilhelm, Borkenhagen, & Brahler, 2006), and up to 13% in psychiatric settings ( Grant, Kim, & Crow, 2001; Phillips, Nierenberg, Brendel, & Fava, 1996; Wilhelm, Otto, Zucker, & Pollack, 1997). BDD is an under-recognized disorder that causes significant suffering, disability, and functional impairment ( Phillips, 2000 and Veale et al., 1996).
Very little is known about the etiology or pathophysiology of BDD, as few studies have addressed this directly. This review of the pathophysiology of BDD explores what has been elucidated thus far from research on the genetics, neuroanatomy, neuropsychology, and psychopharmacology of BDD, as well as secondary BDD symptoms resulting from brain damage and medical illnesses. In addition, the brain networks that mediate body image distortion, self-recognition, and emotional reactions to visual stimuli are reviewed. This information is synthesized to produce preliminary hypotheses of the pathophysiological processes most likely to mediate the symptoms of BDD, in the interest of stimulating further research in this area.
The pathophysiology of BDD by and large still remains unknown. Nevertheless, evidence from studies of brain-damaged patients as well as neuroimaging studies of brain activation patterns for visual perception, body image distortion, and emotional processing have allowed us to develop a tentative model for the neuroanatomical dysfunctions that may underlie the symptoms of BDD. A combination of frontal-striatal circuit dysfunction, hemispheric imbalances (perhaps involving the right PHG, dorsal occipital cortex, IPL, fusiform gyrus, IFG, and greater left prefrontal and temporal activation for processing faces), and hyper-responsiveness of the amygdala and insula may be involved in mediating the symptoms and neuropsychological deficits of BDD (Table 1).
