Can understanding the neurobiology of body dysmorphic disorder (BDD) inform treatment?

Structural neuroimaging

To date, there have been four magnetic resonance imaging (MRI) studies^5–8 and three using diffusion-weighted imaging^9-11 that have examined structural brain changes in BDD compared with healthy controls.

In terms of volumetric or morphometric brain changes, the study from Rauch et al. ⁶ only included eight patients with BDD, all with comorbid conditions and no control group, thus will not be further reviewed. Buchanan et al. ⁵ (n=20) and Atmaca et al. ⁷ (n=12) both reported reductions in brain volumes in BDD in the right orbito-frontal cortex (OFC: a brain region important in decision making) and left thalamus (a brain region that acts as a relay station between the subcortical structures and the cerebral cortex) in comparison with age and sex-matched control groups. Buchanan et al. ⁵ further demonstrated that there were reductions in the left amygdala (a region important in emotional reactions and memory) volume in BDD, as well as a number of other volume reductions, the most significant of which being in the left dorsal anterior cingulate cortex (a region involved in a number of functions including emotion, conflict monitoring and decision making). Feusner and colleagues ⁸ in 12 patients with BDD did not report amygdala volume reductions in BDD compared with healthy controls, but did demonstrate that left amygdala volume was significantly correlated with BDD symptom severity.

Reductions in brain volumes within fronto-striatal brain regions (including the anterior cingulate, important in most executive functions including decision making and behavioural control) are commonly observed in patients with OCD, as confirmed in a recent large multicentre study of over 400 patients with OCD. ¹² In contrast, changes in brain volume in the amygdala are not typically observed in OCD overall, but have been more discretely associated with certain OCD symptom dimensions, especially the harm/checking symptoms. ¹³

The three diffusion studies were all published in 2013. In 14 patients Arienzo et al. ¹¹ reported reduced fractional anisotropy (FA) in the inferior longitudinal fasciculus (ILF: connects the temporal and occipital lobes), which correlated with BDD symptom severity. Reductions in FA values were equated to disruptions in white matter integrity; brain areas with low FA demonstrated sparse, poorly myelinated or divergent white matter tracts. In a different cohort of 14 patients, Feusner ¹⁰ also demonstrated ILF changes in BDD. In a larger cohort of 20 BDD patients, Buchanan ⁹ established more widespread white matter changes which included the ILF as well as superior longitudinal fasciculus (SLF: connects all four of the lobes of the brain), inferior fronto-occipital fasciculus (connects the frontal lobes with the occipital and temporal lobes), the corpus callosum, and uncinate fasciculus (UF: connects the limbic system with the frontal lobe). Taken together, this literature suggests that individuals with BDD show distributed abnormalities in white matter integrity, including overall connections between the hemispheres in the corpus callosum; compromised connections are evident between the occipital and temporal cortices (i.e. via the ILF), as well as impaired connectivity between the prefrontal, parietal, occipital, and temporal regions via the SLF. Fronto-amygdala connectivity (via UF) was also shown to be compromised.

White matter integrity studies in OCD have typically indicated changes within the cingulate bundle, corpus callosum, and internal capsule, ¹⁴ which are consonant with the notion that fronto-striatal circuits are pivotal to the pathogenesis of OCD. The findings from Buchanan and colleagues, ⁹ in the largest sample of BDD patients to date examined with diffusion tensor imaging, would suggest more widespread white matter integrity changes in BDD. Although these results await replication, they suggest a divergence in the neurobiology of the two disorders.

Functional neuroimaging

There have been four published functional magnetic resonance imaging studies (fMRI) in BDD,^15–18 all from the same research group. Given the body-image focused nature of BDD with particular relevance to facial features and clinical observations of detail-oriented bias, the focus of these studies has been on visual processing of faces or other visual stimuli (reviews of visual and cognitive studies in BDD are available^19,20). Each of the four papers reports an extensive set of data and analyses: for brevity, the major findings are summarised here.

Feusner et al. ¹⁵ established that patients with BDD demonstrated increased right amygdala activity to faces of others compared with healthy controls; this finding has yet to be replicated. In an extension to this initial study, Feusner and colleagues ¹⁶ presented patients and controls with photographs of their own face, familiar faces, and unfamiliar faces. Patients with BDD showed lower activity to their own face and familiar faces in the primary and secondary visual cortices, but hyperactivity in the OFC to unfamiliar faces. In follow-up analyses of the same data, Bohon et al. ¹⁸ reported correlations between amygdala activity and anxiety scores for own face stimuli in the BDD cohort. In a separate study, Feusner et al. ¹⁷ presented BDD patients and healthy controls with photographs of houses. They established reduced activity to these visual stimuli within primary and secondary visual cortices of the patients with BDD.

Functional brain imaging studies in OCD have not had such a focus on visual or face processing; in contrast, there has been a major focus in OCD on executive functioning, with differences noted in fronto-cortico-striatal functioning. ⁶ There has not been any work to date comparing OCD or BDD patient cohorts in terms of their neurobiology. As we can see, neuroimaging studies in BDD are still in their infancy, and replication of both structural and functional neuroimaging research is essential to provide further insights into the underlying neurobiology of BDD.

Current treatment options

The most common therapeutic intervention for BDD, as with OCD, involves pharmacological and/or psychological treatments. Phillips and Hollander ²¹ recommended selective serotonin reuptake inhibitors (SSRIs) as the first-line medications of choice for BDD. Efficacy has been demonstrated in open-label trials in BDD of citalopram, ²² escitalopram, ²³ fluvoxamine, ²⁴ and the serotonin-noradrenaline reuptake inhibitor of venlafaxine. ²⁵ Double-blind randomised placebo-controlled and crossover trials are few in BDD; both fluoxetine ²⁶ and clomipramine ²⁷ have shown benefits over placebo. Augmentation with atypical antipsychotics, whilst common in clinical practice, ²⁸ has been subjected to only a handful of rigorous clinical trials: augmentation of fluoxetine using olanzapine or pimozide to target delusions in BDD has met with limited success.^29,30 Psychological interventions for BDD largely employ behavioural (exposure/response prevention) or cognitive behavioural therapy (CBT) strategies, with recent randomised control trial studies confirming the efficacy of CBT in particular.^31,32 Our own experience is that a combination of CBT with acceptance-commitment elements enhances engagement; this approach requires scientific scrutiny.

In terms of understanding the neurobiology of the efficacy of serotonergic agents in BDD, there has been increasing interest in the last few years with regards to the neurobiological networks and functional brain changes associated with SSRI administration. A number of studies report modulation of the amygdala and OFC following acute and continual SSRI administration.^33,34 Further, a recent sophisticated neuroimaging study examining whole-brain functional networks reported improved functional connectivity in fronto-parietal networks after 16 weeks of SSRI treatment in an OCD cohort. ³⁵ Current neurobiological findings in BDD thus appear consistent with such literature, and indeed suggest that SSRIs are normalising activity within the limbic system and possibly frontal-limbic circuits, which potentially assists with symptom amelioration. More work needs to be done to investigate other brain pathways in BDD, notably dopaminergic systems, given the high proportion of BDD patients who hold their beliefs with delusional intensity. ²⁸

In terms of psychological interventions for BDD, our own experience is that enhancement of CBT can be effected by the addition of certain BDD-specific strategies informed by the neurocognitive work outlined above. For example, the functional neuroimaging studies emphasise significant face-processing deficits in BDD, which has definite therapeutic implications. Enhancement of facial affect recognition in persons with BDD could be achieved with a specialised training of affect recognition (TAR) program developed for schizophrenia.^36,37 Guiding BDD patients to use effective eye movement and facial scanning strategies appears to be unique to BDD patients in comparison with those with OCD. Such approaches require rigorous testing in BDD.

Conclusions

Patients with BDD are difficult to treat, due to the chronicity of their problems. There has been very little research in BDD as to the most effective treatment strategies. Recent research using neuroimaging has begun to delineate the neurobiology of BDD, with structural and functional brain changes both being reported. To date, there have been no direct comparisons using neuroimaging techniques between BDD and OCD, thus observations of similarities and differences can only be made across studies. BDD pathophysiology appears to demonstrate greater abnormalities (structurally and functionally) within the limbic system, visual processing areas of the brain, and the OFC, with additional widespread white matter changes. This would suggest that improving visual capabilities through formalised computer packages or more informal guided mirror work should be incorporated into treatment regimes.