Own-body perception in body dysmorphic disorder

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Own-body perception in body dysmorphic disorder Ryan A. Kaplan

a b

David J. Castle

d

, Susan L. Rossell

b c

b

, Peter G. Enticott &

a

School of Psychology and Psychiatry, Monash University, Melbourne, Australia b

Monash Alfred Psychiatry Research Centre, The Alfred and Central Clinical School, Monash University, Melbourne, Australia c

Brain and Psychological Sciences Research Centre, Swinburne University of Technology, Melbourne, Australia d

St Vincent's Hospital and University of Melbourne, Melbourne, Australia Version of record first published: 26 Feb 2013.

To cite this article: Ryan A. Kaplan , Susan L. Rossell , Peter G. Enticott & David J. Castle (2013): Own-body perception in body dysmorphic disorder, Cognitive Neuropsychiatry, DOI:10.1080/13546805.2012.758878 To link to this article: http://dx.doi.org/10.1080/13546805.2012.758878

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Cognitive Neuropsychiatry, 2013 http://dx.doi.org/10.1080/13546805.2012.758878

Own-body perception in body dysmorphic disorder Ryan A. Kaplan1,2, Susan L. Rossell2,3, Peter G. Enticott2, and David J. Castle4

Downloaded by [144.132.181.172] at 14:30 26 February 2013

1

School of Psychology and Psychiatry, Monash University, Melbourne, Australia 2 Monash Alfred Psychiatry Research Centre, The Alfred and Central Clinical School, Monash University, Melbourne, Australia 3 Brain and Psychological Sciences Research Centre, Swinburne University of Technology, Melbourne, Australia 4 St Vincent’s Hospital and University of Melbourne, Melbourne, Australia

Introduction. This paper reviews the literature as it relates to perceptual processes in body dysmorphic disorder (BDD). Methods. A narrative-style review of the literature was undertaken to explore the relationship between BDD and obsessive-compulsive disorder, the empirical evidence for aberrant own-body perception in BDD, and the possible role of the parietal cortex in the disorder. Results. The . extant literature appears to support the postulation that BDD is underpinned by a dysfunction in somatoperception*the process by which individuals formulate a sense of what they look like. Conclusions. Investigation . of somatoperceptive processes in BDD and related brain structures would provide important insight about the development and maintenance of this complex and often neglected psychiatric condition, and, in turn, help improve its treatment.

Keywords: Body dysmorphic disorder; Body image; Proprioception; Selfperception; Somatoperception.

INTRODUCTION The term ‘‘body image disorder’’ may typically invoke connotations of anorexia nervosa, a potentially devastating illness that has been estimated Correspondence should be addressed to Ryan A. Kaplan, School of Psychology and Psychiatry, Monash University, Victoria 3800, Australia. E-mail: [email protected] # 2013 Taylor & Francis


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to affect 0.5% of females and 0.05% of males (American Psychiatric Association, 2000 [DSM-IV-TR]). However, with a prevalence estimated to be up to five times that of anorexia (Bartsch, 2007; Koran, Abujaoude, Large, & Serpe, 2008), it seems surprising that body dysmorphic disorder (BDD) remains relatively unknown among the lay public. BDD is characterised by a preoccupation with a perceived but usually nonexistent defect in appearance that causes significant distress or functional impairment (DSM-IV-TR). In some cases, a slight physical abnormality may be present but it is often almost imperceptible to others and the distress it causes the individual is grossly excessive. Whereas the bodily misperception and preoccupation in anorexia relates to body size and weight (DSM-IV-TR), in BDD the bodily misperception and concern may pertain to any body part or parts*their shapes, sizes, positioning, symmetry, or any other aesthetic element. Studies have found common areas of concern to include the face, skin, hair, nose, breasts, stomach, hips, and thighs (Bartsch, 2007; Buhlmann et al., 2010; Koran et al., 2008; Perugi et al., 1997). Although people with BDD often have around five to six body parts or areas of concern (Bartsch, 2007; Phillips, Menard, Fay, & Weisberg, 2005), the number of concerns has been found to range as high as 12 (Bartsch, 2007). Onset of BDD usually occurs during adolescence (Castle, Rossell, & Kyrios, 2006; Phillips & Diaz, 1997; Phillips, McElroy, Keck, Pope, & Hudson, 1993; Phillips et al., 2005; Veale et al., 1996). Studies have produced BDD prevalence estimates ranging from 0.7% to 13%, depending on methodology, country, and sample characteristics (Bartsch, 2007; Biby, 1998; Bohne, Keuthen, Wilhelm, Deckersbach, & Jenike, 2002; Bohne, Wilhelm, et al., 2002; Buhlmann et al., 2010; Faravelli, Salvatori, Galassi, & Aiazzi, 1997; Koran et al., 2008; Liao et al., 2010; Taqui et al., 2008). These findings indicate that, in terms of prevalence, BDD is as common as, if not more common than, schizophrenia, bipolar disorder, and anorexia nervosa. Such studies have also found the BDD prevalence rate to be equal among men and women (Buhlmann et al., 2010; Koran et al., 2008); an interesting pattern in light of the substantial discrepancy between the sexes in the prevalence of anorexia and rates of nonpathological appearance concerns (Feingold & Mazzella, 1998). Additionally, little is known about the relevance of cultural and ethnic factors in BDD; comparative investigations of cross-cultural prevalence rates are limited to a study by Bohne, Keuthen, and colleagues (2002), who found no significant difference in rates of BDD between university students in Germany and the USA. This is perhaps not surprising given the cultural and economic similarities of the two countries. A US study of BDD among Caucasian, African American, Latino, and Asian American ethnic groups identified some differences between Caucasian and Asian Americans with regards to body parts of concern, but clinical


OWN-BODY PERCEPTION IN BDD

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characteristics of the disorder were otherwise mostly similar across the four groups (Marques et al., 2011). Individuals with BDD typically spend an inordinate amount of time thinking about their appearance (Buhlmann et al., 2010) and often engage in excessive grooming behaviours designed to camouflage their supposed defects (Buhlmann, Reese, Renaud, & Wilhelm, 2008; Phillips et al., 1993, 2005). The majority of BDD sufferers spend extended periods looking at themselves and inspecting their ‘‘defects’’ in mirrors or other reflective surfaces (Buhlmann et al., 2008; Neziroglu & Yaryura-Tobias, 1993; Phillips et al., 1993, 2005; Veale & Riley, 2001). The minority of BDD sufferers who do not engage in mirror gazing tend actively to avoid mirrors (Phillips et al., 1993). As a consequence of these behaviours, the social and occupational functioning of people with BDD is often severely impaired (Phillips et al., 2005). Furthermore, although it is common for people with BDD to seek nonpsychiatric treatments such as plastic surgery and dermatological procedures in order to correct their supposed defects, such treatments usually do not result in remission of BDD symptoms (Crerand, Phillips, Menard, & Fay, 2005; Phillips, Grant, Siniscalchi, & Albertini, 2001; Phillips et al., 1993; Veale, 2000; Veale et al., 1996). In fact, they often lead to a worsening of symptom severity (Crerand et al., 2005; Phillips et al., 2001, 1993; Veale, 2000; Veale et al., 1996) or redirection of the concern to a different body part or parts (Veale, 2000).

PHENOMENOLOGICAL AND NOSOLOGICAL ISSUES Although BDD is classified in DSM-IV-TR as a somatoform disorder, it shares aspects of its symptomatology, phenomenology, and treatment response with disorders from several other classes. For example, body obsession, inaccurate body perception, and often compulsive engagement in corrective behaviours are key features of eating disorders such as anorexia nervosa and bulimia nervosa (Hrabosky et al., 2009; Rosen & Ramirez, 1998; Rosen, Reiter, & Orosan, 1995; Willmuth, Fondacaro, Gross, Leitenberg, & Rosen, 1985). Not only are these disorders often found to be comorbid (Dingemans, van Rood, de Groot, & van Furth, 2012; Grant, Kim, & Eckert, 2002; Ruffolo, Phillips, Menard, Fay, & Weisberg, 2006), but BDD symptoms may precede the development of eating disorders (Jolanta & Tomasz, 2000) or occur following remission of an eating disorder (Pantano & Santonastaso, 1989). BDD also shares key clinical features with social phobia such as social anxiety, excessive social evaluation concerns, and social withdrawal (Phillips, 1991; Wilhelm, Otto, Zucker, & Pollack, 1997), and the suggested relatedness of these two disorders has been discussed at length previously (see Coles


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et al., 2006; Fang & Hofmann, 2010; Lewis-Fernandez et al., 2011; Pinto & Phillips, 2005). Not only are the two disorders frequently comorbid (Brawman-Mintzer et al., 1995; Gustad & Phillips, 2003; Wilhelm et al., 1997), in eastern cultures BDD is regarded as a variant of social phobia (Kleinknecht, Dinnel, Kleinknecht, Hiruma, & Harada, 1997; LewisFernandez et al., 2011). Moreover, BDD severity has been shown to be associated with social anxiety (Pinto & Phillips, 2005) and aspects of social anxiety appear to play a key role in the functional impairment of BDD sufferers (Kelly, Walters, & Phillips, 2010). However, it is the supposed relatedness of BDD and obsessive-compulsive disorder (OCD) that has perhaps garnered the most attention in recent years. Like the compulsions characteristic of OCD, the impulse to inspect themselves in mirrors and repeatedly perform grooming and camouflage behaviours feels, for many BDD sufferers, irresistible (Phillips et al., 1993). Moreover, such behaviours are often accompanied or preceded by intrusive and anxiety-provoking cognitions that have been likened to obsessions (Phillips et al., 1993). Thus, it has been suggested that BDD is more appropriately conceptualised as an ‘‘obsessive-compulsive spectrum disorder’’ (OCSD) than as a somatoform disorder, as is the case in the DSM-IV-TR (Phillips, Stein, et al., 2010; Phillips, Wilhelm, et al., 2010). As well as the similarities in behavioural symptoms, proponents of BDD’s inclusion in an obsessive-compulsive spectrum (OCS) have pointed to high comorbidity rates between BDD and OCD as further evidence for their relatedness (e.g., Hollander & Rosen, 2000). BDD and OCD also respond similarly to selective serotonin reuptake inhibitors (SSRIs; Leonard, 1997; Phillips, 2010) and cognitive-behavioural therapy (CBT) focusing on exposure and response prevention (Podea, Suciu, Suciu, & Ardelean, 2009; Veale, 2010). BDD is expected to be categorised in DSM-5 as an OCSD, but the empirical evidence for this conceptualisation and the support for it in the field is by no means unequivocal (e.g., Castle & Phillips, 2006). Although BDD is indeed characterised by repetitive and time-consuming behaviours, the behaviours differ from those seen in OCD. Whereas the compulsions of OCD are the result of ego-dystonic cognitions, the behavioural symptoms of BDD are considered by some to be the outward manifestation of an egosyntonic preoccupation with the perceived defects (Crino, 2000; Hollander & Rosen, 2000). Furthermore, although the repetitive behaviours of BDD may be intended to reduce anxiety, unlike checking and other compulsive behaviours in OCD they are often unsuccessful in this regard and frequently have the opposite effect: an increase in anxiety and distress (Veale & Riley, 2001). With regards to comorbidity, as critics have noted (e.g., Crino, 2000; Swerdlow, 2000), both BDD and OCD have much higher comorbidity rates



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with other (non-OCS) disorders (e.g., major depressive disorder; Phillips et al., 2005) than with each other. Thus, inferences about the relatedness of OCD and BDD based on these figures are questionable. Moreover, although studies have yielded some support for the efficacy of SSRIs and CBT in treating BDD, they have used outcome measures that assess behavioural and cognitive symptomatology and not the degree of perceptual distortion. Whether these treatments are effective in correcting any perceptual distortion in BDD is therefore not known. Empirical evidence from neuroimaging and genetic studies for the conceptualisation of BDD as an OCSD has been equivocal at best. Consistent with OCD findings (see Rotge et al., 2009, for a review), structural magnetic resonance imaging (MRI) studies have shown caudate nucleus asymmetry (Rauch et al., 2003) and orbitofrontal cortex volume (Atmaca et al., 2010) abnormalities in BDD. However, whereas imaging studies have found reduced mean white matter volume in OCD compared to healthy controls (Jenike et al., 1996), two structural MRI studies have shown an increase in white matter volume in BDD (Atmaca et al., 2010; Rauch et al., 2003). A leftward shift in cerebral laterality has also been observed in BDD (Rauch et al., 2003) and not in OCD, with some evidence suggesting a possible rightward shift in laterality in OCD (Jenike et al., 1996). Additionally, findings indicate smaller anterior cingulate volumes in BDD (Atmaca et al., 2010) but not OCD (Grachev et al., 1998; Rosenberg & Keshavan, 1998; Szeszko et al., 2004). Moreover, one study found an absence of any significant volumetric abnormalities in BDD subjects (Feusner et al., 2009). Interestingly, a study employing single photon emission computed tomography (SPECT) imaging showed occipital perfusion and parietal abnormalities in BDD, neither of which have been implicated in OCD (Carey, Seedat, Warwick, van Heerden, & Stein, 2004). Parietal dysfunction, however, is known to be associated with disturbed body image (Cutting, 1990; Trimble, 1988). Finally, a preliminary genetic study of people with BDD found no association with several candidate genes implicated in OCD (Richter et al., 2004). It did, however, find an association with the GABAA receptor-g2 gene in BDD which has not been implicated in OCD in preliminary genetic investigations (Richter et al., 2009).

PERCEPTUAL ABERRATION IN BDD Despite the nosological complexities, given current best practice treatment approaches, the conceptualisation of BDD as an OCSD has important clinical utility and is thus potentially beneficial to patients. However, such a conceptualisation emphasises the cognitive and behavioural aspects of BDD,


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while deemphasising the importance of perceptual aspects of its phenomenology. Figure 1 illustrates how these three components may contribute to the BDD experience. Thus, reclassifying BDD as an OCSD may draw both clinical and research attention towards its cognitive and behavioural symptomatology and away from its characteristic perceptual distortion, which is the very lynchpin of a BDD diagnosis and the aspect of BDD arguably most in need of empirical attention. Indeed, as Figure 1 highlights, there has been scant investigation of this aspect of the BDD experience to date, and consequently it is poorly understood. Phenomenological studies have largely ignored it (e.g., Perugi et al., 1997; Phillips et al., 1993, 2005) and the majority of intervention studies have used outcome measures that assess cognitive and behavioural symptoms but have neglected to assess whether such interventions are effective in correcting the perceptual distortion (e.g., Aldea, Storch, Geffken, & Murphy, 2009; Greenberg et al., 2010; Wilhelm, Buhlmann, Hayward, Greenberg, & Dimaite, 2010). Indeed, clinical and anecdotal evidence suggests that even if psychopharmacologic and psychotherapeutic treatments are successful in attenuating cognitive and behavioural symptoms of BDD, the bodily misperception associated with the disorder often does not remit (Geremia & Neziroglu, 2001; Khemlani-Patel, Neziroglu, & Mancusi, 2011). Of importance, then, not only to improvements in our understanding of the aetiology and pathogenesis of BDD but also to advancements in intervention, is the investigation of own-body perception in this population. Some of the issues requiring attention include the extent and qualitative nature of distortions in own-body perception in BDD, their association with cognitive and behavioural symptoms, their response to treatment, and their neurobiological cause. Symptoms

Vision Execuve abilies Beliefs

Cognive

Cognions

Checking

BDD

Grooming/camouﬂaging

Behavioural

Reassurance-seeking Social withdrawal

Perceptual

Vision

Somatopercepon

Propriocepon Other somatosensory input Mulsensory integraon

Figure 1. Model indicating our current understanding of BDD symptoms. Ellipse indicates features that require further empirical study in BDD due to a paucity of data.


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BDD AND BODY IMAGE DISTURBANCE IN NEUROPSYCHIATRIC CONDITIONS Although little is known at present about the neurobiology of BDD, the importance of the right hemisphere*and the right parietal lobe in particular*in own-body perception and experience is widely acknowledged and supported by a large literature (see Devinsky, 2000; Giummarra, Gibson, Georgiou-Karistianis, & Bradshaw, 2008; Longo, Azanon, & Haggard, 2010). Indeed, phenomena involving anomalous body perception such as out-of-body experiences, in which a person perceives himself as if he were observing his own body from outside, and autoscopy, in which a person perceives himself outside of his own body, are associated with lesions or dysfunction in the right parietal area, or within networks that include this region (Blanke, Landis, Spinelli, & Seeck, 2004). Lesion studies have implicated the same brain region in asomatognosia, the experience of body parts being missing or having disappeared (Arzy, Overney, Landis, & Blanke, 2006), and unilateral neglect, which is characterised by a lack of awareness of or attention to the contralesional side of the body (Danckert & Ferber, 2006). Right-sided lesions have also been shown to be involved in somatoparaphrenia, the disowning of a body part or parts, often on the contralesional side (Aglioti, Smania, Manfredi, & Berlucchi, 1996; Halligan, Marshall, & Wade, 1995). In many, although not all cases of these conditions, the affected body part is on the contralesional, and thus often the left, side, whereas there appears to be no clear lateralisation with regards to body parts of concern in BDD (Phillips et al., 2005). Moreover, the previously mentioned conditions/ phenomena all differ materially from BDD, as they involve disembodiment, disownership, or unawareness of body. None of these is the case with BDD, which instead involves a misperception of the size, shape, positioning, or symmetry of body parts. Nevertheless, the perceptual aberration in BDD may still be explained by right hemispheric and, indeed, right parietal dysfunction. First, as pointed out by Cutting (1990), although right hemispheric brain lesions can result in somatosensory and own-body perception problems on the left side of the body, the right hemisphere plays an important role not just in perception of the left side, but in own-body perception and processing generally. Indeed, a complex network involving right parietal areas has been implicated in different aspects of selfperception, including body and facial recognition of self (Frassinetti, Maini, Romualdi, Galante, & Avanzi, 2008; Uddin, Kaplan, Molnar-Szakacs, Zaidel, & Iacoboni, 2005), and appears to be central to awareness of, and identification with, one’s own body (Devinsky, 2000). Frassinetti et al. (2008), for example, postulated based on neuropsychological evidence that the right hemisphere plays a critical role in visual processing of the body;


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their findings implicate the right hemisphere in recognition of own body parts, without evidence of a laterality effect. Second, BDD is distinguished from the previously mentioned conditions by what Longo et al. (2010) labelled ‘‘emotion-about-body’’. Not only do people with BDD experience misperception of their bodies, but the misperception is accompanied by a subjective evaluative judgement*a dislike or hatred of the body part(s) concerned. Longo et al. supposed that emotion-about-body is associated with the right hemisphere, especially right parietal and frontal regions, and cited examples of misoplegia and body identity integrity disorder, both of which involve hatred or extreme dissatisfaction with limbs or body parts, as evidence (Blanke, Morgenthaler, Brugger, & Overney, 2009; Loetscher, Regard, & Brugger, 2006). Indeed, of all the neuropsychiatric conditions relating to body image disturbances, misoplegia may be regarded as most closely resembling BDD. Whatever the neural basis, of importance is that BDD has typically been overlooked in reviews and syntheses of the literature about disorders of body image (e.g., Cutting, 1990; Devinsky, 2000; Giummarra et al., 2008; Longo et al., 2010). Perhaps this is precisely because the perceptual disturbance in BDD has simply not yet been afforded due research attention.

STUDIES OF PERCEPTION IN BDD The study of disturbed body perception in BDD is particularly difficult because the objective assessment and quantification of one’s subjective perceptual experiences is inherently challenging. The psychological discipline of psychophysics has produced some rather ingenious methods to this end. Yet the methods of psychophysics are limited in that they typically require the subject to offer comparison judgements of different manipulations of some kind of stimulus*methods that are difficult, if not impossible, to apply to interoceptive experiences (hunger, for example) and such a self-referential endeavour as perception of one’s own body. This process of own-body perception has been termed somatoperception by Longo et al. (2010) and is defined as ‘‘the essentially perceptual process of constructing perceptual representations of the body and somatic stimuli from perceptual input’’ (p. 665). In other words, somatoperception refers to the process through which one acquires a sense of the shape, size, and configuration of one’s own body and its constituent parts. Despite the challenges in its assessment, studies employing inventive means have offered some insight into somatoperceptive processes in BDD. Thomas and Goldberg (1995) used an analogue of the classic psychophysical method of adjustment to determine whether people with BDD demonstrate differences in visual perception of their heads and faces compared to



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nondisordered cosmetic surgery patients and healthy controls. Participants viewed a real-time video image of themselves on a television screen connected to a device that allowed the width of the image to be altered by turning a knob. Beginning from either an extremely thin starting point or an extremely wide starting point, participants were required to use the knob to adjust the image to match what they thought they see when looking in a mirror. When starting from the thin extreme, BDD participants significantly underestimated their facial proportions compared to the other groups. However, when starting from the wide extreme, all groups overestimated their facial proportions but the BDD and cosmetic surgery groups were significantly more accurate than the healthy control group. Overall, BDD participants demonstrated greater accuracy than the other groups. The authors proposed that this may be the result of their increased familiarity with appearance and their mirror-gazing behaviour. Yaryura-Tobias and colleagues (2002) presented BDD, OCD, and nondisordered control participants with nondistorted computerised photographs of themselves. Participants were told that the presented photographs may or may not have been distorted, and, if believed to be distorted, were allowed to correctively modify them using specialised computer software. No control participants made changes to their photos; approximately half the BDD and OCD participants did. Although the study’s small sample size limits the generalisability of the findings, they support the idea of a somatosensorial deficit in BDD. In both these studies, however, participants had to rely on their memories of their appearance and it is thus unclear whether these findings indicate perceptual deficits or differences in the way that people with BDD remember and recall their bodies. Indeed, visual and verbal memory deficits have been shown to be exhibited by BDD sufferers (Deckersbach et al., 2000). Clerkin and Teachman (2008) attempted to deal with this issue by allowing participants in their study to hold a mirror while trying to pick the unaltered photograph of themselves from an array including a series of modified photographs. No difference in accuracy was found between students scoring ‘‘high’’ in BDD-like symptoms and those ‘‘low’’ in such symptoms. However, because of the nonpathological sample, these results may not be applicable to diagnosed BDD patients. Neuropsychological research has also indicated possible differences in visual processing among BDD patients, which may affect somatoperception. A study by Deckersbach and colleagues (2000) using the Rey-Osterrieth Complex Figure Test, which, among other things, assesses organisational and executive strategies using a visual reproduction and recall task, revealed an organisational approach among people with BDD suggestive of more detailed processing as opposed to holistic, configural processing, as observed in healthy controls. Although such findings may indicate problems in


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executive function or executive organisation (as also reported in Dunai, Labuschagne, Castle, Kyrios, & Rossell, 2009), or idiosyncratic attentional qualities, they may also be indicative of problems in visual perceptual processes related to Gestalt perception or configural integration of elements of the visual percept, underpinned by a detail-focused analytical perceptual style. A study employing an identity-matching task offers convergent evidence (Feusner, Bystritsky, Hellemann, & Bookheimer, 2010). In the study, BDD and healthy participants were presented with a photograph of a face with either a neutral or emotional expression. They were then required to pick the previously shown face from a set of two photographs of faces with neutral expressions. Although there were no between-group differences for neutral faces, for emotional faces the BDD group was significantly less accurate than the healthy group and their task reaction times were significantly greater. The authors proposed that, whereas matching two identical faces, as was the case in the neutral expression trials, is achievable using either a configural or detailed approach, attempting to match the identity of an emotional face to a neutral face involves processing of both detailed and configural facial elements. Thus, despite the study’s small sample size and the high rate of comorbid major depressive disorder in the BDD group, which could have contributed to the slowed response times, these between-group differences, taken with the findings of the Deckersbach et al. study, may reflect BDD-related deficits in configural visual processing. Findings that people with BDD are less susceptible to the face inversion effect than people without BDD (Feusner, Moller, et al., 2010; Jefferies, Laws, & Fineberg, 2012) provide further support for this notion. Perhaps the most convincing evidence for a characteristic detail-oriented visual processing approach in BDD comes from neuroimaging studies. Feusner, Townsend, Bytritsky, and Bookheimer (2007) used a similar identity-matching task to that described earlier while conducting functional magnetic resonance imaging (fMRI). In this study three different sets of photographs of faces were used. One set had been altered to contain only high spatial frequency visual information (HSF), the information used in detail processing; a second set was altered to include only low spatial frequency information (LSF), as is used in processing configural aspects of images; and the third set was unaltered. Based on the idea that analytical, detail-oriented perceptual processing occurs predominantly in the left hemisphere, the authors hypothesised that BDD participants would demonstrate elevated left hemispheric activity during the matching task, irrespective of the image set used. This hypothesis was supported by the data. Additionally, as expected, such left-sided activity was evident in healthy controls for only the HSF image set. Although the findings from these studies imply BDD-related visual processing deficits generally and not specifically in relation to one’s own face or body, such general disordered



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visual processing may nevertheless account for the distorted perceptual experience of self, observed in BDD. Indeed, two similar fMRI studies using images of participants’ own faces and images of houses respectively, likewise found aberrant neural activity among people with BDD, suggestive of abnormalities in the processing of configural aspects of their own faces (Feusner, Hembacher, Moller, & Moody, 2011; Feusner, Moody, et al., 2010). Whether any deficits in configural processing are the result of aberrant visual perception or a consequence of problems in higher order perceptual processing is unclear from these studies. However, such detail-oriented visual processing occurs in other conditions without BDD comorbidities, such as autism spectrum disorders (for a review see Behrmann, Thomas, & Humphreys, 2006). Stangier, Adam-Schwebe, Muller, and Wolter (2008) proposed that, amongst individuals with BDD, an analytical perceptual style focusing on detail may underlie an enhanced ability to perceive deviations from appearance standards. To test this hypothesis, they made modifications of different degrees of extremeness to a particular facial feature on an image of a neutral female face. BDD, disfigured, and nondisfigured dermatology patients rated the change from the neutral image on a scale of 1 to 10. BDD participants were more accurate in their ratings than participants in the other two groups. A heightened perceptual aesthetic sensitivity among individuals with BDD was also implicated in a study by Lambrou, Veale, and Wilson (2011) in which, relative to nonartistic healthy controls, BDD participants and artistic healthy controls exhibited a significant preference for highly symmetrical computer-modified images of their own and others’ faces. Interestingly, however, a separate study by Reese, McNally, and Wilhelm (2010) found no differences between BDD, OCD, and healthy participants in facial or dot array symmetry sensitivity or preference. Nevertheless, rather than reflecting aesthetic sensitivity, findings such as those produced by Stangier et al. and Lambrou et al. may point to a visual attentional bias among BDD patients which may contribute to a distorted visual percept. Indeed, Grocholewski, Heinrichs, and Lingnau (2007) used eye-tracking cameras to record how people with BDD and non-BDD cosmetic surgery patients looked at photographs of faces, including their own. Analysis of eye movements showed that the cosmetic surgery patients did not exhibit greater attention to disliked facial areas, but that individuals with BDD did.

SOMATOPERCEPTION BEYOND VISION The eye and the brain are conspirators, and like most conspiracies, theirs is negotiated behind closed doors, in the back room, outside of our awareness. (Gilbert, 2006, p. 210)


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Although vision undeniably plays an important role in somatoperception, and abnormalities in visual perception may therefore contribute to the BDD experience, somatoperception is a complex process that goes beyond simply viewing oneself in a mirror. As with perception generally (Epstein et al., 2001; Gregory, 1997; and, for example, Hollingworth, 2006), somatoperception involves both bottom-up and top-down processing. That is, it results from the integration of afferent multisensory information with expectancies based on an existing complex and multifaceted neural body representation (Epstein et al., 2001; Giummarra et al., 2008; Longo et al., 2010). Additionally, because the body itself is dynamic, the body representation, or at least aspects thereof, must likewise be dynamic. Thus, not only does somatoperception rely upon that body representation, but it plays an important role, through a bidirectional calibration process, in keeping that body representation up to date. Despite the obvious impairments in own-body perception in BDD, beyond the previously mentioned studies of visual perception there has been a dearth of research investigating somatoperception in the disorder. Although the nature and complexity of somatoperception makes it difficult, in and of itself, to study, important insight can be obtained through investigation of the underlying processes, including multisensory integration processes relevant to own-body perception, and proprioception. Proprioception is among the multitude of afferent inputs to the somatoperceptive process and is defined as one’s sense of the current positions of the parts of one’s own body, in space and relative to each other. It is predominantly informed by afferent signals from the muscle spindles, tendons, skin, and joints (Giummarra et al., 2008). However, as well as being informed by these afferent signals, like the somatoperceptive process of which it is a part, proprioception both relies on a neural representation of the body and contributes to the maintenance of that body representation (Longo et al., 2010). In fact, in an illustration of the reciprocal interplay between somatoperception, proprioception, and body representation, Longo et al. (2010) proposed that adolescent clumsiness may be the result of physical growth outpacing ‘‘the ability of somatoperception to update the body [representation] used for proprioceptive localisation’’ (p. 659). Thus, addressing the question of whether proprioceptive abnormalities exist in people with BDD will provide valuable insight into whether somatoperceptive dysfunction is involved in BDD’s characteristic somatic misperception. A particularly useful paradigm for investigation of both proprioception and multisensory integration processes is the rubber hand illusion (RHI). The RHI involves integration of proprioceptive, visual, and tactile signals and is created by synchronously stroking a subject’s real hand and a rubber hand positioned veridically on a table, while the real hand is hidden from view and the subject fixates on the rubber hand. When this is done, subjects



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often experience the illusory sensation that they can feel the touch that is seen on the rubber hand. Although we are unaware of any studies that have used the RHI to investigate somatoperception in BDD, increased susceptibility to the RHI has been shown to be associated with unhealthy body development behaviours in nonpathological individuals (Mussap & Salton, 2006). In addition, a study by Eshkevari, Rieger, Longo, Haggard, and Treasure (2011) found that individuals with eating disorders were more susceptible to the RHI than controls, and illusion strength was positively correlated with a range of eating disorder-related psychopathology variables including body dissatisfaction. These findings are suggestive of an association between body image disturbances and abnormal somatoperceptive processes. They may also be indicative of abnormalities in the parietal lobe functioning of individuals with such disturbances. Indeed, studies comparing RHI experience among people with schizophrenia to healthy controls point to a correspondence between enhanced experience of the illusion and aberrant parietal cortex activity, as measured using EEG (Peled, Pressman, Geva, & Modai, 2003; Peled, Ritsner, Hirschmann, Geva, & Modai, 2000). Further evidence of such an association was produced by Grunwald, Ettrich, Krause, and colleagues (2001), who had anorexic and healthy participants complete a haptic task which involved manual exploration of a series of sunken relief designs with the eyes closed. After exploring each design, participants were asked to reproduce it with their eyes open using paper and pencil. Anorexic patients spent less time exploring the designs with their hands than healthy controls, and their reproductions were significantly poorer, both before and after weight gain. As noted by the authors, such haptic tasks require active exploration by limb movement and therefore, as well as tactile mechanisms, involve the mechanisms utilised in proprioception. The authors proposed that the poor performance of the anorexia group may reflect dysfunction in the cortical integration of the various afferent proprioceptive and tactile signals. Importantly, a similar study in which EEG data were recorded while participants performed the same haptic exploration task found less neural activity in anorexia patients compared to healthy controls in the right hemisphere and, in particular, the right parietal area (Grunwald, Ettrich, Assmann, Dahne, & Krause, 2001). Another study by Grunwald and colleagues (2002) provides further support for this idea. The study required blindfolded participants to adjust a lever with one hand (the ‘‘adjusting’’ hand) to match the angle of a second lever felt by the other hand (the ‘‘feeling’’ hand). Compared to healthy controls, participants with anorexia demonstrated impaired performance on the angle-matching task but only when adjusting the lever with the right hand. This finding was explained in terms of the direct access model which implies that, although the multisensory integration necessary for correct adjustment of the lever occurs in the right parietal cortex irrespective of


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which hand is doing the adjusting, the information sensed by the feeling hand is predominantly processed in the contralateral hemisphere. Thus, there is greater capacitive strain on the right parietal cortex when the feeling hand is the left hand than when it is the right and, as a result of its dysfunction, the right parietal cortex is unable to provide the necessary processing power for accurate task performance. Other studies have found individuals with eating disorders to be more susceptible to proprioceptive illusions. In three studies (Holliday, Tchanturia, Landau, Collier, & Treasure, 2005; Tchanturia et al., 2004; Tchanturia, Serpell, Troop, & Treasure, 2001), individuals with anorexia demonstrated impaired performance relative to healthy controls on the Uznadze illusion (UI; Uznadze, 2009). The UI involves placing wooden balls of the same weight but either equal or differing in size in each hand of a blindfolded participant. The participant is required to say whether both balls are the same size and if the response is in the negative, to say which ball is larger. Although the authors of these studies explained their findings in terms of perceptual rigidity and impairments in set shifting, when considered together with the other proprioceptive findings it is plausible that they reflect proprioceptive dysfunction.

CONCLUSION: TOWARDS A MODEL OF SOMATOPERCEPTIVE DYSFUNCTION IN BDD Although little is known at present about the neuropsychological and neurobiological basis of BDD, the notion that its characteristic somatic misperception is the result of dysfunction in somatoperception, as opposed to being purely cognitive and attitudinal in nature, is both reasonable and plausible. The empirical findings previously discussed have offered evidence of differences in the processing and integration of multisensory information, a fundamental part of somatoperception, among people with disorders with phenomenological overlap with BDD. Past findings have also demonstrated impairments in proprioception in such individuals, which also plays a key role in somatoperception. Associations between susceptibility to the RHI and unhealthy body development behaviours in nonpathological individuals (Mussap & Salton, 2006) may be a preliminary indication of dysfunctional somatoperception in BDD. This somatoperceptive dysfunction may be underpinned by abnormalities in the right parietal cortex, which is known to be associated with disturbances in body image and experience of self (Cutting, 1990; Trimble, 1988), and which is also associated with integration of multisensory information such as is fundamental to somatoperception. Parietal abnormalities in BDD have been postulated elsewhere (YaryuraTobias, Neziroglu, & Torres-Gallegos, 2002), and although neuroimaging



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studies have yet to firmly establish the neurological substrates of BDD, such abnormalities have been preliminarily implicated in this disorder (Carey et al., 2004). Moreover, a burgeoning and fairly robust body of evidence has found support for the idea that people with BDD demonstrate impairments in recognition and processing of emotional facial expressions (Buhlmann, McNally, Etcoff, Tuschen-Caffier, & Wilhelm, 2004; Buhlmann et al., 2002; Feusner, Bystritsky, et al., 2010). These functions have been shown to be dependent on somatosensory mechanisms and, in particular, the parietal cortex (Adolphs, Damasio, Tranel, Cooper, & Damasio, 2000; Adolphs, Damasio, Tranel, & Damasio, 1996). Much research is still required to understand BDD, the roles of somatoperception and proprioception in the disorder, and whether the parietal cortex is among the neurological substrates that are involved. However, the evidence that has accumulated to date indicates that such investigation would provide a valuable contribution to our knowledge about this disorder, especially its pathogenesis, which, in turn, will help inform improvements and innovations in its treatment. Manuscript received 23 August 2011 Revised manuscript received 11 December 2012 First published online 18 February 2013

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