Body Dysmorphic Disorder - SRossell

Current Psychiatry Reviews, 2009, 5, 261-270

261

Body Dysmorphic Disorder: A Review of Current Nosological Issues and Associated Cognitive Deficits Wei Lin Toh*,1, Susan L. Rossell1,2 and David J. Castle1,3 1

Departments of Behavioural Science and Psychiatry, The University of Melbourne, Melbourne, VIC, Australia

2

Cognitive Neuropsychiatry Laboratory, Monash Alfred Psychiatry Research Centre, School of Psychology, Psychiatry and Psychological Medicine, Monash University, Melbourne, VIC, Australia 3

Department of Psychiatry, St. Vincent’s Mental Health, Melbourne, VIC, Australia Abstract: Recent study into body dysmorphic disorder (BDD) has raised questions about the validity of its current diagnostic classification as well as categorical division into ‘psychotic’ and ‘non-psychotic’ variants. Furthermore, though individuals with the disorder are believed to experience cognitive difficulties, the precise nature of these deficits remains unclear. This paper aims to provide a comprehensive review of existing knowledge of BDD in terms of its nosology and cognitive deficits. We evaluate arguments in relation to its inclusion within the obsessive-compulsive spectrum disorders (OCSDs), consider how delusionality is coded in BDD, and also examine recent studies suggesting which specific cognitive deficits may underpin the disorder. There appears to be a sound rationale for considering BDD as part of the OCSDs, though current findings indicate that it is not simply a subtype of obsessive-compulsive disorder (OCD). Evidence also suggests that the degree of delusional beliefs in BDD would be more appropriately theorised on a dimensional basis. In terms of cognitive deficits, research to date has implied that attentional biases and/or abnormalities in basic visual processing may be especially important. Further research is needed to elucidate an inclusive profile of the underlying cognitive deficits in BDD. In turn, these insights could help to clarify current nosological debates surrounding the disorder.

Keywords: Body dysmorphic disorder, nosology, delusionality, cognitive deficits, obsessive-compulsive spectrum disorders. INTRODUCTION Humans are visual creatures and innately drawn to aesthetically pleasing stimuli. Throughout history, individuals possessing inordinate beauty have been highly revered. Despite the fact that the quintessential body ideal has evolved over time, the premium placed on physical attractiveness has remained largely unchanged. Most people thus exhibit some degree of concern about their appearance. However in some individuals, this concern reaches extreme proportions and becomes pathological. Accordingly, the Italian physician, Enrico Morselli, coined the term ‘dysmorphophobia’ in the late nineteenth century to describe such a phenomenon [1]. A hundred years later, it was officially introduced into the Diagnostic and Statistical Manual of Mental Disorders IIIRevised (DSM-III-R) under the label of ‘body dysmorphic disorder’ [2]. WHAT IS BODY DYSMORPHIC DISORDER? According to the current Diagnostic and Statistical Manual of Mental Disorders IV-Text Revised (DSM-IV-TR), body dysmorphic disorder (BDD) is characterised by an excessive preoccupation with an imagined defect or slight physical anomaly in appearance [3]. Where there is indeed an objective physical imperfection, the resultant concern is dispro-

*Address correspondence to this author at the Monash Alfred Psychiatry Research Centre, 1st Floor Old Baker Building, Alfred Hospital, Commercial Road Prahran VIC 3004, Australia; Tel: +613 9076 8650; E-mail: [email protected] 1573-4005/09 $55.00+.00

portionately extreme. Frequent complaints relate to perceived flaws in facial features, especially the shape and size of the nose, quantity of hair, or asymmetry of the head, as well as other body parts, such as condition of the skin, proportion of the limbs, or even the appearance of genitalia. This disorder is differentiated from standard concerns of body image by its severity, chronic nature and the presence of clinically significant distress or functional impairment. Afflicted individuals typically engage in elaborate avoidance strategies, such as camouflage with the aid of make-up or loose clothing, as well as safety behaviours, involving excessive grooming or reassurance seeking from significant others. A unique safety behaviour for BDD relates to the phenomenon of mirror gazing [4]. Some individuals feel compelled to check their appearance repeatedly in mirrors or shiny surfaces, but with an exclusive focus on their perceived flaw to the exclusion of the entirety of their reflection. This produces a confirmatory bias of ‘repulsiveness’, usually making the person feel worse after the act. In contrast, other individuals become highly distressed at any glimpses of their own reflection, and may try to avoid mirrors altogether. On the whole, individuals with BDD have been shown to have markedly impaired psychosocial functioning and quality of life [5, 6]. In the long term, adverse outcomes may include needless cosmetic procedures, acts of self-mutilation, prolonged unemployment, severe social isolation, or even suicide. In fact, available evidence has indicated that up to 80% of these individuals have experienced suicidal ideation, and 26% have actually attempted suicide [7]. © 2009 Bentham Science Publishers Ltd.

262 Current Psychiatry Reviews, 2009, Vol. 5, No. 4

EPIDEMIOLOGY Prevalence rates for BDD have been difficult to establish with certainty, though it is believed that the disorder is somewhat underdiagnosed. This is because individuals with BDD tend to be secretive about their illness, are reluctant to seek psychiatric or psychological treatment, and instead attend dermatology or cosmetic surgery settings. Within the general population, Rief and colleagues [8] placed its prevalence at around 1.7%. An Australian student survey revealed a similar prevalence of 2.3% [9]. In terms of psychiatric samples, varying estimates of 16.0% [10] and 3.2% [11] have been observed in inpatient and outpatient groups respectively. On the contrary, BDD prevalence in aesthetic and beauty clinics has been projected as up to seven times higher relative to community samples; 11.9% of dermatology patients [12] and 9.1% of cosmetic surgery patients [13] were shown to have a diagnosable BDD condition. Most BDD sufferers recount having been hypersensitive about their physical appearance all their lives, though the condition tends to actively manifest in adolescence, with the mean age of onset reported as 16.4 years [14]. Furthermore, the typical course appears to be chronic. Although previous research has indicated 83.8% full or partial remission at fouryear follow-up, caution must be exercised in drawing conclusions from this study, as Phillips and colleagues [15] utilised retrospective chart review methods. A later prospective one-year follow-up revealed a perhaps more realistic prognosis; that is, the probabilities of full and partial remissions were respectively 0.09 and 0.21, but this was accompanied by a 0.15 chance of further relapse [16]. There is a general consensus that BDD afflicts equal numbers of men and women. Yet consistent sex differences have been documented in terms of the specific bodily areas triggering fixation; male distress is predominantly associated with baldness, body build and genitals, whereas major female concerns tend to centre upon skin, breast size, and overall body weight [17, 18]. These disparities reflect culturally mediated norms, and suggest that existing social values not only exert an impact on the content of BDD symptoms, but also influence the specific co-occurrence of other psychological disorders. Accordingly, a clear pattern of psychiatric comorbidities has been observed across the genders; men seemed predisposed to co-occurring bipolar disorder, whereas women were more likely to also suffer from bulimia nervosa, generalised anxiety disorder, or panic disorder [19]. ETIOLOGICAL THEORIES To date, little has been definitively established regarding the etiology of BDD. A number of differing perspectives have attempted to elucidate the mechanisms through which the disorder is developed and maintained. To this end, early psychoanalytic accounts have posited that BDD arises from an unconscious displacement of hidden emotional or sexual conflict based on feelings of guilt and poor self-image [20]. The feature that forms the focus of BDD preoccupation is seen as symbolic of some other body part, and reflective of deep-seated and unresolved psychological difficulties. These descriptions have, however, tended to emerge from single case reports, and lack empirical support.

Toh et al.

Cororve and Gleaves [21] reviewed biological underpinnings to the disorder, and identified organic contributants such as a Darwinian drive for perfection and symmetry, neurological disturbances in the temporal lobe, or dysregulation in the serotonin neurotransmitter system. Indeed, cases of idiopathic secondary BDD have been highlighted as developing after right temporal lobectomy or inflammatory frontotemporal atrophy [22, 23]. This could be because the nondominant temporal lobe is often theorised as mediating perceptions of body image [24]. Hollander and colleagues [25] also uncovered beneficial therapeutic responses to serotonergic antidepressants, thus verifying the role of neurotransmitter irregularities in BDD occurrence, though exact mechanisms remain unspecified. Moreover, genetic factors likely play a pivotal role in the etiology of BDD, given its heritability. For instance, 8% of individuals with BDD have a family member with the same disorder, representing at least a fourfold increase in incidence relative to the general population [26]. Yet scant research has been conducted on the genetics of BDD, although a preliminary study did uncover an association for GABA A-2 and 5-HTTLPR in relation to BDD, but only at a trend level for the latter gene [27]. Cognitive-behavioural models of BDD have received much attention of late, with reasonable empirical validation in the literature [28, 29]. Accordingly, it has been theorised that core dysfunctional schema arise from multiple interactions between genetic vulnerabilities, early childhood experiences, and social factors. Vital learning incidents involving social comparison and feedback instill and reinforce the value of physical beauty, thereby fostering links between personal attractiveness and self-worth. This is especially relevant in adolescence where dramatic physical changes occur alongside a rapidly developing and vulnerable psyche. In support of this, Phillips and colleagues [30] found that the clinical features of BDD in adolescence were largely similar to those in adulthood, with the exception of increased delusional beliefs and suicidality. In addition, specific personality styles involving high negative affect, perfectionism or self-conscious shyness could further exacerbate the situation [31]. Thereafter, a series of critical events, such as episodes of childhood maltreatment or repeated teasing, may trigger the disorder, leading to subsequent avoidant and safety behaviours. In fact, there appears to be a distinct relationship between childhood abuse and the occurrence of BDD [32]. Thus, Didie and colleagues [33] reported elevated rates of emotional and sexual abuse, with a significant association between the severities of sexual abuse and BDD symptoms. Likewise, preliminary research has revealed that individuals with BDD recalled more incidents of both appearance- and competence-related teasing compared to healthy controls [34]. Yet for some individuals, no particular trigger may be identified. This model also does not provide an adequate explanation for why BDD develops in some individuals, but not in others, experiencing similar life circumstances. CURRENT NOSOLOGICAL DEBATES At present, two ongoing nosological debates surround the DSM-IV-TR classification of BDD [3]. The first point of contention relates to the current incorporation of BDD under the category of somatoform disorders, and the second related area of dispute lies with how individuals who hold their BDD beliefs with delusional intensity should be classed [35].

Body Dysmorphic Disorder: A Review of Current Nosological Issues

The major aspects of each of these debates are now reviewed, based on a Medline literature search using the term ‘body dysmorphic disorder’, with a particular focus on papers published from 2007 to the present, following a previous review carried out by similar authors [36]. BODY DYSMORPHIC DISORDER AND THE SOMATOFORM DISORDERS Since its conception, the classification of BDD has been fraught with inconsistencies. For example, early psychiatrists, Emil Kraepelin and Pierre Janet, classed BDD as a compulsive neurosis and an obsessional shame about the body respectively [1]. Moreover, BDD has been variously termed ‘hypochondriacal paranoia’, ‘beauty hypochondria’, and ‘dermatologic hypochondriasis’. Its multiple monikers in association with hypochondriasis have likely left a legacy in terms of its enduring links with the class of somatoform disorders. Though BDD shares several commonalities with the latter, such as exaggerated beliefs about the body or the need to seek excessive reassurance, its focus is centred on perceived physical flaws, rather than concerns with death or disease. As a result, a number of contemporary authors have contended that BDD is uneasily situated within this category and bears little resemblance to the other members of such a heterogeneous cluster [36, 37]. In fact, recurring critiques have provoked a push toward discarding the entire grouping in favour of a multiaxial formulation [38]. In such an event, a further debate has ensued with regard to where exactly BDD should be placed. Links with Mood, Anxiety, Eating and Personality Disorders In terms of Axis I psychopathology, BDD has been closely associated with several disorders, including major depressive disorder (MDD), obsessive-compulsive disorder (OCD), social phobia (SP), and anorexia nervosa (AN) [39]. There is also emerging research documenting links between BDD and Axis II personality disorders (PDs). The links between BDD and OCD form a special case, which is discussed in the next section. Meanwhile, the similarities between BDD and each of these other disorders are considered in turn. BDD and MDD share commonalities in that individuals afflicted with either or both disorders report similar symptoms in terms of lowered mood, loss of self-esteem, a sense of personal guilt and worthlessness, and suicidal ideation. Studies looking at the comorbidity rates of BDD in patients whose primary complaint is MDD have generally yielded inconsistent results ranging from 0% [40] to 13.8% [41]. Research examining the converse however, has ascertained that MDD is the disorder most commonly comorbid with BDD, with an estimated 38.2% of BDD sufferers currently experiencing MDD [42]. In these cases, it has also been found that BDD usually precedes episodes of MDD, implying that the latter possibly emerges as a consequence of the psychological difficulties of living with BDD. On the other hand, Phillips and Stout [43] uncovered bidirectional longitudinal associations, such that improvements in one disorder served as a significant predictor of remission in the other disorder. This was posited as suggestive of a joint affective etiology. An added noteworthy finding is that atypical [44]

Current Psychiatry Reviews, 2009, Vol. 5, No. 4

263

and melancholic [42] subtypes of MDD co-occur more frequently with BDD. Though reasons behind this remain unclear, it perhaps denotes that only specific subtypes of MDD may share etiological links with BDD. In relation to the anxiety disorders, BDD resembles SP in that both are associated with excessive self-focused attention and fears of negative evaluation, with a resultant avoidance of social situations. Indeed, these disorders tend to be characterised by feelings of social defectiveness and shame, as well as related concerns of public humiliation and rejection. This is further corroborated by the Japanese conceptualisation of BDD as a subtype of SP. Specifically, the former is termed shubokyofu or ‘phobia of a deformed body’ [45]. Comorbidity estimates range from 12% of BDD in a sample whose primary diagnosis was SP [46] to 34.3% of SP in a population whose predominant condition was BDD [47]. Furthermore, in almost all cases, SP onset typically preceded BDD. A key differential feature however, is that fears in BDD relate to expectations of aversive reactions in others in response to perceived physical flaws, whereas concerns in SP tend to focus on potential embarrassment engendered by deficits in communication or other forms of social inaptitude. Nevertheless, both disorders share similar clinical features, for instance, in terms of age of onset and gender distribution. Moreover, individuals with comorbid BDD and SP tend to experience elevated social anxiety, increased suicidal ideation, and poorer overall psychosocial functioning [47]. There also appears to be major overlaps between BBD and the eating disorders, especially for AN [48]. The eating disorders entail marked body image disturbance and dissatisfaction, an ensuing drive to ‘enhance’ appearance and an undue emphasis of physical appearance on evaluations of self-worth [49]. It is thus not uncommon to observe individuals with AN being preoccupied with non-weight aspects of their bodies, such as the appearance of their stomach or thighs. Grant and colleagues [50] demonstrated that 39% of those with a predominant diagnosis of AN suffered from comorbid BDD. Likewise, individuals with BDD can at times bear added weight concerns, which may or may not reach diagnostic significance. Accordingly, Kittler and colleagues [51] reported that up to 29% of persons with BDD expressed discontent with their body weight, while Ruffolo and colleagues [52] showed that 1.0% of their BDD sample had a current diagnosable AN condition. It was concluded that comorbid BDD and AN was generally associated with more psychiatric hospitalisations as well as poorer psychosocial outcomes. A further diagnostic dilemma exists as to how to classify persons with symptoms straddling both disorders. For example, when prominent features of BDD and AN co-exist alongside weight concerns that do not clearly meet diagnostic criteria for the latter, it is unclear whether a diagnosis of BDD or Eating Disorder, Not Otherwise Specified (ED-NOS) should be given. There are also major differences between the disorders. In particular, AN engages notable eating and purging behaviours as well as an array of attendant physical health problems, including amenorrhea and malnutrition. Furthermore, a key limitation to conceptualising BDD and AN as variants of a class of body image disorders lies in an inability to explain significant gender differences in prevalence, as the latter is known to primarily affect women.


Toh et al.

Though scant research has been conducted on PDs in relation to BDD, the emerging evidence consistently points toward severe comorbid Axis II psychopathology. Approximately 57% to 87% of individuals with BDD met the criteria for one or more PDs, with the mean number of PD diagnoses ranging from 2.5 to 6.0 [53, 54, 55]. Most widespread are Cluster C PDs, including avoidant, dependent, and obsessive-compulsive, followed by Cluster A PDs, particularly schizotypal and paranoid [56]. Analyses of personality factors revealed high Neuroticism and low Extraversion [57]. Semiz and colleagues [58] recently examined the prevalence of BDD in a sample with borderline personality disorder (BPD), and reported an elevated comorbidity of 54.3%. This was posited as linked to experiences of trauma, which significantly predicted co-occurring BDD with BPD. Overall, it is likely that the existence of PDs will shape BDD treatment response, thereby warranting further investigations into this area. Body Dysmorphic Disorder and Compulsive Spectrum Disorders

the

Obsessive-

Despite various attempts to categorise BDD as either an affective spectrum disorder in line with MDD, a form of SP or a body image disorder along with AN as outlined, these arguments have tended to struggle due to cracks in theoretical formulation or lack of empirical data. The most compelling stance to date probably relates to the case for BDD, along with OCD and several related impulse control disorders, to be classed as part of the obsessive-compulsive spectrum disorders (OCSDs). This line of reasoning arises from numerous similarities between BDD and OCD, especially in terms of phenomenology, symptomatology, comorbidity, familial loading, and treatment outcomes. In general, OCD is characterised by (i) persistent and recurrent thoughts, images, or impulses that are experienced as inappropriate and intrusive, and cause marked anxiety or distress (obsessions) as well as (ii) excessive and repetitive behaviours or mental acts performed in accordance to rigid rules in a bid to neutralise the distress (compulsions) [3]. Akin to OCD, BDD preoccupations are often experienced as recurring cognitions that prompt ritualistic acts carried out in a stereotyped and time-consuming manner. Grant and colleagues [59] introduced pathological skin-picking as one such example that could be a behavioural symptom of BDD and/or OCD. Shared clinical features typically include sex ratio, age of onset as well as obsessionality and compulsivity attributes, to name a few [60, 61]. Examples of differing clinical aspects conversely relate to educational, employment and marital statuses as well as suicidal ideation, for which poorer functioning was usually observed in BDD cohorts [62, 63]. However, two key differences are clinically important, and deserve special mention. First, a discrete pattern of psychiatric comorbidities has been observed; BDD groups reported greater co-occurring bulimia nervosa, MDD, and substance use disorders, whereas OCD groups exhibited more frequent generalised anxiety disorder [64]. Second, BDD groups also have lower levels of insight, and are more likely to be delusional [65, 66]. This latter point is closely linked to the other nosological debate regarding delusionality in BDD, and will be covered in the following section.

Despite these clinical differences, several lines of reasoning do lend partial support to the OCSD classification debate, including increased comorbidity, neurobiological correlates, and comparable therapeutic agents in treatment. In terms of comorbidity estimates, research has mainly focused on the prevalence of BDD in OCD samples, which has ranged from 7.7% [46] to 15.3% [67]. Comorbidity is not only associated with more severe functional impairment and psychopathology in several domains, but also has a specific link to checking, hoarding, somatic, and symmetry concerns, as well as anxious, impulsive, and schizotypal personality traits [68]. The biological links underlying OCD have been well documented. Samuels and colleagues [69] established that the presence of the disorder in a blood relative increased the overall familial risk for OCD and other putative OCSDs. This genetic trend extends to BDD, where familial studies have revealed that 5.8% of first-degree relatives of 200 BDD probands were also diagnosed as having the disorder [14]. In fact, familial aggregation of OCD and BDD has been repeatedly demonstrated. Bienvenu and colleagues [26] examined OCD patients and healthy controls as well as their firstdegree relatives, and discovered that BDD was significantly more prevalent in case probands and their first-degree relatives, regardless of whether the former had the same diagnosis. Previously, Hollander and colleagues [70] established that 17% of family members of 50 BDD probands had OCD as well. A case report likewise described an adolescent onset of BDD followed by a middle-age onset of OCD, faced by a man and his mother alike [71]. In a similar vein, cognitive and neuroimaging research has identified parallel patterns of executive dysfunction and the involvement of similar brain regions in both disorders, consistent with their conceptualisation as OCSDs. In particular, Hanes [72] reported that BDD and OCD groups performed equally poorly on the Stroop task and the New Tower of London task, likely implicating frontal lobe dysfunction. In support of this, Dunai and colleagues [73] uncovered executive function deficits in BDD, especially in relation to the online manipulation, planning and organisation of information. Furthermore, Saxena and colleagues [74] compared treatment response across the two groups, and found that BDD and OCD symptoms responded equally well to intensive multimodal therapy, comprising primarily of selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioural therapy (CBT). The overall conclusion appears to be that BDD is intricately related to OCD, but is not a mere clinical variant of the latter, such that both disorders may potentially be situated amid the OCSDs. Proponents of this debate cite the benefits of a dimensional approach, with its diagnosis and treatment implications, whereas detractors query its clinical utility and gaps in explanatory power [75]. Another limitation is that OCD itself is a highly heterogeneous disorder, and may not form a unitary construct in view of its distinct symptom dimensions, for instance, in relation to hoarding. More research is thus necessary to elucidate the theoretical validity and clinical efficacy of positioning BDD within the OCSDs. DELUSIONALITY IN BODY DYSMORPHIC DISORDER Though their OCD counterparts usually perceive their obsessions as ego-dystonic and irrational, persons with BDD


often accept their cognitions as ‘natural’ and thus retain high levels of conviction as to the veracity of their beliefs. Accordingly, a prominent feature setting BDD apart from the other disorders discussed thus far is that it often achieves delusional proportions. In fact, Phillips and colleagues [76, 77] found that 35.6% to 52.0% of BDD samples had delusional ideation. Despite the fact that these psychotic beliefs tend to be non-bizarre, they often comprise ideas of reference based on the erroneous viewpoint that others are mocking or judging the perceived physical flaw. This raises the question of whether BDD should be classed alongside the psychotic disorders, leading up to the second related nosological debate of how individuals with delusional BDD beliefs should be best accounted for. At present, BDD straddles two discrete diagnostic categories within the DSM-IV-TR, thereby warranting a doublecoding approach [3]. In other words, a standard BDD diagnosis implicates a somatoform disorder, but an option for the ancillary diagnosis of delusional disorder, somatic subtype (DDST) exists, and is assigned if preoccupations reach delusional intensity. In a similar way, the International Classification of Diseases (ICD-10) system terms BDD as dysmorphophobia, incorporating the non-delusional subtype as a hypochondriacal disorder, whilst subsuming the delusional subtype under the label of persistent delusional disorder [78]. These taxonomies however, are rather unhelpful, as fluctuations in either direction in line with life stressors or treatment efficacy are common. Several authors have thus suggested that the psychotic and non-psychotic forms of BDD reflect a single disorder distinguished along the spectrum of insight [36, 76]; the former involves extreme delusional convictions, whereas the latter engages overvalued ideas susceptible to disconfirmation. Empirical corroboration for this stance is based on findings that both groups were remarkably similar in terms of demographics, clinical features and course as well as treatment response, with the exception of heightened symptom severity in the delusional subtype [77, 79]. Though arguments in favour of preserving the DDST concept have been raised [80], the adoption of a dimensional model may pave the way for a more valid and consistent taxonomy of other disorder subtypes characterised along the continuum of insight [81]. Nevertheless, the multidimensional nature of insight and its explicit links to BDD warrant further study. THE ROLE OF COGNITION IN BODY DYSMORPHIC DISORDER The clinical presentation of BDD suggests that it encompasses perceptual and affective elements in that sensory disturbances are manifested as flawed cognitive appraisals of personal ‘ugliness’, which engender negative attitudes toward oneself and feelings of internal aversion. Yet to date, only 12 identified studies have examined cognitive function in BDD [82]. Available research has uncovered a range of deficits in the areas of executive function [72, 73], memory [83, 84], social information processing [85, 86], facial emotion perception [87-90], self-discrepancies [91], and metacognition [92]. Based on the existing literature, Castle and colleagues [35] have proposed two main cognitive mechanisms as likely underlying the etiology and maintenance of BDD.


265

Foremost, selective attentional biases may be responsible. To this end, Buhlmann and colleagues [85] demonstrated that individuals with BDD exhibited a negative interpretive bias when presented with ambiguous body-related, social or general scenarios. For example, someone laughing behind them would tend to be construed as an adverse reaction to their physical appearance. Based on an emotional Stroop paradigm, these individuals were also shown to be vulnerable to distraction by emotional cues, as evidenced by significant interference effects for positive and negative words related to BDD [86]. Maximum Stroop interference was moreover noted for the former, likely representing key disruptions in mechanisms involving higher order attentional control. Extending their investigation via the use of ecologically valid stimuli, Buhlmann and colleagues [87] examined the ability of persons with BDD in terms of (i) discrimination of general facial features, and (ii) identification of facial expressions of emotion. The former involved matching a neutral target face with up to three images of the same person in a six-stimuli array of faces that varied in terms of angles and lighting, whereas the latter comprised the presentation of faces bearing one of seven basic facial emotions, namely anger, disgust, fear, happiness, neutral, sadness, and surprise. Though there were no impairments in overall facial discrimination, deficits were established in the recognition of facial expressions, particularly in terms of the misidentification of disgusted and fearful emotions as angry. Follow-up research uncovered a contemptuous recognition bias in addition to the original angry recognition bias, both of which were only significant for self-referent (eg. ‘Imagine that the bank teller is looking at you, what is his facial expression like?’), as opposed to other-referent (eg. ‘Imagine that the bank teller is looking at a friend of yours, what is his facial expression like?’), scenarios [88]. It was further hypothesised that poor insight and ideas of reference underlay these difficulties. These studies collectively suggest that selective attentional biases may be seen to embody social rejection in BDD, thereby reinforcing misguided notions of personal unattractiveness and social undesirability. An alternative understanding is that anomalies in basic perceptual operations create organisational difficulties that give rise to the disorder. In this way, primary deficits in visual perception may play a key role in the development and maintenance of BDD. Accordingly, Deckersbach and colleagues [83] administered the Rey-Osterrieth Complex Figure Test and the California Verbal Learning Test to a BDD sample, and uncovered deficits on verbal and non-verbal learning and memory indices. In particular, the use of inappropriate scanning and categorisation strategies was interpreted as indicative of deficits in Gestalt organisation; individuals with BDD were believed to only recall isolated elements of stimuli, neglecting the overriding global aspects. It was therefore argued that the failure to correctly identify facial affect could instead be attributed to a restricted focus on specific facial features, thereby distorting overall interpretation. Accordingly, this line of reasoning may serve as a viable alternative explanation for the facial emotion recognition biases found in BDD, but does not explain why no deficits were identified in the general facial discrimination task [87, 88]. Other similarly contradictory findings also exist. In line with the perceptual deficits hypothesis, Yaryura-Tobias and colleagues [90] showed that persons with BDD were


poor at detecting distortions in their own digital facial images and thus, more prone to engaging in computerised facial modification relative to a healthy control group. On the contrary, Stangier and colleagues [89] demonstrated that BDD patients were surprisingly more accurate in recognising subtle manipulations in target features relative to dermatology patients. These findings were based on a facial discrimination task, involving varying degrees of alterations to five target areas of a neutral face that frequently constituted the focus of BDD preoccupations, namely distance between the eyes, size of the nose, pustules of the skin, scars and hair loss. A main difference between the two studies is the use of one’s own face as presentation stimuli in the former versus the faces of others in the latter. Perhaps viewing a close-up facial image of oneself activated the aforementioned selective attentional biases in addition to possible perceptual deficits, thereby yielding greater overall deficits. In fact, it is likely that the contrasting mechanisms of top-down versus bottom-up processing are somewhat interdependent; densely integrated neural networks ensure profound connectivity and dependency amongst disparate cerebral structures. In this sense, the involvement of controlled higher order attentional functions and rudimentary perceptual processes in BDD symptomatology is to be expected. Based on the available literature, other cognitive mechanisms of interest include the role of self-discrepancies, mental imagery, and metacognitive beliefs, all of which may serve as further maintaining factors in BDD. In particular, individuals with BDD displayed significant discrepancies between their actual and ideal selves, as well as their actual and should selves, but negligible discrepancies between self and other domains, implying that the disorder may be perpetuated by a failure to achieve internally generated appearance standards [91]. Furthermore, these persons were shown to experience spontaneously occurring vivid imagery bearing appearance-related themes [84]. These mental images were also more likely to be viewed from an observer perspective and accompanied by negative bodily sensations. In follow-up research, Cooper and Osman [92] investigated metacognitive processing in BDD and identified mental imagery as well as verbal thoughts as underlying cognitive features of the disorder. Neuroimaging Studies Thus far, only three neuroimaging studies are known to have been conducted in relation to BDD. On the whole, it appears that a combination of dysfunctions in the frontalsubcortical circuits, parietal lobe, temporal lobe, and limbic structures likely underlie the characteristic neurocognitive deficits observed in BDD [93, 94]. Morphometric magnetic resonance imaging (MRI) has revealed a leftward shift in caudate asymmetry and greater total white matter volume in eight women with BDD relative to healthy controls [95]. As its primary function is to regulate and filter new information, caudate abnormalities may result in reduced incoming information, thereby partially accounting for the selective attentional biases observed in BDD. Yet it remains unexplained why such a bias may be especially directed toward body-related details. A subsequent single photon emission computed tomography (SPECT) study of six patients with BDD revealed a range of discrepant findings, including relative perfusion deficits in bilateral anterior-medial temporal

Toh et al.

and occipital regions as well as asymmetric perfusion in the parietal lobes [96]. However, the small sample size bearing comorbid conditions, the absence of comparison and control groups as well as a lack of quantitative regional brain activity measurements are several limitations that render firm interpretations from these two studies difficult. A recent functional magnetic resonance imaging (fMRI) study compared the visual processing of faces in 12 patients with BDD relative to healthy controls [97]. In particular, participants were asked to match neutral facial photographs with differing spatial frequencies, namely, low, normal, or high. Accordingly, some photographs had been digitally altered to remove low or high spatial frequency information, thereby generating images containing only detail or configural visual information respectively. Relative to healthy controls, patients with BDD exhibited greater left hemispheric activity, especially in the lateral aspects of the prefrontal cortex and temporal lobe, for all tasks. Moreover, the dorsal anterior cingulate gyrus was activated in BDD patients for the low spatial frequency task, whereas the left prefrontal cortex and dorsal anterior cingulate gyrus were activated in healthy controls for the high spatial frequency task. These findings suggest a predominance of detail encoding and analysis for low spatial frequency and normal faces in BDD that is only found for high spatial frequency faces in healthy controls. In other words, patients with BDD tend to display a bias for local or piecemeal processing as opposed to global or holistic management of visual information. Patients with BDD also showed an abnormal hyperactivation of the amygdala to low and high spatial frequency faces, which likely mediates the aforementioned selective attentional biases. At this point, further replication of neuroimaging research is recommended to provide a firm foundation upon which to draw conclusions regarding the underlying neurobiology of BDD. TREATMENT OF BODY DYSMORPHIC DISORDER As mentioned, individuals with BDD often forgo psychiatric treatment, instead opting for dermatological or cosmetic surgery remedies for their perceived physical defect. Several studies assessing cosmetic procedure outcomes for BDD patients have found that these medical treatments tend to be ineffective for the disorder; BDD diagnoses, psychiatric comorbidities, and high levels of functional handicap still existed at follow-up, despite subjective reports of high patient satisfaction [98, 99, 100]. Though a full review of available treatments for BDD is beyond the scope of the present paper, the most efficacious modalities to date relate to psychopharmacological approaches as well as psychological interventions [101, 102]. Each of these treatments will be broadly briefly reviewed in turn, with the general acknowledgment that a rigorous evaluation of combined psychopharmacological and psychological treatments is called for. Psychopharmacological Approaches Phillips and Hollander [103] have recommended SSRIs as the current medication of choice for BDD. Thus far, openlabel trials of citalopram [104], escitalopram [105], fluvoxamine [106], and venlafaxine [107] have all demonstrated good efficacies. Moreover, fluvoxamine yielded significant improvements in delusionality, whereas venlafaxine was useful for reducing obsessive and compulsive symptoms. Double-blind randomised placebo-controlled and crossover


trials of fluoxetine [108] and clomipramine [25] respectively established their efficacies for BDD treatment. In general, antipsychotic augmentation of fluoxetine using olanzapine and pimozide to target delusional symptoms has met with limited success [109, 110], with the exception of a single case study effectively treated with olanzapine augmentation of paroxetine [111]. Psychological Interventions Though a review has suggested that the literature does not support any one psychological intervention over another [112], the majority of research has converged on the use of some form of cognitive and/or behavioural strategies in the treatment of BDD. Core techniques employed include psychoeducation, social skills training, cognitive restructuring as well as behavioural experiments, especially graded exposure and response prevention (ERP). Accordingly, a number of early studies have specifically examined ERP using imaginary or in vivo exposure techniques with promising results [113, 114]. In terms of CBT, moderate therapeutic success has been demonstrated via a single case study [115], a pilotrandomised controlled trial [116] as well as within a group format [117]. Other research has also investigated pure cognitive [118] or behavioural [119] approaches with modest treatment outcomes. Costa and colleagues [120] have even applied a narrative therapy framework for the successful treatment of a single case study of BDD. On the whole, recent research on psychological interventions for BDD has been lacking, and there is a real need for randomised controlled trials that seek to compare efficacies across diverse treatment modalities for BDD. IMPLICATIONS AND FUTURE RESEARCH Based on the findings of the current review, a number of tentative suggestions may be made in relation to (i) the assessment and treatment of BDD, (ii) its nosological classification in the upcoming Diagnostic and Statistical Manual of Mental Disorders-V (DSM-V), and (iii) future research essential to address current gaps in knowledge surrounding the disorder. In terms of proposed assessment protocols, the covert nature of BDD sufferers coupled with its numerous clinical overlaps with other psychiatric conditions means that clinicians need to be alert and ask candid questions in order to effectively screen for the disorder. Furthermore, practitioners in the cosmetic surgery and dermatology industries need to pay special attention and monitor potential clients for the possibility of BDD, especially since research has shown that these individuals likely yield poorer long-term outcomes after undergoing surgical interventions [98-100]. With regards to management recommendations for BDD, evidencebased treatment options seem limited at present. A combination of psychopharmacological and psychological approaches appears desirable, but randomised controlled trials verifying its efficacy are currently lacking [101, 102]. In addition, variations in individual client presentation in terms of the degree of delusionality exhibited and comorbidities with specific disorders would always necessitate treatment evaluations on a case-by-case basis.


267

Although there appears to be a general consensus that BDD sits uneasily amongst the somatoform disorders [36, 37], with some authors even going as far as to dispute the utility of the category of somatoform disorders as a whole [38], current gaps in knowledge surrounding BDD preclude any definitive recommendations in terms of its nosological classification in DSM-V. Given its numerous overlaps with several clinical disorders, it remains to be seen whether BDD will be subsumed under the OCSDs, grouped alongside the spectrum of psychotic disorders, or perhaps even classed within its own unique category. Based on existing research, much is known about the phenomenology of BDD, but its genetic, cognitive, and neurobiological aspects remain poorly documented. Accordingly, future research should look toward addressing these deficits in knowledge. For instance, cognitive studies may focus on elucidating how selective attentional biases and perceptual deficits intersect and underlie key features of the disorder. Likewise, neuroimaging studies may investigate if structural anomalies exist or if functional brain activation patterns differ in individuals with BDD. Taken together, such research would likely yield a deeper understanding of the neurocognitive mechanisms of the disorder, which would in turn enhance its clinical management. CONCLUSION BDD remains an underdiagnosed and poorly understood disorder. More research needs to be undertaken into its etiological underpinnings as well as associated neurocognitive deficits. Based on these findings, it is hoped that the ongoing nosological debates in relation to its classification may be informed, along with the evolution of treatment plans, involving the design and implementation of earlier and more effective intervention measures. REFERENCES [1] [2]

[3] [4]

[5] [6]

[7] [8] [9]

[10]

Phillips KA. Body dysmorphic disorder: The distress of imagined ugliness. Am J Psychiatry 1991; 148: 1138-49. American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DMS-III-R. Washington, American Psychiatric Association 1987. American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DSM-IV-TR. Washington, American Psychiatric Association 2000. Veale D, Riley S. Mirror, mirror on the wall, who is the ugliest of them all? The psychopathology of mirror gazing in body dysmorphic disorder. Behav Res Ther 2001; 39: 1381-93. Phillips KA, Menard W, Fay C, Pagano ME. Psychosocial functioning and quality of life in body dysmorphic disorder. Compr Psychiatry 2005; 46: 254-60. Phillips KA, Quinn G, Stout RL. Functional impairment in body dysmorphic disorder: A prospective, follow-up study. J Psychiatr Res 2008; 42: 701-7. Phillips KA. Suicidality in body dysmorphic disorder. Prim Psychiatry 2007; 14: 58-66. Rief W, Buhlmann U, Wilhelm S, Borkenhagen A, Brähler E. The prevalence of body dysmorphic disorder: A population-based survey. Psychol Med 2006; 36: 877-85. Bartsch D. Prevalence of body dysmorphic disorder symptoms and associated clinical features among Australian university students. Clin Psychol, 2007; 11: 16-23. Conroy M, Menard W, Fleming-Ives K, Modha P, Cerullo H, Phillips KA. Prevalence and clinical characteristics of body dysmorphic disorder in an adult inpatient setting. Gen Hosp Psychiatry 2008; 30: 67-72.

268 Current Psychiatry Reviews, 2009, Vol. 5, No. 4 [11]

[12] [13]

[14]

[15] [16]

[17] [18]

[19] [20]

[21] [22]

[23] [24] [25]

[26] [27]

[28] [29] [30]

[31] [32]

[33] [34]

[35] [36]

Zimmerman M, Mattia JI. Body dysmorphic disorder in psychiatric outpatients: Recognition, prevalence, comorbidity, demographic, and clinical correlates. Compr Psychiatry 1998; 39: 265-70. Phillips KA, Dusfresne RG Jr, Wilkel CS, Vittorio CC. Rate of body dysmorphic disorder in dermatology patients. J Am Acad Dermatol 2000; 42: 436-41. Aouizerate B, Pujol H, Grabot D, et al. Body dysmorphic disorder in a sample of cosmetic surgery applicants. Eur Psychiatry 2003; 18: 365-8. Phillips KA, Menard W, Fay C, Weisberg R. Demographic characteristics, phenomenology, comorbidity, and family history in 200 individuals with body dysmorphic disorder. Psychosomatics 2005; 46: 317-25. Phillips KA, Grant JE, Siniscalchi JM, Stout R, Price, LH. A retrospective follow-up study of body dysmorphic disorder. Compr Psychiatry 2005; 46: 315-21. Phillips KA, Pagano ME, Menard W, Stout RL. A 12-month follow-up study of the course of body dysmorphic disorder. Am J Psychiatry 2006; 163: 907-12. Phillips KA, Menard W, Fay C. Gender similarities and differences in 200 individuals with body dysmorphic disorder. Compr Psychiatry 2006; 47: 77-87. Taqui AM, Shaikh M, Gowani SA, et al. Body dysmorphic disorder: Gender differences and prevalence in a Pakistani medical student population. BMC Psychiatry 2008; 8: 20. Perugi G, Akiskal HS, Giannotti G, Frare F, di Vaio S, Cassano GB. Gender-related differences in body dysmorphic disorder. J Nerv Ment Dis 1997; 185: 578-82. Sobanski E, Schmidt MH. Body dysmorphic disorder: A review of the current knowledge. Child Psychol Psychiatry Rev 2000; 5: 1724. Cororves MB, Gleaves DH. Body dysmorphic disorder: A review of conceptualisations, assessment, and treatment strategies. Clin Psychol Rev 2001; 21: 949-70. Gabbay V, Asnis GM, Bello JA, Alonso CM, Serras SJ, O’Dowd MA. New onset of body dysmorphic disorder following frontotemporal lesion. Neurology 2003; 61: 123-5. Naga A, Devinsky O, Barr W. Somatoform disorders after temporal lobectomy. Cogn Behav Neurol 2004; 17: 57-61. Saxena S, Feusner JD. Toward a neurobiology of body dysmorphic disorder. Prim Psychiatry 2006; 13: 41-8. Hollander E, Allen A, Kwon J, et al. Clomipramine versus desipramine crossover trial in body dysmorphic disorder: Selective efficacy of a serotonin reuptake inhibitor in imagined ugliness. Arch Gen Psychiatry 1999; 56: 1033-9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: Results from a family study. Biol Psychiatry 2000; 48: 287-93. Richter MA, Tharamalingam S, Burroughs E, et al. A preliminary genetic investigation of the relationship between body dysmorphic disorder and OCD. Neuropsychopharmacology 2004; 29: S200. Neziroglu F, Khemlani-Patel S, Veale D. Social learning theory and cognitive-behavioural models of body dysmorphic disorder. Body Image 2008; 5: 128-38. Veale D. Advances in a cognitive behavioural model of body dysmorphic disorder. Body Image 2004; 1: 113-25. Phillips KA, Didie ER, Menard W, Pagano ME, Fay C, Weisberg RB. Clinical features of body dysmorphic disorder in adolescents and adults. Psychiatry Res 2006; 141: 305-14. Rosen JC. In: Thompson JK Ed, Body image, eating disorders, and obesity. Washington, American Psychological Association, 2003; 149-72. Neziroglu F, Khemlani-Patel S, Yaryura-Tobias JA. Rates of abuse in body dysmorphic disorder and obsessive-compulsive disorder. Body Image 2006; 3: 189-93. Didie ER, Tortolani CC, Pope CG, Menard W, Fay C, Phillips KA. Childhood abuse and neglect in body dysmorphic disorder. Child Abuse Negl 2006; 30: 1105-15. Buhlmann U, Cook LM, Fama JM, Wilhelm S. Perceived teasing experiences in body dysmorphic disorder. Body Image 2007; 4: 381-5. Castle DJ, Rossell SL, Kyrios M. Body dysmorphic disorder. Psychiatr Clin N Am 2006; 29: 521-38. Castle DJ, Rossell SL. An update on body dysmorphic disorder. Curr Opin Psychiatry 2006; 19: 74-8.

Toh et al. [37] [38]

[39] [40]

[41] [42]

[43]

[44] [45] [46]

[47] [48]

[49] [50]

[51] [52]

[53] [54]

[55]

[56]

[57]

[58]

[59] [60]

Phillips KA, Castle DJ. In: Castle DJ, Phillips KA Eds, Disorders of body image. Hampshire, Wrightson Biomedical 2002; 101-20. Mayou R, Kirmayer LJ, Simon G, Kroenke K, Sharpe M. Somatoform disorders: Time for a new approach in DSM-V. Am J Psychiatry 2005; 162: 847-55. Pavan C, Simonato P, Marini M, Mazzoleni F, Pavan L, Vindigni V. Psychopathologic aspects of body dysmorphic disorder: A literature review. Aesthetic Plast Surg 2008; 32: 473-84. Brawman-Mintzer O, Lydiard B, Phillips KA, et al. Body dysmorphic disorder in patients with anxiety disorders and major depression: A comorbid study. Am J Psychiatry 1995; 152: 1665-7. Phillips KA, Nierenberg AA, Brendel G, Fava M. Prevalence and clinical features of body dysmorphic disorder in atypical major depression. J Nerv Ment Dis 1996; 184: 125-9. Phillips KA, Didie ER, Menard W. Clinical features and correlates of major depressive disorder in individuals with body dysmorphic disorder. J Affect Disord 2007; 97: 129-35. Phillips KA, Stout RL. Associations in the longitudinal course of body dysmorphic disorder with major depression, obsessivecompulsive disorder, and social phobia. J Psychiatr Res 2006; 40: 360-9. Nierenberg AA, Phillips KA, Petersen TJ, et al. Body dysmorphic disorder in outpatients with major depression. J Affect Disord 2002; 69: 141-8. Suzuki K, Takei N, Kawai M, Minabe Y, Mori N. Is taijin kyofusho a culture-bound syndrome? Am J Psychiatry 2003; 160: 1358. Wilhelm S, Otto MW, Zucker BG, Pollack MH. Prevalence of body dysmorphic disorder in patients with anxiety disorders. J Anxiety Disord 1997; 11: 499-502. Coles ME, Phillips KA, Menard W, et al. Body dysmorphic disorder and social phobia: Cross-sectional and prospective data. Depress Anxiety 2006; 23: 26-33. Rosen JC, Ramirez E. A comparison of eating disorders and body image disorder on body image and psychological adjustment. J Psychosom Res 1998; 44: 441-9. Grant JE, Phillips KA. Is anorexia nervosa a subtype of body dysmorphic disorder? Probably not, but read on. Harv Rev Psychol 2004; 12: 123-6. Grant JE, Kim SW, Eckert ED. Body dysmorphic disorder in patients with anorexia nervosa: Prevalence, clinical features, and delusionality of body image. Int J Eat Disord 2002; 32: 291-300. Kittler JE, Menard W, Phillips KA. Weight concerns in individuals with body dysmorphic disorder. Eat Behav 2007; 8: 115-20. Ruffolo J, Phillips KA, Menard W, Fay C, Weisberg RB. Comorbidity of body dysmorphic disorder and eating disorders: Severity of psychopathology and body image disturbance. Int J Eat Disord 2006; 39: 11-9. Cohen L, Kingston P, Bell A, Kwon J, Aronowitz B, Hollander E. Comorbid personality impairment in body dysmorphic disorder. Compr Psychiatry 2000; 41: 4-12. Neziroglu F, McKay D, Todaro J, Yaryura-Tobias JA. Effect of cognitive behaviour therapy on persons with body dysmorphic disorder and comorbid Axis II diagnoses. Behav Ther 1996; 27, 6777. Phillips KA, McElroy SL. Personality disorders and traits in patients with body dysmorphic disorder. Compr Psychiatry 2000; 41: 229-36. Bellino S, Zizza M, Paradiso E, Rivarossa A, Fulcheri M, Bogetto F. Dysmorphic concern symptoms and personality disorders: A clinical investigation in patients seeking cosmetic surgery. Psychiatry Res 2006; 144: 73-8. Pavan C, Vindigni V, Semenzin M, et al. Personality, temperament, and clinical scales in an Italian plastic surgery setting: What about body dysmorphic disorder? Int J Psychiatry Clin Pract 2006; 10: 91-6. Semiz U, Basoglu C, Cetin M, Ebrine S, Uzun O, Ergun B. Body dysmorphic disorder in patients with borderline personality disorder: Prevalence, clinical characteristics, and role of childhood trauma. Acta Neuropsychiatrica 2008; 20: 33-40. Grant JE, Menard W, Phillips KA. Pathological skin-picking in individuals with body dysmorphic disorder. Gen Hosp Psychiatry 2006; 28: 487-93. Didie ER, Pinto A, Mancebo M, Rasmussen SA, Phillips KA. A comparison of psychosocial functioning and quality of life in obsessive-compulsive disorder and body dysmorphic disorder. Ann Clin Psychiatry 2007; 19: 181-6.

Body Dysmorphic Disorder: A Review of Current Nosological Issues [61]

[62] [63]

[64]

[65] [66]

[67] [68]

[69] [70] [71]

[72] [73]

[74]

[75]

[76] [77]

[78] [79]

[80] [81] [82] [83]

[84] [85]

McKay D, Neziroglu F, Yaryura-Tobias JA. Comparison of clinical characteristics in obsessive-compulsive disorder and body dysmorphic disorder. J Anxiety Disord 1997; 11: 447-54. Nakata ACG, Diniz JB, Torres AR, et al. Level of insight and clinical features of obsessive-compulsive disorder with and without body dysmorphic disorder. CNS Spect 2007; 12: 295-303. Phillips KA, Pinto A, Menard W, Eisen JL, Mancebo M, Rasmussen SA. Obsessive-compulsive disorder versus body dysmorphic disorder: A comparison study of two possibly related disorders. Depress Anxiety 2007; 24: 399-409. Frare F, Perugi G, Ruffolo G, Toni C. Obsessive-compulsive disorder and body dysmorphic disorder: A comparison of clinical features. Eur Psychiatry 2004; 19: 292-8. Eisen JL, Phillips KA, Coles M, Rasmussen SA. Insight in obsessive-compulsive disorder and body dysmorphic disorder. Compr Psychiatry 2004; 45: 10-5. Marazziti D, Giannotti D, Catena M, et al. Insight in body dysmorphic disorder with and without comorbid obsessive-compulsive disorder. CNS Spect 2006; 11: 494-8. Stewart SE, Stack DE, Wilhelm S. Severe obsessive-compulsive disorder with and without body dysmorphic disorder: Clinical correlates and implications. Ann Clin Psychiatry 2008; 20: 33-8. Simeon D, Hollander E, Stein DJ, Cohen L, Aronowitz B. Body dysmorphic disorder in the DSM-IV field trial for obsessivecompulsive disorder. Am J Psychiatry 1995; 152: 1207-9. Samuels J, Nestadt G, Riddle MA, et al. A family study of obsessive-compulsive disorder. American Journal of Medical Genetics: Neuropsychiatric Genet 2001; 105: 638. Hollander E, Cohen L, Simeon D. Body dysmorphic disorder. Psychiatric Ann 1993; 23: 359-64. Canan F, Kocer E, Yildirim S, Ataogli A. Obsessive-compulsive disorder after body dysmorphic disorder: A report of 2 cases (a man and his mother). Prim Care Compan J Clin Psychiatry 2007; 9: 313-5. Hanes KR. Neuropsychological performance in body dysmorphic disorder. J Int Neuropsychol Soc 1998; 4: 167-71. Dunai J, Labuschagne I, Castle DJ, Kyrios M, Rossell SL. Executive function in body dysmorphic disorder. Paper in submission 2008. Saxena S, Winograd A, Dunkin JJ, et al. A retrospective review of clinical characteristics and treatment response in body dysmorphic disorder versus obsessive-compulsive disorder. J Clin Psychiatry 2001; 62: 67-72. Chosak A, Marques L, Greenberg JL, Jenike E, Dougherty DD, Wilhelm S. Body dysmorphic disorder and obsessive-compulsive disorder: Similarities, differences, and the classification debate. Exp Rev Neurother 2008; 8: 1209-18. Phillips KA, McElroy SL, Keck PE, Hudson JI, Pope HG. A comparison of delusional and non-delusional body dysmorphic disorder in 100 cases. Psychopharmacol Bull 1994; 30: 179-86. Phillips KA, Menard W, Pagano ME, Fay C, Stout RL. Delusional versus non-delusional body dysmorphic disorder: Clinical features and course of illness. J Psychiatr Res 2006; 40: 95-104. World Health Organisation. International classification of diseases10: Clinical descriptions and diagnostic guidelines. Geneva, World Health Organisation, 1992. Buhlmann U, Reese H, Golan E, Wilhelm S. Body dysmorphic disorder: Delusions of physical appearance. Curr Psychosis Ther Rep 2006; 4: 117-20. Fontenelle LF, Mendlowicz MV, Kalaf J, Versiani M. The problem of delusional ugliness: Is it really body dysmorphic disorder? World J Biol Psychiatry 2006; 7: 110-5. Phillips KA. Psychosis in body dysmorphic disorder. J Psychiatr Res 2004; 38: 63-72. Buhlmann U, Wilhelm S. Cognitive factors in body dysmorphic disorder. Psychiatric Ann 2004; 34: 922-6. Deckersbach T, Savage CR, Phillips KA, et al. Characteristics of memory dysfunction in body dysmorphic disorder. J Int Neuropsychol Soc 2000: 6: 673-81. Osman S, Cooper M, Hackmann A, Veale D. Spontaneously occurring images and early memories in people with body dysmorphic disorder. Memory 2004; 12: 428-36. Buhlmann U, Wilhelm S, McNally RJ, Tuschen-Caffier B, Baer L, Jenike MA. Interpretive biases for ambiguous information in body dysmorphic disorder. CNS Spect 2002; 7: 435-43.

Current Psychiatry Reviews, 2009, Vol. 5, No. 4 [86]

[87] [88]

[89] [90]

[91] [92] [93] [94] [95]

[96]

[97] [98]

[99] [100]

[101] [102] [103]

[104] [105] [106] [107]

[108] [109] [110]

[111]

269

Buhlmann U, McNally RJ, Wilhelm S, Florin I. Selective processing of emotional information in body dysmorphic disorder. Anxiety Disord 2002; 16: 289-98. Buhlmann U, McNally RJ, Etcoff NL, Tuschen-Caffier B, Wilhelm S. Emotion recognition deficits in body dysmorphic disorder. J Psychiatr Res 2004; 38: 201-6. Buhlmann U, Etcoff NL, Wilhelm S. Emotion recognition bias for contempt and anger in body dysmorphic disorder. J Psychiatr Res 2006; 40: 105-11. Stangier U, Adam-Schwebe S, Müller T, Wolter M. Discrimination of facial appearance stimuli in body dysmorphic disorder. J Abnorm Psychol 2008; 117: 435-43. Yaryura-Tobias JA, Neziroglu F, Chang R, Lee S, Pinto A, Donohue L. Computerised perceptual analysis of patients with body dysmorphic disorder: A pilot study. CNS Spect 2002; 7: 444-6. Veale D, Kinderman P, Riley S, Lambrou C. Self-discrepancy in body dysmorphic disorder. Br J Clin Psychol 2003; 42: 157-69. Cooper M, Osman S. Metacognition in body dysmorphic disorder: A preliminary exploration. J Cogn Psychother 2007; 21: 148-55. Feusner JD, Yaryura-Tobias J, Saxena S. The pathophysiology of body dysmorphic disorder. Body Image 2008; 5: 3-12. Yaryura-Tobias JA, Neziroglu F, Torres-Gallegos M. Neuroanatomical correlates and somatosensorial disturbance in body dysmorphic disorder. CNS Spect 2002; 7: 432-4. Rauch SL, Phillips KA, Segal E, et al. A preliminary morphometric magnetic resonance imaging study of regional brain volumes in body dysmorphic disorder. Psychiatry Res Neuroimaging 2003; 122: 13-9. Carey P, Seedat S, Warwick J, van Heerden B, Stein DJ. SPECT imaging of body dysmorphic disorder. J Neuropsychiatry Clin Neurosci 2004; 16: 357-9. Feusner JD, Townsend J, Bystritsky A, Bookheimer S. Visual information processing of faces in body dysmorphic disorder. Arch Gen Psychiatry 2007; 64: 1417-26. Crerand CE, Phillips KA, Menard W, Fay C. Non-medical psychiatric treatment of body dysmorphic disorder. Psychosomatics 2005; 46: 549-55. Phillips KA, Grant JE, Siniscalchi JM, Albertini RS. Surgical and non-psychiatric medical treatment of patients with body dysmorphic disorder. Psychosomatics 2001; 42: 504-10. Tignol J, Biraben-Gotzamanis L, Martin-Guehl C, Grabot D, Aouizerate B. Body dysmorphic disorder and cosmetic surgery: Evolution of 24 subjects with a minimal defect in appearance five years after their request for cosmetic surgery. Eur Psychiatry 2007; 22: 520-4. Grant JE, Phillips KA. Recognising and treating body dysmorphic disorder. Ann Clin Psychiatry 2005; 17: 205-10. Williams J, Hadjistavropoulos T, Sharpe D. A meta-analysis of psychological and pharmacological treatments for body dysmorphic disorder. Behav Res Ther 2006; 44: 99-111. Phillips KA, Hollander E. Treating body dysmorphic disorder with medication: Evidence, misconceptions and a suggested approach. Body Image 2008; 5: 13-27. Phillips KA, Najjar F. An open-label study of citalopram in body dysmorphic disorder. J Clin Psychiatry 2003; 64: 715-20. Phillips KA. An open-label study of escitalopram in body dysmorphic disorder. Int Clin Psychopharmacol 2006; 21: 177-9. Phillips KA, McElroy SL, Dwight MM, Eisen JL, Rasmussen SA. Delusionality and response to open-label fluvoxamine in body dysmorphic disorder. J Clin Psychiatry 2001; 62: 87-91. Allen A, Hadley SJ, Kaplan A, et al. An open-label trial of venlafaxine in body dysmorphic disorder. CNS Spect 2008; 13: 13844. Phillips KA, Albertini RS, Rasmussen SA. A randomised placebocontrolled trial of fluoxetine in body dysmorphic disorder. Arch Gen Psychiatry 2002; 59: 381-8. Phillips KA. Olanzapine augmentation of fluoxetine in body dysmorphic disorder. Am J Psychiatry 2005; 162: 1022-3. Phillips KA. Placebo-controlled study of pimozide augmentation of fluoxetine in body dysmorphic disorder. Am J Psychiatry 2005; 162: 377-9. Nakaaki S, Murata Y, Furukawa TA. Efficacy of olanzapine augmentation of paroxetine therapy in patients with severe body dysmorphic disorder. Psychiatry Clin Neurosci 2006; 62: 370.

270 Current Psychiatry Reviews, 2009, Vol. 5, No. 4 [112]

[113]

[114] [115]

Toh et al.

Neziroglu F, Khemlani-Patel S. A review of cognitive and behavioural treatment for body dysmorphic disorder. CNS Spect 2002; 7: 464-71. McKay D, Todaro J, Neziroglu F, Campisi T, Moritz EK, YaryuraTobias JA. Body dysmorphic disorder: A preliminary evaluation of treatment and maintenance using exposure with response prevention. Behav Res Ther 1997; 35: 67-70. Neziroglu F, Yaryura-Tobias JA. Exposure, response prevention, and cognitive therapy in the treatment of body dysmorphic disorder. Behav Ther 1993; 24: 431-8. Schmidt NB, Harrington P. Cognitive-behavioural treatment of body dysmorphic disorder: A case report. J Behav Ther Exp Psychiatry 1995; 26: 161-7.

Received: March 17, 2009

[116]

[117] [118]

[119] [120]

Revised: May 14, 2009

Veale D, Gournay K, Dryden W, et al. Body dysmorphic disorder: A cognitive-behavioural model and pilot randomised controlled trial. Behav Res Ther 1996; 34: 717-29. Wilhelm S, Otto MW, Lohr B, Deckersbach T. Cognitive behaviour group therapy for body dysmorphic disorder: A case series. Behav Res Ther 1999; 37: 71-5. Geremia GM, Neziroglu F. Cognitive therapy in the treatment of body dysmorphic disorder. Clin Psychol Psychother 2001; 8: 24351. Rabinowitz D, Neziroglu F, Roberts M. Clinical application for a behavioural model for the treatment of body dysmorphic disorder. Cogn Behav Pract 2007; 14: 231-7. Costa D, Nelson TM, Rudes J, Guterman JT. A narrative approach to body dysmorphic disorder. J Ment Health Coun 2007; 29: 67-80.

Accepted: May 15, 2009