Body Dysmorphic Disorder

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Practice Essentials

The essential feature of body dysmorphic disorder (BDD) is preoccupation with an imagined defect in appearance or disproportionate concern with a slight physical anomaly. By definition, BDD causes significant distress or impairment in important areas of functioning.

Signs and symptoms

Common areas of perceived imperfections (order of frequency) in BDD include the following:[1]

Body Part of Concern



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The clinical picture typically illustrates many of the following behaviors:

Asking the following 4 questions may be helpful:

  1. Are you worried about how you look? (Yes/No); if you are, do you think about your appearance problems a lot and wish you could think about them less? (Yes/No)
  2. How much time per day, on average, do you spend thinking about how you look? - (a) Less than 1 hour a day; (b) 1-3 hours a day; (c) more than 3 hours a day
  3. Is your main concern with how you look that you aren’t thin enough or that you might become too fat? (Yes/No)
  4. How has this problem with how you look affected your life? - (a) Has it often upset you a lot? (Yes/No); (b) has it often gotten in the way of doing things with friends, your family, or dating? (Yes/No); (c) has it caused you any problems with school or work? (Yes/No); (d) are there things you avoid because of how you look? (Yes/No)

Patients are likely to have BDD if they give the following answers:

See Presentation for more detail.

Diagnosis

No specific laboratory tests or imaging studies are indicated for suspected BDD. Screening questionnaires may be helpful. A mental status examination should be carried out and may include the following findings:

Except for the amount of time and energy spent on the preoccupation, findings from the mental status examination are usually within normal limits.

See Workup for more detail.

Management

Medications that may be employed in treating BDD include the following:

Psychotherapy (especially CBT) and behavioral modification therapy are highly recommended in addition to treatment with SSRIs. Approaches include the following:[2]

General strategies are as follows:

Surgical considerations include the following:

See Treatment and Medication for more detail.

Background

Body dysmorphic disorder (BDD)—formerly referred to as dysmorphophobia, dysmorphic syndrome, dermatologic hypochondriasis, or dermatologic nondisease in various contexts—is a relatively common and often severe psychiatric illness that is likely underrecognized and underreported.[5, 6, 7, 8, 9] It is classified in the category of obsessive-compulsive and related disorders in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5).[10] If left untreated, BDD can become a chronic condition.

The essential feature of BDD is a preoccupation with an imagined defect in appearance or disproportionate concern with a slight physical anomaly. These preoccupations most often involve the nose, the ears, the face, hair, or features related to sexuality (eg, breasts in women or muscular build or penis size in men); however, any body part may occupy the patient’s focus.

Social values and mass media greatly influence body image and, in turn, self-image. Most people have concerns related to appearance; however, this concern is considered pathologic when it interferes with social or occupational functioning. By definition, BDD causes significant distress or impairment in these areas.[11]

BDD usually appears during early adolescence. Parents of children with BDD may seek psychiatric evaluation after witnessing excessive mirror checking, time-consuming grooming, and an inability to be reassured about the perceived flaw. From a developmental perspective, some preoccupation with appearance is common during adolescence; the hallmark of BDD in adolescents is, as noted, clinically significant distress or impairment in functioning.

A key characteristic of BDD is that patients seek actions, such as cosmetic surgery, to correct their perceived malformation. Patients whose symptoms are exclusively focused on a preoccupation with body weight and shape or perceived inappropriateness of sexual characteristics are not diagnosed with BDD and frequently meet criteria for other disorders, such as anorexia nervosa or gender identity disorder.

Data suggest that quality of life and psychosocial functioning are at least as poor in patients with BDD as in those with obsessive-compulsive disorder (OCD).[12] BDD is associated with high rates of hospitalization (48%), as well as high rates of suicidal ideation and attempts.[1, 13] A history of suicidal ideation attributed primarily to BDD is reported in 45–70% of those with BDD, and past suicide attempts are reported in 22–24%.[14]

BDD affects 2.4% of the general population and reportedly affects as many as 7–15% of those undergoing cosmetic surgery.[10, 15, 16, 17] Persons with BDD who choose to undergo plastic surgery are generally unhappy with the results and often subsequently become concerned with another body part. They are often consumed by thoughts about the postoperative site. Surgeons and dermatologists have occasionally been victims of violence, even murder, by BDD patients who are in despair over their procedural outcomes.[18]

Diagnostic criteria (DSM-5)

Specific DSM-5 criteria for BDD are as follows:[10]

The diagnosis may also specify whether muscle dysmorphia is present. In such cases, individuals are preoccupied with the idea that their physical build is too small or not muscular enough. This specifier is used even if individuals are also preoccupied with other body areas.

In addition, the diagnosis may specify patients’ level of insight into their BDD beliefs as follows:

Pathophysiology

At present, the pathophysiology of body dysmorphic disorder (BDD) is understood to only a highly limited extent; however, it remains a subject of continuing research.[19] Studies have highlighted a variety of plausible mechanisms, including such hypotheses as abnormal visual processing and hypo−N-methyl-D-aspartate (NMDA) receptor (NMDAR) signal transduction.[20, 21] A more recent study published in 2018 by Greenberg et al found set-shifting deficits in visuospacial processing compared to controls even when controlling for mood disorder severity, suggesting possibility of co-occuring delusional disorders or an as-yet-unidentified endophenotype.[22] A more robust understanding of BDD’s pathophysiology will surely inform and improve available treatment options.

Patterns of heritability have been noted. Family members of patients diagnosed with BDD show a prevalence rate of BDD that is 4–8 times that found in the general population. There is also a heritable association with BDD in patients with OCD. Accordingly, genetic factors are suspected of playing a role in the pathogenesis of BDD.[23] Unfortunately, the studies that could more fully illuminate the molecular genetic basis of BDD have yet to be done.[24]

A 2000 study by Deckersbach et al found that patients with BDD had impaired verbal and nonverbal memory encoding strategies.[25] This finding suggests an involvement of executive memory deficits with a lesion of the frontostriatal connections. A similar abnormality in memory encoding also occurs in patients with OCD. Additionally, enlarged white matter volume and asymmetry of the caudate nucleus, favoring the left side, have been observed in patients with BDD.

Regarding fear recognition, an fMRI study published in 2018 showed a significant deficit in mPFC-amygdala connectivity compared to healthy controls during repeated exposures to fearful faces. These findings suggest impairment in modulation of fear, especially amygdala to mPFC signaling. However, mPFC to amygdala signaling is intact and may explain why treatment modalities such as exposure techniques may be beneficial.[26] ​ Specific abnormalities in cognitive processing have been identified involving local processing, selective attention, interpretive biases, and memory deficits that all appear to affect perception and fear about oneself and one's self-image.[27]

A 2007 study by Feusner et al found that BDD may be associated with fundamental differences in visual processing of faces.[24] The study also found that subjects with BDD had greater left hemisphere activation and might have a cognitive style that relies more on extraction and processing of details. The authors suggested that BDD patients may process faces in a piecemeal manner, whereas healthy controls’ perception of faces may be more configural and holistic.

Several studies have explored the possible role of disrupted serotonergic transmission in the development of BDD. Many of these are based on evidence that illustrates the effectiveness of selective serotonin reuptake inhibitors (SSRIs) in the treatment of BDD. Overall, the exact role for serotonergic transmission in the etiology of BDD remains the subject of continuing research.[24, 28]

In addition to the neuroanatomic, neurochemical, and genetic models for explaining BDD, several cognitive-behavioral models have been developed. It is recognized that most people are unsatisfied with at least 1 aspect of their appearance; the signal characteristic of people with BDD is that they are obsessed with any such perceived defects.

Individuals with BDD are believed to use maladaptive cognitive processes that overemphasize the importance of perceived attractiveness.[29, 30] By this logic, their disproportionate emphasis on physical attractiveness leads them to view themselves negatively, so that they experience low self-esteem, anxiety, shame, and sadness, commonly reporting to maladaptive coping methods such as mirror-gazing or avoidance.[31]

Etiology

At present, the causes of body dysmorphic disorder (BDD) have not been established, though numerous theories have been advanced.

Heredity may contribute to the development of this condition. The prevalence of BDD is 4 times higher in first-degree relatives of BDD patients than in relatives of probands without the disorder. BDD appears to be related to OCD, in that it occurs frequently in OCD patients and their relatives and responds to the same medications.[32, 33, 34, 35]

Brain anomalies may be important causes. Functional abnormalities in visual processing, frontostriatal, and limbic systems have been documented. Diffusion-weighted magnetic resonance imaging (MRI) of white matter suggested a relation between impaired insight (a clinically important phenotype) and fiber disorganization in tracts connecting visual with emotion/memory processing systems.[36]

Another study found disturbances in whole-brain structural topologic organization in subjects with BDD.[37] The authors also found evidence of abnormal connectivity between regions involved in lower-order visual processing and those involved in higher-order visual and emotional processing, as well as interhemispheric visual information transfer, which may relate to abnormalities in information processing.

A study investigating the potential role of early-life sexual, physical, or emotional abuse in the development of BDD found that subjects with BDD had more retrospective experiences of sexual and physical abuse during childhood or adolescence than healthy control subjects did.[38] Such findings suggest that abuse might be a potential risk factor in the development of BDD.

Epidemiology

United States statistics

Because of frequent comorbidity with other conditions, the diagnosis of body dysmorphic disorder (BDD) is often overlooked. BDD is estimated to affect 1–2% of the general US population.[39, 40] Given that the condition is underdiagnosed, this may be an underestimate. Patients underreport to their physicians because of intense shame. The prevalence of BDD appears to be significantly higher among people receiving dermatologic care—as high as 11.9% in one study.[41]

The prevalence of BDD in patients undergoing plastic or cosmetic surgery ranges from 7% to 15%.[17] Patients who undergo cosmetic surgery do not seem to have increased incidence of generalized body dissatisfaction; however, when surveyed about specific body parts, they have a much higher incidence of specific body part dissatisfaction.[42]

International statistics

The international incidence and prevalence of BDD have not been determined with any precision or accuracy.

BDD is a relatively common disorder among individuals seeking aesthetic surgery in Iran, being seen in about a quarter of those seeking rhinoplasty.[43] In São Paulo, Brazil, the prevalence of BDD in dermatologic patients was evaluated in a sample of 150 patients in a cosmetic group, 150 patients in a general dermatology group, and 50 control subjects; the prevalence in the cosmetic group was 14%, compared with 6.7% for the general group and 2% for the control group.[44]

Age-related demographics

The onset of BDD typically occurs in adolescence or young adulthood (average age of onset, 16–17 years[45] ). The condition may also occur in older adults who are overly concerned with their aging appearance. The course of BDD is usually continuous over time, with waxing and waning symptoms. For many patients, BDD becomes chronic. The body part that is the focus of concern may remain the same or may change over time.

Sex-related demographics

BDD affects men and women with nearly equal frequency; female-to male ratios are in the range of 1:1 to 3:2.[46] In terms of most clinical features, male and female BDD patients appear to be more similar than different,[10] though males and females tend to focus on different types of perceived defects.[47, 1]

Women more often have comorbid anxiety and panic disorder and are obsessed with legs and breasts; they are also more likely to have a comorbid eating disorder. Men, particularly those who engage in weightlifting or body building, are more likely to become preoccupied with their muscle size (so-called muscle dysmorphia).[48] Men are also more likely to have genital preoccupations, to have a diagnosis of substance abuse (50% of cases), and to be single.

Race-related demographics

No data are available on the relationship between BDD and race. However, cultural values and preferences may influence symptom content to some degree. Taijin kyofusho, a syndrome included in the traditional Japanese diagnostic system, has a subtype resembling BDD.[10]

Prognosis

Body dysmorphic disorder (BDD) results in significant suffering, occupational dysfunction, or social malaise. Many patients affected by BDD have comorbid conditions such as OCD, major depression, delusions, or social phobia.

If fully and appropriately treated with both pharmacotherapy and psychotherapy, BDD generally has a good prognosis. A small prospective study of the course of BDD found the probability of full recovery to be relatively high (0.76) and the probability of recurrence after remission to be low (0.14 over 8 years).[49] The presence of a delusional intensity of belief or comorbid conditions may necessitate more extensive and intensive therapy and follow-up.

Of those with a primary diagnosis of BDD, 30% also meet the criteria for OCD. The 2 conditions have many features in common, including repetitive thoughts concerning a perceived defect and activities centered on concealing or confirming the perceived deformity that consume most of the patient’s time. Compared with OCD, BDD has much higher rates of poor insight, ideas of reference, overvalued ideas, and delusions.

Major depression is a common comorbidity, occurring in some 60% of patients with BDD; these patients also are at increased risk for suicide.[50, 51] Suicidal ideation attributed primarily to BDD is reported in 45–70% of those with BDD, and past suicide attempts are reported in 22–24%.[14] In a self-reported German study, young adults and adolescents age 15–21 years who reported suicidal ideation were four times more likely to also report body dysmorphia (36.4% vs. 8.8%).[52] Preliminary data from a pilot study suggest that the annual rate of completed suicide in BDD may be unexpectedly high (at 0.3%).[14]

Individuals with BDD have variable degrees of awareness concerning the psychiatric nature of the illness. Many continue to agonize about an imagined defect even when they are cognizant that their concerns are excessive. Other people with BDD are regarded as delusional and have no insight into their unusual behavioral tendencies.

In many cases, individuals with BDD experience drastic social and occupational dysfunctions that may progress to the point of social isolation. Psychosocial functioning tends to remain poor over time, with few attaining functional remission.[53, 54]

In one study, BDD was evident in almost 50% of subjects with an eating disorder.[55] Accordingly, efforts should be made to recognize BDD in patients with eating disorders, especially because the presence of this disorder will affect treatment.

Patient Education

In both cognitive-behavioral psychotherapy and behavioral modification, patient education is an important component of care; education of family members is also valuable. For patient education resources, see the Depression Center, as well as Anorexia Nervosa and Depression.

A helpful online resource for patients is BDD Central. Helpful online resources for family education include the following:

History

The fundamental issue in body dysmorphic disorder (BDD) is a preoccupation with an imagined defect in appearance or disproportionate concern with a slight physical anomaly. Common areas of perceived imperfections include the following:[1]

Body Part of Concern



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BDD is a chronic disorder that can wax and wane in intensity.[56] The symptoms often start during adolescence. Over the course of a lifetime, new symptoms may be added onto the original presentation, or symptoms may shift from one body part to another. BDD may not be diagnosed for many years after its onset, often because of the patient’s reluctance to reveal the symptoms. In some cases, patients who are ashamed of their symptoms may not identify individual symptoms, referring only to a sense of general ugliness.

BDD may lead to time-consuming unproductive rumination. Patients adopt repetitive, obsessive, and ritualistic behavior and may spend a great deal of time in front of a mirror, repeatedly checking their perceived imperfections or engaging in exorbitant grooming or skin picking. Many people with BDD go to great lengths to conceal their imagined defects, using items such as wigs, hats, and makeup.

BDD is associated with significant social impairment, ranging from diminished social activities to extreme social isolation. In severe cases, individuals may leave home only at night and may avoid job interviews, dating, and peers.

Patients also have a constant need for reassurance about their perceived flaws and can often be extremely demanding of caregivers in their pursuit of perfection. Multiple visits, with resulting unsuccessful treatment, are common. Attempts to explain that the physical defect is either nonexistent or minor will be futile; individuals with BDD will continue to agonize over perceived flaws.

Because of the nature of the symptoms and the perceived solution, patients with BDD commonly present to a plastic or cosmetic surgeon. In such cases, it is critical that the surgeon elicit an appropriate history and consider referral to a psychiatrist. Most of these patients will not consider the possibility that the cause is perception-based and thus more amenable to psychiatric treatment than to surgical treatment; therefore, the referring physician must exercise sensitivity and empathy when making the referral.

Framing the psychiatric referral in the context of standard procedures, as is done with the psychological workup required as part of many elective bariatric procedures, may increase the likelihood that that patient will follow through with the referral, decrease the likelihood that the patient will be disappointed with the referring physician, and possibly decrease the likelihood that the patient will engage in surgeon-shopping.

Screening, identifying, and referring patients with BDD is particularly critical when physicians consider that patients with BDD who undergo corrective surgical procedures are typically unsatisfied with the results and often present with new complaints related to perceived defects ensuing from surgery. Some of these patients become both litigious and violent.

A thorough history focused on symptoms pertinent to BDD is the most reliable clinical tool for making an accurate diagnosis. Several surveys and scales have been developed that can be used to facilitate the process. One such scale, first published in 1997 by Phillips et al, is the Yale-Brown Obsessive Compulsive Scale Modified for Body Dysmorphic Disorder (BDD-YBOCS). This survey is a 12-item semistructured clinician-administered tool that has consistently been shown to be a reliable and valid measure of BDD severity.[57]

In the course of interviewing a patient with BDD, a clinical picture will emerge that illustrates many of the following behaviors:

Patients with BDD tend to find social situations difficult because they fear that people may point out their imagined defect or avoid them. They usually have difficulty maintaining relationships with peers, family, and spouses. Some patients skip school or work repeatedly. Many become housebound: About 30% of BDD patients have been housebound at some point for at least 1 week because of their preoccupation.[46]

Asking the following 4 questions can quickly help clinicians screen for the presence of symptoms pertinent to BDD:

As described on the Butler Hospital’s public website, patients are likely to have BDD if they give the following answers[58] :

Physical Examination

Any body part can be a source of distress in a patient with BDD; however, the body areas noted most frequently are the skin, hair, and nose. Complaints vary widely, including preoccupation with wrinkles, spots, acne, and large pores. Women may be distressed by the appearance or function of their genitalia.[59] The Cosmetic Procedures Screening questionnaire may be helpful in identifying women with BDD among those seeking labioplasty.

Vascular markings, greasiness, scars, paleness, redness, excessive hairiness, and thinning of hair are also common complaints.[60] Folliculitis and scarring may be a product of skin picking and plucking of nonexistent hairs; these often result in exacerbation of distress.[61]

With regard to physical examination, however, the signal characteristic of BDD is the paucity of physical findings in comparison with the patient’s complaint regarding the perceived physical defect. As in other psychiatric illnesses that have a substantive somatic component, the presence of occult medical conditions (eg, a brain tumor or endocrine perturbations) must be ruled out. Accordingly, a thorough physical examination is always warranted.[62]

In addition, all patients should undergo a thorough mental status examination.

Complications

Some BDD patients who are not treated may become delusional or depressed. Moreover, in the treatment of this disorder, attempts to challenge or work with the delusion can make patients even more depressed. In patients with obsessive-compulsive disorder (OCD), the presence of BDD is associated with poor insight into obsessional beliefs and higher morbidity, reflected in a generally higher prevalence of comorbid psychiatric disorders.[63]

People with BDD frequently develop major depressive episodes and are at risk for suicide.[64] They also may exhibit violent behavior toward treatment providers. In a placebo-controlled study evaluating suicidality in BDD patients treated with fluoxetine, there was no significant difference between fluoxetine and placebo with regard to the emergence of suicidality; moreover, fluoxetine appeared to protect against worsening of suicidality.[65]

In many cases, individuals with BDD experience drastic social and occupational dysfunctions that may progress to the point of social isolation. Embarrassment and fear of being scrutinized or mocked cause these individuals to avoid social situations and intimate relationships. Often victims of poor self-image, people with BDD tend to lack sufficient social skills and frequently are single or divorced.

Approach Considerations

No specific laboratory tests are used to diagnose body dysmorphic disorder (BDD). No specific imaging studies are indicated.

Patients undergoing cosmetic surgery should undergo a screening questionnaire to determine whether may have BDD. The Body Dysmorphic Disorder Questionnaire-Dermatology Version (BDDQ-DV) and the Dysmorphic Concern Questionnaire (DCQ) have been validated for the dermatologic surgery setting.[66, 67]

The Multidimensional Body-Self Relations Questionnaire is a self-reported measure of body image that assesses satisfaction with appearance and preoccupation with perceived defects. It is used in clinical trials and may not be practical in routine office settings. A study of 92 patients with BDD who took the questionnaire revealed that patients with this condition differ from population norms with respect to numerous aspects of body image, including perception of illness.[29]

The Body Dysmorphic Disorder Examination Self-Report measures the patient’s level of dissatisfaction with respect to the perceived defect. It is another tool that is used in clinical trials and may not be practical in routine office settings.

The Body Dysmorphic Disorder Symptom Scale (BDD-SS) is another self-report measure  designed to differentiate, for each group of symptoms, the number of symptoms endorsed and their severity. A study of 99 adults with BDD who completed the measure found it showed good reliability and convergent validity.[68]

Mental Status Examination

Key findings from the mental status examination that may be associated with the experience of symptoms consistent with a diagnosis of body dysmorphic disorder (BDD) include the following:

Typical nondelusional patients with BDD display little or no insight. For a brief time, they may admit that they might be wrong about their preoccupation. Often, they have only come to see the psychiatrist because they were coerced by a family member or because they were told to do so by the plastic surgeon.

Delusional BDD patients are firmly attached to false beliefs that they cannot be talked out of, even with given adequate proof that these beliefs are mistaken. Such patients may believe that what they consider their abnormal body part is slowly worsening or that other people are always staring or know about it.

These considerations aside, findings from the mental status examination are usually within normal limits except for the amount of time and energy spent on the preoccupation. Auditory hallucinations or wide mood swings might point to additional diagnoses, such as schizophrenia or bipolar disorder.

Approach Considerations

Treatment of body dysmorphic disorder (BDD) may include cognitive-behavioral therapy (CBT), pharmacologic interventions, and other psychosocial interventions that promote social functioning. The basic goals of treatment are as follows:

The primary treatment modalities for BDD are selective serotonin reuptake inhibitor (SSRI) therapy and CBT.[69] Both modalities are supported by level-2 evidence. One study includes a double-blinded randomized controlled trial with placebo or an active comparison condition.[70]

There are several other published studies that strongly demonstrate efficacy for CBT, two of which are double-blinded randomized controlled trials.[71, 72, 73, 74]  A head-to-head comparison study of CBT and supportive psychotherapy (SPT), the most common psychosocial treatment for BDD, showed that CBT leads to more consistent improvement in symptom severity and quality of life.[75]

Pharmacologic agents are employed on an off-label basis; at present, no medications have been specifically approved by the US Food and Drug Administration (FDA) for the treatment of BDD. Drugs with potential for abuse or addiction must be avoided.

The United Kingdom’s National Collaborating Centre for Mental Health published guidelines on core interventions in the treatment of BDD and obsessive-compulsive disorder (OCD), which may be of interest.[76]

Pharmacologic Therapy

Evidence supports the use of SSRIs such as fluoxetine, fluvoxamine, escitalopram, and citalopram in the treatment of body dysmorphjic disorder (BDD), though caution should be used with citalopram given the FDA dose guidelines regarding QT prolongation, as high dose is frequently needed.[70] The tricyclic antidepressant (TCA) clomipramine has been widely used as well.[77, 78] Other pharmacologic agents, such as neuroleptics, trazodone, lithium, benzodiazepines, TCAs other than clomipramine, and anticonvulsants have been much less beneficial or ineffective.

Clomipramine has adverse effects similar to those of other TCAs (eg, sedation, anticholinergic effects, orthostatic hypotension, sexual dysfunction, weight gain, cardiac conduction slowing, and a potential for fatal overdose). In a study comparing clomipramine with the selective norepinephrine reuptake inhibitor desipramine in patients with BDD, superior results were noted with clomipramine, including improvements in obsessive characteristics, depression, insight, social performance, and disorder severity.[79]

The SSRIs fluoxetine and fluvoxamine usually have milder adverse effect profiles than clomipramine does; however, they may be associated with adverse effects such as initial anxiety or agitation, nausea or other gastrointestinal (GI) disturbance, headache, sexual dysfunction (eg, delayed orgasm or loss of libido), and occasional apathy. In addition, they may be associated with various cutaneous reactions, such as the following:[80]

Cutaneous Reactions Associated with SSRIs



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Because cross-reactions may occur between SSRIs, even those with different chemical structures, switching to another family of antidepressants may be advisable if an SSRI is linked to a serious skin eruption.

Clomipramine and SSRIs often must be given at high dosages and for lengthy treatment periods (eg, 6–16 weeks for SSRIs[81] ) before symptoms improve; drug trials should continue for several months after the target dose is reached. Average time to response for fluoxetine and fluvoxamine is generally 6-9 weeks, while the effect from citalopram and escitalopram was slightly faster at 4–5 weeks.[77] Dosages should be increased gradually to prevent possible adverse effects. Almost 58% of patients with BDD achieve either partial improvement or complete resolution of symptoms with an SRI regimen.

In some situations, patients who show resistance to normal treatment may have positive results when treated with SSRIs in combination with clomipramine. In this case, clomipramine levels should be monitored because SSRIs increase clomipramine concentrations in the blood.

Typical Mean and Maximum Dosing of SSRIs[82]



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*Reflects FDA dosing limit reduction

Even when the patient’s perceptions are distorted to the point where they are felt to be psychotic, the use of neuroleptics may not ameliorate the delusions. Some patients may still benefit from adjunctive antipsychotics. However, when used at higher dosages similar to those used in the treatment of OCD, SSRIs are frequently effective at ameliorating symptoms.[62, 82] The response to SSRIs is often partial rather than complete, and 40-50% of patients may not respond adequately to medication alone.[70]

BDD patients with delusional symptoms may benefit from a therapeutic regimen that includes the antipsychotic agent pimozide in addition to an SSRI. Patient insight may improve with the use of pimozide alone. A pimozide-clomipramine combination may lengthen the QT interval on the electrocardiogram (ECG); therefore, close monitoring of the ECG is required.

Pimozide has the adverse effects common to other typical high-potency antipsychotic medications (ie, extrapyramidal symptoms such as dystonia, parkinsonism, akathisia, neuroleptic malignant syndrome, and tardive dyskinesia). It also can slow cardiac conduction and cause hyperprolactinemia.

For the one third of patients who do not respond to treatment with SSRIs or clomipramine alone, the addition of buspirone may prove helpful.

If all other treatment modalities fail, monoamine oxidase inhibitors (MAOIs) may be given, though their use necessitates the imposition of dietary and other restrictions (eg, avoidance of tyramine-containing foods and certain medications). These drugs probably should be prescribed only by experienced specialists.

An open-label trial of the serotonin-norepinephrine reuptake inhibitor venlafaxine suggested that it may be an effective treatment for BDD.[83]

There is one double-blind, placebo-controlled trial that supports the effectiveness of escitalopram vs placebo with regards to relapse prevention. Escitalopram delayed time to relapse and fewer escitalopram-treated subjects relapsed than did placebo-treated subjects. In addition, body dysmorphic disorder severity significantly improved during the additional six months of escitalopram treatment following acute response, and more than one-third of escitalopram-treated subjects experienced further improvement.[84]  

Use of SSRIs in pediatric patients

Physicians are advised to be aware of the following information and use appropriate caution when considering treatment with SSRIs in the pediatric population.

In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory stating that most SSRIs are not suitable for use by persons younger than 18 years for treatment of “depressive illness.” After review, this agency decided that the risks SSRI treatment poses to pediatric patients outweigh the benefits, except in the case of fluoxetine, which appears to have a positive risk-benefit ratio for the treatment of depressive illness in patients younger than 18 years.

In October 2003, the FDA issued a public health advisory regarding reports of suicidality in pediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. Accordingly, the FDA asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and thus could not be definitively linked to drug treatment.

However, a study of more than 65,000 children and adults treated for depression between 1992 and 2002 by the Group Health Cooperative in Seattle found that suicide risk declines, rather than rises, with the use of antidepressants. To date, this is the largest study to date to address this issue.

Currently, no evidence associates OCD and other anxiety disorders treated with SSRIs with an increased risk of suicide.

Psychiatric and Behavioral Interventions

Psychotherapy (especially CBT) and behavioral modification therapy are highly recommended in addition to treatment with SSRIs.[85, 71, 72, 73, 74] Approaches include systematic desensitization, exposure techniques, self-confrontational techniques, and cognitive imagery.

General strategies include the following:

Predictors of response to CBT for BDD include the following:[86]

Components of CBT for BDD include the following:[3, 4, 2]

Additional approaches include the following:

CBT may be beneficial in situations where patients develop a structured and predictable strategy for identifying cognitive errors and maladaptive thinking. When CBT is efficacious, patients learn to alter cognitive distortions and are able to maintain and generalize more adaptive thought patterns in daily life. Therapy within a group setting and supportive psychotherapy may be adequate for people who are not truly delusional. A few studies have claimed successful results with behavior modification alone.

A small study of CBT in 13 adolescents with BDD found symptoms were improved at 3- and 6-month followup. Treatment was delivered in 12–22 weekly individual sessions.[87]

Two randomized control trials support the efficacy of CBT for BDD. The first included a broad range of patients, including those with delusional BDD beliefs and those with suicidal ideation. Over 24 weeks, they were randomized to either 24 weeks of manualized CBT or  a12-week wait-list, then 24 weeks of CBT. By week 12, 50% of the CBT group were responders compared to 12% of the wait-list group. Post-treatment analysis demonstrated 81% of the intention-to-treat group and 83% of the immediate CBT group were deemed responders.[73] The second randomized control trial did not use a wait-list control group (to control for nonspecific treatment factors such as therapist time and attention) where CBT for BDD was compared to behavioral therapy for anxiety management after 12 weeks of treatment. The CBT group was found to have a better treatment response.[74] ​ A systematic review identified six RCTs from 1996 to 2014, including these two studies, and concluded that CBT continues to show promise in reduction in BDD symptom severity; however, it notes that larger and higher quality RCTs are still needed.[88]

A head-to-head comparison study of CBT and supportive psychotherapy (SPT), the most common psychosocial treatment for BDD, showed that CBT leads to more consistent improvement in symptom severity and quality of life.[75]

Although nonpharmacologic psychiatric treatment is often effective in the treatment of BDD, patients with this condition are likely to try to avoid psychiatric therapy. An on-site psychiatric liaison may be helpful in bridging the gap between dermatologic and psychological treatments.

Therapy with family members, spouses, or significant others should be strongly considered as a means of helping to improve the patient’s outcome. On one hand, people who have a close relationship with the patient may agree with the patient’s perception of the defect and may reinforce his or her maladaptive beliefs and behaviors. On the other, people with a close relationship to the patient may disagree with what the patient thinks is necessary for treatment and may be able to urge a more effective approach. ​

Novel treatment consideration​

An RTC specifically focused on efficacy measures of internet-based CBT for BDD (BDD-NET) has shown evidence for short-term reduction in BDD symptoms using BDD-YBOCS primary outcomes measures. A 2-year follow-up study showed sustained long-term reduction in BDD symptoms. Of the patients in this study, 69% were classified as responders, and of those 56% were classified as in remission (no longer meeting criteria for BDD according to DSM).[89]  

A preliminary randomized double-blind trial in 2019 showed some improved response to CBT when adjunctive treatment with a cognitive enhancer D-cycloserine (DSC) was provided over a 10-week period. Novel treatment modalities continue to be explored for BDD.[90]

A pilot study of 21 patients offering acceptance-based therapy (ACT) has shown a significant (68%) reduction in BDD symptom severity using the BDD-YBOCS scale at the end of a 12-week treatment course.[91]

Surgical Interventions

Patients with body dysmorphic disorder (BDD) frequently consult cosmetic specialists (eg, dermatologists or plastic surgeons) for treatment of their imagined defect. However, cosmetic surgery frequently fails to improve BDD symptoms. Most people with BDD will be displeased with the results, commonly either becoming increasingly preoccupied with the original perceived defect or finding a new one with which to be concerned (such as a surgical blemish or scar from the cosmetic surgery itself).

Given that more than 90% of BDD patients report symptoms that are unchanged and often exacerbated after surgical procedures, plastic or cosmetic surgery intended to correct the perceived defect in BDD is contraindicated. These patients constitute a disproportionate litigious risk for surgeons. Of even greater concern for surgeons considering providing surgical treatment to BDD patients are reports of individuals who become violent after the operation and cause physical harm to their healthcare providers.[92]

In all suspected cases of BDD, any proposed surgical treatment must be thoroughly documented and discussed with patients. Preoperatively, if a surgeon suspects that a patient may meet diagnostic criteria for BDD, referral to a psychiatrist for further evaluation is indicated. A commonly used screening measure for BDD is the Body Dysmorphic Disorder Questionnaire (BDDQ), which has a reported sensitivity of 100% and specificity of 90.3%.[67] Surgeons are advised not to perform surgery on patients who have been definitively diagnosed with BDD.

Consultations

Physicians should refer patients to a psychiatrist for a thorough psychiatric evaluation to confirm a suspected diagnosis of BDD, as well as to assess the patient for possible comorbid psychiatric diagnoses and provide appropriate treatment recommendations.[93, 43] Because many of these patients present to surgeons seeking surgical correction of what they consider a clear physical defect, with little or no awareness of their underlying psychiatric disorder, they may react negatively and angrily to such a referral.[92, 94]

The referring surgeon or other physician is advised to treat the referral to a psychiatrist as they would a referral to any other health professional. Treating the referral as a standard aspect of preoperative care increases the likelihood that the patient follows up with the referral and should mitigate the possibility of patient dissatisfaction with the referring surgeon or physician.[43]

Long-Term Monitoring

Over the long term, patients achieve the best results when treated by a consistent medical and mental health team. They may derive the greatest benefit from a combination of SSRIs and therapy sessions.

As a chronic condition, BDD requires maintenance therapy and monitoring of SSRI tolerance. According to the American Psychiatric Association, patients who are taking maintenance medications should be seen at least 3-4 times per year. Approximately 53% of those with BDD experience relapse within 6 months of discontinuance of treatment.

For long-term management of a chronic disorder such as BDD, it is usually considered prudent to prescribe the same dosages of medications for initial treatment and ongoing maintenance. The concept of lower maintenance dosages is not well supported; the majority of studies have reported higher relapse rates at lower maintenance dosages.

Medication Summary

The goals of pharmacotherapy in patients with body dysmorphic disorder (BDD) are to reduce symptoms and morbidity and prevent complications. Selective serotonin reuptake inhibitors (SSRIs) appear to be useful in the treatment of this condition. For the most part, other classes of drugs, including benzodiazepines, neuroleptics, and anticonvulsants, yield minimal or no improvement, though may be helpful in augmentation. In general, medication use is recommended in conjunction with psychosocial interventions.

Escitalopram (Lexapro)

Clinical Context:  Escitalopram is the S-enantiomer of citalopram. It is used for the treatment of depression. The mechanism of action is thought to be potentiation of serotonergic activity in the CNS resulting from inhibition of CNS neuronal reuptake of serotonin. The onset of depression relief is typically after 1-2 weeks, which is sooner than that noted with other antidepressants.

Citalopram (Celexa)

Clinical Context:  Citalopram enhances serotonin activity through selective reuptake inhibition at the neuronal membrane. Although no head-to-head comparisons of SSRIs exist, citalopram is considered the SSRI of choice for patients with head injury.  Caution is advised with using high doses (which may be needed for BDD) due to the QT prolonging effects.

Fluoxetine (Prozac)

Clinical Context:  Fluoxetine selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine. It is approved by the US Food and Drug Administration (FDA) for OCD and major depressive disorder in children aged 8 years or older. Dosages used to treat OCD are also effective for BDD. A low starting dose and a more gradual increase are advisable in patients sensitive to medications (ie, slow metabolizers).

Fluoxetine is available in 10- and 20-mg capsules and in a 20 mg/5 mL liquid form. Because of its stimulating properties, dosing should be initiated in the morning. If nausea is a problem, it may be helpful to take the medication with food.

Fluvoxamine (Luvox)

Clinical Context:  Fluvoxamine is a potent selective inhibitor of neuronal serotonin reuptake. It does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and thus has fewer adverse effects than TCAs do. In the treatment of BDD, higher doses than those used for depression generally are needed. Fluvoxamine is FDA-approved for children with OCD.

Sertraline (Zoloft)

Clinical Context:  Sertraline selectively inhibits presynaptic serotonin reuptake. It is approved for obsessive-compulsive disorder in children aged 6 years or older.

Paroxetine (Paxil, Pexeva)

Clinical Context:  Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake. It is approved for obsessive-compulsive disorder.

For maintenance dosing, make dosage adjustments to maintain patient on lowest effective dosage, and reassess patient periodically to determine need for continued treatment.

Class Summary

SSRIs are antidepressant agents that are chemically unrelated to TCAs, tetracyclic antidepressants (TeCAs), or other available antidepressants. They inhibit central nervous system (CNS) neuronal uptake of serotonin and may have a weak effect on neuronal reuptake of norepinephrine and dopamine. They have been used to treat patients with BDD, as well as those with anxiety, phobias, or obsessive-compulsive disorder (OCD).

SSRIs are strongly preferred to the other types of antidepressants. Because their adverse effect profile is less prominent, compliance is improved. SSRIs do not have the cardiac arrhythmia risk associated with TCAs. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered in the treatment of a child or adolescent with a mood disorder. All SSRIs are equally efficacious; the choice depends on adverse effects and drug interactions.

Clomipramine (Anafranil)

Clinical Context:  Clomipramine affects serotonin uptake and affects norepinephrine uptake when converted into the metabolite desmethylclomipramine. Because of its sedative properties, nighttime dosing is recommended. Therapy should be initiated at a low dosage to minimize adverse effects. Clomipramine is available in 25-, 50-, and 75-mg capsules.

Imipramine (Tofranil, Tofranil PM)

Clinical Context:  Imipramine inhibits the reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at the presynaptic neuron.

Amitriptyline

Clinical Context:  Amitriptyline increases the synaptic concentration of serotonin or norepinephrine in the central nervous system (CNS) by inhibiting their reuptake by the presynaptic neuronal membrane.

Class Summary

TCAs are used when SSRIs are ineffective. They are structurally related to the phenothiazine antipsychotic agents and exhibit 3 major pharmacologic actions in varying degrees: amine pump inhibition, sedation, and anticholinergic action (peripheral and central). They inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron.

Physicians should be cautious when using TCAs because overdose has the potential to be deadly. Patients with BDD may have a higher risk of suicidal behavior; accordingly, the potential harm to the patient in an overdose situation must be taken into account in choosing the type of antidepressant.

Pimozide (Orap)

Clinical Context:  Pimozide is a centrally acting dopamine-receptor antagonist. In the United States, it is available in 2-mg scored tablets; in Canada, it is available in 2-, 4-, and 10-mg tablets.

Class Summary

Neuroleptic medications reduce psychotic symptoms (eg, hallucinations and delusions).

Author

Iqbal Ahmed, MBBS, FRCPsych(UK), Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of the Health Sciences; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Anton Power, DO, Resident Physician, Department of Pyschiatry, Tripler Army Medical Center; Teaching Fellow, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

David R Bowman, MD, Psychiatrist, Deputy Chief, Joint Behavioral Health Clinic, Multi-Disciplinary Outpatient Clinic, Medical Review Officer, Clinical Practice Guidelines Champion, External Behavioral Health Consultant, Department of Behavioral Health, Moncrief Army Health Clinic

Disclosure: Nothing to disclose.

Chief Editor

David Bienenfeld, MD, Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Lawrence Genen, MD, MBA, Board Certified Psychiatrist; Diplomate, American Board of Psychiatry and Neurology; Founder, The Genen Group - A Multi-Specialty Psychiatry and Psychotherapy Practice

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School

Disclosure: Nothing to disclose.

Thomas Cook, MD, Resident Physician, Department of Psychiatry, University of Hawaii, John A Burns School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Carol Diane Berkowitz, MD Executive Vice Chair, Department of Pediatrics, Professor, Harbor-University of California at Los Angeles Medical Center

Carol Diane Berkowitz, MD is a member of the following medical societies: Alpha Omega Alpha, Ambulatory Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, American Medical Association, American Pediatric Society, and North American Society for Pediatric and Adolescent Gynecology

Disclosure: Nothing to disclose.

O Joseph Bienvenu III, MD, PhD Assistant Professor, Department of Psychiatry, Johns Hopkins University School of Medicine

O Joseph Bienvenu III, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

M Peter Chodynicki, MD Staff Physician, Department of Psychiatry, Johns Hopkins University School of Medicine

M Peter Chodynicki, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Sing-Yi Feng, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, Section of Medical Toxicology, Univerity of Texas Southwestern Medical Center; Staff Toxicologist, North Texas Poison Center, Parkland Memorial Hospital

Sing-Yi Feng, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Caroly Pataki, MD Professor of Clinical Psychiatry and Behavioral Sciences, Department of Psychiatry, Division Chair, Child and Adolescent Psychiatry, Keck School of Medicine of the University of Southern California

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Wanda M Patterson, MD Department of Dermatology, UMDNJ-New Jersey Medical School

Wanda M Patterson, MD is a member of the following medical societies: Sigma Xi

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, New York Academy of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Jagvir Singh, MD Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge

Jagvir Singh, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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WomenMen
SkinSkin
HairHair
NoseNose
LegsBody build
EyesEyes
WeightGenitals
BreastsLegs
StomachPectoral muscles
TeethStomach
HipsLips
Face size/shapeEars
LipsWeight
ChinFace size/shape
CheeksTeeth
HeightChin
JawHead size/shape
Head size/shapeArm/wrist
FeetCheeks
ButtocksHeight
Ugly faceUgly face
ForeheadJaw
EarsForehead
FingersFingers
HandsHands
NeckFeet
ShouldersButtocks
Body buildNeck
Arm/wristFace muscles
EyebrowsEyebrows
WomenMen
SkinSkin
HairHair
NoseNose
LegsBody build
EyesEyes
WeightGenitals
BreastsLegs
StomachPectoral muscles
TeethStomach
HipsLips
Face size/shapeEars
LipsWeight
ChinFace size/shape
CheeksTeeth
HeightChin
JawHead size/shape
Head size/shapeArm/wrist
FeetCheeks
ButtocksHeight
Ugly faceUgly face
ForeheadJaw
EarsForehead
FingersFingers
HandsHands
NeckFeet
ShouldersButtocks
Body buildNeck
Arm/wristFace muscles
EyebrowsEyebrows
Cutaneous Reaction
Spontaneous bruising
Pruritus
Urticaria
Angioedema
Erythema multiforme
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Erythema nodosum
Alopecia
Hypertrichosis
Leukocytoclastic vasculitis
Acneiform eruption
MedicationMean DoseMax Dose
Fluoxetine       67 ± 24 mg     120 mg          
Fluvoxamine308 ± 49 mg450 mg
Sertraline202 ± 46 mg400 mg
Paroxetine55 ± 13 mg90 mg
Citalopram66 ± 36 mg40 mg*
Escitalopram29 ± 12 mg60 mg
Clomipramine203 ± 53 mg250 mg