Case Report

An otherwise healthy 9-year-old Filipino girl presented with a complaint of urticaria precipitated by cold exposure over the preceding 5 weeks. She had no recent illnesses and normal results of a school physical examination performed 2 weeks prior to symptom onset. The patient's medical history was significant only for cat allergy; however, she noted that on multiple occasions, erythema and pruritus appeared on her arms and face after walking through the freezer aisle of a grocery store. Urticaria subsequently developed on regions where she scratched and spontaneously resolved 2 to 3 hours later. On one occasion, urticaria appeared diffusely on the patient while she showered after swimming; it resolved within a few hours after she was given diphenhydramine by her mother. Three days prior to presentation, the patient experienced upper lip angioedema with erythema, globus sensation, and difficulty swallowing after drinking a strawberry slushy. She denied having respiratory complaints at that time, and her symptoms again resolved spontaneously. A day later, the patient tolerated ice cream with no complaints. Her family history was significant for a maternal history of seasonal allergies.

On physical examination, the patient appeared to be well. She had 2 to 3 discrete urticarial lesions on the distal posterior aspect of each calf that, according to her mother, recently began appearing on "cold and rainy" days. The mother attributed them to her daughter's lower legs being exposed because of the length of her pants. Results of the remainder of the examination were unremarkable, and dermatographism was absent.

Laboratory evaluation consisted of a strawberry radioallergosorbent test and cryoglobulins test, both of which had negative results. An ice cube wrapped in plastic was applied to the volar surface of the patient's right forearm for 5 minutes. A 9X6-cm wheal was noted 3 minutes after ice removal (Figure).

PLEASE REFER TO THE PDF TO VIEW THE FIGURE

A diagnosis of cold urticaria with associated angioedema was made. The patient's mother opted for her daughter to use only diphenhydramine as needed; additionally, an epinephrine autoinjector was dispensed. By 3 months after symptom onset, the patient's only complaint was pruritus of her hands if they became too cold. No urticaria was noted. At 6-month follow-up, the patient denied having had symptoms for the preceding 2 months, and the results of an ice cube test were negative. 

Comment

Cold urticaria is a form of physical urticaria that is notable for the development of urticaria and/or angioedema after cold exposure.¹ Cold urticaria syndromes were first described in the 19th century² and are uncommon. However, it has been observed that approximately one third of adult³ and pediatric⁴ patients with cold urticaria have systemic reactions that are mostly hypotensive episodes associated with aquatic activities. Thus, identification of these patients should be a priority.

The prevalence of cold urticaria is not well defined. Cold urticaria is most commonly noted in young adults, with only 11% of cases noted in children under 10 years of age.³ Most forms of cold urticaria are idiopathic (Table); however, some forms can be secondary to underlying conditions such as malignancies, vasculitides, and infectious diseases.⁸ Cryoglobulinemia (primary and secondary to malignancy) often is cited as a cause of secondary cold urticaria.^3,8-11 Mounting evidence indicates that a possible autoimmune mechanism underlies the idiopathic form of this disorder in many patients.¹²

PLEASE REFER TO THE PDF TO VIEW THE TABLE

Although most forms of cold urticaria are considered to be acquired, familial forms have been described,^7,13 some of which have been classified within the hereditary periodic fever syndromes.¹² Diagnosis of cold urticaria primarily is made by evaluating the patient's clinical history; the diagnosis may be confirmed by applying a cold stimulus, most commonly an ice cube wrapped in plastic and applied to the volar aspect of the patient's forearm. A positive reaction is noted by the formation of a wheal during rewarming of the skin. The length of time that a cold stimulus is applied is not standardized; commonly, 3-, 5-, and 10-minute applications are used. Visitsuntorn et al¹⁴ observed the effectiveness of 3- or 5-minute applications in children who had not taken antihistamines for at least 5 days prior. The authors also noted that false-positive results (defined as reddening of the skin and minimal edema) were possible with 10- and 20-minute applications in patients with chronic urticaria not induced by cold. Other studies have observed that the length of time necessary for a cold stimulus to induce wheal formation inversely may be related to the patient's risk of having a systemic reaction.^1,8,12 Specifically, patients who demonstrated wheal formation after the application of a cold stimulus for 3 minutes or less were noted to experience cold-induced hypotension more frequently. Regardless, it should be recognized that all patients with cold urticaria are at risk for hypotensive reactions.

Approximately 20% of patients with cold urticaria lack an immediate response to cold stimulus with an ice cube; these patients have so-called atypical acquired cold urticaria syndromes^1,12 (eg, cold-dependant dermatographism, delayed cold urticaria, systemic cold urticaria). Other forms of cold stimulus testing that can be considered include partially immersing a limb of the patient's in cold water³ or placing the patient in a cold room¹⁵; however, these forms of cold stimulus may put the patient at increased risk for a systemic reaction. Finally, scratching the skin prior to cooling or during cooling also may be of diagnostic value in cases of cold-dependant dermatographism.^9,15

Additional testing should be guided by a patient's history. To determine if a secondary cause is responsible for the clinical presentation of cold urticaria, laboratory studies could include complete blood count, erythrocyte sedimentation rate, antinuclear antibodies titer, infectious mononucleosis serology, syphilis serology, rheumatoid factor, total complement, cold agglutinins, cold hemolysin, cryofibrinogen, and cryoglobulin.¹² Of note, approximately 4% of patients with cold urticaria have been observed to have cryoglobulinemia. Thus, testing for cryoglobulinemia is the most likely laboratory study to yield positive results.^1,16 Beyond evaluation for cryoprecipitates, however, an extensive search for etiology is not indicated unless additional clinical findings warrant investigation.¹⁶

Treatment of patients with cold urticaria can be difficult. Patients and their families should be counseled on the risks of aquatic activities and should be instructed on the proper use of an epinephrine autoinjector. In severe cases, patients may elect to move to warmer climates. Antihistamines sometimes provide benefit, especially at high doses and/or with the more potent formulations, such as doxepin. Cyproheptadine has been shown to be more effective than chlorpheniramine.¹⁷ Second-generation antihistamines also may be considered to minimize sedation. Cetirizine, loratadine, and desloratadine have been shown to be effective and well-tolerated options for treatment.^18,19 Additionally, leukotriene receptor antagonists may have a role in treatment.⁵ Bonadonna et al⁶ demonstrated that cetirizine and zafirlukast in combination are more effective than either drug alone. Adjusting the level of medication so that the patient requires more than 3 minutes of cold stimulus testing before having a wheal response is a recommended goal of therapy that is aimed at minimizing the patient's risk of having a hypotensive reaction.¹²

Cold urticaria is an uncommon disorder that can put patients at significant risk. Taking a thorough history and confirming the condition through the use of cold stimulation tests can lead to a diagnosis in most cases. Although most forms of cold urticaria are idiopathic and acquired, familial and secondary forms also must be kept in mind when considering this diagnosis. In addition to antihistamine therapy, an epinephrine autoinjector and preventive measures play an important role in treating patients with cold urticaria. 

Case Report

An otherwise healthy 9-year-old Filipino girl presented with a complaint of urticaria precipitated by cold exposure over the preceding 5 weeks. She had no recent illnesses and normal results of a school physical examination performed 2 weeks prior to symptom onset. The patient's medical history was significant only for cat allergy; however, she noted that on multiple occasions, erythema and pruritus appeared on her arms and face after walking through the freezer aisle of a grocery store. Urticaria subsequently developed on regions where she scratched and spontaneously resolved 2 to 3 hours later. On one occasion, urticaria appeared diffusely on the patient while she showered after swimming; it resolved within a few hours after she was given diphenhydramine by her mother. Three days prior to presentation, the patient experienced upper lip angioedema with erythema, globus sensation, and difficulty swallowing after drinking a strawberry slushy. She denied having respiratory complaints at that time, and her symptoms again resolved spontaneously. A day later, the patient tolerated ice cream with no complaints. Her family history was significant for a maternal history of seasonal allergies.

On physical examination, the patient appeared to be well. She had 2 to 3 discrete urticarial lesions on the distal posterior aspect of each calf that, according to her mother, recently began appearing on "cold and rainy" days. The mother attributed them to her daughter's lower legs being exposed because of the length of her pants. Results of the remainder of the examination were unremarkable, and dermatographism was absent.

Laboratory evaluation consisted of a strawberry radioallergosorbent test and cryoglobulins test, both of which had negative results. An ice cube wrapped in plastic was applied to the volar surface of the patient's right forearm for 5 minutes. A 9X6-cm wheal was noted 3 minutes after ice removal (Figure).

PLEASE REFER TO THE PDF TO VIEW THE FIGURE

A diagnosis of cold urticaria with associated angioedema was made. The patient's mother opted for her daughter to use only diphenhydramine as needed; additionally, an epinephrine autoinjector was dispensed. By 3 months after symptom onset, the patient's only complaint was pruritus of her hands if they became too cold. No urticaria was noted. At 6-month follow-up, the patient denied having had symptoms for the preceding 2 months, and the results of an ice cube test were negative. 

Comment

Cold urticaria is a form of physical urticaria that is notable for the development of urticaria and/or angioedema after cold exposure.¹ Cold urticaria syndromes were first described in the 19th century² and are uncommon. However, it has been observed that approximately one third of adult³ and pediatric⁴ patients with cold urticaria have systemic reactions that are mostly hypotensive episodes associated with aquatic activities. Thus, identification of these patients should be a priority.

The prevalence of cold urticaria is not well defined. Cold urticaria is most commonly noted in young adults, with only 11% of cases noted in children under 10 years of age.³ Most forms of cold urticaria are idiopathic (Table); however, some forms can be secondary to underlying conditions such as malignancies, vasculitides, and infectious diseases.⁸ Cryoglobulinemia (primary and secondary to malignancy) often is cited as a cause of secondary cold urticaria.^3,8-11 Mounting evidence indicates that a possible autoimmune mechanism underlies the idiopathic form of this disorder in many patients.¹²

PLEASE REFER TO THE PDF TO VIEW THE TABLE

Although most forms of cold urticaria are considered to be acquired, familial forms have been described,^7,13 some of which have been classified within the hereditary periodic fever syndromes.¹² Diagnosis of cold urticaria primarily is made by evaluating the patient's clinical history; the diagnosis may be confirmed by applying a cold stimulus, most commonly an ice cube wrapped in plastic and applied to the volar aspect of the patient's forearm. A positive reaction is noted by the formation of a wheal during rewarming of the skin. The length of time that a cold stimulus is applied is not standardized; commonly, 3-, 5-, and 10-minute applications are used. Visitsuntorn et al¹⁴ observed the effectiveness of 3- or 5-minute applications in children who had not taken antihistamines for at least 5 days prior. The authors also noted that false-positive results (defined as reddening of the skin and minimal edema) were possible with 10- and 20-minute applications in patients with chronic urticaria not induced by cold. Other studies have observed that the length of time necessary for a cold stimulus to induce wheal formation inversely may be related to the patient's risk of having a systemic reaction.^1,8,12 Specifically, patients who demonstrated wheal formation after the application of a cold stimulus for 3 minutes or less were noted to experience cold-induced hypotension more frequently. Regardless, it should be recognized that all patients with cold urticaria are at risk for hypotensive reactions.

Approximately 20% of patients with cold urticaria lack an immediate response to cold stimulus with an ice cube; these patients have so-called atypical acquired cold urticaria syndromes^1,12 (eg, cold-dependant dermatographism, delayed cold urticaria, systemic cold urticaria). Other forms of cold stimulus testing that can be considered include partially immersing a limb of the patient's in cold water³ or placing the patient in a cold room¹⁵; however, these forms of cold stimulus may put the patient at increased risk for a systemic reaction. Finally, scratching the skin prior to cooling or during cooling also may be of diagnostic value in cases of cold-dependant dermatographism.^9,15

Additional testing should be guided by a patient's history. To determine if a secondary cause is responsible for the clinical presentation of cold urticaria, laboratory studies could include complete blood count, erythrocyte sedimentation rate, antinuclear antibodies titer, infectious mononucleosis serology, syphilis serology, rheumatoid factor, total complement, cold agglutinins, cold hemolysin, cryofibrinogen, and cryoglobulin.¹² Of note, approximately 4% of patients with cold urticaria have been observed to have cryoglobulinemia. Thus, testing for cryoglobulinemia is the most likely laboratory study to yield positive results.^1,16 Beyond evaluation for cryoprecipitates, however, an extensive search for etiology is not indicated unless additional clinical findings warrant investigation.¹⁶

Treatment of patients with cold urticaria can be difficult. Patients and their families should be counseled on the risks of aquatic activities and should be instructed on the proper use of an epinephrine autoinjector. In severe cases, patients may elect to move to warmer climates. Antihistamines sometimes provide benefit, especially at high doses and/or with the more potent formulations, such as doxepin. Cyproheptadine has been shown to be more effective than chlorpheniramine.¹⁷ Second-generation antihistamines also may be considered to minimize sedation. Cetirizine, loratadine, and desloratadine have been shown to be effective and well-tolerated options for treatment.^18,19 Additionally, leukotriene receptor antagonists may have a role in treatment.⁵ Bonadonna et al⁶ demonstrated that cetirizine and zafirlukast in combination are more effective than either drug alone. Adjusting the level of medication so that the patient requires more than 3 minutes of cold stimulus testing before having a wheal response is a recommended goal of therapy that is aimed at minimizing the patient's risk of having a hypotensive reaction.¹²

Cold urticaria is an uncommon disorder that can put patients at significant risk. Taking a thorough history and confirming the condition through the use of cold stimulation tests can lead to a diagnosis in most cases. Although most forms of cold urticaria are idiopathic and acquired, familial and secondary forms also must be kept in mind when considering this diagnosis. In addition to antihistamine therapy, an epinephrine autoinjector and preventive measures play an important role in treating patients with cold urticaria. 

Case Report

An otherwise healthy 9-year-old Filipino girl presented with a complaint of urticaria precipitated by cold exposure over the preceding 5 weeks. She had no recent illnesses and normal results of a school physical examination performed 2 weeks prior to symptom onset. The patient's medical history was significant only for cat allergy; however, she noted that on multiple occasions, erythema and pruritus appeared on her arms and face after walking through the freezer aisle of a grocery store. Urticaria subsequently developed on regions where she scratched and spontaneously resolved 2 to 3 hours later. On one occasion, urticaria appeared diffusely on the patient while she showered after swimming; it resolved within a few hours after she was given diphenhydramine by her mother. Three days prior to presentation, the patient experienced upper lip angioedema with erythema, globus sensation, and difficulty swallowing after drinking a strawberry slushy. She denied having respiratory complaints at that time, and her symptoms again resolved spontaneously. A day later, the patient tolerated ice cream with no complaints. Her family history was significant for a maternal history of seasonal allergies.

On physical examination, the patient appeared to be well. She had 2 to 3 discrete urticarial lesions on the distal posterior aspect of each calf that, according to her mother, recently began appearing on "cold and rainy" days. The mother attributed them to her daughter's lower legs being exposed because of the length of her pants. Results of the remainder of the examination were unremarkable, and dermatographism was absent.

Laboratory evaluation consisted of a strawberry radioallergosorbent test and cryoglobulins test, both of which had negative results. An ice cube wrapped in plastic was applied to the volar surface of the patient's right forearm for 5 minutes. A 9X6-cm wheal was noted 3 minutes after ice removal (Figure).

PLEASE REFER TO THE PDF TO VIEW THE FIGURE

A diagnosis of cold urticaria with associated angioedema was made. The patient's mother opted for her daughter to use only diphenhydramine as needed; additionally, an epinephrine autoinjector was dispensed. By 3 months after symptom onset, the patient's only complaint was pruritus of her hands if they became too cold. No urticaria was noted. At 6-month follow-up, the patient denied having had symptoms for the preceding 2 months, and the results of an ice cube test were negative. 

Comment

Cold urticaria is a form of physical urticaria that is notable for the development of urticaria and/or angioedema after cold exposure.¹ Cold urticaria syndromes were first described in the 19th century² and are uncommon. However, it has been observed that approximately one third of adult³ and pediatric⁴ patients with cold urticaria have systemic reactions that are mostly hypotensive episodes associated with aquatic activities. Thus, identification of these patients should be a priority.

The prevalence of cold urticaria is not well defined. Cold urticaria is most commonly noted in young adults, with only 11% of cases noted in children under 10 years of age.³ Most forms of cold urticaria are idiopathic (Table); however, some forms can be secondary to underlying conditions such as malignancies, vasculitides, and infectious diseases.⁸ Cryoglobulinemia (primary and secondary to malignancy) often is cited as a cause of secondary cold urticaria.^3,8-11 Mounting evidence indicates that a possible autoimmune mechanism underlies the idiopathic form of this disorder in many patients.¹²

PLEASE REFER TO THE PDF TO VIEW THE TABLE

Although most forms of cold urticaria are considered to be acquired, familial forms have been described,^7,13 some of which have been classified within the hereditary periodic fever syndromes.¹² Diagnosis of cold urticaria primarily is made by evaluating the patient's clinical history; the diagnosis may be confirmed by applying a cold stimulus, most commonly an ice cube wrapped in plastic and applied to the volar aspect of the patient's forearm. A positive reaction is noted by the formation of a wheal during rewarming of the skin. The length of time that a cold stimulus is applied is not standardized; commonly, 3-, 5-, and 10-minute applications are used. Visitsuntorn et al¹⁴ observed the effectiveness of 3- or 5-minute applications in children who had not taken antihistamines for at least 5 days prior. The authors also noted that false-positive results (defined as reddening of the skin and minimal edema) were possible with 10- and 20-minute applications in patients with chronic urticaria not induced by cold. Other studies have observed that the length of time necessary for a cold stimulus to induce wheal formation inversely may be related to the patient's risk of having a systemic reaction.^1,8,12 Specifically, patients who demonstrated wheal formation after the application of a cold stimulus for 3 minutes or less were noted to experience cold-induced hypotension more frequently. Regardless, it should be recognized that all patients with cold urticaria are at risk for hypotensive reactions.

Approximately 20% of patients with cold urticaria lack an immediate response to cold stimulus with an ice cube; these patients have so-called atypical acquired cold urticaria syndromes^1,12 (eg, cold-dependant dermatographism, delayed cold urticaria, systemic cold urticaria). Other forms of cold stimulus testing that can be considered include partially immersing a limb of the patient's in cold water³ or placing the patient in a cold room¹⁵; however, these forms of cold stimulus may put the patient at increased risk for a systemic reaction. Finally, scratching the skin prior to cooling or during cooling also may be of diagnostic value in cases of cold-dependant dermatographism.^9,15

Additional testing should be guided by a patient's history. To determine if a secondary cause is responsible for the clinical presentation of cold urticaria, laboratory studies could include complete blood count, erythrocyte sedimentation rate, antinuclear antibodies titer, infectious mononucleosis serology, syphilis serology, rheumatoid factor, total complement, cold agglutinins, cold hemolysin, cryofibrinogen, and cryoglobulin.¹² Of note, approximately 4% of patients with cold urticaria have been observed to have cryoglobulinemia. Thus, testing for cryoglobulinemia is the most likely laboratory study to yield positive results.^1,16 Beyond evaluation for cryoprecipitates, however, an extensive search for etiology is not indicated unless additional clinical findings warrant investigation.¹⁶

Treatment of patients with cold urticaria can be difficult. Patients and their families should be counseled on the risks of aquatic activities and should be instructed on the proper use of an epinephrine autoinjector. In severe cases, patients may elect to move to warmer climates. Antihistamines sometimes provide benefit, especially at high doses and/or with the more potent formulations, such as doxepin. Cyproheptadine has been shown to be more effective than chlorpheniramine.¹⁷ Second-generation antihistamines also may be considered to minimize sedation. Cetirizine, loratadine, and desloratadine have been shown to be effective and well-tolerated options for treatment.^18,19 Additionally, leukotriene receptor antagonists may have a role in treatment.⁵ Bonadonna et al⁶ demonstrated that cetirizine and zafirlukast in combination are more effective than either drug alone. Adjusting the level of medication so that the patient requires more than 3 minutes of cold stimulus testing before having a wheal response is a recommended goal of therapy that is aimed at minimizing the patient's risk of having a hypotensive reaction.¹²

Cold urticaria is an uncommon disorder that can put patients at significant risk. Taking a thorough history and confirming the condition through the use of cold stimulation tests can lead to a diagnosis in most cases. Although most forms of cold urticaria are idiopathic and acquired, familial and secondary forms also must be kept in mind when considering this diagnosis. In addition to antihistamine therapy, an epinephrine autoinjector and preventive measures play an important role in treating patients with cold urticaria. 

Identifying which came first—body dysmorphic disorder (BDD) or comorbid anxiety or depressive disorders—can be as complex as treating the disorder’s delusional thinking and high suicide risk. To help you when working alone or with a psychotherapist, we offer strategies we have found useful for:

• diagnosing BDD
• educating patients and families about it
• choosing and dosing medications
• addressing inaccurate perceptions with targeted cognitive-behavioral therapies.

Though many recommendations are based on published data, we also draw on our clinical experience because research on effective BDD treatments is limited.

Box

Assessment

BDD causes patients great distress and disability—often accompanied by major depression—but is easy to miss or misdiagnose (Box).^1-7 Even when suicidal, BDD patients often do not reveal their symptoms to clinicians,² probably because of poor insight or shame about their appearance. When a patient describes being unable to stop thinking about specific aspects of his or her appearance, assess further for BDD.

BDD patients’ conviction that their appearance is defective ranges from good insight to mildly overvalued ideation to frankly delusional.⁸ They often have ideas of reference (such as thinking others may be looking at their “defective” body part) and delusions of reference (such as being convinced others are talking about their “defective” body part). Asking a patient the questions in Table 1 can help establish the diagnosis. BDD also is included in the Structured Clinical Interview for DSM-IV (SCID). Useful assessment tools include:

• Body Dysmorphic Disorder Questionnaire,⁹ a 5-minute, patient-rated scale for screening
• Body Dysmorphic Disorder Examination,¹⁰ to diagnose BDD, survey BDD symptoms, and measure severity
• Yale-Brown Obsessive-Compulsive Scale modified for Body Dysmorphic Disorder (BDD-YBOCS),¹¹ for measuring symptom severity and changes over time.

Comorbidity. Psychiatric comorbidity is common in BDD (Table 2),^6,7,12-14 and deciding which disorder to address first can be difficult. If there is acute mania or non-BDD psychosis, we suggest that you stabilize these before treating BDD. Suicidality or severe substance dependence or abuse may result from BDD and therefore needs to be treated in conjunction with BDD.

If comorbid obsessive-compulsive disorder (OCD) or social phobia symptoms are interconnected with the patient’s BDD, treat concurrently; if not, address sequentially, starting with the more-severe symptoms. For example, symptoms that suggest social phobia (such as fear of public speaking) may be related to BDD, and treatment should focus on BDD. A patient with obsessive fears about how “contaminants” will affect her skin’s appearance may need to have the OCD and BDD addressed concurrently.

For other comorbidities, the treatment hierarchy is less clear. Major depression, for example, may be caused by severe BDD and might not improve until BDD improves. Even when a patient has several concurrent Axis I disorders, don’t over-look treating BDD; otherwise, the patient may remain quite impaired.

Assess suicide risk, as ≥ 25% of BDD patients may attempt suicide in their lifetimes.² Safety measures include frequent monitoring, medication, family involvement, and—if necessary—hospitalization.

Table 1

Patient interview: Questions to help diagnose BDD

Table 2

Lifetime prevalence (%) of comorbid Axis I disorders in BDD

Patient education

Improving insight. Educate patients that BDD is a brain disorder that creates faulty, inaccurate thoughts and perceptions about appearance. Many patients initially resist a BDD diagnosis; delusional thinking and poor insight lead them to assume the “flaw” they see is an accurate perception. They may need to hear about other persons with similar concerns to realize that a psychiatric disorder is causing their distress.

Other helpful resources for improving insight include:

• group therapy
• The Broken Mirror, by Katharine A. Phillips, MD,¹⁵ which contains case examples to which BDD sufferers may relate
• Websites and online forums (see Related resources).

Explaining BDD. Discuss possible causes of BDD, giving patients alternate explanations for the physical defects they perceive. Contributing factors may include:

• neurobiological abnormalities and genetic factors¹⁶
• a history since childhood of shyness, perfectionism, or anxious temperament
• being teased, abused, or in poor family and peer relationships.¹⁷

Emphasize that multiple, different, converging factors cause BDD for each individual.

The obsessive-compulsive cycle. Explain that thoughts create distressing emotions, and that persons with BDD try to relieve or prevent these emotions by performing compulsive behaviors. Compulsions then strengthen the association between intrusive thoughts about appearance “defects” and negative feelings about appearance.

Review a list of common compulsions (Table 3) with BDD patients, as many have engaged in these behaviors for years without realizing they are compulsions.

Table 3

Common BDD compulsions and avoidances

Pharmacotherapy

BDD is a severe and complex disorder that often requires multimodal treatment using cognitive-behavioral therapy (CBT) and medication (algorithm).¹⁸ In our experience, most BDD patients need medication for the disorder and for common comorbidities. We recommend starting medications before or when beginning CBT for patients with moderate to severe BDD (BDD YBOCs ≥ 20).

Serotonin reuptake inhibitors (SRIs) have reduced BDD symptoms in open-label^19,20 and controlled trials.^21,22 As first-line treatments, SRIs decrease distress, compulsions, and frequency and intensity of obsessions about perceived defects; they also can improve insight.^21-24 SRIs appear equally effective for delusional and nondelusional patients;^21,23 whether CBT is similarly effective is unclear.

Relatively high dosages are usually necessary, according to published flexible-dosing trials in BDD,^19-23 a retrospective chart review²⁴ and our experience. Try dosages similar to those used for OCD (Table 4) as tolerated, and monitor for side effects. Twelve to 16 weeks of treatment are often needed for a full therapeutic effect.^20-21

Augmentation. Consider adding another agent if a full SRI trial achieves partial symptom relief. One open-label trial of 13 BDD patients found that 6 (46%) improved when buspirone (mean dosage 48.3 mg/d) was added to SRI therapy.²⁵ In a chart review, Phillips et al²⁴ reported variable response rates of BDD patients treated with augmentation trials of clomipramine (4/9), buspirone (12/36), lithium (1/5), methylphenidate (1/6), and antipsychotics (2/13).

Very few studies have examined antipsychotic use in BDD. Placebo-controlled data are available only for pimozide.²⁷ Conventional antipsychotics are unlikely to be effective, either as monotherapy²⁶ or augmentation.²⁷ As for the atypicals, olanzapine augmentation showed little to no efficacy in one small trial, although the average dosage used was low (4.6 mg/d).²⁸ In our experience, atypicals—such as aripiprazole, 5 to 30 mg/d; quetiapine 100 to 300 mg/d; olanzapine, 7.5 to 15 mg/d; or risperidone, 1 to 3 mg/d—can improve BDD core symptoms and improve insight.

Benzodiazepines can be useful for acute anxiety or agitation. Carefully monitor benzodiazepine use, however, as substance abuse is relatively common in BDD patients.²⁹

Table 4

Recommended SRI dosages for treating BDD*^†

Specialized cbt techniques

Cognitive restructuring. Trying to convince BDD patients there is nothing wrong with their appearance will not be successful. Instead, we use cognitive restructuring to challenge the rationality of their thoughts and beliefs and to find alternate, more rational ones:

Therapist: “I know I cannot convince you that your (body area) is not defective, but can you give me evidence of how this ‘defect’ has affected your life?”

BDD patient: “Well, I haven’t had a date for a long time. I think this is evidence that my (body part) must be ugly, and that no one wants to date me because of it.”

Therapist: “What are some other possible reasons why you haven’t had a date in a long time? You admitted that you have barely left your house for many months. Is it possible that you have not had a date for a long time because you rarely go outside?”

With cognitive restructuring, patients learn to:

• identify automatic thoughts and beliefs that provoke distress
• examine evidence supporting or refuting these beliefs
• de-catastrophize (such as “What is the worst thing that could happen if you left the house today without checking your [body part]? Do you think you would eventually be able to cope with that?”)
• learn to more accurately assess the probability of feared negative consequences
• arrive at rational responses.

In our experience—which is supported by OCD literature—participating in CBT is very hard for patients with frank delusions, and insight determines how effective cognitive restructuring can be.³⁰ If a patient is convinced a body part is defective, she is unlikely to stay in treatment—much less be open to restructuring her thoughts. Even unsuccessful attempts can help you gauge the intensity of patients’ beliefs, however.

During cognitive restructuring, it is important to uncover patients’ core beliefs (underlying, organizing principles they hold about themselves, others, and the world). BDD patients commonly believe that appearance is of utmost importance and that no one could love them because of their “defect.” The therapist can then help the patient challenge the rationality of those core beliefs.

Behavioral therapy. Basic behavioral therapy attempts to normalize excessive response to appearance concerns and to prepare patients for exposure and response prevention therapy (ERP). Having identified their compulsions, the next step is to guide patients in changing these behaviors, such as by:

• decreasing reassurance-seeking
• reducing avoidance of social situations
• decreasing opportunities to use the mirror
• reducing time spent on the Internet seeking cosmetic solutions
• increasing eye contact in social situations
• decreasing scanning of others’ physical features.

For example, suggest that BDD patients stand at least an arm’s length away when using a mirror for normal grooming. Then, instead of focusing on their body part, they will view it within the context of their entire face and body.

Exposure and response prevention

ERP exposes the patient to situations that evoke negative emotions—primarily shame and anxiety in BDD—so that they gradually habituate to these feelings. Individualize exposure exercises, targeting the body parts each person believes are defective. Because these exercises are intended to induce the discomfort patients usually experience, do not attempt ERP until the patient has had extensive education, developed insight, and has consented to treatment.

Create a hierarchy of ERP tasks (Table 5), ranking situations from low- to high-distress. Address items lower on the hierarchy first, and progress to higher items as the lower ones become easier to perform. Do not attempt the highest-distress items until the patient has improved insight and is not severely ill and suicidal.

During exposures, patients must remain in distress-provoking situations—without performing compulsive behaviors—until their negative feelings decrease by at least 50% of the initial subjective, self-rated distress level. Leaving the situation before stress diminishes may reinforce shame and discomfort. Performing compulsive behaviors during or after an exposure will negate the exposure’s effect.

Mirrors and ERP. Some therapists use mirrors for exposure exercises, but this is a complex issue. Mirror-checking is a common BDD compulsion that provides temporary relief but ultimately reinforces negative, intrusive thoughts about the disliked body area. How BDD patients perceive themselves changes from moment to moment; they may stare at and analyze any reflective surface in hopes that their “defect” will not appear as deformed or ugly that day. Thus, one cannot predict whether looking in the mirror at any one time is an exposure or a compulsion.

ERP exercises for BDD need to emphasize behaviors that involve interactions with the outside world, rather than reinforcing the importance of appearance. Using the mirror for ERP could promote checking compulsions and may send the message that appearance is the focal point of treatment. On the other hand, for patients with persistent mirror avoidance, gradual mirror exposures may be useful. A technique called mirror retraining helps patients objectively view their appearance and has been used with success in some individuals.

Table 5

Exposure and response therapy: a BDD patient’s sample hierarchy

Psychosocial development

BDD therapy challenges the disorder’s core theme—that appearance is one’s only important attribute—and helps patients identify and develop qualities not related to appearance. Through social interactions, the BDD patient can:

• develop a multidimensional sense of self
• receive nonappearance-related positive feedback from the outside world.

Explore psychosocial development during the assessment phase and when a patient shows little progress in CBT. In some patients, for example, BDD onset in childhood or adolescence interferes with developmental transition to adulthood.

In our experience, some patients may resist treatment because of conscious and unconscious fears of adult responsibilities and relationships. We focus therapy on making them aware of these phenomena, exploring fears of development, and encouraging them to seek new relationships and responsibilities.

Because a BDD patient’s symptoms often create conflict and distress at home, offer the family support and education about the disorder. Occasionally, forces within the family seem to be working against the individual’s recovery and/or independence.

In some families, an individual with BDD may become the “identified patient,” diverting attention from other dysfunctional family members or relationships. During therapy, the BDD patient’s goal to develop a sense of self that is not appearance-based may run counter to the family’s need to keep him or her in the “sick” role.

If therapy is to succeed, talk to the patient about these dynamics. Consider family therapy if resistance to change is strong. When a patient is not progressing well with CBT, we find understanding the family system can be useful to comprehensive BDD treatment, although this observation remains to be validated.

Preventing and treating relapse

Educate patients that BDD is usually chronic, even when treated with psychotherapy and medication.³¹ Relapse often occurs, especially when patients discontinue medications on their own²⁴ or drop out of therapy early. No guidelines exist, but based on our experience:

• we continue medication for at least 1 year after a patient improves
• psychotherapy is more variable but may need to last 6 to 12 months or more.

When therapy ends, we encourage patients to practice and reinforce everything they learned during treatment. Casting BDD resurgence as normal—and not as failure—will help patients who relapse to resist the downward spiral of low self-esteem, shame, and turning to the mirror for reassurance. Identifying BDD symptom triggers and developing plans to cope with them may also prevent relapse. CBT “booster sessions” scheduled monthly for 3 to 6 months may help patients who have completed therapy.

Related resources

FOR CLINICIANS:

• Phillips KA. “I’m as ugly as the elephant man:” How to recognize and treat body dysmorphic disorder. Current Psychiatry. 2002;1(1):58-65.
• Cororve MB, Gleaves DH. Body dysmorphic disorder: a review of conceptualizations, assessment, and treatment strategies. Clin Psychol Rev. 2001;21(6):949-70.

FOR PATIENTS AND FAMILIES:

• Phillips KA. The broken mirror. New York: Oxford University Press; 2005.
• BDD and body image program, Butler Hospital, Providence, RI. BDD education and support. www.BDDcentral.com.
• Winograd A. Director, Accurate Reflections, Los Angeles, CA. Support group and information on BDD and obsessive compulsive spectrum disorders. www.AccurateReflections.com

Drug brand names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Buspirone • BuSpar
• Citalopram • Celexa
• Clomipramine • Anafranil
• Desipramine • Norpramin
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Lithium • Lithobid, others
• Methylphenidate • Ritalin, Concerta
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Identifying which came first—body dysmorphic disorder (BDD) or comorbid anxiety or depressive disorders—can be as complex as treating the disorder’s delusional thinking and high suicide risk. To help you when working alone or with a psychotherapist, we offer strategies we have found useful for:

• diagnosing BDD
• educating patients and families about it
• choosing and dosing medications
• addressing inaccurate perceptions with targeted cognitive-behavioral therapies.

Though many recommendations are based on published data, we also draw on our clinical experience because research on effective BDD treatments is limited.

Box

Assessment

BDD causes patients great distress and disability—often accompanied by major depression—but is easy to miss or misdiagnose (Box).^1-7 Even when suicidal, BDD patients often do not reveal their symptoms to clinicians,² probably because of poor insight or shame about their appearance. When a patient describes being unable to stop thinking about specific aspects of his or her appearance, assess further for BDD.

BDD patients’ conviction that their appearance is defective ranges from good insight to mildly overvalued ideation to frankly delusional.⁸ They often have ideas of reference (such as thinking others may be looking at their “defective” body part) and delusions of reference (such as being convinced others are talking about their “defective” body part). Asking a patient the questions in Table 1 can help establish the diagnosis. BDD also is included in the Structured Clinical Interview for DSM-IV (SCID). Useful assessment tools include:

• Body Dysmorphic Disorder Questionnaire,⁹ a 5-minute, patient-rated scale for screening
• Body Dysmorphic Disorder Examination,¹⁰ to diagnose BDD, survey BDD symptoms, and measure severity
• Yale-Brown Obsessive-Compulsive Scale modified for Body Dysmorphic Disorder (BDD-YBOCS),¹¹ for measuring symptom severity and changes over time.

Comorbidity. Psychiatric comorbidity is common in BDD (Table 2),^6,7,12-14 and deciding which disorder to address first can be difficult. If there is acute mania or non-BDD psychosis, we suggest that you stabilize these before treating BDD. Suicidality or severe substance dependence or abuse may result from BDD and therefore needs to be treated in conjunction with BDD.

If comorbid obsessive-compulsive disorder (OCD) or social phobia symptoms are interconnected with the patient’s BDD, treat concurrently; if not, address sequentially, starting with the more-severe symptoms. For example, symptoms that suggest social phobia (such as fear of public speaking) may be related to BDD, and treatment should focus on BDD. A patient with obsessive fears about how “contaminants” will affect her skin’s appearance may need to have the OCD and BDD addressed concurrently.

For other comorbidities, the treatment hierarchy is less clear. Major depression, for example, may be caused by severe BDD and might not improve until BDD improves. Even when a patient has several concurrent Axis I disorders, don’t over-look treating BDD; otherwise, the patient may remain quite impaired.

Assess suicide risk, as ≥ 25% of BDD patients may attempt suicide in their lifetimes.² Safety measures include frequent monitoring, medication, family involvement, and—if necessary—hospitalization.

Table 1

Patient interview: Questions to help diagnose BDD

Table 2

Lifetime prevalence (%) of comorbid Axis I disorders in BDD

Patient education

Improving insight. Educate patients that BDD is a brain disorder that creates faulty, inaccurate thoughts and perceptions about appearance. Many patients initially resist a BDD diagnosis; delusional thinking and poor insight lead them to assume the “flaw” they see is an accurate perception. They may need to hear about other persons with similar concerns to realize that a psychiatric disorder is causing their distress.

Other helpful resources for improving insight include:

• group therapy
• The Broken Mirror, by Katharine A. Phillips, MD,¹⁵ which contains case examples to which BDD sufferers may relate
• Websites and online forums (see Related resources).

Explaining BDD. Discuss possible causes of BDD, giving patients alternate explanations for the physical defects they perceive. Contributing factors may include:

• neurobiological abnormalities and genetic factors¹⁶
• a history since childhood of shyness, perfectionism, or anxious temperament
• being teased, abused, or in poor family and peer relationships.¹⁷

Emphasize that multiple, different, converging factors cause BDD for each individual.

The obsessive-compulsive cycle. Explain that thoughts create distressing emotions, and that persons with BDD try to relieve or prevent these emotions by performing compulsive behaviors. Compulsions then strengthen the association between intrusive thoughts about appearance “defects” and negative feelings about appearance.

Review a list of common compulsions (Table 3) with BDD patients, as many have engaged in these behaviors for years without realizing they are compulsions.

Table 3

Common BDD compulsions and avoidances

Pharmacotherapy

BDD is a severe and complex disorder that often requires multimodal treatment using cognitive-behavioral therapy (CBT) and medication (algorithm).¹⁸ In our experience, most BDD patients need medication for the disorder and for common comorbidities. We recommend starting medications before or when beginning CBT for patients with moderate to severe BDD (BDD YBOCs ≥ 20).

Serotonin reuptake inhibitors (SRIs) have reduced BDD symptoms in open-label^19,20 and controlled trials.^21,22 As first-line treatments, SRIs decrease distress, compulsions, and frequency and intensity of obsessions about perceived defects; they also can improve insight.^21-24 SRIs appear equally effective for delusional and nondelusional patients;^21,23 whether CBT is similarly effective is unclear.

Relatively high dosages are usually necessary, according to published flexible-dosing trials in BDD,^19-23 a retrospective chart review²⁴ and our experience. Try dosages similar to those used for OCD (Table 4) as tolerated, and monitor for side effects. Twelve to 16 weeks of treatment are often needed for a full therapeutic effect.^20-21

Augmentation. Consider adding another agent if a full SRI trial achieves partial symptom relief. One open-label trial of 13 BDD patients found that 6 (46%) improved when buspirone (mean dosage 48.3 mg/d) was added to SRI therapy.²⁵ In a chart review, Phillips et al²⁴ reported variable response rates of BDD patients treated with augmentation trials of clomipramine (4/9), buspirone (12/36), lithium (1/5), methylphenidate (1/6), and antipsychotics (2/13).

Very few studies have examined antipsychotic use in BDD. Placebo-controlled data are available only for pimozide.²⁷ Conventional antipsychotics are unlikely to be effective, either as monotherapy²⁶ or augmentation.²⁷ As for the atypicals, olanzapine augmentation showed little to no efficacy in one small trial, although the average dosage used was low (4.6 mg/d).²⁸ In our experience, atypicals—such as aripiprazole, 5 to 30 mg/d; quetiapine 100 to 300 mg/d; olanzapine, 7.5 to 15 mg/d; or risperidone, 1 to 3 mg/d—can improve BDD core symptoms and improve insight.

Benzodiazepines can be useful for acute anxiety or agitation. Carefully monitor benzodiazepine use, however, as substance abuse is relatively common in BDD patients.²⁹

Table 4

Recommended SRI dosages for treating BDD*^†

Specialized cbt techniques

Cognitive restructuring. Trying to convince BDD patients there is nothing wrong with their appearance will not be successful. Instead, we use cognitive restructuring to challenge the rationality of their thoughts and beliefs and to find alternate, more rational ones:

Therapist: “I know I cannot convince you that your (body area) is not defective, but can you give me evidence of how this ‘defect’ has affected your life?”

BDD patient: “Well, I haven’t had a date for a long time. I think this is evidence that my (body part) must be ugly, and that no one wants to date me because of it.”

Therapist: “What are some other possible reasons why you haven’t had a date in a long time? You admitted that you have barely left your house for many months. Is it possible that you have not had a date for a long time because you rarely go outside?”

With cognitive restructuring, patients learn to:

• identify automatic thoughts and beliefs that provoke distress
• examine evidence supporting or refuting these beliefs
• de-catastrophize (such as “What is the worst thing that could happen if you left the house today without checking your [body part]? Do you think you would eventually be able to cope with that?”)
• learn to more accurately assess the probability of feared negative consequences
• arrive at rational responses.

In our experience—which is supported by OCD literature—participating in CBT is very hard for patients with frank delusions, and insight determines how effective cognitive restructuring can be.³⁰ If a patient is convinced a body part is defective, she is unlikely to stay in treatment—much less be open to restructuring her thoughts. Even unsuccessful attempts can help you gauge the intensity of patients’ beliefs, however.

During cognitive restructuring, it is important to uncover patients’ core beliefs (underlying, organizing principles they hold about themselves, others, and the world). BDD patients commonly believe that appearance is of utmost importance and that no one could love them because of their “defect.” The therapist can then help the patient challenge the rationality of those core beliefs.

Behavioral therapy. Basic behavioral therapy attempts to normalize excessive response to appearance concerns and to prepare patients for exposure and response prevention therapy (ERP). Having identified their compulsions, the next step is to guide patients in changing these behaviors, such as by:

• decreasing reassurance-seeking
• reducing avoidance of social situations
• decreasing opportunities to use the mirror
• reducing time spent on the Internet seeking cosmetic solutions
• increasing eye contact in social situations
• decreasing scanning of others’ physical features.

For example, suggest that BDD patients stand at least an arm’s length away when using a mirror for normal grooming. Then, instead of focusing on their body part, they will view it within the context of their entire face and body.

Exposure and response prevention

ERP exposes the patient to situations that evoke negative emotions—primarily shame and anxiety in BDD—so that they gradually habituate to these feelings. Individualize exposure exercises, targeting the body parts each person believes are defective. Because these exercises are intended to induce the discomfort patients usually experience, do not attempt ERP until the patient has had extensive education, developed insight, and has consented to treatment.

Create a hierarchy of ERP tasks (Table 5), ranking situations from low- to high-distress. Address items lower on the hierarchy first, and progress to higher items as the lower ones become easier to perform. Do not attempt the highest-distress items until the patient has improved insight and is not severely ill and suicidal.

During exposures, patients must remain in distress-provoking situations—without performing compulsive behaviors—until their negative feelings decrease by at least 50% of the initial subjective, self-rated distress level. Leaving the situation before stress diminishes may reinforce shame and discomfort. Performing compulsive behaviors during or after an exposure will negate the exposure’s effect.

Mirrors and ERP. Some therapists use mirrors for exposure exercises, but this is a complex issue. Mirror-checking is a common BDD compulsion that provides temporary relief but ultimately reinforces negative, intrusive thoughts about the disliked body area. How BDD patients perceive themselves changes from moment to moment; they may stare at and analyze any reflective surface in hopes that their “defect” will not appear as deformed or ugly that day. Thus, one cannot predict whether looking in the mirror at any one time is an exposure or a compulsion.

ERP exercises for BDD need to emphasize behaviors that involve interactions with the outside world, rather than reinforcing the importance of appearance. Using the mirror for ERP could promote checking compulsions and may send the message that appearance is the focal point of treatment. On the other hand, for patients with persistent mirror avoidance, gradual mirror exposures may be useful. A technique called mirror retraining helps patients objectively view their appearance and has been used with success in some individuals.

Table 5

Exposure and response therapy: a BDD patient’s sample hierarchy

Psychosocial development

BDD therapy challenges the disorder’s core theme—that appearance is one’s only important attribute—and helps patients identify and develop qualities not related to appearance. Through social interactions, the BDD patient can:

• develop a multidimensional sense of self
• receive nonappearance-related positive feedback from the outside world.

Explore psychosocial development during the assessment phase and when a patient shows little progress in CBT. In some patients, for example, BDD onset in childhood or adolescence interferes with developmental transition to adulthood.

In our experience, some patients may resist treatment because of conscious and unconscious fears of adult responsibilities and relationships. We focus therapy on making them aware of these phenomena, exploring fears of development, and encouraging them to seek new relationships and responsibilities.

Because a BDD patient’s symptoms often create conflict and distress at home, offer the family support and education about the disorder. Occasionally, forces within the family seem to be working against the individual’s recovery and/or independence.

In some families, an individual with BDD may become the “identified patient,” diverting attention from other dysfunctional family members or relationships. During therapy, the BDD patient’s goal to develop a sense of self that is not appearance-based may run counter to the family’s need to keep him or her in the “sick” role.

If therapy is to succeed, talk to the patient about these dynamics. Consider family therapy if resistance to change is strong. When a patient is not progressing well with CBT, we find understanding the family system can be useful to comprehensive BDD treatment, although this observation remains to be validated.

Preventing and treating relapse

Educate patients that BDD is usually chronic, even when treated with psychotherapy and medication.³¹ Relapse often occurs, especially when patients discontinue medications on their own²⁴ or drop out of therapy early. No guidelines exist, but based on our experience:

• we continue medication for at least 1 year after a patient improves
• psychotherapy is more variable but may need to last 6 to 12 months or more.

When therapy ends, we encourage patients to practice and reinforce everything they learned during treatment. Casting BDD resurgence as normal—and not as failure—will help patients who relapse to resist the downward spiral of low self-esteem, shame, and turning to the mirror for reassurance. Identifying BDD symptom triggers and developing plans to cope with them may also prevent relapse. CBT “booster sessions” scheduled monthly for 3 to 6 months may help patients who have completed therapy.

Related resources

FOR CLINICIANS:

• Phillips KA. “I’m as ugly as the elephant man:” How to recognize and treat body dysmorphic disorder. Current Psychiatry. 2002;1(1):58-65.
• Cororve MB, Gleaves DH. Body dysmorphic disorder: a review of conceptualizations, assessment, and treatment strategies. Clin Psychol Rev. 2001;21(6):949-70.

FOR PATIENTS AND FAMILIES:

• Phillips KA. The broken mirror. New York: Oxford University Press; 2005.
• BDD and body image program, Butler Hospital, Providence, RI. BDD education and support. www.BDDcentral.com.
• Winograd A. Director, Accurate Reflections, Los Angeles, CA. Support group and information on BDD and obsessive compulsive spectrum disorders. www.AccurateReflections.com

Drug brand names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Buspirone • BuSpar
• Citalopram • Celexa
• Clomipramine • Anafranil
• Desipramine • Norpramin
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Lithium • Lithobid, others
• Methylphenidate • Ritalin, Concerta
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Identifying which came first—body dysmorphic disorder (BDD) or comorbid anxiety or depressive disorders—can be as complex as treating the disorder’s delusional thinking and high suicide risk. To help you when working alone or with a psychotherapist, we offer strategies we have found useful for:

• diagnosing BDD
• educating patients and families about it
• choosing and dosing medications
• addressing inaccurate perceptions with targeted cognitive-behavioral therapies.

Though many recommendations are based on published data, we also draw on our clinical experience because research on effective BDD treatments is limited.

Box

Assessment

BDD causes patients great distress and disability—often accompanied by major depression—but is easy to miss or misdiagnose (Box).^1-7 Even when suicidal, BDD patients often do not reveal their symptoms to clinicians,² probably because of poor insight or shame about their appearance. When a patient describes being unable to stop thinking about specific aspects of his or her appearance, assess further for BDD.

BDD patients’ conviction that their appearance is defective ranges from good insight to mildly overvalued ideation to frankly delusional.⁸ They often have ideas of reference (such as thinking others may be looking at their “defective” body part) and delusions of reference (such as being convinced others are talking about their “defective” body part). Asking a patient the questions in Table 1 can help establish the diagnosis. BDD also is included in the Structured Clinical Interview for DSM-IV (SCID). Useful assessment tools include:

• Body Dysmorphic Disorder Questionnaire,⁹ a 5-minute, patient-rated scale for screening
• Body Dysmorphic Disorder Examination,¹⁰ to diagnose BDD, survey BDD symptoms, and measure severity
• Yale-Brown Obsessive-Compulsive Scale modified for Body Dysmorphic Disorder (BDD-YBOCS),¹¹ for measuring symptom severity and changes over time.

Comorbidity. Psychiatric comorbidity is common in BDD (Table 2),^6,7,12-14 and deciding which disorder to address first can be difficult. If there is acute mania or non-BDD psychosis, we suggest that you stabilize these before treating BDD. Suicidality or severe substance dependence or abuse may result from BDD and therefore needs to be treated in conjunction with BDD.

If comorbid obsessive-compulsive disorder (OCD) or social phobia symptoms are interconnected with the patient’s BDD, treat concurrently; if not, address sequentially, starting with the more-severe symptoms. For example, symptoms that suggest social phobia (such as fear of public speaking) may be related to BDD, and treatment should focus on BDD. A patient with obsessive fears about how “contaminants” will affect her skin’s appearance may need to have the OCD and BDD addressed concurrently.

For other comorbidities, the treatment hierarchy is less clear. Major depression, for example, may be caused by severe BDD and might not improve until BDD improves. Even when a patient has several concurrent Axis I disorders, don’t over-look treating BDD; otherwise, the patient may remain quite impaired.

Assess suicide risk, as ≥ 25% of BDD patients may attempt suicide in their lifetimes.² Safety measures include frequent monitoring, medication, family involvement, and—if necessary—hospitalization.

Table 1

Patient interview: Questions to help diagnose BDD

Table 2

Lifetime prevalence (%) of comorbid Axis I disorders in BDD

Patient education

Improving insight. Educate patients that BDD is a brain disorder that creates faulty, inaccurate thoughts and perceptions about appearance. Many patients initially resist a BDD diagnosis; delusional thinking and poor insight lead them to assume the “flaw” they see is an accurate perception. They may need to hear about other persons with similar concerns to realize that a psychiatric disorder is causing their distress.

Other helpful resources for improving insight include:

• group therapy
• The Broken Mirror, by Katharine A. Phillips, MD,¹⁵ which contains case examples to which BDD sufferers may relate
• Websites and online forums (see Related resources).

Explaining BDD. Discuss possible causes of BDD, giving patients alternate explanations for the physical defects they perceive. Contributing factors may include:

• neurobiological abnormalities and genetic factors¹⁶
• a history since childhood of shyness, perfectionism, or anxious temperament
• being teased, abused, or in poor family and peer relationships.¹⁷

Emphasize that multiple, different, converging factors cause BDD for each individual.

The obsessive-compulsive cycle. Explain that thoughts create distressing emotions, and that persons with BDD try to relieve or prevent these emotions by performing compulsive behaviors. Compulsions then strengthen the association between intrusive thoughts about appearance “defects” and negative feelings about appearance.

Review a list of common compulsions (Table 3) with BDD patients, as many have engaged in these behaviors for years without realizing they are compulsions.

Table 3

Common BDD compulsions and avoidances

Pharmacotherapy

BDD is a severe and complex disorder that often requires multimodal treatment using cognitive-behavioral therapy (CBT) and medication (algorithm).¹⁸ In our experience, most BDD patients need medication for the disorder and for common comorbidities. We recommend starting medications before or when beginning CBT for patients with moderate to severe BDD (BDD YBOCs ≥ 20).

Serotonin reuptake inhibitors (SRIs) have reduced BDD symptoms in open-label^19,20 and controlled trials.^21,22 As first-line treatments, SRIs decrease distress, compulsions, and frequency and intensity of obsessions about perceived defects; they also can improve insight.^21-24 SRIs appear equally effective for delusional and nondelusional patients;^21,23 whether CBT is similarly effective is unclear.

Relatively high dosages are usually necessary, according to published flexible-dosing trials in BDD,^19-23 a retrospective chart review²⁴ and our experience. Try dosages similar to those used for OCD (Table 4) as tolerated, and monitor for side effects. Twelve to 16 weeks of treatment are often needed for a full therapeutic effect.^20-21

Augmentation. Consider adding another agent if a full SRI trial achieves partial symptom relief. One open-label trial of 13 BDD patients found that 6 (46%) improved when buspirone (mean dosage 48.3 mg/d) was added to SRI therapy.²⁵ In a chart review, Phillips et al²⁴ reported variable response rates of BDD patients treated with augmentation trials of clomipramine (4/9), buspirone (12/36), lithium (1/5), methylphenidate (1/6), and antipsychotics (2/13).

Very few studies have examined antipsychotic use in BDD. Placebo-controlled data are available only for pimozide.²⁷ Conventional antipsychotics are unlikely to be effective, either as monotherapy²⁶ or augmentation.²⁷ As for the atypicals, olanzapine augmentation showed little to no efficacy in one small trial, although the average dosage used was low (4.6 mg/d).²⁸ In our experience, atypicals—such as aripiprazole, 5 to 30 mg/d; quetiapine 100 to 300 mg/d; olanzapine, 7.5 to 15 mg/d; or risperidone, 1 to 3 mg/d—can improve BDD core symptoms and improve insight.

Benzodiazepines can be useful for acute anxiety or agitation. Carefully monitor benzodiazepine use, however, as substance abuse is relatively common in BDD patients.²⁹

Table 4

Recommended SRI dosages for treating BDD*^†

Specialized cbt techniques

Cognitive restructuring. Trying to convince BDD patients there is nothing wrong with their appearance will not be successful. Instead, we use cognitive restructuring to challenge the rationality of their thoughts and beliefs and to find alternate, more rational ones:

Therapist: “I know I cannot convince you that your (body area) is not defective, but can you give me evidence of how this ‘defect’ has affected your life?”

BDD patient: “Well, I haven’t had a date for a long time. I think this is evidence that my (body part) must be ugly, and that no one wants to date me because of it.”

Therapist: “What are some other possible reasons why you haven’t had a date in a long time? You admitted that you have barely left your house for many months. Is it possible that you have not had a date for a long time because you rarely go outside?”

With cognitive restructuring, patients learn to:

• identify automatic thoughts and beliefs that provoke distress
• examine evidence supporting or refuting these beliefs
• de-catastrophize (such as “What is the worst thing that could happen if you left the house today without checking your [body part]? Do you think you would eventually be able to cope with that?”)
• learn to more accurately assess the probability of feared negative consequences
• arrive at rational responses.

In our experience—which is supported by OCD literature—participating in CBT is very hard for patients with frank delusions, and insight determines how effective cognitive restructuring can be.³⁰ If a patient is convinced a body part is defective, she is unlikely to stay in treatment—much less be open to restructuring her thoughts. Even unsuccessful attempts can help you gauge the intensity of patients’ beliefs, however.

During cognitive restructuring, it is important to uncover patients’ core beliefs (underlying, organizing principles they hold about themselves, others, and the world). BDD patients commonly believe that appearance is of utmost importance and that no one could love them because of their “defect.” The therapist can then help the patient challenge the rationality of those core beliefs.

Behavioral therapy. Basic behavioral therapy attempts to normalize excessive response to appearance concerns and to prepare patients for exposure and response prevention therapy (ERP). Having identified their compulsions, the next step is to guide patients in changing these behaviors, such as by:

• decreasing reassurance-seeking
• reducing avoidance of social situations
• decreasing opportunities to use the mirror
• reducing time spent on the Internet seeking cosmetic solutions
• increasing eye contact in social situations
• decreasing scanning of others’ physical features.

For example, suggest that BDD patients stand at least an arm’s length away when using a mirror for normal grooming. Then, instead of focusing on their body part, they will view it within the context of their entire face and body.

Exposure and response prevention

ERP exposes the patient to situations that evoke negative emotions—primarily shame and anxiety in BDD—so that they gradually habituate to these feelings. Individualize exposure exercises, targeting the body parts each person believes are defective. Because these exercises are intended to induce the discomfort patients usually experience, do not attempt ERP until the patient has had extensive education, developed insight, and has consented to treatment.

Create a hierarchy of ERP tasks (Table 5), ranking situations from low- to high-distress. Address items lower on the hierarchy first, and progress to higher items as the lower ones become easier to perform. Do not attempt the highest-distress items until the patient has improved insight and is not severely ill and suicidal.

During exposures, patients must remain in distress-provoking situations—without performing compulsive behaviors—until their negative feelings decrease by at least 50% of the initial subjective, self-rated distress level. Leaving the situation before stress diminishes may reinforce shame and discomfort. Performing compulsive behaviors during or after an exposure will negate the exposure’s effect.

Mirrors and ERP. Some therapists use mirrors for exposure exercises, but this is a complex issue. Mirror-checking is a common BDD compulsion that provides temporary relief but ultimately reinforces negative, intrusive thoughts about the disliked body area. How BDD patients perceive themselves changes from moment to moment; they may stare at and analyze any reflective surface in hopes that their “defect” will not appear as deformed or ugly that day. Thus, one cannot predict whether looking in the mirror at any one time is an exposure or a compulsion.

ERP exercises for BDD need to emphasize behaviors that involve interactions with the outside world, rather than reinforcing the importance of appearance. Using the mirror for ERP could promote checking compulsions and may send the message that appearance is the focal point of treatment. On the other hand, for patients with persistent mirror avoidance, gradual mirror exposures may be useful. A technique called mirror retraining helps patients objectively view their appearance and has been used with success in some individuals.

Table 5

Exposure and response therapy: a BDD patient’s sample hierarchy

Psychosocial development

BDD therapy challenges the disorder’s core theme—that appearance is one’s only important attribute—and helps patients identify and develop qualities not related to appearance. Through social interactions, the BDD patient can:

• develop a multidimensional sense of self
• receive nonappearance-related positive feedback from the outside world.

Explore psychosocial development during the assessment phase and when a patient shows little progress in CBT. In some patients, for example, BDD onset in childhood or adolescence interferes with developmental transition to adulthood.

In our experience, some patients may resist treatment because of conscious and unconscious fears of adult responsibilities and relationships. We focus therapy on making them aware of these phenomena, exploring fears of development, and encouraging them to seek new relationships and responsibilities.

Because a BDD patient’s symptoms often create conflict and distress at home, offer the family support and education about the disorder. Occasionally, forces within the family seem to be working against the individual’s recovery and/or independence.

In some families, an individual with BDD may become the “identified patient,” diverting attention from other dysfunctional family members or relationships. During therapy, the BDD patient’s goal to develop a sense of self that is not appearance-based may run counter to the family’s need to keep him or her in the “sick” role.

If therapy is to succeed, talk to the patient about these dynamics. Consider family therapy if resistance to change is strong. When a patient is not progressing well with CBT, we find understanding the family system can be useful to comprehensive BDD treatment, although this observation remains to be validated.

Preventing and treating relapse

Educate patients that BDD is usually chronic, even when treated with psychotherapy and medication.³¹ Relapse often occurs, especially when patients discontinue medications on their own²⁴ or drop out of therapy early. No guidelines exist, but based on our experience:

• we continue medication for at least 1 year after a patient improves
• psychotherapy is more variable but may need to last 6 to 12 months or more.

When therapy ends, we encourage patients to practice and reinforce everything they learned during treatment. Casting BDD resurgence as normal—and not as failure—will help patients who relapse to resist the downward spiral of low self-esteem, shame, and turning to the mirror for reassurance. Identifying BDD symptom triggers and developing plans to cope with them may also prevent relapse. CBT “booster sessions” scheduled monthly for 3 to 6 months may help patients who have completed therapy.

Related resources

FOR CLINICIANS:

• Phillips KA. “I’m as ugly as the elephant man:” How to recognize and treat body dysmorphic disorder. Current Psychiatry. 2002;1(1):58-65.
• Cororve MB, Gleaves DH. Body dysmorphic disorder: a review of conceptualizations, assessment, and treatment strategies. Clin Psychol Rev. 2001;21(6):949-70.

FOR PATIENTS AND FAMILIES:

• Phillips KA. The broken mirror. New York: Oxford University Press; 2005.
• BDD and body image program, Butler Hospital, Providence, RI. BDD education and support. www.BDDcentral.com.
• Winograd A. Director, Accurate Reflections, Los Angeles, CA. Support group and information on BDD and obsessive compulsive spectrum disorders. www.AccurateReflections.com

Drug brand names

• Alprazolam • Xanax
• Aripiprazole • Abilify
• Buspirone • BuSpar
• Citalopram • Celexa
• Clomipramine • Anafranil
• Desipramine • Norpramin
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Lithium • Lithobid, others
• Methylphenidate • Ritalin, Concerta
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft

Disclosures

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

VIENNA — Rituximab successfully induced remission of severe extrarenal systemic lupus erythematosus previously unresponsive to cyclophosphamide and/or mycophenolate in five of six treated patients in a small series, Constantine K. Saadeh, M.D., reported at the annual European congress of rheumatology.

Previous studies of rituximab in SLE have focused on the agent's utility in patients with refractory lupus nephritis. But in Dr. Saadeh's six-patient series, the anti-CD20 chimeric monoclonal antibody targeting mature B cells induced remission in patients with lupus skin, lung, and synovial disease.

All five responders to two 500-mg doses of rituximab given a week apart experienced disease remissions lasting at least 3 months. All five experienced a transient 2- to 3-week drop in their globulin fraction beginning roughly a week after treatment.

The sole rituximab nonresponder had mixed lupus nephritis and chronic glomerulonephritis that continued to deteriorate, requiring hemodialysis, added Dr. Saadeh, an Amarillo, Tex., rheumatologist.

The rituximab nonresponder was also the only one of the six patients who did not have depressed complement levels at baseline. It's possible that this agent requires depressed complement levels in order to be effective in SLE, although that hypothesis will require further investigation, the physician noted at the meeting, which was sponsored by the European League Against Rheumatism.

VIENNA — Rituximab successfully induced remission of severe extrarenal systemic lupus erythematosus previously unresponsive to cyclophosphamide and/or mycophenolate in five of six treated patients in a small series, Constantine K. Saadeh, M.D., reported at the annual European congress of rheumatology.

Previous studies of rituximab in SLE have focused on the agent's utility in patients with refractory lupus nephritis. But in Dr. Saadeh's six-patient series, the anti-CD20 chimeric monoclonal antibody targeting mature B cells induced remission in patients with lupus skin, lung, and synovial disease.

All five responders to two 500-mg doses of rituximab given a week apart experienced disease remissions lasting at least 3 months. All five experienced a transient 2- to 3-week drop in their globulin fraction beginning roughly a week after treatment.

The sole rituximab nonresponder had mixed lupus nephritis and chronic glomerulonephritis that continued to deteriorate, requiring hemodialysis, added Dr. Saadeh, an Amarillo, Tex., rheumatologist.

The rituximab nonresponder was also the only one of the six patients who did not have depressed complement levels at baseline. It's possible that this agent requires depressed complement levels in order to be effective in SLE, although that hypothesis will require further investigation, the physician noted at the meeting, which was sponsored by the European League Against Rheumatism.

VIENNA — Rituximab successfully induced remission of severe extrarenal systemic lupus erythematosus previously unresponsive to cyclophosphamide and/or mycophenolate in five of six treated patients in a small series, Constantine K. Saadeh, M.D., reported at the annual European congress of rheumatology.

Previous studies of rituximab in SLE have focused on the agent's utility in patients with refractory lupus nephritis. But in Dr. Saadeh's six-patient series, the anti-CD20 chimeric monoclonal antibody targeting mature B cells induced remission in patients with lupus skin, lung, and synovial disease.

All five responders to two 500-mg doses of rituximab given a week apart experienced disease remissions lasting at least 3 months. All five experienced a transient 2- to 3-week drop in their globulin fraction beginning roughly a week after treatment.

The sole rituximab nonresponder had mixed lupus nephritis and chronic glomerulonephritis that continued to deteriorate, requiring hemodialysis, added Dr. Saadeh, an Amarillo, Tex., rheumatologist.

The rituximab nonresponder was also the only one of the six patients who did not have depressed complement levels at baseline. It's possible that this agent requires depressed complement levels in order to be effective in SLE, although that hypothesis will require further investigation, the physician noted at the meeting, which was sponsored by the European League Against Rheumatism.

A combination of oral methotrexate and pulsed high-dose corticosteroids significantly improved the visible inflammation in 15 adults with severe localized scleroderma, wrote Alexander Kreuter, M.D., of Ruhr-University Bochum (Germany) and his colleagues.

In a prospective, nonrandomized pilot study, nine women and six men received a weekly oral methotrexate dose of 15 mg. They also received an intravenous methylprednisolone sodium succinate dose of 1,000 mg for 3 consecutive days each month.

Patients were treated for at least 6 months, and the mean treatment duration was 9.8 months (Arch. Dermatol. 2005; 141:847–52). The two treatments have shown effectiveness against severe localized scleroderma when used separately, the researchers noted.

On average, the modified skin scores of the patients dropped significantly, from 10.9 to 5.5, and signs of improvement were visible after 2 months. In addition, the visual analog scores (VAS) for tightness improved in 12 patients. On average, the VAS for tightness decreased significantly, from 65.3 to 27.5.

Follow-up visits occurred every 4 weeks, and a modified skin score was used to assess skin involvement. Ultrasonography was performed at the end of the study to confirm the clinical improvement, and it showed a significant decrease in skin thickness between baseline and the study's end.

The patients also demonstrated significant increases in dermal density at the end of the study, and the dermal collagen structure had returned to normal or near normal levels.

The patients' ages ranged from 18 to 73 years, and the duration of illness ranged from 1 to 36 years. Prior to the study, 11 patients had been treated unsuccessfully with other methods.

Adverse effects included mild nausea and headache in three patients, diabetes mellitus in two patients, and weight gain in one patient, but these effects normalized after treatment ended. None of the patients showed signs of relapse over 6 months of follow-up.

Although the study was limited by its small size and lack of placebo controls, the favorable response and moderate side effects suggest that combination therapy for localized scleroderma merits further study and that the treatment may be effective in less severe cases as well.

A combination of oral methotrexate and pulsed high-dose corticosteroids significantly improved the visible inflammation in 15 adults with severe localized scleroderma, wrote Alexander Kreuter, M.D., of Ruhr-University Bochum (Germany) and his colleagues.

In a prospective, nonrandomized pilot study, nine women and six men received a weekly oral methotrexate dose of 15 mg. They also received an intravenous methylprednisolone sodium succinate dose of 1,000 mg for 3 consecutive days each month.

Patients were treated for at least 6 months, and the mean treatment duration was 9.8 months (Arch. Dermatol. 2005; 141:847–52). The two treatments have shown effectiveness against severe localized scleroderma when used separately, the researchers noted.

On average, the modified skin scores of the patients dropped significantly, from 10.9 to 5.5, and signs of improvement were visible after 2 months. In addition, the visual analog scores (VAS) for tightness improved in 12 patients. On average, the VAS for tightness decreased significantly, from 65.3 to 27.5.

Follow-up visits occurred every 4 weeks, and a modified skin score was used to assess skin involvement. Ultrasonography was performed at the end of the study to confirm the clinical improvement, and it showed a significant decrease in skin thickness between baseline and the study's end.

The patients also demonstrated significant increases in dermal density at the end of the study, and the dermal collagen structure had returned to normal or near normal levels.

The patients' ages ranged from 18 to 73 years, and the duration of illness ranged from 1 to 36 years. Prior to the study, 11 patients had been treated unsuccessfully with other methods.

Adverse effects included mild nausea and headache in three patients, diabetes mellitus in two patients, and weight gain in one patient, but these effects normalized after treatment ended. None of the patients showed signs of relapse over 6 months of follow-up.

Although the study was limited by its small size and lack of placebo controls, the favorable response and moderate side effects suggest that combination therapy for localized scleroderma merits further study and that the treatment may be effective in less severe cases as well.

A combination of oral methotrexate and pulsed high-dose corticosteroids significantly improved the visible inflammation in 15 adults with severe localized scleroderma, wrote Alexander Kreuter, M.D., of Ruhr-University Bochum (Germany) and his colleagues.

In a prospective, nonrandomized pilot study, nine women and six men received a weekly oral methotrexate dose of 15 mg. They also received an intravenous methylprednisolone sodium succinate dose of 1,000 mg for 3 consecutive days each month.

Patients were treated for at least 6 months, and the mean treatment duration was 9.8 months (Arch. Dermatol. 2005; 141:847–52). The two treatments have shown effectiveness against severe localized scleroderma when used separately, the researchers noted.

On average, the modified skin scores of the patients dropped significantly, from 10.9 to 5.5, and signs of improvement were visible after 2 months. In addition, the visual analog scores (VAS) for tightness improved in 12 patients. On average, the VAS for tightness decreased significantly, from 65.3 to 27.5.

Follow-up visits occurred every 4 weeks, and a modified skin score was used to assess skin involvement. Ultrasonography was performed at the end of the study to confirm the clinical improvement, and it showed a significant decrease in skin thickness between baseline and the study's end.

The patients also demonstrated significant increases in dermal density at the end of the study, and the dermal collagen structure had returned to normal or near normal levels.

The patients' ages ranged from 18 to 73 years, and the duration of illness ranged from 1 to 36 years. Prior to the study, 11 patients had been treated unsuccessfully with other methods.

Adverse effects included mild nausea and headache in three patients, diabetes mellitus in two patients, and weight gain in one patient, but these effects normalized after treatment ended. None of the patients showed signs of relapse over 6 months of follow-up.

Although the study was limited by its small size and lack of placebo controls, the favorable response and moderate side effects suggest that combination therapy for localized scleroderma merits further study and that the treatment may be effective in less severe cases as well.