Bodies are not perfect. But the extent to which individuals attend to their own perceived imperfections varies greatly. The variability of this focused attention on specific aspects of the body depends on many factors about which not a great deal is known. Until recently, excessive preoccupation with the appearance of the body or parts of the body was regarded as a special monosymptomatic form of hypochondriasis, referred to as dysmorphophobia. Ladee (1966) referred to it as beauty-hypochondriasis, in which “the self-detested body image in fancied deformity…no mirror and no surgeon can correct”.
Description and Classification
Recognized more than a century ago as an emotional disturbance, sometimes delusional and sometimes not, dysmorphophobia was most often regarded as an obsessive or compulsive reaction to imagined ugliness. Perhaps the most well-known case has been Freud’s Wolf Man, whose compulsive neurosis expanded into a delusional belief about swelling, scarring, and perforation of his nose, related through psychoanalysis to identification with his mother and the presence of a wart on her nose. Another case that challenges diagnostic precision is that of Charles Darwin, whose preoccupation with his hands and lips might have justified the diagnosis of dysmorphophobia, although his pansymptomatology also evoked other diagnoses of somatization, hypochondriasis, and even irritable bowel syndrome.
More recent observers noted that fear is less a factor than obsession in this preoccupation with defectiveness. The disorder that had been described as monosymptomatic hypochondriasis before 1980 included conditions such as parasitosis, or a fear of worm infestation; dysmorphophobia, or obsessional concerns about ugliness or deformity of the body; and bromosis, or fear of emitting foul body odors. Confusion of terminology has hampered treatment decisions.
In 1980, dysmorphophobia was classified as an atypical somatoform disorder; in ICD-10 (World Health Organization 1992), however, it was included under hypochondriacal disorder. Because phobia did not always appear as part of the syndrome, it was renamed body dysmorphic disorder in DSM-III-R and was defined as a preoccupation with some imagined defect in appearance in a normal-appearing person or a grossly excessive concern in the presence of some slight physical anomaly. The DSM-IV criteria for body dysmorphic disorder are listed in
Table 61-2. The continuing difficulty in distinguishing this condition from a true delusional disorder has given rise to much discussion and controversy as to whether more delusional forms are part of the same disorder or merely variants on a single continuum of pathological disorder that also includes eating disorders. Some authors have called attention to the criteria common to obsessive-compulsive disorder, delusional disorder, and body dysmorphic disorder and have called for further studies of these overlaps.
When delusional intensity is detected, as in parasitosis or bromosis, the condition is classified as delusional disorder, somatic subtype. In the current DSM-IV classification, other body image disturbances, such as those accompanying anorexia nervosa or transsexualism, are excluded from the diagnosis.
Further confounding the picture are those instances of pathological self-observation that occur in the presence of detectable peripheral or central neural lesions. The neurologist Schilder (1935/1950) recognized that one’s image of the human body was much more than the picture that was cast on the retina of the eye. He wrote, “The image of the human body means the picture of our own body which we form in our mind, that is to say, the way in which the body appears to ourselves”. In other words, beauty is in the eye of the beholder. Like Freud, Schilder recognized both conscious and unconscious determinants. Freud had said that “the ego is first and foremost a bodily ego…not merely a surface entity, but is itself the projection of a surface”.
Self-perception and identity are inextricably bound to one’s experience of one’s own body. Developmental flaws in the ego can readily predispose one to vulnerabilities in perceptual distortion. One’s personal definition of ugliness is shaped by internal and external forces; cultural views of stature, hair configuration, body shape, and similar features will conspire with one’s self-assessment born of shame, guilt, fear, sexuality, and so on. Other confounding factors include dissociative states, conversion disorder, obsessive-compulsive features, or even developmentally appropriate concern over one’s looks and dress. Perception of one’s body also is affected by personality factors, psychological defenses (e.g., denial), premorbid states, idiosyncratic meanings attributed to the body and its parts, and the effect of individual experience. It is this personalized definition of ugliness that underlies an exaggerated sense of defectiveness about some aspect of one’s own being. Why one person should become obsessed with a sense of defectiveness about one specific body part that is of little or no consequence to another is of clinical and scholarly interest to psychoanalysts and psychologists. Many volumes about body image and the psychological aspects of appearance and dress are available to the interested reader.
Clinical Presentation and Etiology
In body dysmorphic disorder, the focus of concern is most commonly the face: the shape of the nose, mouth, or jaw and the presence or distribution of hair. Less commonly, the concern is about the feet, hands, breasts, back, or other body parts, including erogenous areas. Although shame and embarrassment often keep individuals with this disorder from registering their concerns or seeking help, they often do seek help from plastic surgeons in the form of reconstructive intervention. Others may attempt to alter their appearance through self-administered cosmetics, clothing, or hairstyle; some may request dental or electrolytic treatments.
The literature reveals ongoing controversy over the positive and negative results of surgical efforts to ameliorate perception of bodily ugliness through reconstructive techniques, although there is a dearth of controlled studies to support either viewpoint. Plastic surgeons report cases in which surgical correction appeared to improve self-image, whereas psychiatrists and psychologists address the risks that are apt to accompany purely cosmetic changes. Nonetheless, increased sophistication and screening by surgeons, combined with psychiatrists’ greater interest in this previously neglected disorder, have resulted in increased attention and improved diagnosis. The social withdrawal often accompanying this condition may have resulted in its previous description as a phobic disorder.
Body dysmorphic disorder has been associated with depression, schizophrenia, obsessive-compulsive disorder, personality disorder, psychosis, social phobia, and anxiety. Although no causal links have been established, awareness of comorbidity is essential for accurate diagnosis and appropriate treatment selection.
The etiology of body dysmorphic disorder is poorly understood, but authors of some studies have suggested that fixation on “defective” body parts may be an individual’s defense against more overwhelming anxiety. For example, discomfort with social or sexual function may be rationalized by shyness secondary to physical defectiveness. Results of psychoanalytic studies call attention to mechanisms, such as displacement, that divert anxiety-producing attention from one area of sensitive concern to another of less intensity. Feelings of inferiority, poor self-image, and guilt may be assuaged by the circumscribed attribution of “badness” to one specific bodily area or part. Identification with meaningful objects is sometimes revealed through the body part selected, as in the case of the Wolf Man described earlier in this chapter. Ambivalently experienced sexual impulses may be renounced by a self-perception of ugliness. Early interpersonal experiences (e.g., teasing, criticism, rejection) may establish points of bodily fixation on which subsequent disappointments are layered; the old adage that “sticks and stones will break my bones, but names will never hurt me” is probably invalid.
The complex etiology and comorbidity associated with body dysmorphic disorder require that therapeutic interventions be flexible and eclectic. Careful selection from a variety of treatments (e.g., psychotherapy, pharmacotherapy, cognitive-behavioral approaches, surgical intervention) is based on a thorough biopsychosocial assessment of the patient.
When depression is present, a trial of antidepressant medication is warranted. It is not always clear whether depression precedes or follows the onset of body dysmorphic disorder, and the presence of depression does not necessarily ensure that antidepressants will produce beneficial results. In fact, in their review of the treatment history of 30 patients with body dysmorphic disorder, Phillips et al. (1993) suggested that the most consistently beneficial medications were the serotonin reuptake inhibitors clomipramine and fluoxetine; no remission occurred with monoamine oxidase inhibitors (although one patient improved partially with the addition of amitriptyline) or with drugs other than clomipramine, bupropion, trazodone, or lithium. On the basis of treatment results of their 30 patients, the investigators concluded that major depression was the mood disorder most frequently associated with body dysmorphic disorder and that obsessive-compulsive disorder and social phobia often coexist with this rare condition. It is of interest that the two most effective antidepressants in body dysmorphic disorder - fluoxetine and clomipramine - are also known to have beneficial results in obsessive-compulsive disorder. Serotonin reuptake inhibitors, even in the absence of diagnosable depression, are considered the first line of treatment by several researchers, although other authors have suggested that tricyclic antidepressants and tranylcypromine can be effective. When social anxiety disorder accompanies body dysmorphic disorder, pharmacological treatment must be selected on the basis of history, patient tolerance, adverse side-effect profile, and so on. With treatment-refractory cases, combinations of selective serotonin reuptake inhibitors and augmenting agents such as buspirone or antipsychotics may be effective. Because all results to date are based on open drug trials, confirmatory data await controlled studies.
In those forms of body dysmorphic disorder that appear more delusional or psychotic, antipsychotics sometimes may be effective, although they often do not bring about remission and may actually cause worsening of symptoms. Pimozide, reported by Riding and Munro (1975) to be useful in monosymptomatic hypochondriacal disorder, had minimal effect.
Psychotherapy was tried in 24 of the 30 patients in the study by Phillips et al. (1993), with only an 8% incidence of slight improvement. The nature and duration of the therapy were unclear from the study report, but therapy is usually supportive in this population of relatively non-psychologically minded patients. The challenge of treating these patients is intensified by their tendency to request help late, keep their distress secret, and resist psychological types of treatment. In Phillips et al.‘s (1993) sample, 73% had sought surgical or dental intervention and 80% of these patients were judged to be worse following the latter types of treatment.
Treatment with electroconvulsive therapy has proven ineffective, and treatment with benzodiazepines resulted in remission in only one patient. Fishbain (1991) recommended that treatment for body dysmorphic disorder begin with either pimozide or clomipramine, depending on the prominence of either psychotic or depressive content. If that agent is not effective, Fishbain recommended, based solely on the literature of psychopharmacological treatment, trying haloperidol, then clomipramine (for those in whom pimozide was tried first), fluoxetine, and finally doxepin, other tricyclic antidepressants, or a monoamine oxidase inhibitor (e.g., tranylcypromine); no studies on the effectiveness of this sequential treatment have been reported.
Recent reports on the treatment of body dysmorphic disorder with cognitive-behavioral therapy models, including a pilot randomized controlled trial, offer promise, with evidence that patients receiving cognitive-behavioral therapy for comorbid social anxiety disorder may have lower rates of relapse in the long term. One study reported success in a small number of patients (n = 10) treated with a standard behavior therapy protocol consisting of exposure (in vivo and imaginal) and response prevention. Half of the patients were then assigned to a biweekly structured maintenance program, with the other half serving as the control group. Although both groups remained symptom free at follow-up, only those in the maintenance program continued to improve on measures of avoidance, body dysmorphic disorder symptoms, depression, and anxiety.
Although dysmorphophobia was originally described more than 100 years ago, diagnostic criteria for the disorder have been unclear. Therefore, treatment has been poorly described. With efforts at improved and standardized diagnosis since publication of DSM-III, along with the development of improved pharmacological agents, it is anticipated that treatment trials will increase in this heretofore neglected disorder. In time, controlled studies will shed more light on this curious and fascinating disorder. The importance of correct diagnosis in preventing unnecessary and sometimes harmful treatments cannot be overemphasized.
Both hypochondriasis and body dysmorphic disorder are somatoform disorders characterized by fear or a conviction of serious disease (in hypochondriasis) or body deformity (in body dysmorphic disorder). Earliest reports of both disorders are centuries old, but past treatments have been elusive or ineffective. Improved classification and diagnosis have shed light on the phenomenology of these conditions, thereby permitting a broader approach to therapeutic trials. These include the use of behavioral and cognitive techniques with the objective of converting maladaptive reactions and behaviors to effective coping methods and the introduction of new psychopharmacological agents (e.g., selective serotonin reuptake inhibitors) that show promise in decreasing somatic symptomatology, especially when it accompanies primary depression, anxiety, panic, and obsessive-compulsive disorders. Findings to date have been only empirical, anecdotal, and suggestive and await further rigorously controlled studies for verification.
Current innovations in the physician’s therapeutic armamentarium are heartening, and their use must be assessed within the context of a therapeutic patient-physician relationship that is available, supportive, empathic, understanding, reliable, and trustworthy if the benefits of these new treatments are to be optimized. An appreciation of the psychodynamics of interpersonal relationships allows the therapeutic interaction to be used to enhance personal growth and to improve quality of life and adaptation to stress.
Revision date: June 14, 2011
Last revised: by Janet A. Staessen, MD, PhD