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Chapter: Essentials of Psychiatry: Somatoform Disorders


The essential feature in hypochondriasis is preoccupation with fears or the idea of having a serious disease based on the “mis-interpretation of bodily symptoms”.





The essential feature in hypochondriasis is preoccupation with fears or the idea of having a serious disease based on the “mis-interpretation of bodily symptoms”. (see Table 54.1). This is in contrast to somatization disorder, conversion disorder and pain disorder, in which the symptoms themselves are the predominant focus. There was some debate in the development of DSM-IV as to whether it was necessary that a body complaint be present. On the basis of empirical data, however, it was determined that this requirement was a valid one and helped to distinguish the “disease conviction” of hypochondriasis from “disease fear” as in phobic disorder. Bodily symptoms may be interpreted broadly to include misinterpretation of normal body functions. In hypo-chondriasis, the preoccupation persists despite reassurance from physicians and the accumulation of evidence to the contrary. As in the other somatoform disorders, symptoms must result in clinically significant distress or impairment in important areas of functioning. The duration must be at least 6 months. Hypochon-driasis is not diagnosed if the hypochondriacal concerns are bet-ter accounted for by another psychiatric disorder, such as major depressive episodes or various psychotic disorders with somatic delusions.


Throughout the modern period, there has been contro-versy as to whether hypochondriasis represented an independent, discrete disease entity. Some maintain that hypochondriasis is virtually always secondary to another psychiatric disorder, usu-ally depression. A number of studies suggested that of the many patients with hypochondriacal complaints, few meet criteria for the full diagnosis. Moreover, the lack of bimodality to the com-plaints suggests a continuum rather than a discrete entity.


In the development of DSM-IV, owing to observations that the disease conviction resembled disease phobia or the incorrigi-ble ideas of obsessive–compulsive disorder, placement of hypo-chondriasis with the anxiety disorders was considered. Similarly, a case can be made that disease conviction is on a continuum with somatic delusions of disease, suggesting inclusion with the delu-sional disorders. In the end, such considerations were resolved by keeping hypochondriasis with the somatoform disorders, de-fining it in terms of an idea that one already has a particular ill-ness rather than fears of acquiring one to distinguish it from a disease phobia, and by excluding cases in which the idea was of delusional proportions to differentiate hypochondriasis from delusional disorder, somatic type.




Some degree of preoccupation with disease is apparently com-mon. As reviewed by Kellner (1991), 10 to 20% of “normal” and 45% of “neurotic” persons have intermittent unfounded worries about illness, with 9% of patients doubting reassurances given by physicians. Kellner also estimated that 50% of all patients attend-ing physicians’ offices “suffer either primary hypochondriacal symptoms or have minor somatic disorders with hypochondriacal overlay”. How these relate to hypochondriasis as a disorder is difficult to assess because these estimates do not appear to dis-tinguish between a focus on the symptoms themselves (as in somatization disorder) and preoccupation with the implications of the symptoms (as in hypochondriasis). The Epidemiological Catchment Area study (Robins et al., 1984) did not consider hy-pochondriasis. A 1965 study reported prevalence figures ranging from 3 to 13% in different cultures, but it is not clear whether this represents a syndrome comparable to the current definition or just hypochondriacal symptoms. As already noted, many pa-tients manifest some hypochondriacal symptoms as part of other psychiatric disorders, and others have transient hypochondriacal symptoms in response to stresses such as serious physical illness yet never fulfill the inclusion criteria for DSM-IV hypochondria-sis. Assessment of the incidence and prevalence of hypochondria-sis undoubtedly requires study of general or primary care rather than psychiatric populations, because patients with hypochon-driasis are convinced that they suffer from some physical illness. To date, study of such populations suggests that 4 to 9% of pa-tients in general medical settings suffer from hypochondriasis.


It does appear that hypochondriasis is equally common in males and females.


Etiology and Pathophysiology


Until recently, psychoanalytic hypotheses of etiology predomi-nated. Freud hypothesized that hypochondriasis represented “the return of object libido onto the ego with cathexis of the body” (Viederman, 1985). Subsequently, the cathexis to the body hy-pothesis was elaborated on to include interpretations involving disturbed object relations – displacement of repressed hostility to the body to communicate anger indirectly to others. Dynamic mechanisms involving masochism, guilt, conflicted dependency needs and a need to suffer and be loved at the same time have also been suggested (Stoudemire, 1988). The presence of such “narcissistic” mechanisms has been suggested as the reason that patients with hypochondriasis were “unanalyzable”. Other psy-chological theories involve defense against feelings of low self-esteem and inadequacy, perceptual and cognitive abnormalities, and operant conditioning involving reinforcement for assump-tion of the sick role.


Biological theories have been suggested as well. Hypo-chondriacal ideas have been attributed to a hypervigilance to insult, including overperception of physical problems. This has been posited in particular in reference to hypochondriasis as an aspect of depression or anxiety disorders. Hypochondriasis has been included by some in the posited obsessive–compulsive spectrum disorders along with obsessive–compulsive and body dysmorphic disorders, anorexia nervosa, Tourette’s disorder, tri-chotillomania, pathological gambling and other impulsive disor-ders. All these disorders involve repetitive thoughts or behaviors that patients are unable to delay or inhibit without great difficulty. Evidence for this clustering includes observations of clinical im-provement with SSRIs such as fluoxetine even in nondepressed patients with hypochondriasis, body dysmorphic disorder, obses-sive–compulsive disorder and anorexia nervosa. Because such a response is not evident with nonSSRI antidepressants, some type of common serotonin dysregulation is suggested for these disorders.


Diagnosis and Differential Diagnosis


As shown in Figure 54.1, the first step in approaching patients with distressing or impairing preoccupation with or fears of having a serious disease is to exclude the possibility of explanation on the basis of a general medical condition. Fears that may seem excessive may also occur in patients with general medical conditions with vague and subjective symptoms early in their disease course. These include neurological diseases, such as myasthenia gravis and multiple scle-rosis; endocrine diseases; systemic diseases that affect several organ systems, such as systemic lupus erythematosus; and occult malignant neoplasms. The disease conviction of hypochondriasis may actually be less amenable to medical reassurance than the fears of patients, with general medical illnesses, who may at least temporally accept such encouragement. Hypochondriacal complaints are not often in-tentionally produced such that differentiation from malingering and factitious disorder is seldom a problem.


Exclusion is made if the preoccupation is better accounted for by another psychiatric disorder. DSM-IV lists generalized anxiety disorder, obsessive–compulsive disorder, panic disorder, a major depressive episode, separation anxiety, or another so-matoform disorder as candidates. Chronology will be of utmost importance in such discriminations. Hypochondriacal concerns occurring exclusively during episodes of another disturbance, such as an anxiety or depressive disorder, do not warrant an ad-ditional diagnosis of hypochondriasis. The presence of other psy-chiatric symptoms will also be helpful. For example, a patient with hypochondriacal complaints as part of a major depressive episode will show other symptoms of depression, such as sleep and appetite disturbance, feelings of worthlessness and self-reproach, although depressed elderly patients may deny sadness or other expressions of depressed mood. A confounding factor is that patients with hypochondriasis often have comorbid anxiety or depressive syndromes. Again, characterizing the symptoms by chronology will be useful. Treatment trials may also have diag-nostic significance. Depressed patients who are hypochondriacal may respond to nonSSRI antidepressant medications or elec-troconvulsive therapy (often necessary to reverse a depressive state of sufficient severity to lead to such profound symptoms), with resolution of the hypochondriacal as well as the depressive symptoms.


Hypochondriasis is differentiated from other somatoform disorders such as pain, conversion and somatization disorders by its predominant feature of preoccupation with and fears of having an underlying illness based on the misinterpretation of body symptoms, rather than the physical symptoms themselves. Patients with these other somatoform disorders at times are con-cerned with the possibility of underlying illness, but this will gen-erally be overshadowed by a focus on the symptoms themselves.


The next consideration is whether the belief is of delu-sional proportions. Patients with hypochondriasis, although preoccupied, generally acknowledge the possibility that their concerns are unfounded. Delusional patients do not. Somatic de-lusions of serious illness are seen in some cases of schizophrenia and in delusional disorder, somatic type. In general, patients with schizophrenia that have such delusions also show other signs of schizophrenia, such as disorganized speech, peculiarities of thought and behavior, hallucinations and other delusions. Belief that an underlying illness is being caused by some bizarre proc-ess may also be seen (e.g., “I’m trying not to defecate because it will cause my brain to turn to jelly”). Schizophrenic patients may also show improvement with neuroleptic treatment, at least in the “active” symptoms of their illness, under which somatic delusions are included.


Differentiation from delusional disorder, somatic type, may be more difficult. It is often a thin line between preoccupation and fear that is a conviction and that which is a delusion. Often, the distinction is made on the basis of whether the patient can consider the possibility that the conviction is erroneous. Yet, patients with hypochondriasis vary in the extent to which they can do this. DSM-IV acknowledges this by its inclusion of the specifier with poor insight. In the past, some argued that differ-entiation could be made on the basis of response to neuroleptics, especially pimozide; patients with delusional disorder, but not hypochondriasis, respond.


If it is concluded that the preoccupations are not delusional, the next consideration is whether the duration requirement of 6 months has been met (see Figure 54.1). Syndromes of less than 6 months’ duration are diagnosed under either somatoform dis-order NOS or adjustment disorder if the symptoms are an abnor-mal response to a stressful life event. The reason to make such a distinction is to distinguish hypochondriasis from transient syn-dromes, the longitudinal course of which have been shown to be more variable, suggesting heterogeneity.


Other diagnostic considerations include whether the pre-occupations or fears are restricted to preoccupations with being overweight, as in anorexia nervosa; with the inappropriateness of one’s sex characteristics, as in a gender identity disorder; or with defects in appearance, as in body dysmorphic disorder. The pre-occupations of hypochondriasis resemble the obsessions, and the health checking and efforts to obtain reassurance resemble the compulsions of obsessive–compulsive disorder. However, if such manifestations are health centered only, obsessive–compulsive disorder is not diagnosed. If, on the other hand, nonhealth related obsessions and compulsions are present, obsessive–compulsive disorder may be diagnosed in addition to hypochondriasis.


Course, Natural History and Prognosis


Data are conflicting, but it appears that the most common age at onset is in early adulthood. Available data suggest that approxi-mately 25% of patients with a diagnosis of hypochondriasis do poorly, 65% show a chronic but fluctuating course and 10% re-cover. This pertains to the full syndrome. A much more variable course is seen in patients with just some hypochondriacal con-cerns. It appears that acute onset, absence of a personality disor-der and absence of secondary gain are favorable prognostically.




Until recently, it appeared that patients with hypochondriasis as a primary condition benefited, but only modestly, from psychiatric intervention. Patients referred early for psychiatric evaluation and treatment showed a slightly better prognosis than those continu-ing with only medical evaluations and treatments. Of course, the first step in treatment is getting the patient to a psychiatrist. Pa-tients with hypochondriasis generally present initially to nonpsy-chiatric physicians and are often reluctant to see a psychiatrist. Referral should be done sensitively, with the referring physician stressing to the patient that his or her distress is real and that psy-chiatric evaluation will be a supplement to, not a replacement for, continued medical care.


Initially, the generic techniques outlined for the somato-form disorders in general should be followed. However, it has not been demonstrated that a specific psychotherapy for hypo-chondriasis is available. Dynamic psychotherapy is of minimal effectiveness; supportive–educative psychotherapy is only some-what helpful, and primarily for those with syndromes of less than 3 years’ duration; and cognitive–behavioral therapy, especially response prevention of checking rituals and reassurance seeking, is of only moderate effectiveness at best. All of these techniques seem to lack definitive effects on hypochondriasis itself.


Until recently, this could also be said of pharmacological approaches. Pharmacotherapy of comorbid depressive or anxiety syndromes was often effective, and control of such syndromes aided in general management, yet hypochondriasis itself was not ameliorated. Although controlled trials are lacking, anecdotal and open-label studies suggest that serotoninergic agents such as clomipramine and the SSRI fluoxetine may be effective in amel-iorating hypochondriasis. Similar effects are expected from the other SSRIs. Response to fluoxetine has been reported with doses recommended for obsessive–compulsive disorder, rather than usual antidepressant doses (i.e., 60–80 mg rather than 20–40 mg/ day). Such pharmacotherapy is best combined with the generic psychotherapy recommendations for somatoform disorders, as well as with cognitive–behavioral techniques to disrupt the coun-terproductive checking and reassurance-seeking behaviors.

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