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Psychiatry > Psychosomatic
Hypochondriasis
Article Last Updated: Nov 20, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11
Author: Glen L Xiong, MD, Assistant Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California Davis School of Medicine; Attending Psychiatrist, Sacramento Mental Health Treatment Center; Consulting Staff, Sacramento County Primary Care Clinic
Glen L Xiong is a member of the following medical societies: American Association for Geriatric Psychiatry, American College of Physicians, American Medical Association, American Psychiatric Association, and Sierra Sacramento Valley Medical Society
Coauthor(s):
James A Bourgeois, OD, MD, Alan Stoudemire Professor of Psychosomatic Medicine, Department of Psychiatry, University of California at Davis;
Shayna L Marks, BA, MA, Graduate Assistant, Department of Psychology and Social Behavior Consortium for Integrative Health Studies, University of California Irvine, School of Social Ecology;
Dandan Liu, BA, Student Researcher for Dr. Ladson Hinton, University of California Davis School of Medicine;
Celia H Chang, MD, Associate Health Sciences Clinical Professor, Department of Neurology, University of California at Davis;
Peter M Yellowlees, MD, Professor of Psychiatry, Associate Director, Center for Health and Technology, Director of Academic Information Systems, University of California at Davis;
Donald M Hilty, MD, Associate Professor and Vice-Chair of Faculty Development, Department of Psychiatry and Behavioral Science, University of California at Davis
Editors: Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine; Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin; Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Author and Editor Disclosure
Synonyms and related keywords:
somatoform disorders, body dysmorphic disorder, BDD, depressive disorders, anxiety disorders, obsessive-compulsive disorder, OCD, obsessive compulsive disorder, anorexia nervosa, Tourette disorder, Tourette syndrome, Tourette's syndrome, impulsivity disorders, trichotillomania, neurochemical deficits, selective serotonin reuptake inhibitors, SSRIs, neurasthenia, chronic fatigue syndrome, CFS, hypochondriacs, malingering, hypochondriacal behavior, hypochondriacal disorder, hypochondriacal episodes
Background
Hypochondriasis and the other somatoform disorders are among the most difficult and most complex psychiatric disorders to treat in the general medical setting. On the basis of many new developments in this field, diagnostic criteria have been revised to facilitate clinical care and research. Long-awaited randomized, placebo-controlled treatment approaches have finally emerged. As with all psychiatric disorders, the somatoform disorders demand creative, rich biopsychosocial treatment planning by a team that includes primary care physicians, subspecialists, and mental health professionals.
This article describes hypochondriasis, its diagnosis, and an overview of treatment approaches, with references for details beyond the scope of the article. Finally, the article reviews new developments in psychopharmacologic and psychotherapeutic treatments.
Pathophysiology
Neurochemical deficits associated with hypochondriasis and some other somatoform disorders (eg, somatization, conversion, and body dysmorphic disorders) appear similar to those of mood and anxiety disorders. For example, Hollander et al posited an "obsessive-compulsive spectrum" to include obsessive-compulsive disorder (OCD), body dysmorphic disorder (BDD), anorexia nervosa, Tourette syndrome, and impulse control disorders (eg, trichotillomania, pathological gambling).1 This formulation of obsessive-compulsive (OC) spectrum disorders, while not a part of the consensus psychiatric diagnostic and classification literature, crosses boundaries of several diagnostic categories in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision (DSM-IV-TR). In addition, encountering a patient with more than one of the anxiety spectrum disorders during his or her life is not unusual. Although findings of studies of these neurochemical deficits are only preliminary, such deficits may explain why symptoms overlap, why the disorders are commonly comorbid, and why effective treatments parallel one another (eg, selective serotonin reuptake inhibitors [SSRIs]).
Frequency
United States
The prevalence rates for primary hypochondriasis in the primary care setting are 0.8-4.5%.2 Some degree of preoccupation with disease is apparently common, because 10-20% of people who are healthy and 45% of people without a major psychiatric disorder have intermittent unfounded worries about illness.3
International
International rates are similar to those in the United States.4
Mortality/Morbidity
Hypochondriasis is usually episodic, with hypochondriacal symptoms that last from months to years and equally long quiescent periods. Although formal outcome studies have not been conducted, one third of patients with hypochondriasis are believed to eventually improve significantly. A good prognosis appears to be associated with high socioeconomic status, treatment-responsive anxiety or depression, the absence of a personality disorder, and the absence of a related nonpsychiatric medical condition. Most children are believed to recover by adolescence or early adulthood, but empiric studies have not been carried out. Epidemiological studies are lacking, but patients with hypochondriasis appear similar to those with somatization disorder. These individuals use medical care at high rates, making frequent visits to the emergency department, the doctor, and other health care providers and undergoing frequent physical examinations, laboratory testing, and other costly, invasive, and potentially dangerous procedures.5
Cognitive, social learning, and psychodynamic theories imply that patients have significant psychosocial disturbances in terms of relationship, vocational, and other endeavors. Exacerbations may occur with psychological stressors and in patients with comorbid psychiatric conditions. These high-use patterns differ dramatically from those of nonsomatizing patients and remain true even when comorbid medical conditions and sociodemographic differences are accounted for.6 The medically unexplained complaint is often a symptom of hypochondriasis7 and may well be a presentation of associated abnormal illness behavior8.
Patients with hypochondriasis have a high rate of psychiatric comorbidity.9 In one general medical outpatient clinic, 88% of patients with hypochondriasis had one or more concurrent psychiatric disorders, the most common being generalized anxiety disorder (71%), dysthymic disorder (45.2%), major depression (42.9%), somatization disorder (21.4%), and panic disorder (16.7%). These patients are 3 times more likely to have a personality disorder than the general population.9 Substance abuse or dependence is also a serious comorbid condition, particularly use of benzodiazepines, though epidemiological studies have not assessed the exact frequency of this problem.
Race
This disorder has not been well studied with respect to race and ethnicity. More information is needed, too, with regard to its relationship to other medical disorders needing better definition (eg, neurasthenia, chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivity syndrome).
Sex
Hypochondriasis appears to occur equally in men and women.
Age
Hypochondriasis can begin at any age, but the most common age of onset is early adulthood.
History
Hypochondriasis is classified as one of the somatoform disorders, a class that was formulated to accommodate the differential diagnosis of disorders characterized primarily by physical symptoms for which no demonstrable organic findings exist. The DSM-IV-TR stipulates that the symptoms are not under voluntary control (thus excluding malingering and factitious disorders) and are not fully explained by known physiological causes (excluding psychological factors affecting the medical condition). The disorders in the somatoform class include somatization disorder, conversion disorder, pain disorder, hypochondriasis, BDD, and undifferentiated somatoform disorder.
- The core feature of hypochondriasis is not preoccupation with symptoms themselves, but rather the fear or idea of having a serious disease (see Image 1). The fear or idea is based on the misinterpretation of bodily signs and sensations as evidence of disease. The illness persists despite appropriate medical evaluations and reassurance.
- The diagnosis should be considered strongly if the patient has a history of hypochondriasis (or other somatization disorder) or has had multiple nonproductive clinical workups, and if the patient's complaints are markedly inconsistent with objective findings or the examination yields no abnormal findings. Further psychiatric history should be obtained with regard to a history of hypochondriasis (or corresponding behaviors) in family members or a sudden, unexplained loss of function that spontaneously resolved.
- Diagnostic criteria for hypochondriasis include the following (DSM-IV-TR):
- The patient has a preoccupying fear of having a serious disease.
- The preoccupation persists despite appropriate medical evaluation and reassurance.
- The belief is not of delusional intensity (as in delusional disorder, somatic type) and is not restricted to a concern about appearance (as in persons with BDD).
- The preoccupation causes clinically significant distress or impairment.
- The preoccupation lasts for at least 6 months.
- The preoccupation is not explained better by another mood, anxiety, or somatoform disorder.
Physical
The absence of physical findings, particularly after serial examinations, supports the diagnosis of hypochondriasis. However, the patient must receive a physical examination to make the psychiatric intervention possible. A mental status examination complements the physical examination. - General appearance, behavior, and speech
- Modestly or well groomed, not grossly disheveled
- Cooperative with the examiner, yet ill at ease and not easily reassured
- Possible signs of anxiety, including moist hands, perspiring forehead, strained/tremulous voice, and wide eyes and intense eye contact
- Psychomotor status
- Restlessness
- Frequent shifts in posture
- Agitation
- Slowed, if sleeping poorly
- Mood (the pervasive and sustained emotion that colors the patient's perception of the world) and affect (what the examiner observes)
- Anxious or worried, depressed, or futile mood
- Restricted, shallow, fearful, or anxious affect, with fluctuations and limited depth
- Thought process
- Spontaneous speaking with occasional abrupt changes in topic within an underlying theme
- Circumstantial, scattered at times
- Responds to questions but may divert to next worry or revert to an already expressed concern despite reassurance to the contrary
- No latency unless also depressed
- No thought blocking or looseness of associations
- Concrete focus of thought, but with capacity to abstract in a number of areas when encouraged or tested
- May appear distractible and yet can concentrate independently and with encouragement
- Thought content
- Preoccupation with being ill
- Anxious themes concerning what in the body is wrong, how it is wrong, and how it is experienced
- May have guilt, which is not usually linked to the preoccupations
- May have feelings of despair and/or hopelessness, although these are not usually of significant depth unless little relief has come from seeing multiple providers and/or the patient concurrently depressed
- Catastrophizing tendencies (focused on dire consequences of various symptoms and obtaining more diagnostic testing)
- Uninterested in revealing other aspects of daily functioning or general lifestyle topics at length
- Inflexibility regarding bodily concerns, but only rarely to the point of a delusion (ie, fixed, false belief), and if so, limited to somatic complaints rather than grandiose or persecutory complaints
- No suicidal ideation, unless concurrently depressed
- No homicidal ideation
- Cognitive function
- Attentive
- Oriented fully to time, place, and person
- Rare difficulties with concentration, memory, and other faculties, but functions in the normative range with refocusing and encouragement
- May have some deficits if concurrently depressed; these also tend to be overcome in response to encouragement
- Interestingly, may have selective attention (eg, the patient is distressed by an ongoing bodily complaint but not by a newly sprained ankle)
- Insight
- Able to recognize bodily sensations
- Lacking full understanding of underlying psychological concerns and how they underpin development and maintenance of bodily complaints; tends to see the "trees" rather than the "forest"
- Some awareness of own feelings about people and events, but not always with the ability to translate that into action, sustained change in mood, or lessening of preoccupations
- Judgment
- Capable of social greetings and other behaviors
- Persistence in discussing and evaluating continuing preoccupations (due to limited insight)
- May be impaired if concurrently depressed
Causes
Developmental and other predisposing factors (see Image 2) consistently indicate the importance of parental attitudes toward disease, previous experience with physical disease, and culturally acquired attitudes relevant to the etiology of the disorder.10 Overall however, few demographic and clinical differences have been found between patients with hypochondriasis and the general population. Social position, education level, and marital status do not appear to be factors in this condition.
- A cognitive model of hypochondriasis suggests that patients misinterpret bodily symptoms by augmenting and amplifying their somatic sensations. Patients also appear to have lower-than-usual thresholds for, and tolerance of, physical discomfort. For example, what most people normally perceive as abdominal pressure, patients with hypochondriasis experience as abdominal pain. When they do sustain an injury (eg, ankle sprain), it is experienced with significant anxiety and is taken as confirmation of their worry about being ill. This may be due to a tendency among patients with hypochondriasis to exaggerate their assessment of vulnerability to disease and their appraisal of the risk of serious illness.6
- The social learning theory frames hypochondriasis as a request for admission to the sick role made by a person facing seemingly insurmountable and insolvable problems. This role may allow them to avoid noxious obligations, postpone unwelcome challenges, and be relieved from duties and obligations.11
- The psychodynamic theory implies that aggressive and hostile wishes toward others are transferred via repression and displacement into physical complaints. The hypochondriacal symptoms serve to "undo" guilt felt about the anger and serve as a punishment for being "bad."
- Neurochemical deficits with hypochondriasis and some other somatoform disorders (eg, BDD) appear similar to those of depressive and anxiety disorders. For example, in 1992, Hollander et al posited an obsessive-compulsive spectrum that includes OCD, BDD, anorexia nervosa, Tourette syndrome, and impulse control disorders (eg, trichotillomania, pathological gambling). Although only preliminary data have been reported on these neurochemical deficits, such deficits may explain why symptoms overlap, why the disorders are commonly comorbid, and why treatments may parallel one another (eg, SSRIs).
Anxiety Disorders
Body Dysmorphic Disorder
Conversion Disorders
Delusional Disorder
Depression
Personality Disorders
Schizophrenia
Somatoform Disorders
Other Problems to be Considered
Physical disease must be excluded, which involves evaluation for an extensive number of neurological (eg, myasthenia gravis, multiple sclerosis), endocrinological, and other systemic diseases. The psychiatric differential diagnosis for hypochondriasis includes other somatoform, mood, anxiety, and psychotic disorders. Somatization disorder This disorder is characterized by early onset (<30 y) and recurrent, multiple, physical complaints that result in medical attention or significant impairment. Somatization disorder is best thought of as preoccupation with numerous and/or sequential symptoms, not an underlying explanatory illness. The symptoms must meet a specific pattern to be classified as a somatization disorder, including 4 different sites of pain, 2 different gastrointestinal symptoms, 1 sexual or reproductive symptom other than pain, and 1 neurologic symptom. Somatization disorder is distinguished from physical illness by the involvement of multiple organ systems and a prolonged course without the development of findings consistent with somatic illness. Onset of somatization disorder may be earlier than that of hypochondriasis (eg, <15 y in >50% of cases). Females have a higher lifetime risk of developing somatization disorder, at 2-3%, and the female-to-male ratio is 10:1.12 What differentiates somatization disorder is the patient's focus on symptoms rather than a preoccupation with illness and the accompanying worry. Somatoform pain disorder Patients with pain disorder focus on pain rather than illness more broadly. The 2 types of pain disorders are with (1) psychological factors alone and (2) psychological factors that exacerbate an associated general medical condition. However, pain disorders may have more in common with hypochondriasis than is apparent at first glance because activity induced in the nociceptor and nociceptive pathways may be activated by a psychological state, physical state, or both in combination. Diagnostic criteria include pain in one or more anatomical sites. The pain causes clinically significant distress or impairment. Psychological factors have an important role in the onset, severity, exacerbation, or maintenance of the pain. Conversion disorder This disorder is characterized by a symptom that indicates a deficit of voluntary motor or sensory function (other than pain) and is not explained by a neurological or other general medical condition, the effects of a substance, or a culturally sanctioned experience. These patients do not have a general sense of being ill or concerns about serious disease indicated by pseudoneurological symptoms and, indeed, may have a noticeable lack of worry even about their presenting symptom. Common symptom presentations include impaired coordination, paralysis or weakness, tremor, difficulty swallowing, loss of pain or touch sensation, double vision, seizure, or blindness. Conversion disorder is also more common in females, with female-to-male ratios varying from 2:1 to 10:1.13, 14 Body dysmorphic disorder The essential feature of BDD is a preoccupation with some imagined defect in appearance or a markedly excessive concern with a minor physical anomaly. Complaints include preoccupations with the face, head, hair, skin, genitals, breasts, buttocks, extremities, shoulders, and overall body size or weight. The nose, ears, face, or sexual organs are involved most often.15 Concerns of patients with BDD, unlike those of patients with hypochondriasis, are limited only to bodily appearance, not underlying illness. Mood disorders Depression may be considered in these patients because they often present with somatic symptoms, somatic ruminations, and hypochondriacal preoccupation. However, for a diagnosis of depression, patients must have depressed mood or anhedonia (loss of interest or pleasure in activities) and must have 4 associated symptoms, including any of the following: poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, psychomotor agitation or retardation, poor concentration or indecision, feelings of worthlessness or excessive guilt, or thoughts of death and/or suicide. The patient's appearance is usually consistent with these problems. When depression is treated, the somatic complaints also resolve. Anxiety disorders These disorders are part of the differential diagnosis for hypochondriasis because patients often present with, or have a number of, somatic symptoms. Typically though, the somatic symptoms are alleviated when these disorders are treated. Patients with generalized anxiety disorder have excessive, pervasive, and uncontrollable worries concerning relationships, work, and leisure. However, such worries are generalized and are not limited to worries of being ill. Patients with OCD have obsessions that mimic hypochondriasis in that they are recurrent and persistent and experienced as intrusive, but these worries extend beyond concerns about illness (eg, to fear about a door being unlocked) and are often accompanied by thematically related compulsive compensatory behavior (eg, lock checking). Psychotic disorders A patient with a psychotic disorder (eg, schizophrenia, delusional disorder) may present primarily with a somatic symptom, but the belief has a fixed quality (ie, a delusion) in contrast to the patient with hypochondriasis, who is convinced of his or her concerns but is able to consider the possibility that the specific feared disease is not present. Monosymptomatic hypochondriasis is a term that was previously used to indicate concerns about parasitosis, or the delusions of infestation by parasitic organisms. Now these patients are generally thought to have delusions (ie, diagnosed formally as DSM-IV-TR delusional disorder, somatic type). Personality disorders Some personality disorders/styles overlap with hypochondriasis.9 Characteristics of patients with hypochondriasis include anxiousness, conscientiousness, dependence, narcissism, and avoidance.16 Secondary hypochondriasis Hypochondriasis in the context of another Axis I disorder, a major life stress, or a medical disorder has been described,9 but this description is not recognized in the DSM-IV-TR. Undifferentiated somatoform disorder This is characterized by the presence of one or more clinically significant, medically unexplained somatic symptom or symptoms lasting for 6 months or longer. Proposed alternative terms for this disorder include subsyndromal, forme fruste, or abridged somatization disorder. Some patients meet the criteria for somatization disorder on follow-up evaluation. As discussed earlier, depressive, anxiety, or personality disorders are highly comorbid as secondary consequences of hypochondriasis. Therefore, rather than excluding hypochondriasis when the comorbid disorder is discovered, both disorders should likely be treated concurrently. Evidence to recommend sequential versus concurrent treatment is insufficient. Clinically, the most prominent and disturbing symptoms should be addressed first.
Special PopulationsPrimary care As detailed above, the patient's report of his or her physical symptoms may not be specific, and the physical examination may not support a clear medical diagnosis. A history of “doctor shopping” is common. Because multiple evaluations and workups have been unfruitful, frustration may ensue, as the patient feels the physicians do not care. The task of the primary care physician here involves the development of a caring and professional relationship with the patient and setting realistic expectations. The physician must be firm but supportive to avoid the patient fleeing to another physician.17 Some of the “tests” these patients present are predictable. Often, the patient requests a specific blood test, radiological study, or invasive procedure, or a combination thereof. The patient may question the expertise of the primary physician and request referrals to different specialists and an ongoing workup. Any possible yield of an investigation must be balanced by the potential medical risks as well as the psychological risk of reinforcing the cyclical hypochondriacal pattern. The physician should engage the patient in the decision-making process whenever possible. Premature reflexive reassurance may be interpreted as a physician deflecting responsibility or may serve to feed into the patient’s reassurance-seeking behavior.18 Meanwhile, the physician must not lose sight of more important health care maintenance examinations, annual screening studies, and lifestyle modifications. Pediatric
Hypochondriasis, per se, is infrequent in the pediatric population because of children’s lack of knowledge of specific disorders that may engender concerns or fears. Children generally respond to reassurance from parents and health care professionals.17 On the other hand, somatic disorders as a result of psychological distress do occur (eg, headaches, stomachaches). In childhood, recurrent abdominal pain (RAP) is a common reason for medical consultation, in at least 1 out of 10 school-aged children. The outcomes of RAP among 28 young adults showed higher ratings on the Hypochondriacal Beliefs subscale of the Illness Attitude Scales (IAS).19 As adult, these patients also perceived themselves as more susceptible to illness and expressed more fear of death. A history of childhood somatic symptoms and psychosocial distress appear to increase the risk of hypochondriasis in adulthood.20 Several factors may increase the risk for hypochondriacal presentations. Somatic disorders seem to occur more in children who are conscientious, sensitive, insecure, and anxious. Childhood adversity, especially overt neglect and sexual abuse, are associated with frequent medical consultations.21 Interestingly, childhood memory about health may contribute to the development of hypochondriasis, though these children may not distinguish between memories about their own health and the health of a friend or stranger.22 As children develop a better ability to communicate and more awareness of their emotions, the expression of emotion through somatic symptoms lessens. Geriatric
The diagnosis of hypochondriasis can be particularly challenging in this patient population, since elderly patients may experience both medical and psychiatric disorders as part of aging. Most elderly patients are reluctant to admit to sadness or depressed mood. Instead, the depressive symptoms are expressed as somatic and hypochondriacal symptoms. Additionally, an elderly patient is uniquely faced with loss of loved ones, social isolation, reduced financial resources, restricted freedom, and existential crisis. The hypochondriacal reaction is often an adaptive response to such unfamiliar psychosocial distress. Therefore, hypochondriasis may be difficult to distinguish from reality-based organic diseases, psychiatric disorders, or adjustment to psychosocial changes.23 Hypochondriasis can be found in any particular patient and appears to be unrelated to age. In fact, hypochondriasis, seemingly more prevalent in the elderly, might actually be healthy emotional and behavioral adaptations to aging, social isolation, or depression.24The provider could empathize with the functional value of hypochondriasis in the elderly patient in helping the patient face mounting medical problems and inevitable aging. Other specialties
Hypochondriasis is now being directly or indirectly evaluated in numerous specialties, including cardiology, dermatology, otorhinolaryngology, gastroenterology, infectious disease, obstetrics and gynecology, ophthalmology, and oncology.17
Lab Studies
- In patients with hypochondriasis, the abnormal laboratory findings characteristic of the suggested physical disorder are absent.
Other Tests
Screening tools
- The Health Anxiety Inventory (HAI) (long version; short version of 14 items, 5 min) reliably distinguishes patients with hypochondriasis from patients with anxiety disorders or healthy controls.18
- The Illness Attitude Scale (29 items, 15 min, English only) is used for detection and to assess severity.25
- The Whitely Index of Hypochondriasis (14 items, 5 min, >14 languages) is used for detection, for rating severity, and for measuring change per interventions.26
- The Somatoform Disorders Symptom Checklist (65 yes-or-no items, 20 min, >5 languages) screens for hypochondriasis, somatization disorder, BDD, and others.27
Medical Care
- Basic management principles
- Establish a firm therapeutic alliance with the patient.
- Educate the patient regarding the manifestations of hypochondriasis.
- Offer consistent reassurance.
- Optimize the patient's ability to cope with the symptoms, rather than trying to eliminate the symptoms.
- Avoid performing high-risk, low-yield invasive procedures.
- Close collaboration among all treating providers to prevent investigative duplication
- Physician concerns and influence
- The most powerful therapeutic tool is the physician and his or her team's attention, concern, interest, careful listening, and nonjudgmental stance, which can potentially break a pathological cycle of maladaptive interactions between the patient and movement from physician to physician (see Image 1).
- One difficulty with which physicians struggle is related to countertransference (ie, physicians' own emotional reactions to the patient). Typically, physicians feel angry, hopeless, and/or helpless because their assessments and interventions are not effective and efforts at reassuring the patient are usually met with resistance and even escalation of physical symptoms. These feelings may lead physicians to reject or withdraw from patients with hypochondriasis.
- Numerous other strategies appear to benefit patients with hypochondriasis (see Image 3). These strategies may prevent potentially serious complications, including the effects of unnecessary diagnostic and therapeutic procedures.
- Establish one primary care physician as the patient's main physician.
- Review the patient's medical history to build an alliance and rule out medical disorders.
- Premature reassurance, prescription of psychotropic medications, and referral for mental health services may suggest to the patient that he or she is not being taken seriously. Therefore, while such treatments may be indicated at some time, prematurely offering a diagnosis or psychiatric treatment may, in fact, impair the establishment of a trusting patient-physician relationship.
- Acknowledge the patient's pain and suffering.
- Couple reassurance statements of normal findings with statements that that the patient will not be abandoned. For example, “Mr. Smith, it appears that you are still having pain despite all the workup, which, so far, has not showed any abnormal finding. I will continue to work with you to maximize you overall well-being and health.”
- Explain to the patient that he or she is not crazy and that symptoms are not just "in his or her head."
- Understand the symptoms as a form of emotional communication.
- Reassure the patient that evaluation will be ongoing.
- Search for underlying medical and psychiatric disorders potentially amenable to treatment.
- Use good judgment when deciding whether to perform elaborate diagnostic evaluations.
- Seek consultation or refer the patient to a colleague if establishing an alliance proves difficult.
- Set up regularly scheduled visits approximately every 4-8 weeks and gradually taper visits when the patient is less symptomatic.
- Allow for time-limited structured discussions about somatic concerns.
- Spend sufficient time on health care maintenance issues such as diet, experience, smoking cessation, and cancer detection.
- Treat comorbid psychiatric disorders concurrently.
- Be aware of emotional reactions toward the patient (ie, anger, hopelessness, helplessness) and seek frequent informal consultation when possible.
- Focus on care of the patient and disorder, not on a cure for the disorder.
- Frequent regularly scheduled visits, attentive but “focal” physical examinations, and benign remedies (eg, bandages, lotions, vitamins, heating pads, massage, slings, and vitamins) help to provide tangible evidence of the physician’s interest and acknowledge the patient's suffering.
- Psychotherapy
- Several authors have suggested a cognitive-educational approach to understand the development of the severe anxiety associated with hypochondriasis (see Image 3) and the factors that maintain the long-term anxiety (see Image 4). Randomized controlled trials now suggest that cognitive-behavioral therapy (CBT) is efficacious in the treatment of hypochondriasis28, 29, 30 and may be the recommended treatment for patients with hypochondriasis.
- Treatments target selective attention31, compatibility between distressing physical symptoms and physical health and longevity32, the cycle involving fear and autonomic overactivity31, and explanations for symptoms and fears32.
- In a corollary vein, controlled studies of patients with noncardiac chest pain show that patients who accept psychological factors as the major cause of their symptoms report a significant decrease in pain.33, 34
- In one study, 74% of patients being treated for hypochondriasis indicated psychological therapy would be their first choice for treatment, versus 4% who indicated that medication would be their first choice.35
- Exposure and response prevention and cognitive therapy have been shown to be equally valuable in the treatment of patients with hypochondriasis.29
- In general, patients with hypochondriasis who show little response to cognitive-behavioral therapy interventions have a higher level of preexisting hypochondriasis, more somatic symptoms, more general psychopathology, and greater psychosocial impairment.36
- Group therapy interventions have gained prominence in recent years, including a cognitive-educational approach.37 Positive results have also been shown for community and group therapy interventions.38, 39
- Psychoeducational approaches provide accurate information (ie, somatic symptoms are exceedingly common, with only a small proportion caused by disease and most compatible with physical health). They also explain that selective attention to one part of the body makes a person more aware of sensation in that part than in other parts (eg, paying attention to vague chest pain while ignoring a badly sprained ankle). Accurate information about the relationship of a threatening stimulus and its somatic consequences can influence the severity of autonomic responses, subjective distress, and behavior. Group psychoeducation has demonstrated short- and long-term (follow-up at 6 mo) improvement.38
- Psychotherapy can counter maladaptive iatrogenic beliefs. Evidence indicates that patients frequently either forget information or distort it. Giving a small amount of information at one time and repeating it appears best.
- Complex developmental, environmental (eg, medical care, family, social network supports, work/disability, sociopolitical, institutional), and cultural factors also influence hypochondriasis (see Image 2). Individual, group, and family psychotherapeutic modalities are uniquely qualified to address these factors.
- Individual CBT has been compared to paroxetine and placebo in a recent randomized trial of 112 patients.40
- A number of other psychotherapy methods have been used to treat hypochondriasis. In one study, psychoanalytic psychotherapy achieved satisfactory results for only 4 of 23 patients. Psychodynamically oriented therapies may be less desirable in the treatment of hypochondriasis.
- Behavioral treatments emphasizing exposure, based on the belief that hypochondriasis is a disease phobia, have been examined. Uncontrolled trials suggest that these strategies help a substantial portion of patients. Persuasion techniques, similar to psychoeducation, have been used to convince patients that symptoms are not due to medical illness.
- For patients who do not respond to psychotherapy, some authors have advocated more intensive treatments in specialized inpatient units, including those aimed at changing the patient's habits, motives, and goals.
- In a survey of patients with hypochondriasis, psychological treatment (ie, cognitive-behavioral treatment) was preferred as the first choice by 74% of respondents, medication was preferred by 4%, and an equal preference for both was indicated by 22%. Of respondents, 48% said they would only accept psychological treatment.35
- Pharmacotherapy
- Off-label usage is being studied for primary hypochondriasis. Initial case reports reported positive effects from fluoxetine, clomipramine, fluvoxamine, and imipramine. More recently, additional reports have cited positive effects for fluvoxamine (originally approved for OCD), nefazodone (now off the market), and paroxetine.
- A recent 16-week, randomized, placebo-controlled trial compared CBT, paroxetine, and placebo in 112 patients. In the completer analysis, paroxetine (average dose 40 mg/d) performed better than placebo and was not statistically significant compared to CBT, based on the Whiteley Index scores. The responders in the completer group were paroxetine, 38%; CBT, 54%; and placebo, 12%. The responders in the intention-to-treat analysis (ITT) were paroxetine, 30%; CBT, 50%; and placebo, 14%. Overall, both CBT and paroxetine performed better than placebo. About 75% of this cohort of patients had a comorbid depressive, anxiety, or another somatoform disorder. 40
- In a 12-week double-blind, placebo-controlled trial of fluoxetine in 20 patients, of the 12 patients treated with fluoxetine, 8 responded, compared with 4 of 8 patients on placebo.41
- Consistent with findings from studies in subjects with OCD or BDD, studies in subjects with hypochondriasis indicate that an adequate trial of medication is 3 months before concluding that it is ineffective; moreover, combination pharmacotherapy may be more effective than monotherapy.42
- Pharmacotherapy has also been directed at anxiety or depression coexisting with hypochondriasis. In controlled trials, benzodiazepines, imipramine, phenelzine, propranolol, and alprazolam were found to decrease somatic symptoms in anxious patients. However, some of these medications are associated with significantly more adverse effects, and benzodiazepine could potentially be addictive for those with comorbid substance use disorder.
- Treatment of delusional disorder, somatic type (monosymptomatic hypochondriacal psychosis or parasitosis) has been largely successful via pharmacotherapy. If the hypochondriacal fear is of delusional intensity, treatment with haloperidol, pimozide, thioridazine, risperidone, olanzapine, and other antipsychotics may lead to improvement. For parasitosis, 2 double-blinded, placebo-controlled studies revealed that pimozide is superior to placebo.43
- Open trials have suggested the efficacy of monoamine oxidase inhibitors, tricyclic antidepressants, antipsychotics, and electroconvulsive therapy (ECT).
A survey showed that most patients do not prefer medication treatment. Prematurely prescribing a psychotropic medication to a patient with hypochondriasis could potentially damage the therapeutic relationship. While medication could definitely be helpful, especially in the setting of a comorbid psychiatric disorder, establishing a therapeutic alliance and providing a caring nonjudgmental treatment structure is the foundation to treatment. - Other interventions
- Other treatments for hypochondriasis include exercise, ECT, and psychosurgery. Exercise increases psychological well-being. Patients who are hypochondriacal may be reluctant to follow this advice, but many patients greatly increase their physical activity as treatment progresses. Studies show conflicting results about the efficacy of ECT, which appears to be effective only if a comorbid mood disorder exists. Psychosurgery is only recommended for patients with severe and intractable hypochondriasis.
- A number of psychiatric consultation interventions that have been successful for somatization disorder have yet to be evaluated for hypochondriasis. Efforts have been made to educate primary care physicians on the essentials of psychosocial assessment, interviewing, developing approaches to dealing with patients with a somatoform disorder, or improving referral skills.
- One randomized controlled trial revealed that referral to a psychiatrist was associated with a 12% reduction in health care costs and no deterioration in physical, mental, or general health. Two controlled studies have shown that consultation with a psychiatrist and an instructive letter to the physician about diagnostic and therapeutic measures resulted in a sharp reduction in health care charges and no change in patient satisfaction.
Surgical Care
Psychosurgery is only recommended for patients with severe and intractable hypochondriasis.
Consultations
Primary care physicians generally treat hypochondriasis, with psychiatrists providing consultation.
Diet
Patients with hypochondriasis should eat 3 meals per day to feel as healthy as possible. They should avoid substances that adversely affect mood, exacerbate anxiety symptoms, or reduce the quality of sleep (eg, caffeine, alcohol, nicotine).
Activity
Exercise increases psychological well-being. Patients who are hypochondriacal may be reluctant to follow this advice, but many patients greatly increase their physical activity as treatment progresses. Exercise helps to improve mood, reduce tension, and improve sleep in patients with associated depression, anxiety, or both.
Pharmacotherapy is used as an adjunct to psychotherapy and educational treatments. The goals of pharmacotherapy are to reduce comorbid symptoms and disorders (eg, depression), to prevent complications, and, in a few circumstances, to reduce hypochondriacal symptoms. Each medication has advantages and disadvantages.44
Drug Category: Antidepressants
These are typically used for depression or anxiety comorbid with hypochondriasis, although in some cases they alleviate hypochondriacal symptoms in the absence of another disorder. They are indicated for use in adults with depression, anxiety (eg, panic disorder, OCD, social phobia, generalized anxiety, posttraumatic stress disorders), and bulimia nervosa disorders.
Off-label uses include insomnia, attention-deficit/hyperactivity disorder, premenstrual dysphoric disorder, and other conditions. All SSRIs (eg, fluoxetine [Prozac], sertraline [Zoloft], paroxetine [Paxil], citalopram [Celexa], escitalopram [Lexapro], fluvoxamine [Luvox]), one selective norepinephrine and serotonin inhibitor (ie, venlafaxine [Effexor XR]), 2 TCAs (ie, clomipramine [Anafranil], imipramine [Tofranil]), and one MAOI (ie, tranylcypromine [Parnate]) have been listed; the latter should be used with care because of dietary restrictions and drug interactions. Data on bupropion (Wellbutrin) and mirtazapine (Remeron) are insufficient to warrant listing, but they may also be used.
Initial doses are listed below. The general principle in these patients is to start at a low dose and progress slowly, unless a psychiatric emergency (eg, suicidal ideation) is present. Once established, a well-tolerated and efficacious antidepressant should be continued as indicated for the comorbid condition (eg, 6-12 mo for a single depression or indefinitely for recurrent depression and an anxiety disorder). If used for hypochondriasis alone, for maintenance dosing, adjust the dose to maintain the patient on the lowest effective dosage, and reassess the patient periodically to determine the need for continued treatment.
| Drug Name | Fluoxetine (Prozac) |
| Description | Selectively inhibits presynaptic serotonin reuptake with minimal or no effect on reuptake of norepinephrine or dopamine |
| Adult Dose | 10-60 mg qam PO; start at 10 mg PO qam and increase in 1-2 wk; liquid available |
| Pediatric Dose | <6 years: Not established; liquid available 6-18 years: 5-10 mg PO qam; liquid available >18 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; MAOIs in past 2 wk |
| Interactions | Increases toxicity of diazepam, alprazolam, and trazodone by decreasing clearance; increases levels of MAOIs, carbamazepine, clozapine, cyclosporine, and highly protein-bound drugs (eg, warfarin); can increase levels of concurrently administered TCAs; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); discontinue other serotonergic agents at least 2 wk prior to beginning SSRIs |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
| Precautions | Caution in hepatic impairment and history of seizures; discontinue MAOIs at least 2 wk before initiating therapy; may induce anxiety, nervousness, anorexia, and insomnia; may activate mania or hypomania in bipolar patients; taper over 1-2 wk upon discontinuation |
| Drug Name | Paroxetine (Paxil) |
| Description | Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake |
| Adult Dose | 10-50 mg PO qhs or 12.5-75 mg am for CR; start at 10 mg qhs (or 12.5 CR am) and increase in 1-2 wk to next dose, then q4wk |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; MAOIs in past 2 wk |
| Interactions | Phenobarbital and phenytoin decrease effects; alcohol, cimetidine, sertraline, phenothiazines, and warfarin increase toxicity; serotonin syndrome (see fluoxetine above) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Nervousness, headache, tremors, GI upset, insomnia, sexual dysfunction, adverse anticholinergic effects; taper over 1-2 wk upon discontinuation; caution in history of seizures, mania, renal disease, and cardiac disease |
| Drug Name | Sertraline (Zoloft) |
| Description | Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine, and clinically insignificant inhibition of reuptake of dopamine. |
| Adult Dose | 50-200 mg PO qam; start at 25-50 mg qam; liquid available |
| Pediatric Dose | <6 years: Not established 6-18 years: 25 mg PO qam >18 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; MAOIs in past 2 wk |
| Interactions | Alcohol; MAOIs; may increase digoxin and phenytoin levels; may decrease warfarin levels; serotonin syndrome (see fluoxetine above) |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
| Precautions | Nervousness, headache, tremors, GI upset, insomnia, sexual dysfunction, adverse anticholinergic effects; taper over 1-2 wk upon discontinuation; caution in history of seizures, mania, renal disease, and cardiac disease |
| Drug Name | Venlafaxine (Effexor XR) |
| Description | Selectively inhibits presynaptic serotonin reuptake, norepinephrine (at doses of approximately 150 mg PO qam), and dopamine (at doses of approximately 150-225 mg qam). |
| Adult Dose | 75-225 mg PO qam; start at 37.5 mg PO qam, increase to 75 mg PO qam in 1-2 wk, then by 75 mg q4wk prn |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; MAOIs in past 2 wk |
| Interactions | Cimetidine, MAOIs, sertraline, fluoxetine class IC antiarrhythmics, TCAs, and phenothiazine may increase effects; serotonin syndrome (see fluoxetine above) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Anxiety, anorexia, sedation, dry mouth, nervousness, dizziness, insomnia, headaches, nausea, increased BP, and sexual dysfunction may occur; taper over 1-2 wk upon discontinuation; caution in patients with cardiovascular disorders |
| Drug Name | Clomipramine (Anafranil) |
| Description | Affects serotonin uptake while affecting norepinephrine uptake when converted into its metabolite desmethylclomipramine. |
| Adult Dose | 50-250 mg PO qhs; 25 mg PO qhs initially, followed by gradual incremental increases to 100 mg PO qhs in first 2 wk |
| Pediatric Dose | 25 mg PO qhs initially, followed by gradual incremental increases; not to exceed 3 mg/kg/d or 200 mg/d, whichever is lower |
| Contraindications | Documented hypersensitivity; recent MI; MAOIs within past 2 wk |
| Interactions | Barbiturates, phenytoin, and carbamazepine decrease effects; increases effects of anticholinergics, sympathomimetics, alcohol, and CNS depressants; increases toxicity of MAOIs |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Caution in severe cardiopulmonary or renal impairment and in patients unable to metabolize sorbitol; may induce drowsiness and impair alertness; exercise precaution when driving or operating machinery; may induce weight gain and orthostatic hypotension; adverse anticholinergic effects include constipation, urinary retention, dry mouth, blurred vision, and exacerbation of narrow-angle glaucoma; taper over 1-2 wk upon discontinuation |
| Drug Name | Fluvoxamine (Luvox) |
| Description | Potent selective inhibitor of neuronal serotonin reuptake. Does not bind significantly to alpha-adrenergic, histamine, or cholinergic receptors and, thus, has fewer adverse effects than TCAs. |
| Adult Dose | 50-150 mg PO bid; 50 mg PO qhs initially as single dose and then divide total daily dose into 2 doses; increase dose in 50-mg increments q4-7d, as tolerated, until maximum therapeutic benefit achieved; if doses are unequal, give larger dose qhs |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; MAOIs within past 2 wk |
| Interactions | MAOIs increase risk of hypertensive crisis; potentiates effects of triazolam and alprazolam (when taking concurrently, reduce dose by at least 50%); reduce dose of theophylline by one third, and monitor plasma levels; alcohol, cimetidine, sertraline, phenothiazines, and warfarin increase toxicity; may inhibit metabolism of beta-blockers, including propranolol and metoprolol, resulting in cardiac toxicity; may inhibit metabolism of carbamazepine, clozapine, methadone, haloperidol, lovastatin, and simvastatin, resulting in elevated levels and/or toxicity; serotonin syndrome (see fluoxetine above) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Caution in patients with liver dysfunction or cardiovascular disease, history of seizures, or suicidal tendencies; adverse effects include drowsiness, insomnia, nervousness, and sexual dysfunction; taper over 1-2 wk upon discontinuation |
| Drug Name | Imipramine (Tofranil) |
| Description | Inhibits reuptake of norepinephrine or serotonin at presynaptic neuron. |
| Adult Dose | 50-300 mg PO qhs; start at 50-100 mg PO qhs and increase q2-4wk prn |
| Pediatric Dose | <12 years: Not established, but not recommended because of possible association with arrhythmia >12 years: 30-40 mg PO qhs, increasing prn; not to exceed 100 mg qhs |
| Contraindications | Documented hypersensitivity; narrow-angle glaucoma; during acute recovery phase following MI; MAOIs or fluoxetine in past 2 wk |
| Interactions | Increases toxicity of sympathomimetic agents (eg, isoproterenol, epinephrine) by potentiating effects and inhibiting antihypertensive effects of clonidine; metabolism may be inhibited by drugs metabolized by cytochrome P-450-2D6 isoenzyme, including fluoxetine, paroxetine, quinidine, carbamazepine, propafenone, and cimetidine, leading to increased levels and/or toxicity |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
|
| Precautions | May impair mental or physical abilities required for performance of potentially hazardous tasks; caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, and patients receiving thyroid replacement |
| Drug Name | Phenelzine (Parnate) |
| Description | Usually reserved for patients who do not tolerate or respond to traditional cyclic or second-generation antidepressants. |
| Adult Dose | 60-90 mg/d PO; start with 15 mg PO qam or bid and increase q2-4wk |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; pheochromocytoma; hepatic or renal disease; cardiovascular disease; cerebrovascular defect |
| Interactions | Increases effects/toxicity of barbiturates and CNS depressants; toxicity increased by fluoxetine, methylphenidate, amphetamines, levodopa, meperidine, carbamazepine, buspirone, cyclobenzaprine, dextromethorphan, pseudoephedrine, phenylephrine, disulfiram, and tyramine-containing foods |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Caution in hyperactive or hyperexcitable disorders and glaucoma; avoid foods with high tyramine content, including red wine and cheese (except cottage, cream, and ricotta cheeses); may cause orthostatic hypotension; routinely monitor BP and recognize signs of elevated BP (ie, headaches, nosebleeds); abrupt discontinuation may precipitate withdrawal syndrome; should not be started if patient has had exposure to SSRI within last 2 wk, except in the case of fluoxetine, for which this period is 5 wk |
| Drug Name | Citalopram (Celexa) |
| Description | Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine. |
| Adult Dose | 20-60 mg PO qd; start at 20 mg and titrate upward q4wk |
| Pediatric Dose | <18 years: Not established >18 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; MAOIs in past 2 wk |
| Interactions | Alcohol; MAOIs; may increase digoxin and phenytoin levels; may decrease warfarin levels; serotonin syndrome (see fluoxetine above) |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
| Precautions | Nervousness, headache, tremors, GI upset, insomnia, sexual dysfunction, adverse anticholinergic effects; taper over 1-2 wk upon discontinuation; caution in history of seizures, mania, renal disease, and cardiac disease |
| Drug Name | Escitalopram (Lexapro) |
| Description | Selective serotonin reuptake inhibitor (SSRI) and S-enantiomer of citalopram. Used for the treatment of depression. Mechanism of action is thought to be potentiation of serotonergic activity in CNS resulting from inhibition of CNS neuronal reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is sooner than other antidepressants. |
| Adult Dose | 10 mg PO qd initially; if needed, may increase to 20 mg/d after 1-4 wk
|
| Pediatric Dose | Not established
|
| Contraindications | Documented hypersensitivity; administration within 14 d of receiving MAOI |
| Interactions | Primarily metabolized by CYP450, 3A4, and 2C19; coadministration with alcohol or other centrally acting drugs increases CNS depression; cimetidine increases AUC and maximum serum concentration; coadministration with sumatriptan and SSRIs has caused weakness and hyperreflexia |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Caution with history of seizures, mania, suicide; common adverse effects include insomnia, ejaculation disorder (primarily ejaculatory delay), nausea, sweating, fatigue, and somnolence |
Drug Category: Beta-adrenergic receptor-blocking agents
Compete with beta-adrenergic agonists for available beta-receptor sites. Propranolol inhibits beta-1 receptors (located mainly in cardiac muscle) and beta-2 receptors (located mainly in bronchial and vascular musculature), inhibiting chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
| Drug Name | Propranolol (Inderal) |
| Description | Has membrane-stabilizing activity and decreases automaticity of contractions. |
| Adult Dose | 30-320 mg/d PO in a tid regimen; start with test dose of 10 mg PO qam and ensure diastolic blood pressure and pulse do not drop below 90 mm Hg and 50 bpm, respectively; if not, start at 10 mg PO tid and increase by 30 mg/d q4-7d to response |
| Pediatric Dose | 0.5-2 mg/kg/d PO |
| Contraindications | Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities; COPD; asthma; diabetes, Raynaud disease |
| Interactions | Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; may increase toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines; concurrent clonidine may lead to hypertensive crisis reported after or during withdrawal of either agent |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and closely monitor patient; avoid use in pregnancy, if possible (reports of neonatal complications during delivery include neonatal bradycardia, hypoglycemia, apnea, low birth weight, and low Apgar scores); adverse effects include light-headedness, confusion, and depression |
Drug Category: Benzodiazepines
Indicated for treatment of anxiety disorders and panic attacks, with or without agoraphobia, which are commonly comorbid with hypochondriasis. Use with caution because patients with hypochondriasis may have increased risk of substance abuse or dependence.
| Drug Name | Alprazolam (Xanax) |
| Description | For management of panic attacks. Binds receptors at several sites within CNS, including limbic system and reticular formation. Effects may be mediated through GABA receptor system. |
| Adult Dose | 0.25-0.5 mg PO tid; titrate prn; not to exceed 4 mg/d |
| Pediatric Dose | <18 years: Not established >18 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; severe respiratory depression; narrow-angle glaucoma; preexisting hypotension |
| Interactions | Carbamazepine and disulfiram decrease effects; toxicity increases with cimetidine, lithium, oral contraceptives, erythromycin, isoniazid, azole antifungals, and CNS depressants (including alcohol) |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
|
| Precautions | Withdrawal symptoms, including seizures, may occur upon abrupt discontinuation; use of benzodiazepines during first trimester of pregnancy associated with increased risk of congenital malformations, including cleft lip or palate; may impair mental or physical abilities required for performance of potentially hazardous tasks |
Drug Category: Antipsychotic medications
Have been shown to reduce morbidity associated with this disorder, particularly in presence of comorbid anxiety or hypochondriacal worries that mimic obsessions or delusions. Because of potential for serious long-term adverse effects (eg, tardive dyskinesia), consultation with psychiatrist recommended to evaluate need for antipsychotic medication. Insufficient data to list other antipsychotics, although they have been used in patients with hypochondriasis.
| Drug Name | Pimozide (Orap) |
| Description | Indicated for Tourette syndrome for suppression of motor and phonic tics. Off-label use for psychosis, hypochondriacal delusions and parasitosis, and Huntington chorea. |
| Adult Dose | 1-2 mg/d PO qam or bid; not to exceed 10 mg/d |
| Pediatric Dose | <12 years: Not recommended >12 years: 0.05 mg/kg/d PO, up to 0.2 mg/kg/d; not to exceed 10 mg/d |
| Contraindications | Documented hypersensitivity; cardiac arrhythmias, especially congenital prolonged QT syndrome |
| Interactions | Azole antifungals (eg, itraconazole, fluconazole, ketoconazole), macrolide antibiotics (eg, erythromycin, clarithromycin, azithromycin), fluvoxamine, indinavir, ritonavir, saquinavir, and isoniazid may lead to increased levels/toxicity; thioridazine or mesoridazine may prolong QTc interval |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Prolongs QTc interval of ECG; baseline and routine ECG are recommended to monitor therapy; may induce extrapyramidal reactions, including pseudoparkinsonism, dystonias, akathisia, and tardive dyskinesia |
| Drug Name | Risperidone (Risperdal) |
| Description | Binds to dopamine D2 receptor with 20-times lower affinity than for serotonin receptor. Improves negative symptoms of psychoses and reduces incidence of EPS. Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder mania; also used for sleep. |
| Adult Dose | 2-6 mg PO qhs; start at 0.5 or 1 qhs; may divide into 2 doses/d; liquid available |
| Pediatric Dose | <16 years: Not recommended >16 years: 0.5-1 mg PO bid; not to exceed 6 mg/d |
| Contraindications | Documented hypersensitivity |
| Interactions | Carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels; cimetidine, fluoxetine, paroxetine, quinidine, and ritonavir inhibit CYP3A4 and may increase concentrations |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | May cause extrapyramidal reactions, body temperature dysregulation, hypotension, sedation, tachycardia, and arrhythmias; may cause adverse anticholinergic effects; may elevate prolactin long-term; severe, rare effects include neuroleptic malignant syndrome, seizure, and tardive dyskinesia |
| Drug Name | Olanzapine (Zyprexa) |
| Description | Binds to dopamine D2 and serotonin receptors. Improves negative symptoms of psychoses and reduces incidence of EPS. Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder mania; also used for sleep |
| Adult Dose | 2.5-20 mg PO qhs; start at 2.5 or 5 qhs; SL (Zydis) and IM forms available |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | May enhance effects of antihypertensives; antagonizes effects of dopamine agonists; nicotine, rifampin, carbamazepine, and other inducers of CYP1A2 may lower levels; inhibitors (eg, fluvoxamine) of this system may raise levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | May cause sedation, weight gain, orthostatic hypotension, body temperature dysregulation, and elevation of LFT results; severe, rare effects include neuroleptic malignant syndrome, seizure, and tardive dyskinesia |
Drug Category: Calcium channel blockers
Indicated for angina and hypertension. May have role in reducing mood disturbance (based on use in bipolar disorder) and/or hypochondriacal symptoms (based on pathophysiology)
| Drug Name | Nifedipine (Procardia, Adalat) |
| Description | Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. |
| Adult Dose | 20-30 mg PO tid/qid
|
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; sick sinus syndrome; second- or third-degree AV block without functioning pacemaker |
| Interactions | Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Allergic hepatitis has occurred but is rare; monitor for elevation of hepatic enzymes, especially patients with compromised hepatic function; gradually taper to prevent withdrawal syndrome; nifedipine may cause lower extremity edema |
| Drug Name | Nifedipine (Cardene) |
| Description | Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery. |
| Adult Dose | 20-30 mg PO tid/qid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | May cause lower extremity edema; allergic hepatitis has occurred but is rare |
In/Out Patient Meds
- Continue successful long-term trials of medications for patients with hypochondriasis.
- For patients with comorbid disorders, consider maintenance of those trials because these disorders can initiate and/or exacerbate hypochondriacal symptoms.
Transfer
Physician-to-physician dialogue on the nature of the patient's problems and successful management strategies is useful.
Complications
- Patients who are hypochondriacal may be significant consumers of medical care, undergoing repetitive doctor visits, physical examinations, laboratory testing, and other costly, invasive, and potentially dangerous procedures.
- Physician concerns regarding workups for somatic complaints also may preclude diagnosis of common comorbid disorders (eg, depression) that are quite
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