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. Comparative clinical effectiveness studies are also being developed. 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.[1] 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. See eMedicine articles Somatoform Disorders and Conversion Disorders. For example, Hollander et al posited an "obsessive-compulsive spectrum" to include obsessivecompulsive disorder (OCD)[2, 3] , body dysmorphic disorder (BDD), anorexia nervosa, Tourette syndrome, and impulse control disorders (eg,trichotillomania, pathological gambling).[4] Other authors postulate that somatoform disorders including hypochondriasis may be a learned unconscious behavior that may serve to avoid internal conflicts and external stressors.[5] 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]). In a recent study of biological markers, subjective who met DSM-IV-TR diagnostic criteria for hypochondriasis had decreased plasma neurotrophin 3 (NT-3) level and platelet serotonin (5-HT) levels, compared to healthy control subjects. NT-3 is a marker of neuronal function and platelet 5-HT is a surrogate marker for serotonergic activity.[6]

Epidemiology
Frequency
United States The prevalence rates for primary hypochondriasis in the primary care setting are 0.84.5%.[7] 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.[8] International International rates are similar to those in the United States.[9]

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.[10] Cognitive, social learning, and psychodynamic theories imply that patients have significant psychosocial disturbances in terms of relationships, 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.[11] The medically unexplained complaint is often a symptom of hypochondriasis[12] and may well be a presentation of associated abnormal illness behavior.[13] Patients with hypochondriasis have a high rate of psychiatric comorbidity.[14] 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.[14]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. The long-term prognosis of patients with hypochondriasis is understudied due to the heterogeneity of the disorder. However, higher severity at baseline is likely associated with worse outcome.

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 explanations or physical findings exist. The DSMIV-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 the image below). 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.

Pathological cycle of bodily concern and anxiety in hypochondriasis.

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 Mild-to-moderate 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 mood Restricted, shallow, fearful, or anxious affect, with restricted fluctuations and limited depth

Thought process
Spontaneous speaking with occasional abrupt changes in topic 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 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 perceptual disturbances (eg, hallucinations) 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 the image below) 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.[15] 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.

Mood, cultural, developmental, and environmental factors that influence hypochondriasis.

A cognitive model of hypochondriasis suggests that patients misinterpret bodily symptoms by augmenting and amplifying their somatic sensations. Patients also appear to have lower-thanusual 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.[11] 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.[16] 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).[4] 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). Hypochondriasis has been hypothesized to be an anxiety spectrum disorder. P-wave dispersion (the difference between the maximum and minimum P-wave duration on the electrocardiograph) has been found to be significantly higher in patients with panic disorder and in patients with hypochondriasis, compared with healthy control subjects. The elevated P-wave dispersion may be an indicator of cardiac autonomic dysfunction in anxiety disorders.[17]

Diagnostic Considerations
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 physical symptoms, not a preoccupation with a particular medical 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.[18] 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.[19, 20] 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.[21] 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). On the other hand, OCD may be comorbid with hypochondriasis. Based on family data in studies of OCD, Bienvenu et al found a relationship between OCD and hypochondriasis and body dysmorphic disorder, suggesting comorbidity between OCD and these somatoform disorders.[22] Van den Heuvel et al found similar frontal-striatal alterations during a planning task among OCD, panic disorder, and hypochondriasis, suggesting a common limbic activation pathway among these disorders.[23] 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 hypochondriacal psychosis is a term that was commonly used to indicate concerns about delusional parasitosis, or the delusions of infestation by parasitic organisms. Now these patients are generally thought to have delusions (ie, diagnosed formally as DSM-IV-TRdelusional disorder, somatic type). Personality disorders Some personality disorders/styles overlap with hypochondriasis.[14] Characteristics of patients with hypochondriasis include anxiousness, conscientiousness, dependence, narcissism, and avoidance.[24] Secondary hypochondriasis Hypochondriasis in the context of another Axis I disorder, a major life stress, or a medical disorder has been described,[14] 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. Primary 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.[25] Some of the "tests" 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 patients reassurance-seeking behavior.[26] Meanwhile, the physician must not lose sight of more important health care maintenance examinations, annual screening studies, and lifestyle modifications.[25] Pediatric Hypochondriasis, per se, is infrequent in the pediatric population because of childrens lack of knowledge of specific disorders that may engender concerns or fears. Children generally respond to reassurance from parents and health care professionals.[25] 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).[27] 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.[28] 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.[29] 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.[30] 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.[31]

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.[32] The provider could empathize with the functional value of hypochondriasis in the elderly patient in helping the patient face mounting medical problems and inevitable aging. Chronic Pain Hypochondriasis is associated with Chronic Pain. This has been studied in an evidence-based structured review of 57 studies that examined the relationship between hypochondriasis or somatization and chronic pain. In some patients, hypochondriasis may develop after development of the disorder causing the pain. The more severe the pain, the higher the likelihood that hypochondriasis may develop. In some studies, treatment of pain may improve the severity of hypochondriasis.[33] 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.[25]

Differential Diagnoses

Anxiety Disorders Body Dysmorphic Disorder Conversion Disorders Delusional Disorder Depression Personality Disorders Schizophrenia Somatoform Disorders

Medication Summary
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.[66]

Antidepressants
Class Summary
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.

Fluoxetine (Prozac)
Selectively inhibits presynaptic serotonin reuptake with minimal or no effect on reuptake of norepinephrine or dopamine

Paroxetine (Paxil)
Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake

Sertraline (Zoloft)
Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine, and clinically insignificant inhibition of reuptake of dopamine.

Venlafaxine (Effexor XR)

Selectively inhibits presynaptic serotonin reuptake, norepinephrine (at doses of approximately 150 mg PO qam), and dopamine (at doses of approximately 150-225 mg qam).

Clomipramine (Anafranil)
Affects serotonin uptake while affecting norepinephrine uptake when converted into its metabolite desmethylclomipramine.

Fluvoxamine (Luvox)
Potent selective inhibitor of neuronal serotonin reuptake. Does not bind significantly to alphaadrenergic, histamine, or cholinergic receptors and, thus, has fewer adverse effects than TCAs.

Imipramine (Tofranil)
Inhibits reuptake of norepinephrine or serotonin at presynaptic neuron.

Phenelzine (Nardil)
Usually reserved for patients who do not tolerate or respond to traditional cyclic or secondgeneration antidepressants.

Citalopram (Celexa)
Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine.

Escitalopram (Lexapro)
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.

Beta-adrenergic receptor-blocking agents

Class Summary
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.

Propranolol (Inderal)
Has membrane-stabilizing activity and decreases automaticity of contractions.

Benzodiazepines
Class Summary
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.

Alprazolam (Xanax)
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.

Antipsychotic medications
Class Summary
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.

Pimozide (Orap)
Indicated for Tourette syndrome for suppression of motor and phonic tics. Off-label use for psychosis, hypochondriacal delusions and parasitosis, and Huntington chorea.

Risperidone (Risperdal)
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.

Olanzapine (Zyprexa)
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

Prognosis

Hypochondriasis is a common disorder in primary care settings. The differential diagnosis includes other somatoform, depressive, anxiety (eg, generalized anxiety disorder, OCD), and psychotic disorders. Biopsychosocial treatment is required to manage this complex disorder, and further research is required to better understand its pathophysiology and interface with other psychiatric conditions. Recognizing the biological similarities between these seemingly disparate disorders may be a useful starting point to begin a more systematic study of novel treatments for hypochondriasis.[67] A system review of six studies on hypochondriasis indicated that 30-50% of patients achieve recovery.[59] A good prognosis appears to be associated with high socioeconomic status, treatmentresponsive anxiety or depression, the absence of a personality disorder, and the absence of a related nonpsychiatric medical condition. Most children recover by adolescence or early adulthood. There is a dearth of long-term follow-up studies examining outcomes of patients with hypochondriasis. In a prospective study that examined 58 patients with hypochondriasis who had participated in selective serotonin reuptake inhibitor (SSRI) treatment for 4-16 years (mean 8.64.5 y), 40% continued to meet the diagnosis of hypochondriasis. Predictors of continued diagnosis of hypochondriasis include longer duration of hypochondriasis prior to treatment, history of childhood physical punishment, and lower use of SSRI during the treatment period. A large portion of patients with hypochondriasis who received SSRI treatment were able to achieve remission.[55]

Patient Education

Educational approaches provide accurate information, allowing the patient to realize somatic symptoms are exceedingly common, with only a small proportion caused by disease and most compatible with physical health. Accurate information about the relationship of a threatening stimulus and its somatic consequences can influence the severity of autonomic responses, subjective distress, and behavior. Maladaptive iatrogenic beliefs must be countered. Providing a small amount of information at a time and repeating it is best. For excellent patient education resources, visit eMedicine's Mental Health and Behavior Center, Anxiety Center, or Depression Center. Also, see eMedicine's patient education article Chronic Fatigue Syndrome. For mild and short-lived symptoms, the primary medical provider could provide detailed education (symptoms, course, monitoring, diagnosis, and treatment) about the medical condition about which the patient is concerned. Education should additionally focus on the role of anxiety and how anxiety could increase autonomic activity or arousal and, thereby, cause the body to misattribute certain physical sensations and symptoms. For more persistent and chronic hypochondriasis, especially in situations where the patient has already failed treatment with multiple providers, education needs be delivered in small doses, when the time is right, and after the establishment of a firm patient-provider relationship. The tailoring of education delivery as applied to mild versus severe symptoms has not been systematically studied. Since hypochondriasis may be precipitated by psychosocial stress, family support is likely to be additionally helpful. However, the role of family education requires further investigation. Even in the absence of formal research into family education for hypochondriasis, several practical pointers are recommended:

The patient needs to give permission to involve family members in diagnosis and treatment planning decisions.

Family members need to be told that the physician will not keep secrets from the patient; ie, anything family members tell the physician about the patient will be shared, with direct attribution, to the patient. Family members need to understand that the distress the patient feels is real even if the conviction about illness is false or cannot be substantiated. Family members should not enable overuse of medical services by reinforcing patients requests for excessive interventions. Family members should be encouraged to support the outpatient chronic disease model for hypochondriasis as described above. Family members should be educated on the common psychiatric comorbidity of hypochondriasis and help the patient self-monitor for mood and anxiety symptoms and seek help for these separately. Family or couples therapy should be considered in patients where family and marital discord is a major source of conflict that is contributing to psychological distress. Alternatively, family therapy should be considered in patients whose symptoms have cause major distress to family dynamics that either seem to perpetuate current symptoms. Given that these patients are often comfortable with computer searches, websites specific to hypochondriasis may be helpful to recommend to patients and families: o WebMD, Mental Health: Hypochondriasis o MedlinePlus, Hypochondria o University of Maryland Medical Center, Hypochondriasis