eMedicine Specialties > Psychiatry > Psychosomatic

Hypochondriasis

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; Attending Physician, Sacramento County Primary Care Clinic
Coauthor(s): James A Bourgeois, OD, MD, MPA, Professor, Consultation-Liaison Service, Department Education Coordinator, Vice Chair of Education, Department of Psychiatry and Behavioural Neurosciences, Faculty of Medicine, McMaster University, St Joseph's Healthcare, Centre for Mountain Health Services; 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, Professor of Clinical Psychiatry, Vice-Chair of Faculty Development, Department of Psychiatry and Behavioral Sciences, University of California, Davis School of Medicine
Contributor Information and Disclosures

Updated: Sep 8, 2009

Introduction

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.

Case study

A 45-year-old white male engineer presents to a primary care clinic armed with multiple internet searches on the topic of cancer. He states that he “just knows” he has a GI cancer, “probably the colon or maybe the pancreas.” When asked how long this concern has bothered him he says “for years I have been concerned that I have cancer.” You ask about relevant symptoms and he is a bit vague, saying “I get some pain or pressure right here (he points to the left upper quadrant) but it is not there all the time.” Upon asking about prior workups he says “I have had ultrasounds and colonoscopies but they could find anything. I was initially relieved but a couple of weeks later started to think that they must have just missed something.”

When you ask about the patient's goals for today’s visit he is emphatic “I think what I really need is another colonoscopy and abdominal CT scan.” His examination is unrevealing. When you suggest a less invasive approach, he shows the error rates of the other evaluations and shows literature endorsing how abdominal CT is the criterion standard. He is anxious at baseline and increasingly irritable when you propose less invasive evaluation. He ends the encounter by stating that he will “find another doctor who sees my point and will get me what I need.”

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 obsessive-compulsive 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

Frequency

United States

The prevalence rates for primary hypochondriasis in the primary care setting are 0.8-4.5%.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 hypochondriasis12 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.

Clinical

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 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 Media file 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.

  • Pathological cycle of bodily concern and anxiety ...

    Pathological cycle of bodily concern and anxiety in hypochondriasis.

    Pathological cycle of bodily concern and anxiety ...

    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 Media file 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.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 ...

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

Mood, cultural, developmental, and environmental ...

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-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.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).

More on Hypochondriasis

Overview: Hypochondriasis
Differential Diagnoses & Workup: Hypochondriasis
Treatment & Medication: Hypochondriasis
Follow-up: Hypochondriasis
Multimedia: Hypochondriasis
References

References

  1. Barsky AJ, Klerman GL. Overview: hypochondriasis, bodily complaints, and somatic styles. Am J Psychiatry. Mar 1983;140(3):273-83. [Medline].

  2. Fallon BA, Petkova E, Skritskaya N, et al. A double-masked, placebo-controlled study of fluoxeine for hypochondiasis. J Clin Psychopharmcol. December 2008;6:638-45.

  3. Ravindran AV, da Silva TL, Ravindran LN, Richter MA, Rector NA. Obsessive-compulsive spectrum disorders: a review of the evidence-based treatments. Can J Psychiatry. May 2009;54(5):331-43. [Medline].

  4. Hollander E, Stein DJ, Decaria CM, Cohen L, Islam M, Frenkel M. Disorders related to OCD--neurobiology. Clin Neuropharmacol. 1992;15 Suppl 1 Pt A:259A-260A. [Medline].

  5. Wooley SC, Blackwell B, Winget C. A learning theory model of chronic illness behavior: theory, treatment, and research. Psychosom Med. Aug 1978;40(5):379-401. [Medline].

  6. Brondino N, Lanati N, Barale F, Martinelli V, Politi P, Geroldi D. Decreased NT-3 plasma levels and platelet serotonin content in patients with hypochondriasis. J Psychosom Res. Nov 2008;65(5):435-9. [Medline].

  7. Magarinos M, Zafar U, Nissenson K, Blanco C. Epidemiology and treatment of hypochondriasis. CNS Drugs. 2002;16(1):9-22. [Medline].

  8. Kellner R. Hypochondriasis and somatization. JAMA. Nov 20 1987;258(19):2718-22. [Medline].

  9. Gureje O, Ustum TB, Simon GE:. The syndrome of hypochondriasis: a cross-national study in primary care. Psychol Med;. 1997;27:1001-10.

  10. Barsky AJ, Ettner SL, Horsky J, Bates DW. Resource utilization of patients with hypochondriacal health anxiety and somatization. Med Care. Jul 2001;39(7):705-15. [Medline].

  11. Barsky AJ, Ahern DK, Bailey ED, Saintfort R, Liu EB, Peekna HM. Hypochondriacal patients' appraisal of health and physical risks. Am J Psychiatry. May 2001;158(5):783-7. [Medline].

  12. Holder-Perkins V, Wise TN, Williams DE. Hypochondriacal Concerns: Management Through Understanding. Prim Care Companion J Clin Psychiatry. Aug 2000;2(4):117-121. [Medline].

  13. Lipowski ZJ. Somatization: a borderland between medicine and psychiatry. CMAJ. Sep 15 1986;135(6):609-14. [Medline].

  14. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry. Feb 1992;49(2):101-8. [Medline].

  15. Ball RA, Clare AW. Symptoms and social adjustment in Jewish depressives. Br J Psychiatry. Mar 1990;156:379-83. [Medline].

  16. Jones LR, Mabe PA 3rd, Riley WT. Illness coping strategies and hypochondriacal traits among medical inpatients. Int J Psychiatry Med. 1989;19(4):327-39. [Medline].

  17. Smith RC. Somatization disorder: defining its role in clinical medicine. J Gen Intern Med. Mar-Apr 1991;6(2):168-75. [Medline].

  18. Stefansson JG, Messina JA, Meyerowitz S. Hysterical neurosis, conversion type: clinical and epidemiological considerations. Acta Psychiatr Scand. Feb 1976;53(2):119-38. [Medline].

  19. Toone BK. Disorders of hysterical conversion. In: Bass C, ed. Physical Symptoms and Psychological Illness. London, UK: Blackwell Scientific; 1990:207-34.

  20. de Leon J, Bott A, Simpson GM. Dysmorphophobia: body dysmorphic disorder or delusional disorder, somatic subtype?. Compr Psychiatry. Nov-Dec 1989;30(6):457-72. [Medline].

  21. Hollifield M, Tuttle L, Paine S, Kellner R. Hypochondriasis and somatization related to personality and attitudes toward self. Psychosomatics. Sep-Oct 1999;40(5):387-95. [Medline].

  22. Xiong GL, Bougeois JA, Chang CH, Liu D, Hilty DM. Hypochondriasis: common presentations and treatment strategies in primary care and specialty settings. Therapy. 2007;(4):3:323-38.

  23. Salkovskis PM, Rimes KA, Warwick HM, Clark DM. The Health Anxiety Inventory: development and validation of scales for the measurement of health anxiety and hypochondriasis. Psychol Med. Jul 2002;32(5):843-53. [Medline].

  24. Campo JV, Di Lorenzo C, Chiappetta L, Bridge J, Colborn DK, Gartner JC Jr, et al. Adult outcomes of pediatric recurrent abdominal pain: do they just grow out of it?. Pediatrics. Jul 2001;108(1):E1. [Medline].

  25. Noyes R Jr, Stuart S, Langbehn DR, Happel RL, Longley SL, Yagla SJ. Childhood antecedents of hypochondriasis. Psychosomatics. Jul-Aug 2002;43(4):282-9. [Medline].

  26. Fiddler M, Jackson J, Kapur N, Wells A, Creed F:. Childhood adversity and frequent medical consultations. Gen Hosp Psychiatry. 2004;26:367-77.

  27. Durso FT, Reardon R, Shore WJ, Delys SM:. Memory processes and hypochondriacal tendencies. J Nerv Ment Dis. 1992;179(5):279-83.

  28. Gottlieb GL. Hypochondriasis: A psychosomatic problem in the elderly. Adv Psychosom Med. 1989;19:67-84.

  29. Stein EM. When is hypochondriasis not hypochondriasis? Geriatrics. 2003;58(3):41-2.

  30. Kellner R, Abbott P, Pathak D, Winslow WW, Umland BE. Hypochondriacal beliefs and attitudes in family practice and psychiatric patients. Int J Psychiatry Med. 1983-1984;13(2):127-39. [Medline].

  31. Speckens AE, Spinhoven P, Sloekers PP, Bolk JH, van Hemert AM. A validation study of the Whitely Index, the Illness Attitude Scales, and the Somatosensory Amplification Scale in general medical and general practice patients. J Psychosom Res. Jan 1996;40(1):95-104. [Medline].

  32. Janca A, Isaac M, Bennett LA, Tacchini G. Somatoform disorders in different cultures--a mail questionnaire survey. Soc Psychiatry Psychiatr Epidemiol. Jan 1995;30(1):44-8. [Medline].

  33. Harrington P. Obsessive compulsive disorder with associated hypochondriasis. BMJ. May 10 2008;336(7652):1070-1. [Medline].

  34. Looper KJ, Kirmayer LJ. Behavioral medicine approaches to somatoform disorders. J Consult Clin Psychol. Jun 2002;70(3):810-27. [Medline].

  35. Visser S, Bouman TK. The treatment of hypochondriasis: exposure plus response prevention vs cognitive therapy. Behav Res Ther. Apr 2001;39(4):423-42. [Medline].

  36. Kroenke K, Swindle R. Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom. Jul-Aug 2000;69(4):205-15. [Medline].

  37. Visser S, Bouman TK. Cognitive-behavioural approaches in the treatment of hypochondriasis: six single case cross-over studies. Behav Res Ther. May 1992;30(3):301-6. [Medline].

  38. Kellner R. Psychotherapeutic strategies in hypochondriasis: a clinical study. Am J Psychother. Apr 1982;36(2):146-57. [Medline].

  39. House A. Hypochondriasis and related disorders. Assessment and management of patients referred for a psychiatric opinion. Gen Hosp Psychiatry. May 1989;11(3):156-65. [Medline].

  40. Klimes I, Mayou RA, Pearce MJ, Coles L, Fagg JR. Psychological treatment for atypical non-cardiac chest pain: a controlled evaluation. Psychol Med. Aug 1990;20(3):605-11. [Medline].

  41. Pearce MJ, Mayou RA, Klimes I. The management of atypical non-cardiac chest pain. Q J Med. Sep 1990;76(281):991-6. [Medline].

  42. Walker J, Vincent N, Furer P, Cox B, Kjernisted K. Treatment preference in hypochondriasis. J Behav Ther Exp Psychiatry. Dec 1999;30(4):251-8. [Medline].

  43. Hiller W, Leibbrand R, Rief W, Fichter MM. Predictors of course and outcome in hypochondriasis after cognitive-behavioral treatment. Psychother Psychosom. Nov-Dec 2002;71(6):318-25. [Medline].

  44. Barsky AJ. Hypochondriasis. Medical management and psychiatric treatment. Psychosomatics. Jan-Feb 1996;37(1):48-56. [Medline].

  45. Avia MD, Ruiz MA, Olivares ME, Crespo M, Guisado AB, Sánchez A. The meaning of psychological symptoms: effectiveness of a group intervention with hypochondriacal patients. Behav Res Ther. Jan 1996;34(1):23-31. [Medline].

  46. Ford CV, Long KD. Group psychotherapy of somatizing patients. Psychother Psychosom. 1977;28(1-4):294-304. [Medline].

  47. Bouman TK. A community-based psychoeducational group approach to hypochondriasis. Psychother Psychosom. Nov-Dec 2002;71(6):326-32. [Medline].

  48. Lidbeck J. Group therapy for somatization disorders in primary care: maintenance of treatment goals of short cognitive-behavioural treatment one-and-a-half-year follow-up. Acta Psychiatr Scand. Jun 2003;107(6):449-56. [Medline].

  49. [Best Evidence] Greeven A, van Balkom AJ, Visser S, et al. Cognitive behavior therapy and paroxetine in the treatment of hypochondriasis: a randomized controlled trial. Am J Psychiatry. Jan 2007;164(1):91-9. [Medline].

  50. Thomson A, Page L. Psychotherapies for hypochondriasis. Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD006520. DOI: 10.1002/14651858.CD006520.pub2.

  51. Stone AB. Treatment of hypochondriasis with clomipramine. J Clin Psychiatry. May 1993;54(5):200-1. [Medline].

  52. Wesner RB, Noyes R Jr. Imipramine an effective treatment for illness phobia. J Affect Disord. May-Jun 1991;22(1-2):43-8. [Medline].

  53. Fallon BA, Schneier FR, Marshall R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull. 1996;32(4):607-11. [Medline].

  54. Phillips KA. Body dysmorphic disorder: clinical features and drug treatment. CNS Drugs. 1995;3:30-40.

  55. Fallon BA, Liebowitz MR, Salman E, Schneier FR, Jusino C, Hollander E. Fluoxetine for hypochondriacal patients without major depression. J Clin Psychopharmacol. Dec 1993;13(6):438-41. [Medline].

  56. Cetin M, Ebrinç S, Agargün MY, Yigit S. Risperidone for the treatment of monosymptomatic hypochondriacal psychosis. J Clin Psychiatry. Aug 1999;60(8):554. [Medline].

  57. Hamann K, Avnstorp C. Delusions of infestation treated by pimozide: a double-blind crossover clinical study. Acta Derm Venereol. 1982;62(1):55-8. [Medline].

  58. Reilly TM, Jopling WH, Beard AW. Successful treatment with pimozide of delusional parasitosis. Br J Dermatol. Apr 1978;98(4):457-9. [Medline].

  59. Bursztajn H, Barsky AJ. Facilitating patient acceptance of a psychiatric referral. Arch Intern Med. Jan 1985;145(1):73-5. [Medline].

  60. Medical Economics Staff. Medical Economics. In: Physicians' Desk Reference. 58th ed. Monvale, NJ; 2004.

  61. Kellner R. Prognosis of treated hypochondriasis. A clinical study. Acta Psychiatr Scand. Feb 1983;67(2):69-79. [Medline].

  62. Adler G. The physician and the hypochondriacal patient. N Engl J Med. Jun 4 1981;304(23):1394-6. [Medline].

  63. Fallon BA, Javitch JA, Hollander E, Liebowitz MR. Hypochondriasis and obsessive compulsive disorder: overlaps in diagnosis and treatment. J Clin Psychiatry. Nov 1991;52(11):457-60. [Medline].

Further Reading

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

Contributor Information and Disclosures

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; Attending Physician, Sacramento County Primary Care Clinic
Glen L Xiong, MD is a member of the following medical societies: American College of Physicians, American Psychiatric Association, and Sierra Sacramento Valley Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

James A Bourgeois, OD, MD, MPA, Professor, Consultation-Liaison Service, Department Education Coordinator, Vice Chair of Education, Department of Psychiatry and Behavioural Neurosciences, Faculty of Medicine, McMaster University, St Joseph's Healthcare, Centre for Mountain Health Services
James A Bourgeois, OD, MD, MPA is a member of the following medical societies: Academy of Psychosomatic Medicine, American Neuropsychiatric Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.

Peter M Yellowlees, MD, Professor of Psychiatry, Associate Director, Center for Health and Technology, Director of Academic Information Systems, University of California at Davis
Disclosure: Nothing to disclose.

Donald M Hilty, MD, Professor of Clinical Psychiatry, Vice-Chair of Faculty Development, Department of Psychiatry and Behavioral Sciences, University of California, Davis School of Medicine
Donald M Hilty, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Technology in Psychiatry, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Abbott Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching

Medical Editor

Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland
Sarah C Aronson, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.

CME Editor

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
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
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