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Brian A. Fallon, Arthur J. Barsky: Chapter 40. Hypochondriasis, in Gabbard’s Treatments of Psychiatric Disorders, 4th

Edition. Edited by Glen O. Gabbard. Copyright ©2009 American Psychiatric Publishing, Inc. DOI:

10.1176/appi.books.9781585622986.260536. Printed 5/10/2009 from www.psychiatryonline.com

Gabbard’s Treatments of Psychiatric Disorders > Part VII. Somatoform and Factitious Disorders >

Chapter 40. Hypochondriasis

INTRODUCTION

Hypochondriasis, defined as a fear or conviction of having a disease despite medical reassurance, is

a chronic, debilitating, and prevalent condition (Barsky et al. 1990; Escobar et al. 1998; Kellner

1986). It has three central features: disease conviction, disease fear, and bodily preoccupation

(Pilowsky 1967). The relative balance of each of these features creates different profiles. For

example, if disease conviction predominates, the patient’s adamant determination to find a doctor

who will make the “accurate” diagnosis will lead to doctor shopping and multiple doctor visits. This

patient may also demonstrate a general distrust and disdain about the medical profession because

its practitioners seem to be either incompetent or withholding regarding the true nature of the

patient’s disease. If disease fear predominates, the patient may learn to avoid anxiety-triggering

disease-related environmental cues (e.g., visits to sick relatives, television shows with illness as a

theme) and may also avoid going to doctors for evaluation because of the terror associated with

facing confirmation of the disease that is so dreaded. If bodily preoccupation predominates, the

patient’s primary focus will be on one or more somatic symptoms, and only through probing will the

underlying fear or belief of having a serious disease be revealed. Bodily preoccupation with a focus

on multiple somatic symptoms is common among patients with hypochondriasis in the medical

setting; in one study, 49% of patients with hypochondriasis also met criteria for abridged

somatization (Escobar et al. 1998)—a provisional diagnosis characterized by four medically

unexplained symptoms in men or six such symptoms in women.

Although it would be helpful to have guidelines that recommended specific therapeutic approaches

(e.g., medication, type of psychotherapy) for patients with a particular set of hypochondriacal

symptoms (e.g., higher degree of illness conviction vs. greater avoidance with marked illness fear),

such guidelines would be premature, because the studies have not yet been done to compare the

efficacy of different therapies and to examine whether patients with certain hypochondriacal

features may be better suited to one or another treatment modality. Clinical decision making at this

point should be guided by both the evidence to date (reviewed later) and such variables as patient

preference and the availability of trained practitioners.

It is our purpose in this chapter to describe the various therapeutic modalities and to review the

evidence supporting efficacy. Studies with larger sample sizes and adequate outcome measures are

summarized, with a description of the therapeutic technique. Controlled studies do exist,

particularly in evaluation of the efficacy of the psychotherapeutic approaches. Most often, however,

the comparison group was not another active treatment but a no-treatment waiting list. The lack of

an active comparator leaves us uncertain as to whether the therapy itself has mechanistic aspects

that are uniquely beneficial or whether the efficacy was due to attention alone.

PSYCHOTHERAPIES

Psychodynamic Therapy

Although numerous case reports have indicated therapeutic efficacy for dynamic therapy in the

treatment of hypochondriasis, controlled trials have not been conducted. Ladee’s (1966)

prospective study of 23 patients treated with psychoanalytic therapy resulted in improvement in

only 4 (17%) of the patients. This poor outcome suggests that psychoanalytic therapy, as least as

practiced in the 1960s, is not effective for the majority of patients with hypochondriasis.

A modification of psychoanalytic technique was suggested by Offenkrantz and Tobin (1975) for Print: Chapter 40. Hypochondriasis

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working with hypochondriacal patients. Their approach involved starting off the therapy by

empathically communicating to the patient that his or her suffering was legitimate and would be

taken quite seriously. Galatzer-Levy (1982) used this technique with 10 hypochondriacal

individuals as a means of establishing an effective initial engagement to support the work of

psychodynamic therapy. In the 2 patients with comorbid schizophrenia, their distress was made

worse when the therapist commiserated about being so frightened of a serious medical illness; only

when the fear was labeled as a delusion did the patients’ anxiety lessen. Among the 8

hypochondriacal patients without comorbid schizophrenia, 7 had a good therapeutic outcome. The

initial empathic engagement resulted in rapid symptom remission and strengthening of the

therapeutic relationship. These two reports suggest that although classical psychoanalytic

psychotherapy may not be helpful for patients with hypochondriasis, the use of psychodynamic

principles with initial and consistent empathic commiseration may be helpful. Prospective

controlled trials with well-standardized outcome measures are needed.

Explanatory Therapy

Kellner (1983) reported on the use of a precursor to cognitive-behavioral therapy, referred to as

explanatory therapy, for 45 patients in an uncontrolled prospective study. Largely an educational

approach, this therapy included teaching about selective attention (i.e., focusing on a bodily

symptom amplifies the sensation), providing accurate information about symptoms, guiding the

patient in creating alternative explanations for somatic symptoms, providing reassurance and

clarification, and repeating of these educational guides to help the hypochondriacal individual to

register and retain the material. Nearly two-thirds of the patients did well. Fava et al. (2000) used

these explanatory therapy techniques for eight sessions over 16 weeks in a study of 20 patients

with DSM-IV (American Psychiatric Association 1994) hypochondriasis but added standardized

measures of change. After treatment and at 6-month follow-up, patients given explanatory therapy

had a significantly greater reduction in hypochondriacal fears and beliefs and a greater decrease in

health care utilization than patients randomized to the wait list. Nevertheless, the authors noted

that these subjects had substantial residual symptomatology.

Cognitive-Behavioral Therapy

A variety of uncontrolled series and controlled clinical trials have been conducted demonstrating

the efficacy of approaches that include cognitive restructuring with educational and/or behavioral

strategies (Kroenke and Swindle 2000; Warwick et al. 1996). The common features among the

various iterations of cognitive-behavioral therapy (CBT) relate to the role of faulty cognitions in the

perpetuation of the illness and the adverse effect of selective attention to bodily sensations in

amplifying the symptoms. In addition, most of these therapies have behavioral and educational

components that address the amplifiers of bodily symptoms that propel this hypochondriacal cycle

of disease conviction and symptom amplification. These amplifiers include beliefs involving the

etiology and future course of symptoms, circumstances and situations that exacerbate symptoms,

and illness behaviors that are undertaken in response to the symptoms. Patients are helped to

correct faulty symptom attributions, restructure beliefs and expectations about health and disease,

correct misunderstandings about the medical care process, modify maladaptive illness behaviors

(such as excessive researching of one’s condition, repeated seeking of reassurance, and continual

self-examination), and learn distraction techniques to diminish selective attention.

In the largest treatment study of hypochondriasis to date, Barsky and Ahern (2004) reported on a

randomized, controlled trial of CBT for hypochondriasis in which 187 subjects were randomly

assigned to either the experimental treatment (individual CBT and a consultation letter to their

primary care physicians) or the control condition (medical care as usual). They were assessed with

in-person interviews immediately before, immediately after, and at 6 and 12 months after

treatment. CBT was administered individually in six weekly 75- to 90-minute sessions. Each session

was tightly scripted based on a manual and focused on a single hypochondriacal amplifier of

somatic symptoms: attention, beliefs, circumstances and expectations, behaviors, and mood. Each

session was composed of educational information about the symptom amplifiers, an exercisePrint: Chapter 40. Hypochondriasis

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illustrating its role in hypochondriasis, and a discussion in which the patient made the material

presented personally relevant to his or her particular symptoms and disease concerns. Because it

was thought to be essential to coordinate the patients’ ongoing medical management with the

individual therapy, a standardized consultation letter was sent to each patient’s primary care

physician containing five suggestions for medical management that were compatible with, and

designed to augment, the individual therapy. The primary outcome measure was hypochondriacal

attitudes and beliefs as assessed with the Whiteley Index (Pilowsky 1967). Using an intent-to-treat

analysis, a consistent pattern of statistically and clinically significant treatment effects was found

at both 6- and 12-month follow-up, adjusting for baseline educational level and generalized

psychiatric distress. At 12-month follow-up, CBT patients had significantly lower levels of

hypochondriacal concerns, beliefs, and attitudes and of health-related anxiety. They were also

significantly less impaired in social role functioning and intermediate activities of daily life. The

latter included such activities as shopping, working around the house, and driving or using public

transportation. Hypochondriacal somatic symptoms, however, were not improved significantly by

treatment. Although the magnitude of the treatment effect size was small to medium on the

Whiteley Index (Cohen’s d = 0.25–0.30), this effect is meaningful, particularly because the study

population was indeed quite chronic, having been hypochondriacal for a mean of approximately 11

years before treatment. Additional research is warranted to determine whether greater

symptomatic gains could be obtained via booster sessions or with the addition of other therapeutic

modalities (e.g., medication). This study also had the limitation of relying solely on self-report

measures. The treatment manual used in this study is available from the authors.

CBT given as a group therapy may also be effective. Avia et al. (1996) compared group CBT to a

wait-list control for 17 patients with hypochondriacal complaints (i.e., not DSM diagnosed) and

found CBT to be significantly more effective. A similarly favorable outcome was noted by Bouman

(2002), who conducted an uncontrolled trial using six 2-hour group educational sessions and found

sustained good outcome among the 21 completers with DSM-IV hypochondriasis.

Cognitive-Behavioral Therapy Versus Other Active Therapies

CBT Versus Exposure in Vivo With Response Prevention

In an effort to determine which type of therapy is more effective, Visser and Bouman (2001)

compared “pure” CBT therapy and “pure” behavioral therapy using 12 1-hour sessions for 78

patients with hypochondriasis. The CBT emphasized traditional cognitive strategies: 1)

identification of dysfunctional automatic thoughts (e.g., catastrophic misinterpretations of bodily

symptoms); 2) education of patients (e.g., that irrational thoughts precede fears and distress); and

3) homework assignments with daily diaries to teach patients how to monitor, identify, and label

irrational thoughts and challenge these thoughts with more rational ones to observe the

subsequent reduction in emotional and physical discomfort. The behavioral therapy used traditional

exposure and response prevention (ERP) strategies focusing on typical hypochondriacal behavior

patterns: 1) checking of one’s body, 2) seeking of reassurance, and 3) avoidance of interoceptive

and/or external stimuli or situations that remind one of illness. A hierarchy of exposures is created

and systematically addressed in session (in vivo) and through homework assignments. The three

behavior patterns are countered with response prevention strategies. Examples of in vivo

assignments include watching disease-related videos, having conversations about feared diseases,

visiting hospitals or graveyards, and engaging in physical exercise, which can induce physical

symptoms considered frightening to the patient.

Patients were then prospectively assigned to ERP, CBT, or a wait-list control. This study had 5

treatment settings (mental health institutes and university clinics) and 21 therapists. Treatment

consisted of 12 weekly sessions. The results of this study indicated that the active treatments were

equally effective, that each was more effective than the wait-list control, and that improvement

was maintained at 7-month follow-up. Improvement in the two experimental groups at 1 month

posttreatment compared with pretreatment was noted on the Illness Attitudes Scale (health

anxiety and illness behavior), Somatosensory Amplification Scale, Somatization subscale of thePrint: Chapter 40. Hypochondriasis

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Symptom Checklist–90, depression score on the Beck Depression Inventory, and the

obsessive-compulsive complaints on the Maudsley Obsessive-Compulsive Inventory. Of note, 28.2%

of the enrolled subjects dropped out, but these were equally divided among the three treatment

conditions; dropouts tended to have less serious complaints at baseline. Although no difference in

improvement in hypochondriasis was noted between the two active-treatment groups, the CBT

group did show greater improvement in depression compared with the ERP group (Visser and

Bouman 2001). Limitations of this study include the sole reliance on self-report assessments.

CBT Versus Stress Management Therapy

In a study of 48 patients with hypochondriasis, Clark et al. (1998) randomly assigned patients to

CBT, behavioral stress management therapy, or a wait-list control group. The behavioral stress

management included applied relaxation training, stimulus control techniques to reduce worrying

time, and exposure to health anxiety cues and situations. Active treatments occurred weekly for 16

weeks with 1-hour sessions, and treatments were matched in terms of structured homework

assignments, therapist time, patients’ assessment of treatment legitimacy, and patients’

expectations for improvement. Three booster sessions were provided over the next 3 months.

Evaluations were conducted pretreatment, at 8 weeks (mid-treatment), at 16 weeks (end of

treatment), and at 3-, 6-, and 12-month follow-up. At 16 weeks, significant improvement was noted

in patients from both active treatment groups (but not the wait-list control) in the domains of

hypochondriasis and mood, and this improvement was sustained at 12-month follow-up. Patients

given CBT responded to the treatment more quickly and had a greater degree of improvement in

hypochondriasis (e.g., length of time worrying about illness, level of avoidance of health stressors

[such as visiting a sick relative or watching a television show about disease], degree of conviction

about having an illness) at 8 and 16 weeks than the behavioral stress management group. At 12

months, however, the two groups were still better than they had been before treatment, but no

differences existed between active treatments. In other words, the improvements in the CBT group

noted at 8 and 16 weeks abated while the gains from behavioral stress management therapy were

sustained. This study therefore suggests that both treatments are helpful but that CBT may be more

beneficial during the active phase of treatment itself. Limitations of this study include a sample size

that may have been too small to detect differences and the use of an active control treatment that

included more than stress management (e.g., exposure to health anxiety cues) and thus was not a

“pure” treatment that would allow for a teasing out of the contributions to efficacy of programmatic

versus attentional aspects. Future research needs to address these issues as well as to examine

whether CBT booster sessions over a longer period may be beneficial to maintain the gains noted

during the intensive phase of treatment.

PHARMACOTHERAPY

Prior to 1990, the prevailing view was that there was very little one could do pharmacologically for

patients with primary hypochondriasis—that is, hypochondriasis that was not secondary to a major

mood or anxiety disorder. With the emergence of pharmacological agents with particular efficacy

against obsessional disorders (serotonin reuptake inhibitors [SRIs]), however, the pharmacological

treatment of primary hypochondriasis became more promising. Case reports and clinical case series

emerged indicating that many agents might be helpful for hypochondriasis: clomipramine (Stone

1993), fluvoxamine (Fallon et al. 2003), fluoxetine (Fallon et al. 1991, 1993, 1996; Viswanathan

and Paradis 1991), citalopram (Fallon and Feinstein 2001), and paroxetine (Oosterbaan et al.

2001). Two other agents that are not primarily SRIs have also been reported as helpful: nefazodone

(Kjernisted et al. 2002) and imipramine (Wesner and Noyes 1991). Nefazodone’s mode of action is

primarily postsynaptic on the 5-HT2 receptors, although it does have mild 5-HT reuptake–blocking

properties as well. Imipramine, a tricyclic antidepressant, has both norepinephrine and 5-HT

reuptake blocking properties, although the latter effect is weak when compared with the SRIs in

vitro. Sample sizes in the uncontrolled series were small (10–18 subjects), duration was 8–12

weeks, and responder (“much or very much improved”) rates for treatment completers were high,

ranging from 70% to 88.9%.Print: Chapter 40. Hypochondriasis

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Controlled data on the use of medication in the treatment of hypochondriasis are limited. In a

double-blind, placebo-controlled study of fluoxetine for DSM-IV hypochondriasis, Fallon et al.

(1996) randomly assigned 20 patients to treatment with 12 weeks of either fluoxetine or placebo,

starting at 20 mg/day and increasing by 20 mg/day every 2 weeks to a maximum of 80 mg/day.

Patients were informed that “heightened illness concern” may arise from an imbalance of brain

neurotransmitters and that treatment with an SRI such as fluoxetine may correct a brain problem.

After 12 weeks, among completers, 8 (80%) of 10 patients randomized to fluoxetine versus 3

(60%) of 5 patients given placebo were rated as much improved or better on the Clinical Global

Improvement scale. If restricted to the sample rated as “very much improved” (i.e., the remission

sample), the response rates for fluoxetine and placebo were 50% and 16%, respectively. These

results in this small sample indicate a robust response rate to fluoxetine but also a high placebo

response rate for moderate improvement and a lower placebo response for symptom remission.

When the full sample size of 45 randomized subjects was reported (Fallon 2002), the results

demonstrated that fluoxetine was significantly more effective than placebo when measured

categorically (responders vs. nonresponders) and continuously (clinician-administered

hypochondriasis scales). More than two-thirds of the patients completed the 12 weeks of

treatment, and the dropout rate was not different between placebo- and drug-treated groups. This

study confirmed the efficacy and tolerability of fluoxetine for patients with hypochondriasis but also

demonstrated that symptom improvement, although significant, is only partial for the majority of

patients.

ELECTROCONVULSIVE THERAPY

No studies have been conducted to examine the efficacy of electroconvulsive therapy (ECT) for

patients with primary hypochondriasis. Among patients with secondary hypochondriasis in the

setting of primary depression, however, ECT would be expected to result in improvement in both

depression and hypochondriasis. This expectation is supported by a recent report (Rasmussen et al.

2004) that evaluated response to ECT based on severity of depression. Using the hypochondriasis

item and the somatic anxiety item of the Hamilton Depression Inventory, the authors used the

combined data from 253 unipolar depressed patients from the Consortium for Research in

Electroconvulsive Therapy to examine the relationships between measures of somatic anxiety and

hypochondriasis and ECT response. Among patients with less severe depression, high somatic

anxiety and hypochondriasis predicted a low likelihood of sustained remission with ECT. Among

patients with more severe depression, the presence or absence of these traits was not predictive of

ECT outcome.

PREDICTORS OF COURSE AND OUTCOME

Both Pilowsky (1968) and Kellner (1983) reported that good outcome among patients with primary

hypochondriasis was associated with short duration of illness and absence of a personality disorder.

In a more recent study of 96 hypochondriacal patients treated with CBT, chronicity of illness was

not found to be associated with outcome (Hiller et al. 2002). In a naturalistic study of

hypochondriasis, Robbins and Kirmayer (1996) examined whether there were any features among

patients with hypochondriasis that might distinguish persistent hypochondriasis from transient

hypochondriasis; these authors found that the former was more strongly associated with the

presence of a comorbid depressive or anxiety disorder at presentation, fears of emotional

instability, pathological symptom attributions, and interpersonal vulnerability. However, when the

presence or absence of comorbid Axis I disorders was examined in treatment studies, comorbidity

did not exert a significant effect on outcome. In a controlled fluoxetine trial (Fallon et al. 1996),

patients with comorbid depression were just as likely to have a good response as patients who did

not have comorbid depression. Similarly, comorbidity with other mental disorders was not shown to

influence outcome for patients receiving CBT for hypochondriasis (Barsky and Ahern 2004; Hiller et

1. 2002). The severity of hypochondriasis has been found to be inversely related to the likelihood

of spontaneous remission (Barsky et al. 1993). Pretreatment hypochondriasis severity,

somatization symptoms, and general psychopathology were shown to be inversely related to

improvement after CBT (Hiller et al. 2002). Health care utilization has also been shown to be aPrint: Chapter 40. Hypochondriasis

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negative predictor of outcome for CBT. In Hiller et al.’s study (2002), patients with hypochondriasis

were also less likely to respond to CBT in direct proportion to the degree to which they used the

health care system (as measured by the number of hospital days and costs of inpatient treatments

and medications).

Patient preference about treatment choice has been shown in other disorders to impact both

treatment outcome and compliance. In a study of treatment preference among hypochondriacal

patients (Walker et al. 1999), psychological treatment (e.g., CBT) was indicated as the first choice

by 74% of respondents, medication was chosen by 4%, and 22% indicated an equal preference. No

study of hypochondriasis has yet examined the impact on response of treatment preference prior to

randomization. Similarly, although several studies have investigated the influence of motivation

and compliance on CBT outcome in anxiety disorder patients (Hoogduin and Duivenvoorden 1988;

Keijsers et al. 1994; Lax et al. 1992; O’Sullivan et al. 1991), with all but one finding compliance or

motivation to predict good outcome, no specific study that addresses these issues has been done

among patients with hypochondriasis.

CONCLUSION

A growing number of studies now demonstrate that a variety of therapeutic strategies may lead to

similarly positive results and that gains after treatment are at least partially maintained on

long-term follow-up. The best evidence is for the effectiveness of CBT, ERP, and pharmacotherapy.

Psychodynamic therapy may also be effective, although there are only two studies that provide

information on a series of patients—one favorable, one unfavorable. Alternative therapies, such as

progressive relaxation therapy, may also be helpful, although these have not been studied

adequately. Judging from the therapies that have been well studied, many patients do experience

improvement, although substantial residual symptoms remain. Only a few studies have compared

active treatments with one another. Such studies are important because the therapies may differ in

degree of efficacy, durability over time, and rates of response. In addition, treatments may differ in

their effectiveness for varying aspects of the hypochondriasis spectrum of symptoms. For example,

one type of therapy may be particularly effective in altering hypochondriacal fears, whereas

another may be more effective in reducing intensity of disease conviction. Additionally, although

somatic symptoms may not be very responsive to therapies such as CBT, pain in particular is often

reduced by certain antidepressants and may secondarily lead to an improvement in hypochondriasis

(Onghena and Van Houdenhove 1992). Although not yet tested, it would be valuable to know

whether a therapy that explicitly combines cognitive techniques and ERP strategies is more

effective than an approach that uses either psychological treatment alone. Studies that compare

different modalities (e.g., psychotherapy vs. pharmacotherapy) and that include combined

modalities as another comparator (e.g., psychotherapy with pharmacotherapy) would also be

helpful to determine which may be the most effective therapeutic approaches. Only these direct

head-to-head comparisons of different treatment modalities will provide answers to these critical

questions.

The good news at this point, however, is that patients with hypochondriasis do benefit from

treatment and that because several different approaches are helpful, primary care providers and

mental health practitioners can engage patients in dialogue to determine which therapeutic

approach might be most favored, a dialogue that will likely lead to better compliance and enhanced

outcome.

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