Hypochondriasis

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Hypochondriasis
o Author: Glen L Xiong, MD
o Chief Editor: David Bienenfeld, MD

Overview
Clinical Presentation
Differential Diagnoses
Workup
Treatment & Management
Medication
Follow-up

Overview
Background
Pathophysiology
Epidemiology

Clinical Presentation
History
Physical
Causes

Workup
Laboratory Studies
Other Tests

Treatment & Management

Medical Care
Surgical Care
Consultations
Diet
Activity

Follow-up
Inpatient & Outpatient Medications
Transfer
Complications
Prognosis

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 todays 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.

References

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 Medscape Reference 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]

References

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.

References

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 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.

View Image
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.
References

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

References

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
View Image 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]

References

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

Laboratory Studies
In patients with hypochondriasis, the abnormal laboratory findings characteristic of the
suggested physical disorder are absent.

References

Other Tests
Screening tools

The Health Anxiety Inventory (HAI) (long version; short version of 14 items, 5 min)
reliably distinguishes patients with hypochondriasis from patients with anxiety
disorders or healthy controls.[27]
The Illness Attitude Scale (29 items, 15 min, English only) is used for detection and
to assess severity.[35]
The Whitely Index of Hypochondriasis (14 items, 5 min, >14 languages) is used for
detection, for rating severity, and for measuring change per interventions.[36]
The Somatoform Disorders Symptom Checklist (65 yes-or-no items, 20 min, >5
languages) screens for hypochondriasis, somatization disorder, BDD, and others.[37]
References

Medical Care

Basic management principles

Establish a firm therapeutic alliance with the patient.

Educate the patient regarding the manifestations of hypochondriasis.
Offer consistent reassurance.
Optimize the patient's ability to cope with the symptoms, rather than trying to
eliminate the symptoms.
Avoid performing high-risk, low-yield invasive procedures.
Close collaboration among all treating providers to prevent investigative duplication

Physician concerns and influence

The most powerful therapeutic tool is the physician and his or her team's attention, concern,
interest, careful listening, and nonjudgmental stance, which can potentially break a
pathological cycle of maladaptive interactions between the patient and movement from
physician to physician (see the image below).[38]

Pathological cycle of bodily concern and anxiety in hypochondriasis.

View Image
One difficulty with which physicians struggle is related to countertransference (ie, physicians'
own emotional reactions to the patient). Typically, physicians feel angry, hopeless, and/or
helpless because their assessments and interventions are not effective and efforts at reassuring
the patient are usually met with resistance and even escalation of physical symptoms. These
feelings may lead physicians to reject or withdraw from patients with hypochondriasis.
Inpatient care Psychiatric
As with the other somatoform disorders, inpatient psychiatric hospitalization for the
somatoform disorder itself is rarely necessary. As these patients are at risk for concurrent
mood, anxiety, and personality disorders, a psychiatric admission may be necessary to
manage episodic decompensation of the comorbid psychiatric conditions or suicidal ideation.
If the patient experiences suicidal ideation or makes a suicide act based on comorbid
depression or personality disorder or develops uncontrollable anxiety, then an inpatient
psychiatric hospitalization may be indicated. In such a case, a hypochondriasis diagnosis may
be established in the context of an inpatient admission.
Formal psychometric testing may be of help.
The hypochondriacal patterns of behavior can be addressed in ward therapy interventions.
When patients are discharged following recovery of behavioral stability, the hypochondriasis
treatment model described below may be implemented.
Inpatient care - General Medicine
Patients with hypochondriasis should be admitted to general medicine and surgery services
based on the medical and surgical acuity, not solely to facilitate work-up.

Due to the enigmatic nature of various physical symptoms, occasionally patients with
hypochondriasis are admitted to the general medical-surgical hospital for an extensive workup.
When hypochondriasis is suspected in a medical or surgical inpatient, a psychosomatic
medicine consultation should be performed to elucidate the diagnosis and address psychiatric
comorbidity.
If clinically recommended by the psychosomatic medicine consultant, psychotropic
medication interventions can be started.
As in the outpatient care model, patients should not be exposed to high-risk invasive
procedures.
Numerous other strategies appear to benefit patients with hypochondriasis (see the image
below). These strategies may prevent potentially serious complications, including the effects
of unnecessary diagnostic and therapeutic procedures.

Factors that maintain anxiety in patients with hypochondriasis.

View Image
Establish one primary care physician as the patient's main physician.
Review the patient's medical history to build an alliance and rule out medical disorders.
Premature reassurance, prescription of psychotropic medications, and referral for mental
health services may suggest to the patient that he or she is not being taken seriously.
Therefore, while such treatments may be indicated at some time (in the future), prematurely
offering a diagnosis or psychiatric treatment may, in fact, impair the establishment of a
trusting patient-physician relationship.
Acknowledge the patient's pain and suffering.
Couple reassurance statements of normal findings with statements that that the patient will
not be abandoned. For example, Mr. Smith, it appears that you are still having concern about
having a several medical disorder despite all the workup, which, so far, has not showed any
abnormal finding. I will continue to work with you to maximize you overall well-being and
health.
Reassure the patient that evaluation will be ongoing.
Understand the the fear of having an unknown medical disorder as a form of emotional
communication.
Search for underlying medical and psychiatric disorders potentially amenable to treatment.
Seek consultation or refer the patient to a colleague if establishing an alliance proves
difficult.

Allow for time-limited structured discussions about somatic concerns.

Spend sufficient time on health care maintenance issues such as diet, experience, smoking
cessation, and cancer detection.
Treat comorbid psychiatric disorders concurrently.
Be aware of emotional reactions toward the patient (ie, anger, hopelessness, helplessness) and
seek frequent informal consultation when possible.
Focus on care of the patient with hypochondriasis, not exclusively on a cure for the
disorder.
Psychotherapy
Several authors have suggested a cognitive-educational approach to understand the
development of the severe anxiety associated with hypochondriasis (see thefirst image below)
and the factors that maintain the long-term anxiety (see the second image
below).[39] Randomized controlled trials now suggest that cognitive-behavioral therapy (CBT)
is efficacious in the treatment of hypochondriasis[40, 41, 42, 43, 44] and may be the recommended
treatment for patients with hypochondriasis. Bibliotherapy, using CBT principles, may also
be useful.

References

Surgical Care
Psychosurgery is only recommended for patients with severe and intractable hypochondriasis.

References

Consultations
Primary care physicians generally treat hypochondriasis, with psychiatrists providing
consultation.

References

Diet
Patients with hypochondriasis should eat 3 meals per day to feel as healthy as possible. They
should avoid substances that adversely affect mood, exacerbate anxiety symptoms, or reduce
the quality of sleep (eg, caffeine, alcohol, nicotine).

References

Activity
Exercise increases psychological well-being. Patients who are hypochondriacal may be
reluctant to follow this advice, but many patients greatly increase their physical activity as

treatment progresses. Exercise helps to improve mood, reduce tension, and improve sleep in
patients with associated depression, anxiety, or both.

References

Medication
Medication Summary
Antidepressants
Beta-adrenergic receptor-blocking agents
Benzodiazepines
Antipsychotic medications

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.[45]

References

Antidepressants
Class Summary
Fluoxetine (Prozac)
Paroxetine (Paxil)
Sertraline (Zoloft)
Venlafaxine (Effexor XR)
Clomipramine (Anafranil)
Fluvoxamine (Luvox)
Imipramine (Tofranil)
Phenelzine (Nardil)
Citalopram (Celexa)
Escitalopram (Lexapro)

Fluoxetine (Prozac)

Dosing, Interactions, etc.

Clinical Context: Selectively inhibits presynaptic serotonin reuptake with minimal or no

effect on reuptake of norepinephrine or dopamine

References

Paroxetine (Paxil)

Dosing, Interactions, etc.

Clinical Context: Potent selective inhibitor of neuronal serotonin reuptake. Also has weak
effect on norepinephrine and dopamine neuronal reuptake

References

Sertraline (Zoloft)

Dosing, Interactions, etc.

Clinical Context: Selectively inhibits presynaptic serotonin reuptake, minimal or no effect

on reuptake of norepinephrine, and clinically insignificant inhibition of reuptake of
dopamine.

References

Venlafaxine (Effexor XR)

Dosing, Interactions, etc.

Clinical Context: Selectively inhibits presynaptic serotonin reuptake, norepinephrine (at

doses of approximately 150 mg PO qam), and dopamine (at doses of approximately 150-225
mg qam).

References

Clomipramine (Anafranil)

Dosing, Interactions, etc.

Clinical Context: Affects serotonin uptake while affecting norepinephrine uptake when
converted into its metabolite desmethylclomipramine.

References

Fluvoxamine (Luvox)

Dosing, Interactions, etc.

Clinical Context: Potent selective inhibitor of neuronal serotonin reuptake. Does not bind
significantly to alpha-adrenergic, histamine, or cholinergic receptors and, thus, has fewer
adverse effects than TCAs.

References

Imipramine (Tofranil)

Dosing, Interactions, etc.

Clinical Context: Inhibits reuptake of norepinephrine or serotonin at presynaptic neuron.

References

Phenelzine (Nardil)

Dosing, Interactions, etc.

Clinical Context: Usually reserved for patients who do not tolerate or respond to traditional
cyclic or second-generation antidepressants.

References

Citalopram (Celexa)

Dosing, Interactions, etc.

Clinical Context: Selectively inhibits presynaptic serotonin reuptake, minimal or no effect

on reuptake of norepinephrine.

References

Escitalopram (Lexapro)

Dosing, Interactions, etc.

Clinical Context: 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.

References

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.

References

Beta-adrenergic receptor-blocking agents

Class Summary
Propranolol (Inderal)

Propranolol (Inderal)

Dosing, Interactions, etc.

Clinical Context: Has membrane-stabilizing activity and decreases automaticity of

contractions.

References

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.

References

Benzodiazepines
Class Summary
Alprazolam (Xanax)

Alprazolam (Xanax)

Dosing, Interactions, etc.

Clinical Context: 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.

References

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.

References

Antipsychotic medications

Class Summary
Pimozide (Orap)
Risperidone (Risperdal)
Olanzapine (Zyprexa)

Pimozide (Orap)

Dosing, Interactions, etc.

Clinical Context: Indicated for Tourette syndrome for suppression of motor and phonic tics.
Off-label use for psychosis, hypochondriacal delusions and parasitosis, and Huntington
chorea.

References

Risperidone (Risperdal)

Dosing, Interactions, etc.

Clinical Context: 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.

References

Olanzapine (Zyprexa)

Dosing, Interactions, etc.

Clinical Context: 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

References

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.

References

Inpatient & Outpatient Medications

Continue successful long-term trials of medications for patients with hypochondriasis.

For patients with comorbid disorders, consider maintenance of those trials because
these disorders can initiate and/or exacerbate hypochondriacal symptoms.

References

Transfer
Physician-to-physician dialogue on the nature of the patient's problems and successful
management strategies is useful.

References

Complications

Patients who are hypochondriacal may be significant consumers of medical care,

undergoing repetitive doctor visits, physical examinations, laboratory testing, and
other costly, invasive, and potentially dangerous procedures.
Physician concerns regarding workups for somatic complaints also may preclude
diagnosis of common comorbid disorders (eg, depression) that are quite treatable.
References

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.[46]
A system review of six studies on hypochondriasis indicated that 30-50% of patients
achieve recovery.[47]
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.[48]
References

Author
Glen L Xiong, MD, Associate 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
Disclosure: Lippincott Williams & Wilkins Royalty Book Editor; National Alliance for
Research in Schizophrenia and Depression Grant/research funds Independent contractor
Coauthor(s)
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
Disclosure: Nothing to disclose.
James A Bourgeois, OD, MD, MPA, Clinical Professor, Department of Psychiatry,
University of California, San Francisco, School of Medicine; Faculty Psychiatrist,
Consultation-Liaison Division, Department of Psychiatry, Langley Porter Psychiatric
Institute, University of California, San Francisco, Medical Center
Disclosure: Nothing to disclose.
Peter M Yellowlees, MD, MBBS, Professor of Psychiatry, Director of Health Informatics
Program, University of California, Davis, School of Medicine
Disclosure: Medscape Consulting fee Independent contractor
Specialty Editors
Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case
Western Reserve School of Medicine/University Hospitals of Cleveland
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska
Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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
Disclosure: Novartis Honoraria Speaking and teaching; Sunovion Honoraria Speaking and
teaching; Otsuke Grant/research funds reseach; Merck Honoraria Speaking and teaching
Chief Editor

David Bienenfeld, MD, Professor of Psychiatry, Vice-Chair and Director of Residency

Training, Department of Psychiatry, Wright State University, Boonshoft School of Medicine
Disclosure: Lippincott Williams Wilkins Royalty Author
Additional Contributors
The authors and editors of Medscape Reference gratefully acknowledge the contributions of
previous authors Shayna L Marks, BA, MA; Dandan Liu, BA; and Celia Chang, MD to the
development and writing of this article.
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Pathological cycle of bodily concern and anxiety in hypochondriasis.

Mood, cultural, developmental, and environmental factors that influence

hypochondriasis.

Pathological cycle of bodily concern and anxiety in hypochondriasis.

Factors that maintain anxiety in patients with hypochondriasis.

Pathological cycle of bodily concern and anxiety in hypochondriasis.

Mood, cultural, developmental, and environmental factors that influence

hypochondriasis.

Factors that maintain anxiety in patients with hypochondriasis.

A cognitive model of the development of anxiety with hypochondriasis.