In Review

Somatization Disorder: A Practical Review

Franois Mai, MD, FRCPC, FRCPsych, FRCP(Ed)1

Objective: This paper reviews the present state of knowledge on the etiology, prevalence,
diagnosis, and treatment of somatization disorder (SD).
Method: A comprehensive review of the literature on SD is described under the above
headings.
Results: SD is a common condition that is not well managed by many physicians. Patients
with SD get caught between the cracks of the health care system, with expensive
consequences. SD is a psychiatric disorder, but patients are reluctant to see and be treated
by psychiatrists. They frequently are managed by nonpsychiatric physicians who have
limited understanding of the condition. Cognitive-behavioural therapy (CBT) is the most
efficacious treatment in SD, although antidepressants and supportive psychotherapy also
have a role for some patients.
Conclusions: A cadre of clinicians with training in the theory and practice of CBT for SD
is required. They need to be based both in the community and in tertiary health care
centres, where most patients with this condition are located.
(Can J Psychiatry 2004:49:652662)
Information on author affiliations appears at the end of the article.

Clinical Implications
Somatization disorder (SD) is a common condition.
SD has a major impact on our health care system.
Programs to train clinicians in the use of cognitive-behavioural therapy for SD need to be
established.

Limitations
The diagnostic criteria for SD remain cumbersome.
Long-term outcome studies are rare.

Key Words: somatization disorder, hysteria, Briquets syndrome, somatization, conversion

hen it was still a prevalent condition during the 19th
W and early 20th centuries, syphilis was known in medi-
cine as the great simulator. It could affect so many organs in
the body and present with such a wide variety of symptoms
and signs that it had to be included in the differential diagnosis
of almost any clinical diagnostic problem. Somatization can
present in a similar varied pattern and, with its diverse forms,
has now replaced syphilis as the great medical simulator.
The word somatization was coined, curiously enough, by
the mistranslation of a German word used by the psychoana-
lyst Wilhelm Stekel in the 1920s (1). The word organsprache
literally means organ speecha cumbersome and nebulous
concept. In a well-meaning attempt to simplify Stekels
language, the translator fortuitously coined a word that has
now become ubiquitous. Somatization gained widespread
currency, particularly after 1980, when it was introduced as a
psychiatric diagnostic term by the authors of the DSM-III (2).
Since then, a huge literature has developed on somatization
and its various permutations. The word has caught on partly
because of its neutral connotation and partly because of the
authoritative power of the DSM classificatory system. It
replaced the ancient term hysteria, which was unsatisfac-
tory because of its multiple meanings and because it was so
often used pejoratively. The DSM-III also uses the term
Briquets syndrome as a synonym for somatization disorder
(SD) to honour the contribution made by the great

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19th-century physician, Pierre Briquet (35). However, the
DSM-IV has discarded this eponymous diagnosis (6).
Although the neutrality of the term somatization is advanta-
geous, the long history of the term hysteria must not be forgot-
ten, because many contributions have been made to the
diagnosis and treatment of this condition under the older
terminology.
My interest in and curiosity about this group of conditions was
aroused many years ago, when I worked as a medical intern
with a respected internist at a teaching hospital in London,
England. I was puzzled as to why, at the end of a series of neg-
ative medical investigations, my chief would tell a patient,
There is nothing wrong with you, when there so patently
was something wrong!
Definitions and Diagnosis
Merskey lists at least 7 conditions for which the term
somatization is used (7). These include hypochondriasis, con-
version, psychophysiological events, and SD, among others.
In general terms, somatization refers to the condition wherein
mental states and experiences are expressed as bodily symp-
toms. The term conversion, commonly used as a synonym for
somatization, usually implies that unconscious defence mech-
anisms are operative.
As originally described in the DSM-III, SD was characterized
by a wide variety of somatic symptoms affecting different
organ systems. The number of symptoms and systems was
precisely specified. SD is 1 of the 5 somatoform disorders, the
others being conversion, pain, hypochondriacal, and
dysmorphophobic disorders. They have in common the fea-
ture of presenting with somatic symptomatology, a relative
absence of physical causation, and a presumptive, but often
unstated, psychological cause.
The subjective element of these psychological phenomena
creates nosological difficulties related to the ancient monistic
vs dualistic controversy of mindbody relations. Most psychi-
atrists follow the phenomenological approach exemplified by
the DSM systems, which are based on the presence or absence
of certain clinical symptoms or signs and the monistic impli-
cation that mind and body are one. However, to state that the
practice of dichotomizing illness into mental and physical cat-
egories is archaic and deeply misleading, as does Kendell
(8), ignores the fact that some subjective psychological phe-
nomena crucial to the expression of psychiatric illness cannot
be categorized, as can physical phenomena, and that a science
based on purely mental states must therefore be implausible
(9). Our psychiatric diagnostic systems incorporate into the
diagnostic framework only a part of the subjective and objec-
tive phenomena of illness, namely, that which is observable.
Another partpersonal experiencecannot be categorized.
Although knowledge of current psychiatric classificatory
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Somatization Disorder: A Practical Review
systems is essential, it is worth bearing in mind these practical
limitations of psychiatric diagnosis. Changing sociocultural
variables also have a profound effect on diagnosis: the
definition of disease changes across societies over different
time (10).
The diagnostic concept of SD was based on the work of
Perley, Guze, and Woodruff in the 1960s (1113). Their
objective was to identify a clinical condition that could be
diagnosed in a consistent and replicable manner, and they
used the word stable to emphasize this replicability.
Although the diagnostic criteria were explicit, the number and
variety of symptoms meant that the full-blown condition was
rarely seen in practice. For this reason, the DSM-IV simplified
the criteria (6, Table 1), and they became easier to apply in a
clinical setting.
Conditions that do not meet all the specific symptomatic crite-
ria are characterized as undifferentiated somatoform disorder
when present for 6 months or more and somatoform disorder
not otherwise specified when present for less than 6 months.
Like the DSM-IV system, the ICD-10 also uses the term
somatization disorder and has dropped Briquets syndrome as
a synonym for SD (14). The ICD-10 lists the diagnoses and
provides general diagnostic guidelines, but it does not specify
or describe the symptoms required to make the diagnosis. The
diagnostic terminology of the 2 systems in this domain is
largely interchangeable.
This tabulation of the diagnostic criteria and reliance on num-
bers of symptoms, systems affected, and duration is in keep-
ing with the phenomenological framework and objectives of
the DSM nosological system. However, many practical diffi-
culties of diagnosis remain. Some relate to the continued need
to count the number of symptoms in each category, even
though these are now fewer in number than in the DSM-III.
Other difficulties pertain to the overlap of related conditions,
both organic and psychiatric. An attempt has been made to
further simplify the criteria by developing the concept of
abridged somatization, but further work needs to be done on
the parameters (15).
The conditions most likely to be confused with SD are organic
diseases that present with multiple symptoms affecting sev-
eral bodily systemsdiseases such as multiple sclerosis, sys-
temic lupus erythematosis, and certain endocrine conditions.
It is, of course, essential to identify such conditions when
present, but their presence or the presence of any other medi-
cal disease does not rule out SD, which can coexist with an
organic condition (16). Organic conditions (for example, side
effects from drugs or adhesions following inappropriate
abdominal surgery) may also develop following inappropriate
treatment of SD. The presence of any associated organic
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Table 1 Diagnostic criteria for 300.81 Somatization disorder (from the DSM-IV)

A. A history of many physical complaints beginning before age 30 years that occur over a period of several years and result in treatment
being sought or significant impairment in social, occupational, or other important areas of functioning.

B. Each of the following criteria must have been met, with individual symptoms occurring at any time during the course of the disturbance:
1. Four pain symptoms: a history of pain related to at least 4 different sites or functions (for example, head, abdomen, back, joints,
extremities, chest, rectum, during menstruation, during sexual intercourse, or during urination).
2. Two gastrointestinal symptoms: a history of at least 2 gastrointestinal symptoms other than pain (for example, nausea, bloating,
vomiting other than during pregnancy, diarrhea, or intolerance of several different foods).
3. One sexual symptom: a history of at least 1 sexual or reproductive symptom other than pain (for example, sexual indifference,
erectile or ejaculatory dysfunction, irregular menses, excessive menstrual bleeding, vomiting throughout pregnancy).
4. One pseudoneurological symptom: a history of at least 1 symptom or deficit suggesting a neurological condition not limited to pain
(conversion symptoms such as impaired coordination or balance, paralysis or localized weakness, difficulty swallowing or lump in
throat, aphonia, urinary retention, hallucinations, loss of touch or pain sensation, double vision, blindness, deafness, seizures;
dissociative symptoms such as amnesia; or loss of consciousness other than fainting).

C. Either (1) or (2):

1. After appropriate investigation, each of the symptoms in Criterion B cannot be fully explained by a known general medical condition
or the direct effects of a substance (for example, a drug of abuse, a medication).
2. When there is a related general medical condition, the physical complaints or resulting social or occupational impairment are in
excess of what would be expected from the history, physical examination, or laboratory findings.

D. The symptoms are not intentionally produced or feigned (as in factitious disorder or malingering).

disease complicates treatment and partly explains why physi-
cians manage many patients with SD so poorly.
There is also an overlap between SD and functional medical
syndromes such as fibromyalgia, chronic fatigue, and irritable
bowel (17). These conditions are known to occur together fre-
quently. Recent evidence even questions whether they are dis-
crete conditions or merely part of the same pathophysiological
process (18). Another study found that a diagnosis of either
SD or chronic fatigue was primarily affected by whether psy-
chiatric or physical terminology was used to interpret the
symptoms (19). A related study found that both patients with
chronic fatigue and their spouses were more likely than con-
trol subjects to attribute their symptoms to somatic disease,
even when they had a history of psychiatric illness (20). Both
the psychopathology and the pathophysiology of these condi-
tions are under continued investigation; hence, the criteria dif-
ferentiating them from SD are likely to change as new
research evidence comes to light.
Symptoms of associated psychiatric conditions such as anxi-
ety, mood disorder, hypochondriasis, and malingering
factitious disorder can also cause diagnostic difficulties. The
DSM-IV criteria for SD make no mention of dysphoria, but
symptoms of anxiety or depressed mood are very common in
patients with SD (21). Their presence does not invalidate the
diagnosis. Up to 50% of patients with unexplained medical
symptoms have sufficient criteria for a diagnosis of anxiety or
mood disorder (22). Two studies found a strong positive asso-
ciation between the number of somatic symptoms and overt
psychological distress, and it was concluded that somatic
symptoms were an expression of distress, not a defence
against awareness (23,24). Conversely, it has also been found
that somatic symptoms are common in patients with mood dis-
order (22).
For undifferentiated somatoform disorder, but not for SD, the
differential diagnosis section does specify that the diagnosis
not be made if the symptoms are better accounted for by
another mental disorder (for example, depression, anxiety, or
adjustment disorder). This leaves a substantial grey area
between the diagnoses of SD and the mood disorders. The
presence of dysphoric symptoms has therapeutic implications
(see Treatment below).
SD also largely overlaps with hypochondriasis. Briquet
regarded it (hypochondriasis) as a separate condition from
hysteria, but the conditions are more likely related and over-
lapping. The DSM-IV places them both under the umbrella
category of somatoform disorder. Like SD, hypochondriasis
is characterized by a preoccupation with physical symptoms;
however, a key feature is that it combines the fear with the
conviction that one has an organic disease. This fear may be
based on the misinterpretation of a physiological symptom
such as heartbeat or a relatively minor skin lesion, but the
misinterpretation is not of delusional intensity. In hypo-
chondriasis, the somatic symptoms are usually not multiple,
as they are in SD, but many body systems may be involved
over a period of time. A self-confessed hypochondriac pub-
lished a revealing and highly instructive account of her condi-
tion (25).
Malingering and factitious disorder are conditions that by def-
inition result in symptoms produced consciously and deliber-
ately for the purposes of secondary gain. Sutherland and
Rodin found a factitious disorder prevalence rate of 0.08% in

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a consecutive series of 1288 referrals to a consultation-liaison
service and noted high mortality and morbidity in this group
of patients (26). They also found an association with other
psychiatric conditions, including substance abuse and
somatization. How do clinicians identify the presence of con-
scious manipulation? Clearly, the patient has a vested interest
in concealing or denying its presence. Hence, it is of little
value to confront the patient with this conclusion; its presence
must be identified by implication. The history and examina-
tion will provide useful clues to perspicacious physicians.
Such obvious secondary gain as financial advantage, an
attempt to avoid an untoward legal outcome, and the seeking
of personal attention are suggestive. Another feature is lack of
consistency between the subjective severity of symptoms and
the effect they have on function. For example, the patient who
describes severe somatic symptoms but is able to perform and
function well outside the clinical setting is more likely to be
feigning symptoms than to have SD.
Etiology
One still reads that the etiology of SD is unknown (27). Use of
the phrase unexplained medical symptoms reinforces the
conclusion that we do not know the causes of SD. There is no
single cause for SD; as with most psychiatric conditions, the
disorder is the end result of the interplay between genetic fac-
tors and various events in the antecedent life history of the
individual. Current theories about its causation are grouped
into 3 categories: genetic, organic, and psychosocial.
Genetic
During the 19th century, Briquet found a strong tendency for
family clustering to occur in cases of hysteria (3,4). Of course,
family clustering may be the result of genetic or environmen-
tal influences, and it is likely that both play a role. Cloninger
and others found that male relatives of patients with Briquets
syndrome had increased prevalence of antisocial personality
and alcoholism and that female relatives of a male prison pop-
ulation revealed a high prevalence of Briquets syndrome
(28,29). These authors found that hysteria in women was a
more prevalent and less deviant manifestation of the same
process that causes sociopathy in men and that SD had a dif-
ferent familial pattern in women, compared with men.
Another study of women (n = 859) who had been adopted at
an early age by nonrelatives found that the adoptees had a sig-
nificant excess of somatizers, compared with a nonadopted
control group. The parents of the adoptees were known to
have excess numbers who showed criminal or psychotic
behaviour (30). Some twin studies have found evidence of a
genetic component (31,32), but others have drawn negative
conclusions (33,34). We may therefore conclude that,
although genetic factors may play a role in SD, the effect is a
limited one.
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Somatization Disorder: A Practical Review
Organic
Several studies have investigated a possible connection
between hysteria and cerebral pathology. Both Slater (35) and
Merskey and Buhrich (36) found that a high proportion of
people with hysteria had associated cerebral pathology, in
particular, epilepsy and multiple sclerosis. However, in a
comparable study from a psychiatric rather than a neurologi-
cal hospital setting, Roy found this association in only 3% of
patients (37). It has also been proposed that a dysfunction of
attention and memory associated with inhibition of afferent
stimulation exists in these patients (38) and that bifrontal cere-
bral impairment exists, particularly in the nondominant hemi-
sphere (39). A retrospective neuropsychological study found
evidence of brain dysfunction in 6 of 21 patients diagnosed
with hysteria (40). Patients with SD, compared with control
subjects, have been found to have deficiencies on neuro-
psychological testing (41). In a study comparing magnetic
evoked potentials in patients with psychogenic and organic
limb weakness, Meyer found that the former were associated
with normal values (42). An association between
somatization and elevated 24-hour cortisol levels (physiologi-
cal arousal) has been found (43), as has an association
between somatization and systolic blood pressure (44). Taken
together, these studies strongly suggest a nonspecific associa-
tion between somatization and organic (in particular, cere-
bral) disease. The mechanism by which this effect is mediated
is not clear.
Psychosocial
Illness behaviour is a concept relevant to somatization. It
was developed by Mechanic in the 1970s and refers to the
behaviours that an individual adopts when ill, such as going to
bed, taking medicines, going to see the doctor, or going to an
emergency department (that is, becoming a patient) (45).
Because the individual perceives him- or herself as being ill,
the nature of the illnesswhether it is mild or severe, organic
or psychiatricis not relevant to the development of illness
behaviour; the individual is unaware of the nature or the
severity of the illness.
Learning theory presupposes that behaviour is learned
through experience. Behaviour that is rewarded is thereby
promoted and reinforced and that which is not rewarded is
inhibited. Somatization may therefore be regarded as a
maladaptive way of obtaining social needs that substitutes for
deficits in a patients adaptive behavioural repertoire (46,47).
A child observing a sick parent or sibling may learn illness
behaviour. Previous experience of illness is an important fac-
tor in the pathogenesis of somatization. Through a process of
identification, a child who observes its parent during an illness
of any type, particularly if severe or chronic, may develop a
somatoform disorder when older. It has also been shown that
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Figure 1 Etiology of unexplained medical symptoms (from Gelder and others; 58)

Bodily sensations
physiological processes
minor pathology

Understanding
Cognitive Personality
knowledge experience of
illness
interpretation emotional arousal

Symptoms
behavioral change
disability

the fathers of women with SD are more likely to have an anti-
social personality disorder (28). Whether this effect is medi-
ated by genetic or psychosocial factors, or a combination of
both, is not known. Traditional psychoanalytic factors,
including conflicts with mother or father or difficulties in the
control and regulation of aggression and frustration, may also
play a part in individual cases. However, no experimental sur-
veys have tested the validity of these hypotheses on larger
groups of patients.
Ethnicity, education, and sex are other social factors relevant
to somatization. A high correlation has been found between
somatization and ethnicity (48,49), low social class with less
education (50), and female sex (51,52).
Doctors also play a part in the pathogenesis of SD. If patients
are poorly managed and subjected to unnecessary specialist
referral or expensive, invasive, diagnostic and therapeutic
procedures, this will ensure that complaints become imprinted
and medicalized. In such patients, therefore, iatrogenic fac-
tors must be regarded as part of the etiology.
Personality factors influence the development of SD. Persons
with this condition are more likely to have an underlying per-
sonality disorder or traitsin particular, those belonging to
Cluster B (53,54). Passive-dependent, histrionic, and
sensitive-aggressive traits were 2 times more prevalent
among SD patients than among patients with anxiety and
depression. Conversely, there was a high prevalence of SD in
patients diagnosed with borderline personality disorder. This
association may reflect a similar pattern of social interactions
between SD patients and those with Cluster B personality
disorders.
Life events may precipitate somatization. In a well-designed
study, Craig and others assessed the role played by stressful
life events and secondary gain in psychiatric illness (55). They
found that such events played a part in bringing on all psychi-
atric illness but that secondary gain was more common among
somatizers. They also offered 3 reasons for some patients
expression of dysphoria as a somatic symptom: 1) individual
differences in temperament and physiological response; 2)
social, cultural, and linguistic factors; and 3) previous experi-
ence of illness. As children, these patients had been neglected
and were only given attention when physically ill.
Personality factors, as expressed in the concept of alexi-
thymia, may be relevant to the etiology of SD in another way.
The word was coined by Sifneos (56), is derived from Greek,
and literally means no words for feelings. The term is based
on the psychoanalytic concept that patients somatize because
they are unable to express their feelings in words. There is an
extensive literature on the relation between alexithymia and
somatization (57). Much cross-sectional research has been
carried out, and most studies show a positive correlation
between alexithymia and somatization. However, there is a

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need for verification with longitudinal studies using tech-
niques that distinguish somatization from organic illness.
It needs to be emphasized that there is practical value in estab-
lishing a probable psychopathology in each individual
patient. The predisposingprecipitatingperpetuating
protective framework is a useful format for this
psychopathological construct. Not only does this framework
provide an understanding of the individual and the illness, it
also has therapeutic implications. If precipitating stress or sec-
ondary gain factors are present, for example, the patient is not
likely to improve or recover until these are actively and deci-
sively dealt with.
Gelder and others have provided a useful diagram summariz-
ing their view of the etiology of medically unexplained symp-
toms (Figure 1) (58). It portrays cognitive interpretation as the
final common pathway by which influences originating in
previous experience and in psychological and patho-
physiological factors lead to somatic symptoms. This con-
struct uses a learning theory model, makes sense heuristically,
and has profound implications for both the prevention and the
treatment of SD.
Prevalence
Epidemiologic studies have shown a lifetime prevalence of
somatization disorder that varies between 0.2% and 2.0% in
women (59). In men, the prevalence is likely less than 0.2%.
The reasons for the sex discrepancy are not clear. However,
the prevalence of hypochondriasis, a related condition, is
higher in men; hence, some of the discrepancy may be
explained on the basis of the overlap that exists between these
2 conditions. It was also found that the prevalence was higher
among Mexican Americans. Although SD is most prevalent in
the practice of family doctors, it is also common in specialist
practice, particularly in tertiary health care centres (60,61).
Curiously, epidemiologic studies have found a higher preva-
lence of SD when the interviewers are physicians. Perhaps
this finding is not so surprising and indicates that an inter-
viewee is more likely to describe a medical history to a physi-
cian than to a nonphysician.
The above studies show that SD may be as prevalent in the
community as schizophrenia. In terms of severity and cost to
the community and the health care services, it is also compara-
ble to schizophrenia (6264). A retrospective study of 13 314
consultations in a consultation-liaison service found that SD
caused disability and unemployment more frequently than
any other psychiatric disorder (65). Prevalence and severity
studies indicate a need for action to deal with this neglected
and frequently misdiagnosed condition.
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Somatization Disorder: A Practical Review
Treatment
Many physicians are negative and pessimistic about the treat-
ment of SD. This attitude is reinforced by the use of adjectives
such as chronic or stable to describe the condition. There are
certainly reasons for this attitude. A literature review of the
psychosocial treatments for this condition found that many
studies had methodological shortcomings (66). For example,
standardized diagnostic criteria may not always have been
used. Studies that employ generic terms such as somatization
or unexplained medical symptoms may be examining a subset
of patients different from those examined in studies
investigating a specific condition such as SD. This pessimism
also ignores the fact that poor medical management can aggra-
vate or perpetuate the condition: somatization patients have
an inconsistent pattern of care by their physicians; are dissatis-
fied with their treatment; and are referred inappropriately,
which leads to unnecessary exposure to iatrogenic damage
(67). The huge expense and poor outcome of invasive surgical
and medical procedures for somatizing patients has been well
documented (68).
A close analysis of this situation, however, suggests that this
pessimism is not justified. Effective, evidence-based treat-
ment for these conditions is now available, as reported by
Mayou and Sharpe (69) and Sharpe and Carson (70). These
authors emphasize the need to lead and educate public opinion
positively and nonjudgementally by emphasizing the integrity
of physical, psychological, and social factors in this illness.
They suggest that we return to a neurobiological rather than a
psychological model to manage these patients. We need to
approach them as having a reversible, functional disturbance,
rather than a purely psychogenic one. The effectiveness of
even a single psychiatric consultation that includes specific
treatment recommendations to the family doctor has been
demonstrated (71).
Quill gave 4 reasons for the difficulty doctors experience in
managing patients with SD: ignorance of the condition, the
drive to rule out organic disease, the discomfort of many phy-
sicians when exploring psychological issues, and the fear of
missing an organic disease (72). He emphasized the need for
education, particularly of primary care physicians who often
are the front-line workers in this condition. In a persuasive
study that randomized somatizing patients into treatment and
no-treatment groups, Smith showed that health care costs
declined by 53% when primary care physicians treated their
SD patients appropriately (73).
General Principles
Once SD has been diagnosed, the first step in treatment is to
give diagnostic feedback to the patient. A fascinating paper
has been published on this exact topic (74). The authors stud-
ied a random sample of 68 somatizing patients in a family
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Table 3 Management of somatization disorder

1. General principles
a) Comprehensive clinical assessment (history, mental state, and physical examination).
b) Interview key family member.
c) Minimize number of clinicians involved. Ensure a consistent, coordinated management plan.
d) Minimize invasive diagnostic and therapeutic proceedures.
e) Ensure regular, structured sessions. Avoid as-needed visits to doctors and emergency departments.
f) Recognize reality of symptoms and provide diagnostic feedback to both patient and family member. Where appropriate,
link symptoms to stressful life events.
g) Identify and minimize secondary reinforcers.
h) Treat associated medical and psychiatric conditions appropriately.

2. Cognitive-behavioural therapy
a) Develop treatment contract (listing agreed approximate frequency, duration, and number of sessions).
b) Set realistic short- and long-term goals. Review these regularly.
c) Focus on practical ways of coping with symptoms and limitations.
d) Encourage patient to keep a daily log of thoughts, feelings, and coping behaviours. Review these regularly.
e) Promote daily physical, social, recreational, and occupational activities.
f) Promote daily relaxation activities and exercises.
g) Promote patient control and autonomy.

3. Pharmacotherapy
a) Minimize use of habit-forming drugs.
b) Avoid as-needed medication.
c) Use antidepressant medication where appropriate.

practice setting. Taped transcripts of the explanations that Specific Treatments

doctors gave to patients for their symptoms were analyzed.
The explanations were categorized into 3 types: rejection, col-
lusion, and empowerment. With rejection, the doctor denied
the reality of the symptoms or implied that they had an imagi-
nary source. This approach, found in most of the doctors stud-
ied, is typified by my former chiefs statement (referred to in
this papers introduction), There is nothing wrong with you.
Collusion occurred when the physician explicitly or implicitly
acquiesced to the patients explanation. Finally, with empow-
erment, the physician gave the patient a tangible, rational
explanation for the somatic symptoms, together with an
opportunity for self-management. The doctor legitimized the
patients suffering, removed blame, and created a therapeutic
alliance. The symptom and emotion were thereby linked.
A similar approach was used in a fine paper published earlier
by Goldberg and others (75). These authors identified 3 stages
in the treatment process: 1) feeling understood, in which the
patients symptoms were heard out; 2) changing the agenda,
in which the reality of the symptoms was recognized, as was
the existence of stressful life events; and 3) linking the symp-
toms and life events, in which psychophysiological analogies
(as exemplified by the physiological changes that accompany
anxiety and depression) were provided.
Approaches to the treatment of somatization are psychologi-
cal, pharmacologic, or a combination of both. Table 2 summa-
rizes the treatment modalities that may be used in SD. The
psychological therapies are supportive psychotherapy and
cognitive-behavioural therapy (CBT). Supportive psycho-
therapy is best carried out by a physician who is sympathetic
and understanding toward the patients particular difficulties
and who is able to respond appropriately to both the physical
and the emotional problems presented (76). The advantage of
the therapists being a physician accrues from the fact that
most patients with SD believe they have a medical, as distinct
from a psychiatric, disorder. They are therefore more able to
trust a physician to respond appropriately to their physical
health problems. Therapy sessions must be regular, struc-
tured, and consistent. They need to be sufficiently frequent to
provide support and reassurance but not so frequent that
excessive dependency is fostered. In general, patients should
be discouraged from emergency or as-needed visits to the
doctor or the emergency department and also from extended
therapeutic telephone calls. These serve only to promote and
reinforce illness behaviour and preoccupation with physical
symptomatology. As rapport is established, the interval
between visits can be gradually extended.
A study by Guthrie and others describes the use of
psychotherapeutic intervention limited to 8 sessions in 110

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high users of the psychiatric services, a substantial proportion
of whom had a somatoform disorder (77). Patients were ran-
domized to treatment and to a no-treatment control group. At
6-month follow-up, the treatment group had improved, and
had made less use of services, compared with the control
group. The authors also found that many of the patients
declined therapy and that there was a high dropout rate.
When the tendency to somatize is tenacious, the treatment
contract may need to be long-term. In patients with a
long-standing tendency to somatize, therapeutic objectives
may be limited to stabilizing the behaviour and preventing it
from escalating. Murphy has emphasized that the essence of
the sophisticated management of hysteria is to avoid errors of
commission (78). During therapy sessions, the patients
attention should as far as possible be focused away from
health and symptoms and more toward daily life, activities,
and relationships. This may require the therapist to avoid
inquiring about the presence of specific symptoms; however,
if these are volunteered spontaneously, the response should be
limited to general sympathy and support, and a symptomatic
line of inquiry should not be pursued. It may be of value to
give the patient specific behavioural objectives (for example,
walking a certain distance so many times weekly or joining
particular social or recreational functions). To emphasize
their importance, these objectives can be given as a written
prescription, with the added request that the patient record in a
daily diary when and for how long the activity was performed.
This diary can be brought in to subsequent sessions for inspec-
tion and review. Goldberg and others have described an excel-
lent psychoeducational approach to the treatment of
somatization (75), and Fink and others have more recently
described a 2-day educational course for therapists (79).
Many of the above principles merge into the CBT model of
treatment for the condition. CBT must be regarded as the most
efficacious treatment for SD. A critical review of 31 con-
trolled studies published prior to 2000 concluded that it
should be used either as the first-line treatment or as treatment
for patients who fail simpler strategies (80). An interesting
finding was that the beneficial effect of CBT occurred inde-
pendently of improvement in psychological distress. In other
words, it was not necessary to relieve symptoms of dysphoria
to diminish the intensity and number of somatic symptoms.
Improvement occurred because of better coping, decreased
illness worry, lessened avoidant behaviour, and greater per-
ceived control.
In CBT, the therapist structures the patients social and physi-
cal environment to promote appropriate behaviour (in this
case, healthy social and personal adjustment without
somatization) and discourage inappropriate behaviour (that
is, illness behaviour and preoccupation with physical symp-
toms). Excellent, practical descriptions of CBT techniques are
Can J Psychiatry, Vol 49, No 10, October 2004 W
Somatization Disorder: A Practical Review
available in publications by Sharpe and others (81) and
Kuhlwein (82). These authors emphasize that the way individ-
uals think about their bodily sensations is central to the behav-
ioural model. They note that somatic symptoms cause
emotional distress and that family members and physicians
can unwittingly reinforce the patients illness behaviour.
They also emphasize the need to have treatment goals and a
treatment contract in which issues such as the number and fre-
quency of sessions and the requirement to do homework are
stated clearly. For homework, patients are asked to read cer-
tain relevant literature, keep a diary, record their feelings and
thoughts, and bring these topics back to the treatment sessions
for discussion. Barriers to treatment must be identified and
dealt with.
A randomized controlled trial (RCT) of CBT in the treatment
of unexplained medical symptoms (n = 79) concluded that, at
6-month follow-up, 82% of patients and 64% of control sub-
jects had improved or recovered (a significant difference) and
that this difference was maintained at 12-month follow-up
( 8 3 ) . A n o th e r s tu d y f o u n d th a t a g r o u p - b a s e d
psychoeducational approach combined with relaxation ther-
apy effectively decreased somatic preoccupation, hypochon-
driasis, and medication use in SD patients in a primary care
setting (84). The National Institute of Mental Health is cur-
rently recruiting patients for a randomized, single-blind study
of the efficacy of CBT for SD (85). A second goal is to exam-
ine the effectiveness of CBT among hispanics, since hispanics
have a relatively high prevalence of SD.
Regular structured sessions, discouraging emergency visits,
setting behavioural goals, and avoiding the pursuit of physical
investigations and treatments may all be seen as following the
behavioural principles of management within a supportive,
nonauthoritarian, medical psychotherapeutic framework.
It is also valuable to work with the patients spouse and fam-
ily. They are unwittingly involved in the patients illness and
behaviour and will harbour feelings and reactions that will
have a positive or negative effect on outcome. It is useful to
provide diagnostic feedback to the patient and the spouse or
family together. This ensures that the next-of-kin do not have
to rely on the patients possibly distorted report. Conjoint
feedback also gives family members the opportunity to voice
their concerns, observations, and questions, all of which may
be essential to diagnosis and treatment. Family support is vital
to an effective treatment plan. These arrangements form part
of the CBT process of environmental modification, that is,
structuring or altering the patients social, physical, and occu-
pational surroundings to promote a more therapeutic milieu.
Relaxation therapy may be of value in this group of patients. A
practical description of the technique for instructing patients
in relaxation is available (86). Patients must carry out the exer-
cises regularly, no less than 3 times weekly, and must persist
659
The Canadian Journal of PsychiatryIn Review
in this endeavour. The maximum benefit from relaxation ther-
apy occurs when it is practised frequently over an extended
length of time. Aerobic exercise has been proposed as an aid
to treatment of SD, but an RCT found that it offered no benefit
over nonaerobic exercise (87).
Pharmacologic Therapies
Little work has been done on the use and efficacy of pharma-
cologic agents in SD. However, antidepressants are effective
in patients with unexplained medical symptoms, even in the
absence of dysphoria (88). Some texts either make no mention
of medication or consider that drugs be kept to the minimum
(27,58). The prevalence of psychiatric comorbidity with SD,
including anxiety, phobic, and depressive disorders, suggests
that medication does have a place for at least some patients
with SD. Fluoxetine has been found to be effective in
dysmorphophobic disorder (89) and in hypochondriasis, and
paroxetine has been found to be effective in somatization dis-
order (90). Antidepressants are also widely recommended and
used in other chronic somatoform disorders, such as pain dis-
order. On a priori principles, therefore, it would appear rea-
sonable to give antidepressants to at least some patients with
SD, particularly when dysphoric symptoms are present.
It should be remembered that the tendency to somatize may
increase the sensitivity and probability of side effects. Starting
with a small dosage and titrating gradually can minimize this
tendency. For this reason, it is more appropriate to use selec-
tive serotonin reuptake inhibitors than to use tricyclic anti-
depressants. Monoamine oxidase inhibitors may also have a
role in a small group of drug-resistant patients.
When anxiety and phobic symptoms are present, care must be
taken with the use of anxiolytic drugs. Patients with SD com-
monly have dependent personalities and, hence, easily
become reliant on them. This is particularly likely to occur if
the medication is given as-needed. If needed, anxiolytic drugs
are best given for short periods only and in a fixed-time for-
mat, rather than as-needed.
Conclusions
Clinical experience and a review of the literature on SD indi-
cate that it is a common condition and that it can be severe and
disabling. Because of its clinical characteristics, it falls
between the cracks in management. It is a psychiatric condi-
tion, but patients are reluctant to see psychiatrists, and
nonpsychiatric physicians commonly have little knowledge
and understanding of its psychopathology and treatment.
They may therefore unwittingly aggravate or perpetuate the
condition. SD makes huge demands on the health care ser-
vices. In the pantheon of psychiatric disorders, its relative
neglect by our specialty has allowed SD to compete with
depression and schizophrenia in terms of its clinical and phys-
ical costs to society.
A body of evidence-based knowledge about SD is now accu-
mulating. This shows that it is a treatable condition, particu-
larly in the early stages before its illness-behaviour aspects
have become embedded. A cadre of well-trained therapists
who are knowledgeable in the principles and practice of CBT
660
is required in both family practice and tertiary care settings,
where most SD patients are found.
This review shows that many advances have been made in
recent years, both in our understanding of SD and in its treat-
ment. The task now is to ensure that these advances are widely
disseminated and acted upon. Hopefully, this will lead to SDs
going the way of syphilis when, in the future, a history of the
condition is written.
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Manuscript received and accepted July 2004.
1
Formerly, Chief of Psychiatry, Ottawa General Hospital, Ottawa, Ontario;
now, Consultant, Department of Psychiatry, The Ottawa Hospital, Ottawa,
Ontario; Medical Advisor, Medical Expertise Division, Social
Development Canada, Ottawa, Ontario.
Address for correspondence: Dr F Mai, Medical Advisory Unit, 355 River
Road, Tower B, 3rd Floor, Ottawa ON K1A OL1
e-mail: francois.mai@sdc-dsc.gc.ca
661
The Canadian Journal of PsychiatryIn Review

Rsum : Trouble de somatisation : une analyse pratique

Objectif : Cet article examine ltat actuel des connaissances sur ltiologie, la prvalence, le
diagnostic et le traitement du trouble de somatisation (TS).
Mthode : Une analyse dtaille de la documentation sur le TS est dcrite sous les titres mentionns
ci-dessus.
Rsultats : Le TS est une affection frquente qui nest pas bien traite par nombre de mdecins. Les
patients souffrant de TS ne trouvent pas de crneau dans le systme de sant, et les consquences sont
coteuses. Le TS est un trouble psychiatrique, mais les patients sont rbarbatifs voir un psychiatre et
se faire traiter par lui. Ils sont souvent traits par des mdecins non psychiatriques qui ont une
comprhension limite de cette affection. La thrapie cognitivo-comportementale (TCC) est le
traitement le plus efficace du TS, bien que les antidpresseurs et la psychothrapie de soutien jouent
aussi un rle auprs de certains patients.
Conclusions : Il faut un cadre de cliniciens ayant une formation sur la thorie et la pratique de la TCC
pour le TS. Ils doivent exercer dans les centres de sant communautaire et de soins tertiaires, o se
trouvent la plupart des patients atteints de cette affection.

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