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When it was still a prevalent condition during the 19th and early 20th centuries, syphilis was known in medicine 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 psychoanalyst Wilhelm Stekel in the 1920s (1). The word organsprache literally means “organ speech”—a cumbersome and nebulous concept. In a well-meaning attempt to simplify Stekel’s 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 unsatisfactory because of its multiple meanings and because it was so often used pejoratively. The DSM-III also uses the term “Briquet’s syndrome” as a synonym for somatization disorder (SD) to honour the contribution made by the great 19th-century physician, Pierre Briquet (3–5). However, the DSM-IV has discarded this eponymous diagnosis (6). Although the neutrality of the term somatization is advantageous, the long history of the term hysteria must not be forgotten, 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 negative medical investigations, my chief would tell a patient, “There is nothing wrong with you,” when there so patently was something wrong! Definitions and Diagnosis 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 feature 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 mind–body relations. Most psychiatrists 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 implication that mind and body are one. However, to state that the practice of dichotomizing illness into mental and physical categories is “archaic and deeply misleading,” as does Kendell (8), ignores the fact that some subjective psychological phenomena 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 objective phenomena of illness, namely, that which is observable. Another part—personal experience—cannot be categorized. Although knowledge of current psychiatric classificatory 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 (11–13). 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 criteria 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 Briquet’s 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 numbers of symptoms, systems affected, and duration is in keeping with the phenomenological framework and objectives of the DSM nosological system. However, many practical difficulties 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 several bodily systems—diseases such as multiple sclerosis, systemic 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 medical 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 disease complicates treatment and partly explains why physicians 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 frequently. Recent evidence even questions whether they are discrete 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 psychiatric 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 control 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 conditions are under continued investigation; hence, the criteria differentiating them from SD are likely to change as new research evidence comes to light. Symptoms of associated psychiatric conditions such as anxiety, 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 association 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 disorder (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 overlapping. 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 hypochondriasis, 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” published a revealing and highly instructive account of her condition (25). Malingering and factitious disorder are conditions that by definition result in symptoms produced consciously and deliberately for the purposes of secondary gain. Sutherland and Rodin found a factitious disorder prevalence rate of 0.08% in 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 conscious 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 examination 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. EtiologyOne 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 factors 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 Organic Psychosocial 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 patient’s adaptive behavioural repertoire (46,47). A child observing a sick parent or sibling may learn illness behaviour. Previous experience of illness is an important factor 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 the fathers of women with SD are more likely to have an antisocial personality disorder (28). Whether this effect is mediated 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 surveys 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 factors 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 personality disorder or traits—in 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 psychiatric 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 experience 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 “alexithymia,” 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 need for verification with longitudinal studies using techniques that distinguish somatization from organic illness. It needs to be emphasized that there is practical value in establishing a probable psychopathology in each individual patient. The predisposing–precipitating–perpetuating– 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 secondary gain factors are present, for example, the patient is not likely to improve or recover until these are actively and decisively dealt with. Gelder and others have provided a useful diagram summarizing their view of the etiology of medically unexplained symptoms (Figure 1) (58). It portrays cognitive interpretation as the final common pathway by which influences originating in previous experience and in psychological and pathophysiological factors lead to somatic symptoms. This construct uses a learning theory model, makes sense heuristically, and has profound implications for both the prevention and the treatment of SD.  PrevalenceEpidemiologic 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 prevalence of SD when the interviewers are physicians. Perhaps this finding is not so surprising and indicates that an interviewee is more likely to describe a medical history to a physician 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 comparable to schizophrenia (62–64). 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. TreatmentMany physicians are negative and pessimistic about the treatment 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 aggravate or perpetuate the condition: somatization patients have an inconsistent pattern of care by their physicians; are dissatisfied 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 treatment 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 physicians 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 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 patient’s 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 symptoms and life events, in which psychophysiological analogies (as exemplified by the physiological changes that accompany anxiety and depression) were provided. Specific Treatments
A study by Guthrie and others describes the use of psychotherapeutic intervention limited to 8 sessions in 110 high users of the psychiatric services, a substantial proportion of whom had a somatoform disorder (77). Patients were randomized 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 patient’s 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 inspection and review. Goldberg and others have described an excellent 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 controlled 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 independently 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 perceived control. In CBT, the therapist structures the patient’s social and physical 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 symptoms). Excellent, practical descriptions of CBT techniques are available in publications by Sharpe and others (81) and Kuhlwein (82). These authors emphasize that the way individuals think about their bodily sensations is central to the behavioural model. They note that somatic symptoms cause emotional distress and that family members and physicians can unwittingly reinforce the patient’s illness behaviour. They also emphasize the need to have treatment goals and a treatment contract in which issues such as the number and frequency of sessions and the requirement to do homework are stated clearly. For homework, patients are asked to read certain 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 subjects had improved or recovered (a significant difference) and that this difference was maintained at 12-month follow-up (83). Another study found that a group-based psychoeducational approach combined with relaxation therapy effectively decreased somatic preoccupation, hypochondriasis, and medication use in SD patients in a primary care setting (84). The National Institute of Mental Health is currently recruiting patients for a randomized, single-blind study of the efficacy of CBT for SD (85). A second goal is to examine 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 patient’s spouse and family. They are unwittingly involved in the patient’s 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 patient’s 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 patient’s social, physical, and occupational 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 exercises regularly, no less than 3 times weekly, and must persist in this endeavour. The maximum benefit from relaxation therapy 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 TherapiesLittle work has been done on the use and efficacy of pharmacologic 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 disorder (90). Antidepressants are also widely recommended and used in other chronic somatoform disorders, such as pain disorder. On a priori principles, therefore, it would appear reasonable 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 selective serotonin reuptake inhibitors than to use tricyclic antidepressants. 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 commonly 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 format, rather than as-needed. ConclusionsClinical experience and a review of the literature on SD indicate 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 condition, 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 services. 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 physical costs to society. A body of evidence-based knowledge about SD is now accumulating. This shows that it is a treatable condition, particularly 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 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 treatment. The task now is to ensure that these advances are widely disseminated and acted upon. Hopefully, this will lead to SD’s going the way of syphilis when, in the future, a history of the condition is written. References1. Marin C, Carron R. The origin of the concept of somatization. Psychosomatics 2002;43:249–50. 2. American Psychiatric Association. Diagnostic and statistical manual of psychiatric disorders. 3rd ed. Washington (DC): American Psychiatric Association; 1980. 3. Briquet P. Traité de l’hysterie. Paris: Baillière; 1859. 4. Mai FM, Merskey H. Briquet’s treatise on hysteria. Arch Gen Psychiatry 1980;37:1401–5. 5. Mai FM, Merskey H. Briquet’s concept of hysteria: an historical perspective. Can J Psychiatry 1981;26:57–63. 6. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. 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O’Malley PG, Jackson JL, Santoro J, Tomkins G, Balden E, Kroenke K. Efficacy of antidepressants for physical symptoms: a critical review of the literature. J Fam Pract 1999;48:980–90. 89. Phillips K, Albertini R, Rasmussen S. A randomized placebo-controlled trial of fluoxetine in body dysmorphophobic disorder. Arch Gen Psychiatry 2002;59:381–8. 90. Okugawa G, Yagi A, Kusaka H, Kinoshita T. Paroxetine for treatment of somatization disorder. J Neuropsychiatry Clin Neurosci 2002;14:464–5. Author(s)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
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