Publication
Article
Psychiatric Times
Author(s):
he key manifestations of DSM-IV somatoform disorder are unexplained physical symptoms or complaints that tend to coexist with other psychiatric syndromes or are linked to psychological issues. These symptoms typically lead to repeated medical or emergency department visits; are associated with serious discomfort, dysfunction, and disability; and lead to significant health expenditures.
CHECK POINTS
The key manifestations of DSM-IV somatoform disorder are unexplained physical symptoms or complaints that tend to coexist with other psychiatric syndromes or are linked to psychological issues. These symptoms typically lead to repeated medical or emergency department visits; are associated with serious discomfort, dysfunction, and disability; and lead to significant health expenditures. Despite their frequency and relevance to both primary care and psychiatric practices, the definition, classification, and management of these disorders remain difficult and controversial. Moreover, there are little systematic research data available for these disorders across medical disciplines. Diagnostic changes made on the basis of capricious committee recommendations often become a “moving target,” thus decreasing the ability to compare studies over time.
A Brief History
Dramatic and peculiar somatic manifestations that perplex clinicians have been with us since ancient times. A brief review of their historical evolution shows that they metamorphose as medical paradigms change. For example, labels such as hysteria, hypochondria, spleen, English disease, soldier’s heart, neurocirculatory asthenia, neurasthenia, surmenage, humoral disorders, psychosomatic disorders, and many others have been fashionable or relevant during certain periods, but most eventually faded into oblivion or were replaced by more technical terminology. Despite steady efforts to eradicate them, the survival of some of these terms (hysteria, neurasthenia) is probably proof of their validity.
In psychiatry, the term “somatization” has been used for decades to label these somatic presentations. The classical concept of somatization was coined by Wilhelm Stekel,1 a Viennese psychoanalyst who immigrated to America. He described it as a “deep-seated neurosis” or as the “process by which neurotic conflicts appear as a physical disorder.” In North American psychiatry, this concept was expanded by Zbigniew J. Lipowski,2 who described somatization as the “tendency to experience, conceptualize, and/or communicate psychological states or meanings as corporeal sensations, functional changes, or somatic metaphors.”
The psychogenic view generally considered somatic presentations as ancillary manifestations of psychological discomfort. The more direct and pragmatic approach to somatization that would eventually lead to the atheoretical frame of modern nomenclatures began with French psychopathologist Pierre Briquet,3 who, in 1859, brought an observational or experiential perspective to the study of hysteria during the golden age of French psychopathology. His description of a syndrome inclusive of multiple motor and sensorial symptoms (pseudoneurological symptoms) made possible the separation of somatization from conversion.
In the 1950s, a group of investigators at Washington University–Renard Hospital in St Louis resurrected Briquet’s concept of hysteria in several clinical studies. They formulated criteria for the diagnosis of hysteria that required the presence of a specified number of symptoms from a comprehensive list that included physical and psychological manifestations, personality traits, and behavioral expressions, in addition to the neurological symptoms from the traditional French definition.4,5
With a few modifications, these were the criteria for somatization disorder proposed by Feighner and colleagues6 in 1972 in their seminal paper, “Diagnostic Criteria for Use in Psychiatric Research.” After Robert Spitzer and his colleagues7 coined the term “somatoform disorder” (inclusive of the Greek soma and the Latin form), it officially entered American and world psychiatric terminology with the publication of the International Classification of Diseases criteria in the late 1970s and the DSM-III in the 1980s.
Somatoform Disorders in DSM
Following the publication of DSM-III in the 1980s, somatization disorder (SD) became the key somatoform diagnosis. In DSM-III and its subsequent revisions, SD turned into a simple somatic symptom list that contracted or expanded rather capriciously. Partly because the atheoretical perspective of DSM discarded any presumptions of causality, other manifestations of the syndrome were not included in the criteria.
The list of somatoform disorders kept expanding with the addition of vague categories, such as “undifferentiated somatoform disorder” or “somatoform disorder NOS [not otherwise specified],” which, unfortunately, are the most common diagnoses within the somatoform genre. These terms failed to transcend specialty boundaries. Perhaps as a corollary of turf issues, general medicine and medical specialties started carving these syndromes with their own tools. The resulting list of “medicalized,” specialty-driven labels that continues to expand includes fibromyalgia, chronic fatigue syndome, multiple chemical sensitivity, and many others (Table 1).
Irritable bowel syndrome
Chronic fatigue syndrome
Fibromyalgia
Multiple chemical sensitivity
Nonspecific chest pain
Premenstrual disorder
Non-ulcer dyspepsia
Repetitive strain injury
Tension headache
Temporomandibular joint
disorder
Atypical facial pain
Hyperventilation syndrome
Globus syndrome
Sick building syndrome
Chronic pelvic pain
Chronic whiplash syndrome
These labels fall under the general category of functional somatic syndromes and seem more acceptable to patients because they may be perceived as less stigmatizing than psychiatric ones. However, using DSM criteria, virtually all these functional syndromes would fall into the somatoform disorders category given their phenomenology, unknown physical causes, absence of reliable markers, and the frequent coexistence of somatic and psychiatric symptoms.
Epidemiology
Medically unexplained physical symptoms are extremely common in adults. They are more frequently seen in females, in persons from lower socioeconomic backgrounds, and in certain ethnic groups. These symptoms are also fairly common in childhood and adolescence; a recent study showed that 10% of children surveyed had unexplained headaches, 9% had unexplained abdominal pain, and 4% had unexplained pain in the extremities.8
The Epidemiological Catchment Area Survey of Mental Disorders in the United States reported that fewer than 0.1% of respondents met strict DSM-III criteria for SD, and about 5% met criteria for abridged SD, a less restrictive construct of somatization.9 In Germany, about 20% of a community sample met criteria for undifferentiated SD, but very few (about 1%) met criteria for the more specific somatoform disorders.10
The prevalence of unexplained physical symptoms is much higher in primary care and medical specialty settings. A World Health Organization (WHO) study at 14 primary care sites in Asia, Europe, and the Americas showed that the rates for abridged SD differed widely across countries. They were lowest in Nigeria (7.6%), Italy (8.9%), and the United States (9.8%) and highest in Germany (25.5%), Brazil (32%), and Chile (36.8%).11
In a North American study, patients with SD reported spending an average of 8.8 days sick in bed per month, compared with half a day for those without the disorder. More than 80% of patients with SD stopped working because of “poor health” and their per capita yearly health costs were 9 times higher than average.12 A study of patients with SD who attended a university outpatient service in London showed that 61% were receiving disability benefits, 64% had been treated for spurious physical disorders, 60% had had surgeries with no pathology found, and 16% were using either wheelchairs or crutches without any evidence of organic disorder.13
Unexplained physical symptoms tend to have a chronic, protracted course. For example, in the South London Somatization Study, most patients had a chronic unremitting course. About 80% of these persons still qualified for a somatoform diagnosis 4 years later.14 A follow-up in the WHO study showed that, 1 year later, somatization persisted in about half of the patients.11
The causes of SD are multifactorial. Although no consistent biological (brain) markers have been documented, genetic factors may play a role. Findings from studies of adopted females with SD suggest excessive alcoholism or violent behavior in the biological fathers.15 More recent studies have shown that there is familial clustering of functional syndromes such as fibromyalgia.16 A large number of studies have shown a frequent association between unexplained physical symptoms and early traumatic experiences; medical illness with long hospitalizations; serious medical illness of a parent; natural disasters; or psychological factors such as sensitization processes, specific cognitive styles, or benefits derived from the sick role (secondary gain).17-23
The most common psychiatric conditions that coexist with unexplained physical symptoms are major depression, anxiety, substance use, personality disorders, and posttraumatic stress disorders.24 Averaging data from several studies, about two-thirds of patients with unexplained symptoms also met criteria for at least one of these psychiatric disorders and a large portion of the remaining one-third, who did not fully meet the criteria, had significant symptoms, mainly depression or anxiety.25
Diagnosing and Managing SD
Not surprisingly, patients with unexplained physical symptoms are first seen by primary care or nonpsychiatric specialists, who usually make the initial diagnosis. Unfortunately, only about 1 of 4 primary care physicians acknowledge feeling confident about their ability to treat these patients. The percentage of primary care practitioners who report confidence in managing other mental disorders, such as depression or anxiety disorders, is much higher.26
Assisting primary care providers through instructional sessions and manuals or simply by using a consultation letter has proved to be useful.27,28 Referral of these patients to mental health services is generally unsuccessful unless proper bridges between primary and mental health care are built. This requires patient preparation, careful teamwork, and the presence at the primary care site of trained mental health personnel.
Because of the high level of discomfort associated with unexplained symptoms, to be told that “there is no physical problem” is disconcerting to many patients. For the provider, however, finding no physical abnormality generally brings a sense of relief. In building a good therapeutic relationship, it is important for the therapist not to downplay the patient’s discomfort at being told “there is no problem” or “your symptoms are all psychological.” As in any other field of medicine, empathy and acknowledging the patient’s distress are essential ingredients for a sound therapeutic relationship. Table 2 provides a stepwise list of suggestions for communicating a diagnosis of SD to the patient.
If properly communicated, the diagnosis of SD may offer relief and encouragement to the patient. For example, in a recent study, patients with unexplained symptoms felt that receiving such a diagnosis after a time of worry and uncertainty was an important factor in successfully managing the disorder.
29
Regular patient visits should be scheduled (eg, monthly or bimonthly) independent of fluctuations in symptoms. Treatment goals must be concrete, stepwise, and realistic. Do not aim for an all-or-nothing result, but consider a gradual and incremental response. The goal is to progressively decrease emergency visits and calls.
A routine examination is recommended at every visit to reassure the patient and to ensure that there are no physical abnormalities (remember that paranoid people may have real enemies). However, no new tests or consultations should be ordered unless there is a clear indication. Rather than reassuring patients, unwarranted consultations or tests may feed their belief that they have a serious physical illness.
During the visit, the patient can be allowed to play the “sick role.” Allow him or her to verbalize complaints and concerns without entering into needless arguments on issues related to the reported symptoms. The objective is not to negate the symptoms but to improve functionality and well-being. Briefly discuss current stress factors and other important circumstances, and make sure the patient understands that the unexplained symptoms are elements of a biopsychosocial illness. Table 3 presents a list of goals to work toward.
Treatment Options
Evidence is rapidly growing for the usefulness of modified cognitive-behavioral therapies for somatoform syndromes.30,31 A comprehensive model successfully applied in several studies included relaxation training, behavioral management, cognitive restructuring, emotion identification, emotion regulation, and interpersonal skills training.32 Other types of psychotherapy have not been tested in well-controlled studies. However, it is our impression that intensive or exploratory therapies that focus on internal conflict and mental change may be counterproductive.
As mentioned, mental disorders such as significant depression and anxiety are common in those with SD and should be specifically addressed. However, there is no clear evidence from randomized clinical trials demonstrating the efficacy of psychotropic drugs for the treatment of unexplained physical symptoms. The benefit observed in some studies has been attributed to the effect of medications on anxiety or depressive symptoms and not to a direct effect on somatic symptoms.
On the basis of our clinical experience, patients with SD accompanied by significant depression and anxiety symptoms can be initially treated with an SSRI or a serotonin norepinephrine reuptake inhibitor. Mirtazapine seems to be a reasonable first option for patients with unexplained symptoms who have significant insomnia or anorexia because of the drug’s positive effects on sleep and appetite. In patients with significant fatigue/sleepiness or poor concentration, or those in whom the avoidance of sexual adverse effects is paramount, bupropion may be a good first-line agent.
Because patients with SD may be at a heightened risk for addiction or dependence, caution must be exercised when prescribing medications with addictive potential, such as opiate analgesics and tranquilizers such as benzodiazepines. In patients with SD, pain complaints are very common and include headaches, and joint, abdominal, and pelvic pain. NSAIDs should be used whenever possible for pain relief.
FDA-Approved Medications
The anticonvulsant pregabalin and the antidepressant duloxetine have been recently approved for the treatment of fibromyalgia. Pregabalin has analgesic properties, especially for neuropathic pain, and has also shown some antianxiety effects in randomized clinical trials. Duloxetine, a dual action antidepressant, also seems to exert some analgesic properties similar to those reported for other dual action drugs as well as tricyclic antidepressants.
Lufriprostone has been approved for clinical use in irritable bowel symptoms alternating with chronic idiopathic constipation syndromes. This drug appears to exert a laxative action by increasing the secretion of chloride and fluid in the intestinal epithelium.
Fluoxetine, paroxetine, and sertraline have been approved for the treatment of premenstrual dysphoric disorder/premenstrual syndrome, which have a number of somatic manifestations and also include anxiety and depression symptoms. A recent meta-analysis found that all SSRIs seem to be about equally helpful for premenstrual symptoms, their continuous use is better than intermittent use, and their clinical effect on symptoms seems to be relatively small.33The Future Definition of SD
As we prepare for the new edition of DSM-V, we suggest the following:
• Consider a dimensional approach for unexplained physical symptoms with differences in severity.
• Avoid further expansion of somatoform categories and the mechanistic count of symptoms and systems. There is a need for evidence-based,inclusive, and simpler definitions.
• Do not devalue the psychological, cultural, and social aspects in patients with somatoform disorders; instead, emphasize their character as complex expressions of distress and sickness.
• Do not subordinate somatic presentations to other mental disorders or to purely mental mechanisms. Acknowledge the unique and independent nature of somatoform disorders.
Drugs Mentioned in This Article
Bupropion (Wellbutrin, Zyban)
Duloxetine (Cymbalta)
Fluoxetine (Prozac, Sarafem)
Gabapentin (Neurontin)
Lubriprostone (Amitiza)
Mirtazapine (Remeron)
Paroxetine (Paxil)
Pregabalin (Lyrica)
Sertraline (Zoloft)
References
1.
Stekel W.
Die Sprache des Traumes.
Wiesbaden, Germany: Bergmann; 1911.
2.
Lipowski ZJ. Somatization: the concept and its clinical application.
Am J Psychiatry.
1988;145:1358-1368.
3.
Briquet P.
Traité l’hystérie.
Paris: Baillière; 1859.
4.
Purtell JJ, Robins E, Cohen ME. Observations on clinical aspects of hysteria.
JAMA.
1951;146:902-909.
5.
Perley MJ, Guze SB. Hysteria: the stability and usefulness of clinical criteria.
N Engl J Med.
1962;266: 421-426.
6.
Feighner JP, Robins E, Guze SB, et al. Diagnostic criteria for use in psychiatric research.
Arch Gen Psychiatry.
1972;26:57-63.
7.
Spitzer RL, Endicott J, Robins E. Research diagnostic criteria: rationale and reliability.
Arch Gen Psychiatry.
1978;35:773-782.
8.
Eminson DM. Medically unexplained symptoms in children and adolescents.
Clin Psychol Rev.
2007;27: 855-871.
9.
Escobar JI, Burnam MA, Karno M, et al. Somatization in the community.
Arch Gen Psychiatry.
1987;44: 713-718.
10.
Grabe HJ, Meyer C, Hapke U, et al. Specific somatoform disorder in the general population.
Psychosomatics.
2003;44:304-311.
11.
Gureje O, Simon GE, Ustun TB, Goldberg DP. Somatization in cross-cultural perspective: a World Health Organization study in primary care.
Am J Psychiatry.
1997;154:989-995.
12.
Smith GR, Monson RA, Ray DC. Patients with multiple unexplained symptoms: their characteristics, functional health, and health care utilization.
Arch Intern Med.
1986;146:69-72.
13.
Bass C, Murphy M. Somatisation disorder in a British teaching hospital.
Br J Clin Pract.
1991;45: 237-244.
14.
Craig TK, Boardman AP, Mills K, et al. The South London Somatisation Study, I: longitudinal course and the influence of early life experiences.
Br J Psychiatry.
1993;163:579-588.
15.
Bohman M, Cloninger R, von Knorring AL, Sigvardsson S. An adoption study of somatoform disorders, III: cross-fostering analysis and genetic relationship to alcoholism and criminality.
Arch Gen Psychiatry.
1984;41:872-878.
16.
Buskila D, Neumann L, Hazanov I, Carmi R. Familial aggregation in the fibromyalgia syndrome.
Semin Arthritis Rheum.
1996;26:605-611.
17.
Walker EA, Unutzer J, Rutter C, et al. Costs of health care use by women HMO members with a history of childhood abuse and neglect.
Arch Gen Psychiatry.
1999;56:609-613.
18.
Grunau RV, Whitfield MF, Petrie JH, Fryer EL. Early pain experience, child and family factors, as precursors of somatization: a prospective study of extremely premature and fullterm children.
Pain.
1994;56:353-359.
19.
Hotopf M, Mayou R, Wadsworth M, Wessely S. Childhood risk factors for adults with unexplained symptoms: results from a national birth cohort study.
Am J Psychiatry.
1999;156:1796-1800.
20.
Escobar JI, Canino G, Rubio-Stipec M, Bravo M. Somatic symptoms after a natural disaster: a prospective study.
Am J Psychiatry.
1992;149:965-967.
21.
Wilhelmsen I. Somatization, sensitization, and functional dyspepsia.
Scand J Psychol.
2002;43:177-180.
22.
Rief W, Hiller W, Margraf J. Cognitive aspects of hypochondriasis and the somatization syndrome.
J Abnorm Psychol.
1998;107:587-595.
23.
Craig TK, Drake H, Mills K, Boardman AP. The South London Somatisation Study, III: influence of stressful life events, and secondary gain.
Br J Psychiatry.
1994;165:248-258.
24.
Allen LA, Gara MA, Escobar JI, et al. Somatization: a debilitating syndrome in primary care.
Psychosomatics.
2001;42:63-67.
25.
Escobar JI, Gara M, Silver RC, et al. Somatisation disorder in primary care.
Br J Psychiatry.
1998;173: 262-266.
26.
Hartz AJ, Noyes R, Bentler SE, et al. Unexplained symptoms in primary care: perspectives of doctors and patients.
Gen Hosp Psychiatry.
2000;22:144-152.
27.
GarcÃa-Campayo J, Claraco LM, Sanz-Carrillo C, et al. Assessment of a pilot course on the management of somatization disorder for family doctors.
Gen Hosp Psychiatry.
2002;24:101-105.
28.
Smith GR Jr, Rost K, Kashner TM. A trial of the effect of a standardized psychiatric consultation on health outcomes and costs in somatizing patients.
Arch Gen Psychiatry.
1995;52:238-243.
29.
Servan-Schreiber D, Tabas G, Kolb R. Somatizing patients, part II: practical management.
Am Fam Physician.
2000;61:1423-1428, 1431-1432.
30.
Allen LA, Woolfolk RL, Escobar JI, et al. Cognitive-behavioral therapy for somatization disorder: a randomized controlled trial.
Arch Intern Med.
2006;166:1512-1518.
31.
Escobar JI, Gara MA, Diaz-Martinez AM, et al. Effectiveness of a time-limited cognitive behavior therapy type intervention among primary care patients with medically unexplained symptoms.
Ann Fam Med.
2007;5:328-335.
32.
Woolfolk RL, Allen LA, Tiu JE. New directions in the treatment of somatization.
Psychiatr Clin North Am.
2007;30:621-644.
33.
Shah NR, Jones JB, Aperi J, et al. Selective serotonin reuptake inhibitors for premenstrual syndrome and premenstrual dysphoric disorder: a meta-analysis.
Obstet Gynecol.
2008;111:1175-1182.
34.
Henningsen P, Zipfel S, Herzog W. Management of functional somatic syndromes.
Lancet.
2007;369: 1691-1692.
Evidence-Based References
Escobar JI, Gara MA, Diaz-Martinez AM, et al. Effectiveness of a time-limited cognitive behavior therapy type intervention among primary care patients with medically unexplained symptoms.
Ann Fam Med.
2007;5:328-335.
Smith GR Jr, Rost K, Kashner TM. A trial of the effect of a standardized psychiatric consultation on health outcomes and costs in somatizing patients.
Arch Gen Psychiatry.
1995;52:238-243.