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Somatic Presentations of Mental Disorders (September
6-8, 2006)
The APA, in collaboration with the WHO and NIH, convened a diagnosis-related research
planning conference focusing on somatic presentations of mental disorders in Beijing, China, on
September 6-8, 2006. The conference was the eighth in a series of 12 NIH-funded conferences
on "The Future of Psychiatric Diagnosis: Refining the Research Agenda". The Somatic
Presentations conference co-chairs were Joel Dimsdale, MD, University of California San Diego
(La Jolla, CA), Yu Xin, MD the Institute of Mental Health Peking University Bejing, China), Arthur
Kleinman, MD, Harvard University (Cambridge, MA), and Vikram Patel, PhD, London School of
Hygiene and Tropical Medicine (London, UK). Twenty-eight invited scientists from around the
world participated.
Ricardo Araya MD (Bristol, UK), speaking on the epidemiology and association of somatoform
disorders and common mental disorders in community and primary care settings, noted that it is
impossible not to approach depression and anxiety without considering the presence of
unexplained physical symptoms. He emphasized, however, that the absence of a medical
explanation should not confer automatic psychiatric labeling. With respect to the validity of the
somatoform disorders, he identified several noteworthy issues, including: 1) somatoform
disorders are highly comorbid with depression and anxiety in most community and primary care
studies, although a small group of individuals present with a somatoform disorder alone; 2) in the
WHO-PHC study, mood, anxiety, and somatoform symptoms loaded into one common factor
('internalizing' disorders) in all countries surveyed; and 3) a large longitudinal community survey
in Germany found there was marked mobility over time between somatoform diagnostic
categories. Regarding reliability, recall of symptoms in primary care settings is markedly
inconsistent; in one follow-up study involving individuals who initially reported somatic symptoms,
they could not recall 61% of those symptoms 12 months later. Furthermore, test-retest, inter-rater
reliability, or internal consistency of measures is mostly unknown. The clinical usefulness in
primary care settings also warrants attention; although unexplained somatic symptoms are
common in primary care throughout the world, the complexity of the diagnostic categories
discourages their widespread use in primary care outside developed countries, he reported.
Discussant Roseland Lieb, PhD (Basel, Switzerland) noted the remarkable association (both
current and lifetime) between somatoform disorders (including subclinical forms of somatization
disorders) and anxiety/mood disorders. Among the possible explanations she offered for this
association are symptom overlap across categories, reporting bias(i.e., subjects affected by one
disorder tend to report more symptoms of the other disorder), one disorder causing another
disorder, and shared vulnerability factors. One method for exploring questions of comorbidity is to
compare the age at first onset of the various disorders. The different somatoform disorders
appear to have different patterns of age of onset; for example, undifferentiated somatoform
disorder has an early onset but conversion and pain disorder have a much later onset, typically
after the onset of mood and anxiety disorders. She concluded by pointing out that although there
is no clear empirical distinction between mood, anxiety, and somatoform disorders, lumping them
together cannot resolve the problem of how they fit together.
Elizabeth Lin MD (Seattle, WA) presented on the somatic burden of co-occurring depression and
anxiety in chronic medical illnesses. Depression is highly prevalent in a number of chronic
medical illnesses, including diabetes (10-20%), heart disease (20- 30%), chronic pain (40-60%),
cancer (10-20%), and neurological disorders (10-20%). The question is not which came first, but
how do these interplay? When depression and anxiety co-occur with such illnesses, there is less
treatment adherence and self-care, more functional impairment, higher use of medical services,
and increased complications and mortality. Dr. Lin and colleagues reviewed the literature
focusing on arthritis, heart disease, diabetes, and congestive heart failure
(CHF)/asthma/emphysema. For arthritis, anxiety and depression is strongly linked to pain
severity. Successful treatment of depression results in less pain and less interference with daily
life. For diabetes, anxiety and depression is related to neuropathic pain and to the number of
diabetes symptoms, but not to hemoglobin A1C (a measure of blood glucose control). For
coronary artery disease, depression and anxiety are related to angina and decreased exercise
capacity; after a myocardial infarction, a history of depression is related to increased angina
frequency. In contrast, physiological measures (e.g., ejection fraction and ischemia measures)
were not significantly related to angina. For CHF, asthma, and emphysema, depression and
anxiety were significantly related to dyspnea and fatigue, whereas pulmonary functions tests were
not. Dr Lin concluded that in chronic medical illnesses it is crucial to assess and treat mood and
anxiety disorders.
In his discussion, Yu Xin, MD (Beijing, China) noted that there is a higher prevalence of
somatoform disorders in elderly patients and that health care providers need to take into account
cognitive function, which can influence expression of mood symptoms and communication with
physicians. He also noted that cultural differences were of great importance in the treatment of
patients with somatoform disorder. Language, in particular, is especially important in culture; in
the Chinese language, somatic words are used to indicate emotions: "trouble in heart" means
anxiety, "headache" means feeling annoyed, "suffocation of heart" means depressed mood, and
"body is withered" means fatigue and loss of energy. Furthermore, the symptomatology of
depression and anxiety in chronic medical illness need to be further studied as it may differ from
what we see in "pure depression" in terms of clinical manifestations. For example, studies have
shown that demoralization was more prominent than anhedonia for the diagnosis of depression
concurrent with medical illness.
Joel Dimsdale, MD (La Jolla, CA), in a presentation on biological substrates for somatoform
disorders, began by noting that behind many somatoform patients lurks an undiagnosed disease.
He identified four ways in which unrecognized diseases get labeled as somatoform disorders: 1)
missed diagnoses (in a small sample of fatigued breast cancer patients, 40% had undiagnosed
thyroid disease); 2) new diagnostic tests reveal surprisingly prevalent diseases (e.g., celiac
disease, once considered rare and diagnosed primarily in childhood is quite common); 3) new
insights about fatigue and pain (e.g., sleep disruption contributes to pain and fatigue); and 4) new,
previously unknown diseases are discovered (e.g., SARS, hepatitis C). Dr. Dimsdale stressed the
importance of "getting beyond the black box" and using lab data to try to understand the
underlying somato-psychic phenomena. One area of potentially fruitful study is the process of
somatic amplification and de-amplification, i.e., what determines the "volume level" of distress.
Neural imaging offers enormous potential, particularly for amplification and de-amplification of
pain (e.g., brain regions show similarities and differences during laser and suggestion-induced
pain). Genetic approaches to understanding underlying pathophysiology are also likely to be
helpful (e.g., the CDC international collaboration to study chronic fatigue syndrome is integrating
psychiatric, sleep, genetic, epidemiologic, and neuroendocrine investigations).
In his discussion, Robert Dantzer DVM, PhD (Urbana, IL) described the potential importance to
the experience of physical symptoms of the immune system-to-brain communication pathways.
He proposed a mechanism by which manifestations of physical problems may be mirrored in the
brain: pathogen-associated molecular patterns and bodily danger signals lead to the release of
peripheral cytokines, which are recognized by the brain and lead to brain cytokines (internal
representations of sickness), which, in turn,, which are experienced as non-specific symptoms of
disease (e.g., anorexia, anhedonia, cachexia, pain, GI distress, cognitive disorders, mood
alternations, and fatigue). Normally this system is accurately regulated; that is, it is geared to be
triggered in a temporal manner and is usually transient. Somatic disease with an inflammatory
component would thus induce both dysfunction at the target organ as well as sensitizing brain
sickness systems, leading to internal representation of sickness with an entire array of nonspecific symptoms. If the sickness system is sensitizing the brain, then other systems, such as
psychological conflict, could trigger it as well.
Michael Sharpe MD (Edinburgh, Scotland) in his presentation, considered whether there are
consistently demonstrated psychosocial risk factors for somatoform disorders and, if so, whether
they are shared across syndromes. Risk factors are identifiable factors that make a condition
more likely to occur; it is important to understand that they are not necessarily a cause (i.e., an
understanding of psychosocial risk factors will not explicate the mechanisms involved and are
most helpful in prevention). Specific risk factors for somatoform disorders, given the limited
available data, probably include female sex, childhood experiences, previous history, iatrogenesis
(clinically seen but limited data available), physical stress and trauma, and having a psychological
predisposition. Although most of these risk factors are likely common to all of the somatoform
disorders, there may be some differences (e.g., the relationship between abuse and conversion
disorder). Future research methods should include large surveys and case-control studies,
prospective cohort studies, and studies that integrate psychology with biology (brain imaging and
animal experiments).
In his discussion, Winfried Rief, PhD (Marburg, Germany) wondered whether the above
mentioned risk factors are relevant to the development of symptoms, or rather are risk factors for
maladaptive coping when symptoms occur. Anxiety, depression, and somatoform disorders are
interdependent risk factors; if someone has anxiety or depression, then they are at increased risk
for developing a somatoform disorder. Factors which somatoform, depressive, and anxiety
disorders have in common include comorbidity, traumatization, lower social status, family history,
cultural variations, increased health care use, seeking treatment in primary care, reporting
physical symptoms to general practitioners, and immigration. Possible psychosocial correlates
which may be more specific to somatoform disorders and that should be considered for inclusion
as part of the definition of somatoform disorders include attention-focusing on physical
perceptions, over-interpretation of physical sensations as possible illness signs, illness worries
and rumination, seeking medical reassurance, failure of medical reassurance, demoralization,
negative affectivity, physical deconditioning, and avoidance behavior.
Winfried Rief, PhD (Marburg, Germany) presented on the diagnostic stability of somatoform
symptoms over time. He began by showing the results of several empirical studies that
demonstrated: 1) patients have problems recalling lifetime symptoms; 2) the reduction of physical
functioning in somatoform disorders is a stable feature; 3) patients with multi-somatoform
disorders were less likely to improve over time than patients with fewer medically unexplained
symptoms; 4) the number of symptoms predicts outcome even after correcting for anxiety,
depression, and health anxiety; 5) somatic complaints are a strong predictor of bad outcome in
pharmacological depression trials; 6) the time pattern of recovery is different for depression
symptoms than for pain symptoms; and 7) during antidepressant treatment, depressive mood
disappears, but somatic symptoms tend to persist. Regarding the issue of whether somatoform
symptoms are actually undetected physical disease, in scientific trials less than 10% of the
diagnoses had to be modified because of non-detected medical conditions. Furthermore, the rate
of misdiagnosed organic conditions seems to be comparable between somatoform disorders,
anxiety, and depression. These findings, said Dr. Rief, have the following implications for future
classifications: 1) symptoms may vary, but the syndrome seems to be stable; 2) because of
problems with recalling lifetime symptoms, the classification should focus on present state
symptoms or the last seven days; 3) the term "medically unexplained" should not be used as a
criterion; instead, the criteria should continue to use "the symptoms are not fully accounted by an
(other) known medical condition" and 4) patients with polysomatoform symptoms show different
course and outcome features than patients with depression or anxiety. Dr Rief proposed changes
in the classification of somatoform disorders, including modifying the criteria for somatization
disorder by including further descriptive criteria for the syndrome (attention-focusing; avoidance;
etc.); and modifying the criteria for hypochondriasis by removing the criterion which states: "the
preoccupation persists despite adequate medical reassurance."
In her discussion, Maria Graceiela Rojas Castillo, MD (Santiago, Chile) noted that in the
developing world there is only one prospective study on somatoform disorders; that research on
somatization disorder is difficult because it is expensive; and that there is lack of clarity about the
exclusion criteria. She questioned why a physician should make a diagnosis of somatization
disorder unless he/she has something to offer to the patient.
Athula Sumathipala, MD (London, UK) reviewed treatment intervention studies for somatoform
disorders. Studies of pharmacological interventions support the use of tricyclic antidepressants,
SSRIs, and MAO inhibiters; a systematic review of 94 randomized controlled trials on six
symptom syndromes concluded that antidepressants could be effective for symptoms and
disability but that side effects were an issue. Reviews of studies of psychological interventions
concluded that cognitive-behavioral therapy (CBT) may be efficacious for either defined symptom
syndromes or for the broader category of medically unexplained symptoms. The impact of CBT
ranges from a reduction of physical symptoms to a reduction in psychological distress and
disability. However, further studies with high quality design are needed. Only limited evidence
exists for psychodynamic psychotherapy, family therapy, problem solving approaches,
reattribution, eliciting the patient's explanatory model, and structured care by one therapist.
Moreover, in studies completed to date, limitations include: 1) studies were carried out using
different forms of psychotherapies and adopted divergent selection procedures, interventions,
outcome measures, and instruments, hampering efforts to compare treatment effects between
studies; 2) most trials assessed only short-term outcomes; 3) although medically unexplained
symptoms are much more common in primary care, of the meager number of intervention
studies, none were conducted in primary care; and 4) economic analyses of the cost or benefits
of psychological therapy were non-existent. In her discussion, Susan Levenstein, MD (Rome,
Italy) a general internist, noted that a physical symptom is not a psychiatric disorder even if it is
worsened by stress or distress (so is coronary artery disease) and even if it is medically
unexplained (which is often a code word for MD frustration or ignorance). An overemphasis on
psychological components in functional disorders may breed diagnostic sloppiness and lead to
therapeutic nihilism. When medically managing patients with excessive somatic concerns, the
physician must detect and treat depression, be patient (these problems go on for a long time),
should schedule frequent visits with repeated reassurances, be slow and selective with
psychiatric referrals, and strive to build a strong therapeutic alliance, shifting from conflict to
collaboration with the goal of trying to help the patient feel better. Dr. Levenstein proposed the
following principles for alliance building: 1) take symptoms seriously and empathize with suffering;
2) take an interest in the patient's life situation and psychological state; 3) inquire about the
influence of psychological factors on symptoms; and 4) do not rush to communicate perceived
links between psyche and soma.
Richard Mayou FRCPsych (Oxford, UK) presented on whether treatments for common mental
disorders are also efficacious for somatoform disorders. The most specific treatments of mental
disorders are effective when there is comorbid anxiety or depression; for somatoform disorders
like hypochondriasis and body dysmorphic disorder; and when the treatments have analgesic or
other specific actions. General measures (e.g., explanation, information, guidance, and
reassurance) are effective in mental disorders, functional symptoms and maladaptive reactions to
major physical disorders. Nonspecific, but well-defined interventions have a major role, especially
in early non-specialist phases of care. Regarding issues of classification, Dr Mayou argued that 1)
somatoform disorder have helped to focus attention but have impeded understanding and
effective care, and that classifying physical symptoms on Axis I has been unhelpful; 2)
operational Axis III definitions should be promoted; 3) treatment evidence is consistent with
proposals to reassign certain somatoform disorders to other categories (i.e., hypochondriasis,
BDD); 4) Psychological Factors Affecting Medical Condition (which may need a new name)
should be rewritten, perhaps including Winfried Rief's more psychological criteria for multisomatoform disorder (e.g., attention focusing on physical perception, over-interpretation of
physical sensations as possible illness signs, illness worries, rumination, avoidance behavior,
etc). In his discussion, Ji Jianlin MD (Shanghai, China), noted that the gold standard in the
treatment of patients with somatoform disorders is a long-term empathic relationship with a
primary care physician. The goal of treatment includes: 1) care for the patient, but not necessarily
to "cure" the somatization; 2) ruling out concurrent physical disorders; 3) removing any
conversion or pseudoneurological symptoms; and 4) maintaining or improving the patient's
overall functioning. While it appears that common treatments for mental disorders are also
effective for somatoform disorders, there need to be more randomized controlled trials and
especially trials on the different subtypes of somatoform disorders because these are a spectrum
of disorders rather than a single disorder.
Kurt Kroenke MD (Indianapolis, IN) presented on the evidence for a differential response to
specific treatments for subcategories of somatoform disorders. He reported that CBT has been
studied in all disorders (except conversion) and that it was found beneficial in 13 of 14 studies he
reviewed. For somatization disorder (and its variants), a consultation letter to the general
practitioner (GP) was effective in most studies, whereas the benefits of GP training have not yet
been established. SSRIs are effective for treating body dysmorphic disorder. Antidepressants
have been less well studied for other somatoform disorders. He found no proven therapy for
conversion disorder and no randomized controlled trials for pain disorder or undifferentiated
somatoform disorder. Both CBT and antidepressants are effective for functional somatic
syndromes. In his discussion, Javier Garcia-Campayo, MD (Zaragoza, Spain), noted the many
methodological limitations of these treatment studies, including nosological limitations (e.g.,
agreement between DSM-IV and ICD-10 criteria is low, and most research carried out is on
functional somatic syndromes rather than somatoform disorders); design limitations (e.g., studies
did not control for comorbid depression and anxiety); and, for the psychotherapy studies, the
treatments were not manualized. He concluded that 1) there has been little research on the
treatment of somatoform disorders using DSM/ICD criteria as such; 2) differences in response to
treatments by subcategory support to the nosological validity of these categories; and 3) the
quality of future research can be improved (e.g., evaluate somatic symptoms, psychological
distress, and function, and do two-year follow-up to evaluate decay effects).