Potentially over-inclusive DSM-5 diagnostic categories for somatic disorders can result in a confusing overlap of criteria. These authors sort through the challenges of the differential diagnosis-and map out a well-structured treatment plan.
Table 1 – Diagnostic categories regarding somatoform disorders in DSM-5 and DSM-IV
Table 2 – Andrew’s symptoms as they relate to DSM-5 criteria for somatic symptom disorder
Table 3 – Communication strategies for clinicians who work with patients who have a somatic symptom or related disorder recommended by the Royal College of General Practitioners
Figure 1. Andrew’s case based on the model of somatoform disorders by Kirmayer and Taillefer
Figure 2. Short- and long-term positive and negative consequences of Andrew’s avoidance behavior
PREMIERE DATE: September 20, 2015
EXPIRATION DATE: March 20, 2017
This activity offers CE credits for:
1. Physicians (CME)
To understand how the changes in DSM-5 affect the diagnoses of somatic disorders and how to assess and treat a patient with somatic symptoms.
At the end of this CE activity, participants should be able to:
• Differentiate between DSM-5 somatic symptom and related disorders and DSM-IV somatoform disorders
• Incorporate DSM-5 criteria for somatoform disorder into their practice
• Understand the role of medically unexplained symptoms in somatic disorders
This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.
CME Credit (Physicians): This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians.
CME Outfitters designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
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“I have somatic problems, I am not crazy!”
-Andrew’s story of pain
During his first psychiatric consultation, Andrew reported enduring pain in his left shoulder that spread to his chest and was accompanied by strong palpitations. When Andrew experienced this pain for the first time 8 years ago, he was terrified that he was having a heart attack, but no organic causes were found. In the following years, the pain persisted with slightly varying intensity. As a consequence, Andrew had many appointments with medical specialists and started several treatments-none of them helped.
A year ago, a cardiologist identified cardiac arrhythmias. Andrew underwent surgery, and the arrhythmias were completely cured. However, the pain in his shoulder and chest continued. Andrew’s primary care physician confirmed that the pain was not explained by arrhythmias.
Andrew was formerly an athlete. As a single father with a full-time job, he was used to a full schedule. The pain in his shoulder was distressing and impaired his day-to-day functioning. Moreover, because of the pain, he was rarely able to exercise or get together with friends.
At the end of the intake session, Andrew stated that after talking about his symptoms he felt better. He felt that he was being taken seriously for the first time in years; nevertheless, he was convinced that a psychiatrist would diagnose his pain as a somatic disorder. “I am not crazy!” he said.
DSM-5 and somatic disorders
In DSM-5, the term “somatoform disorders” to describe medically unexplained symptoms was abolished. Instead, somatic symptom and related disorders was created. Medically unexplained symptoms are now not distinguished from medically explained symptoms. The somatic symptom disorder (SSD) as a central diagnosis replaces the former somatization disorder, undifferentiated somatoform disorder, and pain disorder. This broad diagnostic category also covers most patients who have hypochondriasis or a medical condition that is accompanied by psychological features.
According to DSM-5, SSD requires at least one distressing and impairing somatic symptom-independently of being medically explained or unexplained (criterion A). Criterion B specifies the need for at least 1 of 3 symptom-associated psychological features. Including health anxiety as one of these features makes sense because many patients with a former somatization disorder often experience health anxiety.1 In addition, health anxiety seems to be a significant predictor of the persistence of somatoform disorders and of illness behaviors such as health care use.2
SSD covers patients who fulfill the criteria of what was formerly hypochondriasis. However, health anxiety is not necessarily apparent in patients who have chronic somatic symptoms. Under criterion B, the psychological feature “disproportionate and persistent thoughts about the seriousness of one’s symptoms” has less empirical support and is difficult to distinguish from health anxiety. Contrary to expectations, many patients are able to accept psychosocial explanations of their symptoms.3
The validity of the third psychological feature, “excessive time and energy devoted to these symptoms or health concerns,” has been questioned.4,5 It is unclear in which cases “excessive time and energy” can be considered as appropriate. For example, if a patient has a serious illness that requires complex medical treatment, it is appropriate that he or she spend a substantial amount of time with health care services; this should not be considered a criterion of a mental disorder.
Although in SSD the single somatic symptom does not have to be present continuously, according to criterion C, symptoms should typically last for at least 6 months. This persistence-related criterion is difficult to distinguish from a specifier of SSD that defines the disorder as “persistent” when symptoms are present for longer than 6 months.
Another specifier classifies patients “with predominant pain” when symptoms primarily involve pain. The importance of pain syndromes could be misjudged by degrading them as a specifier of another disorder only, but not as a distinct diagnostic category.4 Pain symptoms are the most frequent and persisting somatoform symptoms, and they are important predictors of severe disability. SSD also includes a specifier for symptom severity.
The category of Illness Anxiety Disorder was introduced in DSM-5 to classify patients with former hypochondriasis that cannot be fully covered by SSD because there are no somatic symptoms. A criterion is preoccupation with “having or acquiring a serious illness.” However, it does not allow the presence of somatic symptoms, except when they are mild in intensity.
Finally, the diagnostic category of Conversion Disorder has been carried over with no essential changes. The exception is that symptoms no longer have to be associated with conflicts or other distressing events.
An essential change in DSM-5 is the merging of Psychological Factors Affecting Medical Conditions with Factitious Disorder into one diagnostic group. Table 1 contrasts the diagnostic categories of DSM-IV and DSM-5. In Table 2, the new diagnostic criteria are transferred to our case example, Andrew, who fulfills the criteria for SSD.
Challenges in applying DSM-5 criteria
Challenges to the new concept of SSD began even before DSM-5 was published. It was assumed that renaming somatoform disorders as Somatic Symptoms and Related Disorders would help communicate the diagnosis to patients in a non-stigmatizing way. However, renaming the diagnosis does not sufficiently address the original problem of underdiagnosing somatoform complaints.
The problem is not the label but rather that physicians avoid the diagnosis because it is so difficult to explain to patients. For example, Andrew might find it less disturbing to talk about SSD instead of a somatoform disorder if he understands how a psychological intervention can help him. Providing training to physicians might help them communicate the diagnosis more easily.4 Another problematic issue is that the terms “disorder” and “symptom” are used synonymously under one diagnostic label. Consequently, patients might have a problem understanding whether they have a “real” disorder or just a “symptom.”
It is hard to distinguish diagnoses in this large group of somatic symptom and related disorders from each other. For example, patients with medically explained symptoms could fulfill criteria of SSD but also of psychological factors affecting other medical conditions. Another example is that patients who have a diagnosis of conversion disorder often also fulfill criteria for SSD.
Mental health clinicians may see problems in abolishing the distinction between medically explained symptoms and medically unexplained symptoms. Apart from the advantage of avoiding body-mind dualism, there is the danger of over-inclusivity-physically ill patients may be mislabeled as mentally disordered. American psychiatrist Allen Frances6 illustrates this problem: “If you have a medical illness, you can get a diagnosis of DSM-5 SSD just by worrying about it a lot.”
As it stands, whether Andrew has had a heart attack in the past does not matter. With or without a previous heart attack, he would receive a diagnosis of SSD. Distinguishing between medically explained symptoms and medically unexplained symptoms can have implications for treatment. An additional specifier indicating explained and unexplained medical symptoms would make an essential difference in making treatment decisions-in Andrew’s case, whether the risk of cardiac disease needs to be addressed in therapy.
Criterion B for SSD has several problematic implications for clinical practice. For example, specific affective and cognitive symptoms that play an important etiological role are not explicitly mentioned (eg, rumination about physical symptoms, catastrophizing thoughts) or are completely absent (eg, self-concept of bodily weakness, subjective low symptom tolerance, somatosensory amplification, negative affectivity). Finally, criterion B completely ignores one important class of features of somatoform disorders-illness behaviors such as reassurance seeking, and checking or avoidance behaviors. Some of the illness behaviors that Andrew exhibits can be classified with SSD criterion B (Table 2). However, it would be difficult to classify Andrew’s avoidance behaviors (avoiding sports and social activities).
The potential over-inclusiveness of somatic symptom and related disorders diagnostic categories may result in an overlap of criteria that makes differential diagnosis and creating a well-structured therapy plan difficult. A thorough examination of the patient’s somatic symptoms (eg, with symptom lists) and examination of the physical symptoms continue to play an important role.
Medically unexplained symptoms
The Cochrane Collaboration recently published 2 review articles on psychological and pharmacological interventions for medically unexplained symptoms and somatoform disorders. The first includes 21 studies that evaluated cognitive-behavior therapy (CBT), mindfulness-based cognitive therapy, psychodynamic therapy, and integrative therapy.7 The number of therapeutic sessions ranged from 1 to 13. CBT was the only intervention that has been adequately studied to allow tentative conclusions for clinical practice. A moderate effect was seen with CBT (g = 0.58; 95% confidence interval [CI], 0.38, 0.77). Effects were stable within and after 1 year of follow-up. Results for CBT in regard to secondary outcomes, such as quality of life (g = 0.15; 95% CI, −0.06, 0.37) and depression (g = −0.09; 95% CI, −0.31, 0.13), however, showed low or nonsignificant effect.
The second review consisted of 26 studies and examined the efficacy of TCAs, atypical antidepressants, and natural products (eg, St John’s wort).8 The duration of the pharmacological treatments ranged between 2 and 12 weeks. The atypical antidepressants demonstrated predominantly moderate efficacy in reducing the severity of somatic symptoms (g = 0.74; 95% CI, 0.31, 1.17), depression (g = 0.56; 95% CI, 0.25, 0.88), and functional impairment (g = 0.52; 95% CI, 0.04, 1.00). The natural products appeared to be moderately effective in reducing the severity of somatic symptoms (g = 0.74; 95% CI, 0.51, 0.97) and depression (g = 0.64; 95% CI, 0.41, 0.87). Most of the discontinuations due to adverse effects were seen with the antidepressants. Long-term efficacy was not examined in any of the studies.
Although the results of both reviews show comparable effects for pharmacological treatments and psychological interventions, results have to be interpreted against the background of 3 critical issues. First, factors such as study design, assessment tools, and patient features vary considerably between the pharmacological and psychological studies, thus making it nearly impossible to compare results without head-to-head trials. Second, for the moderately effective atypical antidepressants, the rates of adverse effects were high. Especially in a population of patients with somatoform symptoms, adverse effects can amplify the effects of symptom perception. Third, nothing is known about the long-term efficacy of pharmacotherapy for somatoform disorders.
To date there are no internationally accepted treatment guidelines for somatoform disorders. However, a German guideline published in 2013 recommends the use of different classes of antidepressants only for severe syndromes dominated by pain symptoms with or without comorbid depressive symptoms.9 For severe syndromes not determined by pain, the guideline recommends antidepressants only if there is comorbid depression. Furthermore, the guideline discourages the use of anxiolytic drugs (eg, benzodiazepines), tranquilizers or hypnotics, and antipsychotics when there is no comorbidity that justifies the use of these agents. It should be taken into consideration that this guideline recommends treating somatoform disorders with a combination of psychosocial interventions and pharmacotherapy.
CBT has the best evidence as an intervention for hypochondriasis. Thomson and Page10 reviewed 6 studies comprising 440 participants who were randomized to various psychotherapies. The number of sessions ranged from 6 to 19. Regarding the primary outcome of illness anxiety, depression, and anxiety, moderate to high effects were identified (0.78 ≤ g ≤ 0.96). For severity of somatic symptoms, the effects were rather small (g = 0.41; 95% CI, 0.13, 0.96).
There are few studies of pharmacotherapeutic efficacy for anxiety. Three placebo-controlled studies showed the efficacy of fluoxetine and paroxetine for hypochondriasis.11-13 One study showed that the efficacy of the SSRIs was comparable to that of CBT.13 However, the results have to be interpreted carefully because dropout rates were high in all 3 studies. Moreover, the stability of effect after medication discontinuation cannot be judged because of the lack of follow-up results. There are no internationally accepted treatment guidelines for hypochondriasis, although a German guideline of psychological interventions recommends CBT as first-choice treatment.14
CBT for somatoform disorders
The following modules are optional, not obligatory, parts of CBT for somatoform disorders. They can be tailored to individual patients. At the beginning of a psychological treatment, it is important that the patients’ subjective illness perceptions and their adherence to psychological interventions are thoroughly explored. Enriching therapy with self-experiential exercises can make it easier for patients to get involved.
The focus at the beginning of Andrew’s therapy was on psychoeducation. This was challenging because Andrew had problems with accepting psychosocial explanations of his symptoms. Applying helpful communications skills can facilitate this part of the therapy (Table 3). To explain why psychological interventions may be helpful, we used a model proposed by Kirmayer and Taillefer15 (Figure 1).
Andrew entered therapy following many years of stressful events (eg, divorce, raising 2 children as a single parent, working full-time). Therefore, we provided psychoeducation on the effects of persistent stress on the body. Completing a diary over several weeks helped him understand the relationship between stressful events and his physical symptoms. We followed the stress model of Lazarus and Launier16 and talked with him about his appraisal of stressful events. In this part of the therapy, clinicians often have to deal with rigid cognitive schemes. For example, Andrew exhibited perfectionist thoughts, such as “I only leave a good impression when I accomplish things perfectly.” The patient has to be questioned and his perceptions addressed with cognitive restructuring techniques. Finally, the patient is trained in stress management techniques (eg, progressive muscle relaxation).
Using an imagining exercise, we asked Andrew to switch his attention between different parts of his body. Consciously focusing attention on his body brought up physical perceptions that Andrew had not noticed earlier. In another exercise, Andrew had to hold a heavy object in his hand with his arm outstretched, first with an attention-focusing instruction and then with a distracting instruction. He learned that distraction changes pain sensation. Additional distraction strategies were also practiced.
Biased symptom-related cognitions
This therapeutic module asks the patient to imagine that he is biting into a lemon. Andrew was surprised to realize that just by imagining this, his body responded by producing physical symptoms such as salivation and muscle constrictions in his mouth. This exercise helps patients see the relationship between physical symptoms, cognitions, emotions, and behaviors.
The patient’s dysfunctional beliefs were identified, questioned, and restructured in the next steps. Cognitive restructuring can be combined with behavioral exercises that induce physical symptoms. For example, we had Andrew walk up and down the stairs several times until he was out of breath before we started talking about his symptom-related cognitions.
It is important to discuss long- and short-term effects of illness behaviors with the patient-regardless of whether they are positive or negative. Andrew and his therapist worked out the consequences of his avoidance behavior (Figure 2). Andrew easily found short-term positive effects of his behavior but no long-term positive effects, which explains how avoidance behavior is maintained. Exposure-based interventions play an important role in reducing a patient’s doctor shopping and body checking to a reasonable level.
In the treatment of patients who have hypochondriasis, 2 kinds of exposure-based interventions play an important role. One is based on the exposure therapy for agoraphobia and panic disorder and is indicated for patients who avoid fear-inducing situations (eg, talking with friends about illnesses) or places (eg, hospitals).17,18 First, the exposure rationale is explained to the patient. Then, the patient is exposed to the fear-inducing situation until a previous level of anxiety habituation is reached.
The other exposure-in sensu exposure-is based on a treatment concept for generalized anxiety disorder.19 The patient is asked to pick one of his most fear-inducing worries. The patient writes a worst case scenario script of what he imagines. The therapist reads the script out loud while the patient listens and imagines the worst outcomes. This procedure continues until the patient’s anxiety is reduced.
Regardless of which exposure is used, a thorough analysis with the patient follows. These exposure approaches can be complemented by modern concepts of inhibitory learning. Such concepts include expectation strategies that try to break the biased expectations regarding the frequency and intensity of aversive outcomes.20
PLEASE NOTE THAT THE POST-TEST IS AVAILABLE ONLINE ONLY ON THE 20TH OF THE MONTH OF ACTIVITY ISSUE AND FOR A YEAR AFTER.
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Dr KleinstÃ¤uber is Assistant Professor of Clinical Psychology and Dr Rief is Professor of Clinical Psychology in the department of clinical psychology and psychotherapy at Philipps-UniversitÃ¤t Marburg, Germany.
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3. Rief W, Nanke A, Emmerich J, et al. Causal illness attributions in somatoform disorders: associations with comorbidity and illness behavior. J Psychosom Res. 2004;57:367-371.
4. Rief W, Martin A. How to use the new DSM-5 somatic symptom disorder diagnosis in research and practice: a critical evaluation and a proposal for modifications. Annu Rev Clin Psychol. 2014;10:339-367.
5. Hiller W, Rief W. Abolishing the somatoform disorders by DSM-5-an academic piece of bungling? Psychotherapeut. 2014;59:448-455.
6. Frances A. DSM-5 somatic symptom disorder. J Nerv Ment Dis. 2013;201:530-531.
7. van Dessel N, den Boeft M, van der Wouden JC, et al. Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults. Cochrane Database Syst Rev. 2014;11:CD011142.
8. KleinstÃ¤uber M, WitthÃ¶ft M, Steffanowski A, et al. Pharmacological interventions for somatoform disorders in adults. Cochrane Database Syst Rev. 2014;11:CD010628.
9. Hausteiner-Wiehle C, SchÃ¤fert R, Sattel H, et al. New guidelines on functional and somatoform disorders [in German]. Psychother Psychosom Med Psychol. 2013;63:26-31.
10. Thomson AB, Page LA. Psychotherapies for hypochondriasis. Cochrane Database Syst Rev. 2007; 4:CD006520.
11. Fallon BA, Petkova E, Skritskaya N, et al. A double-masked, placebo-controlled study of fluoxetine for hypochondriasis. J Clin Psychopharmacol. 2008;28:638-645.
12. Fallon BA, Schneier FR, Marshall R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull. 1996;32:607-611.
13. Greeven A, van Balkom AJ, Visser S, et al. Cognitive behavior therapy and paroxetine in the treatment of hypochondriasis: a randomized controlled trial. Am J Psychiatry. 2007;164:91-99.
14. Martin A, HÃ¤rter M, Henningsen P, et al. Evidence-Based Guideline for Psychotherapy for Somatoform Disorders. GÃ¶ttingen, Germany: Hogrefe; 2012.
15. Kirmayer LJ, Taillefer S. Somatoform disorders. In: Turner SM, Hersen M, eds. Adult Psychopathology and Diagnosis. 3rd ed. New York: Wiley; 1997:333-383.
16. Lazarus RS, Launier R. Stress-related transactions between person and environment. In: Pervin LA, Lewis M, eds. Perspectives in International Psychology. New York: Plenum Press; 1978:287-327.
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18. Warwick HM. A cognitive-behavioural approach to hypochondriasis and health anxiety. J Psychosom Res. 1989;33:705-711.
19. Borkovec TD, Ray WJ, StÃ¶ber J. Worry: a cognitive phenomenon intimately linked to affective, physiological, and interpersonal behavioral processes. Cognitive Ther Res. 1998;22:561-576.
20. Craske MG, Treanor M, Conway CC, et al. Maximizing exposure therapy: an inhibitory learning approach. Behav Res Ther. 2014;58:10-23.
21. Royal College of General Practitioners. Guidance for Health Professionals on Medically Unexplained Symptoms (MUS); January 2011. http://www.rcpsych.ac.uk/pdf/CHECKED%20MUS%20Guidance_A4_4pp_6.pdf. Accessed July 14, 2015.