8.2 Somatic Symptom Disorders

During the course of her illness, Anna O. developed medical symptoms that her doctors could not explain. For instance, she saw an eye doctor for problems with her vision, but he was unable to identify the cause (Breuer & Freud, 1895/1955). Similarly, doctors were unable to find a medical explanation for her chronic cough. How might persistent medically unexplained physical symptoms such as these arise? How should they best be treated? Such bodily symptoms (also called somatic symptoms) may fall under the category of somatic symptom disorders in DSM-5.

Somatic Symptom Disorders: An Overview

The hallmark of somatic symptom disorders is complaints about physical well-being along with cognitive distortions about bodily symptoms and their meaning; the focus on these bodily symptoms causes significant distress or impaired functioning. With these disorders, it is the person’s response to bodily symptoms that is notable and excessive. Common bodily complaints of patients with somatic symptom disorders are listed in TABLE 8.7.

Symptoms of somatic symptom disorders have existed for millennia and were written about in the Papyrus Ebers, an ancient Egyptian medical document dating to 1600 B.C.E. However, the Egyptians believed that these symptoms had an underlying medical cause.

University Library, Leipzig, Germany/Archives Charmet/The Bridgeman Art Library

Somatic symptom disorders are relatively rare in the general population but are the most common type of psychological disorder in medical settings (Bass et al., 2001). The medical costs of caring for patients with somatic symptom disorders are substantial; according to one estimate, these costs come to over $250 billion each year in the United States alone (Barsky et al., 2005).

Somatic symptom disorders are not new phenomena; they have a long history, although different labels have been given to them over time. They were described by the ancient Greek philosopher Hippocrates, who thought that somatic symptoms—generally reported by women—were caused by a wandering uterus, from which the term hysteria is derived (hystera is Greek for “uterus”; Phillips, 2001). Hysteria was often used to refer to bodily symptoms that lack a medical explanation, as was true of Anna O.; in addition, patients with hysteria typically describe their symptoms dramatically.

One somatic symptom disorder that must be distinguished from the others is factitious disorder, mentioned in Chapter 3, in which people intentionally induce symptoms or falsely report symptoms that they do not in fact have in order to receive attention from others. People who have any of the other somatic symptom disorders neither pretend to have symptoms nor intentionally induce physical symptoms for any type of gain. (However, in DSM-5, factitious disorder is considered a somatic symptom disorder because bodily symptoms may be among those feigned.)

Putting aside factitious disorder, somatic symptom disorders share two common features (Looper & Kirmayer, 2002):

1. bodily preoccupation, which is similar to the heightened awareness of panic-related bodily sensations experienced by people with panic disorder (see Chapter 6), except that with somatic symptom disorders, the patient can be preoccupied with any aspect of bodily functioning; and
2. symptom amplification, or directing attention to bodily symptoms such as those in TABLE 8.7, which in turn intensifies the symptoms (Kirmayer & Looper, 2006; Looper & Kirmayer, 2002). A common example of symptom amplification occurs when someone with a headache pays attention to the headache—and, invariably, the pain worsens.

In the following sections, we focus on three of these disorders in turn—somatic symptom disorder, conversion disorder, and illness anxiety disorder.

Somatic Symptom Disorder

The hallmark of somatic symptom disorder (SSD) is at least one somatic symptom that is distressing or disrupts daily life, about which the person has excessive thoughts, feelings, or behaviors (American Psychiatric Association, 2013). For example, Anna O.’s eye problems and her cough were both physical symptoms that disrupted her daily life. Because the name of the disorder and this category of disorders are so similar (the former is singular and the latter plural), we will abbreviate the disorder as SSD.

To be diagnosed with SSD according to DSM-5 criteria, the person must have at least one distressing or impairing bodily symptom and respond excessively to it. Examples of an excessive response are unrealistic thoughts about the seriousness of the symptoms, significant anxiety about the symptoms or health in general, or devoting excessive amount of time and energy to it—such as seeing multiple doctors when such visits aren’t necessary. For instance, a man who had a heart attack might become preoccupied with his heart rate and be afraid to go up and down stairs, lest he increase his heart rate and have another heart attack—despite his doctor’s assuring him that walking on stairs would be okay. Sometimes the single bodily symptom is pain (American Psychiatric Association, 2013). TABLE 8.8 lists the DSM-5 diagnostic criteria for SSD.

A clinician diagnoses SSD only if the person’s response to the symptoms is more extreme than what would be expected based on the medical assessment. SSD must be distinguished from various other disorders, including anxiety disorders. Many laboratory tests and visits to doctors may be required to rule out other medical and psychological diagnoses, which is necessary before a diagnosis of SSD can be made (Hilty et al., 2001). TABLE 8.9 lists additional facts about SSD.

People with SSD may avoid certain activities that they believe are associated with their bodily symptoms, such as any type of exercise. In so doing, patients attempt to minimize the physical sensations associated with the disorder. As a result, they may become so out of shape that even normal daily activities, such as walking to a store from the parking lot, may lead them to experience bodily symptoms—which creates a vicious cycle of avoidance and increased bodily symptoms, impairing daily life. For people with SSD, these symptoms impair daily life, which is what happened to Edward in Case 8.4.

SSD can be fully understood only by considering multiple factors, including genetics, bodily preoccupation, symptom amplification and catastrophic thinking, and other people’s responses to illness.

Neurological Factors: Genetics

Most of the progress in understanding the neurological factors that underlie SSD has been in the area of genetics. For example, in a large-scale twin study, researchers found that genetic effects may account for as much as half of the variability in SSD (Kendler, Walters, et al., 1995). Note, however, that this finding does not imply that the disorder itself is necessarily inherited; it could be that temperament or other characteristics that are influenced by genetics predispose a person to develop the disorder in certain environments. (This same point can be made about most findings that link genes to disorders.) Kendler and colleagues (1995) also reported that characteristics of families have no consistent effect on whether members of the family develop this disorder. This finding suggests that, in addition to genes, specific experiences of a particular person—not shared experiences among members of a family—affect whether a person develops the disorder.

In an effort to minimize their bodily symptoms, people with somatic symptom disorder may restrict their activities. If this model were suffering from somatic symptom disorder, his inactivity could create additional symptoms (such as back pain) or make existing symptoms worse (such as increased heart rate or difficulty breathing).

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Psychological Factors: Misinterpretation of Bodily Signals and Coping

Like all other somatic symptom disorders, SSD involves bodily preoccupation and symptom amplification, as well as catastrophic thinking—in this case, about physical sensations or fears of illness. These patients may believe, for example, that headaches indicate a brain tumor. Their mental processes—particularly attention—focus on bodily sensations, including the beating of their hearts (Barsky, Cleary, et al., 1993, 1994), leading to symptom amplification and catastrophic thinking. These effects also arise in part from faulty beliefs about their bodies and bodily sensations. For example, people with SSD may erroneously believe that health is the absence of any uncomfortable physical sensations (Rief & Nanke, 1999). People who do not have a somatic symptom disorder do not habitually develop catastrophic misinterpretations of such sensations.

Somatic symptoms can also serve as a coping strategy, leading the person to focus attention away from a stressor and onto a bodily sensation. This observation can help to explain why somatic symptom disorders, including SSD, sometimes develop after the death of a loved one (as happened to Anna O. after her father died) or after another significant stressor (Hiller et al., 2002).

Social Factors: Observational Learning and Culture

Observational learning may also play a role in SSD. Such learning can explain the finding that people with SSD are more likely than those without the disorder to have had an ill parent (Bass & Murphy, 1995; Craig et al., 1993). In these cases, an ill parent may have inadvertently modeled illness behavior. Moreover, operant conditioning can also be at work, when people reinforce a person’s illness behavior: During the patient’s childhood, family members may have unintentionally reinforced illness behavior by paying extra attention to the child or buying special treats for the child when he or she was ill (Craig et al., 2004; Holder-Perkins & Wise, 2001). Similarly, adults with SSD may be reinforced for their symptoms by the attention of medical personnel, family, friends, or coworkers (Maldonado & Spiegel, 2001).

Children whose parents have chronic pain may be more likely to report pain themselves.

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In addition, in many cultures—including in the United States—somatic symptoms may be regarded as an acceptable way to express helplessness, such as by those who experienced abuse during childhood (Walling et al., 1994). The use of somatic symptoms to express helplessness may explain the bodily symptoms of Anna O. and other upper-middle-class women of the Victorian era, whose lives were severely restricted by societal conventions. However, although symptoms of SSD occur around the globe, the nature of the symptoms differs across cultures. For instance, symptoms of burning hands or feet are more common in Africa and South Asia than in Europe or North America (American Psychiatric Association, 2000).

Feedback Loops in Understanding Somatic Symptom Disorder

It is common for people with SSD to have had a disease, an illness, an accident, or another form of trauma prior to developing the disorder. In fact, people with this disorder are more likely to report a history of childhood abuse than are other medical patients (Brown et al., 2005). People who are genetically predisposed to SSD (neurological factor), interpret the bodily sensations caused by an illness or accident as signaling a catastrophic illness (psychological factor). In turn, this misinterpretation may cause the person to change his or her behavior in a way that ultimately becomes dysfunctional, restricting activities and straining relationships.

Such misinterpretations may initially grow out of modeling. For example, children whose parents have chronic pain are more likely to report abdominal pain themselves and to use more pain relievers than a comparison group of children (Jamison & Walker, 1992). These children’s experiences with their ill parent (social factor) may influence their body via their brains (perhaps they have more stomach acid because they are more anxious and stressed; neurological factor), their attention to and attributions for bodily sensations (psychological factors), and their reporting of pain (social factor).

Moreover, a patient’s symptoms may have been unintentionally reinforced by friends and family members (social factor). And, as with panic disorder (see Chapter 6), the arousal that occurs in response to stress can increase troubling bodily sensations that then become the focus of preoccupations (see Figure 8.1).

FIGURE 8.1 • Feedback Loops in Understanding Somatic Symptom Disorder

Conversion Disorder

Conversion disorder involves sensory or motor symptoms that are incompatible or inconsistent with known neurological or medical conditions.

Patients who have conversion disorder do not consciously produce the symptoms they experience (as in factitious disorder or malingering), and these patients are significantly distressed or their functioning is impaired by the symptoms (see TABLE 8.10). Conversion disorder is similar to SSD in that both involve physical symptoms; however, conversion disorder is limited to sensory and motor symptoms that appear to be neurological (that is, related to the nervous system) but, on closer examination, are inconsistent with the effects of known neurological or medical disorders (see Figure 8.2). A diagnosis of conversion disorder can be made only after physicians rule out all possible medical causes—and this process can take years. Conversion disorder is sometimes referred to as functional neurological symptom disorder because the neurological symptom relates to the functioning of some aspect of the nervous system but not to an underlying medical cause of the symptom.

FIGURE 8.2 • Conversion Disorder: Glove Anesthesia Patients who suffer from conversion disorder have sensory or motor symptoms that at first may appear to be neurological but on further investigation do not correspond to true neurological damage. One example is glove anesthesia, in which the person reports that his or her hand—and only the hand—has no sensation, as shown in (a). However, the neural pathways that would create such an anesthesia in the hand would also create a lack of sensation in the arm (b); the color-coded regions show the areas served by different nerves. Thus, conversion disorder may be the appropriate diagnosis when a patient reports glove anesthesia in the absence of anesthesia of the arm.

Conversion disorder is characterized by one or more of three types of symptoms (American Psychiatric Association, 2000; Maldonado & Speigel, 2001):

• Motor symptoms. Examples include tremors that become worse when the person pays attention to them, tics or jerks, muscle spasms, swallowing problems, staggering, and paralysis (sometimes referred to as pseudoparalysis, which may also involve significant muscle weakness).
• Sensory symptoms. Examples include blindness, double vision, deafness, auditory hallucinations, and lack of feeling on the skin that doesn’t correspond to what is produced by malfunctioning of an actual nerve path.
• Seizures. Examples include not only the motor symptoms of twitching or jerking of some part of the body but also loss of consciousness with uncontrollable spasms of the large muscles in the body, causing the person to writhe on the floor. These seizures are often referred to as nonepileptic seizures because they do not have a neurological origin and are not usually affected by medication for seizures. The nonepileptic seizures are likely to occur when other people are present.

Anna O. had both motor conversion symptoms (paralysis of her neck, arm, and legs) and sensory conversion symptoms (problems with vision, a lack of sensation in her elbows). Breuer did not report any seizure-like symptoms.

In conversion disorder, symptoms do not correspond to what would be produced by the relevant nerve pathways, but rather they arise from the patients’ (perhaps unconscious) ideas about what would happen if certain nerve pathways were disrupted. Thus, a patient may not be able to write but can scratch an itch, which would be impossible with true paralysis of the hand muscles. Similarly, when the sensory symptom of blindness occurs in conversion disorder, medical tests reveal that all parts of the visual system function normally, as was true for Mary, described in Case 8.5.

People with conversion disorder may react in radically different ways to their symptoms and to what they might imply: Some seem indifferent whereas others respond dramatically. Anna O.’s response was “a slight exaggeration, alike of cheerfulness and gloom; hence she was sometimes subject to moods” (Breuer & Freud, 1895/1955, p. 21). TABLE 8.11 provides more facts about conversion disorder.

Both the diagnosis of conversion disorder and its placement among the somatic symptom disorders are controversial (Brown & Lewis-Fernández, 2011). Some researchers have suggested that conversion disorder is not a distinct disorder but rather a variant of SSD; these researchers point out that both disorders may involve the bodily expression of psychological distress (Bourgeois et al., 2002). Other researchers believe that conversion symptoms in general, and nonepileptic seizures in particular, are more like dissociative symptoms than like symptoms of other somatic symptom disorders (Kihlstrom, 2001; Mayou et al., 2005). As they note, dissociation can not only affect memory and the sense of self but also can disrupt the integration of sensory or motor functioning.

Research on neurological factors in conversion disorder focuses on how brain systems operate differently in people with the disorder than in other people.

Neurological Factors: Not Faking It

When considering making a diagnosis of conversion disorder, clinicians must rule out simple malingering, or faking of symptoms, which is difficult to do (Stone et al., 2010). Could all cases of conversion disorder just be faking? Neuroimaging findings suggest that muscle weakness arising from conversion disorder is not the same as consciously simulated muscle weakness. For example, Stone and colleagues (2007) scanned the brains of patients with conversion disorder and of healthy control participants while their ankles were flexed. The patients with conversion disorder all reported weakness in the manipulated ankle prior to the study; during the study, participants in the control group were asked to pretend that their ankles were weak. The results were clear: Some brain areas were more activated in the patients than in the controls (such as the insula, which is involved in registering bodily sensations), and some brain areas (including areas in the frontal lobes) were less activated in the patients than in the controls. These findings are good evidence that the patients in this study were not simply faking their disorder.

In addition, some patients with chronic pain develop sensory deficits, a kind of “psychological” anesthesia. In one study, researchers scanned the brains of four such patients, using fMRI, while sharp plastic fibers were pressed into the skin (Mailis-Gagnon et al., 2003). These patients had apparent sensory deficits in only one limb, and thus the researchers could directly compare stimulation of the normal and affected limbs. When the researchers stimulated the normal limb, the sharp plastic fibers activated a brain network that registers pain, as is normal. In contrast, this network was not activated when the researchers stimulated the affected limb, as is shown in Figure 8.3. These findings indicate that the “psychological” anesthesia actually affected the brain and inhibited activation in the brain areas that register sensation and pain.

FIGURE 8.3 • Brain Activation in Conversion Disorder: Healthy Limb Versus Affected Limb Brain areas activated when the skin of the healthy, nonaffected limb was stimulated (top row) compared to those activated when the skin of the affected limb was stimulated (bottom row); arrows show the key areas of activation (Mailis-Gagnon et al., 2003). It’s clear that the scans in the bottom row show much less activation.

Source: A. Mailis-Gagnon, M.D., et al., Neurology 2003;60:1501–1507. © 2003 American Academy of Neurology.

Other studies have shown that conversion disorder is not a direct consequence of abnormal functioning of brain areas that register peripheral sensations but rather reflects abnormal functioning of brain areas that interpret sensations and manage other brain areas (that is, areas that are involved in “executive functions”) (Hoechstetter et al., 2002; Lorenz et al., 1998). At least in some cases, abnormal processing in brain areas responsible for executive functions might inhibit brain areas that process sensation and pain or that produce movements, which in turn causes them to fail to function properly.

Symptoms of conversion disorder may be more common after significant psychological stressors, such as military combat. This soldier is displaying muscular spasms as part of his conversion disorder. Such symptoms among soldiers are thought to resolve a conflict between their loyalty to comrades and their fear of battle: Soldiers with such symptoms are unable to fight (Spiegel, 1974).

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Psychological Factors: Self-Hypnosis?

There is no generally accepted explanation for how psychological factors might produce the selective bodily symptoms in conversion disorder (Halligan, Athwal, et al., 2000). But self-hypnosis offers one possible explanation—that the disorder is the result of unintended self-hypnotic suggestion. According to this theory, patients have, consciously or unconsciously, “suggested” to themselves that they have symptoms (Kozlowska, 2005); that is, particular sensations have become dissociated. This theory receives support from the fact that people with conversion disorder are unusually hypnotizable (Roelofs, Hoogduin, et al., 2002) and from the finding that areas of the brain activated by hypnotically induced paralysis are similar to those activated by paralysis in patients with conversion disorder (Halligan, Bass, & Wade, 2000; Oakley, 1999).

Social Factors: Stress Response

Life stressors, such as combat, can trigger conversion disorder. Moreover, the greater the severity or number of stressors, the more severe the conversion symptoms (Roelofs et al., 2005). As we saw with SSD, somatic symptoms can be a culturally accepted way to express feelings of helplessness (Celani, 1976), which may explain why some soldiers develop conversion disorder in combat. Conversion disorder can also be a way to obtain the attention associated with being sick. This was certainly true for Anna O., as well as for many other women of the Victorian era.

Illness Anxiety Disorder

People who are diagnosed with illness anxiety disorder have either no or minor medical symptoms but nonetheless are preoccupied with a fear or belief that they have a serious disease; they engage in excessive behaviors related to this belief, such as repeatedly checking their bodies for sign of an illness or avoiding medical care. Despite the fact that physicians cannot identify a medical problem, patients with illness anxiety disorder persist in clinging strongly to their conviction that they have a serious disease. This diagnosis is in some ways similar to the DSM-IV diagnosis of hypochondriasis. However, in DSM-IV the disorder hypochondriasis included two groups of people—those without any significant medical symptoms (now classified as illness anxiety disorder) and those with at least one medical symptom but whose psychological response to the symptom is excessive (now classified as somatic symptom disorder). Although people with SSD and those with illness anxiety disorder share a focus on bodily symptoms, only people with illness anxiety disorder believe that they have a serious illness, despite reassurance from doctors and minimal physical symptoms, if any.

Patients with illness anxiety disorder may or may not realize that their worries are excessive for the situation; when they do not, they are said to have poor insight into their condition. Consider a man who sees floating “spots” and does not believe his eye doctor when told that such floaters are normal and nothing to worry about. The man probably doesn’t think that the doctor is lying about the spots, but he may believe that the doctor didn’t do a thorough enough eye examination; he may think that the floaters indicate that he is going blind or that he has a tumor. His worries about this problem are distressing and preoccupying to the point that he functions less well at work—not because of the floaters but because of his frequent thoughts about the floaters.

People with this disorder may spend hours on the Internet, searching for illness-related information to reassure themselves, only to become more anxious or worried (Starcevic & Berle, 2013). To be diagnosed with this disorder, this kind of preoccupation with a perceived health problem must cause significant distress or impair the person’s functioning and must have continued for at least 6 months (see TABLE 8.12). Because illness anxiety disorder is a newly defined disorder and most people (75%) previously diagnosed with hypochondriasis would now be diagnosed with somatic symptom disorder, additional facts about illness anxiety disorder, such as prevalence and course, are not known at this time. However, two thirds of people with this disorder are estimated to have at least one other psychological disorder, commonly anxiety or depressive disorders, and the disorder typically begins in early to middle adulthood (American Psychiatric Association, 2013).

Like people with SSD, those with illness anxiety disorder don’t understand that even healthy people sometimes have aches and pains and other bodily discomforts. Instead, like the woman in Case 8.6, they unrealistically believe that having “good health” implies not having any unpleasant bodily symptoms (Barsky, Coeytaux, et al., 1993).

Illness anxiety disorder has many features in common with anxiety disorders. In fact, certain forms of illness anxiety disorder and anxiety disorders are so similar that some researchers have advocated moving illness anxiety disorder from the category of somatic symptom disorders to the category of anxiety disorders (Mayou et al., 2005). Illness anxiety disorder, phobias, and panic disorder are all characterized by high levels of fear and anxiety, as well as a faulty belief of harm or danger. However, with illness anxiety disorder and panic disorder, the perceived danger is from an internal event that is thought to be producing a bodily sensation, whereas with phobias, it is from an external object (such as a snake) or a situation (such as giving a speech; Fava, Mangelli, & Ruini, 2001). People with panic disorder, phobias, and illness anxiety disorder all may try to avoid certain stimuli or situations; with panic disorder and illness anxiety disorder, what is avoided may be an elevated heart rate (Hiller et al., 2002).

In addition, both patients with illness anxiety disorder and those with obsessive-compulsive disorder (OCD) have obsessions and compulsions (Abramowitz & Braddock, 2006). In particular, patients with illness anxiety disorder obsess about possible illnesses or diseases they believe they might have. They may compulsively ask doctors, friends, or family members for reassurance or compulsively “check” their body for particular sensations. People with some forms of illness anxiety disorder spend hours compulsively consulting medical websites. It’s important to keep in mind that some medically related Internet chat rooms or websites can spread false or misleading information.

Because illness anxiety disorder is a diagnosis new to DSM-5, most research related to this disorder studied people diagnosed with hypochondriasis. Hence we use the term hypochondriasis when discussing studies of people with that diagnosis, and the term illness anxiety disorder when discussing experiences and symptoms that clearly apply to the new disorder. Most research has examined psychological factors, and not enough is known about neurological and social factors to understand the feedback loops among the types of factors.

Neurological Factors

Some researchers have suggested that the neurotransmitter serotonin does not function properly in at least some cases (King, 1990). As we’ll see in the section on treatment, there is some indirect support for this hypothesis, based on the observation that SSRIs (which selectively affect serotonin reuptake) appear to improve the disorder. That is, the mere fact that SSRIs can improve the symptoms is evidence that the symptoms arise, at least in part, from disruption of the activity of serotonin. In addition, results from one twin study suggest that genetic differences contribute to hypochondriasis (Gillespie et al., 2000).

Psychological Factors: Catastrophic Thinking About the Body

People with hypochondriasis have specific biases in their reasoning: Not surprisingly, given their disorder, they both tend to seek evidence of health threats and also may fail to consider evidence that such threats are minimal or nonexistent (Salkovskis, 1996; Smeets et al., 2000). For instance, a man with illness anxiety disorder who notices a bruise on his leg might interpret it as evidence that he has leukemia rather than try to remember whether he recently bumped into something that could cause a black-and-blue mark.

In addition, people afflicted with illness anxiety disorder focus attention closely on unpleasant sensations. They commonly focus on the functioning of body parts (such as the stomach or the heart), minor physical problems (such as a sore throat), and ambiguous physical sensations (such as “aching veins”). Moreover, they interpret bodily sensations as abnormal, pathological, and symptomatic of disease (Barsky, 1992; Barsky et al., 2000). In fact, like patients with SSD, patients with hypochondriasis (and likely with illness anxiety disorder) may engage in catastrophic thinking about their physical sensations or fears of illness, just as the woman in Case 8.6 did when she interpreted physical sensations as signs of “crippling illness.”

Concern for one’s health is normal. How do we begin to assess when the concern is excessive?

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As is the case with many anxiety disorders, people with illness anxiety disorder may engage in behaviors that temporarily reduce their anxiety. For example, they may repeatedly take their blood pressure, perform urine dipstick tests, feel body parts for cancerous lumps, or call their doctor about new symptoms. Such behaviors maintain their faulty beliefs and can, through negative reinforcement, sustain their anxiety in the long term.

Social Factors: Stress Response

As with other somatic symptom disorders, research has shown that stressful events can precipitate hypochondriasis (Fallon & Feinstein, 2001). In addition, such people are more likely than people without the disorder to report having experienced traumatic sexual contact, physical violence, or major familial upheaval (such as their parents’ divorce) (Barsky, Wool, et al., 1994). Moreover, through their attention and concern, relatives and friends may unintentionally reinforce patients’ symptoms.

Treating Somatic Symptom Disorders

When treating any of the three somatic symptom disorders (SSD, conversion disorder, or illness anxiety disorder), clinicians target neurological, psychological, and social factors—individually or in combination. As we discuss below, cognitive-behavior therapy is generally the treatment of choice for somatic symptom disorders.

Perhaps the most effective treatment for leg paralysis due to conversion disorder may be the simplest: Educate the patient about the nature of the symptoms. At least for three patients in one study, simply showing them their normal test results and contradictions from their physical exam did the trick. These patients walked out of the hospital unaided immediately after these results were given to them (Letonoff et al., 2002).

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There has not been much rigorous research on neurologically-based treatments for somatic symptom disorders in general; the studies that have been reported have rarely included appropriate control groups, such as a placebo group or a wait-list control group to determine whether the disorder spontaneously improves with time. Some treatments target specific symptoms. For instance, medications, such as an SSRI, or St. John’s wort may be used to treat some anxiety-related symptoms of somatic symptom disorders. As with anxiety disorders, however, when the medication is stopped, the anxiety-related symptoms usually return. Other types of treatments, such as biofeedback, target muscle tension.

Were Anna O. to be treated by a mental health clinician today, she might receive medication. Anxiety or depression may have contributed to her symptoms, and if medication for these disorders did not alleviate her hallucinations, the clinician might recommend an antipsychotic medication (Martorano, 1984). Note that Anna O. was given medications frequently used at that time: morphine (typically given for pain relief) and chloral hydrate (a narcotic used to induce sleep). She became addicted to both of these substances, and after her “talking cure” with Breuer ended, she needed inpatient treatment to end her addiction.

Research indicates that the treatment of choice for most somatic symptom disorders is cognitive-behavior therapy (CBT). As shown in TABLE 8.13, the cognitive and behavioral methods used to treat each of the disorders vary because each disorder has different symptoms. Cognitive methods focus on identifying and then modifying irrational thoughts and shifting attention away from the body and bodily symptoms (Gropalis et al., 2013). Behavioral methods focus on decreasing compulsive behaviors and avoidance.

Patients with any of the somatic symptom disorders can be helped, in part, merely by feeling that someone understands the pain and distress they feel (Looper & Kirmayer, 2002). For SSD and conversion disorder, the therapist strives to understand the context of the symptoms and of their emergence and the way the symptoms affect the patient’s interactions with others (Holder-Perkins & Wise, 2001); with these two disorders, treatment may focus on helping the patient communicate more assertively—which can help to relieve the social stressors that contribute to the disorders.

Treatment may also focus on the family—educating family members about the disorder and the ways they may have inadvertently contributed to or reinforced the patient’s symptoms. The therapist may teach family members how to reinforce positive change and to extinguish behavior related to the symptoms (Looper & Kirmayer, 2002; Maldonado & Spiegel, 2001). For instance, if the patient has SSD, family members may be asked not to inquire about the patient’s bodily symptoms. In addition, support groups may help patients feel less alone and isolated (Looper & Kirmayer, 2002).

CBT can provide new skills and new ways to interpret the sensations and modify the preoccupying thoughts, which in turn can decrease the bodily symptoms (neurological factor) and the attention paid to them (psychological factor). Similarly, although biofeedback and medication primarily target neurological factors, these techniques can in turn affect the type and quality of attention paid to bodily sensations and can change the meaning made of bodily sensations (psychological factors). In addition, the relationship with a therapist (social factor) can provide reassurance and support; as family members change how they respond to the patient’s symptoms (social factor), positive change can be enhanced. Figure 8.4 shows how successful treatment of somatic symptom disorders affects the different types of factors directly and through their feedback loops.

FIGURE 8.4 • Feedback Loops in Treating Somatic Symptom Disorders