Psychosomatic Conditions: Somatic Symptom and Related Disorders, Functional Somatic Syndromes, and Deception Syndromes

Somatic Symptom Disorder

Somatic symptom disorder (SSD) is the prototype diagnosis of the category bearing its name. In contrast to the smorgasbord approach that required a somewhat arbitrary and arcane multidomain symptom array in its predecessor, somatization disorder, SSD requires only that “one or more” symptoms form the focus of the patient's attention. Thus, in a rare display of “lumping” diagnoses, this change in DSM-5 obviates the need for the previous edition's pain and undifferentiated somatoform disorders. For a full “cross-walk” between DSM-IV Somatoform Disorders and DSM-5 Somatic Symptom and Related Disorders, see Figure 16-1 .

The patient with SSD is characterized by preoccupation, anxiety, and “time and energy devoted” to their symptom(s) that are disproportionate to their severity, as determined by providers. This determination can be a very difficult task of cross-matching objective findings, clinical experience, and patient reports, as in the case of back pain and spinal imaging. Still and unavoidably, the crux of this disorder is nonetheless “abnormal illness behavior” or a mismanagement of the “sick role” by the patient. While these characteristics are found to varying degrees in all of the SSD and related disorders, they are the crux of SSD. A major component of Parsons' sociologic conceptualization of the sick role is that the sick person justly acquires a degree of blamelessness for their symptoms, relief from duties incompatible with their malady, and an entitlement to care; these are balanced by an obligation to pursue health along with the help of one's providers. When one considers the plight of the guilt-ridden, overburdened, and unloved person, sickness can be “one-stop-shopping” from a primary gain point of view. From that same sociologic view, the pathology of SSD can be seen as a desperate clinging to the benefits of the sick role without fulfillment of the duty, that, along with sickness, purchases those benefits. This imbalance may be the cause of the variable consternation, and desperate indulgence that many providers and family members exhibit toward the SSD patient.

Etiologic theories in SSD seem to exist in proportion to “schools” of psychiatry and cannot be given full justice here. Psychodynamic theories, originating in conversion hysteria as noted above, tend to hinge on defense mechanisms that “convert” unbearable or unacceptable feelings and impulses into bodily sensations. Originally coined by Nemiah, alexithymia comes in and out of fashion as an explanation for why patients who are unable to recognize and describe their own emotions might instead experience them somatically. A cognitive model applied to somatization and hypochondriasis is presumed to still be applicable. Here, the symptom-amplifying patient is one who, already having a low threshold of detection for bodily sensations and variations, applies medical significance to those sensations, and behaves accordingly. This behavior often includes limiting activities and seeming to relentlessly seek medical validation (and, usually unsuccessfully, functionally meaningful relief) of their suffering. This mechanism is borne out by studies of the cognitive biases about health found in symptom-amplifying patients, and overlaps with biological theories as represented in studies of the phenomenon of central sensitization.

Epidemiology of SSD is yet to be determined. Extrapolating from prior conditions, SSD would be expected to be overrepresented among women, those with low education, low socioeconomic status, and a high rating in the personality trait of neuroticism. SSD must be present for 6 months to be diagnosed and is generally considered to be a chronic condition.

Illness Anxiety Disorder

Whereas the patient with SSD is preoccupied with symptoms, the patient with illness anxiety disorder (IAD) is preoccupied with the idea of having or contracting a major illness. He or she may not even have any active symptoms at a given point in time, and instead beset providers with requests for unwarranted screening tests such as “full body scans,” or serially and progressively make restrictive lifestyle alterations based on the 11 o'clock news' “fear segments” or fringe health media. Alternatively, and as opposed to the above portrayal of stoicism, a person with IAD may avoid the healthcare system altogether, afraid of finding out something he does not wish to know. Thus, DSM-5 divides IAD into “care-seeking” and “care-avoidant” types.

In the formative days of DSM-5, there was some debate as to whether IAD was better sorted among the anxiety or somatic symptom disorders, with arguments in favor of the latter coming out on top. It is felt to map best onto the DSM-IV diagnosis of hypochondriasis, though the DSM-5 committee predicts that it will capture only about 25% of these patients, leaving the rest to SSD. Again, the presence or absence of somatic disease is immaterial to this diagnosis; the crux being the disproportionate nature of the patient's anxiety.

Extrapolating from studies of hypochondriasis, patients with IAD hold to a “restrictive concept of good health,” as evidenced by their responses on scales such as the Health Norms Sorting Task, which asks if a person could be considered “healthy” while experiencing a variety of different somatic sensations. A cognitive-behavioral model, much like that described above, minus the heightened symptom detection, is thought to hold sway over these patients and informs some promising psychotherapeutic approaches that may be adaptable to other SSDs. As with any illness beliefs and behaviors, the patient's cultural and familial upbringing will have had a major influence, and (as with all SSDs) it is worth asking about family illness experiences/models, particularly in childhood.

Unlike the SSD patient, at any particular point in their illness, a patient with IAD may be amenable to reassurance and dutiful clinical attention. Depending on how often this attention is required and how impactful the maladaptive health beliefs are over time, this “patchwork” approach to the patient's problems may be of limited use.

Conversion Disorder

In a sense, psychiatry's original somatic symptom disorder, conversion disorder involves a loss or change in sensory or motor function that is suggestive of a neurological disorder, but lacks examination and laboratory/imaging results compatible with said change. DSM-5 accounts for non-neurologic presentations, such as pseudocyesis, separately under the heading of “Other Specified Somatic Symptom and Related Disorder.” As with other somatic symptom disorders, incompatibility between signs and exam, laboratory, or radiologic findings does not necessarily mean complete absence of abnormality. The best example of this point is the oft-reported (though sometimes overblown) overrepresentation of conversion seizures (note: the standard term, “psychogenic nonepileptic seizures” [PNES], implies an unsubstantiated etiology) among patients with electrographic evidence of separate epileptic seizures.

The possibility of psychiatric–neurologic co-existence can become a point of contention between psychiatrists and neurologists unless both are aware of it, and each has some basic knowledge of the others' work. On the subject of psychiatrists' attitudes towards conversion disorder work-ups, two other issues worth noting are that: (1) the idea that up to 30% of conversion disorders are later found to have neurologic disease has been debunked and the rate of false-positives for this diagnosis (about 5%) appears to be no higher than for other neurologic disorders; (2) the idea of conversion disorder being a “diagnosis of exclusion” does not mean that psychiatrists should only be consulted at the end of a patient's work-up. For example, it has been convincingly argued that psychiatric consultation should occur on the day of admission to an epilepsy monitoring unit (where rates of PNES are generally found to be 20% to 30% ), so as to normalize the possibility of conversion disorder early on.

DSM-5, in an effort to reduce the perceived underdiagnosis of conversion disorder, removed proof of unintentional sign production from the diagnostic criteria. The subsequent text addressing conversion disorder nonetheless clearly indicates that unintentional production is assumed, and that if feigning is suspected strongly enough, the differential shifts to factitious disorder or the non-disorder, malingering. Another important change in the DSM-5 criteria is the elimination of the need to identify a proximate psychological stressor presumably triggering conversion disorder. The previous requirement of this usually highly presumptive piece of detective work was not only an impediment to diagnosis, but also made an unsubstantiated psychodynamic etiologic assumption about all cases of conversion disorder.

The proximate-stressor requirement also runs counter to the longitudinal course of conversion disorder. More often than not, conversion disorder does not follow a stressor–conversion–relaxation–resolution pattern. Instead, conversion disorder frequently follows a relapsing–remitting or chronic course, which may vary depending on the type of presentation. For example, unilateral sensory and motor signs may persist for several years in the vast majority of hospitalized neurological patients. PNES frequency/presence similarly waxes and wanes in many patients.

Often referred to as “functional” deficits, the signs seen in conversion disorder ought to be looked at less as misleading than as misunderstood. The original historic meaning of “functional” in medicine, meant hidden or physiologic, as distinguished from visible, anatomic disease. The physiologic underpinnings of conversion disorder remain “hidden,” and are difficult to study given their protean nature (e.g., should conversion disorder patients with conversion blindness, hemiparesis, and “psychogenic” non-epileptic seizures be grouped together in the same study?). Still, an emerging literature suggests abnormal recruitment and connectivity between brain areas involved in arousal, planning, and execution of movements. Hypothesized to represent disruptions in self-monitoring and agency, these findings may also reflect the pathophysiologic underpinnings of the association between conversion disorder and trauma.

Conversion disorder is seen more often in women. Age of onset is variable across most of the life span and across different manifestations of the illness. PNES may peak in the third decade and motor signs may peak in the fourth. Treatment of conversion disorder is understudied. Suggestion of recovery is often employed, with hospitalized patients in particular often offered the prediction of a non-abrupt, progressive pattern of functional recovery. This technique likely has its heritage in psychoanalytically informed ideas about conversion “hysteria” and the theory/hope that a patient pathologically subject to suggestion will also be open to its therapeutic application. It is important that the psychiatric consultant emphasize the importance of physical therapy to patient and consultee alike, disconnecting this intervention from etiology and connecting it instead to deficit and recovery. Psychodynamic therapies are often recommended, and consultees often seem to assume this is a proven, effective, and standard treatment. Cognitive-behavioral therapies, including paradoxical approaches in which patients are coached through the precise, conscious simulation of their conversion signs, are under investigation.

Psychological Factors Affecting Medical Illness

This diagnosis refers to abnormal illness behaviors that are adversely affecting the course or treatment of a conventionally defined and diagnosed medical condition. Psychological factors affecting medical illness exist on a range of severity from “mild” (i.e., increasing risk) to “extreme” (i.e., causing life-threatening risk), and encompassing just about any psychological state or personality trait (aside from those associated with a distinct psychiatric co-morbidity). It could be said that just about all of us have this condition, since just about none of us refrain from all behaviors detrimental to health, and that hypothetical person who unerringly behaves in a health-directed manner probably has illness anxiety disorder anyway. Perhaps conspicuously, this “diagnosis” does not end in the word “disorder.”

Factitious Disorders

Factitious disorders are discussed later in this chapter, in the section on “Deception Syndromes.” It is simply noted here that in previous iterations of the DSM, factitious disorders occupied a category of its own, “Factitious Disorders.” Under this heading could be found factitious disorders with physical symptoms or psychological symptoms, and factitious disorder by proxy. Despite the preservation of its possible expression through psychological symptoms (e.g., lying about or simulating psychosis, reporting false suicidal ideation, or reporting non-lethally intended self-injury as a suicide attempt for “primary gain”), this diagnosis has been moved to the “Somatic Symptom and Related Disorders” category.

Depressive Disorders

The first consideration in patients with physical symptoms that seem out of proportion to objective findings is whether the patient is depressed. Major depressive disorder has a somatic dimension, and everything hurts more in the setting of depression.

Indeed, 75% of primary care patients with MDD or panic disorder seek treatment from their physicians for exclusively somatic symptoms. The vegetative symptoms of MDD include insomnia, fatigue, anorexia, and weight loss; and depressed patients report more functional somatic symptoms (aches and pains, constipation, dizziness, etc.) than do other patients. Among primary care patients, disabling chronic pain was present in 41% of those with MDD compared with 10% of those without MDD. Those patients with both chronic pain and MDD tended to have more severe affective symptoms and a higher prevalence of panic disorder. Even across cultures, the majority of patients with MDD spontaneously report only somatic symptoms; when pressed, however, 89% will also offer psychological symptoms.

When MDD is diagnosed in the context of unexplained bodily complaints, depression should be treated promptly. Both affective and somatic symptoms may abate with systematic antidepressant treatment. Of course, MDD (as well as generalized anxiety disorder) is also a major comorbidity of somatic symptom disorders, seemingly present in a majority of these patients. So, one must also be on guard against the false hope that, “if I just treat the depression, the ‘somatizing’ will disappear.” Further, MDD itself can be difficult to diagnose in patients prone to amplified experiences and reporting of somatic symptoms. There is reason to believe they may also be prone to amplify certain psychological “symptoms” as well. (For further coverage of affective disorders, see Chapter 9 .)

Anxiety Disorders

Anxiety frequently co-occurs with functional somatic symptoms, distorting the cognitive appraisal of somatic symptoms and making even benign bodily sensations seem ominous and alarming. Anxious patients tend to catastrophize normal physiologic sensations and ailments. As noted in Chapter 13 , many of the symptoms of panic disorder are somatic; they include dyspnea, palpitations, chest pain, choking, dizziness, paresthesias, hot and cold flashes, sweating, faintness, and trembling. As a result, patients in the midst of a panic attack may feel that they are unable to breathe or that they are dying. Patients with panic disorder may focus on the most prominent symptom and find the appropriate subspecialist; therefore, patients with medically unexplained symptoms and panic disorder present with chest pain in cardiology, nausea or diarrhea in gastroenterology, and dizziness in neurology. Anxiety is also one of the most common features of MDD.

When co-morbid with pain, anxiety can lower the pain threshold dramatically. In fact, some patients cannot distinguish anxiety from pain (“No, I am not frightened; I hurt!”). Pleas for pain relief may be related to anxiety rather than addiction or the neediness associated with personality disorder.

Substance Use Disorders

Physicians should always consider the diagnosis of alcohol abuse in a patient with multiple, vague somatic symptoms. Whether the patient consciously conceals alcohol dependency or fails to make the connection, the diagnosis may be elusive. Information from the patient's family may help (“What he calls headache and chest pains, Doctor, I call a hangover.”). Because alcohol abuse systematically disrupts sleep, patients may begin using sedative–hypnotic substances as well. Insomnia, morning cough, pains in the extremities, dysesthesias, palpitations, headache, gastrointestinal (GI) symptoms, fatigue, bruises—none are strangers to the alcoholic. The effects of other addictive drugs may be similarly confounding. (See Chapters 14 and 15 , for the diagnosis and treatment of substance abuse disorders.)

Psychotic Disorders

Sometimes a somatic complaint has the rigid, stereotyped character of a delusion and presents in a patient with a psychotic disorder. Here the key is to consider a psychotic disorder as a possibility from the perspective of a fuller mental status exam and a fuller past history. Patients with psychotic depression may have particularly negatively flavored somatic delusions (such as the conviction that one's abdominal organs are decomposing).

Delusional disorder of the somatic type presents a particular diagnostic challenge since the delusions of delusional disorder are, by definition, non-bizarre, at least insofar as they follow the laws of biology and physics. Patients with delusional disorder of the somatic type tend to be more circumscribed about the nature of their medical complaint in terms of its content, even as its consequences increasingly consume their lives. A (to some) controversial, yet prototypical example of this kind of somatic delusion is Morgellons disease which involves specific convictions about dermal infestation. Formerly known as Ekbom's syndrome, Morgellons disease, as with other specific delusions and fringe beliefs, is increasingly difficult to pin down because of the spread of ideas and cohesion of sufferers through on-line resources.

In contrast to delusional disorder, the somatic delusions of schizophrenia are generally so bizarre and idiosyncratic (e.g., that foreign bodies are inside an organ or orifice, that body parts are missing or deformed, or that a more mundane somatic issue is being caused by other parties at a distance) as to be easily recognized. But when a patient with schizophrenia complains of a symptom that is not bizarre (e.g., a headache or weakness), the rigid delusional dimension of psychosis may be missed. Making such a diagnosis with a thorough psychiatric history and examination is ordinarily no problem. Patients with schizophrenia can also have conversion symptoms (e.g., hemiparesis).

Nonetheless, physical symptoms in a patient with psychotic disorder must be taken seriously. The premature mortality in this seriously mentally ill population is significant. What component of this is due to symptoms being dismissed by providers distracted or biased by a psychotic disorder diagnosis is not entirely clear, but the fact that a schizophrenia diagnosis means a life foreshortened by an average of 15 years, is! It may be more common not to hear out a patient with schizophrenia and to miss a straightforward medical complaint.