Are those in which the physical symptoms of a disorder can be produced or exacerbated by psychological factors?

Differential Diagnosis and Testing

In the emergency department [ED], the brevity of the clinical encounter and a diagnostic focus on life threats make accurate identification of patients with somatoform disorders difficult. Even when demonstrable medical disease is present, symptoms and severity are modulated by the psychologic well-being of the patient. Even though it stands to reason that many patients somatize to some degree, clearly a subset exists in whom such behavior represents a disorder.

The goals when evaluating somatoform illness are identification of the condition and appropriate referral. In the ED, life-threatening conditions on the differential diagnosis are excluded first, other potentially serious medical illnesses are excluded second, and somatoform causes are excluded last, if at all.

Classic findings can make one suspect a somatoform illness; however, such behavior is insufficient for psychiatric diagnostic criteria. Synopses of the characteristics of somatoform disorders can be found inTable 198.1. It is useful to categorize these illnesses as nondeliberate [somatization, conversion disorder, and hypochondriasis] and deliberate [factitious disorders and malingering].

The symptoms experienced by a patient with a nondeliberate somatoform illness are perceived as very real. Diligent history taking often uncovers telling patterns. Useful questions to consider include the following: Are these complaints chronic? Do they correlate with identifiable stressors? Does the patient hold a conviction of a particular illness or imminent death? Does the patient have a lifelong history of “illness”? What has been done for this patient in previous visits, by previous providers? What is new today? Obtaining answers to these questions, along with a careful physical examination, can help direct the emergency evaluation while at the same time reassuring patients that they are being taken seriously. Respect ultimately aids in disposition because these patients are far more likely to comply with a plan when they believe that a provider has their best interests at heart.

Concerns about making the diagnosis of a somatoform illness should not preclude a thorough ED evaluation because many medical conditions can be mistaken for somatization, particularly when the findings are atypical.Box 198.3 provides examples of medical conditions that can mimic somatoform behavior.

As a general rule, patients with nondeliberate somatoform illness acquiesce to invasive diagnostic testing, whereas those with factitious disorders and malingerers are more reluctant. The presence of two or more of the following features is suggestive of malingering behavior: mention of a medicolegal context of the visit, discrepancy between subjective and objective assessment of the degree of stress and disability, poor compliance with evaluation and treatment, and antisocial personality disorder.19 Malingering is very difficult to prove, even in the presence of high clinical suspicion and deliberate investigation, and surveillance of the patient is often required.22 Determination of malingering is usually the purview of specialists such as neuropsychologists.

E. Psychologic Aspects

Psychosomatic disease should be considered mainly in patients with no precipitating history [childbirth, infection], negative workup, noncyclic pain, or evidence of depression/anxiety. Depression and physical abuse are concerns in CPP patients. It is important to ask women suffering CPP about a history of domestic violence and sexual abuse [17]. An interesting finding common to CPP, fibromyalgia, chronic fatigue syndrome, and asthma is adrenocortical hyporesponsiveness. Obviously, further work in this area is needed [18].

Coping with CPP can lead to maladaptive behavior with depressive symptoms and decreased quality of life. Patients with CPP report difficulty maintaining employment [19], difficulty with family relationships, and difficulty with travel [20].

Pitfalls in the Diagnosis and Management of Abnormal Illness Behavior

In Case 4, no organic cause was found to explain his severe abdominal pain and weight loss. This led a gastroenterologist to suspect a psychiatric explanation for the patient’s symptoms, and a psychiatrist was consulted. After taking a psychiatric history and observing the patient, the psychiatrist made a diagnosis of “psychogenic pain,” a term that implies that pain is caused primarily and maintained by emotional distress. This diagnosis was fully accepted by the gastroenterologist, and the patient was transferred to a psychiatric unit of the hospital.

The thought processes were erroneous for 2 reasons. First, physical [or organic] disease cannot be excluded with certainty, and failure to discover an organic disease to explain severe abdominal pain did not constitute evidence for a psychiatric etiology in this case. Moreover, there were no clues suggesting positive evidence for abnormal illness behavior. Although consulting a psychiatrist to help manage any associated depression may have been wise, the gastroenterologist should have known that a psychiatrist cannot accurately diagnose emotional distress as the primary cause of severe abdominal pain by performing a psychiatric evaluation. Second, the psychiatrist should have known that secondary gain is part of normal illness behavior, and he should have recognized that there was no supporting evidence for abnormal illness behavior. He should not have made a diagnosis of “psychogenic pain,” which closed the door to a further search for a medical cause of this patient’s severe abdominal pain, which was classic abdominal angina.90

In this regard, the advice of Nadelson rings true: “The psychiatrist must encourage the referring physician to confront the patient on the basis of clinical evidence, recognizing that the psychiatrist’s own diagnostic acumen may fall short of divining the hidden truth.”91 According to our interpretation of this advice, a diagnosis of abnormal illness behavior as the primary cause of physical symptoms should be based on clinical evidence [such as that discussed inBoxes 23.1 and23.2], rather than on information gained from a psychiatric evaluation. In this case, the negative clinical evidence could have been compiled by either the gastroenterologist or the psychiatrist. Unfortunately, no one did it.

Full references for this chapter can be found onwww.expertconsult.com.

PSYCHOGENIC FACTORS

Psychosomatic factors first were implicated in the pathogenesis of UC in the 1930s,95 but there is no good direct evidence to support this concept. Since the introduction of glucocorticoids for the treatment of patients with UC and the focus on immunologic aspects of the pathogenesis of the disease in the 1950s, this previously widely held notion has diminished in popularity.

Experimental studies have helped identify mechanisms of the proinflammatory potential of stress in animal models of colitis.95 When rats are exposed to stress before proinflammatory stimuli are introduced, the severity of colonic inflammation is increased. This particular response has been shown not to be mediated by either vasopressin or corticotropin-releasing factor. In addition, stress has been shown to directly increase intestinal permeability in rats, an action mediated by cholinergic nerves, and to potentiate intestinal inflammation in this particular situation. There are indeed studies reporting that psychosocial stress increases the risk of relapse in patients with quiescent UC.96,97 Conversely, many of the psychological features observed in patients with UC are likely secondary to this chronic disease process, a phenomenon physicians must be aware of when managing these patients.

Stress and Psychosomatic Disorders

Psychologic conditions, particularly psychosocial stress, have been implicated as risk indicators for periodontal disease.88 The most notable example is the documented relationship between stress [e.g., experienced by soldiers at war or by students during examinations] and acute necrotizing ulcerative gingivitis [seeChapters 20 and29]. The presence of necrotizing ulcerative gingivitis among soldiers stressed by wartime conditions in the trenches led to one of the early diagnostic terms used to describe this condition: “trench mouth.” Despite this well-known association between stress and necrotizing ulcerative gingivitis, confirming the connection between psychologic conditions and other forms of periodontal disease [e.g., chronic periodontitis] has been elusive. These relationships are difficult to elucidate, because, as with many common diseases, the etiology and pathogenesis of periodontal disease is multifactorial, and the role of individual risk factors is difficult to define.

Some studies have failed to recognize a relationship between psychologic conditions and periodontal disease despite specific efforts to identify them. In a study of 80 patients [40 with aggressive periodontitis and 40 with chronic periodontitis], Monteiro da Silva and colleagues failed to find a relationship between psychologic factors and periodontal disease.180 The researchers were able to identify depression and smoking as marginally significant in the aggressive periodontitis group. Their inability to find a relationship may be attributed to a lack of significant differences in psychologic characteristics between the two groups in the study. In an earlier study, the same researchers identified depression and loneliness as significant factors associated with aggressive periodontal disease in 50 patients as compared with 50 periodontally healthy individuals and 50 individuals with chronic periodontitis.179 Another challenge when defining the relationship between psychosocial status and periodontitis is the myriad confounding factors and the difficulty of controlling for them.68

Categories of Psychodermatologic Disorders

Q35.1 Other than personality disorders, in which pharmacotherapy has limited usefulness, most psychodermatologic disorders can be classified into four categories: [1] psychophysiologic disorders, [2] primary psychiatric disorders, [3] secondary psychiatric disorders, and [4] cutaneous sensory disorders. A fifth ‘category’ of use for psychotropic agents in dermatology is for purely dermatologic [i.e., nonpsychiatric or nonpsychodermatologic] cases [Fig. 35.1].

Psychosomatic Disorders

Psychosomatic disorders were previously thought to be a separate group of disorders in which stress and psychological distress led to disease. Examples were peptic ulcer, arthritis, and dermatitis. It is now recognized that all diseases may have social, psychological, and behavioral aspects as well as physical organic features. The World Health Organization defines psychosomatic medicine as “the study of biological, psychological and social variables in health and disease.”

This is best illustrated by the example of heart disease. Heart disease is caused by many factors. These include inherent biological factors, including age, sex, and genetic enhancement, that increase the chances of a heart attack; physiological factors, such as raised blood pressure, smoking, alcohol consumption, and increased blood cholesterol level; and psychological and social factors, which include depression, anxiety, and certain forms of stress, which are associated with an increased chance of developing a heart attack or increased chance of dying thereafter. Stress may lead to anxiety or depressive disorders, which can lead to a fast heart rate and increased chance of irregular heart beats, which may be fatal soon after a heart attack. Lack of social support – in the form a close person with whom all difficulties or problems can be shared – also contributes to increased chance of further heart attacks.

Thus, the modern view of psychosomatic mechanisms includes a role for stress, depression, and lack of social support alongside biological factors in the causation or outcome of disease. The relative importance of environmental stress varies in different conditions.

Treatment

Most physicians see psychosomatic disorders as untreatable, and their negative expectation is self-fulfilling. Yet a flexible approach can be very effective.16 Chapter 24 outlines psychotherapeutic approaches to somatoform disorders. The following focuses on medical treatments of specific symptoms. Such treatment is better done with a strong liaison between a neurologist and psychiatrist. Although medicalized explanations of psychogenic symptoms may seem more appropriately delivered by the neurologist than the psychiatrist, many neurologists are counterproductively hesitant to manage psychosomatic or emotional aspects of their patients' illness. Sometimes the consulting psychiatrist can diplomatically provide concrete strategies for how the neurologist might better fill this role.

Patients with psychogenic disorders often have fraught relations with medications, either overly hesitant to try them [“I'm very sensitive to medicines”], or so eager to continue them that they end up with multidrug interactions that contribute to their symptoms, or some combination of both relations. Most patients referred to a psychiatrist for potentially psychogenic movement symptoms have already had a failed trial of an antidepressant. The patients may take it as proof that their symptom is not from depression, not “all in my head.” There are many reasons for such failures. In a patient whose depression or anxiety is on the bipolar spectrum, the antidepressant may have worsened the patient's agitation. Patients given a TCA for associated pain often cannot tolerate the sedation. Patients may have received inadequate doses, sometimes because their associated PTSD makes them somatically hypervigilant about side effects. But whatever the cause of the failure, this creates a nocebo effect, in which future trials of similar treatment can fail simply because of the patient's negative expectation. One approach to circumventing this is to work hard to convince the patient to complete a long treatment trial of the new medicine, since placebo and nocebo effects are generally transient. A second approach is to present a new treatment as significantly different in kind [e.g., a patch rather than oral delivery, or for pain rather than depression], so that the patient's expectations are less negative.

Because most psychiatric medications have neurological indications as well, treatments can serve a dual function, and can be presented as having a medical indication that is acceptable to the patient.

Table 80-7 lists a number of drugs that may be helpful in this regard. Duloxetine in particular can be useful for somatic preoccupations. It decreases pain independent of its antidepressant and anxiolytic effect. Its tendency to be stimulating rather than sedating separates it from other neuropathic pain medications. Fatigue is an important and often neglected aspect of many psychogenic syndromes. Patients' excessive use of caffeine may not only worsen their anxiety and cause somatic symptoms [such as tachycardia or tremor], but also worsen their fatigue through its rebound hypersomnolence. Modafinil can sometimes help patients wean from caffeine.

The functional imaging evidence for right frontoparietal hyperactivity in conversion disorder suggest that transcranial magnetic stimulation [TMS] over this region may help somatization. This technique is noninvasive and has few side effects, but its effects are generally short-lived. There are preliminary reports of its effectiveness for hysterical hemiparesis, PTSD, and somatization. Much more investigation of these very early results is needed, but the growing evidence for benefit from targeted electrical and magnetic therapies in other neurological and psychiatric conditions makes the approach worthy of consideration.

INSOMNIA

Insomnia is a symptom that reflects a perception, by the patient or the caregiver, that it takes too long to fall asleep or that it is difficult to maintain sleep. Terms such as sleeplessness, insomnia, and restlessness may be the actual words used. Different people may notice different clinical features. For example, the parent of a child may comment on the child's nocturnal difficulties, whereas the school teacher might notice that the sleep-deprived child falls asleep in class or demonstrates features of hyperactivity.

Children can have disorders in any of the major categories listed in Table 2-1. The clinician decides which ones are most likely to be encountered and pursues a diagnosis.

Alteration in HPA Axis and Glucocorticoid Receptors in Depression

HPA axis dysfunctionality in psychosomatic and psychiatric disorders includes both hyperactivity and hypoactivity of the system, leading to dysregulation of stress-related responses and associated changes in GR sensitivity.26,57 Most clinical studies point to hyperactivity of the HPA axis, in association with reduced GR sensitivity, as the most prevalent abnormality [see below for further discussion of HPA axis hypoactivity].

Elevated levels of glucocorticoids are observed in a significant proportion of patients with major depression and are believed to be involved in both etiology and pathogenesis of the disease. Indeed, almost half of the depressed patients show increased levels of cortisol in cerebrospinal fluid, plasma, and urine, and enlargement of pituitary and adrenal glands.50 The hyperactivity of the HPA axis in depressed patients appears to reflect an impaired ability of glucocorticoid hormones to exert their physiological effects: that is, a reduced GR sensitivity, also called “glucocorticoid resistance,” which not only leads to an impairment of the negative feedback regulation of the axis but also diminishes glucocorticoid antiinflammatory actions at the periphery. Glucocorticoid resistance is also reflected by reduced GR function in peripheral blood cells35 and in the skin,19 and by the lack of Cushing-like stigmata in hypercortisolemic depressed patients,34 suggesting that GR dysfunction is not confined to the HPA axis tissues. Indeed, a variety of studies report that depressed patients show HPA axis hyperactivity in the presence of GR resistance and reduced expression and receptor number, as discussed extensively before.48,50

Although the mechanisms leading to glucocorticoid resistance are not yet clear, some studies suggest that prolonged inflammation has a direct effect in reducing GR sensitivity through the interaction of cytokine signaling pathway with GR signaling pathway.35,68 Proinflammatory cytokines may generate glucocorticoid resistance by directly affecting functional capacity of the GR at multiple levels. Apart from the above-mentioned overexpression of GRβ modulating the sensitivity of GRα, cytokines trigger glucocorticoid resistance by reducing GR ligand and DNA-binding capacities, inhibiting GR translocation to the nucleus and influencing GR protein–protein interactions; for example, activation of the mitogen-activated protein kinase [MAPK] signaling pathway in cytoplasm leads to phosphorylation of the GR, thus diminishing its transcriptional activity.10,42,53

Despite the extensive evidence supporting HPA axis hyperactivity and overproduction of glucocorticoids in depression, insufficient glucocorticoid signaling through hypoactivity of the HPA axis is also believed to contribute to the pathogenesis of depression, in at least some subgroups of patients. The evidence suggests that inadequate signaling capacity of glucocorticoids could be due not only to impaired GR-mediated signal transduction, but also to reduced glucocorticoid bioavailability itself.35,57 For example, the study by Nikkheslat et al.35 has recently shown reduced cortisol awakening response together with impaired GR sensitivity in elderly depressed patients with coronary heart disease.35 In atypical depression, HPA hypoactivity probably contributes to the fatigue and reversed neurovegetative symptoms presented in this specific subtype.36