CHAPTER 24 Functional Somatic Symptoms and Somatoform Disorders
OVERVIEW
Called by Lipowski1 “the borderland between medicine and psychiatry,” somatization presents a fascinating challenge to psychiatrists. It is defined here as experiencing and complaining about physical symptoms for which there are no discoverable organic causes. Kellner2 noted that 60% to 80% of the general nonpatient population experiences one or more somatic symptoms in any given week. When a patient approaches a physician with a somatic complaint, no organic cause can be found between 20% and 84% of the time. Commonest among these functional somatic symptoms are palpitations, chest pain, headache, fatigue, and dizziness. For patients who persist in searching for a medical cause for their functional symptoms, the dangers of invasive diagnostic procedures, unnecessary surgery, and misdirected therapeutic drug trials can be life-threatening, and the unwarranted costs of these measures further strain limited medical resources.
The approach to patients with many unexplained symptoms must include a thorough history and examination: medical history, personal and family psychiatric history, psychosocial history, current medications, and current laboratory examination results. In fact, one of the clinician’s first questions in creating a differential diagnosis should be, “What organic disease could account for these symptoms?” Even when presented with functional somatic symptoms, it is crucial to recall that such symptoms often occur in the context of serious medical illness. Reading both the current and (too often formidable) old medical records is an indispensable beginning. One of the main reasons that a psychiatrist may end up diagnosing a physical disease is because something about the patient (e.g., personality, behavior, affect, or odd cognition) has effectively distracted the primary physician and other consultants. Old pathology reports and other objective documentation are invaluable. As with any condition, a systematic differential diagnostic approach is required. Table 24-1 lists the diagnoses most likely to produce somatized complaints.
Table 24-1 Differential Diagnosis of Functional Somatic Symptoms: Diagnoses Producing Somatoform Complaints
| Physical Disease | Personality Disorders |
|---|---|
| Depressive disorders | Dependent |
| Anxiety disorders | Passive-aggressive |
| Substance abuse disorders | Antisocial |
| Psychotic disorders | Borderline |
| Organic mental disorders | Narcissistic |
| Voluntary symptom production | Compulsive |
| Malingering | Histrionic |
| Factitious disorders | Paranoid |
| Somatoform disorders | Schizoid |
| Schizotypal |
DIFFERENTIAL DIAGNOSIS OF FUNCTIONAL SOMATIC SYMPTOMS
Depressive Disorders
Asked to evaluate a patient whose somatic symptoms do not seem to have a physical cause or that seem out of proportion to any abnormalities found, psychiatrists should not think of somatoform disorders first. Major depressive disorder (MDD) is found far more often. Indeed, half of all the primary care patients who ultimately receive a psychiatric diagnosis have exclusively somatic symptoms,3 and 75% of those with MDD or panic disorder on a diagnostic interview seek treatment from their physicians for exclusively somatic symptoms.4,5
The vegetative symptoms (e.g., insomnia, fatigue, anorexia, and weight loss) of MDD are physical in nature. Moreover, depressed patients have more functional somatic symptoms (aches and pains, constipation, dizziness, and the like) than do other patients. Among primary care patients in an American health maintenance organization,6 disabling chronic pain was present in 41% of those with MDD compared to 10% of those without MDD. Those patients with both chronic pain and MDD tend to have more severe affective symptoms and a higher prevalence of panic disorder. Older patients with MDD are also more preoccupied with somatic symptoms. Even across cultures, the majority of patients with MDD have only somatic symptoms, half of these with multiple unexplained symptoms; however, if they are asked, 89% will also offer psychological symptoms.7
When MDD is diagnosed, it should be treated first. Ordinarily both affective and somatic symptoms improve with treatment, although, as shall be discussed, sometimes only the affective illness remits, leaving functional somatic symptoms still to be managed. (For further coverage of affective disorders, see Chapter 29.)
Anxiety Disorders
Symptoms of anxiety intermingle with functional somatic symptoms. Anxiety draws attention toward dangerous and threatening perceptions. It also distorts the cognitive appraisal of somatic symptoms, making them seem more ominous and more alarming. Anxious patients thus tend to catastrophize normal physiological sensations and trivial ailments. As noted in Chapter 32, many of the symptoms of panic disorder are somatic (e.g., dyspnea, palpitations, chest pain, choking, dizziness, paresthesias, hot and cold flashes, sweating, faintness, and trembling).
Although anxiety is not as likely as depression to escape the notice of the primary physician, panic disorder often goes unrecognized. It is far more prevalent among patients with medically unexplained symptoms than was once thought, especially in cardiology, gastroenterology, and neurology practices.8 Anxiety is also one of the most common features of MDD.9 It is important to remember that when co-morbid with pain, anxiety can lower the pain threshold dramatically. Moreover, some patients cannot distinguish anxiety from pain (“No, I am not frightened; I hurt!”). Some caregivers therefore mistakenly attribute the marked discrepancy between pain complaints and objective findings to drug abuse or personality disorder.
Substance Abuse Disorders
Alcohol abuse should always be considered in a patient who continues to have multiple, vague somatic symptoms. Whether the patient consciously tries to conceal alcohol dependency or simply 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 symptoms, fatigue, bruises—none are strangers to the alcoholic. The effects of other addictive drugs may be similarly confounding. (See Chapters 26 and 27 for the diagnosis and treatment of substance abuse disorders.)
Personality Disorders
Although included in the differential diagnostic list of Table 24-1, personality disorders do not “cause” functional somatic symptoms. Rather, for the patient with an Axis II disturbance, the somatic symptom is a means to an end. For the individual with an antisocial personality, pain may be a means to get narcotics, to get out of work, or to escape trial. For the person with a dependent personality, functional weakness gains the attention and nurturance of others.10 The borderline patient’s somatic symptoms can become the focus for physicians and nurses, who may engage in a sadomasochistic struggle with the patient. The process begins with a helping relationship and ends with the rejection of a disappointed and outraged patient accused of wrongdoing. The “end” for this patient is the emotionally charged (usually hostile) relationship, and the failure to palliate the symptoms means to the patient that the physician simply does not care enough. Sometimes symptoms are reinforced by personality styles. Somatic symptoms are exaggerated by patients with a histrionic personality and may be the object of such intense fixations by those with compulsive, paranoid, schizotypal, and schizoid personalities as to make these patients take on a hypochondriacal character.
Somatoform Disorders
Conversion Disorder
Conversion disorder is perhaps the classic somatoform disorder; it involves a loss or change in sensory or motor function that is suggestive of a physical disorder but that is caused by psychological factors. Common symptoms include paralysis, aphonia, seizures, disturbances of gait and coordination, blindness, tunnel vision, and anesthesia. The primary evidence for the psychological cause consists of a temporal relationship between symptom onset and psychologically meaningful environmental precipitants or stressors. A patient who developed conversion blindness, for instance, may have seen her husband with another woman before she complained of being unable to see. The conversion symptom is not under voluntary control, although the patient may be able to modulate its severity. A patient with a functional gait disturbance or a weak arm, for example, may, with intense concentration, be able to demonstrate slightly better control or strength. DSM-IV has eliminated pain and sexual dysfunction as conversion symptoms. Reviewing conversion, Ford and Folks11 recommended that it be considered as a symp-tom rather than as a primary diagnosis. In children with conversion symptoms, the gender ratio is equal; in adults, conversion is two to five times more common in women than men.
Predisposing factors are important considerations for both diagnosis and treatment. A prior medical illness is a common source for the symptom. If a viral illness is accompanied by vertigo while a patient is under stress, the illness may bring secondary benefits of attention and support from loved ones. At a later time, when stress recurs, the symptom of vertigo may recur, this time as a conversion symptom. By definition, the symptom is not intentionally produced or feigned. It is presumed that the unconscious secondary benefit of the condition that alleviates conflict sustains the condition. Patients with seizures, especially complex partial seizures (in which consciousness is preserved), are repeatedly exposed to a phenomenon that removes them from responsibility, evokes sympathy, and brings help from a loved one. Pseudoseizures commonly coexist with true seizures and can be exceedingly hard to discriminate, particularly when the electroencephalogram (EEG) fails to demonstrate spiking activity or shows only nonspecific slowing. Epileptic and nonepileptic seizures can be temporally related, and in patients with partial seizures, organic ictal changes may also facilitate the development of conversion symptoms.12
Conversion symptoms may be precipitated by exposure to others with specific symptoms. Such “figures of identity” may be psychologically important people in the patient’s life (such as a parent who has just died), or they may be strangers whose symptoms the patient observes under extreme and sudden stress, as occurs in mass psychogenic illness (“epidemic hysteria”). Extreme psychosocial stress may be the most important of all precipitating factors. Some authors have presented evidence for a predominance of conversion symptoms, when unilateral, on the nondominant side in females.13,14 More recently, the tendency for motor and sensory symptoms to occur on the nondominant left has been questioned.15
The diagnosis of conversion cannot rest comfortably only on the absence of organic disease. Caution in diagnosing conversion symptoms is based on early reports that 13% to 30% of those with this diagnosis went on to develop an organic condition that, in retrospect, was related to the original symptom.16 The rate of misdiagnosis of conversion has dropped; a recent report found only 4% who were subsequently found to have a documented medical illness.17
Functional brain imaging has added another dimension to the study of patients with conversion disorder; there have been reports of functional neuroanatomical abnormalities in patients with conversion (i.e., sensorimotor loss).18 Black and co-workers19 have summarized the lessons from neuroimaging, suggesting that conversion results from dynamic reorganization of neural circuits that link volition, movement, and perception. Disruption of this network may occur at the stage of preconscious motor planning, modality-specific attention, or right frontoparietal networks subserving self-recognition and the affective correlate of selfhood.19
Conversion symptoms are usually sustained, but sometimes only for a certain activity. The patient who cannot lift his leg adequately in walking may be observed to cross it over his good one during conversation. Deviation of the eyes toward the ground, no matter which side the “semicomatose” patient lies on, is functional, and sometimes demonstrates lack of an organic disorder.20 One may lead the patient with functional blindness around obstacles (e.g., chairs); the patient with conversion usually avoids them (a malingerer is more likely to bump into them). Carefully watching the “blind” patient’s eyes and face while taking a roll of money out of one’s wallet, or suddenly menacing (being careful to avoid creating a draft or noise) or making a face at the patient is another way to assess vision. Sensory testing on the patient in both prone and supine positions checks for consistency. A malingerer is more likely to become hostile and uncooperative during the examination, probably in the hope of shortening it.
Prognosis and Treatment.
The literature supports an optimistic outlook for these patients, at least in the first few years. Folks and co-workers21 recorded a complete remission rate of 50% by discharge in those with conversion disorder in a general hospital. However, the long-term course is less favorable because a sizable fraction of these patients develop recurrent conversion symptoms (20% to 25% within 1 year). Unilateral functional weakness or sensory disturbance diagnosed in hospitalized neurological patients persisted in more than 80% (of 42 patients over a median of 12.5 years).22 Patients with one conversion symptom may also develop other forms of somatization or eventually meet criteria for somatization disorder.
The most common form of treatment is to suggest that the conversion symptom will gradually improve. This ordinarily begins with reassuring news that tests of the involved body system show no damage and therefore that recovery is certain. Predicting that recovery will be gradual, with specific suggestions (e.g., vague shapes will become visible first; weight bearing will be possible and then steps with a walker; standing up straight will come before full steadiness of gait; strength in squeezing a tennis ball will be followed by strength at the wrist and then elbow joints; and feeling will return to the toes first) usually succeeds, provided that the diagnosis is conveyed with serene confidence and the suggestions provided with supportive optimism. Lazare16 pointed out that the psychiatrist should also discuss the patient’s life stresses and try to detect painful affects to assess the nonverbal interpersonal communication embodied by the symptom.
Confrontation is seldom helpful. Patients are particularly sensitive to the idea that an authoritative person has dismissed their suffering; their anger and sensitivity may be based on a history of abuse or neglect. Stonnington and associates23 suggested that the best context for discussion of the diagnosis of pseudoseizure comes after the patient and the family have agreed that key representative events have been captured by video EEG monitoring.
Further intervention may not be necessary. However, if the conversion symptom persists, if the precipitating stress is chronic, or if there is massive secondary gain, resolution of the situation becomes a target of the intervention. Because the stresses are often social, couples or family therapy may be instrumental in achieving a final resolution. Treatment, for instance, for nonepileptic seizures, should consider risk factors, including perpetuating and triggering events. Co-morbid psychiatric diagnoses should be treated. Behavioral interventions, physical therapy, and reassurance are crucial, particularly for less verbal patients.23
Somatoform Pain Disorder
The predominant feature of somatoform pain disorder (termed simply pain disorder in DSM-IV) is chronic, severe, and preoccupying pain that has no adequate medical explanation. Either there is no medical disease at all, or the patient’s pain is grossly disproportionate to demonstrable histopathological findings. The pain is severe enough to warrant clinical attention and to impair role function. It is constant and often inconsistent with known neuroanatomical innervation. Psychological factors must be judged to play a significant role in the precipitation, maintenance, or exacerbation of the pain, but it is neither intentionally produced nor feigned. Pain is the subject of Chapter 78. Patients with somatoform pain disorder are often severely disabled by their symptoms, live like invalids, and work infrequently. They have long histories of medical care and many surgical interventions. They are often completely preoccupied with their pain and view it as the sole source of all their difficulties. Depression is commonly co-morbid with somatoform pain disorder.
In practice, the problem is often that organic causes of pain cannot be completely disregarded. Co-morbid medical illness, concerns about neuropathic pain, myofascial pain, or an undiagnosed medical problem, challenge the diagnosis of the psychiatric disorder. Questions about substance abuse and personality disorder complicate the picture. A multiaxial record of the data related to a patient may help clarify the course, treatment effectiveness, and relative contributions of medical and psychiatric data. Mayou and associates24 have suggested a method of somatoform classification that would include medical diagnoses, the presence or absence or depressive or anxiety disorder, history of narcotic use, health beliefs, illness behavior, stressors, and social benefits (e.g., disability payments or unemployment). Each parameter could be followed over time to shed light on the patient’s condition.
Somatization Disorder
Originally termed hysteria or Briquet’s syndrome and now given the DSM-IV designation of somatization disorder, this condition has been solidly established as clinically and epidemiologically distinct. It is a chronic syndrome of recurring multiple somatic symptoms that are not explainable medically and are associated with psychosocial distress and with medical help–seeking behaviors. The disorder is much more common in women than it is in men, and it tends to occur in those of low socioeconomic status, often nonwhite and rural, at a 1-year prevalence rate of 0.3% in the general population, even with a criterion of clinical significance.25–27 Of first-degree female relatives, 10% to 20% suffer the same disorder, whereas male relatives show an increased incidence of alcoholism and sociopathy.28
Women with this disorder tend to have histories as children of missing, disturbed, or defective parents, and of sexual or physical abuse.29–32 The tendency to somatization has been linked to childhood trauma via insecure attachment and maladaptive patterns of interpersonal communication in seeking care.33,34
These women marry sociopathic men more often than chance would predict, and they tend to be poor parents themselves.29–31 Given these unfortunate circumstances, and their roughly 75% chance of having one or more additional psychiatric diagnoses (the most common being an affective or anxiety disorder, or drug and alcohol abuse35), it is no surprise that marital discord and unsatisfactory work histories are also the rule.
The diagnostic symptoms are numerous and can be cumbersome for the busy clinician. Othmer and DeSouza36 have attempted to deal with the first problem by developing an abbreviated list of seven symptoms that can be employed to screen for the disorder. If two or more of the symptoms in their clever mnemonic (Table 24-2) are present, there is a high likelihood of somatization disorder. The presence of three symptoms accurately identified 91% of the patients with somatization disorder with a sensitivity of 87% and a specificity of 95%. However, despite this list of symptoms, the clinical diagnosis almost always requires review of past records; these tend to be voluminous, scattered among a host of hospitals, lost, or a combination of the three. In the absence of the chart, contact with prior treating physicians or family members may help in establishing the symptom count. Notoriously poor historians, these patients will be unable to recall past admissions or clinic visits, and they will deny a history of a symptom that the chart lists as a chief complaint on a past visit.
Table 24-2 Seven-Symptom Screening Test for Somatization Disorder
| Mnemonic | Symptom | System |
|---|---|---|
| Somatization | Shortness of breath | Respiratory |
| Disorder | Dysmenorrhea | Female reproductive |
| Besets | Burning in sex organ | Psychosexual |
| Ladies | Lump in throat (difficulty swallowing) | Pseudoneurological |
| And | Amnesia | Pseudoneurological |
| Vexes | Vomiting | Gastrointestinal |
| Physicians | Painful extremities | Skeletal muscle |
From Othmer E, DeSouza C: A screening test for somatization disorder (hysteria), Am J Psychiatry 142:1146-1149, 1985.
During the interview, the patient usually presents complaints in a histrionic fashion (“Why I bled so much—I’ve never seen so much blood!!—that I passed out on the bed and my family said I was in a coma for 3 days!”), with symptoms so exaggerated that a psychogenic cause may be suspected from the outset. The other consistent trait these patients possess is a peculiar communication style. Histories are vague and details are either elusive or downright inconsistent. Efforts at clarification may be fruitless and frustrating. (“Is your pain worse in the morning?” “Yes, and it’s worse in the afternoon, too.”) Emotional distress is openly expressed (“I’m not getting anywhere, Doctor! No one can tell me anything! What’s happening to me?”), but if one tries to identify the emotion, for example, telling the patient she seems very anxious, that emotion is more likely to intensify (“Well, wouldn’t anybody be? It’s been a whole month and nobody—nobody, Doctor—knows what’s going on with me!”). This type of response tends to drive the physician back to a cognitive search—onset, duration, radiation, intensifying or relieving factors—only to encounter once again the fogbound and trackless wastes of imprecision, inconsistency, and lapsing memory.
Contemporary medicine’s shift from clinical to economic priorities has only heightened attention to somatization disorder. Smith and associates37 have documented that the typical patient with this disorder spends an average of 7 days per month sick in bed (compared with 0.48 days for the average person), and accrues (mostly unnecessary) annual hospital care rates many times higher than those of the average person in the population between the ages of 15 and 64 years. This happens despite their remarkably stable clinical course, with a 90% probability of not developing a new medical or psychiatric disorder in the subsequent 6 to 8 years following diagnosis.
Treatment.
The management of somatization disorder has been well formulated by Murphy.38 It is best carried out by primary care physicians according to a conservative plan based on being a consistent care provider, preventing unnecessary or dangerous medical procedures, and inquiring in a supportive manner about the areas of stress in the patient’s life. The last occurs during the physical examination, without inferring that the real cause for the increase in the patient’s somatic complaints is psychosocial stress (which is what most authors believe). The basic goal is to help the patient cope with the symptoms rather than to eliminate them completely. In short, the aim is palliation, rather than outright cure. Psychotropic medication and prescription analgesics generally are not very helpful, except when used to treat a clear-cut, co-morbid psychiatric condition, such as major depression or panic disorder.
Smith and associates39 codified treatment recommendations in a letter to the primary care physicians of somatization disorder patients. These included regularly scheduled appointments (e.g., every 4 to 6 weeks); a physical examination performed at each visit to look for true disease; the avoidance of hospitalization, diagnostic procedures, surgery, and the use of laboratory assessments, unless clearly indicated; and advice to avoid telling patients, “It’s all in your head.” In a randomized controlled trial (RCT), this intervention reduced quarterly health care charges by 53%, largely as a result of decreases in hospitalization.40 Neither the health of the patients nor their satisfaction with their care was adversely affected by implementation of the advice.
A cognitive-behavioral therapy (CBT) program, when compared to standard medical care, has also reduced symptoms, ratings of disorder by evaluators, and health care costs. The intervention focused on stress management, activity regulation, emotional awareness, cognitive restructuring, and interpersonal communication.41
Undifferentiated Somatoform Disorder
The diagnostic criteria for somatization disorder are quite restrictive, and most chronic somatizing patients in medical practice do not cross this stringent threshold. In an attempt to provide a diagnostic home for such patients, DSM-IV now includes the entity undifferentiated somatoform disorder. This diagnosis requires one or more physical symptoms that persist for at least 6 months and are medically unexplained. Several researchers, including Kroenke and co-workers42 and Escobar and associates,43,44 have sought to define a more inclusive entity that requires fewer somatic symptoms than are required for somatization disorder, but that nonetheless identifies patients who have the clinical and behavioral features characteristic of the disorder. Multisomatoform disorder is based on current unexplained symptoms. It requires three or more unexplained symptoms within the past 2 weeks out of a list of 15, along with a 2-year history of somatization. Escobar’s abridged somatization disorder is based on at least six lifetime unexplained symptoms in women and four in men. Multisomatoform disorder has a high concordance with somatization disorder and perhaps a more efficient diagnostic algorithm. It is less correlated with abridged somatization disorder, but all three diagnoses are associated with similar medical utilization rates and declining physical function over a year.45
Hypochondriasis
While extensive research has helped to crystallize the concept of somatization disorder, the nosology of hypochondriasis remains more ambiguous. Concern about health is common, and the point at which preoccupation becomes pathological is not always clear. Hypochondriacal thinking may occur in the form of a primary disorder or as a nonspecific correlate of other Axis I illnesses, including affective and anxiety disorders. Tendencies to amplify benign, unpleasant symptoms and to misconstrue them as pathological have both traitlike and statelike properties. In a study of a military population, Noyes and colleagues46 found that personality measures, mainly neuroticism, explained much of the variance in hypochondriacal concerns. Based on evidence such as this, some nosologists have argued that hypochondriasis is better thought of as a personality disorder to be denoted on Axis II.47
DSM-IV identifies the predominant feature of hypochondriasis as a preoccupation with the fear or belief that one has a serious, undiagnosed disease. This concern is based on a misinterpretation of benign physical signs and symptoms as evidence of disease. Other diagnostic criteria include the absence of a physical disorder that accounts for the patient’s symptoms; persistence of the disease fear or belief despite appropriate medical reassurance; clinically significant distress or role impairment; and duration of at least 6 months. By this definition, hypochondriasis is quite prevalent. It is found in approximately 5% of medical outpatients and occurs equally between the genders.48
The origins of hypochondriasis are not fully understood. Both genes and early upbringing may serve as conditioning factors. There is evidence, for instance, that hypochondriacal patients tend to amplify and augment somatic and visceral sensations more than nonhypochondriacal patients.49,50 Predisposing events in childhood include disease in the patient or in a family member, and adversity, including neglectful and abusive parents.51 Context also plays a role. The onset of the syndrome can be triggered by illness or by the death of a loved one.
Prognosis and Treatment.
Hypochondriasis can be a chronic and disabling disease. Barsky and Ahern52 note a time course of approximately 11 years in the group they studied; Kenyon53 found that among hospitalized patients with hypochondriasis, only 20% were judged as recovered or much improved at the time of discharge, and twice that many were either unchanged or worse than on admission. There may be some room for optimism, however, particularly when the illness has lasted less than 3 years and is not co-morbid with a personality disorder.54
When confronted with hypochondriasis, a treater’s first step should be to screen for co-morbid affective and anxiety disorders (including obsessive-compulsive disorder [OCD]). These are likely easier to treat, and their resolution may greatly diminish or bring an end to exaggerated disease fears. Isolated hypochondriasis is more difficult to cure. Although there have been a few reports suggesting a role for selective serotonin reuptake inhibitors (SSRIs),55–57 the most successful psychiatric interventions for primary hypochondriasis are cognitive, behavioral, and educational.58,59 Barsky and Ahern52 have recently shown that the treatment combination of education of the primary care physician and time-limited CBT for the patient improves a range of hypochondriacal symptoms, with modest treatment effect. The manualized treatment for the patient targets cognitive and perceptual mechanisms of illness, including hypervigilance to visceral experience, beliefs about symptom etiology, context in which the hypochondriasis occurs, sick role behaviors, and mood.
Patients with hypochondriasis tax the general physician. Such patients are difficult to reassure; their care is both time-consuming and expensive; and they often provoke strong negative reactions in their frustrated providers.53 Psychiatrists can be instrumental in easing anxieties and offering management recommendations. An internist’s goals when treating a hypochondriacal patient should be threefold58: to avoid unnecessary diagnostic tests and to obviate overly aggressive medical and surgical intervention; to help a patient tolerate the symptoms, rather than striving to eliminate them; and to build a durable patient-doctor relationship based on the physician’s interest in the patient as a person and not just in the symptoms. Once a physician views his or her task as palliative, not curative, the patient-physician relationship becomes less contentious and adversarial. Further, the patient is likely to loosen the grip on symptoms when he or she feels that the physician has acknowledged and accepted them as real.
Monosymptomatic Hypochondriasis and Body Dysmorphic Disorder
Monosymptomatic hypochondriasis refers to several distinct syndromes characterized by a single, fixed, false belief that one is diseased. The disease conviction is generally delusional, and grossly disproportionate to any objective disease or deformity. This belief is tightly circumscribed; no other thought disorder is present; and the remainder of the patient’s personality remains intact and unaffected.60 Body dysmorphic disorder (BDD), formerly termed dysmorphophobia, is one of the most common of these syndromes, and it is singled out in the DSM-IV as a separate diagnosis under somatofom disorder.61,62 Other forms of monosymptomatic hypochondriasis include the delusional belief that one is infested with a parasite or insect and the delusion that one emits an offensive odor (olfactory reference syndrome).
The patient with BDD believes he or she is physically misshapen and unattractive, although objective appearance is unremarkable. Self-reported prevalence of the disorder in the German population is 1.7%.63 The defect or deformity in appearance is most commonly in the face, breasts, or genitals. The average age of onset for these patients is younger than age 20, with males and females equally represented. Typical males seek plastic surgeons with the conviction that their noses are too large or disfiguring. The typical female, convinced that her facial skin is “scarred,” making her appearance grotesque, will seek a plastic surgery or dermatological consultation. BDD is commonly accompanied by a mood disorder (including atypical depression with rejection sensitivity), social phobia, OCD, and substance use disorders. The rate of suicidal ideation, suicide attempts, and completed suicide is notable,64 and the course chronic with a remission rate probably lower than that reported for mood and anxiety disorders alone.65
Treatment.
SSRIs and clomipramine (a tricyclic antidepressant [TCA]) are the agents of choice in the treatment of BDD, with doses in the upper therapeutic range. BDD may remit along with major depression, but treatment often fails or is only partially effective. Olanzapine, but not pimozide, has been shown to be effective to augment fluoxetine.66,67 Electroconvulsive therapy (ECT) has also been used successfully when the patient was frankly delusional.
Maintenance therapy is generally necessary.61 Even with successful pharmacotherapy, most patients retain some concern about their problem, but its intensity is blunted sufficiently to permit them to lead more normal lives. One may never be able to get some patients to acknowledge the delusional nature of their symptom, even after significant improvement. Hard-pressed to justify the recommendation of a neuroleptic, the physician may even tell the patient that these insects or odors are best “cleansed” from within the system, hence the need for a drug. On the other hand, a few patients will accept the notion that the body is more vulnerable to parasitic infestation or odor generation during times of greater stress. When major depression is present in BDD, medication is more readily accepted.
Functional Medical Syndromes
Although somatoform disorders are characterized by complaints that seem far out of proportion to any abnormalities found, common functional medical syndromes also lack laboratory confirmation. Like the diagnoses in DSM-IV, these diagnoses depend on consensus criteria, description of symptoms, and a natural course of illness. There is substantial overlap in the phenomenology, epidemiology, and co-occurrence of these various syndromes.68,69
The principles of care for somatoform disorders apply here as well. Rule out organic disease. Diagnose and treat affective disorder, substance abuse, and the other psychiatric diagnoses. Knowing the patient, listening with respect for his or her suffering, setting limits, and keeping an ear for changes in medical complaints remain pivotal concepts. CBT is emerging from a number of rigorous intervention trials as an effective treatment for many of these syndromes.70–72 The status of antidepressant pharmacotherapy for them has been systematically reviewed.73
Chronic Fatigue Syndrome
Many more patients complain of chronic fatigue without a medical cause than meet formal criteria for CFS. Fatigue itself is a vague symptom that requires exploration of exacerbating factors, timing, mood, and meaning. Patients with MDD have fatigue that is worse in the morning. They have difficulty initiating activity, as do patients with Parkinson’s disease. Sometimes fatigue actually turns out on exploration to be agoraphobic avoidance of leaving home, or a tendency to avoid the risk of social embarrassment. Fatigue may also mean daytime sleepiness, seen in sleep apnea. Fatigue with dysphoria is central to a mood disorder. Apathy—lack of motivation and lack of dysphoria—is more characteristic of a neurological disorder or hypothyroidism. Patients who value their productivity and strength are especially frustrated by fatigue, and its personal meaning will exacerbate the symptom.
By consensus, CFS is defined by several features: self-reported, clinically evaluated, unexplained, persistent or relapsing chronic fatigue with a definite onset, that lasts more than 6 months. It is not due to exertion or relieved by rest, but it substantially reduces the patient’s activities; and it includes four or more other symptoms (impaired memory or concentration, sore throat, tender cervical or axillary lymph nodes, muscle pain, multijoint pain without joint swelling or redness; new headaches, unrefreshing sleep, and postexertional malaise lasting more than 24 hours), which came after onset of fatigue.74
Although fatigue may follow a viral infection, no single virus has been shown to cause persistent, debilitating CFS. In the primary care setting, patients with postinfectious fatigue after 6 months are more likely to have had fatigue and psychological distress before the infection.75 A history of dysthymia and more than eight medically unexplained symptoms not already listed in CFS criteria may predict prolonged disability in CFS patients.76
Suggested screening laboratory tests include a complete blood count, a sedimentation rate, liver and renal function tests, calcium, phosphate, glucose, thyroid-stimulating hormone (TSH), and urinalysis. Further tests, such as a magnetic resonance imaging (MRI) scan of the head to search for multiple sclerosis, should be guided by clinical findings. Lyme disease, for instance, is unlikely to cause fatigue as the only finding.77 Acute mononucleosis in adolescence might produce a similar picture, but it is not likely later on in life. The acute diagnosis could be documented by antibody evidence of recent infection.
There is no specific medical treatment for formal CFS. The choice of antidepressant for co-morbid mood disorder depends on its capacity to improve sleep but limit sedation. Graduated aerobic exercise programs are important to improve physical conditioning. CBT programs increasingly appear to have established their effectiveness.78,79 The goal is to help the patient achieve maximal function.
Fibromyalgia
FM is a syndrome of generalized muscle pain and tenderness at specific trigger points, detected by physical examination.80 To make the diagnosis, pain must be bilateral, above and below the waist, and include the axial-cervical spine, chest, or lower back. Criteria require 11 of 18 (9 bilateral) trigger points. Secondary FM occurs with rheumatoid arthritis and Lyme disease.
For FM, amitriptyline (25 to 50 mg/day) and cyclobenzaprine (10 to 30 mg at bedtime) (both TCAs) to relieve pain and improve sleep seem to work at least briefly in some fraction of patients.81,82 There have been single RCTs of fluoxetine, duloxetine, and venlafaxine.
Irritable Bowel Syndrome
Functional gastrointestinal disorders are recurrent medical syndromes without known biochemical or structural abnormalities. Irritable bowel symptoms occur in 15% to 20% of the population, but the small subset that seek medical help compose a major component, 25% to 50%, of referrals to gastroenterologists.83
The international criteria for IBS include continuous or recurrent symptoms (for at least 3 months) of abdominal pain or discomfort relieved by defecation, or associated with a change in stool frequency or consistency and an irregular pattern of defecation at least 25% of the time (three or more of the following): altered stool frequency; hard, loose, or watery stool; straining, urgency, or feeling of incomplete evacuation; passage of mucus; and bloating or a feeling of abdominal distention.84
Those who visit physicians have more severe symptoms and are more likely to have co-morbid psychiatric diagnoses than those who do not. Mood disorder,85 panic with agoraphobia (especially fear of leaving the house because of diarrhea),86 and a history of childhood abuse are more prevalent among patients than among the general population.87
Again, diagnosis depends on criteria, natural history of illness, and absence of laboratory confirmation of another diagnosis. The clinical approach to IBS is similar to that for the somatoform disorders: rule out organic and psychiatric diagnoses. In the context of a relationship in which the physician continues to learn about the patient, the physician chooses somatic treatments that target the predominant symptom of pain, constipation, or diarrhea. A TCA has an analgesic effect at low doses but tends to cause constipation and be preferable for a patient with recurrent diarrhea. An SSRI seems the better choice for co-morbid panic disorder or OCD,88 particularly in patients with constipation. No one is preferable, but paroxetine is most studied. If the patient tends to have diarrhea, loperamide, a constipating agent, may be useful. Fiber and dietary adjustments may relieve constipation. The principles of pain management in IBS parallel the principles of management in somatoform pain disorder.
CBT and interpersonal psychodynamic therapy appear to be effective for improving well-being and quality of life.89–91 Education about amplification of visceral symptoms and the vicious circle of anxiety, increased vigilance for symptoms, and resultant increase in symptoms and pain; relaxation training; and stress management techniques are helpful to both individuals and groups.
CONCLUSIONS
When one thinks of psychologically driven somatic symptoms, the somatoform disorders may be the first diagnostic category to come to mind. But among general hospital inpatients and outpatients, other psychiatric diagnoses (particularly affective disorders, anxiety disorders, and organic mental syndromes) are more likely to be discovered at the end of the history and examination. These require specific treatment, and when the psychiatric disorder remits, the somatic symptoms usually subside. The diagnostic tests we find helpful are the Minnesota Multiphasic Personality Inventory (MMPI), an excellent screening device for conversion or a somatoform disorder, and Axis II parameters; projective tests, to help both physician and patient understand conflicts in the patient’s life that may not be in the patient’s awareness; and full neuropsychological test batteries, which delineate precise areas of cognitive deficiency (see Chapters 7 and 8).
In the case of complex medical patients, some have suggested that disorders defined solely by unexplained somatic symptoms should be described as a multidimensional functional medical diagnosis without reference to etiology. Disorders such as chronic pain, FM, or IBS would be listed as medical diagnoses. Somatic symptoms associated with depression would be classified with depression, and those associated with anxiety would be classified with anxiety. A multiaxial diagnostic system would allow anxiety disorders, anxiety/hypochondriasis, and specific illness fears to be listed together. Personality disorders, including those seen in somatization disorder, would be on a personality axis, and specific stressors (including difficult interactions with the health care system) could be specified. A multidimensional descriptive system for somatic symptoms should document the type and number of somatic symptoms and the nature of the acute, chronic, or recurrent course. Known organic disease pathology should be listed as well as health beliefs, illness behavior, associated psychiatric disorders, and social factors such as employment or social benefits.24
The treatment ultimately depends on the diagnosis. Smith and associates39 have shown that an intervention with the primary care physician significantly reduced costly and potentially harmful medical interventions for somatizing patients without compromising the health or satisfaction of these patients. Psychological treatments such as CBT that focus on initiating and perpetuating factors improve the outcome.
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