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.
