CHAPTER 16
Somatic Symptom and Related Disorders*
Patients with somatic symptom and related disorders continue to suffer from both medically explained and unexplained ailments, which cause significant medical and psychiatric disability. Physicians and health systems remain challenged by this patient population, as somatic symptoms are often chronic, are difficult to treat, and increase health care utilization. The interrelationship of mind and body is well established and increasingly accepted within medicine. However, the complexity of this connection creates a daunting task for physicians when making diagnoses and finding effective treatments. Previous DSM editions attempted to capture the pathological manifestations of the mind-body connection with many well-known diagnoses, including somatization disorder, conversion disorder, and hypochondriasis.
The DSM-5 Work Group on Somatic Symptom Disorders introduced several important changes into the organization of DSM-5 (American Psychiatric Association 2013) that have refocused the classification of these disorders. The previous emphasis on absence of medical explanations for symptoms has been reduced throughout this new system, as simply having an unexplained symptom is not a sufficient cause for establishing a psychiatric diagnosis. Additionally, the presence of a well-documented medical symptom does not exclude the possibility of a dysfunctional psychological reaction that would be an appropriate focus for treatment. Also, deemphasizing medically unexplained symptoms helps to discredit dualistic mind-body concepts that may have been reinforced by previous diagnoses. Assumptions about the exact origin of the symptoms have generally been removed, in keeping with this goal. This reconceptualization aims to destigmatize illness, to prevent patients from feeling blamed for their somatic symptoms, and to improve diagnostic accuracy across medical disciplines. The total number of somatic symptom and related disorders has been reduced, and efforts have been made to clarify boundaries between diagnoses, consistent with a goal of making these diagnoses more understandable and useful to nonpsychiatrist physicians. Somatization disorder, pain disorder, and hypochondriasis have been eliminated from DSM-5, and somatic symptom disorder and illness anxiety disorder have been introduced. Factitious disorder, formerly in a DSM chapter of its own, is now grouped with the somatic symptom and related disorders. Psychological factors affecting other medical conditions was previously listed in the DSM-IV chapter "Other Conditions That May Be a Focus of Clinical Attention" but is included as a diagnosis in Somatic Symptom and Related Disorders in DSM-5. Body dysmorphic disorder has been included in DSM-5 as part of the Obsessive-Compulsive and Related Disorders chapter.
The core feature of somatic symptom disorder is the presence of multiple physical complaints that are not fully explained by physical factors and that result in medical attention or significant impairment.
The DSM-5 diagnosis of somatic symptom disorder replaces the previous DSM-IV (American Psychiatric Association 1994) and DSM-IV-TR (American Psychiatric Association 2000) diagnoses of somatization disorder and undifferentiated somatoform disorder. Somatic symptom disorder is defined by the presence of somatic symptoms, as in the older classifications. However, the DSM-5 criteria for somatic symptom disorder (Box 16-1) do not require that the symptoms be medically unexplained, nor are specific numbers or types of symptoms needed to meet the diagnosis. Rather, the additional core feature of this diagnosis is presence of abnormal thoughts, feelings, and behaviors associated with the somatic symptoms. These changes have been made in an effort to better capture the variability in the relationship between somatic symptoms and psychopathology and to shift scrutiny away from the medical plausibility of symptoms and toward the distress and maladaptive thoughts, feelings, and behaviors associated with those symptoms.
Box 16-1. DSM-5 Criteria for Somatic Symptom Disorder |
300.82 (F45.1) |
Specify if: With predominant pain Specify if: Persistent Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Hypochondriasis has been eliminated from DSM-5, but it is likely that many patients who previously met that diagnosis would now meet criteria for somatic symptom disorder. Others who previous qualified for a hypochondriasis diagnosis may more appropriately receive the diagnosis of illness anxiety disorder, if prominent somatic symptoms are not present. Pain disorder has also been eliminated from DSM-5, but the specifier "with predominant pain" may be applied to the diagnosis of somatic symptom disorder to characterize patients whose somatic symptoms predominantly involve pain. Somatic symptom disorder is diagnosed in patients who have significant somatic symptoms. Multiple symptoms are commonly present, but a single severe symptom (such as pain) can be sufficient to establish the diagnosis. The diagnosis may be appropriate for some individuals in association with a medical illness.
Many of the culture-bound syndromes described in earlier DSM editions have a prominent somatic component. Culturally based somatic symptom presentations have even been described as "idioms of distress," because symptoms may have particular meanings and may be attributed to specific causes in a given cultural or ethnic group (see Chapter 36 in this volume, "Treatment of Culturally Diverse Populations," by Lu et al.). The complex and dynamic interplay between culture and expression of somatic symptoms continues to be an area of developing knowledge, but it may be safely assumed that culture will have a significant impact on the presentation and course of somatic symptom disorder. Kirmayer and Sartorius in 2007 provided a detailed review of the influence of cultural models on multiple aspects of somatic symptoms, including symptom reporting, interpretation of symptoms, modes of coping, and helpseeking behaviors.
The differential diagnosis for DSM-IV/DSM-IV-TR somatization disorder included many of the "great imitator" medical disorders that were notorious for their widely varying and unpredictable symptom presentations. However, because the new DSM-5 criteria for somatic symptom disorder emphasize maladaptive thoughts, feelings, and behaviors associated with symptoms, the differential diagnosis now focus on a number of psychiatric conditions that feature similar maladaptive patterns.
Other somatic symptom and related disorders should be considered in the differential diagnosis of somatic symptom disorder. Illness anxiety disorder may include similar maladaptive thoughts and behaviors but would not include the presence of significant somatic symptoms. The essential feature of conversion disorder (functional neurological symptom disorder) is a loss of function rather than the presence of maladaptive thoughts, feelings, and behaviors related to one's symptoms.
Depressive disorders may include features similar to somatic symptom disorder. The cognitive distortions that may accompany depression in the setting of medical illness may appear similar to the "disproportionate and persistent thoughts about the seriousness of one's condition" (Criterion Bl) that characterize somatic symptom disorder. Somatic symptoms and preoccupations are also frequently associated with depression. However, the core depressive symptoms of low (dysphoric) mood and anhedonia must be present to establish a diagnosis of major depressive disorder.
Anxiety disorders and obsessive-compulsive disorder also must be distinguished from somatic symptom disorder. Panic disorder patients often have heightened sensitivity to bodily sensations combined with catastrophic thinking about illness, resulting in frequent workups for cardiac complaints, dyspnea, and near-syncope in emergency and outpatient settings. Although panic disorder includes an intense focus on somatic concerns, such preoccupations tend to occur as acute episodes. Generalized anxiety disorder typically includes worries related to a number of domains, not solely focused on somatic symptoms. Obsessive-compulsive disorder could result in excessive time and energy being devoted to health concerns or somatic symptoms, but obsessions would be accompanied by compulsions focused on reducing anxiety.
Extensive literature on the natural history of somatic symptom disorder is not yet available. However, the DSM-IV/DSM-IV-TR diagnosis of somatization disorder was well studied over decades, and it can be assumed that some of its observed natural history will continue to be relevant for patients with somatic symptom disorder.
Robins and O'Neal (1953) found somatization disorder to be unusual in children younger than 9 years. In most cases, characteristic symptoms begin during adolescence, and the criteria are satisfied by the mid-20s.
Somatization disorder, a chronic illness with fluctuations in the frequency and diversity of symptoms, was previously thought to remit only in rare cases. The most active symptomatic phase is usually early adulthood, but aging does not lead to total remission. Pribor et al. (1994) found that patients with somatization disorder age 55 years and older did not differ from younger patients in terms of the number of somatization symptoms or the use of health care services. Early longitudinal prospective studies showed that 80%-90% of patients diagnosed with somatization disorder retained the diagnosis over many years (Cloninger et al. 1986). However, newer studies have yielded much higher rates of remission, suggesting that as many as 50% of patients experience remission within 1 year (Creed and Barsky 2004).
The most frequent and important complications of somatization disorder are repeated surgical operations, drug dependence, suicide attempts, and marital separation or divorce, according to Goodwin and Guze (1996). These authors suggested that the first two complications are preventable if the disorder is recognized and the patient's symptoms are managed appropriately. Generally, because of awareness that somatization disorder is an alternative explanation for various pains and other symptoms, invasive techniques (which have the potential to cause iatrogenic illness) can be withheld or postponed when objective indications are absent or equivocal. There is no evidence of excess mortality in patients with somatization disorder.
Avoiding the prescribing of habit-forming or addictive substances for persistent or recurrent complaints of pain should be paramount in the mind of the treating physician. Suicide attempts are common, but completed suicide is not. It is unclear whether marital or occupational dysfunction can be minimized through psychotherapy.
The lifetime risk, prevalence, and incidence of somatic symptom disorder are unclear pending further research. Older studies of DSM somatization disorder estimated the lifetime risk at about 2% in women when age at onset and method of assessment were taken into account (Cloninger et al. 1975).
Somatization disorder was diagnosed predominantly in women and rarely in men. Some suggested that this sex difference might be an artifact of bias in the diagnostic criteria, because of the inapplicability of pregnancy and menstrual complaints. The former DSM diagnosis of undifferentiated somatoform disorder was estimated to have a higher over-all prevalence. Escobar et al. (1991) used a construct requiring six somatic symptoms for women and four for men and reported that in the United States 11% of non-Hispanic whites and Hispanics, as well as 15% of blacks, fulfilled the criteria. In Puerto Rico, 20% met the criteria. A preponderance of women was evident in all groups except the Puerto Rican sample. Later studies using this abridged criteria for somatization disorder found less consistent associations with female sex, with 8 of 14 studies reporting a significant effect (Creed and Barsky 2004).
The etiology of somatic symptom disorder is not well understood. Research on the former DSM diagnoses of somatization disorder and undifferentiated somatoform disorder suggested several contributing factors. Temperamental factors, comorbid anxiety and depression, fewer years of education, psychological abuse in childhood, and recent stressful life events have been identified as important risk and prognostic factors.
A familial pattern to these disorders has been demonstrated. In a study by Guze et al. (1986), approximately 20% of the female first-degree relatives of patients with somatization disorder also met criteria for the disorder.
A link to personality disorders has also been posited. Cloninger et al. (1997) identified similarities and even over-lap between somatization disorder and borderline personality disorder. These findings support the interpretation that the life course in somatization disorder is more similar to that in personality disorders than to that in other psychiatric disorders, considering the early onset, non-remitting nature, and pervasiveness of symptoms. More recent research has identified the trait of neuroticism as being associated with an increase in the total number of reported somatic symptoms (Creed et al. 2012).
Experimental neuropsychological testing has indicated that individuals with somatization disorder have difficulty with information processing related to problems with attention and memory. Other theories have been propounded in an attempt to explain the characteristics of patients with somatization disorder. In particular, Horowitz (1977) suggested that "hysterical" information processing might be responsible for many of the clinical features. The information-processing deficit may be the basis for the somatic complaints, mental status findings of vagueness and circumstantiality, and many social, interpersonal, and occupational problems prominent in these patients and their biological relatives. Quill (1985) postulated a social communication model based on the theory that individuals with somatization disorder learn to somatize as a means of expressing emotion (i.e., distress) in their family constellation, evoking support and care from significant individuals. Further research is needed to more completely characterize these theories.
Somatic symptom disorders can be broadly viewed as a pattern of illness behavior by which bodily idioms of distress serve as symbolic means of social regulation as well as protest or contestation. As yet, however, there is little (if any) empirical evidence for such theories.
Somatization disorder is difficult to treat, and there appears to be no single superior treatment approach. In short, patients require an empathic, supportive, and functional approach to address their suffering, although physicians should be cautious about ordering repetitive, unnecessary, and invasive medical/surgical workups, which can cause iatrogenic illness.
Primary care physicians generally can manage patients with somatization disorder adequately, but the expertise of a consulting psychiatrist has been shown to be useful. In a prospective, randomized, controlled study, Smith et al. (1986) found a reduction in health care costs for patients with somatization disorder who received a psychiatric consultation as opposed to those who did not receive a consultation. Reduced expenditures were largely the result of decreased rates of hospitalization. These gains were accomplished with no decrement in medical status or in patient satisfaction, suggesting that many of the evaluations and treatments otherwise provided to patients with somatization disorder are unnecessary. Smith et al. (1986) suggested that treatment include regularly scheduled visits with an appropriate physician. The frequency of visits should be determined on the basis of support for the patient, not in response to the frequency or severity of complaints.
Scallet et al. (1976) reviewed the earlier psychiatric literature on treatment of hysteria and reported the success rates of various approaches. The most effective treatment involved "reeducation, reassurance, and suggestion." This approach accords well with the general principles of treatment recommended by Cloninger (1994). Three important suggestions emerge from review of these reports: 1) establish a firm therapeutic alliance with the patient, 2) educate the patient about the manifestations of somatization disorder, and 3) provide consistent reassurance. Implementation of these principles may greatly facilitate clinical management of somatization disorder and prevent potentially serious complications, including the effects of unnecessary diagnostic and therapeutic procedures (iatrogenic illness). The superiority of more specific treatment approaches has not yet been documented in controlled trials.
During the late 1990s and early 2000s, cognitive-behavioral approaches embodying some of the principles just described were applied to "somatization" patients and yielded tentatively positive results in small studies (Kroenke and Swindle 2000). In 2001, the National Institute of Mental Health funded a single-blind, active-control, parallel-assignment interventional study of cognitive-behavioral therapy (CBT) for somatization disorder in the primary care setting. In this study, Allen et al. (2006) found that CBT with psychiatric consultation was more effective in improving symptoms and functioning than psychiatric consultation alone.
The clinician should develop a relationship with the patient's family. This facilitates attaining a better appreciation of the patient's social structure, which may be crucial to understanding and managing the patient's often-chaotic personal lifestyle. When appropriate, the clinician must place firm limits on excessive demands, manipulations, and attention seeking.
Illness anxiety disorder is a new diagnosis in DSM-5 characterized by a preoccupation with having or acquiring a serious illness. A key feature of the disorder is the absence of significant somatic symptoms; the patient's distress derives not from any specific physical complaints but rather from anxiety surrounding the possibility of having a dreaded illness. Two types of illness anxiety disorder are recognized in DSM-5: care-seeking type (in which medical care is frequently used) and care-avoidant type (in which medical care is rarely accessed). This diagnosis is expected to capture a minority of patients previously diagnosed with hypochondriasis, which is not included as a DSM-5 diagnosis.
Patients with illness anxiety disorder are most commonly encountered in medical settings but may present to psychiatrists for treatment of anxiety. These patients' excessive concerns about undiagnosed disease are unlikely to be alleviated by medical reassurance or negative diagnostic tests; in some patients, this anxiety is further heightened by exposure to illness in others or medical news stories. The symptoms may re-emerge periodically as a characteristic response to various stressors. The DSM-5 diagnostic criteria for illness anxiety disorder are shown in Box 16-2.
Box 16-2. DSM-5 Criteria for Illness Anxiety Disorder |
300.7 (F45.21) |
Specify whether: Care-seeking type Care-avoidant type |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Various other conditions may share the diagnostic features of illness anxiety disorder, particularly mood and anxiety disorders. Somatic symptom disorder is characterized by the presence of at least one significant symptom. Adjustment disorder should be considered in patients whose symptoms have not met the criteria for duration or severity and are clearly in response to a specific event. This maybe particularly relevant when the event leading to the adjustment disorder is health related. Generalized anxiety disorder typically involves persistent worrying about topics aside from those that are strictly health related. Obsessive-compulsive disorder would be expected to focus on a fear of getting the disease in the future as opposed to a focus on current symptoms, and would also generally involve additional obsessions or compulsions. Because patients with major depressive disorder frequently report anxious and somatic preoccupations, depressive disorders may over-lap with the symptoms of illness anxiety disorder; however, the former would include other mood, vegetative, and cognitive symptoms consistent with common mood disorders.
The development and course of illness anxiety disorder is not yet well understood. Previous studies of hypochondriasis suggested that approximately one-fourth of the patients with a diagnosis of hypochondriasis do poorly, two-thirds show a chronic but fluctuating course, and one-tenth recover. However, such predictions may not reflect advances in psychopharmacology. It also must be remembered that such findings pertain to the full syndrome. A much more variable course is seen in patients with some hypochondriacal concerns. Approximately 25%-50% of patients have a more transient form of hypochondriasis that is associated with less severity (American Psychiatric Association 2013).
Because illness anxiety disorder is newly defined in DSM-5, detailed epidemiological studies with the exact criteria are unavailable. However, illness anxiety symptoms and the former DSM diagnosis of hypochondriasis have been studied. In a 2005 survey in the United States, 7.0% of respondents reported significant distress or impairment related to illness worry, with 6.9% of the general population reporting illness anxiety symptoms lasting 6 months or more (Noyes et al. 2005).
Multiple environmental factors appear to be associated with the development of excessive illness worry or hypochondriasis. These factors include early exposure to illness, parental over-protection, and exposure to childhood trauma. In considering hypochondriasis as an aspect of depressive or anxiety disorders, it has been posited that these conditions create a state of hypervigilance to bodily insult, including over-perception of physical problems (Barsky and Klerman 1983).
Hypochondriasis has also been classified by some as falling within the posited obsessive-compulsive spectrum disorders, which include, in addition to obsessive-compulsive disorder, body dysmorphic disorder, anorexia nervosa, Tourette's disorder, and certain impulsive disorders (e.g., trichotillomania and pathological gambling). This clustering is based in part on the phenomenological similarity of repetitive thoughts and behaviors that are difficult or impossible to delay or inhibit (Martin and Yutzy 1997).
Treatment of illness anxiety disorder has yet to be thoroughly researched, but research on and clinical experience with hypochondriasis remains relevant. Patients referred early for psychiatric evaluation and treatment of hypochondriasis appear to have a better prognosis than those receiving only medical evaluations and treatments. As with other somatic symptom and related disorders, psychiatric referrals should be made with sensitivity and awareness of stigma related to mental illness. Perhaps the best guideline to follow is for the referring physician to emphasize that the patient's distress is serious and that psychiatric evaluation will be a supplement to, not a replacement for, continued medical care. Patients may feel dissatisfied by reassurance that their symptoms are "not serious" and may avoid psychiatric referral due to anger over being told that the symptoms "are all in their head."
Because illness anxiety disorder shares many features with other anxiety disorders, it can be expected that selective serotonin reuptake inhibitor (SSRI) pharmacotherapy may have some utility. In patients with hypochondriasis, research has suggested that SSRI treatment is useful for both acute and long-term treatment, with significant proportions of patients achieving remission (Schweitzer et al. 2011).
Investigators have tried many psychotherapeutic approaches in treating hypochondriasis. Stoudemire (1988) suggested an approach featuring consistent treatment, generally by the same primary physician, with supportive, regularly scheduled office visits not focused on the evaluation of symptoms. Hospitalization, medical tests, and medications with addictive potential are to be avoided if possible. During office visits, the clinical interview should gradually shift in content from symptoms to social and/or interpersonal difficulties. Psychotherapeutic approaches may be enhanced greatly by effective pharmacotherapy. CBT was found to be effective in a 2004 study in which 57% of CBT-treated patients showed a reduction in hypochondriacal beliefs at 12-month follow-up (Barsky and Ahern 2004). Preventing adoption of the sick role and chronic invalidism should be a guiding principle for clinicians when treating patients with illness anxiety symptoms.
The essential feature of conversion disorder is the presence of symptoms of altered motor or sensory function that (as evidenced by clinical findings) are incompatible with any recognized neurological or medical condition and not better explained by another medical or mental disorder. Specific symptoms mentioned as examples in DSM-5 include motor symptoms such as weakness or paralysis, abnormal movements (e.g., tremor, dystonic movements), gait abnormalities, and abnormal limb posturing; and sensory symptoms including altered, reduced, or absent skin sensation, vision, or hearing. There may also be episodes of abnormal generalized limb shaking with apparent impairment or loss of consciousness that resemble epileptic seizures (also called psychogenic or nonepileptic seizures); episodes of unresponsiveness resembling syncope or coma; and other symptoms including reduced or absent speech volume (dysphonia/aphonia), altered articulation (dysarthria), a sensation of a lump in the throat (globus), and diplopia. Single episodes usually involve one symptom, but longitudinally, other conversion symptoms will be evident as well. Psychological factors generally appear to be involved, because symptoms often occur in the context of a conflictual situation that may in some way be resolved with the development of the symptom.
In conversion disorder, as in other somatic symptom and related disorders, the symptom or deficit cannot be fully explained by a known physical disorder. This criterion is perhaps the most important diagnostic consideration. The DSM-5 criteria for conversion disorder (Box 16-3) explicitly require neurological examination findings that are inconsistent with known neurological disease. Many examples of these types of findings have been referenced in the literature, some of which are listed below.
Box 16-3. DSM-5 Criteria for Conversion Disorder (Functional Neurological Symptom Disorder) |
Specify symptom type: (F44.4) With weakness or paralysis (F44.4) With abnormal movement (F44.4) With swallowing symptoms (F44.4) With speech symptom (F44.5) With attacks or seizures (F44.6) With anesthesia or sensory loss (F44.6) With special sensory symptom (F44.7) With mixed symptoms Specify if: Acute episode Persistent Specify if: With psychological stressor Without psychological stressor |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
DSM-5 does not include a requirement that the symptoms be produced unintentionally, as absence of feigning is difficult to determine reliably. Although the symptoms of conversion disorder often occur in association with an identifiable stressor, the DSM-IV-TR criterion that required identification of associated psychological factors has been removed.
Psychogenic nonepileptic seizures (PNES) have been researched extensively, and a multitude of terms have been used to describe these events. A conversion disorder diagnosis may be appropriate for certain patients experiencing such episodes who meet the other criteria. Diagnosis of PNES is currently most reliably established by ruling out epilepsy using video EEG monitoring to capture a typical seizure event without an electrographic ictal pattern. Despite the cost and difficulty of identifying PNES in this manner, current research suggests that timely recognition of PNES yields over-all cost savings and reduced utilization of services (Ahmedani et al. 2013).
Symptoms that are fully explained by culturally sanctioned behaviors or practices and that do not involve clinically significant impairment would not qualify for the diagnosis of conversion disorder. Examples of such symptoms include seizure-like episodes occurring in conjunction with certain religious ceremonies, as well as culturally expected responses from other persons present.
Conversion symptoms usually suggest physical illness at first, and therefore patients usually consult primary care and emergency department physicians initially. Neurologists are frequently consulted because most conversion symptom presentations suggest neurological disease (hence the term "functional neurological symptom disorder"). One major problem with conversion symptoms is the risk of applying a conversion disorder diagnosis when a true illness is present. Earlier studies found that among patients initially diagnosed as having conversion symptoms, up to 50% (Slater and Glithero 1965) had a neurological disorder diagnosis on followup. However, more recent studies have suggested a misdiagnosis rate of around 4% (Stone et al. 2005). Also noteworthy is the fact that misdiagnosis may happen in reverse, with patients with multiple sclerosis ultimately being diagnosed with conversion disorder (Hankey and Stew-art-Wynne 1987). The trend toward less misdiagnosis may reflect growing sophistication in neurological diagnosis. Nevertheless, physicians should consider the risks of misdiagnosis when making a diagnosis of conversion disorder.
Symptoms of various neurological illnesses may seem to be inconsistent with known neurophysiology or neuropathology and may suggest conversion disorder. Diseases to be considered include multiple sclerosis (blindness secondary to optic neuritis with initially normal fundi), myasthenia gravis, periodic paralysis, myoglobinuric myopathy, polymyositis, other acquired myopathies (all of which may include marked weakness in the presence of normal deep-tendon reflexes), and Guillain-Barre syndrome (in which early weakness of the arms and legs may be inconsistent). As reviewed by Ford and Folks (1985), more than 13% of actual neurological cases are diagnosed as "functional" before the elucidation of a neurological illness. Initial evidence of some neurological disease is predictive of a subsequent neurological explanation.
Complicating diagnosis is the fact that physical illness and conversion (or other apparent psychiatric over-lay) are not mutually exclusive. Patients with incapacitating and frightening physical illnesses may appear to exaggerate their symptoms. Patients with documented neurological illness also may have "pseudo-symptoms"; for example, patients with epilepsy may also have PNES, previously described as "pseudoseizures" (Dickinson and Looper 2012).
Longitudinal studies indicate that the most reliable predictor that a patient with apparent conversion symptoms will not later be shown to have a physical disorder is a history of conversion or other unexplained symptoms. Conversion symptoms that first occur in middle age or later warrant increased suspicion of an occult physical illness.
Several other psychiatric conditions may share features with conversion disorder. Additionally, a diagnosis of conversion disorder may be made in the presence of other DSM-5 diagnoses, such as somatic symptom and related disorders, dissociative disorders, or mood disorders. Panic disorder may involve neurological symptoms but would not include amnesia or tonic-clonic movements in most cases. Depressive disorders may feature complaints of fatigue or heaviness in the limbs but also would include prominent depressed mood or anhedonia. Although the DSM-5 criteria for conversion disorder do not include a requirement that the symptoms be unintentional, clear evidence of intentional production of symptoms would lead the clinician to the diagnostic categories of factitious disorder or malingering.
Onset of conversion disorder is generally from late childhood to early adulthood. Conversion disorder is rare before age 10 years and seldom first presents after age 35 years. As previously mentioned, symptom onset in middle or late life is associated with a higher likelihood of a neurological or other medical cause.
Onset of conversion disorder is generally acute, but it may be characterized by gradually increasing symptomatology. The typical course of individual conversion symptoms is generally short; half to nearly all patients show a disappearance of symptoms by the time of hospital discharge. However, 20%-25% will relapse within 1 year. Factors traditionally associated with good prognosis include acute onset, presence of clearly identifiable stress at the time of onset, short interval between onset and institution of treatment, and good intelligence. One study noted a better outcome for patients with affective illnesses and a poor prognosis for those with personality disorders (Mace and Trimble 1996). The study also reported that a diagnosis of somatization disorder at follow-up was especially associated with chronicity. Symptoms of blindness, aphonia, and paralysis have been noted to have a relatively good prognosis, whereas seizures and tremor were identified to be more persistent.
Generally, individual conversion symptoms are self-limited and do not lead to physical changes or disabilities. Occasionally, physical sequelae such as atrophy may occur, but this is rare. Morbidity in terms of marital and occupational impairment appears to be less than that in somatization disorder (Kent et al. 1995).
Conclusions regarding the epidemiology of conversion disorder are compromised by methodological differences in diagnostic boundaries as well as by ascertainment procedures from study to study. Vastly different estimates have been reported. Lifetime prevalence rates of treated conversion symptoms in general populations have ranged from 11 in 100,000 to 500 in 100,000 (Ford and Folks 1985). A marked excess of women compared with men develop conversion symptoms. More than 25% of healthy postpartum and medically ill women report having had conversion symptoms sometime during their lives (Cloninger 1994).
Approximately 4%-15% of neurology outpatients, 5%-24% of psychiatric outpatients, 5%-14% of general hospital patients, and l%-3% of outpatient psychiatric referrals have a history of conversion symptoms (Cloninger 1994; Ford 1983; Stone et al. 2010; Toone 1990).
Conversion disorder has been linked with lower socioeconomic status, lower education, lack of psychological sophistication, and rural setting. The disorder appears to be diagnosed more often in women than in men, with ratios varying from 2:1 (Stefansson et al. 1976) to 10:1 (Raskin et al. 1966). In part, this variance may relate to referral patterns, and there may be significant underreporting of some of these symptoms in men; however, more recent reports confirm that more women than men develop conversion symptoms (Bodde et al. 2009).
An etiological hypothesis is implicit in the term conversion. The term, in fact, is derived from the hypothesized conversion of psychological conflict into a somatic symptom. Several psychological factors have been implicated in the pathogenesis, or at least pathophysiology, of conversion disorder. However, as the following discussion will show, such etiological relationships are difficult to establish.
Several terms have historically been used in describing aspects of conversion disorder. In primary gain, anxiety is theoretically reduced by keeping an internal conflict or need out of awareness by symbolic expression of an unconscious wish as a conversion symptom. However, individuals with active conversion symptoms often continue to show marked anxiety, especially on psychological tests. Symbolism is infrequently evident, and its evaluation involves highly inferential and unreliable judgments. Interpretation of symbolism in persons with occult medical disorder has been noted to contribute to misdiagnosis. Secondary gain, whereby conversion symptoms allow the person to avoid noxious activities or to obtain otherwise unavailable support, also may be apparent in persons with medical conditions, who often take advantage of such benefits (Watson and Buranen 1979). La belle indifference refers to a lack of concern regarding the symptoms that has at times been observed, but this presentation is no longer thought to be of sufficient specificity to aid with a diagnosis of conversion disorder (American Psychiatric Association 2013).
Only limited data suggest that conversion symptoms are more frequent in relatives of individuals with conversion disorder. In one distant nonblinded study, rates were 10 times greater than similarly derived general population estimates in female relatives and approximately 5 times the corresponding rate in male relatives (Ljungberg 1957).
If not directly etiological, many factors have been suggested as predisposing individuals to conversion disorder. In many instances, preexisting personality disorders are diagnosable and may predispose some individuals to conversion disorder. In regard to the association with personality disorders, it has been hypothesized that individuals with less healthy defense mechanisms and poor coping are at greater risk for conversion symptoms. Several psychosocial factors in addition to a history of abuse may be involved. Preliminary functional imaging studies postulate an association among conversion disorder, depression, and posttraumatic stress disorder (Ballmaier and Schmidt 2005). Individuals with existing neurological disorders also appear to be predisposed to conversion disorder. Patients with neurological disorders are likely to observe a variety of neurological symptoms in themselves as well as others, and they may at times simulate such symptoms as conversion symptoms.
Generally, the initial aim in treating conversion disorder is the removal of the symptom. The pressure behind accomplishing this goal depends on the distress and disability associated with the symptom. If the patient is not in particular discomfort and the need to regain function is not great, direct attention may not be necessary. In any situation, direct confrontation is not recommended. Such a communication may cause a patient to feel even more isolated. A conservative approach of reassurance and relaxation is effective. Reassurance need not come from a psychiatrist but can be performed effectively by the primary physician. After physical illness is excluded, prognosis for conversion symptoms is good. Folks et al. (1984), for example, found that half of 50 general hospital patients with conversion symptoms showed complete remission by the time of discharge.
If symptoms do not resolve with a conservative approach and there is an immediate need for symptom resolution, other techniques have historically been attempted, including narcoanalysis (e.g., amobarbital interview), hypnosis, and behavior therapy. It does appear that prompt resolution of conversion symptoms is important in that the duration of conversion symptoms is associated with greater risk of recurrence and chronic disability.
Anecdotal reports exist of positive response to somatic treatments such as phenothiazines, lithium, and even electroconvulsive therapy (EGT). Of course, in some cases, such a response again may be attributable to suggestion. In others, it may be that symptom removal occurred because of resolution of another psychiatric disorder, especially a mood disorder. Interestingly, even without a diagnosable mood disorder, antidepressants may be helpful (Hurwitz 2004).
Thus far, the discussion on treatment of conversion disorder has centered on acute treatment primarily for symptom removal. Longer-term approaches involve a pragmatic, conservative approach that entails support for and exploration of various areas of conflict, particularly interpersonal relationships. Ford (1995) suggested a treatment strategy based on "three Ps," wherein predisposing factors, precipitating stressors, and perpetuating factors are identified and addressed. A certain degree of insight may be attained, at least in terms of appreciating relationships between the onset or presence of various conflicts and stressors and the development of symptoms. More ambitious goals have been adopted by some in terms of long-term, intensive, insight-oriented psychotherapy, especially of a psychodynamic nature. Reports of such approaches date from Freud's work with Anna O (Breuer and Freud 1893-1895/1955). At least three studies involving a series of patients treated with psychoanalytic psychotherapy have reported success (Merskey 1989).
The relationship between psychological factors and medical illness is familiar to many clinicians, and often to their patients as well. This relationship has been researched extensively, and a number of specific associations are also well known. Many of the treatment challenges faced by primary care and hospital-based physicians are further complicated by patient factors such as poor adherence to treatment plans, maladaptive coping styles, and persistent high-risk behavior. While these factors (defined loosely) are present in many patients, the DSM-5 diagnosis is reserved for cases in which patient psychological factors are judged to have a clinically significant impact on a medical condition.
Many examples of common combinations that this diagnosis may take are available. Some of these combinations have been historically recognized, such as the relationship between asthma and anxiety or between stress and peptic ulcer disease. Others, such as the link between coronary artery disease and depression, have only recently become a widespread focus of clinical attention. Additional areas of mind-body connection have wide resonance and interest among laypersons, such as the role of psychological factors in cancer treatment. The management of chronic medical conditions such as diabetes requires coping with intense psychological factors for many patients. Additionally, lifestyle risk factors such as cigarette smoking, alcohol abuse, obesity, or high-risk sexual behavior are of paramount importance in the development of many medical illnesses.
The core feature of this diagnosis is the presence of a psychological or behavioral factor that adversely affects a medical condition by increasing the risk for suffering, disability, or death. The most common types of psychological factorsmental disorders, psychological symptoms, personality traits, coping styles, and maladaptive health behaviorswere included as specifiers in DSM-IV-TR. At times a given psychological factor's influence on a medical condition may be evident from the close temporal relationship between the factor and either emergence or worsened course of the condition. The factors may also directly inhibit treatment, most commonly through poor adherence to treatment plans. In other cases, the psychological factors constitute a well-established health risk for the individual. Culturally specific behaviors such as use of faith healers must be excluded when applying this diagnosis, as a variety of health practices exist as a normal pattern within certain cultures and represent attempts to treat illness rather than to perpetuate it. Box 16-4 presents the DSM-5 criteria for psychological factors affecting other medical conditions.
Box 16-4. DSM-5 Criteria for Psychological Factors Affecting Other Medical Conditions |
316 (F54) |
Specify current severity: Mild Moderate Severe Extreme |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Several other somatic symptom and related disorders must be differentiated from psychological factors affecting other medical conditions. Somatic symptom disorder may include the same psychological distress or maladaptive behaviors that would help to meet criteria for the psychological factors affecting other medical conditions diagnosis. However, the core of the latter diagnosis is the presence of a medical condition, the course of which has been adversely altered by the psychological factors. By contrast, a diagnosable medical condition need not be present in somatic symptom disorder; instead, the focus is on the maladaptive thoughts, behaviors, and feelings associated with a symptom. Illness anxiety disorder shares a relationship between a psychological symptom and health concerns, but in that diagnosis, no serious medical illness is present. DSM-5 includes the diagnosis other specified mental disorder due to another medical condition (in the chapter "Other Mental Disorders") to capture presentations in which a medical condition is judged to be causing symptoms of a mental disorder through direct physiological means. An adjustment disorder diagnosis may also be appropriate in cases where the stress of coping with a medical illness has led to significant psychological or behavioral symptoms.
The essential feature in factitious disorder is falsification of physical or psychological signs or symptoms, or induction of injury or disease, with evidence of deceptive intent. This disorder has been described in medical writing throughout history (Feldman et al. 1994; Gavin 1843) and throughout the world (Bappal et al. 2001; Mizuta et al. 2000). The concept became firmly established in modern medical thinking, in 1951 when Asher (1951) described what was later classified as a subtype of factitious disorder known as Munchausen syndrome (which in DSM-5 is now classified as factious disorder imposed on self). Factitious disorder may remain undiagnosed, and even when recognized, it often goes untreated. Yet factitious disorder causes significant morbidity and mortality (Folks 1995), consumes an astonishing amount of medical resources (Feldman 1994), and produces significant emotional distress in the patients themselves, in their caregivers, and in their close relationships (Feldman and Smith 1996).
The DSM-5 criteria for factitious disorder have undergone minor changes from previous criteria. The DSM-IV criterion requiring that the behavior be motivated by a desire to assume the sick role has been removed. However, the requirement that identifiable external incentives for the behavior be absent has been retained in DSM-5. Additionally, the DSM-5 criteria explicitly require that the falsification of symptoms be associated with identified deception.
DSM-5 criteria for factitious disorder are presented in Box 16-5. Criterion A, falsification of physical or psychological signs or symptoms, distinguishes factitious disorder from somatic symptom disorder, in which physical symptoms are viewed as unconsciously produced. Criterion B accounts for the presentation of the symptoms in a manner designed to mimic illness, which hints at the eliminated DSM-IV-TR Criterion B requiring that the behavior be motivated by a desire to assume the sick role. However, the assumption that such motivation can be reliably determined may be problematic, and the new DSM-5 Criterion B can more reliably be established (Turner 2006). Criterion C helps to distinguish factitious disorder from malingering by excluding from the diagnosis those patients with identifiable secondary gain. The DSM-IV-TR codes for subtyping the presentation as involving predominantly psychological, predominantly physical, or combined psychological and physical signs and symptoms have been removed. However, the DSM-5 diagnostic criteria include separate categories for factious disorder imposed on self and factitious disorder imposed on another (previously factitious disorder by proxy).
Box 16-5. DSM-5 Criteria for Factitious Disorder |
300.19 (F68.10) |
Factitious Disorder imposed on Self
Specify: Single episode Recurrent episodes Factitious Disorder Imposed on Another (Previously Factitious Disorder by Proxy)
Note: The perpetrator, not the victim, receives this diagnosis. Specify: Single episode Recurrent episodes |
Illness falsification can take many forms. Patients may exaggerate symptoms, for example, by claiming that occasional tension headaches are continual crippling migraines. They may interfere with diagnostic instruments to give false readings, for example, by manipulating electrocardiogram leads to simulate arrhythmia (Ludwigs et al. 1994) or by rubbing thermometers to fake fevers. Patients may also tamper with laboratory specimens (e.g., by adding blood to urine) to falsely indicate an abnormality. They may purposefully injure themselves by active methods such as selfcatheterization, self-induced infection of wounds or skin with bacteria, injection of unneeded or excessive insulin, or ingestion of thyroid hormones or anticoagulants. Finally, dissimulators may temporarily avoid necessary medical treatment to exacerbate existing conditions.
Given the duplicity inherent in the presentation of factitious disorder, establishing the diagnosis and differentiating this disorder from other conditions may be difficult. Malingering can be distinguished from factitious disorder by the presence of personal gain resulting from the symptoms. Although self-harm behaviors such as the cutting common in borderline personality disorder might appear similar to the deliberate induction of injury in factitious disorder, such self-injurious behaviors would not possess the required association with identified deception. Similarly, somatic symptom disorder lacks evidence of feigned symptoms, instead being defined by maladaptive thoughts, behaviors, and feelings associated with a symptom. Conversion disorder also is not characterized by duplicity and is associated with functional neurological deficits. Finally, the presence of a true medical condition does not exclude the possibility of co-occurring factitious disorder.
Factitious disorder is thought to follow a course characterized by intermittent episodes throughout life. Onset is generally in early adulthood, often after hospitalization for a medical or psychiatric condition. Patients can be difficult to track longitudinally due to the duplicity inherent in the disorder, but the pattern of seeking medical care for falsified symptoms often continues throughout the individual's life (American Psychiatric Association 2013).
Data on incidence and prevalence rates for factitious disorder are difficult to gather, vary considerably, and must be viewed with a critical eye. The covert nature of the disorder can lead to missed diagnosis and underestimation of rates or, conversely, to the same case being counted twice (Ifudo and Friedman 1993) and inflating apparent rates. Sutherland and Rodin (1990) diagnosed factitious disorder in 0.8% of all psychiatric consultation-liaison service referrals of medical or surgical inpatients. Bhugra (1988) found 0.5% of psychiatric admissions to have Munchausen syndrome. Rates are higher in more specialized treatment settings. Whereas most reported cases have been in patients in their 20s to 40s, Munchausen syndrome has been reported in children, adolescents, and geriatric populations (Angus et al. 2007; Libow 2000).
Psychodynamic explanations for these paradoxical disorders have been provided by several authors. Many have noted the apparent prevalence of histories of early childhood physical or sexual abuse, with disturbed parental relationships and emotional deprivation. Histories of early illness or extended hospitalizations also have been noted. Nadelson (1979) conceptualized factitious disorder as a manifestation of borderline character pathology rather than as an isolated clinical syndrome. The patient becomes both the "victim and the victimizer" by garnering medical attention from physicians and other health care workers while defying and devaluing them. Projection of hostility and worthlessness onto the caregiver occurs as he or she is both desired and rejected. Plassmann (1994b, 1994c) viewed the disorders as a "symptom of a psychic problem complex." Early traumas are dealt with narcissistically and through dissociation, denial, and a type of projection. The patient's body, or part of the body, becomes perceived as an external object or as a fused symbiotic combination of self and object, which then comes to represent negative affects (hate, fear, pain), the associated negative object concepts, and negative self-concepts. In the face of early deprivation and assaults, the "body self" is split off to preserve the "psychic self" (Hirsch 1994). When subsequent life events activate these affects or concepts, the result is extreme anxiety and growing derealization. Eventually, the patient acts out or involves the medical system in a type of countertransference identification, which leads to manipulations of the body of the patient. The manipulation results in emotional relief, albeit transient and incomplete, in the manner of most repetitious compromises. Other intrapsychic, cognitive, social learning, and behavioral theories have been advanced as well (Feldman et al. 2001; Ford 1996).
Neuropathological foundations for factitious disorder also have been suggested on the basis of abnormal findings on single photon emission computed tomography, computed tomography, and magnetic resonance imaging scans and neuropsychological testing. No consistent findings have yet been reported. Intriguing, however, is the suggestion that pseudologia fantastica may be a syndrome related to but distinct from factitious disorder, with its own associated pathology.
Although many cases of factitious disorder are chronic, the stressor of recurrent object loss, or fear of loss, occurs over and over in the literature as an antecedent of a factitious episode. For example, Carney (1980) found that 74% of his patients with factitious disorder experienced severe sexual or marital stress prior to developing factitious signs or symptoms.
Treatment of factitious disorder can be divided into acute and long-term methods. Initially the diagnosis must be confirmed. An erroneous diagnosis of factitious disorder can itself result in trauma and may be perpetuated in medical records. Previously used methods of confirming the diagnosis, such as searching patients' belongings for paraphernalia used in producing symptoms, may continue to be tempting for clinicians, but such methods violate ethical and most likely legal boundaries. Because of this and the potentially strong countertransference reactions engendered by these patients, some authors have endorsed early involvement with hospital administration when a diagnosis of factitious disorder is suspected (Wise and Rundell 2005). Treatment team meetings are recommended to help coordinate efforts between providers and to allow for management of negative emotions toward patients (Eisendrath and Feder 1996). As Feldman and Feldman (1995) described, countertransference can lead to several adverse consequences. "Therapeutic nihilism" on the part of the treatment system may lead to an unexamined assumption that the patient cannot or should not be treated, with subsequent failure to diagnose or refer. Anger and aversion can rupture any therapeutic alliance, undermine the unity of a treatment team, or lead to punitive acting-out against the patient. Genuine comorbid or concomitant illness may be over-looked. Nonemergent breaches of confidentiality may ensue in the diagnostic hunt or in the supposed effort to "warn" colleagues. Overidentification with the patient or activation of rescue fantasies can sabotage treatment efforts and may paradoxically reinforce continued factitious behaviors.
Once the contribution of general medical illness has been factored out, the patient must be informed of a change in the treatment plan, and an attempt must be made to enlist him or her in that plan. The literature generally refers to this process (perhaps alluding to its countertransference aspects) as containing an element of "confrontation." There is now general agreement that treatment begins at this point and that it is best done indirectly, with minimal expectation that the patient "confess" or acknowledge the deception. It is a delicate process, with patients frequently leaving the hospital against medical advice or otherwise leaving treatment. Guziec et al. (1994) aptly likened this process to making a psychodynamic interpretation. Eisendrath (1989) described techniques for reducing confrontation, such as using inexact interpretations, therapeutic double binds, and other strategic and face-saving techniques to allow the patient tacitly to relinquish the factitious signs and symptoms.
Some authors recommend inpatient psychiatric hospitalization, often protracted and/or involuntary (Plassmann 1994a). However, others (Guziec et al. 1994) recommend treatment initiation in the general medical inpatient setting where the factitious disorder has been diagnosed and continuing in the psychiatric outpatient setting. Although the patient with Munchausen syndrome is regarded as less likely to engage in treatment (Eisendrath 1989), and the patient with general factitious disorder is seen as more available for intervention, there are case reports of Munchausen patients responding favorably to treatment (Feldman 2006; Rothchild 1994).
No comparative studies of therapeutic approaches are available, although several different techniques have been described. Regardless of modality, treatment must be collaborative and involve some level of communication among all of the patient's treatment providers. The psychodynamic approach to treatment (Plassmann 1994a) generally focuses not on the factitious behaviors themselves but rather on the underlying dynamic issues, with the therapist taking a neutral stance toward the factitious nature of the behaviors. As indicated, strategic-behavioral approaches also have been used (Teasell and Shapiro 1994), implementing standard behavioral techniques as well as the therapeutic double bind, in which the only way out is to abandon the target factitious behaviors. Pharmacotherapy, when used, targets specific symptoms, such as depression, transient psychosis, or comorbid disorders. Some patients cease factitious behaviors on their own as a result of unanticipated life change (e.g., marriage or involvement in a church group that provides the requisite attention and support). Perceiving an "addictive" quality to their factitious behaviors, others have creatively evolved personal "12-Step" programs that have helped them end the deceptions.
Insufficient studies have been conducted to address conclusively the prognostic factors in factitious disorder, but children, patients with major depressive disorder, and patients without personality disorders may have better prognoses (Li-bow 2000). Recent reviews have considered many of these treatment issues and have called for more coordination between clinicians treating this disorder in an effort to improve research of this diagnosis (Eastwood and Bisson 2008). The literature on the disorder is certainly ample, and it implies that the factitious disorder patient, although requiring considerable therapeutic skill, may be approached with a cautious hope for improvement.
Two additional somatic symptom and related disorder diagnostic categories are provided in DSM-5. The categories of other specified somatic symptom and related disorder and unspecified somatic symptom and related disorder may be applied to presentations that are characteristic of a somatic symptom and related disorder and that cause clinically significant impairment but do not meet full criteria for any of the disorders in this diagnostic class. For an "other specified" diagnosis, the clinician records the specific reason that full criteria are not met; for an "unspecified" diagnosis, no reason need be given. Use of the latter category should be reserved for exceptionally uncommon situations in which there is insufficient information to make a more specific diagnosis.
DSM-5 provides four examples of presentations for which an other specified somatic symptom and related disorder designation might be appropriate:
The treatment of patients with somatic symptom pathology remains challenging across medical specialties. These patients often feel blamed for their somatic symptoms, and invasive medical workups often place patients at higher risk of medically induced illness. The updated DSM-5 criteria aim to help physicians accurately diagnose these disorders and to protect patients with these conditions from undue interventions and stigma. Careful application of these updated criteria will encourage compassionate care while adhering to one of the fundamental precepts of the medical profession, primum non nocere.
Key Clinical Points
* The 6th Edition Textbook revision of this chapter has combined diagnoses that were previously included in three different chapters, in keeping with the updated organization of DSM-5. The authors would like to acknowledge and thank the authors of the chapters in previous editions of this textbook that provided the framework for this updated chapter. Sean H. Yutzy, M.D., and Brooke S. Parish, M.D., provided the previous Somatoform Disorders material. Martin Leamon, M.D., and his colleagues contributed the foundation for the Factitious Disorder section. Much of the material included for Psychological Factors Affecting Other Medical Conditions stems from the 5th Edition Textbook chapter by James Levenson, M.D., and readers are referred to that text for a more thorough discussion of the topic than is included in the current edition.
Ahmedani BK, Osborne J, Nerenz DR, et al: Diagnosis, costs, and utilization for psychogenic non-epileptic seizures in a US health care setting. Psychosomatics 54:28-34, 2013
Allen L, Woolfolk R, Escobar J, et al: Cognitive-behavioral therapy for somatization disorder. Arch Intern Med 166:1512-1518, 2006
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Arlington, VA, American Psychiatric Association, 1994
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA, American Psychiatric Association, 2013
Angus J, Affleck AG, Croft JC, et al: Dermatitis artefacta in a 12-year-old girl mimicking cutaneous T-cell lymphoma. Pediatr Dermatol 24:327-329, 2007
Asher R: Munchausen's syndrome. Lancet 1(6):339-341, 1951
Ballmaier M, Schmidt R: Conversion disorder revisited. Funct Neurol 20(3):105-113, 2005
Bappal B, George M, Nair R, et al: Factitious hypoglycemia: a tale from the Arab World. Pediatrics 107:180-181, 2001
Barsky AJ, Ahern DK: Cognitive behavior therapy for hypochondriasis. JAMA 291:1464-1470, 2004
Barsky AJ, Klerman GL: Overview: hypochondriasis, bodily complaints, and somatic styles. Am J Psychiatry 140:273-283, 1983
Bhugra D: Psychiatric Munchausen's syndrome: literature review with case reports. Acta Psychiatr Scand 77:497-503, 1988
Bodde NM, Brooks JL, Baker GA, et al: Psychogenic non-epileptic seizuresdiagnostic issues: a critical review. Clin Neurol Neurosurg 111:1-9, 2009
Breuer J, Freud S: Studies on hysteria (1893-1895), in The Standard Edition of the Complete Psychological Works of Sigmund Freud, Vol 2. Translated and edited by Strachey J. London, Hogarth, 1955, pp 1-311
Carney MW: Artefactual illness to attract medical attention. Br J Psychiatry 136:542-547, 1980
Cloninger CR: Somatoform and dissociative disorders, in The Medical Basis of Psychiatry, 2nd Edition. Edited by Winokur G, Clayton P. Philadelphia, PA, WB Saunders, 1994, pp 169-192 Cloninger CR, Reich T, Guze SB: The multifactorial model of disease transmission, III: familial relationship between sociopathy and hysteria (Briquet's syndrome). Br J Psychiatry 127:23-32, 1975
Cloninger CR, Martin RL, Guze SB, et al: A prospective follow-up and family study of somatization in men and women. Am J Psychiatry 143:873-878, 1986
Cloninger CR, Bayon C, Przybeck TR: Epidemiology and Axis I comorbidity of antisocial personality, in Handbook of Antisocial Behavior. Edited by Stoff DM, Breiling J, Maser JD. New York, Wiley, 1997, pp 12-21
Creed FH, Barsky A: A systematic review of the epidemiology of somatisation disorder and hypochondriasis. J Psychosom Res 56:391-408, 2004
Creed FH, Davies I, Jackson J, et al: The epidemiology of multiple somatic symptoms. J Psychosom Res 72:311-317, 2012
Dickinson P, Looper KJ: Psychogenic nonepileptic seizures: a current over-view. Epilepsia 53:1679-1689, 2012
Eastwood S, Bisson JI: Management of factitious disorders: a systematic review. Psychother Psychosom 77:209-218, 2008
Eisendrath SJ: Factitious physical disorders: treatment without confrontation. Psychosomatics 30:383-387, 1989
Eisendrath SJ, Feder A: Management of factitious disorders, in The Spectrum of Factitious Disorders. Edited by Feldman MD, Eisendrath SJ. Washington, DC, American Psychiatric Press, 1996, pp 195-213 Escobar JI, Swartz M, Rubio-Stipec M, et al: Medically unexplained symptoms: distribution, risk factors, and comorbidity, in Current Concepts of Somatization: Research and Clinical Perspectives. Edited by Kirmayer LJ, Robbins JM. Washington, DC, American Psychiatric Press, 1991, pp 63-78
Feldman MD: The costs of factitious disorders. Psychosomatics 35:506-507, 1994
Feldman MD: Recovery from Munchausen syndrome. South Med J 99:1398-1399, 2006
Feldman MD, Feldman JM: Tangled in the web: countertransference in the therapy of factitious disorders. Int J Psychiatry Med 25:389-399, 1995
Feldman MD, Smith R: Personal and interpersonal toll of factitious disorders, in The Spectrum of Factitious Disorders. Edited by Feldman MD, Eisendrath SJ. Washington, DC, American Psychiatric Press, 1996, pp 175-194
Feldman MD, Ford CV, Reinhold T: Patient or Pretender: Inside the Strange World of Factitious Disorders. New York, Wiley, 1994
Feldman MD, Hamilton JC, Deemer HN: A critical analysis of factitious disorders, in Somatoform and Factitious Disorders. Edited by Phillips KA. Washington, DC, American Psychiatric Publishing, 2001, pp 129-166
Folks DG: Munchausen's syndrome and other factitious disorders. Neurol Clin 13:267-281, 1995
Folks DG, Ford CV, Regan WM: Conversion symptoms in a general hospital. Psychosomatics 25:285-295, 1984
Ford CV: The Somatizing Disorders: Illness as a Way of Life. New York, Elsevier, 1983
Ford CV: Conversion disorder and somatoform disorder not otherwise specified, in Treatments of Psychiatric Disorders, 2nd Edition. Edited by Gabbard GO. Washington, DC, American Psychiatric Press, 1995, pp 1737-1753
Ford CV: Lies! Lies!! Lies!!! The Psychology of Deceit. Washington, DC, American Psychiatric Press, 1996
Ford CV, Folks DG: Conversion disorders: an over-view. Psychosomatics 26:371-383, 1985
Gavin H: On Feigned and Factitious Diseases, Chiefly of Soldiers and Seamen, on the Means Used to Simulate or Produce Them, and on the Best Mode of Discovering Imposters: Being the Prize Essay in the Class of Military Surgery, in the University of Edinburgh, Session, 1835-6, With Additions. London, John Churchill Princess Street Soho, 1843
Goodwin DW, Guze SB: Psychiatric Diagnoses, 5th Edition. New York, Oxford University Press, 1996
Guze SB, Cloninger CR, Martin RL, et al: A follow-up and family study of Briquet's syndrome. Br J Psychiatry 149:17-23, 1986
Guziec J, Lazarus A, Harding JJ: Case of a 29-year-old nurse with factitious disorder: the utility of psychiatric intervention on a general medical floor. Gen Hosp Psychiatry 16:47-53, 1994
Hankey GJ, Stewart-Wynne EG: Pseudo-multiple sclerosis: a clinicoepidemiological study. Clin Exp Neurol 24:11-19, 1987
Hirsch M: The body as a transitional object.
Psychother Psychosom 62:78-81, 1994
Horowitz MJ: Hysterical Personality. New York, Jason Aronson, 1977
Hurwitz TA: Somatization and conversion disorder. Can J Psychiatry 49:172-178, 2004
Ifudo O, Friedman EA: Kidney-related Munchausen's syndrome and the Red Baron (letter). N Engl J Med 328:61, 1993
Kent D, Tomasson K, Coryell W: Course and outcome of conversion and somatization disorders: a four-year follow-up. Psychosomatics 36:138-144, 1995
Kirmayer L, Sartorius N: Cultural models and somatic syndromes. Psychosom Med 69:832-840, 2007
Kroenke K, Swindle R: Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom 9:205-215, 2000
Libow J: Child and adolescent illness falsification. Pediatrics 105:336-342, 2000
Ljungberg L: Hysteria: clinical, prognostic and genetic study. Acta Psychiatr Neurol Scand Suppl 112:1-162, 1957
Ludwigs U, Ruiz H, Isaksson H, et al: Factitious disorder presenting with acute cardiovascular symptoms. J Intern Med 236:685-690, 1994
Mace CJ, Trimble MR: Ten-year prognosis of conversion disorder. Br J Psychiatry 169:282-288, 1996
Martin RL, Yutzy SH: Somatoform disorders, in Psychiatry. Edited by Tasman A, Kay J, Lieberman JA. Philadelphia, PA, WB Saunders, 1997, pp 1119-1155
Merskey H: Conversion disorder, in Treatments of Psychiatric Disorders: A Task Force Report of the American Psychiatric Association, Vol 3. Washington, DC, American Psychiatric Association, 1989, pp 2152-2159
Mizuta I, Fukunaga T, Sato H, et al: A case report of comorbid eating disorder and factitious disorder. Psychiatry Clin Neurosci 54:603-606, 2000
Nadelson T: The Munchausen spectrum: borderline character features. Gen Hosp Psychiatry 1:11-17, 1979
Noyes R, Carney CP, Hillis SL, et al: Prevalence and correlates of illness worry in the general population. Psychosomatics 46:529-539, 2005
Plassmann R: Inpatient and outpatient long-term psychotherapy of patients suffering from factitious disorder. Psychother Psychosom 62:96-107, 1994a
Plassmann R: Munchausen syndromes and factitious diseases. Psychother Psychosom 62:7-26, 1994b
Plassmann R: Structural disturbances in the body self. Psychother Psychosom 62:91-95, 1994c
Pribor EF, Smith DS, Yutzy SH: Somatization disorder in the elderly. Am J Geriatr Psychiatry 2:109-117, 1994
Quill TE: Somatization disorder: one of medicine's blind spots. JAMA 254:3075-3079, 1985
Raskin M, Talbott JA, Meyerson AT: Diagnosis of conversion reactions: predictive value of psychiatric criteria. JAMA 197:530-534, 1966
Robins E, O'Neal P: Clinical features of hysteria in children, with a note on prognosis; a two to seventeen year follow-up study of 41 patients. Nerv Child 10:246-271, 1953
Rothchild E: Fictitious twins, factitious illness. Psychiatry 57:326-332, 1994
Scallet A, Cloninger CR, Othmer E: The management of chronic hysteria: a review and double-blind trial of electrosleep and other relaxation methods. Dis Nerv Syst 37:347-353, 1976
Schweitzer PJ, Zafar U, Pavlicova M, et al: Long-term follow-up of hypochondriasis after selective serotonin reuptake inhibitor treatment. J Clin Psychopharmacol 31:365-368, 2011
Slater ETO, Glithero C: A follow-up of patients diagnosed as suffering from "hysteria." J Psychosom Res 9:9-13, 1965
Smith GR Jr, Monson RA, Ray DC: Psychiatric consultation in somatization disorder: a randomized controlled study. N Engl J Med 314:1407-1413, 1986
Stefansson JH, Messina JA, Meyerowitz S: Hysterical neurosis, conversion type: clinical and epidemiological considerations. Acta Psychiatr Scand 59:119-138, 1976
Stone J, Smyth R, Carson A, et al: Systematic review of misdiagnosis of conversion symptoms and "hysteria." BMJ 331:989, 2005
Stone J, Carson A, Duncan R, et al: Who is referred to neurology clinics? The diagnoses made in 3781 new patients. Clin Neurol Neurosurg 112:747-751, 2010
Stoudemire GA: Somatoform disorders, factitious disorders, and malingering, in The American Psychiatric Press Textbook of Psychiatry. Edited by Talbott JA, Hales RE, Yudofsky SC. Washington, DC, American Psychiatric Press, 1988, pp 533-556 Sutherland AJ, Rodin GM: Factitious disorders in a general hospital setting: clinical features and a review of the literature. Psychosomatics 31:392-399, 1990
Teasell RW, Shapiro AP: Strategic-behavioral intervention in the treatment of chronic nonorganic motor disorders. Am J Phys Med Rehabil 73:44-50, 1994
Toone BK: Disorders of hysterical conversion, in Physical Symptoms and Psychological Illness. Edited by Bass C. London, Black-well Scientific, 1990, pp 207-234
Turner MA: Factitious disorders: reformulating the DSM-IV criteria. Psychosomatics 47:23-32, 2006
Watson CG, Buranen C: The frequency and identification of false positive conversion reactions. J Nerv Ment Dis 167:243-247, 1979
Wise MG, Rundell JR: Clinical Manual of Psychosomatic Medicine: A Guide to Consultation-Liaison Psychiatry. Washington, DC, American Psychiatric Publishing, 2005
Dimsdale JE, Patel V, Xin Y, Kleinman A: Somatic presentationsa challenge for DSM-V. Psychosom Med 69:829, 2007
http://www.dsm5.org/about/Pages/DSMVOverview.aspx
http://www.dsm5.org/ProgressReports/Documents/Guidelines-for-Making-Changes-to-DSM_l.pdf
http://www.psychiatry.org/practice/dsm/dsm5