Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis

Author
Donna B Greenberg, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Donna B Greenberg, MD Nothing to disclose. Joel Dimsdale, MD Nothing to disclose. David Solomon, MD Nothing to
disclose.
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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Mar 25, 2015.
INTRODUCTION Somatization is a syndrome of physical symptoms that are distressing and may not be fully explained
by a known medical condition after appropriate investigation. In addition, the symptoms may be caused or exacerbated by
anxiety, depression, and interpersonal conflicts, and it is common for somatization, depression, and anxiety to all occur
together [1-5]. Somatization can be conscious or unconscious and may be influenced by a desire for the sick role or for
personal gain [1].
Somatization often occurs in primary care patients [5]. It increases use of medical services independent of any
accompanying psychiatric or nonpsychiatric disorder and leads to frustration in both the patient and the clinician [4,6-9].
This topic reviews the following issues related to somatization: epidemiology, pathogenesis, clinical features, medical
evaluation, and diagnosis of specific disorders. Treatment of somatization and prognosis are discussed separately.
(See "Somatization: Treatment and prognosis".)
TERMINOLOGY AND DSM-5 The term "somatization" as used in this topic refers to a syndrome consisting of physical
symptoms that cause substantial distress and psychosocial impairment, and in some instances, are not explained by a
known general medical disease. Somatization has also been referred to as medically unexplained symptoms and
functional somatic symptoms.
Somatization is an overarching term that encompasses many different illnesses and terms including somatoform
disorders, which is a group of disorders that are recognized in the World Health Organization's International Classification
of Diseases-10th Revision (ICD-10) [10], and were previously described in the American Psychiatric Association's
Diagnostic and Statistical Manual, Fourth Edition, Text Revision (DSM-IV-TR) (table 1) [11]. (See 'Somatoform
disorders' below.)
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) does not use the term somatization, and
has eliminated the category of diagnoses called somatoform disorders. DSM-IV-TR described somatoform disorders as
illnesses with physical symptoms that were not explained by a general medical condition [11]. Psychiatric nosology has
evolved such that in DSM-5, the centrality or prominence of medically unexplained symptoms has been deemphasized,
because it is difficult to prove that a symptom is not caused by a general medical disorder [12]. Many of the somatoform
diagnoses lacked validity, due to insufficient evidence for a discrete, characteristic cluster of symptoms and a predictable
longitudinal course of illness [9,13]. In addition, the criteria or cut-off points used to distinguish cases often appeared
arbitrary [9].
For patients with prominent somatic symptoms that cause distress and impair psychosocial functioning, DSM-5 has
replaced the category of somatoform disorders with a category called somatic symptom and related disorders [12].
(See 'Somatic symptom and related disorders' below.)

EPIDEMIOLOGY Somatization is common in the general population. More than 50 percent of patients presenting to
outpatient medical clinics with a physical complaint do not have a medical condition [14-17].
Somatization, defined in one study as four or more unexplained physical symptoms in men and six or more unexplained
physical symptoms in women, occurred in 17 percent of patients in primary care settings and 4 percent of the general US
population [9]. Risk factors for somatization include:
Female sex
Fewer years of education
Minority ethnic status
Low socioeconomic status
A systematic review of 21 European studies found the median 12-month prevalence rate for any somatoform disorder was
6 percent of the general population [18]. (See'Somatoform disorders' below.)
Health care utilization Somatization increases use of medical services independent of any accompanying psychiatric
or nonpsychiatric medical disorder [6,7,9]. One study found primary care patients with somatization visited their outpatient
clinic more often during five years of follow-up compared with patients without somatization (34 versus 23 visits) [19].
Another study identified somatization (with a high likelihood of being formally diagnosed with a somatoform disorder) in
about 20 percent of 1500 consecutive patients who made scheduled visits to primary care physicians in urban and
suburban hospital-based practices [8]. Somatizing patients had significantly more annual primary care visits (4.9 versus
3.4), specialist visits (8.1 versus 4.9), emergency room visits (1.3 versus 0.5), and hospital admissions (0.3 versus 0.1),
even after adjusting for sociodemographic characteristics, major medical morbidity, and comorbid anxiety and depression.
Overall, patients with somatization utilized medical services (outpatient and inpatient) twice as often compared to
nonsomaticizing patients, and generated twice the costs for medical care. The difference in costs between the two groups
represented 16 percent of the total costs for the entire 1500 patients.
Psychosocial functioning Somatization is consistently associated with impaired functioning and disability,
independent of any existing psychiatric and nonpsychiatric medical comorbidity [20]. As an example, studies in primary
care settings that compared somatizing patients to nonsomaticizing patients found significantly higher rates of
unemployment (29 versus 15 percent) and impaired occupational functioning (55 versus 14 percent) [20,21].
ETIOLOGY Controversy exists regarding whether somatization is to be considered a purely psychiatric disorder (eg, a
learned pattern of behavior), or if it should be viewed as a syndrome of multiple unexplained symptoms that complicate
the presentation of a general medical condition [22-25].
The genetic basis for somatization is not clear. Some, but not all studies, indicate a familial pattern for somatization. The
familial aggregation may be due to genetic or environmental factors, or both. In addition, a genetic influence may
represent an inherited predisposition to general distress, and not specifically to somatization [26]. Representative studies
include the following:
In one study of patients with somatization disorder, about 20 percent of the female first-degree relatives also had
the disorder [27]. Male relatives were more likely to have a substance use disorder or antisocial personality disorder.
A family study examined 72 first-degree relatives of 19 patients with hypochondriasis and 97 relatives of 24
controls. There was no increase in the rate of hypochondriasis among the relatives of hypochondriasis patients
compared with the relatives of controls [28].
Childhood sexual abuse and recent exposure to physical or sexual violence are consistently associated with somatization
in adult women [29-31]. A systematic review and meta-analysis involving 4640 patients found an association between a
history of sexual abuse and lifetime diagnosis of functional gastrointestinal disorders (OR 2.4, 95% CI 1.4-4.3),
nonspecific chronic pain (OR 2.2, 1.5-3.2), psychogenic seizures (OR 3.0, 1.1-4.7), and chronic pelvic pain (OR 2.7, 1.74.3) [32]. For victims of rape, associations were observed between rape and a lifetime diagnosis of fibromyalgia (OR 3.4,
1.5-7.5), chronic pelvic pain (OR 3.3, 1.02-10.53), and functional gastrointestinal disorders (OR 4.0, 1.9-8.6).

Physical symptoms may offer a means to express distress when patients do not easily express emotions in words
(alexithymia) [33]. Patients may also come to the clinician with physical complaints when psychiatric symptoms have great
stigma. The interpersonal model of somatization hypothesizes that somatic symptoms represent care-seeking behavior in
patients with insecure attachment [34]. In addition, somatization may involve an over-inclusive or unrealistic concept of
good health, increased attention to bodily processes to detect possible signs of illness, catastrophic interpretations of
bodily sensations, lack of external stimulation, expectations, operant conditioning, and difficulty with information
processing [35].
The patient's perception of symptoms affects how they are reported, and perception is influenced by attitudes, beliefs, and
psychologic distress [36,37]. In addition, some patients may be more prone to amplify symptoms [38].
Having a family member with a chronic illness during childhood may be a precursor to somatization [35]. The tendency to
report functional or somatic symptoms tends to persist from childhood to adulthood [39,40].
Once somatization has been established, behavior around the symptoms and sick role add another psychologic
dimension [36]. The symptoms offer benefits such as social support, escape from obligations, disability payments, and a
compromise for internal conflicts. At the same time, the symptoms are associated with loss of work, status, and
independence.
The tendency to somatize does not vary from culture to culture, and there are no significant cross-cultural differences in
the rate and sociodemographic correlates of somatoform disorders [41]. One study of somatic symptoms of depressive
disorder in 15 primary care centers in 14 countries did not show cultural variability [42]. Although the frequency of
somatoform disorders is similar across cultures, culture-specific manifestations are often present [43].
CLINICAL PRESENTATION The essential feature of somatization is a history of physical symptoms that the patient
attributes to a nonpsychiatric disease [4,44]. The symptoms may be unexplained.
Somatizing patients present with a wide array of symptoms:
Pain symptoms, including headache, back pain, dysuria, joint pain, diffuse pain, and extremity pain
Gastrointestinal symptoms, including nausea, vomiting, abdominal pain, bloating, gas, and diarrhea
Cardiopulmonary symptoms, including chest pain, dizziness, shortness of breath, and palpitations
Neurologic symptoms, including fainting, pseudoseizures, amnesia, muscle weakness, dysphagia, double or
blurred vision, difficulty walking, difficulty urinating, deafness, and hoarseness or aphonia
Reproductive organ symptoms, including dyspareunia, dysmenorrhea, and burning in sex organs
Preoccupation with symptoms may indicate somatization. Among first-time referrals to a neurology service, clinician
recognition of this preoccupation was the primary identifying factor for patients with somatization [45]. Asking about
multiple symptoms beyond those related to the presenting neurological complaint added to detection of a somatoform
disorder. (See 'Somatoform disorders' below.)
The number of somatic symptoms can aid detection of somatoform disorders [45], and is related to health status. In a
study that used data from nine population studies (n >28,000) and controlled for confounders (eg, age, sex, anxiety,
depression, and general medical illness), disability was greater among individuals with a greater number of somatic
symptoms [46,47].
Somatizing patients can also be recognized by the multiple unexplained symptoms, vague and inconsistent history,
underlying sense of anguish, persistent unspoken demands, lack of factors that exacerbate or alleviate symptoms, and
lack of positive findings on physical examination. These patients often elicit negative feelings from their clinician and are
viewed as "difficult patients" [48,49].
Somatization can occur in the context of general medical illness. As an example, psychogenic nonepileptic seizures can
be comorbid with epileptic seizures, and psychogenic seizures are often underestimated in patients with a known seizure
disorder [50]. (See "Psychogenic nonepileptic seizures".)

Somatization occurs along a spectrum of expression ranging from the exaggeration of common symptoms to unrelenting,
disabling symptoms. The same principles of management apply to patients across the spectrum. (See "Somatization:
Treatment and prognosis".)
Coexisting psychiatric disorders Somatization is strongly associated with anxiety and depression [4,5,9,16,19,51]. In
a group of nearly 300 somatizing patients who visited primary care physicians in urban or suburban hospital-based
practices, 58 percent had a comorbid anxiety or depressive disorder [8]. In a study of 10,000 primary care patients, those
with somatization were six times more likely to manifest anxiety or depression compared to those without somatization (30
versus 5 percent) [52].
The number of physical symptoms, rather than the specific type of symptoms, is important in predicting a comorbid
anxiety or depressive disorder [4,51]. A systematic review of 47 studies found that as the number of somatic symptoms
increased, so did the number of anxiety and depression symptoms [9]. There are many other predictors of anxiety or
depression in patients with somatization (table 2).
One study found that a patient was more apt to report psychologic symptoms to a primary care clinician if the patient
already had a relationship with that clinician [42]. Among those who presented with somatic symptoms of depression, 60
percent acknowledged other depressive symptoms, such as depressed mood or guilt, when the clinician asked.
In addition to depression and anxiety, somatization is often associated with personality disorders. A study of 94
somatization patients, using structured interviews, found that 61 percent had at least one personality disorder [53]. The
most common were avoidance, paranoia, self-defeating, and obsessive-compulsive. (See "Personality disorders".)
It is unclear whether there is an association between somatization and substance use disorder, with contradictory findings
in several studies [54].
GENERAL MEDICAL EVALUATION The evaluation of a patient presenting with possible somatization includes taking
a history, performing a physical examination, reviewing laboratory data, and communicating with other clinicians. A
general medical illness may not be recognized because of insufficient attention to the history, physical examination, or
laboratory tests; insufficient use of contemporary diagnostic techniques; the medical illness is due to iatrogenic adverse
effects; or a new disease has yet to be identified [55].
A medical and a psychosocial etiology for a patient's symptoms should be explored simultaneously so that the patient has
confidence that medical needs are being addressed. In addition, patients who present with a new illness episode may be
more willing to discuss psychosocial concerns at the onset of their evaluation, rather than after all medical examinations
have failed to identify a cause for their symptoms [56]. Many of these patients will have seen several clinicians.
Establishing trust and minimizing the chance of humiliation is essential. The patient needs to feel respected and
understood.
A thorough examination will help the clinician and patient feel comfortable that no important diagnosis will be missed.
Ancillary testing should be conservative. It is often clinicians who initially offer further diagnostic tests, even when patients
offer cues that the etiology is psychiatric [57,58].
History of present illness In taking a history, clinicians should pay attention to how the physical symptoms are related
to the patient's emotions and social situation, and if any stressful personal events such as losses have occurred. The
pattern of pain should be assessed. The clinician should determine what exacerbates or alleviates the symptoms, and
why the patient believes he or she is suffering. The patient may be convinced she has a specific disease, is seriously ill, or
is dying. Assess whether the patient can be reassured.
The patient should be asked about medications, including over-the-counter, prescription, and complementary medications.
Additionally, patients should be questioned about substance use, including alcohol.
It is important to ask whether the patient has experienced physical or sexual abuse, whether the patient feels safe in her
current relationships, and whether she feels threatened or afraid in any way, either at home or in other settings.

Past medical illness Some patterns of somatization are characterized by a longitudinal course beginning in childhood.
Patients may report that their parents were attentive only when they were sick.
Ask about a lifetime history of anxiety disorder, depressive disorder, or multiple unexplained symptoms. In addition, prior
treatment with psychotropic medications should be assessed.
It is important to examine past medical records. The past history should be sufficient to document whether there is a
pattern of suspected ailments, which were not confirmed pathologically, or a pattern of symptom preoccupation in different
organ systems. A history of multiple surgical procedures without pathologic confirmation of disease raises the likelihood of
somatization.
The patient may have a history of changing doctors frequently or leaving the hospital against medical advice. Ask about
compliance with a systematic evaluation of symptoms.
Family history The family history should be examined for a model of disability or somatization, and the presence of
depression or anxiety disorder.
Social history Consider the social context in which the physical symptoms appear, including likely stresses at the
patient's stage of development (eg, desire to have children or care for children, work pressures, grief). Financial
pressures, work, unemployment, disability history, history of arrests, time in prison, probation, and legal suits may provide
context for the symptoms.
Physical examination The physical examination should satisfy the clinician that the patient does not have a medical
disease. The examination provides a baseline for detecting change over time. Additionally, patients believe their
complaints are taken seriously when a physical examination is performed.
Clinicians should include a complete neurologic examination when they suspect the specific diagnosis of conversion
disorder. Although the rate of misdiagnosis of conversion disorder was 29 percent in the 1950s, studies since the 1970s
show that only 4 percent of patients diagnosed with conversion are subsequently found to have a documented medical
illness [59]. (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis", section on 'Neurologic
and general medical disorders'.)
Laboratory evaluation Laboratory testing should be judicious when evaluating current and new physical symptoms.
Often, extensive testing has previously been done to look for a diagnosis.
Diagnostic tests are often ordered for patients with a low pretest probability of serious disease to provide reassurance, as
well as to rule out illnesses [60]. However, studies indicate that testing does not reassure patients. A meta-analysis of
three open label randomized trials compared initial diagnostic testing (eg, cranial magnetic resonance imaging) with no
testing in 757 patients with a low probability of disease based upon the presenting symptoms (eg, headache) [61]. Illness
worry (concern that symptoms may represent serious illness) was comparable for both groups in the short term (3
months) and long term (>3 months); heterogeneity across studies was low. Additional analyses found that testing did not
reduce nonspecific anxiety or resolve symptoms, but did lead to a small decrease in the number of subsequent clinic
visits.
Psychologic testing (eg, the Minnesota Multiphasic Personality Inventory [62,63]) or neuropsychologic testing is helpful to
identify psychiatric illness such as depression for patients in whom there is diagnostic uncertainty following the clinical
interview. Additionally, psychologic testing can help assess the patient's strengths, decide which treatments are indicated,
and monitor the impact of treatment over time [64-67].
DIAGNOSIS Somatization encompasses many different illnesses, including disorders that were previously used in the
Diagnostic and Statistical Manual, Fourth Edition, Text Revision (DSM-IV-TR) [11], and continue to be used in the
International Classification of Diseases-10th Revision (ICD-10) [10] (table 1). However, the Diagnostic and Statistical
Manual, Fifth Edition (DSM-5) does not use the term somatization, and has eliminated some of the disorders described in
DSM-IV-TR and ICD-10. As an example, DSM-5 has abandoned the term somatoform disorders, as well as the specific
diagnoses of somatization disorder and hypochondriasis [12]. (See'Terminology and DSM-5' above.)

Naming the illness Clinicians should avoid the debate of whether symptoms are due to psychiatric or nonpsychiatric
illness. Directly challenging the patient's belief that symptoms are caused by a medical condition may unintentionally
undermine the relationship with the patient. It is more reasonable for clinicians to explain there is no evidence of a lifethreatening illness (which is presented as good news), but rather, the patient has a well-described, although not wellunderstood, condition which results in the set of symptoms [68].
Patients often feel better if they can have a name to describe a constellation of symptoms, but a specific psychiatric
diagnosis may serve no purpose, and may even be detrimental [69]. Patients diagnosed with a psychiatric illness can be
informed that their condition is most likely treatable, especially mood and anxiety disorders. Clinicians should
acknowledge the patient's physical and emotional suffering, emphasize that they regard the symptoms as real (eg, they
are not "in your head"), and should assure the patient that the presence of a psychiatric disturbance or disorder does not
negate the reality of his or her suffering [70]. This approach may facilitate the patient's acceptance of a formal psychiatric
intervention. Patients may nevertheless react defensively if clinicians raise the possibility that there is psychopathology
that needs to be addressed and treated.
Somatic symptom and related disorders In DSM-5, the category of somatic symptom and related disorders
encompasses disorders that are marked by prominent somatic symptoms as well as substantial
distress and/or psychosocial impairment [12]. The category includes the following specific disorders:
Somatic symptom disorder
Illness anxiety disorder
Conversion disorder (functional neurological symptom disorder)
Psychological factors affecting other medical conditions
Factitious disorder
Somatic symptom disorder A DSM-5 diagnosis of somatic symptom disorder requires each of the following criteria
[12]:
One or more somatic symptoms that cause distress or psychosocial impairment
Excessive thoughts, feelings, or behaviors associated with the somatic symptoms, as demonstrated by one or
more of the following:
Persistent thoughts about the seriousness of the symptoms
Persistent, severe anxiety about the symptoms or ones general health
The time and energy devoted to the symptoms or health concerns is excessive
Although the specific somatic symptom may change, the disorder is persistent (usually more than six months)
The diagnosis of somatic symptom disorder subsumes approximately 75 percent of patients previously diagnosed with
DSM-IV-TR hypochondriasis. The Somatic Symptom Scale-8 (table 3), an eight item, self report measure, may facilitate
diagnosis of somatic symptom disorder and quantify the burden of somatic symptoms [71,72]. A score of 0 to 3 indicates
no to minimal burden, 4 to 7 low burden, 8 to 11 medium burden, 12 to 15 a high burden, and a score of 16 to 32 indicates
a very high burden.
Illness anxiety disorder A DSM-5 diagnosis of illness anxiety disorder requires each of the following criteria [12]:
Preoccupation with having or acquiring a serious, undiagnosed illness
Somatic symptoms are mild or nonexistent at most
Substantial anxiety about health and a low threshold for becoming alarmed about ones health
Either excessive behaviors related to health (eg, repeatedly checking oneself for signs of illness), or maladaptive
avoidance of situations or activities (eg, exercise) that are thought to represent health threats
The illness preoccupation is present for at least six months
The illness preoccupation is not better explained by other mental disorders (eg, somatic symptom disorder,
generalized anxiety disorder, or somatic type of delusional disorder)

The diagnosis of illness anxiety disorder subsumes approximately 25 percent of patients previously diagnosed with DSMIV-TR hypochondriasis.
Conversion disorder Conversion disorder (functional neurologic symptom disorder) involves symptoms of altered
voluntary motor or sensory function that cause substantial distress or psychosocial impairment [12]. The diagnosis rests
upon positive clinical findings that indicate the symptom is incongruent with anatomy, physiology, or known diseases, or
the symptom is inconsistent at different times (eg, no ankle dorsiflexion while lying down, but the ability to stand on
tiptoes).
Conversion disorder is discussed separately. (See "Conversion disorder in adults: Terminology, diagnosis, and differential
diagnosis" and "Conversion disorder in adults: Clinical features, assessment, and comorbidity" and "Conversion disorder
in adults: Epidemiology, pathogenesis, and prognosis" and "Conversion disorder in adults: Treatment".)
Psychological factors affecting other medical disorders Psychological factors affecting other medical conditions is
a disorder that is diagnosed when a general medical condition is adversely affected by psychological or behavioral factors;
the factors may precipitate or exacerbate the medical condition, interfere with treatment, or contribute to morbidity and
mortality [12]. The clinical features, assessment, diagnosis, and management of psychological factors affecting other
medical conditions are discussed separately. (See "Psychological factors affecting other medical conditions: Clinical
features, assessment, and diagnosis" and "Psychological factors affecting other medical conditions: Management".)
Factitious disorder The essential feature of factitious disorder is intentionally faking symptoms in order to assume the
sick role, ie, to be a patient [12]. In addition, there are no obvious external benefits such as financial gain, or avoiding work
or criminal prosecution. Patients with factitious disorder tend to have some medical knowledge, and common
presentations include wound healing problems, excoriations, infection, bleeding, hypoglycemia, and gastrointestinal
ailments. An extreme presentation (Munchausen syndrome) occurs in a subgroup of patients who feign disease, move
from hospital to hospital, and submit to repeated procedures for an illness they have voluntarily manufactured [42,73,74].
A clue that patients are feigning includes varying accounts of symptoms to different clinicians. However, it is possible to
establish feigning only if the patient acknowledges deliberately producing symptoms, or if other evidence demonstrates a
major inconsistency between reported and observed function (eg, a patient who reports an inability to walk is
subsequently observed on a video recording playing tennis).
Additional information about factitious disorder is discussed separately. (See "Factitious disorder imposed on self
(Munchausen syndrome)".)
Somatoform disorders Somatoform disorders are a group of illnesses, each of which is marked by physical
symptoms that are not explained by a general medical condition [11]. The term somatoform disorders was used in DSMIV-TR [11] and continues to be used in ICD-10 [10] (table 1), but has been abandoned in DSM-5 because it is difficult to
prove that a symptom is medically unexplained [12]. (See 'Terminology and DSM-5' above.)
The somatoform disorders category includes the following diagnoses:
Somatization disorder (table 4)
Undifferentiated somatoform disorder (table 5)
Pain disorder (table 6)
Hypochondriasis (table 7) (see "Hypochondriasis: Epidemiology, clinical presentation, assessment, and diagnosis")
Primary care and other clinicians can screen for these somatoform disorders with a brief instrument such as the Primary
Care Evaluation of Mental Disorders Patient Health Questionnaire [75]. This instrument screens for and provides
categorical DSM-IV diagnoses for somatoform, depressive, anxiety, alcohol and eating disorders. It was specifically
designed for use in primary care, is fully self-administered by the patient, has good diagnostic validity (sensitivity 75
percent, specificity 90 percent), and the median physician time to review the results is one to two minutes (table 8).
In ICD-10, the somatoform disorders category emphasizes the repeated presentation of physical symptoms with
persistent requests for medical investigations, despite repeated negative findings and reassurances by clinicians that the

symptoms have no physical basis [10]. ICD-10 includes the diagnoses of somatization disorder, undifferentiated
somatoform disorder, pain disorder, and hypochondriasis, which were also included in DSM-IV-TR [11]. In addition, ICD-10
includes [10]:
Somatoform autonomic dysfunction The patient believes a physical disorder is causing symptoms that involve a
particular organ or system under autonomic control, ie, the cardiovascular, gastrointestinal, respiratory, or
genitourinary system. The diagnosis requires both symptoms that are based upon objective signs of autonomic
arousal (eg, palpitations, sweating, and tremor) and symptoms that are more subjective (eg, intermittent pain,
burning, heaviness, or tightness).
Other somatoform disorders This refers to symptoms that are not caused by a medical condition and are limited
to specific systems or parts of the body not controlled by the autonomic nervous system. Examples include
sensations of swelling, movements of the skin, and paresthesias.
Other proposed diagnoses Other disorders have been proposed for patients with prominent somatic symptoms, but
are not recognized by DSM-5 or ICD-10 [10,12]:
Abridged somatization disorder Defined as at least six lifetime, unexplained, physical symptoms in women, and
four in men [76]
Multisomatoform disorder Defined as three or more currently bothersome, medically unexplained physical
symptoms, which are present for at least two years [19]
Malingering The essential feature of malingering is intentionally faking or exaggerating symptoms for an obvious
external benefit (eg, money, housing, medications, or avoiding work or criminal prosecution) [12]. Malingering is a
behavior and not a psychiatric disorder.
Clinicians should consider the possibility of malingering if any of the following are present:
History notable for multiple inconsistencies and vague responses
Eagerly or dramatically describing symptoms
Conditional threats (eg, Ill kill myself if you dont admit me)
Inconsistency between the history and mental status examination (eg, patient appears calm and relaxed while
reporting symptoms that are distressing)
Marked discrepancy between the patient's claimed distress or disability and the objective findings (eg, emergency
department patient reports depression but is joking with the security staff, eating every meal, and sleeps throughout
the night)
Using technical medical terms (eg, I have command auditory hallucinations)
Demanding specific medications, such as benzodiazepines and opiates
Nonadherence with diagnostic evaluation or treatment
Antisocial personality disorder
Medical-legal context (eg, patient is referred by an attorney for evaluation)
It is possible to establish feigning only if the patient acknowledges deliberately producing symptoms, or if other evidence
demonstrates a major inconsistency between reported and observed function (eg, a patient who reports an inability to
walk is subsequently observed on a video recording playing tennis).
The motivation for intentionally producing symptoms in malingering is an external incentive, whereas in factitious disorder
the motivation is to assume the role of patient.
DIFFERENTIAL DIAGNOSIS The symptoms that occur in somatization occur in many other general medical and
psychiatric conditions. Somatization and these other conditions can occur together.
Depression Physical symptoms can occur in depressive disorders, and patients may have both somatization as well
as depression. However, diagnosis of major depression requires dysphoric mood or anhedonia, and persistent depressive
disorder (dysthymia) requires dysphoria. (See "Unipolar depression in adults: Assessment and diagnosis".)

Panic disorder Panic attacks are accompanied by a variety of somatic symptoms [12]. These include palpitations,
tachycardia, chest pain, sweating, tremulousness, shortness of breath, sensation of smothering, choking, abdominal
distress or nausea, diarrhea, dizziness, lightheadedness, feeling faint, paresthesia (numbness or tingling), chills, and
flushing. Panic attacks are characterized by discrete, episodic periods of fear during which four or more symptoms
develop abruptly and reach a peak within minutes (eg, 10 minutes). In somatization, the somatic symptoms and anxiety
are more persistent. (See "Panic disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and
diagnosis".)
Substance use disorder Physical symptoms can occur in substance intoxication and withdrawal as well as
somatization [54]. These include weakness, fatigue, headaches, nausea, chest pain, vomiting, ataxia, tremors, blurred
vision, and fasciculations. Substance use disorder is established by the history of using a substance. (See "Substance
use disorder: Principles for recognition and assessment in general medical care".)
Syndromes of unclear etiology Patients may have a variety of syndromes including fibromyalgia, chronic fatigue
syndrome, premenstrual dysphoric disorder, temporomandibular joint disorder, and idiopathic environmental intolerance
(multiple chemical sensitivity) that incorporate many unexplained symptoms. (See "Clinical manifestations and diagnosis
of fibromyalgia in adults" and "Clinical features and diagnosis of chronic fatigue syndrome (systemic exertion intolerance
disease)" and"Clinical manifestations and diagnosis of premenstrual syndrome and premenstrual dysphoric
disorder" and "Temporomandibular disorders in adults" and "Overview of idiopathic environmental intolerance (multiple
chemical sensitivity)".)
Nonpsychiatric medical conditions Somatization disorder (table 4) overlaps with many medical conditions. A
diagnosis of somatization disorder is more likely if symptoms involve multiple organ systems, and there is an early onset
and chronic course in the absence of physical signs, structural abnormalities, and laboratory abnormalities. Medical
conditions with vague symptoms and episodic or diffuse pain that may be confused with somatization disorder include
multiple sclerosis, systemic lupus erythematosus, acute intermittent porphyria, and hemochromatosis [27]. Oncologic
disorders often have clear symptoms due to the illness, but may also carry vague unexplained symptoms that can be
considered somatization [77].
SUMMARY
Somatization is a syndrome of physical symptoms that cause substantial distress or psychosocial impairment, and
in some instances, are not explained by a known general medical disease after appropriate investigation. The term
somatization is an overarching term that encompasses many different illnesses; the term is not used in the
Diagnostic and Statistical Manual, Fifth Edition (DSM-5). (See 'Terminology and DSM-5' above.)
Risk factors for somatization include female sex, fewer years of education, ethnic minority status, and low
socioeconomic status. (See 'Epidemiology' above.)
The essential feature of somatization is a history of physical symptoms that the patient attributes to a
nonpsychiatric disease [4,44]. The symptoms may be unexplained. Somatizing patients may present with almost any
symptom that occurs in patients with a nonpsychiatric disorder. (See 'Clinical presentation' above.)
Somatization should be suspected in cases where the patient is preoccupied with symptoms, the history is vague
or inconsistent, there is a lack of exacerbating or alleviating physical factors, and symptoms are not related to
findings on the physical examination. (See 'Clinical presentation' above.)
Patients with somatization sometimes have comorbid depressive, anxiety, and personality disorders.
(See 'Coexisting psychiatric disorders' above.)
Patients with prominent somatic symptoms should receive a history and physical examination. Ancillary laboratory
testing should be judicious, and ordered only when specific diagnoses are suspected. (See 'General medical
evaluation' above.)
Clinicians should avoid the debate of whether somatization is a psychiatric or nonpsychiatric illness, assure the
patient there is no evidence of a life-threatening illness, emphasize the symptoms are real but are not well
understood, and assure the patient that the presence of a psychiatric disturbance or disorder does not negate the
reality of his or her suffering. (See 'Naming the illness' above.)

Somatization is an overarching term that encompasses many different illnesses described in DSM-5 and its
previous edition, as well as ICD-10 (table 1). DSM-5 disorders include somatic symptom disorder, illness anxiety
disorder, conversions disorder, psychological factors affecting other medical conditions, and factitious disorder.
(See 'Somatic symptom and related disorders' above.)
The differential diagnosis of somatization includes depression, panic disorder, and substance use disorder. Medical
conditions that may be confused with somatization disorder include multiple sclerosis, systemic lupus
erythematosus, acute intermittent porphyria, and hemochromatosis. (See 'Differential Diagnosis'above.)
Use of UpToDate is subject to the Subscription and License Agreement.

Somatization: Treatment and prognosis

Author
Donna B Greenberg, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Donna B Greenberg, MD Nothing to disclose. Joel Dimsdale, MD Nothing to disclose. David Solomon, MD Nothing to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multilevel review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: May 18, 2015.
INTRODUCTION Somatization is a syndrome of nonspecific physical symptoms that are distressing and may not be
fully explained by a known medical condition after appropriate investigation. This syndrome has also been called
"medically unexplained symptoms," "medically unexplained physical symptoms," "functional somatic symptoms," and
"somatic symptom disorders." The symptoms are associated with distress and may be caused or exacerbated by anxiety,
depression, and interpersonal conflicts [1-4]. Somatization can be conscious or unconscious and may be influenced by a
desire for the sick role or for personal gain [1].
Somatization often occurs in primary care patients [5]. It increases use of medical services independent of any
accompanying psychiatric or nonpsychiatric disorder, and leads to frustration in both the patient and the clinician [4,6-9].
This topic reviews the treatment and prognosis of somatization. The epidemiology, pathogenesis, clinical features, and
medical evaluation of somatization; diagnosis of specific disorders; and the treatment and prognosis of hypochondriasis
and conversion disorder are discussed separately. (See "Somatization: Epidemiology, pathogenesis, clinical features,
medical evaluation, and diagnosis" and "Hypochondriasis: Treatment and prognosis" and "Conversion disorder in adults:
Treatment".)
TERMINOLOGY AND DSM-5 The term "somatization" as used in this topic refers to a syndrome consisting of physical
symptoms that cause substantial distress and psychosocial impairment, and in some instances, are not explained by a
known general medical disease. The syndrome has also been referred to as medically unexplained symptoms and
functional somatic symptoms. Somatization can be viewed as a dimensional syndrome with a spectrum of expression
ranging from the exaggeration of common symptoms to unrelenting disabling symptoms [10]. The same principles of
management apply to patients across the spectrum.
Somatization is an overarching term that encompasses many different illnesses and terms including somatoform
disorders, which is a group of disorders that are recognized in the World Health Organization's International Classification
of Diseases-10th Revision (ICD-10) [11], and were previously described in the American Psychiatric Association's

Diagnostic and Statistical Manual, Fourth Edition, Text Revision (DSM-IV-TR) (table 1) [12]. (See "Somatization:
Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis", section on 'Somatoform disorders'.)
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) does not use the term somatization, and
has eliminated the category of diagnoses called somatoform disorders. DSM-IV-TR described somatoform disorders as
illnesses with physical symptoms that were not explained by a general medical condition [12]. Psychiatric nosology has
evolved such that in DSM-5, the centrality or prominence of medically unexplained symptoms has been deemphasized,
because it is difficult to prove that a symptom is not caused by a general medical disorder [13]. Many of the somatoform
diagnoses lacked validity, due to insufficient evidence for a discrete, characteristic cluster of symptoms and a predictable
longitudinal course of illness [14,15]. In addition, the criteria or cut-off points used to distinguish cases often appeared
arbitrary [14].
For patients with prominent somatic symptoms that cause distress and impair psychosocial functioning, DSM-5 has
replaced the category of somatoform disorders with a category called somatic symptom and related disorders [13]. The
somatic symptom and related disorders include the following specific diagnoses:
Somatic symptom disorder
Illness anxiety disorder
Conversion disorder (functional neurological symptom disorder)
Psychological factors affecting other medical conditions
Factitious disorder
The somatic symptom and related disorders are discussed separately. (See "Somatization: Epidemiology, pathogenesis,
clinical features, medical evaluation, and diagnosis", section on 'Somatic symptom and related disorders'.)
TREATMENT Psychotherapy and pharmacotherapy are each beneficial for patients with somatization. These
treatments may also be combined, but there are no data to suggest which particular patients should receive both
treatments. The choice of treatment depends upon availability and preferences, and the different options can be
presented to the patient over time to help overcome resistance to treatment.
Clinicians should set a goal with patients to improve occupational and interpersonal functioning. Physical symptoms
should be treated conservatively. Symptom relief, rather than elimination, should be set as a goal in order to avoid
excessive and possibly harmful treatment.
Major depression or panic disorder are commonly comorbid in patients with somatization and should be treated with
persistence. Somatization frequently resolves when the comorbid disorder is treated with appropriate pharmacotherapy
[16]. (See "Generalized anxiety disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and
diagnosis" and "Unipolar major depression in adults: Choosing initial treatment" and "Serotonin-norepinephrine reuptake
inhibitors (SNRIs): Pharmacology, administration, and side effects" and "Pharmacotherapy for panic disorder".)
General principles We suggest clinicians use the following general principles to manage patients with somatization,
based upon clinical experience [1-3]:
Schedule regular visits
Establish a collaborative, therapeutic alliance with the patient
Acknowledge and legitimize symptoms
Communicate with other clinicians
Evaluate for and treat diagnosable medical disease
Limit diagnostic testing and referrals to specialists
Reassure that grave medical diseases have been ruled out
Assess and treat the patient for psychiatric disorders
Educate patients about coping with physical symptoms
Explicitly set the goal of treatment as functional improvement

Evaluate and treat substance abuse and addiction

A key part of management is to regularly schedule outpatient visits with the primary care clinician, so that symptoms are
not required for the patient to receive clinical attention [17]. This is less stressful for the patient and clinician than
symptom-driven visits, avoids reinforcing the sick role, and enables the clinician to provide reassurance on the basis of
focal physical examinations and to remain vigilant for the same diseases that can befall any patient. The visit interval
depends upon the individual patient. The goal is to find the right interval that avoids inappropriate emergency visits or
telephone calls. It is reasonable to initially try monthly visits. Patients should be discouraged from going to the emergency
department before consulting with their primary clinician since this often leads to a litany of unnecessary and costly tests.
Crises must be managed firmly so that the multiple chronic or recurrent symptoms do not elicit excessive evaluation. The
clinician must be supportive but firm, and adhere to the agreed upon schedule of visits for recurrent problems.
Clinicians should emphasize functioning and coping [2]. The focus of treatment should be the restoration and
maintenance of functioning at work, home and in social circles through rehabilitation. Clinicians should encourage patients
to take an active role in treatment by working on specific, realistic, incremental goals that include observable behaviors.
This will help to discourage patients from assuming the sick role. One example of a useful treatment plan is a graduated
exercise program.
Specific treatment recommendations depend upon the extent of the patient's illness belief and degree of impairment.
Some patients will be interested only in specific treatment for a specified disorder or symptom management, such as
antidepressant medication. Other patients may be receptive to entering a formal behavior modification program to improve
their social and occupational functioning.
It is common for patients with somatization to consult one doctor after another ("doctor shopping"). Thus, communication
among clinicians is vital.
When malingering is suspected (ie, somatization in order to pursue a tangible benefit such as Workers Compensation in
the United States), it is important to understand the motivations for symptom production to manage these patients. We
suggest confronting the individual in a manner that allows him or her to save face. As an example, the clinician may state,
"Your symptoms are not consistent with a known illness and I wonder if there is another reason for them" [18].
To engage the patient in treatment, metaphors can be helpful [17]. The symptoms, which are not amenable to medical or
surgical intervention, can be compared to a radio channel that cannot be changed. The patient needs to gain greater
control over the volume knob and the sensitivity of the antenna (ie, factors that increase or decrease symptoms).
Not all patients are ready for treatment. Clinicians may find that some patients adamantly believe their symptoms are
caused by a nonpsychiatric medical condition and refuse to work with clinicians who do not confirm this belief. We suggest
clinicians take a long-term perspective and let such patients know that the clinician is always available to provide
treatment when the patient is ready.
Structure of visits Caring for patients with somatization requires time to listen to the patients. This should occur at
regularly scheduled office visits not contingent upon complaint, so that patients can voice concerns without feeling the
need to make telephone calls or emergency visits.
New symptoms and current stressors should be explored at these visits. Familiarity with the patient allows judicious
evaluation of new symptoms. It is important to remember that the patient with somatization, as with all patients, remains at
risk for developing new and potentially serious medical conditions. After treatable medical conditions are excluded,
clinicians can express empathy for the patient's predicament, and shift the focus away from the physical symptoms and
toward the social situation in which new symptoms occur.
A physical examination should be performed at each visit, at least in the initial period of patient management [4]. It may be
tempting to use diagnostic tests and specialty consultations for the sole purpose of reassuring the patient; however,
procedures may cause additional complications and negative findings rarely provide lasting reassurance [6]. A study of
420 audiotaped general practice consultations with patients with unexplained symptoms revealed that doctors were more
likely to propose physical interventions than respond to patient cues about psychological needs [7].

Pharmacotherapy Systematic reviews of controlled trials support the use of antidepressant medication to treat
somatoform disorders and medically unexplained symptoms [8,9]. A meta-analysis of 94 controlled trials of
antidepressants found a large benefit for treating unexplained symptoms and symptom syndromes [19]:
Improvement in patients occurred more than three times as often with antidepressants compared with placebo (OR
3.4, 95% CI 2.6-4.5).
Treatment of approximately three patients with antidepressants yielded a beneficial response in one additional
patient that would not have occurred with placebo (number needed to treat of three).
The meta-analysis found tricyclic antidepressants were beneficial in treating somatization in significantly more studies
compared with selective serotonin reuptake inhibitors (76 versus 47 percent of studies), but there was an insufficient
number of trials of selective serotonin reuptake inhibitors to draw a firm conclusion about the relative efficacy of the two
classes of antidepressants. In addition, 50 of the 94 trials involved patients with chronic headache, and tricyclics are
beneficial for these patients (see "Overview of chronic daily headache", section on 'Treatment' and "Chronic migraine",
section on 'Management').
Selective serotonin reuptake inhibitors are beneficial for treating the specific somatoform disorders hypochondriasis and
body dysmorphic disorder [20]. (See"Hypochondriasis: Treatment and prognosis", section on 'Pharmacotherapy'.)
St. John's wort has been shown to be efficacious for treating somatoform disorders independent of any existing
depression, and also well tolerated and safe. Use of St. John's wort is discussed separately. (See "Clinical use of St.
John's wort", section on 'Somatoform disorders'.)
Psychotropic agents should be initiated at low doses in patients with somatization and increased slowly as tolerated to
achieve a therapeutic dose. A typical antidepressant regimen should start with fluoxetine 20 mg per day or another
selective serotonin reuptake inhibitor in the morning, titrating the dose every four weeks as needed and tolerated, in order
to minimize side effects. These side effects may become another source of complaint. Alternatively, it is reasonable to
start withnortriptyline, desipramine, imipramine, or amitriptyline 25 mg at bedtime, titrating the dose up every four weeks
as needed and tolerated. One report suggests that adding a low dose antipsychotic may be beneficial [21]. (See "Unipolar
major depression in adults: Choosing initial treatment" and "Serotonin-norepinephrine reuptake inhibitors (SNRIs):
Pharmacology, administration, and side effects" and "Tricyclic and tetracyclic drugs: Pharmacology, administration, and
side effects".)
Some patients with somatization may resist taking "chemicals" to treat their psychiatric disorders and others will report
intolerance to relatively low levels of medication.Nortriptyline, desipramine, imipramine, amitriptyline, and fluoxetine are
available as a 10 mg pill for patients vulnerable to side effects.
Symptoms of somatization, depression, and anxiety should be reassessed regularly, to evaluate the response to
medication and adjust the dose as needed. Clinicians should also monitor compliance with medication.
Pain Clinicians should avoid opioid analgesics or other potentially addictive medications as much as possible.
A meta-analysis of 11 randomized trials treating patients with somatoform pain disorder and psychogenic pain found
antidepressants decreased pain intensity significantly more compared with placebo, and the clinical effect size was
moderate [22]. A second meta-analysis of 39 randomized trials found antidepressants were efficacious in treating chronic
nonmalignant pain, with a moderate to large clinical effect [23].
Antidepressants that act upon both noradrenergic and serotonergic receptors, such as tricyclics and serotoninnorepinephrine reuptake inhibitors, may have more analgesic effects than other antidepressants [23-27].
Patients with chronic pain and depression benefit from any form of depression treatment. An observational study found
that individuals with chronic pain and depression who received any depression treatment were significantly less likely to
report that pain interfered with their work compared to those who received no treatment (OR 0.57, 95% CI 0.34-0.96) [28].
The treatment of chronic pain due to a general medical condition is discussed separately. (See "Overview of the treatment
of chronic pain".)

Psychotherapy Clinicians should consider psychotherapy to treat somatization, especially cognitive behavioral
therapy [29-37]. Other psychotherapies include family therapy, psychoeducation, supportive therapy, stress management,
and psychodynamic psychotherapy. These can all be provided individually or in a group format, and may be provided in a
primary care or psychiatric setting.
Guidelines for short-term treatment of patients with somatization include [38]:
Clearly explain the structure of the treatment plan
Teach meaningful skills relevant to daily life
Training in these skills should continue until they are mastered in the therapist's office
Patients need to practice these skills outside of the office
Clinicians should attribute improvement to the patient's increased skills
Evidence supporting the use of psychotherapy includes a meta-analysis of 10 randomized trials and 6 observational
studies that compared psychotherapy (primarily cognitive behavioral therapy or psychodynamic therapy) with treatment as
usual, in 1438 patients with somatization (somatoform disorders) [39]. The mean length of physical symptoms was >8
years, and the median length of treatment for both groups was nine weeks. Improvement of physical symptoms and
functioning was superior with psychotherapy than treatment as usual, whereas improvement of psychological symptoms
(eg, depression and anxiety) was comparable for the two groups.
The use of psychotherapy to treat hypochondriasis is discussed separately. (See "Hypochondriasis: Treatment and
prognosis", section on 'Psychotherapy'.)
Cognitive behavioral therapy Clinicians should consider cognitive behavioral therapy (CBT) to treat somatization
because the evidence supporting CBT is stronger than it is for any other psychotherapy.
Systematic reviews consistently find CBT is efficacious for treatment of somatoform disorders and medically unexplained
symptoms [8,9]. In a review of 13 controlled CBT trials for treatment of somatoform disorders, CBT was beneficial in 85
percent of the trials [8]. In a second review of 31 controlled trials of CBT, physical symptoms appeared to be more
responsive to therapy than did psychologic distress and functioning [40]. The median number of treatment sessions was
eight, and benefits achieved by the end of treatment persisted for up to 24 months. Group CBT was as efficacious as
individual CBT. A subsequent 10 week randomized trial compared CBT with usual care in 152 patients with medically
unexplained physical symptoms; improvement was greater with CBT and the benefits were sustained at the 12 month
follow-up assessment [41].
CBT directs patients to reexamine their health beliefs and expectations, and to look at how the sick role affects their
symptoms [2]. Behavioral techniques are used to improve role functioning and minimize sick role behaviors. These
techniques include response prevention, systematic desensitization, progressive muscle relaxation, cognitive
restructuring, and graduated exercise programs. A practical guide for providing CBT is shown (table 2) [3,42].
Primary care providers have successfully provided CBT to patients with somatization. In one study, patients were
randomly assigned to group CBT or a control group waiting list, and general practitioners administered eight weekly
sessions of CBT [43]. Each three-hour session consisted of an educational lesson explaining stress and coping, followed
by a general discussion and then relaxation training. Patients who received CBT showed significantly more improvement
than controls six months post treatment in the perception of their illness, somatic preoccupation, hypochondriasis, and use
of medications. There were no significant differences in depression, anxiety, sleep quality, or perception of social
problems.
The use of CBT is limited when a patient is unable to rationally discuss cognitive distortions [36].
(See "Overview of psychotherapies", section on 'Cognitive and behavioral therapies'.)
Relaxation training Relaxation training may be useful for somatization. A randomized trial compared relaxation
training (three sessions that included progressive muscle relaxation and diaphragmatic breathing) with CBT (three
sessions; patients not responsive to three sessions received six additional sessions) in 89 patients with somatization [44].

Treatments were administered by primary care physicians. Both treatment groups improved from baseline, and follow-up
at 6 and 12 months showed that improvement was comparable for relaxation training and CBT.
Family therapy There are several reasons to involve family members in treatment. Family members can help
clinicians better understand the patient's symptoms and social structure. In addition, genuine concern leads family
members to unintentionally reinforce the patient's problematic behaviors. Difficulties with specific family functions and
processes such as communication and problem solving may also exacerbate the patient's illness. Family members may
be struggling to cope with the patient's illness and may require help for themselves.
Family therapy has not been studied in a systematic fashion for the treatment of somatization.
(See "Overview of psychotherapies", section on 'Family therapy'.)
Psychoeducation Education is effective for treating patients. In one study, primary care clinicians treating 70 patients
with somatization disorder all received a consultation letter offering treatment recommendations [45]. Patients were
randomly assigned to receive eight group therapy sessions focused on education or to treatment as usual. The
experimental group reported significantly better physical and mental health, and generated 52 percent less healthcare
costs over a one-year period. (See 'Psychiatric referral' below and "Overview of psychotherapies".)
Psychiatric referral Primary care clinicians suspecting somatization should consider sending their patients to a
psychiatrist for a one-time consultation. A systematic review of six randomized trials (449 patients with somatization)
compared a consultation letter (from a psychiatrist to the primary care clinician) with treatment as usual, and found that
the letter reduced the severity of symptoms, improved physical and social functioning, and reduced medical costs [46].
For patients diagnosed with somatization or a specific somatoform disorder, the consultation letter describes the diagnosis
and prognosis, and makes the following recommendations for management:
Tell patients that their symptoms are taken seriously
Avoid describing symptoms as entirely psychogenic (all in your head)
Avoid further referrals and laboratory tests unless there is a clear indication of a general medical disorder
Schedule regular visits
Perform a physical exam at each visit
Thus, the primary care clinician remains the responsible caregiver, and the psychiatrist's advice reduces diagnostic
uncertainty and potentially harmful procedures and interventions.
Primary care clinicians may decide to refer patients with somatization to a mental health clinician for other reasons. A
mental health specialist can help establish the diagnosis of a comorbid depressive and anxiety disorder. In addition, most
primary care clinicians do not have the time or training to provide specific treatments such as cognitive behavioral therapy
or family therapy.
Some patients will resist a psychiatric referral. The clinician should offer the referral in such a way that the patient does
not feel stigmatized or dismissed. The patient's willingness to accept a psychiatric referral will likely depend upon the
patient's conviction that the referring clinician will not abandon him or her.
Other interventions Systematic reviews of controlled trials for treatment of somatoform disorders and medically
unexplained symptoms have found evidence to support using other interventions [8,9]. These include training primary care
clinicians to manage somatizing patients and using a nurse care intervention.
In addition, a controlled trial compared aerobic exercise versus stretching for primary care patients with somatization, and
found both were helpful [47]. Each intervention included 20 group sessions, each session lasting one hour. Both forms of
exercise led to a significant reduction in the number of physical symptoms, clinician visits, and medication prescriptions at
six-month follow-up, compared with baseline.
PROGNOSIS The course of illness in patients with the specific types of somatization described in DSM-IV-TR and ICD10 are often chronic [13,48]. However, effective treatment of depressive or anxiety disorders makes a difference. Even
when the course is chronic, it is possible for clinicians to develop and maintain relationships with patients, and help them

to improve their psychosocial functioning and rely less upon diagnostic tests, medications, consults, and treatment by
medical specialists.
Some patients with somatization improve over the short-term [49]. A systematic review of medically unexplained
symptoms found that 50 to 75 percent of patients improved or even recovered during follow-up lasting 6 to 15 months
[50]. A subsequent study of 32 primary care patients with somatization defined as three or more bothersome, medically
unexplained symptoms found that after five years, 78 percent no longer met criteria for the condition, although it is not
clear how many still had one or two bothersome symptoms [51].
DSM-IV-TR and ICD-10 describe the specific diagnoses of hypochondriasis and somatization disorder as chronic but
fluctuating conditions that remit only occasionally [13,48]. Systematic reviews have found that improvement and even
remission from hypochondriasis and somatization disorder does occur in short-term studies [14,50]. One review found that
between 33 to 85 percent of patients with hypochondriasis no longer met criteria for the disorder in studies that mostly
lasted approximately one year or less. In another review, more than 50 percent of patients with somatization disorder no
longer met criteria over a one-year period. However, it's important to note that simply because a patient no longer meets
criteria for these disorders, that does not mean all symptoms have completely and permanently resolved. In addition,
patients may well again meet criteria for the disorder at a subsequent time point. It is also important to note that the
diagnostic terms hypochondriasis and somatization disorder have been abandoned in DSM-5 [13]. Many of the patients
previously diagnosed with hypochondriasis or somatization disorder would now be classified as somatic symptom disorder
or illness anxiety disorder. (See 'Terminology and DSM-5' above and "Somatization: Epidemiology, pathogenesis, clinical
features, medical evaluation, and diagnosis", section on 'Diagnosis'.)
Conversion disorder can also be chronic; the prognosis of conversion disorder is discussed separately. (See "Conversion
disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Prognosis'.)
A few prognostic factors have consistently been identified across different studies. Two systematic reviews both found
improvement in somatization was more likely in patients with fewer physical symptoms and better functioning at baseline
[14,50]. These predictors are nonspecific and similar to the factors that predict improvement of other psychiatric disorders.
The reviews found other nonspecific factors associated with improvement of somatization included less pain, anxiety, and
depression at baseline.
There are no data on the rate of recurrence among patients who recover from somatization. It is our experience that even
when symptoms improve or even remit, other symptoms may arise.
SUMMARY AND RECOMMENDATIONS
Somatization is a syndrome of physical symptoms that cause substantial distress or psychosocial impairment, and
in some instances, are not explained by a known general medical disease after appropriate investigation. The term
somatization is an overarching term that encompasses many different illnesses; the term is not used in the
Diagnostic and Statistical Manual, Fifth Edition (DSM-5). (See 'Terminology and DSM-5' above.)
Principles for managing somatization, based upon clinical experience, include scheduling regular visits,
acknowledging symptoms, communicating with other clinicians, assessing and treating diagnosable medical and
psychiatric disorders, limiting tests and referrals, reassuring the patient that grave medical diseases have been ruled
out, and making functional improvement the goal of treatment. (See 'General principles' above.)
Patients with somatization often have comorbid depressive and anxiety disorders. Somatization frequently resolves
when these psychiatric syndromes are appropriately treated. (See 'General principles' above.)
Pharmacotherapy and psychotherapy are each beneficial, and there is no evidence to indicate one is better than
the other. The choice of treatment, including the combination of pharmacotherapy and psychotherapy, depends upon
availability and preferences. (See 'Treatment' above.)
When pharmacotherapy is selected for the treatment of somatoform disorders, we suggest initial treatment
with fluoxetine 20 mg per day or another selective serotonin reuptake inhibitor in the morning, titrating the dose
every four weeks as needed and tolerated (Grade 2B). Alternatively, it is reasonable to start with a tricyclic

antidepressant such as nortriptyline, desipramine, imipramine, or amitriptyline 25 mg at bedtime, titrating the dose up
every four weeks as needed and tolerated. (See 'Pharmacotherapy' above.)
For treatment of somatoform pain disorder, we suggest antidepressants with both a noradrenergic and serotonergic
profile (Grade 2C). We also suggest clinicians avoid opioids (see 'Pain' above).
For patients in whom psychotherapy is selected for the treatment of somatoform disorders, we suggest cognitive
behavioral therapy (Grade 2B). A practical guide for providing CBT is shown (table 2). (See 'Psychotherapy' above.)
We suggest a one-time psychiatric referral as an effective intervention for patients with somatization (Grade 2B).
The referral can clarify the diagnosis and its nonlethal nature, and make specific recommendations for management,
such as limiting tests. (See 'Psychiatric referral' above.)
Somatization follows a chronic and fluctuating course. Short-term studies show that 50 percent or more of patients
improve and no longer meet criteria for a specific type of disorder, but this is not the same thing as complete and
permanent resolution of all medically unexplained symptoms. (See 'Prognosis' above.)
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Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis

Authors
Jon Stone, FRCP, PhD
Michael Sharpe, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Jon Stone, FRCP, PhD Nothing to disclose. Michael Sharpe, MD Nothing to disclose. Joel Dimsdale, MD Nothing to
disclose. David Solomon, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multilevel review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Feb 04, 2015.
INTRODUCTION Conversion disorder (functional neurologic symptom disorder) is characterized by neurologic
symptoms (eg, weakness, abnormal movements, or nonepileptic seizures) that are inconsistent with a neurologic disease,
but nevertheless cause distress and/or psychosocial impairment [1]. The disorder is common in clinical settings and often
has a poor prognosis [2-5].
This topic reviews the terminology, diagnosis, and differential diagnosis of conversion disorder. The epidemiology,
pathogenesis, prognosis, clinical features, assessment, and treatment are discussed separately, as are specific subtypes
of conversion disorder (psychogenic nonepileptic seizures and psychogenic movement disorders):
(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis".)
(See "Conversion disorder in adults: Clinical features, assessment, and comorbidity".)
(See "Conversion disorder in adults: Treatment".)
(See "Psychogenic nonepileptic seizures".)
(See "Functional movement disorders".)
TERMINOLOGY Many terms are used to describe neurologic symptoms or syndromes in the absence of disease
pathology, including [6,7]:
Conversion disorder (consistent with DSM-5 [1]), somatization, somatoform, or psychogenic, meaning that
the symptoms are psychological and possibly caused by a remote or recent stressor. These terms are consistent
with referral to psychiatric services, but they introduce etiologic assumptions that often cannot often be proven; as an
example, the term conversion disorder is based upon the unproven psychoanalytic hypothesis that overwhelming
affect, psychological conflict, or stress are unconsciously converted into symptoms that suggest a neurologic
disorder [8]. In addition, terms such as psychogenic may also connote faking or crazy behavior and thus alienate
patients [9].
Functional (also consistent with DSM-5 [1]), meaning that the symptoms arise from abnormal nervous system
functioning in the absence of structural pathology (eg, functional weakness). This term is etiologically neutral and
usually acceptable to patients [10,11]. However, it may seem vague and does not indicate that psychosocial factors
may be important.
Dissociative (motor, sensory, or seizure) disorder (consistent with ICD-10 [12]), meaning sensation or control of
movement is separated from awareness. The term is particularly useful to describe the trance-like state seen in
nonepileptic seizures, but also implies that patients are suffering depersonalization or derealization (which is
frequently not true).

Medically unexplained, meaning that the etiology is unknown. The term is neutral and accurate, but may imply
that the clinician does not know what is wrong and is incapable of rendering a diagnosis and treatment [11]. In
addition, it is difficult to prove that a symptom cannot be medically unexplained [1].
Psychosomatic, meaning that the symptom is due to the interaction between the mind and body. However, this
term is often interpreted to mean the same thing as somatization or psychogenic.
Nonorganic or pseudoneurologic, meaning that the patient does not have a disease with a known pathologic
basis. The terms emphasize what patients do not have rather than what is present, and ignore the central nervous
system underpinning of psychological phenomena.
Hysteria, which originally meant that symptoms were due to uterine pathology and implied that the disorder was
exclusive to females. More recent definitions include emotional excess, overwhelming fear, and psychiatric
symptoms involving disturbances of mental, sensory, vasomotor, and visceral functions. This term is generally
considered a historic artifact.
DIAGNOSIS In patients with neurologic symptoms (eg, abnormal movements or seizures) that are not caused by
neurologic disease, the diagnosis of conversion disorder (functional neurologic symptom disorder) should be made after
the neurologist has established positive clinical findings that are incompatible with disease or are inconsistent across
different parts of the examination [7,10]. In addition, clinicians and researchers frequently diagnose conversion disorder
subtypes such aspsychogenic/functional movement disorders or psychogenic nonepileptic seizures.
Prior to 2013, conversion disorder could be diagnosed according to the criteria in either the American Psychiatric
Associations Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) [13], or
the World Health Organization's International Classification of Diseases-10th Revision (ICD-10) [12]. However, neither
nosologic system was widely used in its entirety because many patients did not fulfill all of the criteria [10]. In particular,
both nosologies stipulated that conversion symptoms were associated with or caused by psychologic factors. For many
patients, psychologic factors are not identifiable, and even when they are identified, its not always clear that they are
etiologically relevant [10].
In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the diagnosis of conversion disorder
does not require that clinicians identify psychological factors associated with the conversion symptoms [1]. (Nevertheless,
clinicians should continue to look for psychological factors where relevant.) In addition, clinicians no longer need to
establish that the symptom is not feigned; by contrast, DSM-IV-TR required that the symptom was not intentionally
produced [13]. DSM-5 classifies conversion disorder among the somatic symptom and related disorders, which are
marked by somatic symptoms that are associated with distress and psychosocial impairment.
Diagnostic and Statistical Manual, Fifth Edition (DSM-5) A DSM-5 diagnosis of conversion disorder requires each of
the following criteria (table 1) [1]:
One or more symptoms of altered voluntary motor or sensory function
Clinical findings that demonstrate incompatibility between the symptom and recognized neurologic or general
medical conditions (eg, Hoover's sign of functional limb weakness or a positive entrainment test for functional
tremor)
The symptom or deficit is not better explained by another medical or mental disorder
The symptom or deficit causes significant distress, psychosocial impairment, or warrants medical evaluation
The diagnosis rests upon positive clinical findings that indicate the symptom is incongruent with anatomy, physiology, or
known diseases, or is inconsistent at different times (eg, a paralyzed limb will move inadvertently when the patient is
distracted by performing movements in their unaffected limb) [1].
DSM-5 describes several subtypes of conversion disorder that are based upon the presenting symptom or deficit [1]:
Seizures or attacks These events are also called psychogenic nonepileptic seizures, and are marked by
abnormal generalized limb shaking and apparent impaired or loss of consciousness resembling epileptic attacks or
fainting (syncope) (see "Psychogenic nonepileptic seizures")
Weakness or paralysis

Abnormal movement Includes dystonic movement, gait disorder, myoclonus, and tremor (see "Functional
movement disorders")
Anesthesia or sensory loss Includes symptoms such as loss of touch or pain sensation
Special sensory symptom Includes visual (eg, double vision, blindness, or tubular visual field [tunnel vision]),
hearing (eg, deafness), or olfactory disturbance
Swallowing symptom This symptom is also called globus sensation or globus pharyngeus and is characterized by
the sensation of a lump in the throat (see"Globus sensation")
Speech symptom Includes dysphonia and slurred speech
Mixed symptoms Two or three different subtypes of symptoms are present (eg, paralysis plus blindness)
More common conversion disorder subtypes include nonepileptic attacks, sensory loss, weakness and paralysis, and
abnormal movement [14].
Conversion disorder should not be diagnosed primarily because the patient has a history of other psychiatric disorders
(eg, major depression or a personality disorder) or because laboratory tests are normal [1,7]. Clinicians must ensure that
the symptoms are not better explained by a neurologic or other general medical disease, and should bear in mind that our
knowledge of neurologic disease, anatomy, and physiology is incomplete. Neurologic and general medical disorders that
are included in the differential diagnosis are discussed separately. (See 'Neurologic and general medical
disorders' below.)
However, conversion disorder can be diagnosed in patients who have comorbid neurologic diseases, provided there is
evidence that the diseases do not better explain the conversion symptoms. (See "Conversion disorder in adults: Clinical
features, assessment, and comorbidity", section on 'Neurologic and general medical disorders'.)
In diagnosing conversion disorder, it is not necessary to identify conflicts or other stressors associated with conversion
symptoms (although doing so may help patient management) [1,10,15,16]. Psychological factors are frequently observed
in patients with conversion symptoms, but this is not always the case. In addition, when psychological factors are present,
it is difficult to establish the etiologic relationship between these factors and conversion disorder because psychological
factors are ubiquitous [1,10]. Trauma, conflicts, and stressors may have a specific etiologic relationship with conversion
disorder, a nonspecific relationship (ie, psychologic factors may contribute to onset of psychiatric disorders in general), or
the presence of psychological factors may be coincidental. However, a close temporal relationship between a stressor and
onset or worsening of conversion symptoms may aid diagnosis (eg, hand dystonia after signing an unwelcome
document [15]), especially if there is a prior history of conversion symptoms under similar circumstances [1]. Additional
information about premorbid clinical factors and the etiology of conversion disorder is discussed separately.
(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Premorbid clinical factors'.)
The diagnosis of conversion disorder does not require clinicians to establish that the symptom is not intentionally
produced [1,10,15-17]. However, there is evidence that suggests most patients with conversion disorder are not feigning,
including the consistency among different patients in how they report their symptoms, the common pattern of comorbidity
and physical evidence (eg, abnormal shoe wear, disuse atrophy, and contractures) across patients, and the distress and
disability that is observed in follow up studies [7]. It is also worth noting that awareness of what is happening may not be
all or nothing; rather, there may be gradations of awareness along a continuum, and the patients level of awareness
may change over time [6,7].
Exposure to a common precipitant may lead to shared conversion symptoms in a group of people (mass hysteria) [1820]. Conversion disorder is diagnosed only in those individuals manifesting significant distress or impairment.
International Classification of Diseases - 10th Revision (ICD-10) As stated above (see 'Diagnosis' above), the ICD10 criteria are often not used in their entirety because many patients with the disorder do not fulfill all of the criteria [10],
particularly the criterion that stipulates conversion symptoms are caused by psychological factors.
The ICD-10 classifies conversion disorder among the dissociative disorders, which are characterized by disruption of
awareness, memory, identity, sensations, and control of body movements [12]. Diagnostic equivalents to conversion
disorder within ICD10 include:

Dissociative motor disorders

Dissociative anaesthesia and sensory loss
Dissociative convulsions
Mixed dissociative disorders
Dissociation in this context often includes a feeling of disconnection from ones own body (depersonalization) or from
ones environment (derealization) [7].
Diagnosis of ICD10 conversion disorder equivalents requires each of the following criteria [12]:
Symptoms suggesting the specific dissociative disorder (motor, sensory, convulsions, or mixed)
No evidence of neurologic or general medical disorders that explain the symptoms
Evidence that the specific dissociative disorder is caused by psychological factors such as stressful events,
intractable problems, or interpersonal difficulties
Although ICD-10 does not explicitly require clinicians to exclude feigning of symptoms to diagnose dissociative movement
or sensation disorders or dissociative seizures, the need to do so is implied in the supporting text that discusses the
differential diagnosis and the difficulty in distinguishing dissociation from conscious simulation of loss of movement and
sensation [12].
DIFFERENTIAL DIAGNOSIS The differential diagnosis for conversion disorder (functional neurologic symptom
disorder) includes neurologic and general medical disorders, psychiatric disorders, and malingering [1].
Neurologic and general medical disorders The differential diagnosis for conversion disorder includes many general
medical disorders and all neurologic diseases, including multiple sclerosis, myasthenia gravis, movement disorders,
stroke, epilepsy, and spinal disorders [1,12]. Clinicians faced with symptoms that are difficult to interpret should exercise
caution in diagnosing conversion disorder, no matter how much the psychiatric history suggests it. Patients may notice
symptoms of an occult disease during its early stage when signs on physical examination or laboratory test abnormalities
are not readily apparent. In addition, more unusual neurologic diseases such as stiff person syndrome, autoimmune limbic
encephalitis, and frontal lobe epilepsy may present with unusual features such as symptom variability, bizarre behavior
(eg, cycling leg movements or pelvic thrusting), or other symptoms (eg, emotional lability) that might lead the unwary to
consider a psychogenic disorder. The effects of a neurologic disease can be frightening, which may lead patients to
exaggerate their symptoms to convince a doctor about their problem [21]. The probability that apparent conversion
symptoms are actually the harbinger of neurologic/general medical disease may be greater in patients with gait disorders
or comorbid psychiatric disorders [22].
However, a balance must be struck between not missing neurologic/general medical disorders and failing to positively
diagnose conversion disorder. The frequency of erroneously diagnosing conversion disorder in patients who are
subsequently found to have a neurologic illness (that with hindsight explained the initial symptoms) is generally regarded
as low [15]:
A systematic review of 27 studies (mostly retrospective; median duration of follow-up was five years) found that
among 1466 patients initially diagnosed with conversion symptoms, the frequency of misdiagnosis was
approximately 4 percent [22].
A subsequent study prospectively followed a group of 209 patients initially diagnosed with conversion disorder, who
were part of 1030 neurology outpatients with symptoms that were considered somewhat or not at all explained by a
recognizable neurologic disease [14]. After a median follow-up of 19 months, the investigators determined that the
initial diagnosis was wrong in none of the conversion disorder patients and in 0.4 percent of the entire group.
By contrast, misdiagnosis of other psychiatric and neurologic disorders occurs in 6 to 23 percent of patients [23-25].
In addition, many patients have both conversion disorder and a neurologic condition [26]. As an example, many patients
with psychogenic nonepileptic seizures also have epilepsy. (See "Psychogenic nonepileptic seizures", section on
'Concurrent or past epilepsy'.)

The differential diagnosis of conversion disorder includes all neurologic diseases, including:
Multiple sclerosis Multiple sclerosis and conversion disorder both can involve motor and sensory symptoms, but
patients with conversion disorder will have inconsistent limb movements, whereas, patients with multiple sclerosis alone
will not. Multiple sclerosis is also distinguished by characteristic lesions on magnetic resonance imaging (MRI).
(See "Diagnosis of multiple sclerosis in adults", section on 'Diagnosis'.)
Myasthenia gravis Myasthenia gravis and conversion disorder can both present with weakness that changes over
time, but patients with conversion disorder will have positive evidence of inconsistency without fatigue. Myasthenia gravis
is often associated with bulbar symptoms, diplopia, and ptosis, which are rare in conversion disorder; myasthenia gravis is
also differentiated by findings on serologic tests for autoantibodies and on electrophysiologic studies (repetitive nerve
stimulation studies and single-fiber electromyography) that are not present in conversion disorder. (See "Diagnosis of
myasthenia gravis".)
Movement disorders Psychogenic movement disorders and movement disorders due to defined neurologic disease
both present with abnormal movements; however, psychogenic movement disorders are characterized by several clinical
features, especially signs and symptoms that are inconsistent over time and incongruent with recognizable neurologic
disease. (See "Functional movement disorders".)
Stroke Stroke and conversion disorder can both manifest with weakness, but patients with conversion disorder have
inconsistent limb movements, whereas patients with stroke alone do not. (See "Overview of the evaluation of stroke".)
Spinal disorders Spinal disorders (eg, cervical myelopathy or lumbar nerve root entrapment) and conversion disorder
may each cause weakness or sensory disturbance. However, patients with conversion disorder have inconsistent limb
weakness whereas patients with spinal disorders should not.
Epilepsy Epilepsy and psychogenic nonepileptic seizures both manifest with unresponsive behavior and motor
movements that suggest a generalized convulsion or complex partial seizure. However, psychogenic nonepileptic
seizures and epileptic seizures are distinguished by recording an event on video electroencephalography and analyzing
the clinical and electrographic features. (See "Psychogenic nonepileptic seizures".)
In addition, some examples of more unusual neurologic diseases to consider in the differential diagnosis of conversion
disorder include:
Autoimmune limbic encephalitis Limbic encephalitis and conversion disorder may present with seizures, cognitive
problems, and mood changes. Positive findings on neuroimaging, electroencephalography (EEG), lumbar puncture, or
serologic testing for antibodies are generally found in limbic encephalitis but not conversion disorder. (See "Paraneoplastic
and autoimmune encephalitis".)
Stiff person syndrome Impaired ambulation, variable limb stiffness, and spasms can occur in both stiff person
syndrome and conversion disorder. However, stiff person syndrome is usually denoted by the presence of anti-glutamic
acid decarboxylase antibodies in association with this clinical picture. (See "Stiff-person syndrome".)
Laryngeal dystonia Dysphonia (manifesting with whispering or hoarseness) can occur in both laryngeal dystonia
(spasmodic dysphonia) and conversion disorder (functional dysphonia). Laryngeal dystonia may be either a primary
pathologic phenomenon or secondary to illnesses such as Parkinson disease or multiple systems atrophy. Clues that the
speech impairment may be due to conversion disorder include the presence of a normal cough or singing voice. The
diagnosis of conversion disorder is confirmed by normal vocal cord movement on laryngoscopy. (See "Classification and
evaluation of dystonia", section on 'Spasmodic dysphonia' and"Hoarseness in adults", section on 'Spasmodic dysphonia'.)
Psychiatric disorders The differential diagnosis for conversion disorder includes somatic symptom
disorder, depersonalization/derealization disorder, and factitious disorder [1].
Somatic symptom disorder Somatic symptom disorder subsumes the disorders previously identified as
hypochondriasis and somatization disorder, but also includes patients with somatic symptoms that are explained by
disease [1]. Somatic symptoms that cause distress and/or impairment can occur in both somatic symptom disorder and

conversion disorder, and some patients may warrant both diagnoses. Patients with somatic symptom disorder suffer from
an excessive response to somatic symptoms, but do not typically have loss of function that is clearly incompatible with
anatomy, physiology, and recognized neurologic or general medical illnesses; the disorder can thus occur in patients
whose symptoms are explained by recognized diseases. By contrast, conversion disorder is characterized by evidence of
inconsistency between the clinical findings and recognized disease. Also, the excessive thoughts, feelings, and behaviors
that occur in somatic symptom disorder may not be present in conversion disorder.
Depersonalization/derealization disorder Depersonalization (feeling disconnected from ones own
body) and/or derealization (feeling disconnected from ones environment), which
characterize depersonalization/derealization disorder, can also occur in conversion disorder, and some patients warrant
both diagnoses [1]. However, conversion disorder presents with symptoms of altered voluntary motor or sensory function,
and clinical findings that demonstrate incompatibility between the symptoms and recognized neurologic conditions,
whereas depersonalization/derealization disorder does not.
Factitious disorder Neurologic symptoms that are not due to disease are present in conversion disorder, and can
occur in factitious disorder as well. The primary distinction is that patients with factitious disorder deliberately feign
symptoms and deceive clinicians to be a patient and obtain medical care. In conversion disorder, there is no clear
evidence that symptoms have been simulated for the purpose of receiving medical care [1,10,15-17].
A clue that patients are feigning includes varying accounts of symptoms to different clinicians. However, it is possible to
establish feigning only if the patient acknowledges deliberately producing symptoms, or if other evidence demonstrates a
major inconsistency between reported and observed function (eg, a patient who reports an inability to walk is
subsequently observed on a video recording playing tennis). Minor discrepancies are in keeping with the variable nature
of conversion symptoms, which tend to worsen when attention is paid to them.
Additional information about factitious disorder is discussed separately. (See "Factitious disorder imposed on self
(Munchausen syndrome)".)
Malingering Malingering and conversion disorder are both characterized by symptoms that lack a pathologic basis [1].
The essential feature of malingering is intentionally faking or exaggerating symptoms for an obvious external benefit, such
as money, housing, medications, or avoiding work or criminal prosecution. Malingering is a behavior and not a psychiatric
disorder. In conversion disorder there is no evidence of intentionally producing symptoms [1,10,15-17].
Clinicians should consider the possibility of malingering if any of the following is present:
Multiple inconsistencies in the patients history
Nonadherence with diagnostic evaluation or treatment
Antisocial personality disorder
Medical-legal context (eg, patient is referred by an attorney for evaluation)
Other clues that patients are feigning symptoms are discussed above. (See 'Factitious disorder' above.)
SUMMARY
Many terms are used to describe neurologic symptoms or syndromes in the absence of disease pathology,
including: conversion disorder, functional, somatization, somatoform, psychogenic, dissociative disorder, medically
unexplained, psychosomatic, nonorganic, pseudoneurologic, and hysteria. (See 'Terminology' above.)
The diagnosis of conversion disorder according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition (DSM-5) is summarized in the table (table 1). (See 'Diagnosis' above.)
The differential diagnosis for conversion disorder includes:
Neurologic and general medical disorders (eg, multiple sclerosis, myasthenia gravis, movement disorders,
stroke, spinal disorders, and epilepsy)
Psychiatric disorders (eg, somatic symptom disorder, depersonalization/derealization disorder, and factitious
disorder)

Malingering
(See 'Differential diagnosis' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
Conversion disorder in adults: Treatment
Authors
Jon Stone, FRCP, PhD
Michael Sharpe, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Jon Stone, FRCP, PhD Nothing to disclose. Michael Sharpe, MD Nothing to disclose. Joel Dimsdale, MD Nothing to
disclose. David Solomon, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multilevel review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Jun 10, 2014.
INTRODUCTION Conversion disorder (functional neurologic symptom disorder) is characterized by neurologic
symptoms (eg, weakness, abnormal movements, or nonepileptic seizures) that are inconsistent with a neurologic disease,
but cause distress and/or impairment [1]. The disorder is common in clinical settings and often has a poor prognosis [2-5].
This topic reviews treatment of conversion disorder. The terminology, diagnosis, epidemiology, prognosis, clinical features,
and assessment are discussed separately, as are specific subtypes of conversion disorder (psychogenic nonepileptic
seizures and psychogenic movement disorders):
(See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)
(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis".)
(See "Conversion disorder in adults: Clinical features, assessment, and comorbidity".)
(See "Psychogenic nonepileptic seizures".)
(See "Functional movement disorders".)
GENERAL PRINCIPLES For patients with conversion disorder (functional neurologic symptom disorder), the primary
treatment is education about the illness [6]. Second line treatment for patients unresponsive to education is cognitivebehavioral therapy (CBT); for patients with motor symptoms, we typically offer physical therapy in addition to CBT, or
physical therapy alone if CBT is declined, not indicated, or not available. No head-to-head trials have compared first and
second line treatments.
For patients with conversion disorder who are treated by neurologists or primary care clinicians but do not respond to
education, referral to a psychiatrist can be helpful [7]. A consultation liaison psychiatrist or neuropsychiatrist is preferred
over a general psychiatrist. Patients may be more inclined to accept referrals if they are told that the psychiatrist has
experience in treating conversion symptoms and that the referral does not mean that the patient is crazy. Additional
information about psychiatric referrals is discussed separately. (See "Somatization: Treatment and prognosis", section on
'Psychiatric referral'.)
Comorbid anxiety or depressive disorders should be treated concurrently with conversion symptoms [8]. Treatment of
these comorbid disorders is discussed separately. (See "Pharmacotherapy for panic disorder" and "Pharmacotherapy for
generalized anxiety disorder" and "Unipolar major depression in adults: Choosing initial treatment".)

Multidisciplinary treatment Physical and psychological treatments for conversion disorder can be combined as
multidisciplinary treatment. A retrospective study found that at three year follow-up, symptom improvement or resolution
occurred in more patients who received multidisciplinary care administered by a neurologist and psychiatrist (10 out of 12
patients [83 percent]), compared with patients who received usual care (4 out of 11 [36 percent]) [9].
Inpatient treatment Treating patients with severe conversion disorder on specialist inpatient units may be beneficial:
A retrospective study (chart review) evaluated 33 patients who were hospitalized on a specialist neuropsychiatry
unit for severe conversion disorder (weakness and paralysis subtype, mean duration of symptoms 4 years) and
treated with a combination of cognitive behavioural therapy, occupational therapy, and physiotherapy administered
by a multidisciplinary team [10]. The median length of stay was 101 days, and improvement was demonstrated in
overall physical function and activities of daily living.
A retrospective study assessed 26 patients who were hospitalized on a specialist unit for severe conversion
disorder (weakness and paralysis subtype, duration of symptoms typically exceeded 3 years) and received a
multidisciplinary program that included physiotherapy, occupational therapy, cognitive behavioral therapy,
neuropsychiatry assessment, and neurology input as required [11]. The median length of stay was 24 days; follow-up
occurred a median of seven years after discharge. At both discharge and the follow-up assessment, the program
was rated as beneficial by 15 patients (58 percent), but there was no improvement in the rate of employment.
FIRST LINE TREATMENT First line treatment for conversion disorder (functional neurologic symptom disorder) is
education about the diagnosis, based upon observational studies [12,13]. As an example, a prospective study of 54
patients with psychogenic nonepileptic seizures found that after the diagnosis was explained, recovery occurred
immediately in 44 percent [14]. However, some patients subsequently suffered a recurrence.
A credible explanation of the diagnosis that creates a therapeutic alliance with the patient is an essential platform for any
further treatment that is required [15]. Patients who do not believe the diagnosis are unlikely to cooperate with additional
treatment; rather, they may continue the search for a more convincing disease explanation from another doctor. Treatment
failures can often be attributed to insufficient attention to education.
Therapeutic engagement of patients with conversion disorder often requires repeated explanations of the rationale for the
diagnosis. Thus, clinicians who administer treatment should understand how the diagnosis was made on the basis of the
physical characteristics of the symptoms. If multiple clinicians (eg, primary care physician, neurologist, psychiatrist, and
physical therapist) are treating the patient, the explanation of the diagnosis must be consistent [16]. With successful
engagement, patients become more willing to take some responsibility with the aid of clinicians for getting better, which
can reduce feelings of powerlessness, frustration, and mistrust for both patients and clinicians.
Presenting the diagnosis There is a consensus that treatment of conversion disorder begins with education about the
syndrome [8,12,13]. An explanation of the diagnosis along with encouragement may be all that is necessary for recovery.
In discussing the diagnosis of conversion disorder, we generally [7,8,15-17]:
Ask patients what they think is wrong and whether the problem is caused by damage to their body
State that the symptoms are taken seriously and are real rather than feigned
Confidently give a diagnostic label rather than tell patients that There is no disease. There are several diagnostic
terms; the choice depends upon how the clinician conceptualizes the disorder:
Functional neurologic symptom disorder
Conversion disorder
Dissociative disorder
Somatization
Psychogenic
It is best to avoid a struggle with patients over which term is used. How the term is used is probably more important
than the specific choice. Additional information about the terminology for conversion disorder is described separately.
(See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis", section on 'Terminology'.)

Discuss how the diagnosis was made, including the clinical features and physical signs that are inconsistent with
neurologic disease. As an example, patients with a positive Hoovers sign can be told that the examination confirms
that when they try to move the affected limb, the brain does not transmit messages correctly to the leg, but the
movement seen in the affected limb when they move their unaffected leg shows that none of the neurologic
pathways are damaged [15]. Hoovers sign is discussed separately. (See "Conversion disorder in adults: Clinical
features, assessment, and comorbidity", section on 'Examination'.)
Emphasize the mechanism underlying the symptoms rather than the cause. As an example, patients can be told
that although there is no structural damage to the nervous system, it is not functioning properly. Alternatively,
symptoms can be described as a software problem rather than a hardware problem.
Explain that the patient does not have a neurologic disease such as multiple sclerosis, epilepsy, or stroke; this is
presented as good news
Emphasize that the symptoms are potentially reversible (unlike many neurologic diseases). Patients can be told
that although their bodies are not functioning properly, improvement is possible because there is no structural
damage.
Acknowledge concerns about a psychiatric label if used, and difficulties in understanding the diagnosis
Discuss that it is important to identify and treat comorbid depression and anxiety because they can worsen
conversion symptoms
Explain that understanding and accepting the diagnosis often leads to improvement because it allows proper
engagement with rehabilitation rather than being stuck wondering or worrying about what is wrong
Attempt to enlist family members in helping patients understand the diagnosis
Tell patients that although they did not bring about the symptoms, they need to actively participate in their
rehabilitation (eg, working on graded exercise or distraction techniques) in order to improve
Acknowledge any prior treatment that was unsatisfactory
Arrange a follow-up consultation with the clinician responsible for making the diagnosis to:
Assess the extent to which the patient understands and believes the diagnosis
Provide further explanation
Answer additional questions from the patient and family
For patients with conversion symptoms who want to know the cause, we generally acknowledge that although it is
possible to speculate, the causes are complex and often uncertain. However, we emphasize that despite this uncertainty
we can nevertheless diagnose and treat the problem [7]. In addition, we state that the etiology is unknown for many other
illnesses, such as primary epilepsy and migraine.
Information for patients As part of education about conversion disorder, we typically provide written information that
patients can review at home and share with family and friends [8]. General information about conversion disorder that can
be downloaded and printed is available at the website www.neurosymptoms.org; information specific to psychogenic
nonepileptic seizures is available at www.nonepilepticattacks.info. In addition, for those patients who are treated by
primary care clinicians and have consulted a psychiatrist or neurologist, a copy of the letter from the consultant to the
primary care clinician can be given to patients.
Further information about conversion disorder is provided in a book that is intended for patients and family members:
Overcoming Unexplained Neurological Symptoms: A Five Areas Approach, written by Professor Christopher Williams,
Catriona Kent, Dr. Sharon Smith, Dr. Alan Carson, Professor Michael Sharpe, and Dr. Jonathan Cavanagh (ISBN
9781444138344, published by Hodder Arnold, 2011). One of the authors of this book is also an author of this topic.
SECOND LINE TREATMENT Conversion disorder (functional neurologic symptom disorder) often does not respond to
education. For these patients, we suggest cognitive-behavioral therapy (CBT), especially for psychogenic nonepileptic
seizures. (See "Psychogenic nonepileptic seizures", section on 'Treatment'.)
For patients with functional motor symptoms, we suggest CBT plus physical therapy. However, psychologically informed
physical therapy alone is a reasonable alternative [18,19]. Some patients decline psychotherapy because they refuse to

accept that talking treatments can be beneficial for physical symptoms; indeed, in some cases psychotherapy is not
effective.
Cognitive-behavioral therapy CBT for conversion disorder combines cognitive therapy and behavioral therapy and
thus resembles other forms of CBT that are used to treat anxiety disorders, mood disorders, and chronic fatigue
syndrome. Cognitive therapy attempts to modify dysfunctional thoughts and illness beliefs about conversion symptoms;
one technique is cognitive restructuring, which involves reframing distorted thoughts by empirically testing them and
considering more benign explanations. Behavioral therapy aims to change problematic behavioral responses to
symptoms, dysfunctional thoughts, and environmental stimuli; specific techniques include desensitization (administering
progressively greater exposure to feared and avoided situations and symptoms), problem solving (identifying the problem,
generating multiple solutions, considering the consequences of each solution, choosing one solution, and acting upon it),
progressive muscle relaxation, abdominal breathing exercises, and physical exercise. CBT principles and techniques are
typically taught to therapists according to a manual.
Evidence supporting CBT for conversion disorder includes randomized trials:
A trial compared CBT plus usual care with usual care alone in 125 patients with functional neurologic symptoms
[20]. CBT was administered in a self-guided format in which patients received a workbook and up to four sessions
(each lasting 30 minutes) with a clinician who provided guidance. The book explained that functional symptoms were
the result of changes in nervous system functioning due in part to psychological and behavioral factors, gave
examples of common functional symptoms and their associated anatomy and physiology, discussed how functional
symptoms are diagnosed, and suggested self-help techniques to reduce dysfunctional thoughts and improve coping
with symptoms. At six months, the presenting symptoms improved in more patients who received CBT plus usual
care than usual care alone (47 versus 30 percent). In addition, adjunctive CBT led to better physical functioning and
less anxiety.
A trial in 66 patients with psychogenic nonepileptic seizures found that seizure frequency decreased more with CBT
than standard care [17]. CBT for psychogenic nonepileptic seizures is discussed separately. (See "Psychogenic
nonepileptic seizures", section on 'Treatment'.)
Systematic reviews of trials indicate that CBT is usually efficacious for somatoform disorders in general [21,22]
Psychotherapy for conversion disorder requires an initial assessment of the predisposing, precipitating, and perpetuating
factors to generate a case formulation (table 1) [16]. A practical guide for administering CBT is shown in the table (table 2).
Examining the association between current conversion symptoms and prior life events may be helpful. However, this is
often difficult to achieve and may be appropriate only later in treatment, if at all [7]. It is not always necessary or desirable
to provide a complete psychological explanation of conversion symptoms to improve them. If treatment eventually
uncovers psychological problems or life events that predated the conversion symptoms, we generally avoid reattributing
the conversion symptoms to the stressors; rather, we emphasize that psychological issues may worsen conversion
symptoms. Patients may also disengage from psychotherapy because therapists are overzealous in attributing current
symptoms to past traumas. This can harm patients at a point when they need help understanding their symptoms.
Physical therapy For patients with conversion motor symptoms that do not respond to education, we typically offer
physical therapy in addition to CBT, or physical therapy alone if CBT is declined, not indicated, or not available. Physical
therapy is essential for patients who acquire a physical disability (eg, contractures).
Several studies support the use of physical therapy for conversion symptoms [18,23-25]. As an example, a three-week
randomized trial compared physical therapy (that included an education) with a waiting list control condition in 60
hospitalized patients with psychogenic gait disorder (mean duration of symptoms 10 months) [19]. Ambulation and
functional independence improved more with physical therapy, and the benefits were maintained at the one year followup. Additional information about education for conversion disorder is discussed elsewhere in this topic. (See 'First line
treatment' above.)

The essential element of physical therapy for motor conversion symptoms is to encourage normal movement and to
ignore deficits or abnormal movements as much as possible [18,24,26]. Attention to the affected limb tends to worsen
function, whereas exercises involving distraction (eg, tapping the fingers of the unaffected hand in a patient with unilateral
functional tremor or bouncing a balloon while working on trunk stability and balance) may be useful. It is generally more
beneficial to address activities such as transfers and walking than impairments such as weakness [27]. For patients who
have fallen, therapy emphasizes increasing confidence in standing and walking. In addition, graded exercise consistent
with the same principles that are used for chronic fatigue syndrome may be helpful [28].
THIRD LINE TREATMENT Conversion disorder (functional neurologic symptom disorder) often does not respond to
first or second line treatments; for these refractory patients, we suggest, in order of preference: pharmacotherapy,
hypnosis, or brief psychodynamic psychotherapy. Pharmacotherapy is more widely available and easier to administer than
hypnosis and psychodynamic psychotherapy. In addition, many patients decline hypnosis and psychotherapy, often
because they believe their illness is not amenable to these treatments. Hypnosis is easier to administer than
psychodynamic psychotherapy, and psychodynamic psychotherapy entails the risk of causing harm if the therapist is not
experienced in treating conversion disorder.
Pharmacotherapy Patients with conversion disorder may possibly benefit from medications [29,30]; the most
commonly used drugs are antidepressants [31]. As an example, an observational study of 10 patients with psychogenic
movement disorders (mean duration of illness 55 months) who were treated with antidepressants (citalopram, paroxetine,
or venlafaxine) found that improvement of motor symptoms and psychosocial functioning occurred in 8 patients, including
7 patients who remitted [32]. In addition, systematic reviews suggest that antidepressants are useful for somatoform
disorders in general [21,22]. Additional information about the efficacy of antidepressants for conversion disorder is
discussed separately in the context of psychogenic nonepileptic seizures. (See "Psychogenic nonepileptic seizures".)
For patients with conversion disorder, medications (especially antidepressants) are typically indicated for treating
comorbid anxiety and depressive disorders. (See"Pharmacotherapy for panic disorder" and "Pharmacotherapy for
generalized anxiety disorder" and "Unipolar major depression in adults: Choosing initial treatment".)
Hypnosis During hypnosis, concentration and physical relaxation are induced by asking the patient to focus upon an
external object. In this relaxed, trance-like state, patients are thought to be more susceptible to suggestions aimed at
alleviating symptoms or expressing emotions [33,34]. Hypnosis can be used to demonstrate the diagnosis of conversion
disorder to patients if the symptoms disappear under hypnosis. Some patients can be trained to use self-hypnotic
techniques to change their bodily sensations and functions.
Evidence supporting the use of hypnosis for conversion disorder includes low-quality randomized trials:
A three-month trial compared hypnosis (at least 10 weekly sessions as well as daily self-hypnosis homework) with
a waiting list control group in 44 outpatients with conversion symptoms and found that improvement was greater in
patients who received hypnosis [35]. Follow-up assessments of the active treatment group six months posttreatment
suggested that treatment gains were sustained.
A two-month trial compared adjunctive hypnosis (eight weekly sessions as well as daily self-hypnosis) with
adjunctive psychotherapy that focused upon stressors (eight weekly sessions as well as daily writing about
stressors) in 45 hospitalized patients with conversion symptoms who all received multidisciplinary treatment [36].
Improvement was comparable for both groups.
Psychodynamic psychotherapy Brief, individual, psychodynamic psychotherapy has been adapted for patients with
conversion symptoms and is based upon the assumption that the disorder is caused or exacerbated by a pattern of
dysfunctional interpersonal relationships that typically originates earlier in life [37]. In administering therapy, clinicians
make tentative suggestions about the link between symptoms and relationships, offer support, avoid confrontation, and
encourage patients to change their problematic interpersonal behavior and to express emotions more effectively
(particularly with regard to unresolved past issues such as abuse, neglect, or losses). The goal is to develop insight and
reduce the use of conversion symptoms as a defense against anxiety and conflict. Additional information about
psychodynamic psychotherapy is discussed separately in the context of unipolar major depression. (See "Unipolar
depression in adults: Psychodynamic psychotherapy".)

It is not clear if brief psychodynamic psychotherapy is beneficial for conversion symptoms. Evidence supporting
psychotherapy includes prospective observational studies:
A study in 63 patients found that therapy (median of six sessions, each lasting 50 minutes) was associated with
improved psychosocial functioning, less overall psychopathology, and a reduced number of physical symptoms [37]
A study in 47 patients with psychogenic nonepileptic seizures found that response (50 percent or greater reduction
in the number of nonepileptic seizures) occurred in 66 percent of patients [38]
However, a small randomized trial compared short term psychodynamic psychotherapy with neurologic observation in 15
patients with functional movement disorder; the study was characterized by high dropout rates and found no advantage
for active treatment [39].
Systematic reviews of randomized trials indicate that for somatic symptom and related disorders in general,
psychodynamic psychotherapy may be beneficial [21,22].
OTHER INTERVENTIONS For patients with conversion disorder (functional neurologic symptom disorder) who do not
respond to consecutive trials of first, second, and third line treatments, we suggest adding sedation (and perhaps
abreaction), family therapy, or group therapy.
Sedation and abreaction Sedation may transiently improve conversion symptoms. A retrospective study examined 11
patients with functional motor symptoms who received therapeutic sedation with propofol and were followed for a median
of 30 months; substantial improvement or recovery occurred in 5 (45 percent) [40]. In addition, a case report described
using sedation to help persuade a patient that the symptoms were reversible, and to provide an experience of moving a
limb that was functionally paralysed [41].
Abreaction (narcotherapy) is a rarely used technique that takes sedation one step further and involves interviewing
patients who are lightly sedated (relaxed but not drowsy) with a drug administered intravenously [33,42]. During the
procedure, patients may become more receptive to explanations about the nature of their disorder, which may lead to
improvement. A meta-analysis of 55 mostly older observational studies in 116 patients with conversion disorder found that
recovery occurred in 79 percent [43].
Based upon clinical experience, a positive therapeutic relationship should be established prior to using sedation or
abreaction.
Family therapy Patients with conversion disorder may possibly benefit from an assessment of family functioning in
domains such as communication, problem solving, and roles. Identified problems (eg, expression of suppressed affect)
that perpetuate symptoms can then be addressed in short-term, structured, family therapy. A review of observational
studies found that family therapy may perhaps improve symptoms [8]. Assessment of family functioning and
administration of family therapy are discussed separately in the context of unipolar major depression. (See "Family and
couples therapy for treating depressed adults".)
Group therapy Group therapy can reinforce education about conversion disorder and allows patients to learn from
each other [8]; mixed results have been found in observational studies of patients with psychogenic nonepileptic seizures.
(See "Psychogenic nonepileptic seizures", section on 'Treatment'.).
Repetitive transcranial magnetic stimulation (TMS) Repetitive transcranial magnetic stimulation (TMS) can be used
diagnostically to stimulate movement in psychogenic paralysis and demonstrate normal integrity of the upper and lower
motor neuron pathways [44]. In addition, preliminary studies suggest that repetitive TMS may be useful for treatment [45].
A retrospective study in 70 patients with conversion paralysis examined low frequency repetitive TMS of the motor cortex
contralateral to the corresponding paralysis (generally one session with 30 stimuli); recovery occurred in 76 percent, and
outcome was better for patients treated <30 days from symptom onset [44]. Another retrospective study of 24 patients with
functional movement disorder (median duration of symptoms was three years) showed improvement >50 percent in 75
percent of patients [46]. However, further work is required to confirm whether repetitive TMS is a useful adjunct to other
treatments in conversion disorder, and whether the benefit is due to changing illness beliefs in the patient or directly
altering neural substrates of symptoms.

Techniques to avoid We avoid treatment techniques in which patients are subjected to reverse psychology (also
called paradoxical intention; eg, You are not allowed to get up from that wheelchair [47]), are told that they have a spinal
cord concussion [26], or are told that full recovery constitutes proof of a physical etiology and failure to recover constitutes
conclusive evidence of a psychiatric etiology [48]. Although some clinicians report that these techniques can be effective,
we think that comparable or better results are possible without deceiving patients and risking the loss of trust that can
arise from these questionable approaches.
PERSISTENTLY ILL PATIENTS Patients with conversion disorder (functional neurologic symptom disorder) often do
not improve with consecutive trials of first, second, and third line treatments as well as other interventions. It is not realistic
to expect that patients will necessarily improve because they do not have recognizable disease pathology. Persistently ill
patients should generally be treated by primary care clinicians with a conservative approach that avoids excessive
investigations and treatments, and includes regular visits to monitor for general medical and psychiatric illnesses.
Management of patients with chronic somatic symptoms by primary care clinicians is discussed separately.
(See "Somatization: Treatment and prognosis", section on 'Treatment'.)
Conversion disorder may not respond to treatment for several reasons, including [7,49]:
Symptom severity and chronicity Symptoms may be so severe or chronic that they are not amenable to treatment
Diagnostic doubt Many patients eventually acknowledge that they never accepted the diagnosis and continued to
seek additional opinions, investigations, and medical or surgical solutions to their symptoms
Poor motivation to improve Patients have often resigned themselves to living with their symptoms
Disability payments comparable to money earned at an unpleasant job
Litigation in pursuit of disability payments
Symptoms that engage others to provide social support
Inexperienced clinicians Patients are easily alienated by clinicians who may inadvertently worsen the situation. A
common mistake is to attribute conversion symptoms to psychological issues that are not related to the symptoms,
or to point out the connection between symptoms and psychological issues before patients are ready to consider
such explanations.
Misdiagnosing conversion disorder in patients with:
Factitious disorder (willfully feigning symptoms to obtain medical care) (see "Factitious disorder imposed on
self (Munchausen syndrome)")
Malingering (faking symptoms to obtain obvious benefits such as money)
Recognizable disease with a known pathologic basis
The differential diagnosis and prognosis of conversion disorder are discussed separately. (See "Conversion disorder in
adults: Terminology, diagnosis, and differential diagnosis", section on 'Differential diagnosis' and "Conversion disorder in
adults: Epidemiology, pathogenesis, and prognosis", section on 'Prognosis'.)
SUMMARY AND RECOMMENDATIONS
For patients with conversion disorder (functional neurologic symptom disorder), we suggest education about the
diagnosis as first line treatment rather than other therapies (Grade 2C). (See 'First line treatment' above.)
Education about conversion disorder includes eliciting how patients conceptualize their symptoms, stating that the
symptoms are real and taken seriously, giving a diagnostic label, discussing how the diagnosis was made,
explaining that the patient does not have a neurologic disease, emphasizing that the symptoms are potentially
reversible, reassuring patients that understanding the diagnosis can lead to improvement, enlisting family members
to help patients understand the diagnosis, describing self-help techniques that can foster improvement,
acknowledging prior treatment that was unsatisfactory, and providing at least one follow-up visit. (See 'Presenting
the diagnosis' above.)
Written information describing the diagnosis and management of conversion disorder is often helpful.
(See 'Information for patients' above.)

For patients with conversion disorder who do not respond to education, we suggest CBT as second line treatment
rather than other therapies (table 2) (Grade 2B). For patients with motor symptoms, we suggest physical therapy in
addition to CBT, or physical therapy alone if CBT is declined, not indicated, or not available, rather than other
treatments (Grade 2C). (See 'Second line treatment' above.)
Refractory patients with conversion disorder who do not respond to first or second line treatment may possibly
benefit from pharmacotherapy, hypnosis, or brief psychodynamic psychotherapy as third line treatment. Other
treatments that may be used adjunctively include sedation (with or without abreaction), family therapy, and group
therapy. (See 'Third line treatment' above and 'Other interventions' above.)
Patients with conversion disorder who do not respond to first, second, and third line treatments as well as other
adjunctive interventions should generally be treated by primary care clinicians with a conservative approach that
avoids excessive investigations and treatments, and includes regular visits to monitor for general medical and
psychiatric illnesses. (See 'Persistently ill patients' above and "Somatization: Treatment and prognosis", section on
'Treatment'.)
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Conversion disorder in adults: Clinical features, assessment, and comorbidity

Authors
Jon Stone, FRCP, PhD
Michael Sharpe, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Jon Stone, FRCP, PhD Nothing to disclose. Michael Sharpe, MD Nothing to disclose. Joel Dimsdale, MD Nothing to
disclose. David Solomon, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multilevel review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Oct 06, 2014.
INTRODUCTION Conversion disorder (functional neurologic symptom disorder) is characterized by neurologic
symptoms (eg, weakness, abnormal movements, or nonepileptic seizures) that are inconsistent with a neurologic disease,
but cause distress, and/or impairment [1]. The disorder is common in clinical settings and often has a poor prognosis [2-5].
This topic reviews the clinical features, assessment, and comorbidity of conversion disorder. The terminology, diagnosis,
differential diagnosis, epidemiology, pathogenesis, prognosis, and treatment are discussed separately, as are conversion
disorder with attacks or seizures (functional or psychogenic nonepileptic seizures) and conversion disorder with abnormal
movements (functional or psychogenic movement disorders):
(See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)
(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis".)
(See "Conversion disorder in adults: Treatment".)
(See "Psychogenic nonepileptic seizures".)
(See "Functional movement disorders".)
CLINICAL FEATURES AND ASSESSMENT
General principles Conversion disorder can present with [6]:

Nonepileptic seizures (see "Psychogenic nonepileptic seizures")

Weakness and paralysis
Movement disorders (see "Functional movement disorders")
Speech disturbances
Globus sensation (see "Globus sensation")
Sensory complaints
Visual symptoms
Cognitive symptoms
These symptoms may be episodic or sustained, and acute or chronic [7].
Assessment of patients presenting with possible conversion disorder includes a medical history, physical examination, and
indicated laboratory tests, as well as the psychiatric history and mental status examination. It is essential to look for
neurologic and other general medical conditions, particularly early stage diseases [1,8,9]. The clinician evaluating the
patient should consider diseases that explain the patients symptoms better than conversion disorder, as well as diseases
that are comorbid (eg, in about 10 percent of cases, epileptic patients also have psychogenic nonepileptic seizures, or
patients with multiple sclerosis also have functional weakness) [10]. Comorbid psychiatric disorders may initially be
difficult to discern because patients emphasize physical symptoms rather than symptoms of depressive and anxiety
disorders.
Avoid indirect and fragmentary discussions of the diagnosis during the assessment [11]; instead, clinicians should
understand that presenting the diagnosis to patients is a fundamental aspect of treatment. (See "Conversion disorder in
adults: Treatment", section on 'Presenting the diagnosis'.)
Obtaining prior medical records can help provide information about previous symptoms or problems that patients have
forgotten [12]. In addition, patients may withhold information because they believe that they are less likely to be taken
seriously if they are forthcoming about previous medical encounters and psychiatric diagnoses.
Patients diagnosed with conversion symptoms should be reevaluated periodically because a general medical etiology
may take years to become evident.
History Clinicians taking the history of patients with a possible diagnosis of conversion disorder should ask about
[12,13]:
All current somatic symptoms Making a complete list of the symptoms at the beginning of the assessment can
prevent new symptoms from popping up later. It is also therapeutic as patients may feel understood and
unburdened. We routinely ask about fatigue, pain, dizziness, sleep disturbance, and impaired memory and
concentration if the patient does not volunteer these. After the list is complete, return to each symptom as necessary.
Multiple current conversion symptoms (mixed symptoms subtype of conversion disorder, eg motor and sensory
symptoms) are often found in conversion disorder [1,14]. In a prospective study of 54 patients with conversion
disorder, mixed symptoms occurred in 35 percent [15], and a randomized trial of 127 patients with conversion
disorder found that the mean number of functional symptoms was 2.5 [16].
Patients with conversion disorder often report a large number of current or prior unexplained physical symptoms,
dissociative symptoms, or unexplained syndromes (eg, irritable bowel syndrome, fibromyalgia, or chronic fatigue
syndrome), in addition to conversion symptoms [17-19]. As an example, one prospective study found that the mean
number of physical symptoms was greater in patients with functional weakness (n = 107) than patients with
weakness due to recognizable neurologic disease (n = 46) (9 versus 5 symptoms) [20]. The more physical
symptoms that are present, the less likely it is that the primary conversion symptom is due to a recognized disease.
Circumstances at onset Clinical features that are commonly observed at onset of conversion symptoms include
panic attacks, migraine headache, or pain, as well as physical injury. A systematic review of 132 observational
studies of conversion disorder (869 patients) found that physical injury occurred immediately prior to onset in 37

percent [21]. Although subsequent studies are consistent with this finding [22], it is not known whether recent
physical injury is specific to conversion disorder. In addition, both functional (psychogenic) nonepileptic seizures and
conversion motor symptoms may occur after general anesthesia [23,24].
In addition, onset of conversion symptoms is often sudden. As an example, a prospective study of 107 patients with
functional weakness found that sudden onset (6 hours to maximal onset) while awake occurred in 46 percent, or
upon waking from sleep or general anaesthesia in 15 percent [23].
Dissociation Dissociation in the form of depersonalization (feeling disconnected from oneself) or derealization
(feeling detached from the environment) may be present in patients with conversion disorder, particularly at onset of
the disorder [25]. Patients may describe dissociative symptoms as feeling outside of myself, spaced out, far
away, or unreal.
Disability Asking What is a typical day like? or Do you spend much time out of bed or the house? may be
more informative than asking patients what they cannot do [13]
Illness beliefs Asking patients what they think is causing their conversion symptoms and what should be done to
treat them enables clinicians to tailor the explanation of the diagnosis in such a way that it is more likely to be
accepted. Patients who believe that they have multiple sclerosis need an explanation that differs from patients who
believe that symptoms are related to stress.
Patients frequently believe that conversion symptoms are not due to psychologic factors [26]. As an example, one
prospective study (n = 153) found that the belief that stress was a possible cause of the illness occurred in fewer
patients with functional weakness than patients with weakness due to recognizable neurologic disease (24 versus 56
percent) [20].
However, other illness beliefs in patients with conversion disorder are often comparable to the beliefs of patients with
recognizable neurologic disease, including the conviction that a disease with a known pathologic basis is present
and that symptoms are causing major consequences [20,26].
Psychosocial functioning The relationship between conversion symptoms and psychosocial functioning is
bidirectional (each can affect the other) [13,26].
Family history Illnesses in parents, siblings, and children are common in patients with conversion disorder. As
an example, one prospective study (n = 60) found that general medical disorders in first degree relatives were more
common among patients with conversion disorder than patients with recognizable neurologic disease (80 versus 37
percent of patients) [17]. In addition, psychiatric disorders were more common in relatives of conversion disorder
patients. However, it is not established that patients with conversion disorder mimic the symptoms of others.
(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Premorbid clinical
factors'.)
Course of illness Asking When did you last feel well is a useful way of determining when onset of conversion
symptoms occurred, particularly for patients who have been ill for several years. In addition, a large amount of
information can be condensed by drawing a graph with time on the x axis, severity of symptoms on the y axis, and
adding life events or treatments (figure 1). The intensity of conversion symptoms may fluctuate [20].
Previous conversion symptoms The presenting symptom is more likely to represent conversion disorder if
there is a past history of conversion symptoms [27]
Prior hospitalization Previous hospitalization may be associated with conversion symptoms. As an example,
one prospective study (n = 60) found a history of hospitalization in more patients with conversion disorder than
patients with recognizable neurologic disease (70 versus 13 percent) [17].
Prior clinicians Patients may complain about prior clinicians, and provide clues as to which explanations of the
disorder and treatments are likely to be rejected. In addition, this part of the assessment demonstrates that one is
interested in the patients suffering and frustration.
Recent psychological stressors Although adverse life events are common in patients with conversion
symptoms [17], many patients do not have obvious life events and stressors [26]. In addition, psychological factors
at onset are not necessarily specific to conversion disorder and can thus be diagnostically misleading.

(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Premorbid clinical
factors'.)
Comorbid psychiatric symptoms and disorders We typically leave questions about depression and anxiety
until the end of the assessment (unless the patient volunteers it). Many patients with conversion disorder become
understandably defensive regarding questions of anxiety and depression if they think that their symptoms will be
blamed on a mental disorder. For many patients, attributing physical symptoms to a mental disorder is the same as
suggesting that the symptoms are fake. It may thus be helpful to avoid using terms such as depression or anxiety
and frame the questions in terms of the presenting symptoms. As an example, we may ask Does your weakness
ever make you feel down or frustrated? instead of Have you been feeling depressed? Anxiety and dysphoria are
often but not always present in patients with conversion disorder [3]. (See 'Psychiatric disorders' below.)
Physical and sexual abuse Questions about abuse, like those for comorbid psychiatric disorders, are often best
left to the end of the assessment. Patients may be more forthcoming after trust has been established during the
preceding phases of the assessment. It is important to provide patients enough time to discuss the issue if they
volunteer information about abuse; clinicians pressed for time will be better served by asking about abuse during a
subsequent interview or leaving this to a different clinician [12].
A prior history of aversive childhood experiences (abuse or neglect) is more common in patients with conversion
disorder than healthy and disease controls [28,29]. However, it is not clear that a history of sexual abuse is more
common in conversion disorder than patients with other psychiatric disorders, and most patients with conversion
disorder have not experienced abuse or neglect. (See "Conversion disorder in adults: Epidemiology, pathogenesis,
and prognosis", section on 'Premorbid clinical factors'.)
Other clinical features previously identified as specific to conversion disorder include la belle indifference and a
predominance of left sided symptoms; however, the evidence indicates that these two features are not specific to patients
with conversion disorder [20,30].
La belle indifference, which refers to an incongruous lack of concern (indifference) about significant symptoms, has no
validity in discriminating conversion disorder from recognizable neurologic disease. In a systematic review of 11
prospective or retrospective studies, the median frequency of la belle indifference was comparable for patients with
conversion disorder (n = 356) and patients with defined neurologic disease (n = 157) (21 versus 29 percent) [31]. In our
experience, la belle indifference often indicates that patients are trying to appear brave or cheerful in the presence of
actual distress (to avoid receiving a psychiatric diagnosis such as depression), or may less often suggest factitious
disorder [20].
Unilateral conversion symptoms do not appear to be more common on one side of the body than the other. Although a
meta-analysis of 90 observational studies (1139 patients with conversion symptoms) found that left sided symptoms
occurred in more patients than right sided symptoms (58 versus 42 percent), this finding appeared to be due to reporting
bias [30]. A separate analysis was conducted in the 78 studies (553 patients) in which laterality was reported incidentally
in the study text and did not appear in the title; a left sided preponderance of symptoms was found in only 53 percent of
patients.
Examination For patients who present with symptoms that may represent conversion disorder, the principles of
assessment are to look for evidence of [1,12]:
Inconsistency at different points in the examination (eg, a patient with no ankle dorsiflexion while supine on the
examination table is able to stand on tip toes). In addition, observing patients before and after the formal
examination can be revealing. As an example, compare the patients gait entering and leaving the exam room, what
occurs when patients take their clothes off and put them on, or what occurs when they retrieve something from their
bag.
Incongruity between the symptoms and recognized disease (ie, symptoms do not conform to known anatomical
pathways and physiologic mechanisms).

Thus, the diagnosis of conversion disorder rests upon positive clinical findings, which are described below.
(See 'Weakness and paralysis' below and 'Sensory symptoms'below.)
It should be noted that patients with recognizable neurologic disease may also display these positive findings (called
functional overlay) [20]. In addition, inconsistent signs may be produced consciously (as in factitious disorder or
malingering).
Additional information about the medical evaluation for conversion disorder is discussed separately in the context of
somatization. (See "Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis",
section on 'General medical evaluation'.)
Subtypes of conversion disorder The clinical features and assessment of each conversion disorder subtype are
described below, and are listed as follows from most to least common [2].
Nonepileptic seizures Conversion disorder seizures (also called dissociative seizures/attacks or psychogenic
nonepileptic seizures/attacks) are marked by abnormal generalized limb shaking, apparent impaired or loss of
consciousness, different clinical features from one convulsion to the next, and the lack of paroxysmal activity on
electroencephalograms (EEGs) [1]. A positive sign of conversion disorder with seizures is closed eyes with resistance to
opening. Psychogenic nonepileptic seizures are discussed separately. (See "Psychogenic nonepileptic seizures".)
Weakness and paralysis Weakness is common in patients with conversion disorder; a randomized trial with 127
patients found that weakness occurred in 31 percent [16]. Patients often report a history of dropping things, or dragging
or sudden buckling of the affected leg. Unilateral, hemiparetic symptoms are most frequent, but weakness in just one limb
or in both legs also occurs [17,20]. Patients commonly report that the affected limb doesnt feel part of them or belong
to them, which can be interpreted as a form of depersonalization. Other dissociative symptoms as well as panic attacks,
physical injury to the affected limb, and pain are commonly associated with onset of conversion weakness [21,23].
The key diagnostic finding in conversion weakness or paralysis is that the deficit is inconsistent at different times in the
examination [20]. Positive signs of functional (psychogenic) weakness on physical examination include the following
[12,13,32]:
Obvious inconsistencies Examples include:
No ankle dorsiflexion while lying down, but the ability to stand on tip toes
Inability to move arm during examination, but able to use arm to take something out of a bag or put shoes
back on
Hoovers sign The test is based upon the principle that the hip is extended when the contralateral hip is flexed
against resistance [33]. In weakness due to conversion disorder, hip extension is weak in the affected leg with the
patient lying down supine or seated. (This in itself is unusual in a disease process, but is common in psychogenic
weakness.) Hoovers sign (indicating conversion disorder) occurs when hip extension in the affected leg returns to
normal during contralateral hip flexion against resistance in the unaffected leg (figure 2 and picture 1). Ask the
patient to concentrate on their good leg when flexing it. However, pain may result in a false positive.
Hip abductor sign Comparable to Hoovers sign, hip abduction weakness in the affected leg returns to normal
during contralateral hip abduction against resistance in the unaffected leg [34]. However, pain may result in a false
positive.
Co-contraction sign Co-contraction is the simultaneous contraction of agonist and antagonist muscles. During
muscle strength testing of the agonist (eg, the biceps) in patients with conversion disorder, the clinician may be able
to detect contraction of the antagonist (eg, the triceps) [32,35]
Give-way or collapsing weakness The patient is asked to exert force in a particular direction, and as the examiner
lightly exerts force in the opposite direction, the examiner feels an abrupt decrease in resistance as the patients
extremity gives way suddenly [20]. In weakness due to neurologic disease, give-way weakness is less common.
However, give-way weakness is a soft sign of functional (psychogenic) weakness; other causes of give-way
weakness include chorea, pain, joint problems, and failure to understand instructions.

A delayed, slow, or jerky descent when the clinician positions the outstretched arm in front of the patient and then
releases it
A global or inverted pyramidal pattern of weakness in the legs (eg, extensors weaker than flexors) [20]
Facial spasm due to excessive contraction of orbicularis oculus (sometimes associated with photophobia) may be
mistaken for ptosis (facial weakness) [36]. In the lower face, excessive contraction of the platysma may pull the
mouth down or the jaw to one side and be mistaken for facial weakness.
Drift without pronation sign If patients with functional upper limb weakness are asked to hold their arms in the air
with their palms facing upwards, fingers adducted, and eyes closed, the affected arm may drift downwards but
without accompanying pronation commonly seen in patients with upper motor neuron lesions [37].
Sternocleidomastoid test Patients are asked to rotate their head against resistance [38,39]. In functional
weakness, patients exhibit difficulty rotating to the affected side, whereas patients with neurologic disease usually
manifest no weakness.
One study of 20 patients and 20 controls found that Hoovers sign, co-contraction sign, give-way weakness, and drift
without pronation sign were the most reliable of these signs [39]
Abnormal movement Conversion disorder with motor symptoms or deficits can manifest as movement disorders.
There are several functional (psychogenic) movement disorder syndromes that are based upon the presenting symptoms,
including:
Psychogenic tremor
Psychogenic dystonia
Psychogenic gait disorder
Psychogenic myoclonus
Psychogenic Parkinsonism
Psychogenic movement disorders, including their common clinical characteristics, the specific clinical features of each
syndrome, and their management are discussed separately. (See "Functional movement disorders".)
Speech symptoms The most common conversion speech symptom is functional dysphonia, which usually presents as
whispering or hoarseness, often after an episode of viral laryngitis has remitted. Clues that the speech impairment is
functional (psychogenic) include the presence of a normal cough or singing voice. The diagnosis of conversion disorder is
confirmed by normal vocal cord movement on laryngoscopy.
Patients with conversion motor symptoms also commonly complain of intermittent slurred speech; more severe dysarthria
or mutism may also occur.
Globus sensation (swallowing symptoms) Globus sensation (also called globus pharyngeus) describes the
conversion symptom of a lump or ball in the throat. The sensation is usually most pronounced at times other than
during swallowing. Globus pharyngeus is discussed separately. (See "Globus sensation".)
Sensory symptoms Sensory disturbance (eg, anesthesia or sensory loss) is common in conversion disorder; a
randomized trial with 127 patients found that paresthesias occurred in 50 percent and numbness in 41 percent [16]. In
addition, patients often report a feeling of being cut in half (midline splitting) or that one side or part of their body doesnt
belong to them, and may report a mixture of pain, sensory disturbance, and weakness [13].
Sensory symptoms in conversion disorder may be incongruent with known nerve pathways. As an example, patients may
describe sensory loss where the arm ends at the shoulder, or the leg ends at the groin, which is incompatible with
dermatomal or cortical sensory loss [12].
There are several physical signs that suggest a diagnosis of functional (psychogenic) sensory loss, but none are
conclusive because the signs are not specific to conversion disorder, patients may misunderstand the clinicians
instructions, and the signs can be found in patients with sensory problems due to neurologic disease with a known
pathologic basis [40]. These signs include [12,13,32]:

Altered vibration sense across the forehead or sternum (which generally should not occur in recognizable disease
because these are single bones)
Midline splitting (figure 3), in which sensation is split exactly in the midline (cutaneous branches of the intercostal
nerves overlap such that sensory loss should occur 1 to 2 cm from the midline; however, midline splitting can occur
in thalamic stroke)
Patients with complete sensory loss who respond when they are asked to say yes if they feel a stimulus and no
if they dont
Inconsistent responses when sensation in the hands is tested with the fingers interlocked behind the back
Visual symptoms Functional (psychogenic) visual disturbance is common; a randomized trial with 127 patients found
that functional visual symptoms occurred in 16 percent [16]. Conversion visual symptoms include intermittent blurred
vision, double vision (due to spasm of convergent eye movements), nystagmus, visual field defects, and complete
blindness [12].
Complete blindness, as with complete paralysis, is associated with an increased probability that the symptom is factitious.
In patients with complete binocular blindness, specific tests for conversion disorder with visual symptoms include the
following [12,41]:
Fingertip test, which is performed by asking the patient to touch the tips of their index fingers together. Whereas
blind people can readily do so using proprioception, patients with conversion disorder tend to have difficulty bringing
their fingers together.
Signature test, which is a nonvisual task that blind people can perform. Patients with conversion disorder may have
difficulty writing their signature.
Menace reflex, which involves presenting a visual threat (eg, a closed fist) to the eye. Flinching or blinking is
generally observed in conversion disorder. This test does not exclude a cortical visual problem.
Tearing reflex, which consists of tearing in response to suddenly presenting strong illumination in front of the
patient; the reflex requires intact vision. This test does not exclude a cortical visual problem.
Optokinetic test, which consists of holding a large rotating drum with black and white vertical stripes on it close to
the patients eyes. Optokinetic nystagmus indicates that at some level the brain can detect the stripes; however, this
test does not exclude a cortical visual problem.
Other tests for functional visual symptoms include the following [12,41]:
Tubular visual field defect; as an example, tunnel vision of the same width when the patients is examined at 1
meter and 2 meters (figure 4)
Convergent spasm leading to hyperadduction of one eye during convergent testing, which can resemble a sixth
nerve palsy
A pattern of spiraling on Goldmann automated visual field testing. This occurs because at the start of an
automated visual test, peripheral vision is present. However, as the test progresses and the stimuli rotate, the patient
typically develops increasing tunnel vision resulting in a spiral.
Fogging test of reduced visual acuity Lenses of increasing diopter are placed over the patients unaffected eye
(without the patients awareness) while reading a Snellen chart until any remaining acuity must be coming from the
affected eye
Other special sensory symptoms Conversion symptoms may rarely take the form of olfactory or hearing
disturbances [1].
Cognitive symptoms Cognitive symptoms are not described as part of conversion disorder [1]; however, some
authorities think that they should be included [42]. Based upon our clinical experience, cognitive symptoms that are
commonly encountered in patients with conversion disorder include those seen in anxiety and depressive disorders:
Poor concentration and memory
Impaired fluency

Jumbling of words when speaking

Word finding difficulty
Variability in speed of response
More marked cognitive symptoms may occur in bedside tests of cognition and on neuropsychological testing [42]:
Marked loss of remote autobiographical memory
Inability to perform over-learned skills such as reading, spelling, or simple arithmetic
Ability to perform complex implicit cognitive tasks in the presence of poor performance on simple explicit tasks
Performance inconsistent with observed behavior
Performance inconsistent at different points in the examination or across repeated evaluations
Impaired performance on tests of effort specifically designed to assess validity of cognitive performance (although
poor performance on these tests does not distinguish between intentional and unintentional poor performance)
As with all findings in conversion disorder, these cognitive symptoms may be intentionally produced as part of factitious
disorder or malingering. Some of these symptoms may also be attributable to anxiety or depressive disorders.
Amnesia may occur as a symptom of conversion disorder [13]. Short periods of amnesia are integral to psychogenic
nonepileptic seizures (during which the patient is unresponsive and amnesic for events rather than unconscious) and may
also accompany the onset of motor conversion symptoms. Isolated psychogenic amnesia presents with a dense and well
demarcated focal retrograde memory loss for a period ranging from weeks to years with preservation of anterograde
memory function (ability to make new memories).
Laboratory and radiologic studies Laboratory, radiologic, and neurophysiologic tests are generally required to
seek neurologic/general medical disorders that either explain the presenting symptoms or are comorbid [20]. However, the
diagnosis of conversion disorder generally rests upon findings at the bedside; although negative test results are consistent
with the diagnosis, many patients with neurologic disorders have normal test results [27]. Although we perform tests if we
or the patient is uncertain about the diagnosis, negative results may reassure patients only temporarily [12]. The brief
relief may be reinforcing and lead patients to repeatedly request additional tests.
Investigations should be performed as quickly as possible; protracted testing may encourage diagnostic uncertainty in
patients, who then focus upon finding a disease rather than rehabilitation [12]. We are explicit about why we are ordering
the tests, and predict the results will be normal when this is reasonable [13].
We warn patients that testing may uncover abnormalities that are unrelated to the presenting symptoms (but which derail
treatment). As an example, incidental findings occur on 10 to 15 percent of all magnetic resonance images [13]. However,
tests can also yield false negatives.
COMORBID DISORDERS Comorbidity is common in conversion disorder, and patients may have multiple comorbid
disorders.
Psychiatric disorders Psychiatric comorbidity may occur in up to 90 percent of patients with conversion disorder
[14,15,43-45]. As an example, a prospective study found that the lifetime prevalence of psychiatric disorders was greater
in patients with functional weakness (n = 107) than patients with weakness due to recognizable neurologic disease (n =
46) (95 versus 71 percent of patients) [20]. Based upon our clinical experience, patients may not divulge their comorbid
psychiatric symptoms.
Many studies suggest that the frequency of comorbid depressive disorders and anxiety disorders in patients with
conversion disorder exceeds the frequency in patients with defined neurologic disease by approximately 20 to 30 percent
[17,44,46]. As an example, a prospective study found higher rates of comorbid depression and/oranxiety in patients with
functional weakness (n = 107) compared to patients with weakness due to a neurologic disease such as multiple sclerosis
(n = 46) [20]:
Unipolar major depression 32 versus 7 percent
Generalized anxiety disorder 21 versus 2 percent

Panic disorder 36 versus 13 percent

Dissociative disorders are also common in patients with conversion disorder. A prospective study of 38 patients found a
dissociative disorder in 47 percent [45].
Compared with patients who have defined neurologic disease, patients with conversion disorder are more likely to have
personality disorders, especially [14,44,47]:
Borderline personality disorder
Histrionic personality disorder
Narcissistic personality disorder
As an example, a prospective study found that a comorbid personality disorder was present in more patients with
conversion disorder (n = 30) than patients with recognizable neurologic disease (n = 30) (50 versus 17 percent) [17].
Suicide attempts occur often in conversion disorder. A prospective study of 38 patients found a history of suicide attempts
in 34 percent [45].
Psychotic disorders and substance use disorders do not appear to be associated with conversion disorder [6,46].
Neurologic and general medical disorders A current or prior neurologic disorder may be found in many patients with
conversion disorder [1]. The presence of neurologic or other general medical disorders do not preclude a diagnosis of
conversion disorder if the conversion symptoms are not fully explained by the general medical disorder.
SUMMARY
Conversion disorder can present with different symptoms, such as:
Nonepileptic seizures
Weakness and paralysis
Abnormal movement
Speech disturbances
Globus sensation (swallowing symptoms)
Sensory symptoms
Visual symptoms
Cognitive symptoms
(See 'General principles' above and 'Subtypes of conversion disorder' above.)
Assessment of patients presenting with possible conversion disorder includes a medical history, physical
examination, and indicated laboratory tests, as well as the psychiatric history and mental status examination. It is
essential to look for neurologic and other general medical conditions, particularly early stage disease. (See'General
principles' above.)
Clinicians taking the initial history of patients with a possible diagnosis of conversion disorder should ask about all
current somatic symptoms, circumstances at onset, dissociation, disability, illness beliefs, psychosocial functioning,
family history, course of illness, previous conversion symptoms, prior hospitalization, prior clinicians, recent
psychological stressors, and comorbid psychiatric symptoms and disorders. Questions about physical and sexual
abuse are often best deferred until trust has been established during the preceding phases of the assessment.
(See 'History' above.)
For patients who present with symptoms that may represent conversion disorder, clinicians should look for
evidence of inconsistency at different points in the examination as well as incongruity between symptoms and
recognized disease. (See 'Examination' above.)
The clinical features that are found on assessment of patients with conversion disorder are described for each
subtype. (See 'Subtypes of conversion disorder'above.)

Laboratory and radiologic tests are generally required to seek neurologic/general medical disorders that either
explain the presenting symptoms or are comorbid. (See'Laboratory and radiologic studies' above.)
Psychiatric comorbidity, especially depressive, anxiety, dissociative, and personality disorders, exceeds that found
in defined neurologic diseases. (See 'Psychiatric disorders' above.)
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Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis
Authors
Jon Stone, FRCP, PhD
Michael Sharpe, MD
Section Editor
Joel Dimsdale, MD
Deputy Editor
David Solomon, MD
Disclosures: Jon Stone, FRCP, PhD Nothing to disclose. Michael Sharpe, MD Nothing to disclose. Joel Dimsdale, MD Nothing to
disclose. David Solomon, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multilevel review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Aug 03, 2014.
INTRODUCTION
Conversion disorder (functional neurologic symptom disorder) is characterized by neurologic symptoms (eg, weakness,
abnormal movements, or nonepileptic seizures) that are inconsistent with a neurologic disease, but cause
distress and/or impairment [1]. The disorder is common in clinical settings and often has a poor prognosis [2-5].
This topic reviews the epidemiology, pathogenesis, and prognosis of conversion disorder. The terminology, diagnosis,
differential diagnosis, clinical features, assessment, and treatment are discussed separately, as are specific subtypes of
conversion disorder (psychogenic nonepileptic seizures and psychogenic movement disorders):
(See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)
(See "Conversion disorder in adults: Clinical features, assessment, and comorbidity".)
(See "Conversion disorder in adults: Treatment".)
(See "Psychogenic nonepileptic seizures".)
(See "Functional movement disorders".)
EPIDEMIOLOGY The prevalence of conversion disorder (functional neurologic symptom disorder) has been more
widely studied in clinical settings than in the general population.
General population A review found that the estimated incidence of conversion disorder across disparate geographical
settings was 4 to 12 per 100,000 per year (0.004 to 0.012 percent), and the community prevalence of conversion disorder
based upon case registries was 50 per 100,000 per year (0.05 percent) [6].
Clinical settings The point prevalence of conversion symptoms in clinical settings ranges from 2 to 6 percent:
A prospective study of 157 internal medicine inpatients found that conversion disorder was present in 2 percent [7]
A prospective study of 3781 neurology outpatients found that conversion disorder was present in 6 percent [2]
A retrospective study of 7836 outpatients evaluated by one neurologist found that conversion disorder was present
in 4 percent [8]

Sociodemographic correlates It is not clear if there are any established sociodemographic correlates of conversion
disorder, per se. However, a prospective study compared 1144 neurology outpatients with symptoms somewhat or not at
all explained by a recognizable neurologic illness (including 209 patients with conversion disorder) with 2637 patients
whose symptoms were explained by a neurologic illness [3]. Unexplained symptoms were associated with:
Younger age
Female sex
Greater disability, including physical, role, and social functioning
Conversion disorder has been reported in patients of all ages, from early childhood to old age, but is rare before age 10
years [9,10]. A prospective study of 50 patients with conversion disorder found that the mean age of onset was later for
psychogenic weakness and movement disorders, compared with psychogenic nonepileptic seizures (39 versus 27 years)
[11]. Nevertheless, there have been reports of nonepileptic seizures with onset in an older age group (mean age 61 years,
n = 26), amongst whom comorbid disease was prominent [12].
Many studies have found that conversion disorder is more likely to occur in females than males [3,13]. However, the
preponderance of females may vary by the subtype of the disorder. A pooled analysis of 52 studies that included 2270
patients with conversion disorder found that the proportion of females was less for psychogenic weakness than
psychogenic nonepileptic seizures (48 versus 74 percent) [11].
ETIOLOGY AND PATHOGENESIS The etiology and pathogenesis of conversion disorder (functional neurologic
symptom disorder) are not known [14]. However, there are many biological, psychological, and social factors that are
more common in patients with functional symptoms than patients with comparable symptoms due to recognizable disease
[15]. These factors may predispose patients to conversion disorder or precipitate and/or perpetuate symptoms (table 1).
Premorbid clinical factors Psychological factors or life events such as trauma, interpersonal conflicts, and recent or
old stressors may be associated with onset of conversion disorder [1]. However, psychological factors are not always
reported, nor are they specific to conversion disorder [16]. In a prospective study that compared 54 patients with
conversion disorder and 50 with a mood or anxiety disorder, the mean number of life events in the year prior to onset of
symptoms was similar (4.2 and 3.8) [17]. Another study of 40 patients with psychogenic nonepileptic seizures, 20 patients
with epilepsy, and 40 healthy controls found that the frequency of stressful life events was comparable for the three
groups [18].
Childhood sexual abuse is associated with conversion disorder in many but not all studies. As an example, a metaanalysis of 19 studies found that a history of childhood sexual abuse was more common in patients with psychogenic
nonepileptic seizures (n = 717) compared with controls (n = 931, generally patients with epilepsy) (37 versus 16 percent)
[19]. However, a subsequent prospective study compared 64 patients with psychogenic movement disorder, 39 patients
with focal hand dystonia, and 39 healthy controls, and found no difference in childhood sexual abuse [16]. Another study
also found that sexual abuse was comparable in 54 patients with conversion disorder and in 50 patients with mood or
anxiety disorders (24 and 14 percent) [20].
Pre-existing disorders and symptoms may predispose patients to developing conversion disorder; in some cases, this
process is considered symptom amplification [21]. Compared with controls with recognizable disease, patients with
conversion disorder are more likely to have a history of pre-existing psychiatric disorders (eg, depressive, anxiety, and
personality disorders) and unexplained symptoms (eg, pain, fatigue, and cognitive impairment) [11,22]. In addition,
conversion disorder is often preceded by neurologic illnesses (eg, migraine, peripheral nerve pathology, or stroke) that
appear to trigger, but do not explain the conversion symptoms [23]. Physical injury may also precede conversion
symptoms [24,25].
An excess of symptom modeling (copying the symptoms of others) has been reported in some studies of conversion
disorder [26-28] but not others [29-31].
Perpetuating factors Conversion symptoms may be perpetuated by beliefs that there is an irreversible neurologic
disease, which may create a powerful obstacle to rehabilitation. Clinicians may also make things worse by failing to give a
clear explanation and positive diagnosis of the symptoms [32], excessively investigating symptoms [33], prescribing

inappropriate drugs and appliances (eg, braces and wheelchairs) [34], performing unnecessary operations, and
misattributing symptoms to recognizable disease or to irrelevant radiologic or laboratory findings (eg, age-related
degenerative changes in the vertebrae) [35]. In addition, conversion symptoms may be perpetuated by physical
deconditioning, comorbid psychiatric disorders, disability-related financial benefits, and litigation [15,36]. Another potential
perpetuating factor is life stress (eg, work or family) that was relieved by onset of the disorder and would probably recur if
the patient was to recover from conversion disorder [37].
Hypotheses Several hypothetical models attempt to explain how conversion symptoms develop; these models are not
mutually exclusive.
Cognitive-behavioral models Multiple overlapping cognitive-behavioral models have been proposed to explain the
etiology and pathogenesis of conversion disorder.
One cognitive-behavioral model is based upon findings that processing of perception and behavior mostly occurs outside
of awareness, and proposes that conversion symptoms may result from psychological influences at these lower levels of
processing [6]. It is suggested that patients with conversion disorder initially encounter (in themselves or others) a
stimulus for a particular symptom, such as mild weakness from migraine. This generates a mental representation or
memory of paralysis. Excessive anxiety about becoming paralyzed, and hypervigilance in looking for evidence (eg,
weakness) of paralysis in oneself, may activate the mental representation to the point that it overrides sensory input and
distorts awareness and behavior. Selective attentional bias leads patients to persistently focus upon evidence that they
are paralyzed and avoid evidence that they are not [38]. Some studies suggest that patients with conversion disorder may
lack explicit awareness of their own emotional symptoms, such as anxiety [39,40].
Another cognitive-behavioral model proposes that conversion disorder involves dissociative experiences [6]. Dissociation
is subjectively perceived as disconnection from oneself (depersonalization) or the environment (derealization). During
dissociation, awareness and integration of thoughts, feelings, memories, and identity is altered, as is integration of
somatic experiences and functions, and patients lose functioning of motor control or sensory awareness [41]. Dissociation
may occur as a consequence of fatigue, panic attacks [42], physical injuries [24,25,43], recognizable diseases [23,44],
iatrogenic triggers such as general anesthesia [42,45], or drug side effects [25]. In this model, the symptom of paralysis or
abnormal movement arises during the dissociated state when the patient is depersonalized and generally loses feelings
of ownership over body movements. Attention paid asymmetrically to this experience, combined with fear of what the
symptom might represent (eg, stroke), may intensify and cause more localized depersonalization, thus prolonging the
symptom. In nonepileptic seizures, prodromal symptoms of panic attacks may become so unbearable that patients
respond by losing awareness in an apparent blackout [46,47], with subsequent nonepileptic seizures occurring as a
conditioned response to unpleasant thoughts, feelings, and situations, even in the absence of a prodrome.
Some cognitive behavioral models hypothesize that conversion disorder is perpetuated by maladaptive thoughts.
Evidence for this hypothesis includes findings that recovery can be impeded by thoughts that conversion symptoms are
due to a disease process with a known pathologic basis and beliefs that psychological factors are not involved [9,22,48].
In addition, beliefs that symptoms are caused by recognizable disease and are therefore not reversible appear to be a
more powerful predictor of poor prognosis than the number of conversion symptoms or severity of disability [49].
Neurobiologic model Conversion disorder may involve abnormalities in neural networks of grey matter brain regions
rather than a disturbance in one specific structure [6]. These networks are thought to include frontal (orbitofrontal and
anterior cingulate cortex) and subcortical (limbic) structures that are activated by emotional stress, and in turn provide
input to inhibitory basal ganglia-thalamocortical circuits that reduce conscious motor or sensory processing [50]. One
hypothesis is that overly sensitive amygdala responses to fear (ie, abnormal responses to stimuli, including those that are
objectively neutral) lead to changes in networks mediating sensory and motor function. In the setting of abnormal selfdirected attention (eg, depersonalization), these changes produce sensations or movements that are associated with an
abnormal sense of self control and are interpreted as involuntary symptoms of a disease [6,38].
Neuroimaging of patients with conversion disorder reveals central nervous system changes. Structural magnetic
resonance imaging studies that compared patients with conversion disorder (weakness subtype) to healthy controls have
found evidence of altered brain structure in patients (eg, reduced thalamic volume and increased cortical thickness)

[51,52]. In addition, functional magnetic resonance imaging of patients with conversion disorder (weakness subtype) and
healthy controls during recall of traumatic events shows differences in regional brain activity (eg, prefrontal cortex and
hippocampus) [53]. However, it is not known if the differences represent etiologic causes, confounding comorbidities, or
sequelae of the disorder.
Psychodynamic models The classic psychodynamic hypothesis, which gives conversion disorder its name, is that
patients experience an unconscious conflict that is converted into a somatic symptom [15,54,55]. The symptom serves as
a defense against anxiety and distress, which are reduced by the conflict remaining unconscious [41]. In this model, the
conversion symptom symbolizes the conflict and may help the patient avoid an overwhelming situation [56]. The
hypothesis is difficult to test scientifically, has been hard to apply clinically, and thus has little empirical support [41].
Subsequent psychodynamic hypotheses emphasize abnormal interpersonal relationships that develop in the context of
problematic early relationships (eg, poor parenting) or traumatic events [15]. In these models, a new conflict or traumatic
event leads to recurrence of previous patterns of abnormal behavior and the development of physical symptoms. The
physical symptoms are regarded as a coping response, secondary to emotional dysregulation. As an example, somatic
symptoms that lead to contact with clinicians may enable patients to meet dependency needs established earlier in life.
Such hypotheses are also hard to test.
PROGNOSIS Prognosis for conversion disorder (functional neurologic symptom disorder) is generally poor. Reviews of
observational studies suggest that symptoms persist or worsen in approximately 40 to 66 percent of patients [4,6]. In one
retrospective study of 42 patients with functional weakness and/or sensory disturbances, symptoms were still present
after a median of 12 years in 83 percent [57]. In addition, a median of nine other physical symptoms (eg, fatigue,
arthralgias, myalgias, and nausea) were present, psychosocial functioning was poor, and emotional distress was
common.
Among the subtypes of conversion disorder:
Sensory symptoms [57,58] may have a better prognosis than weakness/paralysis [57], dystonia [59], and tremor
[1,4]
The prognosis of psychogenic nonepileptic seizures varies, but is often poor. A systematic review found that in 10
out of 18 observational studies, seizure remission occurred in 40 percent or fewer patients [5]. However, prognosis
may be better if the disorder is diagnosed early. A prospective study of 54 patients with new onset psychogenic
nonepileptic seizures found that within three months of diagnosis, remission had occurred in 50 percent [60].
Baseline predictors of outcome in patients with conversion symptoms vary between studies, and much of what is known
comes from studies that included not only patients with conversion disorder, but other somatic symptom and related
disorders as well. Across different studies with follow-up ranging from 8 months to 12 years [4,6,23,49,57,61-65]:
Factors associated with a poor outcome included:
Multiple physical symptoms
Long-standing symptoms
Poor physical functioning
Comorbid personality disorder
Beliefs that symptoms are irreversible and caused by a disease with a known pathologic basis
Illness-related financial benefits
Factors associated with a positive outcome included:
Early diagnosis
Good response to initial treatment
Comorbid anxiety or depression
Subsequent change in marital status
Good therapeutic alliance with the clinician

The interpretation of most prognostic studies is hampered because patients with conversion symptoms were not
compared with controls with recognizable neurologic disease.
SUMMARY
The estimated prevalence of conversion disorder (functional neurologic symptom disorder) in community studies
ranges from 0.004 to 0.2 percent, and in clinical settings, from 2 to 6 percent. Sociodemographic correlates of
conversion disorder may include younger age, female sex, and greater disability. Onset of conversion disorder rarely
occurs prior to age 10 years. (See 'Epidemiology' above.)
The etiology and pathogenesis of conversion disorder are not known. However, many factors have been identified
that may predispose patients to conversion disorder or precipitate and/or perpetuate symptoms (table 1).
(See 'Etiology and pathogenesis' above.)
Psychological factors or life events such as trauma, interpersonal conflicts, and recent or old stressors may be
associated with onset of conversion disorder. However, psychological factors are not always reported, nor are they
specific to conversion disorder, and many patients with conversion symptoms may not have identifiable
psychological factors. (See 'Premorbid clinical factors' above.)
Pre-existing psychiatric disorders and functional somatic symptoms may predispose patients to developing
conversion disorder. In addition, conversion disorder may be triggered by physical injury and neurologic illnesses.
(See 'Premorbid clinical factors' above.)
Conversion symptoms may be inadvertently perpetuated by clinicians who fail to give a clear explanation and
positive diagnosis of the symptoms, excessively investigate symptoms, prescribe inappropriate drugs and
appliances, perform unnecessary operations, and misattribute symptoms to recognizable disease or to irrelevant
radiologic or laboratory findings. (See 'Perpetuating factors' above.)
Several hypothetical models attempt to explain how conversion symptoms develop and are not mutually exclusive:
The psychodynamic hypothesis is that patients experience an unconscious conflict that is converted into a
somatic symptom. The symptom is a defense against anxiety and distress, which are reduced by the conflict
remaining unconscious. Subsequent psychodynamic hypotheses emphasize abnormal interpersonal
relationships that develop in the context of problematic early relationships or traumatic events.
(See 'Psychodynamic models' above.)
Cognitive-behavioral models emphasize factors such as processing of perception and behavior outside of
awareness, selective attentional bias that amplifies minor physiological stimuli and asymmetries, dissociation,
and maladaptive thoughts that perpetuate symptoms. (See 'Cognitive-behavioral models' above.)
The neurobiologic model hypothesizes that abnormalities in neural networks of grey matter brain regions
involving frontal and subcortical structures are activated by emotional stress, and in turn provide input to
inhibitory basal ganglia-thalamocortical circuits that reduce conscious motor or sensory processing.
(See 'Neurobiologic model' above.)
Prognosis for conversion disorder is generally poor. Factors associated with poor outcome include the presence of
multiple physical symptoms, long-standing symptoms, poor physical functioning, comorbid personality disorder,
beliefs that symptoms are irreversible and caused by a disease with a known pathologic basis, and illness-related
financial benefits. Factors associated with a positive outcome in conversion disorder include a good response to
initial explanation and treatment, comorbid anxiety or depression, change in marital status, and a good therapeutic
alliance with the clinician. (See 'Prognosis' above.)
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