AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Conversion disorder, as stated in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), involves symptoms or deficits affecting voluntary motor or sensory function that suggest a neurological or other general medical condition. Yet, following a thorough evaluation, which includes a detailed neurological examination and appropriate laboratory and radiographic diagnostic tests, no neurological explanation exists for the symptoms, or the examination findings are inconsistent with the complaint.

Examples of conversion symptoms include blindness, diplopia, paralysis, seizures, anesthesia, aphonia, amnesia, unresponsiveness, and difficulty walking. Conversion disorder represents one type of somatoform disorder. The essential element of all somatoform disorders is the presence of physical symptoms or signs that cannot be explained by a medical condition. Unlike factitious disorders and malingering, the symptoms of somatoform disorders are not intentional or under voluntary control.

Pathophysiology

Conversion symptoms suggest a physical disorder but are the result of psychological factors. According to the psychodynamic model, the symptoms are a consequence of emotional conflict, with the repression of conflict into the unconscious. In the late 1880s, Freud and Breuer suggested that hysterical symptoms resulted from the intrusion of "memories connected to psychical trauma" into the somatic innervation. This mind-to-body process was referred to as "conversion."

It has been postulated that the patient derives primary and secondary gain. With primary gain, the symptoms allow the patient to express the conflict that has been suppressed unconsciously. With secondary gain, symptoms allow the patient to avoid unpleasant situations or garner support from friends, family, and the medical system that would otherwise be unobtainable. According to sociocultural theories, the direct expression of emotions is impermissible and somatization takes its place. In behavioral models, conversion symptoms are viewed as a learned maladaptive behavior that is reinforced by the environment.

The idea that conversion disorder does not have an organic basis has become entrenched. However, some evidence supports the opposite notion. Studies on the natural history of conversion disorder indicate that many patients subsequently develop or are found to have preexisting neurological disease. In fact, conversion disorders may be more frequently observed in patients with a past history of a central nervous system injury. The simultaneous occurrence of organic brain disease with conversion symptoms also is observed, most notably in observation of high rates of organic seizure syndromes associated with psychogenic nonepileptic seizures. Familial studies have also shown that conversion symptoms in first-degree female relatives are up to 14 times greater than in the general population.

Frequency

United States

Stefansson et al report that the annual incidence of conversion reactions is 22 cases per 100,000 persons per year in Monroe County, New York. However, the reported rates vary widely. In a study of 100 consecutive women following a normal full-term pregnancy, 33 were noted to have a past history of conversion symptoms. In a study of 100 randomly selected patients from a psychiatry clinic, 24 were noted to have unexplained neurological symptoms. It is reported to be more common in rural populations, in individuals with lower socioeconomic status, and in individuals with less medical knowledge.

International

Stefansson et al report that the annual incidence is 11 cases per 100,000 persons per year in Iceland.

Mortality/Morbidity

• Individual conversion symptoms generally are self-limiting and do not lead to physical changes or disabilities.
• Morbidity is often an iatrogenic manifestation of unnecessary diagnostic or therapeutic interventions.
• Patients with chronic conversion symptoms (rarely) may develop atrophy, frozen joints, and contractures from disuse.

Sex

• The female-to-male ratio is 2-10:1.

Age

• The typical onset is between the second and fourth decades.
• The reported range is from children to individuals in their ninth decade of life.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Conversion symptoms are those that suggest neurological disease, but no explanation of these symptoms is found following physical examination and diagnostic testing. Conversion symptoms are seen in various clinical settings and include conversion disorder; somatization disorder; affective disorders; antisocial personality disorder; alcohol or drug abuse; or organic, neurological, or medical illnesses. In some situations, an immediate precipitating source of stress may be disclosed, such as a loss of employment or divorce. The patient may have a discordant home life. A history of sexual or physical abuse is not uncommon and can be seen in as many as one third to one half of patients with dissociative disorder, respectively. Therefore, a complete and comprehensive psychosocial history is important. It has been stated that patients with conversion disorder have a relative lack of concern about the nature or implications of the symptoms (la belle indifference). This is not a helpful diagnostic

characteristicbecause it is not specific or sensitive for conversion.

• Diagnostic criteria for conversion disorder as per the DSM-IV-TR are as follows:
• • One or more symptoms or deficits are present that are affecting voluntary motor or sensory function and suggest a neurological or other general medical condition.
  • Psychological factors are judged to be associated with the symptoms or deficits because the initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors.
  • The symptom or deficit is not produced intentionally or feigned, as in factitious disorder or malingering.
  • The symptoms or deficit cannot, after appropriate investigation, be explained fully by a general medical condition, by the direct effects of a substance, or as a culturally sanctioned behavior or experience.
  • The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.
  • The symptom or deficit is not limited to pain or sexual dysfunction, does not occur exclusively during the course of somatization disorder, and is not better accounted for by another mental disorder.
• Possibilities to consider when a patient presents with symptoms of probable psychogenic origin include the following:
• • Symptoms are exclusively a function of somatoform disorder, factitious disorder, or malingering.
  • Symptoms are secondary to other psychiatric etiologies such as panic disorder or depression.
  • Symptoms coexist with a physical disorder.
  • The symptoms are an unusual manifestation of a physical disorder.
• The DSM-IV-TR lists strict criteria for diagnosing conversion disorder. However, 2 of the listed conditions may be determined only by a person with expertise in neurological conditions, neuroanatomy, and the recognized clinical patterns of disease in correlation with the lesion location. This usually is a neurologist. The psychiatric assessment can differentiate conversion disorder from other somatoform disorders, factitious disorder, and malingering and can elucidate the psychodynamics that are very important in treatment. The neurologist must recognize the nonorganic process and rule out imitators while avoiding potentially dangerous diagnostic or therapeutic interventions.
• Patients with conversion disorder may present with hemiparesis, paraparesis, monoparesis, alteration of consciousness, visual loss, seizurelike activity, pseudocoma, abnormal gait disturbance, aphonia or dysphonia, lack of coordination, or a bizarre movement disorder. Patients who are more medically naïve typically have more implausible presenting symptoms. The presenting symptoms depend on the cultural milieu, the degree of medical sophistication, and the underlying psychiatric issue.
• Patients with conversion disorder typically deny any emotional problem and resist a consultation with a psychiatrist. Therefore, responsibility lies with other medical personnel to perform the initial management prior to conveying the diagnosis.

Physical

A full physical examination with attention to the mental status (indifferent affect) and neurological examination should be performed. Certain principles are used during the neurological examination to distinguish psychogenic deficits from neurological ones. The pattern of deficits usually does not conform to known anatomic pathways. For example, patients who present with monoparesis will not have weakness in a corticospinal tract or neuropathic or a myopathic distribution. In addition, no changes may be seen in reflexes or tone that typically would be expected.

The physician should contrast formal examination from functional observations. Patients who do not move a limb when asked on examination may be observed to use that limb inadvertently while dressing or talking. Patients who do not dorsiflex the foot while seated may walk on the heels when asked to do so. Another example might be a patient who cannot stand on one leg who may be observed to do so while putting on pants.

Observations when the patient is unaware of being examined are helpful. Patients with psychogenic movements may have no such movements when observed in the waiting room. Multiple examinations by one or more practitioners may disclose variable results. However, caution is necessary when applying these rules. No single feature is absolute. The knowledge pertaining to neuroanatomy and the clinical deficits that arise from abnormalities is not completely known, thus resulting in limitations of the neurological examination. In addition, patients can embellish on organic deficits. Therefore, only a presumptive diagnosis can be made after the initial evaluation.

Further complicating the assessment is the knowledge that up to 30% of patients with conversion disorder develop a physical illness that may account for their symptoms if followed longitudinally. It also is not uncommon for patients with conversion disorder to have a comorbid medical or neurological illness. An example is the patient who exhibits both epileptic seizures and psychogenic nonepileptic seizures, a clinical situation not uncommon to epilepsy referral centers.

Other specific details to help diagnose 3 different conversion symptoms include the following:

• Psychogenic hemiparesis
• • Unilateral weakness or hemiparesis is one manner in which the patient with conversion disorder may present.
    • Classic hemiparesis represents a deficit of the corticospinal tract. In an acute lesion of the corticospinal tract, a patient may demonstrate flaccidity of the weak limbs, which is associated with decreased reflexes. In more chronic lesions, the patient may develop spasticity of the affected limbs, hyperreflexia, and an extensor toe sign (positive Babinski). The patient with hemiparesis from a corticospinal tract lesion may demonstrate weakness of the extensor muscles to a greater extent than the flexor muscles and may show greater weakness distally than proximally.
    • None of these findings would likely be seen in the patient with conversion disorder. In psychogenic hemiparesis, the muscle contractions are poorly sustained and may weaken abruptly as the patient resists the force exerted by the examiner. This is felt clinically as a "give-way" or ratchet-like weakness, unlike the fluid weakness throughout the range of motion usually felt by the examiner in an upper or lower motor neuron lesion.
  • The Hoover sign also may be elicited. When a patient in the recumbent position flexes the thigh and lifts the leg, the downward movement of the contralateral leg is automatic. The examiner places a hand beneath the heel and asks the patient to raise the paretic leg. In feigned weakness, no appreciable downward movement is evident. In addition, when the patient is asked to raise the normal leg, the downward movement is appreciated from the "paretic" leg.
  • Another helpful tool is examining the sternocleidomastoid muscle. Normal contraction of this muscle results in the face rotating in the opposite direction. The patient with psychogenic weakness therefore may display weakness of the contralateral sternocleidomastoid (ie, weakness in turning the face towards the hemiparetic side).
  • Recognizing the patient with psychogenic hemiparesis includes observing the following:
    • No changes in reflexes
    • No changes in tone
    • Give-way quality of weakness
    • Extensor and flexor muscles equally weak
    • Contralateral sternocleidomastoid weakness
    • Positive Hoover sign
    • Difference between formal examination and general observations
• Psychogenic nonepileptic seizures
• • Distinguishing between a psychogenic nonepileptic seizure, or pseudoseizure, and an epileptic seizure is challenging. The manifestations of each are diverse, and the clinical diagnosis rests on historical information from witnesses with varying observational skills. Simultaneous video electroencephalogram (EEG) monitoring has significantly improved the accuracy of diagnosis, but this technique is expensive and not routinely available. Psychogenic seizures may constitute up to 20% of all patients in an epilepsy referral center. Refer to the article on Psychogenic Seizures in the eMedicine Neurology section for more details.
  • Classic clues that suggest nonepileptic seizure include the following:
    • Ineffectiveness of multiple antiepileptic drugs
    • Induced by stress or emotional upset
    • Lack of physical injury
    • Lack of headache or myalgias following convulsions
    • Lack of incontinence
    • Biting the tip of the tongue as opposed to the side or the lip
    • History of sexual or physical abuse
    • Signs or symptoms suggestive of another conversion
    • Memory of a generalized ictal event
  • Ictal characteristics that suggest nonepileptic seizure include the following:
    • Gradual onset of ictus
    • Prolonged duration (>4 min)
    • Atypical or excessive motor activity such as thrashing, rolling from one side to the other, pelvic thrusting, or arrhythmic (out-of-phase) jerking such as alternating side flexion and extension of the arms
    • Waxing and waning amplitude
    • Intelligible speech
    • Bilateral motor activity with preserved consciousness
    • Clinical features that change from one spell to the next (ie, nonstereotyped)
    • Lack of postictal confusion
    • Postictal crying or cursing
    • Directed violent acts
    • Eyes closed during the ictus
    • Resistance to eye opening
    • Purposeful resistance to passive movements
• Psychogenic movement disorders
• • Conversion disorder can imitate the entire spectrum of movement disorders and include tremor, chorea, myoclonus, dystonia, tics, parkinsonism, and a host of bizarre gait disturbances. A commonly used term for a type of this last phenomenon is an astasia-abasia gait pattern, in which the patient will make wild movements of the trunk and arms during a gait evaluation but does not fall or err from a stressed gait such as a tandem or toe gait.
  • Clinical symptoms or signs that may help distinguish psychogenic movements from organic ones include the following:
    • Abrupt onset of symptoms
    • Character of movements atypical of recognized patterns and have inconsistent amplitude, frequency, and distribution
    • Characteristics of movements change over time
    • Entrainment of the tremor to the rate requested by the examiner
    • Spontaneous remissions
    • Movements disappear with distractions
    • Movements increase with attention
    • Response to placebo, psychotherapy, or suggestion
    • Paroxysmal symptoms
    • Nonobjective weakness or sensory changes also present
    • Obvious secondary gain (eg, litigation, health insurance claim, military service)

Causes

• Neuroimaging studies of conversion disorders indicate hypofunction of the dominant hemisphere and a consequent overactivity in the nondominant side. Other neuroanatomic findings have been seen with conversion disorder. Marshall et al reported changes in regional cerebral blood flow (rCBF) in a female patient with a left leg paralysis and intact sensory modalities for which no anatomic cause of her weakness could be found. Attempting to move her paralyzed leg did not show activation of contralateral motor cortex, but rather contralateral orbit-frontal and anterior cingulated cortex were activated. This implied an anatomic inhibition of primary motor cortex in one case of hysterical paralysis.
• Neuropsychological testing shows evidence of impaired attention and short-term memory.
• Psychodynamic theory postulates that conversion symptoms are the result of conversion of anxiety regarding an unconscious intrapsychic conflict into somatic symptoms.
• Learning theorists believe that such symptoms develop from conditioning that occurs during childhood and that these learned behaviors arise again when the person is subjected to overwhelming stress later in life.
• Such symptoms also can be viewed as a form of physical communication of an emotionally charged idea or feeling when one is unable to verbalize the conflict because of personal or social taboos.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

The differential diagnosis of conversion disorders is highly dependent on the manner in which the patient presents. Organic etiologies must be excluded. For example, the differential for psychogenic hemiparesis includes tumor, stroke, multiple sclerosis, and many others.

Other problems to be considered include the following:

Epileptic seizures
Syncope - Cardiogenic, hypovolemia, orthostasis
Syncopal convulsion
Movement disorders - Tics, startle attacks, tremors, myoclonus
Sleep disorders - Narcolepsy, night terrors, restless legs syndrome, rapid eye movement sleep behavioral disorder
Other psychiatric disorders - Panic disorder, intermittent explosive disorder, dissociative disorder
Malingering

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Hemiparesis
• • MRI of brain with diffusion-weighted imaging
  • MRI of cervical region
• Pseudoseizure
• • MRI of brain
  • EEG
  • Prolonged video-EEG monitoring
  • Provocative EEG with placebo induction
  • Echocardiogram
  • Holter monitor
  • Tilt-table test
  • Prolactin level 30 minutes after the event: An elevation above baseline can occur with partial seizures, generalized seizures, or syncope, but not with pseudoseizures.
• Psychogenic movement disorders
• • MRI of brain
  • Twenty-four–hour urine copper, serum ceruloplasmin, and slit lamp examination for evidence of Kayser-Fleisher rings to look for evidence of Wilson disease
  • Thyroid-stimulating hormone, thyroid peroxidase antibodies, thyroglobulin antibodies
  • CBC count with smear for acanthocytes
  • Erythrocyte sedimentation rate, antinuclear antibody, extractable nuclear antibody, anticardiolipin antibody, lupus anticoagulant
  • HIV antibody, Lyme antibody, anti-streptolysin O (ASO) antibody
  • Human chorionic gonadotropin

Procedures

• Hypnosis or amobarbital interview
• • To ensure diagnosis
  • To disclose underlying psychiatric issues
• Brain PET scan - Has demonstrated evidence of left dorsolateral prefrontal cortex hypofunction
• SPECT scan - Has shown decrease in regional blood flow in the thalamus and basal ganglia contralateral to the deficit

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Current understanding of the phenomenon of conversion disorder implicates some role of the unconscious in the pathophysiology of this condition. It is therefore less likely to respond to treatment when the manifestations of the conversion are confronted directly as a unitary method of therapy. Many patients who experience a conversion disorder are unable to understand this inner conflict, which is perhaps occurring on an unconscious level. They may achieve resolution of the conflict, and their physical symptoms, once they are gently made aware of this connection. Once the patient is aware of this, the psychologic currency of the symptom loses value, and the symptom may be allowed to improve.

• Consider hospital admission: The patient may not return for follow-up after being given a psychiatric diagnosis. A more rapid completion of the diagnostic workup is possible. In addition, a parallel investigation of physical and psychologic factors can and should be pursued. One caveat to note is that the clinical situation may be worsened by providing the patient with the secondary gain he or she is seeking.
• Avoid invasive diagnostic and therapeutic interventions.
• Tactful presentation of the diagnosis to the patient includes the following:
• • Avoid giving the patient the impression that you feel there is nothing wrong with them.
  • Do not inform the patient of the diagnosis on the first encounter.
  • Reassure the patient that the symptoms are very real despite the lack of a definitive organic diagnosis.
  • Provide socially acceptable examples of diseases that often are deemed stress-related (eg, peptic ulcer disease, hypertension).
  • Provide common examples of emotions producing symptoms (eg, queasy stomach when talking in front of an audience, sweaty palms when asking someone for a date).
  • Provide examples of how the subconscious influences behavior (eg, nail biting, pacing).
  • Provide reassurance that no evidence of an underlying neurological disorder is present based on the tests that were performed and that the prognosis for recovery is very good.
  • Provide positive reinforcement that the symptoms can improve spontaneously.
  • Inform patients that the symptoms are not volitional, and no one believes that they are faking.
  • Provide a graceful way for the patient to improve from the symptoms. (Allow for the symptom to get better over time, just as an organic entity might improve.)
• No specific pharmacologic therapy is available for conversion disorder; however, medications for comorbid mood and anxiety disorders should be considered. Care should be taken to avoid dependence-producing psychotropic agents.
• Physical therapy may be warranted.
• Institute patient and family education sensitively in order to not make the patient feel worse.
• Regular follow-up appointments with a neurologist or a psychiatrist should be provided to limit ER visits, which may lead to contact with multiple healthcare providers and, in turn, unnecessary diagnostic/invasive tests.

Consultations

• Neurologist: This is the primary evaluation for differentiating conversion disorders from neurological diseases.
• Cardiologist: Consultation is warranted if the patient has episodic alterations of consciousness.
• Physical therapist: Consultation may be warranted.
• Psychiatrist: This generally is indicated when the symptoms persist. This can aid in identification of psychologic stressors symbolically linked to the symptoms and other risk factors for conversion disorder. The patient must be informed about the consultation before the psychiatrist does the interview. Psychiatric treatments that have demonstrated effectiveness include the following:
• Psychodynamic therapy: Patients with borderline intelligence, lack of motivation or introspection capabilities, important secondary gains, or those with a tendency for behavioral acting out likely are poor candidates.
• Behavioral therapy: The inappropriate behavior no longer is rewarded or may even be punished. An advantage is that neither normal intelligence nor insight is necessary for success. A disadvantage is that behavioral therapy relies on controlling the environmental conditions, which may not be feasible.
• Psychologist: Psychosocial interventions that may be helpful include paradoxical intention therapy and hypnosis.
• Family therapist: Interactions and communication within the family are emphasized rather than only focusing on the individual patient.

FOLLOW-UP

Section 7 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Prognosis

• Spontaneous resolution in most - Approximately 75%
• Recurrence of same or different conversion symptoms - Approximately 25% in 15-year follow-up studies
• False-positive diagnosis of conversion disorder
• • Approximately 25% are diagnosed with neurological disease in 10-year follow-up that could account for presenting symptoms.
  • Multiple sclerosis, neurodegenerative diseases, structural myelopathy, peripheral neuropathy, and myopathy accounted for the false-positive diagnoses.
• Good prognostic factors - Acute onset of symptoms, short duration of symptoms, healthy premorbid functioning, higher intelligence, absence of coexisting psychopathology, presence of an identifiable stressor
• Poor prognostic symptoms - Pseudoseizure, psychogenic tremor

Patient Education

• Sensitively review the disorder with the patient and the family in such a way to not make them feel blamed and to not worsen the condition. During such follow up for review of completed imaging and other studies, continuing to emphasize the importance of, as well as your concern for the patient's pain or other symptom is important. The physician may at the same time reassure the patient that the negative test results are good news for their eventual recovery. Frequent office visits to ensure the expected resolution of their symptoms may be helpful.

MISCELLANEOUS

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Delay in diagnosing organic disease due to lack of appropriate evaluation
• Unnecessary interventional diagnostic tests resulting in iatrogenic illness
• Overly direct or confrontational presentation of the diagnosis, which may entrench the symptom and lead to prolonged patient disability

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  French neurologist Jean Martin Charcot shows colleagues a female patient with hysteria at La Salpêtrière, a Paris hospital.
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Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Multimedia
• References

• American Psychiatric Association. Somatoform disorders. In: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC:. APA Press;2000.
• Boffeli TJ, Guze SB. The simulation of neurologic disease. Psychiatr Clin North Am. Jun 1992;15(2):301-10. [Medline].
• Bourgeois JA, Chang CH, Hilty DM. Clinical Manifestations and Management of Conversion Disorders. Curr Treat Options Neurol. Nov 2002;4(6):487-497. [Medline].
• Carter AB. The prognosis of certain hysterical symptoms. Br Med J. 1949;1:1076-9.
• Cloninger CR, Martin RL, Guze SB, Clayton PJ. A prospective follow-up and family study of somatization in men and women. Am J Psychiatry. Jul 1986;143(7):873-8. [Medline].
• Cohen RJ, Suter C. Hysterical seizures: suggestion as a provocative EEG test. Ann Neurol. Apr 1982;11(4):391-5. [Medline].
• Devinsky O, Thacker K. Nonepileptic seizures. Neurol Clin. May 1995;13(2):299-319. [Medline].
• Fahn S. Psychogenic movement disorders. In: Movement Disorders. Vol 3. Oxford, UK: Butterworth-Heinemann; 1994:. 359-72.
• Gould R, Miller BL, Goldberg MA, Benson DF. The validity of hysterical signs and symptoms. J Nerv Ment Dis. Oct 1986;174(10):593-7. [Medline].
• Leis AA, Ross MA, Summers AK. Psychogenic seizures: ictal characteristics and diagnostic pitfalls. Neurology. Jan 1992;42(1):95-9. [Medline].
• Lesser RP. Psychogenic seizures. Neurology. Jun 1996;46(6):1499-507. [Medline].
• Ljungberg L. Hysteria: A clinical, prognostic and genetic study. Acta Psychiatr Scand Suppl. 1957;112:1-162.
• Marjama J, Troster AI, Koller WC. Psychogenic movement disorders. Neurol Clin. May 1995;13(2):283-97. [Medline].
• Marshall JC, Halligan PW, Fink GR. The functional anatomy of a hysterical paralysis. Cognition. 1997;64:B1-B8.
• Merskey H. Conversion symptoms revised. Semin Neurol. Sep 1990;10(3):221-8. [Medline].
• Ruddy R, House A. Psychosocial interventions for conversion disorder. Cochrane Database Syst Rev. 2005;CD005331. [Medline].
• Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry. Dec 2004;161(12):2271-6. [Medline].
• Sar V, Kundakci T, Kiziltan E. Differentiating dissociative disorders from other diagnostic groups through somatoform dissociation in Turkey. J Trauma Dissociation. 2000;1:67-80.
• Schrag A, Lang AE. Psychogenic movement disorders. Curr Opin Neurol. Aug 2005;18(4):399-404. [Medline].
• Shen W, Bowman ES, Markand ON. Presenting the diagnosis of pseudoseizure. Neurology. May 1990;40(5):756-9. [Medline].
• Spence SA, Crimlisk HL, Cope H. Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement. Lancet. Apr 8 2000;355(9211):1243-4. [Medline].
• Stevens H. Is it organic or is it functional. Is it hysteria or malingering?. Psychiatr Clin North Am. Jun 1986;9(2):241-54. [Medline].
• Vuilleumier P, Chicherio C, Assal F. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain. Jun 2001;124(Pt 6):1077-90. [Medline].

Article Last Updated: Apr 12, 2006