Conversion disorder

Author(s): Gary Goldberg, MD

Originally published:11/27/2012

Last updated:03/27/2017

1. DISEASE/DISORDER:

Definition

Conversion disorder (CD) is a condition now also referred to as Functional Neurological Symptom Disorder (FNSD) classified in DSM-5 as related to Somatic Symptom Disorder (SSD).  Other conditions in this category include Medically Unexplained Symptoms, Pain Disorder, and Factitious Disorder.  CD/FNSD presents with motor and/or sensory symptoms initially suggesting identifiable neurologic pathology as the potential cause. However, subsequent diagnostic evaluation fails to reveal neurological disease as the etiological explanation for the symptoms.1  When CD/FNSD presents primarily as an abnormality of voluntary movement—either a lack or an excess of movement—the term Functional or Psychogenic Movement Disorder (PMD) has been employed.  Presentation is typically acute in onset and symptoms may develop consequent to a psychologically conflictual situation although anticipated psychological distress linked to the potentially ominous somatic symptoms may not be evident.  A source of psychological conflict may or may not be disclosed.  More often, symptoms occur in the context of an undisclosed underlying psychological conflict, unmet need or harrowing traumatic experience(s) precipitating overwhelming anxiety that obstructs direct verbal disclosure.  As such, symptoms may be interpreted in a biosemiotic framework as the product of a less direct but more attainable subconscious process for communicating a meaningful plea for medical remediation.2-4  In contrast to Factitious Disorder (FD), symptoms are not simulated through conscious intention in CD/FNSD, although specific symptom form and plausibility may be influenced by the patient’s prior experiences, degree of medical sophistication, and cultural background.  The clinical distinction between CD/FNSD and the consciously simulated symptomatology of FD is difficult and can often only be definitively made with a confession of deceit or when the patient is caught out in a broader deception or with covert surveillance.5  When, in addition to being aware of willful simulation of symptoms, the patient consciously intends the presentation of symptomatology for the purpose of tangible secondary gain, then the patient meets criteria for a diagnosis of malingering.

A partial list of more common CD symptoms includes paralysis or paresis, involuntary movements, abnormal gait, blindness, sensory alteration, and psychogenic nonepileptic seizures (PNESs).

Diagnostic criteria for CD/FNSD based on the DSM-5 include:

  1. One or more symptoms of altered voluntary motor or sensory function.
  2. Clinical findings providing evidence of incompatibility between the symptom(s) and recognized neurological or medical conditions.
  3. The symptom(s) or deficit(s) are not better explained by another medical or mental disorder.
  4. The symptom(s) or deficit(s) cause clinically significant distress or impairment in social, occupational, or other important areas of functioning, and/or warrant medical evaluation.

It should be noted that the diagnosis of CD/FNSD does not definitively exclude the possibility of coexistent and potentially overlapping organic disease.

Etiology

Etiologic perspectives include psychodynamic, behavioral, and neurophysiologic formulations.  Breuer and Freud used the term ‘conversion’ to describe a process through which the ‘unbearable affect’ of existential anguish linked to a repressed upsetting psychological conflict overflows or ‘converts’ into somatic symptoms symbolically and implicitly (ie. nonverbally) referencing the source of the internal dissonance.   This ‘as-if’ mode of indirect communication then leads to a subconscious emotional decompression, diffusion of affect and resultant ‘escape’ from the original overwhelming provocation—the patient is released from the bind of having a pressing issue about which they long to communicate but cannot.6     Others view CD/FNSD as a rational but maladaptive learned behavior that facilitates coping with an otherwise intolerable situation.7

Anxiety reduction is the adaptive primary gain. Empathic response bestowed and attention given by worried friends and family as well as concern from medical personnel regarding possible physical illness or injury can reinforce the subconscious motive and become a source of fortifying secondary gain.

Epidemiology including risk factors and primary prevention

Epidemiologic studies are limited by inconsistencies in case definition (eg, MUPS vs true CD/FNSD) and inaccurate case ascertainment.  Some associated factors are given in Table 1.

Table 1.  Epidemiology of CD/FNSD

Overall incidence rate 4-12 / 100,000
In general hospital patients 5 – 14%
In psychiatric clinic patients 5 – 25%
In neurology clinic patients ~6%
Gender RRR in adults women:men = 2:1 to 6:1
Gender RRR in children girls:boys = 1:1
History of sexual abuse8 Up to 33%
History of physical abuse8 Up to 50%
Associated factors seen in

adult males

Antisocial personality disorder; occupational injury; severe combat stress.
Most frequent age at initial onset Between 2nd and 4th decades

RRR: relative risk ratio

An increased incidence in relatives of probands with CD has been reported suggesting a genetic predisposition.  Psychogenic seizures may occur in up to one fifth of patients referred for assessment to an epilepsy treatment center.9

Patho-anatomy/physiology

Functional neuroimaging studies suggest impaired communication between brain systems linking emotion to volition, movement, and perception, suggesting a mechanism through which elevated anxiety may be converted into physical symptoms.10 Patients with motor CD show increased responsivity and reduced habituation in the amygdala to emotionally provocative stimuli. An abnormally strong functional linkage between the amygdala and the supplementary motor area (SMA) of the nondominant right hemisphere has been identified in functional neuroimaging.11  The SMA is involved in voluntary movement selection and the regulation of internally generated action.  A recently published systematic review and meta-analysis of neuroimaging studies in CD patients reports that multiple ‘areas that are important for motor-planning, motor-selection or autonomic response seem to be especially relevant.’12

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

As noted, onset is frequently correlated with acute psychologic stress or a personal social crisis associated with discordant home life.

Symptoms may be dramatic and can demonstrate variable intensity depending on who is attending to them.  For the majority of cases, the acute condition is self-limited, and symptoms resolve within a few hours to a month with reassurance and intensive supportive counseling.   Chronicity may relate to severity and persistence of the underlying stress, untreated superimposed or coincident psychiatric difficulties, the comorbid presence of a personality disorder, or continuing environmental reinforcement.

Specific secondary or associated conditions and complications

CD is a diagnosis to be entertained only after excluding an organic etiology for the symptoms. In less than 5% of cases, an organic condition eventually surfaces.13 Psychiatric comorbidities, including axis I psychiatric conditions (eg, mood disorder) and axis II personality disorders (eg, passive-aggressive/dependent), are frequently seen.14 Patients usually deny emotional difficulty, and resist psychodynamic formulation and psychiatric consultation. Over-aggressive pursuit of a medical explanation with multiple diagnostic tests or initiation of inappropriate medical treatments can precipitate iatrogenic complications.

2. ESSENTIALS OF ASSESSMENT

History

A comprehensive psychosocial history is critically important. Precipitating stressors or past traumatic experiences may be disclosed if a trusting patient-provider relationship can be established. A careful comprehensive history can identify if there may be a viable organic etiology to be considered and excluded. History can reflect symptom severity and the extent to which symptoms currently interfere with daily function.  Besides conversion disorder, conversion symptoms can be seen in conjunction with other clinical conditions including somatization disorder, substance abuse, affective disorder, and can overlap with co-morbid organic neurologic or medical illnesses.

Physical examination

Physical examination with attention to mental status and neurologic signs should be completed. The distribution and type of impairment often is not consistent with neuroanatomical pathways. Inconsistencies occur between findings on formal examination and behavior in functional situations. For example, a patient who is unable to balance on one foot during the examination may do so while dressing. Specific signs (eg, Hoover’s sign, give-way quality of weakness, contralateral sternocleidomastoid weakness) can help distinguish organic impairment from functional illness but cannot differentiate between CD and malingering. Pathologic reflexes indicate organic etiology.  Patients may embellish or functionally exaggerate manifestations of underlying organic deficit further complicating the assessment and adding to variability of clinical observations across different examiners.

Functional assessment

Observation of gait and movement show inconsistent limitations or highly atypical and sometimes bizarre nonphysiologic patterns of motor impairment. Patients may show blunted or incongruent emotional responses regarding grim implications of reported symptoms, or may fluctuate inappropriately between inordinate preoccupation with symptoms and benign indifference.  Insight and judgment are often limited or impaired.

Laboratory studies

Laboratory studies should be judiciously utilized to exclude organicity. Sensory-evoked potentials can document normal physiologic pathway transmission. With PNESs, electroencephalography with simultaneous video monitoring may be considered, although a normal result does not exclude organic seizures. A prolactin level drawn 30 minutes after a seizure is elevated after organic but not after nonepileptic seizures.

Imaging

Normal imaging of the brain and spinal cord can help eliminate organic conditions, such as multiple sclerosis.

Supplemental assessment tools

Abreaction, which involves the interview of a patient permitting the disclosure and therapist-guided exploration of repressed experiences and associated affect while the patient is under the influence of an anxiolytic medication—typically an intravenous barbiturate or benzodiazepine—was once a common treatment for CD.15  Well-designed studies to definitively determine efficacy as well as circumstances and methods favoring the success of this intervention, however, are lacking.

Early predictions of outcomes

Between 50% and 90% of CD patients exhibit rapid resolution of symptoms after reassurance, although as many as 25% then relapse or develop new conversion symptoms over time.16  Longer duration of symptoms, expectation of nonrecovery, untreated psychiatric comorbidity, tremor or nonepileptic seizures, and receipt of health-related benefits at the time of initial consultation are associated with worse prognosis.

Environmental

Environmental factors play an important role in the precipitation of CD. Mass psychogenic illness occurs when CD develops simultaneously in multiple individuals in a particular locale. An isolated social group environment, shared environmental stressors, development of acute symptoms in key index high-profile cases, and a rapid spread of the problem to others through relational networks are typical contributing factors.17

Social role and social support system

The depth and breadth of the individual’s relational communication and support matrix, including intrapersonal, interpersonal, and sociocultural factors, determines when and how the patient seeks assistance and engages in recommended treatment and, to some extent, the eventual functional outcome and prognosis.

Professional Issues

Discord between patient and provider may result from disagreement regarding etiology. Persisting symptoms can engender feelings of powerlessness, mistrust, as well as provider frustration, which can undermine therapy.18  Owens and Dein emphasized the importance of not labeling patients as “manipulative, dependent or as exaggerating their difficulties,” in order to preserve a functional therapeutic alliance.19  Avoid confronting the patient.  Assume an empathic approach that affirms symptom veracity while focusing on a course of functional improvement rather than an exhaustive search for an ever-elusive organic explanation. Avoid placating with unnecessary interventions and tests. Take care in discussing the diagnosis with the patient.18

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

A recently published multidisciplinary guideline on treatment of MUPSs recommended a multidisciplinary collaborative approach to this complex clinical problem.20,21  Additional guidelines and recommendations are provided in the extended Bibliography below.

At different disease stages

New onset/acute

  • Patients seen in the emergency department with acute CD can be managed with reassurance, education, and psychologic support. Treatment of comorbid psychiatric conditions is often necessary for symptom resolution. A treatment approach that combines cognitive-behavioral therapy focused on adaptive coping and stress management with conventional physical rehabilitation provides the patient with a program that legitimizes and addresses the physical symptoms while providing an acceptable pathway to symptom resolution.22,23

Subacute

  • In cases of chronic CD, a combination of strategic (double-bind) and behavioral therapy becomes necessary.23 The patient is told that symptoms are either because of a psychiatric condition that will require long-term psychotherapy, or because of an organic cause that will respond to the provided specialized rehabilitation treatment plan. This places the patient in a bind, where the only acceptable way that organicity can be demonstrated is if the patient recovers with treatment. This approach is generally successful in most cases of chronic CD.24

Chronic/stable

  • A small percentage of patients relapse. An approach that incorporates intermittent follow-up review sessions and assistance with stress self-management and mindfulness practices can be helpful.25

Coordination of care

Effective treatment of CD/FNSD is best undertaken with a multidisciplinary team in the context of an integrative relational model implementing a collaborative program, recognizing that comprehensive treatment requires interdisciplinary collaboration providing holistic patient-centered care.21

Patient & family education

Transparent treatment includes education of the patient and caregivers regarding the nature of the problem and its management.  This includes constructive explanations of physical symptoms linked to strategies for reducing their functional impact.26  It is important to ensure that caregivers are aware of how they can assist the patient by reinforcing progress toward independence rather than rewarding symptom manifestation.

Emerging/unique Interventions

Standardized health status questionnaires and symptom inventories can assess outcomes. Depression scales and anxiety measures can help assess psychiatric comorbidity.   The use of a scale to assess occurrence of stressful life events can help to identify associated sources of stress.27  Measures of health care utilization can assess reduced dependence on provider services.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  • CD is often self-limited and resolves with education, reassurance, and psychologic counseling.
  • Do not confront patients about the psychologic nature of their symptoms.
  • Intravenous sedative (eg. Thiopental) may help induce revelation of a major disruptive and actively repressed conflict or trauma.
  • Insight-oriented psychotherapy or short-term cognitive-behavioral therapy in conjunction with conventional rehabilitation therapies can be of benefit.
  • More resistant chronic cases may require strategic double-bind behavioral therapy.
  • Care should be patient-centered, multidisciplinary and collaborative, creating an expectation for recovery and return to full independence.
  • Keep the focus on pragmatic recovery of meaningful function with the expectation for functional improvement and effective symptom management in spite of not being able to determine a specific causative mechanism.
  • Pay attention to contributing environmental and contextual psychosocial factors.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Smith and Dwamena proposed a comprehensive approach to patients with MUPSs, including CD.28  Patients are classified according to 3 dimensions: symptom severity (mild, moderate, and severe), duration (acute, subacute, and chronic), and comorbidity (psychiatric, medical, or both).  Clinical management decisions, such as the extent to which one should pursue diagnosis of an underlying organic disease, can then be guided by this scheme.  The authors propose that this approach facilitates successful and cost-effective symptom management.

Recent research suggests distorted interoception and a disturbance involving the ‘sense of body ownership’ and ‘sense of agency’ in patients with CD/FNSD.  Patients demonstrate reduced interoceptive-based bodily awareness with a retained sense of body ownership similar to dissociative disruption seen in other disorders of self-awareness, embodiment and agency.  Other studies suggest that it is the sense of agency that is impaired in PMD as evidenced by decreased action-effect binding.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Patients as ‘persons’ suffer from illness understood as a disturbance in their experiential self-perceived phenomenological state of subjective well-being and embodiment.29  This disturbance develops in the semiotic context of meaningful and significant social relationships and an internal enculturated belief system framing what the illness experience means to them and how it is perceived and evaluated in their intra- and interpersonal (ie. intersubjective) context.2,3,30  Medical providers diagnose and treat diseases, understood as context- and value-free isolated mechanistic pathology disrupting the function and/or structure of body organs and systems. This reductionistic latter approach is woefully insufficient and often misleading in addressing CD/FNSD and related SSDs.31 Eisenberg recommended that “it is essential to reintegrate ‘scientific’ and ‘social’ concepts of disease and illness as a basis for a functional system of medical research and care.”32 A philosophical post-Cartesian framework that transcends mind-body dualism and very tightly integrates the experiential/relational ‘subjective’ social perspective with the observational/rational ‘objective’ scientific perspective has been proposed for improving treatment of psychosomatic conditions.33

REFERENCES

  1. Aybeck S, Kanaan RA, David AS. The neuropsychiatry of conversion disorder.  Curr Opin Psychiatry.  2008;21:275-280.
  2. Burnum JF. Medical diagnosis through semiotics.  Giving meaning to the sign.  Ann Intern Med. 1993;119:939-943.
  3. Adler RH, von Uexküll T, Hermann JM. The two faces of medical evidence.  Swiss Med Wkly. 2002;132:397-400.
  4. Rafieian S. Cybersemiotic medicine.  A framework for interdisciplinary medicine.  Cybernetics and Human Knowing. 2010;17:65-93.
  5. Allin M, Streeruwitz A, Curtis V. Progress in understanding conversion disorder. Neuropsychiatr Dis Treat. 2005;1:205-209.
  6. Breuer J, Freud S. Studies on hysteria. In: Strachey J, Strachey A, eds. The Standard Edition of the Complete Psychological Works of Sigmund Freud. Vol. II. London, England: Hogarth Press and the Institute of Psycho-Analysis; 1955:vii-xxxi, 1-311.
  7. Rofe Y, Rofe Y. Conversion disorder.  A review through the prism of the rational-choice theory of neurosis.  Eur J Psychol 2013;9:832-868.
  8. Roelofs K, Spinhoven P, Sandijck P, Moene FC, Hoogduin KA. The impact of early trauma and recent life-events on symptom severity in patients with conversion disorder. J Nerv Ment Dis. 2005;193:508-514.
  9. Benbadis SR, Allen Hauser W. An estimate of the prevalence of psychogenic non-epileptic seizures.  2000;9:280-281.
  10. Black DN, Seritan AL, Taber KH, Hurley RA. Conversion hysteria. Lessons from functional imaging. J Neuropsychiatry Clin Neurosci. 2004;16:245-251.
  11. Voon V, Brezing C, Gallea C, et al. Emotional stimuli and motor conversion disorder. Brain. 2010;133:1526-1536.
  12. Boekle M, Liegl G, Jank R, Pieh C. Neural correlates of conversion disorder:  overview and meta-analysis of neuroimaging studies on motor conversion disorder.  BMC Psychiatry.  2016;16:195.  Published online 2016 Jun 10. doi:  1186/s12888-016-0890-x
  13. Stone J, Smyth R, Carson A, et al. Systematic review of misdiagnosis of conversion symptoms and “hysteria”. BMJ. 2005;331:989-994.
  14. Binzer M, Andersen PM, Kullgren G. Clinical characteristics of patients with motor disability due to conversion disorder: a prospective control group study. J Neurol Neurosurg Psychiatry. 1997;63:83-88.
  15. Poole NA, Wuerz A, Agrawal N. Abreaction for conversion disorder:  systematic review with meta-analysis.  Br J Psychiatry. 2010;197:91-95.
  16. Hafeiz HB. Hysterical conversion: a prognostic study. Br J Psychiatry. 1980;136:548-551.
  17. Jones TF. Mass psychogenic illness. Role of the individual physician. Am Fam Physician. 2000;62:2649-2653.
  18. Stonnington CM, Barry JJ, Fisher RS. Conversion disorder.  Am J Psychiatry. 2006;163:1510-1517.
  19. Owens C, Dein, S. Conversion disorder: the modern hysteria. Adv Psychiatr Treat. 2006;12:152-157.
  20. van der Feltz-Cornelis CM, Hoedeman R, Keuter EJ, Swinkels JA. Presentation of the Multidisciplinary Guideline Medically Unexplained Physical Symptoms (MUPS) and Somatoform Disorder in the Netherlands: disease management according to risk profiles. J Psychosom Res. 2012;72:168-169.
  21. Smith HE, Rynning RE, Okafor C, et al. Evaluation of neurologic deficit without apparent cause:  the importance of a multidisciplinary approach.  J Spinal Cord Med. 2007;30:509-517.
  22. Heruti RJ, Levy A, Adunski A, Ohry A. Conversion motor paralysis disorder: overview and rehabilitation model. Spinal Cord. 2002;40:327-334.
  23. Teasell R, Shapiro A. Rehabilitation of conversion disorders: a programmatic experience. Phys Med Rehab. 2002;16:45-52.
  24. Shapiro AP, Teasell RW. Behavioural interventions in the rehabilitation of acute v. chronic nonorganic (conversion/factitious) motor disorders.  Br J Psychiatry. 2004;185:140-146.
  25. Fjorback LO, Arendt M, Ornbøl E, et al. Mindfulness therapy for somatization disorder and functional somatic syndromes: randomized trial with one-year follow-up.  J Psychosom Res. 2013;74:31-40.
  26. Burton C, Weller D, Marsden W, Worth A, Sharpe M. A primary care symptoms clinic for patients with medically unexplained symptoms: pilot randomized trial. BMJ Open. 2012;2:e000513.
  27. Nicholson TR, Aybek S, Craig T, et al. Life events and escape in conversion disorder.  Psychol Med. 2016;46:2617-2626.
  28. Smith RC, Dwamena FC. Classification and diagnosis of patients with medically unexplained symptoms. J Gen Intern Med. 2007;22:685-691.
  29. Fuchs T, Schlimme JE. Embodiment and psychopathology:  a phenomenological perspective.  Curr Opin Psychiatry. 2009;22:570-575.
  30. Kleinman A, Benson P. Culture, moral experience and medicine.  Sinai J Med.  2006;73:834-839.
  31. Schwartz MA, Wiggins OP. Science, humanism and the nature of medical practice: a phenomenological view. Perspect Biol Med. 1985;28:331-366.
  32. Eisenberg L. Disease and illness. Distinctions between professional and popular ideas of sickness. Culture Med Psychiatry. 1977;1:9-23.
  33. Schwartz MA, Wiggins OP. Psychosomatic medicine and the philosophy of life. Philos Ethics Humanit Med. 2010;5:2.

Bibliography

Blakemore RL, Hyland BI, Hammond-Tooke GD, Anson JG. Distinct modulation of event-related potentials during motor preparation in patients with motor conversion disorder.  PLoS One. 2013;8:e62539.

Blakemore RL, Hyland BI, Hammond-Tooke GD, Anson JG. Deficit in late-stage contingent negative variation provides evidence for disrupted movement preparation in patients with conversion paresis.  Biol Psychol. 2015;109:73-85.

Carson AJ, Brown R, David AS, et al. Functional (conversion) neurological symptoms. Research since the millenium. J Neurol Neurosurg Psychiatry. 2012;83:842-850.

Dallocchio C, Marangi A, Tinazzi M. Functional or psychogenic movement disorders:  an endless enigmatic tale.  Front Neurol.  http://dx.doi.org/10.3389/fneur.2015.00037.

Demartini B, Petrochilos P, Ricciardi L, et al. The role of alexithymia in the development of functional motor symptoms (conversion disorder).  J Neurol Neurosurg Psychiatry. 2014;0:1-6.

Demartini B, Ricciardi L, Crucianelli L, et al. Sense of body ownership in patients affected by functional motor symptoms (conversion disorder).  Conscious Cogn.  2016;39:70-76.

Ellenstein A, Kranick SM, Hallett M. An update on psychogenic movement disorders. Curr Neurol Neurosci Rep. 2011;11:396-403.

Evens A, Vendetta L, Krebs K, Herath P. Medically unexplained neurologic symptoms:  a primer for physicians who make the initial encounter.  Am J Med. 2015;128:1059-1064.

Feinstein A. Conversion disorder: advances in our understanding. 2011;183:915-920.

Gelauff J, Stone J, Edwards M, Carson A. The prognosis of functional (psychogenic) motor symptoms:  a systematic review.  J Neurol Neurosurg Psychiatry.  2014;85:220-226.

Hurwitz TA. Somatization and conversion disorder.  Can J Psychiatry. 2004;49:172-178.

Kanaan R, Carson A, Wesely SC, et al. What’s so special about conversion disorder?  A problem and proposal for diagnostic classification.  Br J Psychiatry.  2010;196:427.

Kranick SM, Moore JW, Yusuf N, et al. Action-effect binding is decreased in motor conversion disorder:  Implications for sense of agency.  Mov Disord. 2013;28:1110-1116.

Kranick SM, Hallett M. Neurology of volition.  Exp Brain Res. 2013;229:313-327.

Neilsen G, Ricciardi L, Demartini B, et al. Outcomes of a 5-day physiotherapy programme for functional (psychogenic) motor disorders.  J Neurol. 2015;26:674-681.

Nicholson TR, Stone J, Kanaan RA. Conversion disorder: a problematic diagnosis. J Neurol Neurosurg Psychiatry. 2011;82:1267-1273.

Ricciardi L, Demartini B, Crucianelli L, et al. Interoceptive awareness in patients with functional neurological symptoms.  Biol Psychol.  2016;113:65-74.

Stone J, Sharpe M. Conversion disorder in adults.  Multiple sections available at http://www.uptodate.com/contents/

Stone J, Perthen J, Carson AJ. ‘A leg to stand on’ by Oliver Sacks: a unique autobiographical account of functional paralysis. J Neurol Neurosurg Psychiatry. 2012;83:864-867.

Stone J, Warlow C, Sharpe M. Functional weakness: clues to mechanism from the nature of onset. J Neurol Neurosurg Psychiatry. 2012;83:67-69.

Stone J, Warlow C, Sharpe M. The symptom of functional weakness: a controlled study of 107 patients. Brain. 2010;133:1537-1551.

Stone J, Zeman A, Simonotto E, et al. FMRI in patients with motor conversion symptoms and controls with simulated weakness. Psychosom Med. 2007;69:961-969.

Stone J, Carson A, Duncan R, et al. Which neurological diseases are most likely to be associated with “symptoms unexplained by organic disease.”  J Neurol. 2012;259:33-38.

Stone J. We must tell our patients what is wrong with them even if we don’t know why they have symptoms.  Pract Neurol. 2011;11:98-99.

Voon V, Gallea C, Hattori N, Bruno M, Ekanayake V, Hallett M. The involuntary nature of conversion disorder. Neurology. 2010;74:223-228.

Original Version of the Topic

Gary Goldberg, MD. Conversion disorder. 11/27/2012.

Author Disclosure

Gary Goldberg, MD
Nothing to Disclose

Related Articles