Vision Loss

Sudden Vision Loss: A Case Report and Overview of Conversion Disorder

Abdul Ahad Qazizada, MD

James C. Higgins, DO, CAPT, MC, USN, Ret.,

ABSTRACT: Conversion disorder (CD) is a mental health condition in which the patient experiences sudden neurologic symptoms that are not feigned and cannot be explained by any physical findings during a medical evaluation, making diagnosis difficult. Patients’ symptoms are often debilitating and involve motor or sensory functions, such as ambulation, sight, speech, or hearing. This article reports a case of CD in a patient who suddenly lost vision following a series of stressful situations. It also provides an overview of CD, reviewing its classification, etiology, pathophysiology, epidemiology, risk factors, diagnosis, prognosis, and treatment.

Conversion disorder (CD), also known as functional neurological disorder, Briquet’s syndrome, hysteria, hysterical neurosis, somatization disorder, somatoform disorder, and psychogenic disease, is a condition that manifests sudden neurologic symptoms that cannot be explained by any physical examination or neurologic findings. These symptoms often occur directly after a stressful event and are not feigned or deliberately produced, but are postulated to represent the “conversion” of underlying emotional distress into physical symptoms.  

Reports of CD date back to antiquity, with the first descriptions originating with the ancient Greeks and Egyptians, who observed the condition in women and attributed the symptoms to the uterus.1,2 Greek physician Hippocrates surmised that the uterus in these patients became dry and roamed their bodies in search of moisture, causing symptoms by compressing other organs during its migration.1 In fact, most illnesses in women at that time were attributed to the womb and classified as hysteria, which is derived from the Greek word hysterika, meaning uterus.1 It was not until the 17th century that CD was given psychological roots.2 At that time, CD was classified as a form of melancholy.2 During the 19th century, Paul Briquet built on this idea when he described CD as a dysfunction of the central nervous system, which originated the term Briquet’s syndrome3,4; however, Freud was the first to use the term conversion to refer to the disorder.5,6 Freud suggested that the condition manifested when the psychological distress of a repressed conflict converted into somatic symptoms,5,6 which is the conceptualization still largely recognized today.

Despite CD’s long-documented history, the condition remains poorly understood and difficult to diagnose. It is often confused with other psychological disorders, and even modern classifications systems are not in complete agreement about how to classify CD. This article includes a case report that serves to illustrate how CD might present and provides an overview of this condition, focusing on its classification, etiology, pathophysiology, epidemiology, risk factors, diagnosis, prognosis, and treatment.
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A 23-year-old white female nutrition assistant was brought to the emergency department by her family after experiencing sudden neurologic symptoms. She had been delivering food while working in a local retiree resident facility when she reported “suddenly passing out for a couple of seconds while on the elevator.” She stated that she woke up with blurred vision that developed into loss of vision in both eyes. She also reported an inability to stand due to weakness in her left leg. 

While in the emergency department, the patient described seeing only shadows. She stated that she was generally in good health without significant medical issues or any history of chronic medical conditions or surgeries, which was confirmed by her mother. The patient had no reported mental health history and no history of aversive childhood experiences (ie, abuse or neglect). She had never been seen by a psychiatrist or been on any psychiatric medications (eg, narcotics, hypnotics, antipsychotics, anxiolytics). There was also no reported use of tobacco, alcohol, herbal supplements, or over-the-counter or illicit drugs. The patient’s family history was not significant for medical or psychiatric diseases, including anxiety, depression, or psychosis; however, the patient’s mother reported that her daughter was experiencing significant situational stressors from working 2 jobs, attending school, being a single parent to a 4-year-old child, experiencing significant financial difficulties, and having a difficult relationship with her child’s father.

On physical examination, the patient was alert, awake, and oriented to person, time, and place. Her vital signs were stable with a blood pressure of 122/70 mm Hg and no orthostatic changes, a heart rate of 80 beats per minute, and a temperature of 97.6ºF. A thorough systemic examination was normal, including of her cardiovascular system, with no abnormalities detected on her electrocardiogram. 

On neurologic examination, her speech was normal, her pupils were slightly sluggish but reactive, she was able to see light that was shined into her eyes, and she demonstrated a full range of eye movement, but there was no visual acuity to hand motion or finger counts. The patient had no facial asymmetry and had normal strength in her upper extremities. She had some trouble lifting her left leg off the bed but was able to walk with assistance. No sensory deficits were noticed. A Mini-Mental State Examination yielded a score of 30, indicating normal cognition.

All laboratory work was normal, including a complete blood count, comprehensive metabolic panel, blood glucose test, and drug screening. Imaging studies—including CT scan, contrast-enhanced CT angiogram of the brain,  MRI, and magnetic resonance angiography of the head and neck—were normal. 

The patient was admitted to the hospital and observed for 23 hours, during which time neurology and ophthalmology consultants examined her. Their evaluation revealed no clear anatomical cause for her vision loss or left leg weakness, prompting consultation with the psychiatry department. The psychiatrist who examined her made a diagnosis of CD based on the findings of unexplained vision loss (ie, it was not associated with an identifiable lesion in her visual pathway); normal physical examination and patient history; and observations of the patient and her family. Following the diagnosis, the psychiatrist engaged the patient in a brief session of cognitive behavioral therapy and supportive therapy, to which she responded well. The following day, she reported feeling less stressed, was able to walk normally, and her eyesight gradually improved but was still blurry. The patient was referred for outpatient psychotherapy. After a few days, she was in complete remission per a follow-up visit with her primary care physician.


Two modern classification systems currently categorize CD: the American Psychiatric Association’s 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the 10th revision of the World Health Organization’s International Classification of Diseases (ICD-10). The challenge is that these systems are not in agreement on how to categorize CD. The DSM-5 considers CD a somatoform disorder,7 whereas ICD-10 considers it a dissociative disorder, with somatoform disorders comprising a separate category of conditions.8 Using the DSM-5, the diagnosis rests upon positive clinical findings that indicate the patient’s symptoms are incongruent with his or her 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 his or her unaffected limb).7 ICD-10 characterizes CD as a disruption of awareness, memory, identity, sensation, and control of body movements.8 Diagnostic equivalents to CD within ICD-10 include the following8:

•Dissociative motor disorders

•Dissociative anesthesia andsensory loss

•Dissociative convulsions

•Mixed dissociative disorders.

Dissociation in this context often includes feelings of disconnection from one’s own body (depersonalization) or from one’s environment (derealization).9 Despite these differences in classification, both the DSM-5 and ICD-10 require nonorganic neurologic symptoms to occur in isolation for a diagnosis of CD to be made.


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As previously noted, CD is attributed to psychological conflicts or recent stressors. The symptoms produced may lead to primary and secondary gains for the patient. The primary gain is the channeling or conversion of emotional arousal into physical symptoms (eg, absence of movement of one limb, loss of vision), which takes the focus away from the emotional conflict and reduces anxiety. According to psychodynamic theory, these unconsciously produced symptoms help defend against unacceptable impulses.5 Patients with CD may also experience secondary gains, which are the external benefits derived from having symptoms (eg, change in the stressful situation).10 For example, a patient’s sudden loss of vision enables her to obtain financial compensation and receive extra help; however, unlike with malingering or factitious disorder, the patient’s symptoms are not consciously produced to derive these benefits. Learning theory attempts to explain how secondary gains can serve to maintain conversion symptoms, emphasizing the concept that the environment shapes behaviors. It considers conversion symptoms to be maladaptive operant behaviors that act on the environment to produce reinforcing consequences (secondary gains) that are then sustained by the rewards of these behaviors.11 

Although the conversion hypothesis has long been dominant, there are other etiological hypotheses,12 particularly as imaging modalities have improved. Functional neuroimaging studies have indicated a neurophysiological basis for CD, albeit triggered by psychological stressors.13 Data from these studies suggest that primary perception is intact during conversion reactions, but that modulation of sensory and motor planning is impaired by disruption of the anterior cingulate cortex, orbitofrontal cortex, and limbic brain regions.13,14 When examining specific CD symptoms, various distinct neurophysiological changes have been observed, including reduced activation of the frontal and subcortical areas involved in motor control during conversion paralysis,15 reduced activation in somatosensory cortices during conversion anesthesia,16 and reduced activation in the visual cortex during conversion blindness.17 Although neural circuits linking volition, movement, and perception have been found to be disrupted in patients with CD,14 definitive conclusions cannot be drawn due to these studies having small, heterogeneous study populations and varying study designs. 


CD prevalence rates vary depending on the population studied, the setting of the population studied, and whether the study assessed the frequency of conversion symptoms or required an actual CD diagnosis for inclusion.10 Factors that increase the risk of CD include recent significant stress or emotional trauma, female sex (with a female to male ratio ranging from 2:1 to 10:1), family history of CD, and a personal history of having another mental health condition (eg, anxiety disorder), a neurologic disease that causes similar symptoms (eg, epilepsy), and/or a history of physical or sexual abuse, particularly during childhood.7 Although CD may present at any age, it is rarely encountered in children younger than 10 years or in adults older than 35 years.18 Prevalence may also be influenced by societal and cultural factors. It has been reported that those with less than a high school education, those of lower socioeconomic status, and those living in rural areas have a higher prevalence of CD and other somatoform disorders.11 A study that compared the prevalence of mental disorders among persons living in Puerto Rico with those of individuals living in the United States found that somatoform disorders and its symptoms were significantly more common in Puerto Rico.19 Such disparities in prevalence between cultures has been postulated to occur as a result of certain cultures prohibiting the direct expression of intense emotions, predisposing individuals to manifest their emotions physically.11 

When examining individual symptoms of conversion in the general hospital setting, a prevalence of 20% to 25% has been reported,20 but only 5% of these patients fully meet the criteria for CD.21 With the presence of other neurologic disorders being a risk factor for CD and many patients with CD symptoms receiving neurologic evaluations, it is not surprising that the prevalence increases in neurologic settings. In a study of 100 consecutive patients newly admitted to a neurology ward, 40% had no objective evidence of a neurologic disorder.22 In another study that included 300 new referrals to an outpatient neurology clinic, 11% had symptoms that were rated as “not at all explained” by organic disease and 19% had symptoms that were only “somewhat explained” by organic disease, indicating that 30% of new referrals to general neurology clinics have symptoms that are poorly explained by identifiable organic diseases.23 When examining prevalence data from psychiatric services, they paint yet another picture. In this setting, individual symptoms of CD have been reported to be ubiquitous.24 



In the United States, the DSM-5 criteria are predominantly used to diagnose conversion disorder (Table 1).7 When diagnosing CD, it is not necessary to identify conflicts or other stressors associated with conversion symptoms.7,12 Although psychological factors are frequently observed in patients with conversion symptoms, this is not always the case. When patients present with symptoms that may represent CD, assessment requires evaluating for the following25,26:

• Inconsistency at different points in the examination. For example, how is the patient’s gait when entering the examination room versus when leaving it? What occurs when the patient takes off his or her clothing and puts them back on? What occurs when the patient retrieves something from his or her bag?

• Incongruity between the symptoms and recognized disease (ie, symptoms do not conform to known anatomical pathways and physiological mechanisms; Table 2).

The diagnosis of CD should be considered when neurologic signs are atypical, do not conform anatomically, or are at odds with the result of clinical investigations. Observations when the patient is unaware that he or she is being examined are helpful. Patients with psychogenic movements may have no such movements when observed in the waiting room or may show variability in these movements during multiple examinations by one or more practitioners.27 Two common findings in patients with CD that warrant further discussion are weakness and psychogenic visual disturbance, both of which were encountered in our patient.

Weakness. Weakness is one of the most common motor symptoms encountered in patients with CD. A randomized trial that included 127 patients with functional symptoms rated by neurologists as “not at all” or only “somewhat” explained by organic disease found weakness in 31% of these patients.28 In addition to facial weakness (Table 2), patients with CD may present with hemiparesis (unilateral weakness or paralysis) or weakness and paralysis of their entire body. In psychogenic hemiparesis, the muscle contractions are poorly sustained and may weaken abruptly as the patient resists the force extended by the examiner. This is felt clinically as a “give way” or “ratchet-like weakness.”27 In contrast, classic hemiparesis occurs as a result of a deficit in the corticospinal tract. If an acute lesion is present in the tract, a patient may demonstrate flaccidity of the weak limbs and decreased reflexes. The patient may also demonstrate weakness of the extensor muscles to a greater extent than that of the flexor muscles, and/or show greater weakness distally than proximally. Such findings are unlikely to be observed in the patient with CD. 

In patients with leg paresis, Hoover’s sign may be to distinguish an organic disease process from nonorganic neurologic symptoms. When a patient in a recumbent position flexes the thigh and lifts the leg, the downward movement of the contralateral leg is automatic. In feigned weakness, no appreciable downward movement is evident.29

Psychogenic visual disturbance. Vision disturbances are among the most common sensory symptoms experienced by patients with CD. Visual symptoms may include intermittent blurred vision, double vision (due to spasm of convergent eye movements), nystagmus, visual field defects, and complete blindness.25 A randomized trial that included 127 patients found that functional vision loss occurred in 16%.28 Complete blindness, as with complete paralysis, is associated with an increased probability that the symptom is factitious. In patients presenting with complete binocular blindness, the following tests can be used to determine organic disease processes from CD25,30:

Fingertip test. The fingertip test requires the patient to touch the tips of his/her index fingers together. Blind people can readily do this using proprioception, whereas patients with CD tend to have difficulty bringing their fingers together. 

Menace reflex. The menace reflex involves presenting a visual threat (eg, a closed fist) to the eyes. Patients with CD tend to flinch or blink; however, this test does not exclude the possibility of cortical visual impairment.

Mirror test. This test requires the patient to look at a large mirror placed in front of him or her while having both eyes open. The examiner observes the patient’s eyes while moving the mirror slightly from side to side in front of the patient. If the patient tracks himself/herself in the mirror, it indicates that he/she can see. 

Optokinetic test. The optokinetic test consists of holding a large rotating drum with black and white vertical stripes on it close to the patient’s eyes. If optokinetic nystagmus results, it indicates that the brain can at some level detect the stripes; however, this test does not exclude the possibility of cortical visual impairment.

Signature test. This test requires the patient to write his/her signature. This is another nonvisual task that blind people can readily perform, but that patients with CD may have difficulty with.

Tearing reflex. The tearing reflex suddenly presents strong illumination in front of the patient’s eyes, which should lead to tearing. This test requires intact vision, but does not exclude the possibility of cortical visual impairment. 

conversion disorder


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Diagnosing CD is difficult, particularly because the differential diagnosis includes a variety of neurologic disorders, general medical disorders, psychiatric disorders, and the behavioral disorder of malingering.7,27 What follows are brief descriptions of some common neurologic and medical disorders that should be considered, as well as strategies for distinguishing these conditions from CD:

Epilepsy. Epilepsy and the psychogenic nonepileptic seizures that may occur with CD both manifest with unresponsive behavior and motor movements that suggest a generalized convulsion or complex partial seizure. However, recording an event on video electroencephalography and analyzing the clinical and electrographic features can help distinguish between psychogenic nonepileptic seizures and epileptic seizures.

Movement disorders. Patient with psychogenic movement disorders and those with movement disorders due to defined neurologic diseases can both present with abnormal movements. However, several clinical features characterize psychogenic movement disorders, most notably that its signs and symptoms are inconsistent over time and incongruent with recognizable neurologic diseases. 

Multiple sclerosis. Both multiple sclerosis and CD can produce motor and sensory symptoms, such as numbness or weakness of the legs and visual disturbances. Patients with CD-related leg numbness/weakness have inconsistent leg movements, whereas patients with multiple sclerosis alone do not. In addition, characteristic lesions on MRI can distinguish multiple sclerosis from CD. 

Myasthenia gravis. Myasthenia gravis and CD can both present with weakness that changes over time, but patients with CD will demonstrate inconsistency without fatigue. In addition, myasthenia gravis is often associated with bulbar symptoms, diplopia, and ptosis, which are rare in CD. Serologic tests that screen for autoantibodies and electrophysiologic studies (repetitive nerve stimulation studies and single-fiber electromyography) can be used to confirm a diagnosis of myasthenia gravis. 

Spinal disorders. Spinal disorders (eg, cervical myelopathy, lumbar nerve root entrapment) and CD may each cause weakness and/or sensory disturbance; however, patients with CD have inconsistent limb weakness, whereas patients with spinal disorders generally do not. Depending on the patient’s symptoms, organic causes should be excluded via laboratory and imaging studies.

Stroke. Stroke and CD can both manifest with weakness, but patients with CD have inconsistent limb movements, whereas patients with stroke do not. An MRI should be performed in all patients with a suspected stoke to ensure an accurate diagnosis is made. 

Several psychiatric disorders, including depersonalization/derealization disorder, factitious disorder, and somatic symptom disorder, as well as the behavioral disorder of malingering, also require careful consideration when diagnosing CD. The section that follows describes how to distinguish these disorders from CD7

Depersonalization-derealization disorder. Depersonalization (feeling disconnected from one’s own body) and/or derealization (feeling disconnected from one’s environment) characterize depersonalization-derealization disorder and can also occur in CD, with some patients warranting both diagnoses.7 Although both depersonalization-derealization disorder and CD can present suddenly, particularly after a traumatic event, patients with CD experience physical symptoms of altered motor and sensory functions (eg, blindness, paralysis), whereas patients with depersonalization-derealization disorder present with psychological symptoms, such as feeling unreal, disconnected from reality, and disconnected from loved ones.27

Factitious disorder. Although neurologic symptoms that are not due to disease can occur in both persons with CD and factitious disorder, the primary distinction is that patients with factitious disorder deliberately feign symptoms and deceive clinicians to obtain medical care. In CD, there is no clear evidence that symptoms have been simulated for the purpose of receiving medical care or any secondary gains.7,12,30 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.27

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.7 Somatic symptoms that cause distress and/or impairment can occur in both somatic symptom disorder and CD, and some patients may warrant both diagnoses. Patients with somatic symptom disorder experience 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; thus, the disorder can occur in patients whose symptoms are explained by recognized diseases. In contrast, CD is characterized by evidence of inconsistency between the clinical findings and recognized disease. In addition, the excessive thoughts, feelings, and behaviors that occur in somatic symptom disorder may not be present in CD.27 

Malingering. Malingering and CD are both characterized by symptoms that lack a pathologic basis.7 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 considered a behavior and not a psychiatric disorder. In CD, there is no evidence of intentionally producing symptoms.7,12,30 Clinicians should consider the possibility of malingering if any of the following are present:        

• Multiple inconsistencies in the patient’s history

• Nonadherence with diagnostic evaluation or treatment

• Antisocial personality disorder

• Medical–legal context (eg, patient is referred by an attorney for evaluation).


For most patients, acute symptoms of CD resolve within 1 week, but 20% to 25% of patients may have recurring symptoms within a year, often in association with a stressful event.10 Good prognostic signs include an acute onset and short duration of symptoms, a clearly identifiable stressor, access to a therapist, and a psychologically minded patient (ie, those with a capacity for self-examination, self-reflection, and introspection). A 2009 study of how neurologists view CD showed that some clinicians fail to understand their patients psychologically and may not distinguish their patients’ symptoms from feigning; however, how these attitudes influence prognosis remains unknown.31


CD prognosis has been linked to the duration of symptoms and accessibility to a therapist; thus, it is essential for physicians to rule out neurologic causes as quickly as possible and to refer patients with suspected CD to a psychiatrist or psychologist for further evaluation and treatment. In the presence of often complex symptoms and causes, a multidisciplinary approach to treatment using pharmacotherapy, psychotherapy, physiotherapy, and intervention by a social worker is ideal, despite the empirical data supporting such an approach being limited.10 When multiple healthcare providers are involved in the management of CD, good communication between the treating clinicians is required to maintain a consistent approach to treatment. The primary care physician can play a pivotal role in facilitating a multidisciplinary approach and in improving the care of patients with CD by using the strategies outlined in Table 3.

Currently, empirical data regarding actual CD treatments are lacking, but preliminary findings from studies with small study populations suggest that antidepressants/anxiolytics,32,33 behavioral therapy,34 paradoxical intention,35 and transcranial magnetic stimulation (TMS)36 may be effective; however, these results require validation in larger studies. 

Antidepressants/anxiolytics. Patients with CD often have depression and/or anxiety. In one study that assessed 100 patients with CD for anxiety and depressive symptoms using the Hospital Anxiety and Depression Scale (HADS), anxiety was found in 35% of cases, depression in 29% of cases, and both conditions in 31% of cases.32 Overall comorbidity from anxiety and depressive symptoms in CD was high, affecting 95% of patients. Based on these findings, the investigators suggest that patients with CD need to be better assessed and treated for anxiety and depressive symptoms to optimize outcomes. 

In a small study that assessed antidepressant treatment outcomes of psychogenic movement disorders, 8 of the 10 patients with primary CD showed marked motor and global improvements upon taking antidepressants, and there were 7 complete remissions.33 All of the patients with primary CD had a current or previous depressive or anxiety disorder. It has been postulated that successfully treating depression and anxiety may improve or resolve CD because it removes the primary gain that underpins the conversion reaction; however, pharmacotherapies may not always be necessary. In some cases, other treatments for CD, such as behavioral therapy and transcranial magnetic stimulation (TMS), may be sufficient to treat the underlying anxiety and/or depression.  

Behavioral therapy. Behavioral therapy is a form of psychotherapy that strives to reinforce desirable behaviors and eliminate unwanted or maladaptive ones. Many different behavioral therapy techniques are available, but it is unclear which are most effective for CD. 

In a UK study that included patients with acute and chronic nonorganic motor disorders, 8 of 9 acute patients and 1 of 28 chronic patients successfully underwent a standard behavioral program.34 Using a crossover design, 21 of these chronic patients proceeded to receive a strategic-behavioral treatment in which they and their families were told that full recovery constituted proof of an organic etiology and failure to recover was definitive proof of a psychiatric etiology. By discharge from the rehabilitation facility, 13 patients with chronic nonorganic motor disorders were symptom-free, indicating that behavioral interventions—like all interventions—need to be adjusted and tailored to the patient.

Paradoxical intention. Paradoxical intention therapy strives to overcome neurotic thoughts or habits by having patients confront their source of fear. In a study that included 30 patients with CD who were admitted to the emergency department for pseudoseizures, 15 received paradoxical intention treatment and 15 received diazepam.35 Both groups had similar anxiety scores at the beginning of the study (z=1.08; P=.28). Of the 15 patients who completed paradoxical intention, 14 (93.3%) responded favorably to this treatment. In contrast, 9 of the 15 patients who completed diazepam therapy (60%) responded well to this therapy, with the remaining 6 still experiencing their conversion symptoms at the end of 6 weeks. In this small study, paradoxical intention–treated patients appeared to have greater improvements in anxiety scores (z=2.43; P<.015) and conversion symptoms (t=2.27; P=0.034) than their diazepam-treated counterparts, indicating paradoxical intention may be a promising treatment for CD.

Transcranial magnetic stimulation. TMS is a noninvasive procedure that uses magnetic fields to stimulate nerve cells in the brain. It has been used to treat depression, but data indicate that it might also be a promising therapy for CD. TMS has been reported to “turn on” regions of the brain (eg, motor and sensory cortices) that have been deactivated by unconsciously driven limbic activity.10 This observation corresponds with the functional MRI data elucidating the functional neuroanatomy of conversion.10 

A study that investigated the effect of repetitive TMS in four patients with nonorganic limb paralysis found the therapy to improve most patients’ motor function.36 In the study, TMS was applied over 5 to 12 weeks to the contralateral motor cortex, providing a daily total number of stimuli of 4000. By the end of the study, 1 patient had complete restoration of motor function, 2 patients had marked improvement in their motor function, and 1 patient did not improve, but this patient was identified to be a malingerer. Based on their findings, the authors conclude that repetitive TMS may have a therapeutic effect in CD patients with motor deficits36; however, it is unclear whether TMS may have benefits for patients who have sensory deficits.

conversion disorder


CD is often misunderstood and challenging to diagnose; however, prompt intervention is essential to improve outcomes and avoid prolongation of distressing symptoms. After neurologic diseases and other medical conditions are ruled out as the cause of a patient’s symptoms, psychoanalysis should be undertaken. In most cases, an event causing acute psychological stress will be found to have precipitated the conversion symptoms, as occurred with our patient. Once the diagnosis is made, treatment generally warrants a multidisciplinary approach that is supportive and includes a mental health professional.  ■


1. Traniello V. Hysteria and the wandering womb. Accessed July 7, 2014.

2. Allin M, Streeruwitz A, Curtis V. Progress in understanding conversion disorder. Neuropsychiatr Dis Treat. 2005;1(3):205-209. 

3. Ford CV, Folks DG. Conversion disorders: an overview. Psychosomatics. 1985;26(5):371-374, 380-383.

4. Mace CJ. Hysterical conversion. I: a history. Br J Psychiatry. 1992;161:369-377. 

5. Breuer J, Freud S. Studies on Hysteria. New York, NY: Basic Books; 1957:21. Accessed July 1, 2014.

6. Powsner S. Conversion disorder in emergency medicine. Medscape. Accessed July 7, 2014.

7. American Psychiatric Association. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric Publishing. Accessed April 13, 2013. 

8. World Health Organization. The ICD-10 classification of mental and behavioural disorders: clinical descriptions and diagnostic guidelines. Accessed June 08, 2014.

9. Stone J. The bare essentials: functional symptoms in neurology. Pract Neurol. 2009;9(3):179-189.

10. Feinstein A. Conversion disorder: advances in our understanding. CMAJ. 2011;183(8):915-920.

11. Owens C, Dein S. Conversion disorder: the modern hysteria. Advances in Psychiatric Treatment. 2006;12:152-157. Accessed July 1, 2014.

12. Stone J, LaFrance WC Jr, Levenson JL, Sharpe M. Issues for DSM-5: conversion disorder. Am J Psychiatry. 2010;167(6):626-627.

13. Stonnington CM, Barry JJ, Fisher RS. Conversion disorder. Am J Psychiatry. 2006;163(9):1510-1517. 

14. Black DN, Seritan AL, Taber KH, Hurley RA. Conversion hysteria: lessons from functional imaging. J Neuropsychiatry Clin Neurosci. 2004;16(3):245-251.                                                  

15. Spence SA, Crimlisk HL, Cope H, Ron MA, Grasby PM. Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement. Lancet. 2000;355(9211):1243-1244.

16. Mailis-Gagnon A, Giannoylis I, Downar J, et al. Altered central somatosensory processing in chronic pain patients with “hysterical” anesthesia. Neurology. 2003;60(9):1501-1507.

17. Werring DJ, Weston L, Bullmore ET, Plant GT, Ron MA. Functional magnetic resonance imaging of the cerebral response to visual stimulation in medically unexplained visual loss. Psychol Med. 2004;34(4):583-589.

18. Schwingenschuh P, Pont-Sunyer C, Surtees R, Edwards MJ, Bhatia KP. Psychogenic movement disorders in children: a report of 15 cases and a review of the literature. Mov Disord. 2008;23(13):1882-1888.

19. Canino G, Bird H, Rubio-Stipec M, Bravo M. The epidemiology of mental disorders in the adult population of Puerto Rico. P R Health Sci J. 1997;16(2):117-124.

20. Engl GL. Conversion symptoms. In: McBride CM, ed. Signs and Symptoms: Applied Pathologic Physiology And Clinical Interpretation. 5th ed. Philadelphia, PA: JB Lippincott; 1970:650-668.

21. Folks DG, Ford CV, Regan WM. Conversion symptoms in a general hospital. Psychosomatics. 1984;25(4):285-289, 291, 294-295.

22. Ewald H, Rogne T, Ewald K, et al. Somatization in patients newly admitted to a neurology department. Acta Psychiatr Scand. 1994;89(3):174-179.

23. Carson AJ, Ringbauer B, Stone J, McKenzie L, Warlow C, Sharpe M. Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient clinics. J Neurol Neurosurg Psychiatry. 2000;68(2):207-210.

24. Woodruff RA Jr, Clayton PJ, Guze SB. Hysteria: an evaluation of specific diagnostic criteria by the study of randomly selected psychiatric clinic patients. Br J Psychiatry. 1969;115(528):1243-1248.

25. Stone J, Carson A, Sharpe M. Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry. 2005;76(Suppl 1):i2-12.

26. Haque R, Alavi Z. Mr. Smith is falling every day: conversion disorder in an elderly man. Annals of Long-Term Care: Clinical Care and Aging. 2012;20(11):30-35. Accessed July 11, 2014.

27. Stone J, Sharpe M. Conversion disorder in adults. UpToDate. Updated June 10, 2014. Accessed July 1, 2014.

28. Sharpe M, Walker J, Williams C, et al. Guided self-help for functional (psychogenic) symptoms: a randomized controlled efficacy trial. Neurology. 2011;77(6):564-572.

29. Liepert J, Hassa T, Tüscher O, Schmidt R. Electrophysiological correlates of motor conversion disorder. Mov Disord. 2008;23(15):2171-2176.                

30. Kanaan RA, Carson A, Wessely SC, Nicholson TR, Aybek S, David AS. What’s so special about conversion disorder? A problem and a proposal for diagnostic classification. Br J Psychiatry. 2010;196(6):427-428.

31. Feinstein A. Psychogenic aphonia: spectacular recovery after motor cortex transcranial magnetic stimulation. J Neurol Neurosurg Psychiatry. 2009;80(1):4.

32. Khan MN, Ahmad S, Arshad N, Ullah N, Maqsood N. Anxiety and depressive symptoms in patients with conversion disorder. J Coll Physicians Surg Pak. 2005;15(8):489-492.

33. Voon V, Lang AE. Antidepressant treatment outcomes of psychogenic movement disorder. J Clin Psychiatry. 2005;66(12):1529-1534.

34. Shapiro AP, Teasell RW. Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders. Br J Psychiatry. 2004;185:140-146.

35. Ataoglu A, Ozcetin A, Icmeli C, Ozbulut O. Paradoxical therapy in conversion reaction. J Korean Med Sci. 2003;18(4):581-584.

36. Schönfeldt-Lecuona C, Connemann BJ, Viviani R, Spitzer M, Herwig U. Transcranial magnetic stimulation in motor conversion disorder: a short case series. J Clin Neurophysiol. 2006;23(5):472-475.