Conversion Disorders

Updated: Jul 20, 2021
Author: Scott A Marshall, MD; Chief Editor: David Bienenfeld, MD 



Conversion disorder (Functional Neurological Symptom Disorder) is categorized under the new Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) category of Somatic Symptom and Related Disorders.[1] It involves symptoms or deficits affecting voluntary motor or sensory function that suggest a neurologic or other general medical condition. Yet, following a thorough evaluation, which includes a detailed neurologic examination and appropriate laboratory and radiographic diagnostic tests, no neurologic explanation exists for the symptoms, or the examination findings are inconsistent with the complaint. In other words, symptoms of an organic medical disorder or disturbance in normal neurologic functioning exist that are not referable to an organic medical or neurologic cause.[2]

Common examples of conversion symptoms include blindness, diplopia, paralysis, dystonia, psychogenic nonepileptic seizures (PNES), anesthesia, aphonia, amnesia, dementia, unresponsiveness, swallowing difficulties, motor tics, hallucinations, pseudocyesis and difficulty walking.

Reports of less common manifestations of conversion disorder abound in the literature and include camptocormia, clenched fist syndrome, recumbent gait, odd vocalizations, and pseudo foreign accent syndrome.[3, 4, 5, 6, 7]

Multiple symptoms suggest a somatization disorder. Conversion disorder is a type of somatoform disorder where physical symptoms or signs are present that cannot be explained by a medical condition. Very importantly, unlike factitious disorders and malingering, the symptoms of somatoform disorders are not intentional or under conscious control of the patient. This can be difficult to ascertain during the initial history and work up of the patient. See the image below.

French neurologist Jean Martin Charcot shows colle French neurologist Jean Martin Charcot shows colleagues a female patient with hysteria at La Salpêtrière, a Paris hospital.

Case study

A young woman’s family brings her to the hospital and she presents with a chief complaint of “spells.” It seems that over the past several weeks, the patient has suffered from attacks of bilateral arm jerking, followed by bilateral leg jerking after she lowers herself to the floor. Often, her head shakes violently side to side and her eyes are seen to "roll back in her head" followed by forced eye closure. These incidents follow episodes of emotional outbursts, and the patient is fortunately able to warn others that “I’m about to have a seizure!” After hearing this, her family grabs the patient and places her in a chair or on the ground until the spell is over, which sometimes can wax and wane for 20-30 minutes with varying intensity.

These spells are not accompanied by loss of bladder or bowel continence, but often the patient bites the tip of her tongue and kicks over tables or strikes family members during an episode. This most recent spell occurred while the patient was driving her car, in which she warned of an impending seizure and pulled the car to the shoulder just before losing consciousness; her spell was much more intense than she has had in the past.

She has no significant past medical history and takes no medications. She reports a past history of childhood sexual abuse from a paternal uncle several years ago. On exam, her vital signs are normal and her neurologic evaluation is without significant findings. She is not orthostatic. Laboratory work-up, including urine toxin screen, is negative.


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. Others have introduced attachment theory as a means to understanding conversion disorder in terms of the freeze response and the appeasement defense behavior seen in animal subjects.[8]

The patient has been postulated to derive 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. A review of imaging correlates in patients with motor and sensory conversion symptoms is referenced.[9, 10] Studies on the natural history of conversion disorder indicate that many patients subsequently develop or are found to have preexisting neurologic 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 is also observed, most notably in observation of high rates of organic seizure syndromes associated with psychogenic nonepileptic seizures (PNES). Familial studies have also shown that conversion symptoms in first-degree female relatives are up to 14 times greater than in the general population.

That the diagnosis of a conversion reaction or disorder represents a failed diagnosis of an organic syndrome, perhaps with psychogenic overlay that obscures exam and other findings is a valid concern. A recent meta-analysis including more than 1400 cases with follow-up over 5 years reported missed organic diagnosis rates of less than 5%.[11] This correlates with similar reports for the diagnosis of motor neuron disease or schizophrenia.[12] Past rates of misdiagnosis were reported as considerably higher.[11]



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.[13] 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 neurologic symptoms. A report by Carson found that 30% of patients at a neurology clinic had "unexplained symptoms."[14]  Older reports have estimated that up to 20% of all patients in neurologic clinic settings have symptoms of conversion.[15]  Population estimates on incidence range from 4 to 12 cases per 100,000.[16]

Overall, conversion disorder is reported to be more common in rural populations, in individuals with lower socioeconomic status, lack of education, and low psychological sophistication.[17] The increased rate of conversion in patients with a past history of sexual or physical abuse is well described.[18, 19]  Women are more commonly diagnosed with conversion disorder.[20]

Stefansson et al report that the annual incidence is 11 cases per 100,000 persons per year in Iceland.[13]


Individual conversion symptoms are generally self-limiting and do not lead to physical changes or disabilities. In the case of PNES, patients may have driving privileges removed by medical practitioners and may self-limit other activities due to concern over having a paroxysmal event. The symptoms related to the conversion disorder may lead to decreases in quality of life if they are perceived as egodystonic.

Morbidity is often an iatrogenic manifestation of unnecessary diagnostic or therapeutic interventions aimed at establishing an organic diagnosis for the patient's symptoms.

Patients with chronic conversion symptoms rarely may develop atrophy, frozen joints, and contractures from disuse.

Sex- and age-related demographics

Classically, the female-to-male ratio is 2-10:1.

Recent work with PNES reports that males make up approximately 40% of cases. This is a departure from past work, where females made up 80% of cases of PNES in some series.[21]

Overall, female-to-male ratio is variable, but the occurrence of conversion disorder is likely higher in females overall.[20]

The typical onset is between the second and fourth decades.

The reported range is from children to individuals in their ninth decade of life.


Prognosis is generally poor, although presentation at a young age and early diagnosis in the course of the conversion symptoms are reasons for significant optimism.[22]

  • 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, dystonia, and myopathy accounted for the false-positive diagnoses.

  • Additional positive prognostic factors - Acute onset of symptoms, short duration of symptoms, healthy premorbid functioning, higher intelligence, absence of coexisting psychopathology, presence of an identifiable stressor, male gender, change in marital status (marriage or divorce), isolated sensory symptoms, very young age, and good premorbid medical health status.[2]

  • Poor prognostic symptoms - Pseudoseizure (psychogenic nonepileptic seizure), psychogenic tremor, subclinical (undiagnosed) personality pathology, concomitant medical illness, the presence of a stuffed animal brought to the hospital by the patient,[23]  poor perception of own well-being, motor symptoms, and pending litigation.[2]  Others have shown increased symptom longevity to be associated with a poor prognosis.[24]

  • Recent retrospective study of psychogenic nonepileptic seizure over a 5-year period showed 47% of patients were unemployed, 26% were not living independently, and only 16% were seizure free at 21 months post diagnosis of psychogenic nonepileptic seizure.[25]

  • Of children with a diagnosis of conversion disorder, 85% are symptom free at 5 years with a reported improvement in status in another 5%.[26]

Patient Education

Sensitively review the disorder with the patient and the family in such a way as to not place blame. During such follow-up for review of completed imaging and other studies, continue to emphasize the importance of pain or other symptoms that the patient may be having.

Continue to reassure the patient that the negative test results are good news and bode well for their eventual recovery.

Frequent brief office visits to ensure the expected resolution of their symptoms may be helpful.

Websites that may provide further information and support for patient and family education include the following:

  •, Conversion disorder

  • Mental Health Forum

  • Psych Forums




Conversion symptoms are those that suggest neurologic disease, but no explanation of these symptoms is found following physical examination and diagnostic testing. The presentation is acute in onset and may follow a psychologically conflictual situation. 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, neurologic, 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 of vital importance. Patients with conversion disorder are said to have a relative lack of concern about the nature or implications of the symptoms; Freud described this as la belle indifference. This is not a helpful diagnostic characteristic because it is not specific or sensitive for conversion and should have no isolated role in separating organic from psychiatric disease.[12] Systematic reviews on this subject found the frequency of this finding at 21% among those with a conversion disorder and 29% among those with organic disease.[27]

Diagnostic criteria (DSM-5)

Diagnostic criteria for Conversion Disorder (Functional Neurological Symptom Disorder) as per the DSM-5 are as follows:[1]

  • One or more symptoms of altered voluntary motor or sensory function.

  • Physical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions.

  • The symptom or deficit is not better explained by another medical or mental disorder.

  • The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Specify symptom type:

  • With weakness or paralysis
  • With abnormal movement (e.g., tremor, dystonic movement, myoclonus, gait disorder)
  • With swallowing symptoms
  • With speech symptoms (e.g., dysphonia, slurred speech)
  • With attacks or seizures
  • With anesthesia or sensory loss
  • With special sensory symptom (e.g., visual, olfactory, or hearing disturbance)
  • With mixed symptoms

Specify if:

  • Acute episode:  Symptoms present less than 6 months
  • Persistent:  Symptoms occurring for 6 months or more

Specify if:

  • With psychological stressor (specify stressor)
  • Without psychological stressor

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 depressive disorder or anxiety disorders.

  • Symptoms coexist with a medical condition.

  • The symptoms are an unusual manifestation of a medical condition.

The DSM-5 lists strict criteria for diagnosing conversion disorder. It is important to remember that the diagnosis of conversion disorder is made based on the overall clinical picture and not a single clinical finding.[1]  This usually requires a multispecialty approach. For example, some conditions may be determined only by a person with expertise in neurologic conditions, neuroanatomy, and the recognized clinical patterns of disease in correlation with the lesion location—a neurologist.  The neurologist must also recognize the nonorganic process and rule out imitators while avoiding potentially dangerous diagnostic or therapeutic interventions. The psychiatric assessment can differentiate conversion disorder from other somatoform disorders, factitious disorder, and malingering, and can elucidate the psychodynamics that are important in treatment. The neurologist and psychiatrist are thus prepared to diagnose conversion disorder best when working in concert.[12]

Patients with conversion disorder may present with neurological symptoms such as: hemiparesis, paraparesis, monoparesis, alteration of consciousness, visual loss, seizure like 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 and vice versa. The presenting symptoms depend on the cultural milieu, the degree of medical sophistication, and the underlying psychiatric issue. 

The presentation of conversion disorder may be associated with stress or trauma, either psychological or physical in nature. These patients may present with symptoms we usually associate with trauma (e.g., deporesonalization, derealization, dissociative amnesia).[1]  Patients with conversion disorder may deny any emotional problems and commonly resist consultation with psychiatry. Therefore, responsibility lies with other medical personnel to perform the initial management prior to conveying the diagnosis.


A full physical examination with attention to the mental status and neurologic examination should be performed. Certain principles are used during the neurologic examination to distinguish psychogenic deficits from neurologic ones. The pattern of deficits usually does not conform to known anatomic pathways. For example, patients who present with monoparesis do not have weakness in a corticospinal tract or neuropathic or 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. Importantly, one should differentiate inability to move a limb on command from spontaneous movements. This may imply a receptive aphasia rather than a conversion disorder. 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 certain abnormalities is not completely known, thus resulting in limitations of the neurologic examination. In addition, patients can embellish on organic deficits, thereby making clinical assessment difficult and further introduction of variability between examiners.

Of concern, older data, most notably by Eliot Slater in 1965, published rates of 33% for patients with conversion disorder ultimately developing a physical illness that may account for their symptoms.[28] Patients with conversion disorder not uncommonly have a comorbid medical or neurologic illness. An example is the patient who exhibits both epileptic seizures and psychogenic nonepileptic seizures, a clinical situation accounting for up to 10-20% of referrals to epilepsy referral centers.[29, 30] Although current rates of misdiagnosis are low, this remains a valid concern among practitioners.[11]

Assessment of mental status during examination is paramount. The following mental status examination example focuses only on the possible presentation of a patient with conversion symptoms. In a clinical setting, one would likely see the comorbid psychiatric presentations as well. These may be hard to distinguish and separate from the conversion symptoms (eg, hallucinations and delusions may be a conversion symptom or symptoms of a psychotic disorder).

Mental status examination

See the list below:

  • Appearance - Normal dress; appropriate eye contact; normal hygiene

  • Gait/station - Normal or ataxia, some type of psychogenic paresis, pseudochorea, astasia-abasia pattern of gait (ie, inability to walk due to weakness or balance deficits but can hop on 1 leg back and forth to the bathroom)

  • Attitude - Appropriate

  • Behavior - Could be preoccupied with symptoms or indifferent

  • Speech - May be normal or have evidence of the conversion disorder such as aphonia, dysphonia, verbal tics, stuttering

  • Attention/concentration - May be decreased due to preoccupation with symptoms or may be normal

  • Memory - Normal or impaired[31]

  • Orientation - Likely oriented to person, place, and time

  • Mood - Perhaps anxious about condition; perhaps indifferent

  • Affect - May be restricted; labile or mood incongruent

  • Thought process - Could also vary from concrete and perseverative to normal; obsessive component also possible

  • Thought content - Not likely suicidal or homicidal unless comorbid conditions present

  • Hallucinations - Possible hallucinations present (The patient usually retains some insight that these are not real. The conversion hallucinations often involve multiple modalities [verbal, tactile, visual]. Compared with hallucinations in psychosis that usually involve a single modality, these hallucinations are often psychologically significant [ie, "I heard my ex-boyfriend's voice telling me that he had made a big mistake."]. Often they are imaginative and childish in nature and often presented as a story.[17] Please note that if the hallucinations are better accounted for by post traumatic stress disorder or dissociative identity disorder, a diagnosis of conversion disorder should not be made.)[17]

  • Insight - Limited to poor

  • Judgment - Varies from case to case

Other specific details to help diagnose 3 different common 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. Note that many of these type of signs have been shown to not be specific for conversion, including give-way weakness.[32]

    • The Hoover sign may also 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. This is felt to be a reasonably reliable indication of a possible conversion disorder.[12]

    • Another helpful tool is examining the sternocleidomastoid muscle. Normal contraction of this muscle results in the face rotating in the opposite direction. Therefore, the patient with psychogenic weakness 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 side-to-side changes in reflexes or tone

      • Give-way quality of weakness[32]

      • Extensor and flexor muscles equally weak

      • Contralateral sternocleidomastoid weakness

      • Positive Hoover sign[33]

      • Difference between formal examination and general observations (ie inconsistency)[12]

  • 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.[34] Please refer to the article on Psychogenic Seizures in the eMedicine Neurology section for more details.

    • Classic clues that may be suggestive of a psychogenic 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[19]

      • Signs or symptoms suggestive of another conversion

      • Memory of a generalized ictal event

    • Ictal characteristics that suggest nonepileptic seizure include the following:[12]

      • 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[35]

      • 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, knee buckling, and a host of other bizarre gait disturbances. A commonly used term for a type of this last phenomenon is an astasia-abasia gait pattern, in which the patient makes 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.[36]

    • Variations of astasia-abasia have been described. Psychogenic camptocormia is a conversion reaction manifest by patients ambulating with a severe forward flexion posture at the waist. This was originally described with military personnel during the early 20th century.[6] A recumbent-type gait has also been reported in which a patient was found to walk normally with her eyes open; however, when her eyes were closed, she would continue to walk while falling backward into the arms of examiners. Interestingly, the patient would continue to exhibit a steppage gait as an attempt at walking. When her eyes were opened, she would appear bewildered to be lying on the floor.[5]

    • The clenched fist syndrome has been described as a classic conversion reaction. This is manifested by patients who exhibit a tightly closed fist posture with resistance to all distal hand movement due to severe pain. A finding to alert the clinician to this is paradoxical stiffness, in which a change in finger flexion with motion of the wrist does not occur. Clenched fist syndrome is seen after minor trauma with associated pain and swelling.[7]

    • 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)


Neuroimaging studies of conversion disorders indicate hypofunction of the dominant hemisphere and a consequent overactivity in the non-dominant 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 contra lateral motor cortex, but rather contra lateral orbit-frontal and anterior cingulated cortex were activated. This implied an anatomic inhibition of primary motor cortex in one case of hysterical paralysis.[37]

Others have shown via rCBF analysis that the left temporal region has decreased rCBF. rCBF studies have also implicated the thalamus, putamen, and caudate on the side opposite the motor and sensory conversion symptoms. Published reports show improved rCBF with resolution of the conversion symptoms.[9]  Another study showed decreased rCBF in the basal ganglia and thalamus on the opposite site from the study patient's sensorimotor neurologic deficit. Interestingly, the findings normalized with improvement in the patient's symptoms.[38]

Functional MRI (fMRI) studies have implicated the orbitofrontal cortex and the anterior cingulate gyrus as active in mediating an inhibitory effect on movement and sensation in patients with psychogenic motor and sensory complaints.[39]  Other fMRI research shows that in patients with either sensory or motor conversion symptoms, activation in the anatomically respective areas of the brain is abnormally reduced or absent.[40]

Neuropsychological testing shows evidence of impaired attention and short-term memory.

Psychoanalytic theory postulates that conversion disorder is caused by the repression of unconscious intrapsychic conflicts and conversion of anxiety into physical symptoms.

Learning theorists believe that such symptoms develop from classical conditioning that occurs during childhood and that these learned behaviors arise again as coping mechanisms 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.



Diagnostic Considerations

The differential diagnosis of conversion disorders is highly dependent on the manner in which the patient presents. Organic etiologies must be excluded. Some have suggested that conversion disorder not be considered a diagnosis of exclusion,[2] although a thorough medical and neurologic clinical evaluation and appropriate diagnostic testing is warranted prior to making the diagnosis of conversion. If, for example, a diagnosis of psychogenic hemiparesis is considered, organic etiologies such as tumor, stroke, multiple sclerosis, and others should be ruled out. As in working up any disease, the clinician must weigh the risks and benefits of diagnostic testing to the patient's overall condition.

Other problems to be considered include the following:

  • Epileptic seizures including frontal lobe epilepsy

  • 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 - Depressive disorders, anxiety disorders, panic disorder, posttraumatic stress disorder (PTSD), dissociative disorders, psychotic disorders, other somatic disorders, factitious disorder, intermittent explosive disorder

  • Malingering

  • Medications - Toxicity (eg, tremors from high levels of valproic acid), akathisia (from neuroleptics and possibly antidepressants), EPS from neuroleptics, withdrawal from medications such as benzodiazepines, opiates, and occasionally with antidepressants such as SSRIs or SNRIs

  • Environmental exposures to chemicals or heavy metals

  • Drugs of abuse (inhalants, hallucinogens)



Laboratory Studies

Lab tests for hemiparesis include the following:

  • MRI of brain with diffusion-weighted imaging

  • MRI of cervical region

Lab tests for pseudoseizure (PNES) include the following:

  • MRI of brain

  • EEG

  • Prolonged video-EEG monitoring

  • Echocardiogram

  • Holter monitor

  • Tilt-table test

  • Serum lactic acid

  • Prolactin level 30 minutes after the event: An elevation above baseline can occur with partial seizures, generalized seizures, or syncope, but not with pseudoseizures.

  • Provocative EEG with placebo induction is no longer routinely performed in many centers.

Lab tests for psychogenic movement disorders include the following:

  • MRI of brain

  • Twenty-four hour urine studies for 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

  • Urine and serum toxin screen for stimulant or illicit drug use

  • Drug levels (ie, anticonvulsants, digoxin)


The Amytal interview was once commonly used for diagnosing conversion disorder. This procedure carries significant risk and should be carried out by experienced physicians.[41] Sodium Amytal is a barbiturate and carries risk of respiratory depression. It is contraindicated in cases of upper respiratory infection or airway edema, hemodynamic instability, significant liver or kidney dysfunction, and porphyria. A CPR cart with medications and personnel trained in their use should be available in case of emergency.[42] This is cited in the literature as a technique that may occasionally be used to help facilitate the gathering of data but is not routinely performed in many centers.

Hypnosis is used on occasion and may also facilitate the data gathering process. This technique may also help alleviate the patient's anxiety and aid in relaxation.

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.

Advanced imaging is not diagnostic of conversion disorder, and routine use for this purpose is not currently standard of care.

See Causes for rCBF studies.[9]



Medical Care

Current understanding of the phenomenon of conversion disorder implicates some role of the unconscious in the pathophysiology of this condition.[12, 43] 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, as well as 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.

Hospital admission may be considered in some cases. For example, for a patient that seems likely to not return for follow-up after being given a psychiatric diagnosis. A more rapid completion of the diagnostic workup is possible in the hospital setting. In addition, a parallel investigation of physical and psychologic factors can concomitantly 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, heart racing when asking someone for a date).

  • Provide examples of how the subconscious influences behavior (eg, nail biting, pacing, foot tapping).

  • 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.) This is perhaps the most important point. A patient admitted to the neurology ward with a psychogenic gait disorder should not be discharged suddenly once any mild improvement is seen. It may be the better part of valor to hold a patient a day or so to ensure that the treatment is taking hold.

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 and is often helpful in providing the patient an ego-syntonic way out as they are being provided a benign treatment to which they can respond and improve.[44, 45]

Institute patient and family education sensitively.

Regular short follow-up appointments with a neurologist or a psychiatrist should be provided to limit ED visits and unnecessary diagnostic or invasive tests.

The best evidence for treatment of conversion is with cognitive behavioral therapy. A review of available data is encouraging for use of this modality across a broad spectrum of somatoform disorders.[46]


A multidisciplinary approach to the treatment of conversion disorder is beneficial.[43]

  • Neurologist: This is the primary evaluation where a conversion disorder is differentiated from neurologic diseases.

  • Cardiologist: Consultation is warranted if the patient has episodic alterations of consciousness due to concern over cardiogenic syncope.

  • Physical therapist: Consultation may be warranted for those with motor or gait symptoms.[44]

  • Psychiatrist: This is generally 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:

    • Insight Oriented Supportive therapy: Offers the client support and helps the patient to gain insight into their condition and possible triggers.

    • Behavioral therapy: Examines the patient's symptoms and teaches techniques to help them better cope and alleviate the symptoms (eg, biofeedback techniques). This is ideal for those lacking intelligence and insight.

    • Psychodynamic therapy: This may be used further in the treatment process as a means to help the patient gain insight. However, patients with borderline intelligence, lack of motivation or introspection capabilities, important secondary gains, or those with a tendency for behavioral acting out are likely poor candidates.

  • Psychologist: Psychosocial interventions that may be helpful include paradoxical intention therapy and hypnosis.[18]

    • Family therapy: Interactions and communication within the family are emphasized rather than only focusing on the individual patient.[2]

  • Whatever the type of therapy, the most important element is a good relationship with a confident, supportive therapist.



Medication Summary

Sparse evidence exists for use of medications for the independent treatment of conversion. Medications that have been tried with success include tricyclic antidepressants, haloperidol, and also treatment with electroconvulsive therapy (ECT).[47, 48] Treatment of coexisting psychological or psychiatric disease is warranted.