Pediatric Conversion Disorder

Updated: Dec 11, 2018
Author: Neelkamal S Soares, MD; Chief Editor: Caroly Pataki, MD 


Conversion disorder is included in a newly defined category in the fifth edition of the American Psychiatric Association's (APA)Diagnostic and Statistical Manual of Mental Disorders (DSM-5) called Somatic Symptom and Related Disorders.[1] It first appeared as part of the group of somatoform disorders in the 1980 DSM third edition (DSM-III).

Until the fourth edition (DSM-IV), somatoform disorders were characterized by persistent physical symptoms without an identifiable medical or physiologic explanation and symptoms that were supposed to be linked to psychological factors or conflicts.[2] However, there was significant overlap across the somatoform disorders and a lack of clarity about their boundaries. Therefore, in DSM-5, several of the diagnoses were removed, replaced, and some renamed. However, conversion disorder remains in the new edition.

Diagnostic criteria were established for adults predominantly, and these criteria generally are extended to children; there are no separate child-specific criteria. Diagnoses in children and adolescents are more difficult because the expression of emotional distress in the form of physical complaints is developmentally appropriate in younger children, who lack the capacity to accurately verbally report symptoms and emotional distress. However, when physical symptoms are persistent and a child's functioning deteriorates, a somatic symptom disorder can be considered.


Background and Nomenclature

Historical models of conversion

The term "hysteria" was attributed either to ancient Egyptians or to Hippocrates and the Greeks (hysterika is Greek for uterus), with a belief that female ailments could be the result of a wandering uterus applying pressure internally on organs and nerves leading to symptoms.[3] This social belief reflected the patriarchal nature of society and the different views of male and female health and illness.

In the 17th century, Rene Descartes postulated mind-body dualism, in which mind and body are distinct substances that could not exist in unity, with the body subject to mechanical laws, but not the mind.[4] This led to the development of a reductionist medical model with a dualist outlook influencing management of conversion symptoms.

By the 19th century, reflex theory asserted that every organ can influence every other organ, independent of the mind and will. Charcot opined that hysteria had some psychogenic component and was influenced by environmental conditions, with psychological and medical symptoms of disease along a continuum.[5]

Around the same time, Myers and Janet developed psychological frameworks for understanding “psychological automatisms,” which emphasized the coexistence of separate mental systems that would normally be integrated into person's consciousness, identity, and physical self.[6] This concept is recently reemerging as neodissociation theory.

In the 20th century, thinking was influenced by Freud's psychoanalysis model, and he and Breuer speculated on possible neurological mechanisms of conversion symptoms and coined the term "conversion" to signify the substitution of somatic symptoms for repressed emotions.[7]

In behavioral models, conversion symptoms are viewed as a learned maladaptive behavior that is reinforced by the environment. Although these theories did not provide an explanation of the mechanism for conversion symptoms, they highlighted important contextual factors.[8]

Early neurobiological models

Kretschmer suggested that conversion reactions were related to the instinct for self-preservation and that the continued association of a particular behavior with relief from danger or fear would result in habituation and automation of the behavior. Whitlock argued that the lack of attention to conversion symptoms was the result of a selectively reduced awareness of a body function that was neurobiological in origin.[8]

Empirical research in this area has tended to lag behind theoretical speculation, although advances in functional imaging and neuropsychological testing offer the opportunity to confirm hypotheses in psychoanalytical theory through neurobiological explanations.[9]

Current perspectives

Hilgard’s “neodissociation theory” conceptualizes cognitive hierarchy with executive structure responsible for intentionality and awareness linked with various subordinate structures in the nervous system, with disruption of communication between centers being responsible for negative and positive symptoms. However, failure to demonstrate an underlying biologic pathway and implications for intervention limited its acceptance.[8]

Oakley's attentional control model presents conversion in a neurobiologic substrate with a hierarchy in the prefrontal cortex handling high-level attention, conscious volition, and effort; lower level functions of routine or automatic behaviors anchored by low-level attentional and representational systems in frontal cortices’ executive system; and active representation of internal and external phenomena. However, independent verification of the hypotheses cannot be done, with only partial support from neuroanatomic correlates of cognitive processes.[8]

Newer models also converge on the conceptualization of conversion as reflecting errors in information processing and representation in the cognitive and neural systems as underpinnings of the processes. Brown hypothesizes that conversion symptoms reflect the selection of inappropriate cognitive representations by low-level attention, where sensory information automatically triggers multiple related representations in memory.[8]

Kozlowska offered a developmental framework for understanding conversion reactions with roots in innate defensive behaviors. In the context of a significant threat, behavioral and somatosensory components of emotional responses are activated automatically, manifesting as medically unexplained symptoms (pain, motor or sensory). However, this proposed developmental model requires empirical testing in larger populations.[8]

Kozlowska also reported that conversion disorder was not a single diagnostic entity, but two distinct subtypes of conversion patients existed: first used psychological inhibition, while the second used psychological coercion-preoccupation, whose symptoms fell into discrete clusters. Identification of the neural mechanisms underlying these processes requires further research.[10]

More recently, Stonnington and colleagues hypothesized that conversion may related to Theory of Mind (ToM), with a deficit in the encoding and reporting of emotion when the emotional content of the stimulus is conveyed in action. Difficulty with “conversion” from implicit (action, somatic) to explicit (representational) processing of emotions, exacerbated by anxiety, may constitute a mechanism for somatic symptoms.[11]

Nomenclature changes

In 1952, the original DSM was published. Subsequently, 4 editions have followed over the next 60 years, with the latest in 2013. The International Classification of Diseases,10th edition,(ICD-10) published by the World Health Organization (WHO) came into effect in 1994, with the 11th edition due out in 2018. The nomenclature has changed as outlined below:

  • 1952 DSM - Conversion reaction

  • 1968 DSM-II - Hysterical neurosis (conversion type)

  • 1980 DSM-III - Conversion disorder

  • 1987 DSM-III-R - Conversion disorder

  • 1994 DSM-IV - Conversion disorder

  • 1994 ICD-10 - Dissociative (conversion) disorder

  • 2013 DSM-5 - Conversion disorder (functional neurological symptom disorder)[12, 13]


Diagnostic Criteria

Diagnostic criteria for conversion disorder in DSM-5 are listed below.[1]

One or more symptoms of altered voluntary motor or sensory function are present.

Clinical 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.[14]

The type of symptom or deficit should be specified as follows:

  • With weakness or paralysis

  • With abnormal movement (eg, tremor, dystonic movement, myoclonus, gait disorder)

  • With swallowing symptoms

  • With speech symptom (eg, dysphonia, slurred speech)

  • With "attacks" or seizures

  • With anesthesia or sensory loss

  • With special sensory symptom (eg, visual, olfactory, hearing disturbance)

  • With mixed symptoms

Specify if acute (< 6 months) or persistent (>6 months).

Specify if with or without psychological stressor (specify stressor).

Table 1. DSM-IV and DSM-5 Criteria for Conversion Disorder [1, 2] (Open Table in a new window)




Rationale for Change[15]

Psychological association

Psychological factors are judged to be associated with the symptom or deficit because the initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors

No longer included

Psychological factors may not be readily evident, not reported historically, or patients may be reluctant to discuss them; even if present, may not be easily related to conversion symptoms

Focus on clinical findings

No comparable criterion

Clinical findings provide evidence of incompatibility between symptom and recognized neurological or medical conditions

Stress on internal inconsistency at examination with a requirement about thorough clinical investigation is more evident in newer edition; list of such findings included in manual (see Diagnostic Considerations)

Intention of symptoms

Symptom or deficit not intentionally produced or feigned (as in factitious disorder or malingering)

No longer included

No good evidence that patients with conversion symptoms are more likely to be feigning symptoms than patients with other disorders; criterion is difficult to reliably validate and suggests that one should be especially suspicious of patients with conversion symptoms, which is empirically unfounded

Making the diagnosis

The symptom or deficit, after appropriate investigation, cannot be explained by a general medical condition, the direct effects of a substance, or as a culturally sanctioned behavior or experience

Symptom or deficit is not better explained by another medical or mental disorder

Absence of a general medical disease is not easily determined by mental health specialists, as usually physical examinations and other investigations are the domain of neurologists and other physicians; physical signs must be used in conjunction with a careful assessment by experienced clinician; assumption also made that coexisting medical condition and conversion symptoms cannot happen; using "not better explained by a disease" allows for a comorbid disease to be present


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

Identical criterion




Case definition and case ascertainment of conversion disorder have been barriers to an accurate description of prevalence rates. Many studies characterize referred clinical populations rather than general population ascertainment, and many patients continue to undergo medical evaluations and thus have not been concluded to have conversion disorder. Lifetime prevalence in the general population is quite varied, at about 11-22 cases per 100,000 people. It is more common in rural areas, among uneducated people, and in the lower socioeconomic classes.[15] Another study put the 12-month prevalence at 0.2% in a large cohort of Germans aged 14-24 years.[16] Higher prevalence is seen in general hospitalized patients (1-3%)[17] and higher at 5-6% in neurological clinics.[18]

Conversion disorder is supposed to be rare in young children, with an onset generally from late childhood to early adulthood, and seldom seen after the fourth decade of life. No specific childhood prevalence figures are available. Most studies of conversion disorder in children are limited to case reports and case series. There are epidemiological methodological challenges to investigating conversion disorder in children, notably the limited availability of valid diagnostic interviews and the difficulties in obtaining information from multiple sources.[19] Further, clinicians feel obliged to rule out organic etiologies in children, potentially preventing accurate estimates. A pediatric surveillance in Australia over a 2-year period yielded a prevalence of conversion disorder at 2.3-4.2 cases per 100,000 children in a specialist pediatric practice.[19] Prevalence in an inpatient child psychiatric setting has been reported as 1-2%.[20]

The prevalence is reportedly higher (2-3 times) in women than in men. One study found that the lifetime prevalence of conversion symptoms among Turkish women in the general population was extremely high (48.7%),[21] but there are few other studies reflecting this. This may be due to cultural considerations, as conversion symptoms have been reported commonly as a presentation of psychiatric disorder in non-Western clinical settings. An example is differing prevalence rates in Turkey and Germany using similar methodology (lifetime prevalence of 5.6% in former and 1.4% in latter).[22] However, with psychogenic nonepileptic seizures (PNES), some studies have shown a greater male prevalence (up to 40%), with the sexual distinction appearing only after age 13 years.[23]

Limited data suggest that conversion disorder frequently occurs in relatives of individuals with conversion disorder. Symptoms are often modeled from affected family members. Genetic factors, including temperament (personality traits), may be associated, as are nongenetic factors, such as sexual abuse in childhood, which may be associated with an increased risk for conversion disorder.


Diagnostic Considerations

Developmental considerations

Developmentally, typical young patients can have apparent paresis without a demonstrated physiologic cause for a few hours or days after a minor injury. Difficulty expressing emotional distress verbally is widely thought to underlie the presentation of physical symptoms that cannot be explained in medical terms. Symptoms may elicit increased attention from parents and other caregivers, leading to secondary gain. These symptoms are considered normal behavior for children in this age group, and the role of psychological stressors is minimal.[24]

Psychological considerations

In psychodynamic theory, primary gain refers to the extent to which a conversion symptom diminishes the unpleasant emotion and anxiety and keeps the conflict internal. Secondary gain is achieved when the symptom presentation serves to help the individual avoid the situation generating the conflict. Gaining attention and emotional support from persons in the environment is an example of secondary gain. However, identification of secondary gain is not pathognomonic of conversion disorder.

More recent studies suggest that patients with conversion disorders are mobilized defensively and that this defensive mode of organization is reflected on multiple levels of organization: neural, hormonal, and psychological. Hypervigilance to emotional stimuli may put certain individuals at higher risk for activating stress responses and for being less able to switch it off.[25]

Neuroscience considerations

Recently, functional imaging and electrophysiologic studies have attempted to delineate the neuroscience underpinnings of conversion disorder. However, the heterogeneous nature of symptoms seen in conversion disorder and the varying methodologies used makes comparison between studies difficult. Generally, normal evoked potentials are now thought to be a hallmark of conversion disorder, although limited evidence exists that conversion disorder is neurophysiologically distinct from feigning, but analogous to symptoms seen in right parietal lesions.[9]

Some studies hypothesize a multifocal network, including premotor, primary sensorimotor, superior parietal, cingulate cortex, and cerebellar areas involved in functional sensory disorders with enhanced cortical and subcortical inhibition in the hemisphere contralateral to the functionally impaired limb. Similar networks appear to be involved in enhanced inhibition in the motor system in functional motor paresis symptoms.[26]

At present, the evidence available suggests a broad hypothesis that frontal cortical and limbic activation associated with emotional stress may act via inhibitory basal ganglia–thalamocortical circuits to produce a deficit of conscious sensory or motor processing. Functional imaging and neurophysiological evidence to support the distinction between conversion and factitious disorders is limited.[9]

Making the diagnosis

Conversion disorder can co-occur with several medical and psychiatric conditions, thus complicating diagnostic processes that focus on an “exclusion” of the latter. Typical comorbid diagnoses include mood disorders, panic disorder, generalized anxiety disorder, posttraumatic stress disorder, dissociative disorders, social or specific phobias, and obsessive-compulsive disorders.[27]

Furthermore, patients with physical illnesses may exaggerate symptoms. An example is prevalence of PNES in children with suspected epilepsy, which varies from 1-9%.[28] In PNES, depression is common (12-100%), as are anxiety disorders (11-80%), other somatoform disorders (42-93%), and personality disorders (33-66%).[27]   DSM-5 criterion of symptoms "not better explained by another medical or mental disorder" allows for comorbidity presence while continuing exploration of a conversion disorder.

There is no substitute for a good history and interview of the patient and family. Nondirective interviewing while obtaining a detailed medical and symptom history should be undertaken, while noting language and delivery of symptom reporting. For example, using exaggerated reporting or  medical jargon should alert the interviewer, as should affect mismatch. Family history, psychosocial stressors, school and peer factors should also be considered. Care should be taken to avoid leading questions suggesting a cause-and-effect relationship between the patient's feelings and presenting symptoms. Encouraging talk about life events helps adolescents to volunteer personal feelings associated with somatic symptoms.[29]

A physical examination, with particular attention to the symptomatic site, should be completed. The following specific maneuvers are suggested to test the internal inconsistency of presentation[30] :

  • Hoover sign: In a patient with leg weakness, weakness of hip extension that returns to normal with contralateral hip flexion against resistance strongly suggests conversion weakness.

  • Tremor entrainment test: In a patient with a unilateral arm tremor, when asked to make a voluntary rhythmical movement with the unaffected arm, he or she is either unable to perform this voluntary movement or the rhythm of the affected hand entrains to the rhythm of the voluntary movement, which is evidence of a conversion tremor.

  • Hip abductor sign: Hip abduction weakness returns to normal with contralateral hip abduction against resistance.

  • Weakness of ankle plantar flexion on the bed but patient able to walk on tiptoes

  • Global and give-way patterns of weakness on examination

In general, conversion disorder should not be considered a diagnosis of exclusion. Clinicians suspecting a conversion disorder must use judgment in regards to conducting exhaustive diagnostic tests, which may not allay fears and may exacerbate anxiety in some patients. At the same time, clinicians should avoid premature diagnosis of conversion disorder without an attempt to explore medical conditions. This balance depends on the individual clinician’s level of comfort and expertise, but it can be addressed through collaboration with other specialists (especially psychiatrists and neurologists) and including a mental health examination, laboratory and radiologic tests. In general, misdiagnosis rates have been stable at around 4% for every decade since the 1970s.[31]


Clinical Features

Conversion symptoms are most typically related to voluntary motor or sensory functioning.

Motor conversion disorders are most common and primarily involve weakness, which presents as paralysis, paresis, and gait disturbance. Paralysis can occur for a prolonged period without atrophy, with normal reflexes and involving one, some or all limbs. Dystonic presentations include spasmodic dysphonia, torticollis, tremor, and gait disturbance. Additional symptoms may include ptosis, chorea, ataxia, globus hystericus (difficulty swallowing), and astasia-abasia (the inability to stand or sit upright but an ability to move the legs when lying down or sitting). There is no conclusive finding of lateralization of motor conversion symptoms. Generally conversion motor symptoms differ from  nonconversion motor disorders by the presence of sensory symptoms, especially pain.[32]

Sensory symptoms may include anesthesia and paresthesia, especially in extremities. Often, distribution is inconsistent with either central or peripheral neurological disease (eg, stocking-and-glove anesthesia, hemianesthesia beginning precisely along the midline) Other sensory symptoms include diplopia, blindness, deafness (which may be unilateral or bilateral), and auditory or visual hallucinations. Often, these exist with intact sensory pathways on neurological examination.

PNES, previously known as "pseudoseizures" (a pejorative term), is included under conversion disorder in the somatic symptom and related disorders in DSM-5, but ICD-10 classifies them as a dissociative disorder. They resemble sudden convulsive events but are not associated with electroencephalgraphic (EEG) evidence of a seizure, and they do not follow the typical pattern of a seizure disorder.[23] PNES can appear as convulsive type, atonic drop attack, or as unresponsiveness with complicated automatic behavior.

Diagnosis often involves testing to confirm exclusion of epilepsy, although patients with confirmed epilepsy may also have comorbid PNES. The criterion standard for ruling out epilepsy is video EEG, which coincides observation of typical seizures with the recorded activity. However, this does not hold true for all forms of epilepsy and a diagnosis of PNES is never definitive. History or eyewitness accounts of PNES may be no better than random descriptions, and reliance on such accounts may not be helpful.

Onset and course

The onset is generally acute, but symptoms may gradually increase. Generally, in adults, symptoms ameliorate in more than half of all hospitalized patients with this disorder at the time of their discharge, with a 20-25% relapse rate in one year. Childhood conversion disorder is believed to be associated with a good outcome; however, in one series, 15% failed to recover from their conversion symptoms and 35% were eligible for a DSM diagnosis of mood or anxiety disorder 4 years after diagnosis.[33]


Generally, prognosis is supposed to be better in children than in adults with conversion disorder; follow-up studies indicate eventual full recovery in 85-97% of children. With early recognition of the nature of the condition and prompt intervention, some recover within a few weeks or even days of the onset of symptoms. Prognosis is good in cases with monosymptomatic manifestation and a good premorbid personality and is worse when symptoms have been present for a long time, with comorbid psychiatric disorders, when there is a history of sexual abuse, and in multisymptomatic patients.[34]

Associated features

Sometimes, conversion disorder can present with hallucinations (pseudohallucinations), which can be differentiated from hallucinations in psychotic disorders by the absence of disordered thought processes, awareness that the hallucinations are not real, and revelation that they are often psychologically meaningful rather than bizarre. However, given that comorbid conditions often exist, vigilance must be maintained for emergence of other signs of psychosis in a diagnosed case of conversion disorder. Dissociative disorder and posttraumatic stress disorder can also present with hallucinations.

Table 2. Differences between PNES and Epileptic Seizure [23, 28] (Open Table in a new window)



Epileptic Seizure

Onset of condition

Generally later than epilepsy, but earlier than motor conversion

No pattern


Obvious emotional precipitant including difficulties in school and family/interpersonal conflict, and sometimes sexual or physical abuse

Precipitant may be present but not obvious


Awareness during ictal phase, better memory for event, generally no postepisode confusion

Unaware in ictal phase, amnesia for event; sleep or postictal confusion or transient paralysis

Onset and duration of episode

Gradual onset; duration variable but long (>2 min)

Abrupt onset; generally shorter (unless status epilepticus)

Eye feature

Eyes closed tight or fluttering during episode; resistance to eye opening

Opening or widening of eyelids

Sleep association

Does not occur in sleep

May occur in sleep


Usually preserved with bilateral motor activity; may be fluctuating but some responsive to pain

Lost and unresponsive to pain


Waxing and waning tempo of motor activity; side-to-side head or body movement; opisthotonic posturing or rigidity for extended periods

Generalized tonic-clonic movements; brief rigidity


Readily induced or stopped on command/voluntarily; not readily induced by sleep, photic stimuli, sleep deprivation, or hyperventilation

Not readily induced or stopped or precipitated by sleep, photic stimuli, sleep deprivation, or hyperventilation

Provocative methods

Psychiatric interview, suggestion, placebo medication, or hypnosis

Hyperventilation, photic stimuli, or sleep deprivation

Neuropsychology testing

More abnormal on personality tests and higher on emotional dysregulation tests compared with epileptic patients



No epileptic-form discharge, though may be abnormal in PNES comorbid with epilepsy

Epileptic changes in most patients (though normal EEG does not exclude frontal lobe epilepsy or deep epileptic foci


Other Diagnoses to Consider

Medical conditions

Conversion disorder may coexist with medical disorders, such as:

  • Myasthenia gravis (with muscle weakness)

  • Periodic paralysis (with muscle weakness)

  • Myopathies (with muscle weakness)

  • Polymyositis (with muscle weakness)

  • Guillain-Barré syndrome (motor and sometimes sensory)

Psychiatric conditions

If another mental disorder better explains the symptoms, that diagnosis takes precedence. However, conversion disorder may coexist with other psychiatric conditions, such as:

  • Anxiety disorder

  • Depressive disorder

  • Panic disorder

  • Body dysmorphic disorder

  • Other somatic symptom disorders



Primary care physician

Generally, children and adolescents with conversion disorder first present to the primary care physician (PCP) because the presentation of illness is almost always medical, physical, or both. Family members and patients initially believe that an undiagnosed medical cause for the symptoms is responsible, and they are not comfortable with a provisional diagnosis of conversion disorder from their physician. Fear of litigation related misdiagnosis can delay diagnosis of conversion disorder as extensive medical evaluations are pursued.

The PCP should provide education about conversion disorder while carefully ruling out contributing medical conditions and attending to the views of the patient and his or her family. Patients and families can be educated about how physical symptoms of distress in the absence of serious disease are common and considered to be quite real by healthcare professionals, and they should be reassured that practical help is available. Discussing the relationship between mind and body and the false dichotomy implied by separate systems of care of physical and mental disorders can also be useful.[35]

The PCP should enter into a therapeutic partnership with the family where roles and responsibilities are delineated.  A concurrent physiopsychological approach is best, with physician comfort in the completeness of the physical evaluation and judicious of the organic workup. Reassurance that a serious physical disease is not present is often a necessary, but rarely sufficient, step in the treatment process, but excessive reassurance may prove counterproductive and, reassurance does not help probe the psychological source of the symptoms.[35]


After initial diagnostic exploration, if no medical condition is detected that satisfactorily explains the symptoms, appropriate referrals should be made to child and adolescent psychiatrists or developmental-behavioral pediatricians, community mental health centers, other mental health professionals, and community social support agencies. Modalities used to treat conversion disorder may include individual psychotherapy, family therapy, behavioral, and pharmacologic approaches to manage specific symptoms.[36]

Cognitive-behavioral approaches use teaching cognitive coping skills training in association with differential reinforcement of healthy behavior and self-monitoring techniques (similar to anxiety management: progressive muscle relaxation, visual imagery, and biofeedback). Randomized controlled trials have shown that cognitive-behavioral therapy is effective in some somatic symptom disorders, but there are limited data on its use in conversion disorder.

Psychodynamic techniques help a child gain insight into unconscious conflicts and understand how psychological factors have helped to maintain symptoms. Rehabilitative approaches focus on functional return to usual activities, discouraging illness-related behaviors, and developing coping mechanisms. Data on psychodynamic treatment are sparse and limited to case reports. Results from 2 trials of hypnosis have been contradictory, and studies with small sample sizes exploring transcranial magnetic stimulation need to be replicated.[37] Family and group therapy can work on building self-esteem, promoting assertiveness, and improving communication with family and peer groups.

In a systematic review of studies to investigate the efficacy of psychosocial intervention on conversion disorder, only 3 small studies were found, most with methodological problems and inconclusive results.[38]

Pharmacologic interventions may be needed to treat comorbid depressive and anxiety disorders, but studies supporting their effectiveness in somatic symptom disorders are limited. Hospitalization is sometimes indicated if outpatient therapy is not effective. This approach may be helpful in removing the child from his or her environment and allow for controlled observations. It can also be used to target specific investigations to rule out organic issues. However, the clinical situation may worsen as it can unintentionally provide the patient the attention to symptoms that he or she may be seeking.