eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics

Somatoform Disorder: Conversion

Author: Neelkamal S Soares, MD, FAAP, Assistant Professor, Department of Pediatrics, University of Kentucky; Consulting Staff, Department of Pediatrics, Kentucky Clinic
Coauthor(s): Linda Grossman, MD, Associate Professor, Division Head, Department of Pediatrics, Division of Behavioral and Developmental Pediatrics, University of Maryland School of Medicine
Contributor Information and Disclosures

Updated: Nov 28, 2007

Introduction

Conversion disorder is part of the group of somatoform disorders that were first delineated as a class of psychiatric disorders in 1980 in the American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM), 3rd edition (DSM-III).1

Somatoform disorders are characterized by persistent physical symptoms without a demonstrable organic pathology or physiologic explanation along with clinical indications that symptoms are linked to psychological factors or conflicts.

Diagnostic criteria for the somatoform disorders were established for adults, and the same criteria, in general, are applied to children. Diagnosing somatoform disorders in children and adolescents is often more difficult because the expression of emotional distress in the form of physical complaints is developmentally appropriate in younger children. However, when physical symptoms are persistent and a child's functioning deteriorates, consideration of a somatoform disorder is indicated.

Background And Nomenclature

Historical models of conversion

The ancient Egyptians attributed somatoform disorders to a "wandering uterus." Rene Descartes' 17th-century paradigm of separation between the psyche and the soma guided the development of reductionist medical model with a dualist outlook influencing management of conversion symptoms.

The 18th-century theories of disease included humoral theory (ie, disease is result of imbalance of humors and temperament) and master-organ theories (ie, the brain influenced by the master organs consisting of the uterus, digestive system, or nerves).

In the 19th century, reflex theory asserted that every organ can influence every other organ, independent of the mind and will. Charcot conceptualized hysteria as an inherited CNS disease caused by functional lesions in the nervous system that could not be localized. By the end of the 19th century, the concept of dissociation was referred to as psychological automatisms and emphasized the coexistence of separate mental systems that would normally be integrated into person's consciousness, identity, and physical self. This concept is recently reemerging as somatoform dissociation and neodissociation theory.

In the 20th century, thinking was influenced by Freud's psychoanalysis model. In addition, early neurobiological models suggested that conversion reactions were related to conflicts, including dangerous conflicts associated with fear. Behavioral models described conversion symptoms as diseases of communication or a social construct with disagreement or lack of empathy between patient and doctor.

Freud coined the term conversion to signify the substitution of somatic symptoms for repressed emotions. Historically, the terms conversion, hysteria, and conversion hysteria were used interchangeably to describe a condition characterized by a single somatized symptom, often a pseudoneurologic one (eg, blindness).

Current perspectives

Hilgard's neodissociation theory conceptualizes cognitive hierarchy with executive structure responsible for intentionality and awareness linked with various subordinate structures in CNS, with disruption of communication between centers being responsible for negative and positive symptoms. However, its lack of explanation of an underlying biologic pathway and of guidance for intervention limited its acceptance.

More recently, Oakley's attentional control model attempts to anchor the cognitive processing substrate in a neurobiologic substrate with a hierarchy in the cerebral cortex then the executive system, followed by 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. Newer models also converge on the conceptualization of conversion as reflecting errors in information processing and representation in the cognitive and neural systems are underpinnings of the processes.

Nomenclature changes

In 1952, the original DSM was published. Subsequently, 4 editions have followed and include the 2nd edition (DSM-II) in 1968, the DSM-III in 1980, the DSM-III revised edition (DSM-III-R) in 1987, and the 4th edition (DSM-IV) published in 1994.1 The International Classification of Diseases, 10th edition, (ICD-10) was published in 1992. The nomenclature has changed through time are listed in the following:

  • 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
  • 1992 ICD-10 - Dissociative (conversion) disorder

The DSM-III expanded the concept of conversion to generalized symptoms involving the loss of, or alteration in, physical functioning suggestive of a physical disorder, along with a clinical indication that the conversion was an expression of psychological conflict or need. This concept was retained in the revised edition of the DSM-III (DSM-III-R).

Diagnostic Criteria

Diagnostic criteria for conversion disorder DSM-IV 300.11 are as follows:

  • One or more symptoms or deficits affecting voluntary motor or sensory function suggest a neurologic or other general medical condition.
  • Psychological factors are judged to be associated with symptom or deficit because initiation or exacerbation of symptom or deficit is preceded by conflicts or other stressors.
  • The symptom or deficit is not intentionally produced or feigned (as in factitious disorder or malingering).
  • The symptom or deficit cannot, after appropriate investigation, be fully explained by a general medical condition or by the direct effects of a substance or as a culturally sanctioned behavior or experience.
  • The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.
  • The symptom or deficit is not limited to pain or sexual dysfunction, does not occur exclusively during the course of somatization disorder, and is not better accounted for by another mental disorder.

The type of symptom or deficit should be specified as follows: (1) with motor symptom or deficit, (2) with sensory symptom or deficit, (3) with seizure or convulsions, or (4) with mixed presentation.

Table 1. Somatoform Disorder (DSM-IV)

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Table
Somatoform Disorder (DSM-IV)General DescriptionTemporal and Other RequirementsExclusions By Other Psychiatric IllnessOther Exclusions
Somatization disorderHistory of many physical complaints; 4 pain sites or functions: 2 nonpain GI, 1 sexual or reproductive, 1 pseudoneurologicOnset <30 y of ageNot specifiedNot explained by general medical condition or substance effect
Undifferentiated somatoform disorderOne or more physical complaintsDuration >6 moNot accounted for by another mental disorderNot explained by medical condition or pathophysiologic mechanism
Conversion disorderSymptoms affecting voluntary motor and/or sensory function suggesting neurologic and/or medical conditionAssociated psychological factorsNot limited to pain or sexual dysfunction; not exclusively during course of somatization disorder; not better accounted for by other mental disorderNot intentionally produced or feigned; not explained by other neurologic or medical condition, substance effect, or culturally sanctioned behavior and/or experience
Pain disorderPain is predominant focus; severe enough to warrant clinical attentionPsychological factors in important roleNot better accounted for by mood, anxiety, or psychotic disorder; does not meet criteria for dyspareuniaNot specified
HypochondriasisPreoccupation with fear of having or idea that one has serious disease based on misinterpretation of bodily symptoms; persistent fear and idea despite medical evaluation and reassuranceDuration >6 moNot exclusively during obsessive compulsive disorder (OCD), generalized anxiety, panic disorder, major depressive episode, separation anxiety, or other somatoform disorderNot of delusional intensity; not restricted to circumscribed concern about appearance
Body dysmorphic disorderPreoccupation with imagined defect in appearance or excessive concern about slight physical anomalyNot applicableNot better accounted for by other mental disorderNot specified
Somatoform disorder, not otherwise specifiedSomatoform symptomsCan be <6 mo durationDoes not meet criteria for any other somatoform disorderNot specified
Somatoform Disorder (DSM-IV)General DescriptionTemporal and Other RequirementsExclusions By Other Psychiatric IllnessOther Exclusions
Somatization disorderHistory of many physical complaints; 4 pain sites or functions: 2 nonpain GI, 1 sexual or reproductive, 1 pseudoneurologicOnset <30 y of ageNot specifiedNot explained by general medical condition or substance effect
Undifferentiated somatoform disorderOne or more physical complaintsDuration >6 moNot accounted for by another mental disorderNot explained by medical condition or pathophysiologic mechanism
Conversion disorderSymptoms affecting voluntary motor and/or sensory function suggesting neurologic and/or medical conditionAssociated psychological factorsNot limited to pain or sexual dysfunction; not exclusively during course of somatization disorder; not better accounted for by other mental disorderNot intentionally produced or feigned; not explained by other neurologic or medical condition, substance effect, or culturally sanctioned behavior and/or experience
Pain disorderPain is predominant focus; severe enough to warrant clinical attentionPsychological factors in important roleNot better accounted for by mood, anxiety, or psychotic disorder; does not meet criteria for dyspareuniaNot specified
HypochondriasisPreoccupation with fear of having or idea that one has serious disease based on misinterpretation of bodily symptoms; persistent fear and idea despite medical evaluation and reassuranceDuration >6 moNot exclusively during obsessive compulsive disorder (OCD), generalized anxiety, panic disorder, major depressive episode, separation anxiety, or other somatoform disorderNot of delusional intensity; not restricted to circumscribed concern about appearance
Body dysmorphic disorderPreoccupation with imagined defect in appearance or excessive concern about slight physical anomalyNot applicableNot better accounted for by other mental disorderNot specified
Somatoform disorder, not otherwise specifiedSomatoform symptomsCan be <6 mo durationDoes not meet criteria for any other somatoform disorderNot specified

Note.—To qualify for this category of diagnoses, the symptoms must cause clinically significant distress or impairment in social, occupational, or other areas of functioning.

Epidemiology

Lifetime prevalence rates in the general population are estimated to be 11-300 cases per 100,000 people.

Varying estimates of the prevalence of conversion disorders depend on methodologic differences in diagnosis as well as on procedures used to confirm the disorder in different studies.

Frequency

The prevalence is 5-14% of general hospitalized patients, 1-3% of patients referred to outpatient psychiatric clinics, and 5-25% of psychiatric outpatients. No specific childhood prevalence figures are available.

Sex

The prevalence is higher in women than in men, with a female-to-male ratio of 2-10:1. Approximately 25% of emotionally normal postpartum and medically ill women report conversion symptoms sometime during their lives.

Socioeconomic and psychological factors

Low socioeconomic status and low levels of psychological sophistication are associated with high prevalences, as evident in developing countries compared with developed countries. The prevalence may be as high as 31% in some developing nations.

Familial pattern

Limited data suggest that conversion disorder frequently occurs in relatives of individuals with conversion disorder. Symptoms are often modeled from affected family members. Therefore, a thorough family history of medical conditions is essential. Case series show an increased risk in monozygotic but not dizygotic twins.

Nongenetic familial factors, such as incestuous sexual abuse in childhood, may be associated with an increased risk for conversion disorder. The conversion disorder may be the only mechanism for communication that remains available to the child or adolescent.

Onset

The onset is generally from late childhood to early adulthood, and the disorder rarely occurs in children younger than 10 years. Conversion disorder seldom develops for the first time after the fourth decade of life. The onset is generally acute, but symptoms may gradually increase.

Course

Data suggest that symptoms ameliorate in more than one half of all hospitalized patients with this disorder at the time of their discharge. However, 20-25% have a relapse in one year. In general, individual conversion symptoms are self-limited and do not lead to permanent sequelae or disabilities.

Prognosis

Factors associated with a good prognosis include the following:

  • Acute onset
  • Clearly identifiable stressors at time of onset
  • Short interval between onset and starting treatment
  • Good cognition and intelligence
  • Symptoms of aphonia, paralysis, and/or blindness (as opposed to seizures and tremor, which are associated with a poor prognosis)

Diagnostic Considerations

Developmental considerations

Conversion disorder usually begins in the adolescent years and after. Preschool-aged children who are developmentally healthy often have apparent paresis without a demonstrated physiologic cause for a few hours or days after a minor injury.

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. Psychiatric comorbidity has been poorly studied, as reflected in both the child and adolescent and the adult literature.

Psychological considerations

Conversion reactions represent a form of communication of the uncomfortable or, as Engel writes, "a psychic mechanism whereby an idea, fantasy, or wish is expressed in bodily rather than verbal terms and is experienced by the patient as a physical symptom rather than as a mental symptom." Hollender states, "Conversion symptom is a code which conceals the message from the sender as well as from the receiver." Conversion symptoms are experienced by the patient as involuntary and are often mysterious and frightening to the patient.

Primary gain refers to the extent to which a conversion symptom diminishes the unpleasant emotion and communicates symbolically the unconscious wish by keeping the internal conflict out of awareness. Secondary gain is achieved when the patient has been removed from the uncomfortable situation by virtue of the symptom. Interference with daily activities also provides secondary gain to the patient because attention and emotional support are often elicited from concerned parents and friends.

However, identification of secondary gain from decreased functioning is not pathognomonic of a diagnosis of conversion disorder. Conversion symptoms are more readily exhibited in the presence of those individuals meaningful to the patient because perpetuation of secondary gain is contingent on concern from others significant to the patient and the underlying causes of the symptom.

Neuroscience considerations

Attempts have been recently made, with the advent of functional imaging studies, to delineate the neuroscience underpinnings of conversion disorder. One hypothesis is that conversion is the result of dynamic reorganization of neural circuits that link volition, movement, and perception. Early electrophysiological studies implicate the anterior cingulate gyrus and possibly orbitofrontal cortex as responsible in "active inhibition". However, functional MRI (fMRI) and single-photon emission computed tomography (SPECT) studies are still few and involve few subjects; hence, they are at a preliminary stage and cannot be used to definitively propose a neurobiological basis for conversion disorder. 

Making the diagnosis

Complicating factors in making the diagnosis of conversion disorder include the higher-than-average probability of the presence of a coexisting physical illness because the 2 conditions are not mutually exclusive. Patients with incapacitating and frightening physical illnesses may appear to exaggerate symptoms. At the same time, patients with actual neurologic illnesses may also exhibit conversion symptoms.

More than one third of individuals with conversion symptoms have a current or prior neurologic condition (eg, children with a seizure disorder may also have pseudoseizures). Thus, physicians must recognize a possible comorbidity of conversion disorder along with a medical condition when faced with a symptom profile that is difficult to interpret.

A presentation of possible conversion symptoms mandates a thorough evaluation for the potential underlying organic disease. The extent of this evaluation involves the physician's judgment. When the symptoms suggest the possibility of conversion disorder, the evaluation should include mental health examination in addition to laboratory and radiologic tests. In early studies, general medical etiologies were later found in one fourth to one third of persons initially identified as having conversion symptoms.

A systematic review of misdiagnosis of conversion symptoms in patients who were ultimately identified as an organic medical condition has improved over time. On average, studies in the 1950s revealed misdiagnosis rates around 29% which improved to 17% in the 1960s and has been stable at around 4% for every decade since then. Possible explanations for this include better quality of studies, and cannot be completely accounted for by improvements in medical diagnostic technology.

History

No substitute for a good history and interview is known. Physicians should elicit family history, stressors, family illness, conflicts in relationships, and unresolved grief over loss or separation. School performance and peer relationships should also be considered. A healthcare provider might inquire about change of school, examinations, and new social experiences.

Nondirective interviewing is more rewarding than direct questioning because it provides insights into emotions that the patient associates with the symptoms. Care should be taken to avoid 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.

Clinical Features

Conversion symptoms are most typically related to voluntary motor or sensory functioning and therefore are referred to as pseudoneurologic symptoms. These are the most common type of conversion symptoms. Conversion symptoms typically do not conform to known anatomic pathways and physiologic mechanisms; instead, they follow the individual's conceptualization of a medical condition. Symptoms are often inconsistent (eg, a paralyzed extremity is moved inadvertently when the patient dresses or when his or her attention is directed elsewhere).

Motor conversion disorders primarily involve the major muscle groups. Weakness occurs more frequently than dystonia. Presentations of weakness include paralysis, paresis, and gait disturbance. In conversion motor symptoms, paralysis can occur for a prolonged period without atrophy. Dystonic presentations include spasmodic dysphonia, torticollis, torsion, tremor, equinovarus, 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).

Sensory symptoms may include loss of touch or pain sensation, double vision, blindness, deafness, and hallucinations.

Pseudoseizures are the most commonly reported conversion symptoms in the child and adolescent psychiatric literature. They resemble sudden convulsive events but are not associated with EEG evidence of a seizure, and they do not follow the typical pattern of a seizure disorder. Pseudoseizures can appear as the convulsive type, as hysteroepilepsy (including the classic arc-de-cercle opisthotonic posture, as an atonic drop attack, or as unresponsiveness with complicated automatic behavior and myoclonus.

Table 2. Differences between Pseudoseizure and True Seizure

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Table
FeaturePseudoseizureTrue Seizure
History
PatternNo neurophysiologic patternSame pattern
PrecipitantObvious emotional precipitant and occurrence in presence of othersPrecipitant may be present but not obvious; not associated with presence of others
Sleep associationDoes not occur in sleepMay occur in sleep
TreatmentIntractable despite adequate medicationOften responds to medication
Other featuresHistory of sexual or other abuseHistory of incontinence or self-injury
Observations
OnsetGradualAbrupt
DurationDuration variable but long (10-15 min)Short duration <1-2 minutes
ConsciousnessUsually preserved with bilateral motor activity; may be fluctuating but some responsive to painLost and unresponsive to pain
AuraUnusual except for symptoms of hyperventilationUsual
MoaningSwoon or faint; may moan, cry, scream, or weepMonotonous, epileptic cry
MovementsNonsynchronous out-of-phase movements (may be mild, jerky, side-to-side head movements, pelvic thrusting, limping, motionless, unresponsive); opisthotonic posturing or rigidity for extended periodsGeneralized tonic-clonic movements starting with fast, small amplitude movements to slow, large movements; brief rigidity, supplementary movements (eg, arms in abduction).
During sleepUncommon during physiologic sleepMay occur
InjurySelf-protection before fall; seldom self-injuryFrequent self-injury (eg, bite tongue, hit head, hurt limb)
ReflexesNo pathologic reflexesBabinski reflex and pupillary constriction after seizure
Postictal confusionLittle and patient is unconcernedPostictal confusion or transient paralysis
AmnesiaBetter memory for event; non-organic amnesiaAmnesia
In front of significant othersUsually occursUnconcerned
Independent witnessAbsentPresent
Induction by suggestionReadily induced or stoppedNot readily induced or stopped
 Not readily induced by sleep, photic stimuli, sleep deprivation, hyperventilationPrecipitated by sleep, photic stimuli, sleep deprivation, hyperventilation
Other observationsAvoidance behavior, arm drop, eye opening, genotropic movementSeeking help, tiredness, blank look, pupillary reflexes
Testing
pH immediately after attackNormalMay change
Creatinine kinase after attackNormalRises (significant if positive)
Prolactin after attackNormalRises (significant if positive)
EEGNo epileptic-form discharge, maintenance of alpha rhythm with only discontinuous muscle activity record during attack and absence of slowing with immediate reappearance of previous alpha rhythm; EEG may be abnormal in 10-53%, with prompt clinical and EEG recovery from a generalized convulsive episodeEpileptic changes in most patients (video-monitored EEG [VEEG] preferred); takes time to recover (VEEG useful)
Provocative methodsPsychiatric interview, suggestion, placebo medication, or hypnosisHyperventilation, photic stimuli, or sleep deprivation
FeaturePseudoseizureTrue Seizure
History
PatternNo neurophysiologic patternSame pattern
PrecipitantObvious emotional precipitant and occurrence in presence of othersPrecipitant may be present but not obvious; not associated with presence of others
Sleep associationDoes not occur in sleepMay occur in sleep
TreatmentIntractable despite adequate medicationOften responds to medication
Other featuresHistory of sexual or other abuseHistory of incontinence or self-injury
Observations
OnsetGradualAbrupt
DurationDuration variable but long (10-15 min)Short duration <1-2 minutes
ConsciousnessUsually preserved with bilateral motor activity; may be fluctuating but some responsive to painLost and unresponsive to pain
AuraUnusual except for symptoms of hyperventilationUsual
MoaningSwoon or faint; may moan, cry, scream, or weepMonotonous, epileptic cry
MovementsNonsynchronous out-of-phase movements (may be mild, jerky, side-to-side head movements, pelvic thrusting, limping, motionless, unresponsive); opisthotonic posturing or rigidity for extended periodsGeneralized tonic-clonic movements starting with fast, small amplitude movements to slow, large movements; brief rigidity, supplementary movements (eg, arms in abduction).
During sleepUncommon during physiologic sleepMay occur
InjurySelf-protection before fall; seldom self-injuryFrequent self-injury (eg, bite tongue, hit head, hurt limb)
ReflexesNo pathologic reflexesBabinski reflex and pupillary constriction after seizure
Postictal confusionLittle and patient is unconcernedPostictal confusion or transient paralysis
AmnesiaBetter memory for event; non-organic amnesiaAmnesia
In front of significant othersUsually occursUnconcerned
Independent witnessAbsentPresent
Induction by suggestionReadily induced or stoppedNot readily induced or stopped
 Not readily induced by sleep, photic stimuli, sleep deprivation, hyperventilationPrecipitated by sleep, photic stimuli, sleep deprivation, hyperventilation
Other observationsAvoidance behavior, arm drop, eye opening, genotropic movementSeeking help, tiredness, blank look, pupillary reflexes
Testing
pH immediately after attackNormalMay change
Creatinine kinase after attackNormalRises (significant if positive)
Prolactin after attackNormalRises (significant if positive)
EEGNo epileptic-form discharge, maintenance of alpha rhythm with only discontinuous muscle activity record during attack and absence of slowing with immediate reappearance of previous alpha rhythm; EEG may be abnormal in 10-53%, with prompt clinical and EEG recovery from a generalized convulsive episodeEpileptic changes in most patients (video-monitored EEG [VEEG] preferred); takes time to recover (VEEG useful)
Provocative methodsPsychiatric interview, suggestion, placebo medication, or hypnosisHyperventilation, photic stimuli, or sleep deprivation

Associated features

La belle indifference is defined as a relative lack of concern about the nature or implications of the symptom manifested on the part of the patient. More commonly observed in adults, la belle indifference is rarely observed in children and adolescents (as few as 8%). Children and adolescents may typically express fear and hopelessness regarding their lack of voluntary control over the symptoms. La belle indifference may be present in individuals with combinations of medical conditions and conversion disorders. Occasionally, individuals with conversion symptoms may present in a dramatic or histrionic fashion.

However, evidence from published literature suggests that la belle indifference is not an useful clinical sign for distinguishing conversion symptoms from organic disease. Recommendations have been made to abandon its use as a clinical sign until more rigorous studies are done to clarify its definition and use in diagnostics. Its use has endured, regardless, due to its "cache" name and possibility of a link to biological right hemisphere dysfunction that has yet to be proven with functional imaging studies.

Differential Diagnoses

Medical conditions

Medical conditions that may mimic conversion symptoms include the following:

  • Multiple sclerosis (with blindness secondary to optic neuritis)
  • 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

Psychiatric conditions that must be differentiated include the following:

  • Dissociative disorder
  • Psychotic disorders
  • Mood disorders
  • Factitious disorders and malingering
  • Pain disorder or sexual dysfunction
  • Somatization disorder
  • Undifferentiated somatoform disorder

Considering other somatoform disorders while attempting to make a diagnosis of conversion disorder is always important.

Differentiation of hallucinations in conversion and other psychiatric disorders

In general, conversion disorder hallucinations differ from psychotic hallucinations and sometimes are referred to as pseudohallucinations.

Table 3. Hallucinations in Conversion Disorder Versus Other Psychiatric Disorders

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Table
CharacteristicConversion DisorderPsychotic Disorder
Other psychotic symptomsTypical absence of other psychotic symptoms (eg, disordered thought process)Disordered thought process
Insight into hallucinationsInsight retained that hallucinations are not realTypical lack of insight about unreality of hallucinations
Scope of hallucinationsHallucinations involving more than one sensory modalityTypical hallucinations involving single sensory modality, especially auditory and secondarily tactile or visual
Psychological meaning of hallucinationsHallucinations often psychologically meaningfulHallucinations often bizarre and unrelated to psychological factors
CharacteristicConversion DisorderPsychotic Disorder
Other psychotic symptomsTypical absence of other psychotic symptoms (eg, disordered thought process)Disordered thought process
Insight into hallucinationsInsight retained that hallucinations are not realTypical lack of insight about unreality of hallucinations
Scope of hallucinationsHallucinations involving more than one sensory modalityTypical hallucinations involving single sensory modality, especially auditory and secondarily tactile or visual
Psychological meaning of hallucinationsHallucinations often psychologically meaningfulHallucinations often bizarre and unrelated to psychological factors

Vigilance must be maintained for emergence of other signs of psychosis in a diagnosed case of conversion disorder; psychotic hallucinations may share some of the features of conversion hallucinations.

Dissociative identity disorder and posttraumatic stress disorder and schizophrenia are psychiatric disorders with hallucinations that must be differentiated from conversion disorder.

Treatment

Primary care physician

Most commonly, children and adolescents with conversion disorder present to the pediatrician or primary health care provider because the presentation of illness is almost always medical, physical, or both. Children usually undergo varying degrees of medical workup depending on their presenting symptoms and on the level of comfort and expertise of the provider.

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. The tasks of a primary care physician's include providing education about conversion disorder while carefully ruling out contributing medical conditions and attending to the views of the patient and his or her family.

A discussion of the interplay between emotional and physical stress can be helpful to the patient and his or her family. The clinician should encourage the family to openly communicate about the diagnostic tests that they would like performed and about the medical conditions that they believe are causing the symptoms. Explain to the family that, even while the symptoms persist, the goal is to help the child or adolescent to maintain normal daily functioning in school and in their social life with peers. Referral to a professional trained in mental health diagnosis and treatment may be necessary if progress is not made in coping with symptoms.

The physician should discuss with the patient and the families the close interrelation between physical and emotional factors. Every individual has an emotional response to a physical stress. Similarly, everyone has a physical way of responding to emotional stress. The physician can provide the example of headaches developing when individuals become upset. People without medical training can easily understand this example. The empathetic approach and open acknowledgment of this interplay by the physician can help the family volunteer information about psychosocial functioning.

Focusing on organic diagnosis alone suggests that psychological involvement is unlikely, unimportant, and improbable. By looking at psychological issues alone, the physician implies that this is the last resort because the physician was unable to ascertain an organic cause. Hence, the concurrent physiopsychological approach is best. The physician must be satisfied with the completeness of the physical evaluation and should use discretion regarding the extent of the organic workup.

Although patients with conversion disorder are suggestible, reassurance that symptoms will go away is rarely effective; this reassurance does not help probe the psychological source of the symptoms. On the contrary, suggesting that symptoms will persist may provide time to establish therapeutic relationships. Use of placebo medication is usually ineffective and ethically questionable. The patient should be allowed to eliminate the symptoms and/or signs as slowly as is needed and with dignity.

A pediatrician who encounters a conversion disorder in a child or adolescent is most successful when he or she advocates a team approach, including other healthcare providers who can openly communicate and work together.

Referrals

Appropriate referrals are made to behavioral pediatricians, child and adolescent psychiatric clinics, community mental health centers, private mental health professionals, and community social support agencies.

Mental health professionals

Referrals to psychiatrists, psychologists, and behavioral pediatricians usually come from school personnel, court officials, and children's welfare agencies. Primary physicians may refer patients after the initial workup is completed if an organic condition cannot be documented.

Modalities used to treat conversion disorder may include individual psychotherapy, group and family therapy, and pharmacologic approaches to manage specific symptoms.

Psychodynamic techniques help a child gain insight into unconscious conflicts and understand how psychological factors have helped to maintain symptoms. Cognitive-behavioral approaches and behavior modification plans have also been attempted. Paradoxical intention, which is encouraging the patient to deliberately engage in the unwanted behavior, has been studied as has hypnosis. Therapists also use antianxiety approaches in the form of progressive muscle relaxation, visual imagery, and biofeedback, as well as antianxiety medication.
Case reports have detailed interventions as diverse as spa treatment, surgery, electroconvulsive therapy, physiotherapy, and inpatient psychiatric care.

However, few studies show the effectiveness (or lack thereof) of psychosocial interventions. In a systematic review of studies to investigate efficacy of psychosocial intervention on conversion disorder, only 3 small studies were found, most with methodological problems and inconclusive results.

Goals of family and group therapy include building self-esteem, promoting assertiveness, improving communication with family and peer groups, and teaching nonsomatic ways to express distress. Group therapy is particularly helpful in learning social skills, decreasing dependency on the family, and learning coping strategies.

Educational and pharmacologic interventions may be needed to treat underlying depressive and anxiety disorders, as well as educational problems. Hospitalization is sometimes indicated if outpatient therapy is not effective. Some clinicians advocate inpatient therapy as the primary site to initiate treatment because it removes children from their environments. Inpatient treatment may facilitate a more appropriate level of functioning and more adaptive responses. Inpatient treatment is geared toward ruling out significant organic issues and promoting certain types of functioning away from the home environment.

Prognosis

Follow-up studies indicate an eventual full recovery in 85-97% of children. Early recognition and prompt intervention are often associated with speeded recovery. Favorable prognostic features are a recent onset of symptoms, a monosymptomatic manifestation, and a good premorbid personality. Prognosis has been suggested to be poorer with nonepileptic attacks, tremor, or amnesia rather than hysterical blindness, aphonia, and motor disorders.

Keywords

hysteria, conversion hysteria, pseudoneurologic symptom, persistent physical symptom, physical complaint, conversion disorder, psychiatric disorder, somatoform disorder, psychological automatisms, dissociative disorder, pain disorder, hypochondriasis, body dysmorphic disorder, multiple sclerosis, myasthenia gravis, periodic paralysis, polymyositis, psychotic disorders, mood disorders, spasmodic dysphonia, torticollis, torsion, tremor, equinovarus, ptosis, chorea, ataxia, globus hystericus, astasia-abasia, hysteroepilepsy, pseudoseizures, la belle indifference, hallucinations, posttraumatic stress disorder, schizophrenia

 


More on Somatoform Disorder: Conversion

References

References

  1. APA. Somatoform disorders. Conversion disorder. In: Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Press; 1994:452-7.

  2. Bhatia MS. Pseudoseizures. Indian Pediatr. Jul 2004;41(7):673-9. [Medline].

  3. Ford CV, Folks DG. Conversion disorders: an overview. Psychosomatics. May 1985;26(5):371-4, 380-3. [Medline].

  4. Fritz GK, Fritsch S, Hagino O. Somatoform disorders in children and adolescents: a review of the past 10 years. J Am Acad Child Adolesc Psychiatry. Oct 1997;36(10):1329-38. [Medline].

  5. Ghaffar O, Staines WR, Feinstein A. Unexplained neurologic symptoms: an fMRI study of sensory conversion disorder. Neurology. Dec 12 2006;67(11):2036-8. [Medline].

  6. Kozlowska K. Healing the disembodied mind: contemporary models of conversion disorder. Harv Rev Psychiatry. Jan-Feb 2005;13(1):1-13. [Medline].

  7. Krem MM. Motor conversion disorders reviewed from a neuropsychiatric perspective. J Clin Psychiatry. Jun 2004;65(6):783-90. [Medline].

  8. Mailis-Gagnon A, Giannoylis I, Downar J, et al. Altered central somatosensory processing in chronic pain patients with "hysterical" anesthesia. Neurology. May 13 2003;60(9):1501-7. [Medline].

  9. Martin R, Yutzy S. Somatoform disorders. In: American Psychiatric Press Textbook of Psychiatry. 3rd ed. Washington, DC: American Psychiatric Press; 1999.

  10. Minuchin S, Baker L, Rosman BL, et al. A conceptual model of psychosomatic illness in children. Family organization and family therapy. Arch Gen Psychiatry. Aug 1975;32(8):1031-8. [Medline].

  11. Nemiah JC. Somatoform disorders. In: Sadock BJ, Sadock VA, eds. Kaplan and Sadock's Comprehensive Textbook of Psychiatry. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1985:924-42.

  12. Nemzer E. Somatoform disorders: treatment and outcome. In: Lewis M, ed. Child and Adolescent Psychiatry: Comprehensive Textbook. Philadelphia, PA: Lippincott Williams and Wilkins; 1996.

  13. Pehlivanturk B, Unal F. Conversion disorder in children and adolescents: a 4-year follow-up study. J Psychosom Res. Apr 2002;52(4):187-91. [Medline].

  14. Prazar G. Conversion reactions in adolescents. Pediatr Rev. Mar 1987;8(9):279-86. [Medline].

  15. [Best Evidence] Ruddy R, House, A. Psychosocial interventions for conversion disorder (Review). Cochrane Database Systematic Reviews. Oct 2005;19 (4):[Medline].

  16. Stone J, Smyth R, Carson A, et al. Systematic review of misdiagnosis of conversion symptoms and "hysteria". BMJ. Oct 29 2005;331(7523):989. [Medline].

  17. Stone J, Smyth R, Carson A, Warlow C, Sharpe M. La belle indifference in conversion symptoms and hysteria: systematic review. Br J Psychiatry. Mar 2006;188:204-9. [Medline].

Further Reading

Keywords

hysteria, conversion hysteria, pseudoneurologic symptom, persistent physical symptom, physical complaint, conversion disorder, psychiatric disorder, somatoform disorder, psychological automatisms, dissociative disorder, pain disorder, hypochondriasis, body dysmorphic disorder, multiple sclerosis, myasthenia gravis, periodic paralysis, polymyositis, psychotic disorders, mood disorders, spasmodic dysphonia, torticollis, torsion, tremor, equinovarus, ptosis, chorea, ataxia, globus hystericus, astasia-abasia, hysteroepilepsy, pseudoseizures, la belle indifference, hallucinations, posttraumatic stress disorder, schizophrenia

Contributor Information and Disclosures

Author

Neelkamal S Soares, MD, FAAP, Assistant Professor, Department of Pediatrics, University of Kentucky; Consulting Staff, Department of Pediatrics, Kentucky Clinic
Neelkamal S Soares, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Kentucky Pediatric Society, and Society for Developmental and Behavioral Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Linda Grossman, MD, Associate Professor, Division Head, Department of Pediatrics, Division of Behavioral and Developmental Pediatrics, University of Maryland School of Medicine
Linda Grossman, MD is a member of the following medical societies: Ambulatory Pediatric Association
Disclosure: Nothing to disclose.

Medical Editor

Carol Diane Berkowitz, MD, Executive Vice Chair, Department of Pediatrics, Professor, Harbor-University of California at Los Angeles Medical Center
Carol Diane Berkowitz, MD is a member of the following medical societies: Alpha Omega Alpha, Ambulatory Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, American Medical Association, American Pediatric Society, and North American Society for Pediatric and Adolescent Gynecology
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation

Managing Editor

Caroly Pataki, MD, Professor of Clinical Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Division Chair of Child and Adolescent Psychiatry, Director of Training, Child and Adolescent Psychiatry Residency Program, University of Southern California Keck School of Medicine
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

CME Editor

Carrie Sylvester, MD, MPH, Director of Education in Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Pediatrics, Northwestern University Medical School
Carrie Sylvester, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics, American Medical Women's Association, American Psychiatric Association, and American Society for Adolescent Psychiatry
Disclosure: Nothing to disclose.

Chief Editor

Caroly Pataki, MD, Professor of Clinical Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Division Chair of Child and Adolescent Psychiatry, Director of Training, Child and Adolescent Psychiatry Residency Program, University of Southern California Keck School of Medicine
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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