What is the usual underlying cause in patients with conversion disorder

Conversion disorder is defined as one or more neurological symptoms that cause dysfunction and cannot be explained by a medical condition.

From: Essential Emergency Medicine, 2007

Conversion Disorder, Psychosomatic Illness, and Malingering

James G. Adams MD, in Emergency Medicine, 2013

Classic Features

Somatization is exhibited by patients who are chronically and persistently “sick” with numerous vague complaints and symptoms involving many organ systems; review of systems is often globally “positive.” Patients’ symptoms are distressing to them, and their suffering is authentic even if medically inexplicable. Patients maintain a very strong conviction of illness despite multiple negative diagnostic work-ups, hospital admissions, specialist referrals, and surgical procedures. An example of the breadth of symptoms associated with somatoform disorders can be seen in the diagnostic criteria listed inBox 198.1.

Patients withhypochondriasis, like somatizers, are convinced that they are gravely ill. Although a somatizer focuses on symptoms, a patient with hypochondriasis focuses on disease states and invests great personal energy in seeking multiple extensive reassurances from the health care system. Patients with hypochondriasis are typified by health anxiety leading to strong convictions of illness and fixation with the body and its functions. Ominous implications are often attributed to mundane or insignificant findings, and symptoms are exaggerated out of proportion to any actual organic illness.

Conversion disorder, in contrast to somatization disorder, is the acute, often episodic onset of one symptom or sign involving limited body parts or organ systems. Complaints are generally sensory or motor in nature and often occur in response to an identified stressor. Unlike malingering or factitious disorders, the malady is not consciously feigned or deliberate. Examples of conversion disorder typically seen in the ED include pseudoseizures, altered mental status, paralysis, and movement disorders.17 Other common conversion symptoms are presented inBox 198.2.

One of the more unusual conversion disorders ispseudocyesis, or “hysterical pregnancy,” which includes the physical symptoms of pregnancy [even amenorrhea] in the absence of a true gestation.

La belle indifférence, a seemingly incongruous disinterest in one's illness, is classically associated with conversion reactions. However, la belle indifférence may be seen with organic disease states such as stroke. La belle indifférence should not be used alone to differentiate between conversion and organic disorders.18

Patients whomalinger and those who havefactitious disorder tend to limit themselves to exaggerations of symptoms of a previously diagnosed illness or to symptoms that are difficult to investigate and disprove; examples include pain of any variety, psychiatric conditions such as suicidality, and the pseudoneurologic symptoms of tingling, amnesia, and seizures. Less commonly, patients with factitious disorder inflict injury or disease on themselves. Deliberate misuse of medications such as hypoglycemic agents has been described in health care workers.10

Pediatric Neurology Part II

P.M. Leary, in Handbook of Clinical Neurology, 2013

Clinical profiles

During childhood, conversion disorder occurs most commonly in the 10–15 year age range. Girls outnumber boys in a ratio of 2:1 [Anon, 1991]. In a majority of cases symptoms are of abrupt onset and date from a minor illness or injury. Comprehensive history taking will in many instances reveal evidence of domestic stress, poor intrafamilial communication, unresolved grief [Malony, 1980], unhappiness at school, and feelings of parental rejection [Binzer and Eisemann, 1998]. In a study of 51 children and adolescents with conversion disorder Pehlivanturk and Unal [2000] found comorbid depression in 16% and a comorbid anxiety disorder in 37%. Other predisposing factors are a rigid obsessional personality trait [Wynick et al., 1997] and previous sexual abuse [Roelofs et al., 2002]. There may be an adult family member or acquaintance with obvious disability as a result of stroke, accident, or other cause. This individual could act as a role model for the patient.

The most common symptoms involve motor function. There may be paralysis of one or more limbs, gait disturbance, incoordination, tremor, loss of speech, or a combination of several of these. Sensory symptoms include apparent loss of all modalities of sensation in a limb, paresthesiae intractable pain, tunnel vision, and blindness. Other common presenting features are daily incapacitating headache, unremitting fatigue, and pseudo-seizures. Cultural factors may influence the mode of presentation. A study in India [Ghosh et al., 2007] found that psychogenic nonepileptic seizures were the commonest presenting feature, and in certain areas of southern Africa a state of apparent agitated dementia is recognized.

Detailed physical examination of the patient with conversion disorder will usually reveal incongruities that suggest the diagnosis. Normal tendon reflexes are found in the presence of flaccid paralysis. Position sense is unimpaired and normal flexor plantar responses are elicited despite apparent total anesthesia of a lower limb. Reciprocal muscle contraction is palpable during attempts to use paralysed muscle groups. Abnormal gaits are bizarre and do not conform to those seen in children with hemiplegia, diplegia, athetoid cerebral palsy, cerebellar dysfunction, peripheral neuropathy or lower motor neuron damage. Falls are carefully choreographed and seldom result in injury. Video filming of the subject will reveal variations day-to-day in the pattern of a movement disorder. Sensory loss does not conform to dermatome or glove-and-stocking distribution and may involve only touch and pain and not other modalities such as temperature, position sense, and vibration. Diplopia may be present in all three directions and when one eye is occluded. Tunnel vision due to organic disease [e.g., retinitis pigmentosa] is extremely rare in childhood. In apparent blindness collisions and injuries do not occur and humorous incidents on television may be seen to evoke evidence of amusement. Pseudoseizures occur only when the child is awake and in company. They may last for prolonged periods [15–20 minutes] and include repetitive pelvic thrusting movements and head shaking, which are not seen in true seizures. Incontinence of urine is not a feature.

Some children with conversion disorder exhibit an attitude of tranquil acceptance both of apparent severe disability and of significant loss of school time. This attitude [“la belle indifférence”] is not pathognomonic [Stone et al., 2006] but is seldom seen in otherwise healthy children who are sidelined by fractures or intercurrent infection. It may be interpreted by family members as brave stoicism in the face of serious illness. The duration and degree of disability may be increased if the patient has an ally, either a family member or a healthcare professional, who champions the notion that symptoms are due to organic disease. In all forms of conversion disorder there may be short “remissions” when the patient is alone and “emergencies” arise such as urgent need for sustenance or the toilet.

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Psychiatric Pain–Associated Co-morbidities

Stephen B. McMahon FMedSci, FSB, in Wall & Melzack's Textbook of Pain, 2013

Conversion Disorder

Conversion disorder is characterized by the presence of a symptom or deficit affecting voluntary motor or sensory function that suggests a neurological or general medical condition. The two criteria for this disorder are the presence of the symptom and judgment by the psychiatric examiner that psychological factors are associated with initiation [preceded by conflict or other stressors] or exacerbation of the symptom. As noted later in the section on Waddell’s signs, non-dermatomal sensory abnormalities [NDSAs] and muscle weakness [paresis] are frequently found in CPPs and make the CPP a candidate for a diagnosis of conversion disorder. For example,Fishbain and co-authors [1986] reported that 37.8% of their CPPs had NDSAs. Motor deficits [paresis] are less frequent but are seen regularly.

There is now significant evidence that NDSAs are a neurophysiological central phenomenon. In rodent models of mononeuropathy, stocking or glove hypoesthesia is the result of extraterritorial sensory loss secondary to overlapping receptive fields of adjacent neurons in the spinal cord. Recent positron emission tomography scanning studies [Egloff et al 2009] indicate that CPPs with NDSAs have decreases in cerebral blood flow in the thalamus and basal ganglia contralateral to the deficit and in cortical and subcortical areas. These cerebral blood flow problems resolve after recovery from the pain. Pain induction studies using fMRI have demonstrated that CPPs with NDSAs fail to activate brain areas normally responding to pain stimuli [Mailis-Gagnon et al 2003]. In addition, pain treatment studies have demonstrated that reduction of pain removes the NDSAs implicating pain in the phenomenon. Finally, NDSAs have been shown, in a statistically significant manner, to occur only on the painful site or limb [Fishbain et al 2003b].

Pain has also been implicated in the paresis conversion problem. Motor conversion is almost always associated with the presence of pain in the affected extremity. If a painful limb is compared with a non-painful one, a 20–30% reduction in strength is observed. Muscle pain reduces maximal voluntary contraction and endurance time during submaximal contractions. In pain induction studies, motor unit firing rates are inversely related to reports of pain in rapidly activated painful and pain-free synergistic muscle.

Overall, this research indicates that the neurophysiological phenomena of pain are intimately involved in the generation of these two “conversion” symptoms and are not caused by behavioral issues as the diagnosis implies. Consequently and because the second criterion is essentially a value judgment, it may be inappropriate to apply this diagnosis to any CPP with these conversion symptoms, especially since there are medicolegal consequences in wrongfully applying this diagnosis [Fishbain and Goldberg 1991].

Functional Neurologic Disorders

K. Roelofs, J. pasman, in Handbook of Clinical Neurology, 2016

Abstract

Conversion disorder [CD] has traditionally been ascribed to psychologic factors such as trauma, stress, or emotional conflict. Although reference to the psychologic origin of CD has been removed from the criteria list in DSM-5, many theories still incorporate CD as originating from adverse events.

This chapter provides a critical review of the literature on stressful life events in CD and discusses current cognitive and neurobiologic models linking psychologic stressors with conversion symptomatology. In addition, we propose a neurobiologic stress model integrating those cognitive models with neuroendocrine stress research and propose that stress and stress-induced changes in hypothalamus–pituitary–adrenal [HPA] axis function may result in cognitive alterations, that in turn contribute to experiencing conversion symptoms. Experimental studies indeed suggest that basal as well as stress-induced changes in HPA axis responding lead to alterations in attentional processing in CD. Although those changes are stronger in traumatized patients, similar patterns have been observed in patients who do not report a history of traumatic events.

We conclude that, whereas adverse events may play an important role in many cases of CD, a substantial proportion of patients do not report a history of traumatization or recent stressful events. Studies integrating effects of stress on cognitive functioning in CD are scarce. We propose that, instead of focusing research on defining etiologic events in terms of symptom-eliciting events, future research should work towards an integrated mechanistic account, assessing alterations in cognitive and biologic stress systems in an integrated manner in patients with CD. Such an account may not only serve early symptom detection, it might also provide a starting point for better-targeted interventions.

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C – Clinical Algorithms

Fred F. Ferri MD, FACP, in Ferri's Clinical Advisor 2022, 2022

Coma

ICD-10CM # R40.20 Unspecified coma

FIG. 55. Natural course of acute coma.

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

FIG. 56. Management of acute coma.CT, Computed tomography.

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

TABLE 13. Characteristic Clinical Features of Disorders of Consciousness and Locked-In Syndrome

DisorderConsciousnessCognitionReceptive LanguageExpressive LanguageVisual PerceptionMotor FunctionStructure Injured
Coma No sleep-wake cycles None None None None Primitive reflexes only RASor Diffuse brain damage
Vegetative state Intermittent periods of wakefulness None None None Variable visual startle responses Involuntary movements only Cerebral cortexThalamocortical pathway ± RAS
Minimally conscious state Intermittent periods of wakefulness Inconsistent but clear behavioral signs of self or environmental awareness Inconsistently one-step command following Aspontaneous and ranging from single words or short phrases Visual pursuitObject recognition Localize to noxious stimuliObject manipulation
Automatic movement sequences
Normal to variable lesion in RAS
Akinetic mutismAbulia Normal or depressed Normal or depressed Normal or depressed Normal or depressed Normal Delayed, slow responses HypothalamicBasal forebrain
Acute confusional state Extended period of wakefulness Confusion and disorientation Consistent one-step command following Yes-no responsesPerseverative
Short sentences
Confused
Object recognition No functional deficit Normal to variable lesions in RAS
Brain death Absent Absent None None None Preserved postural and motor reflex Global brain damage
Locked-in syndrome Normal sleep-wake cycles Normal to near-normal Normal Aphonic Normal Quadriplegia Bilateral ventral pons

RAS, Reticular activating system.

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

TABLE 14. Etiologies and Clinical Features of Different Causes of Impaired Consciousness

EtiologyClinical Features for Differential Diagnosis
Supratentorial lesion

Destructive: Ischemic infarct, hemorrhage [SAH, SDH, ICH]

Compressive lesion: Ischemic infarct, hemorrhage, aneurysm, vascular malformation, tumor, venous thrombosis, abscess

Head injury, concussion

Initial focal cerebral dysfunction

Dysfunction progresses rostral to caudal

Signs reflect cortical dysfunction, often multifocal

Often asymmetric cortical involvement and presentation

Infratentorial lesion

Destructive: Ischemic infarct, hemorrhage [SAH, ICH]

Compressive lesion: Ischemic infarct, hemorrhage, aneurysm, vascular malformation, tumor, venous thrombosis

Symptoms of brainstem dysfunction or sudden onset coma [posturing]

Brainstem signs precede/accompany coma

Cranial nerve and oculovestibular dysfunction: Ocular bobbing, vertical pendular oscillation [pons], monocular movement [midbrain]

Early onset of abnormal respiratory pattern

Diffuse brain lesion

Traumatic brain injury

Anoxic injury

Toxic encephalopathy

Seizure, nonconvulsive, postictal

Primary neuronal disorder

Infectious encephalitis [prion disease, progressive leukoencephalopathy]

Inflammatory encephalitis [ADEM]

Vasculitis

Often asymmetric in presentation

Focal signs depending on main brain lesion

Metabolic coma

Hypoglycemia

Nutritional [thiamine, niacin, pyridoxine, cyanocobalamin, folic acid], Wernicke encephalopathy

Hepatic encephalopathy

Uremia and dialysis

CO2 narcosis

Exocrine pancreatic encephalopathy

Endocrine: Addison disease, pheochromocytoma, diabetes

Paraneoplastic

Drug poisoning

Thermal injury

Electrolyte/acid-base imbalance

Confusion/stupor precede motor signs

Motor signs usually symmetric

Pupil responses generally preserved

Myoclonus, asterixis, tremulousness, and generalized seizures common

Acid-base imbalance common with compensatory ventilator changes

Periodic alternating gaze deviation

Systemic: Altered mental state with normal brainstem function [especially normal pupils]. Possible triphasic waves on EEG

Stimulant-induced coma [cocaine, amphetamine, phencyclidine, tricyclic antidepressant]

Fever, mydriasis [except miosis with phencyclidine], and seizure

Sedatives [alcohol, benzodiazepine, barbiturates, antiepileptics]

Ataxia, impaired eye movements but normal pupils

Opiate-induced miosis

Psychiatric

Conversion disorder

Depression

Psychosis—catatonia

Forced eye closure

Pupils reactive or dilated, nonreactive

Unpredictable oculocephalic reflex: Nystagmus on caloric test

Normal or inconsistent motor tone

No pathologic reflexes

Awake-pattern EEG

ADEM, Acute disseminated encephalomyelitis;CO2, carbon dioxide;EEG, electroencephalogram;ICH, intracranial hematoma;SAH, subarachnoid hemorrhage;SDH, subdural hematoma.

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

TABLE 15. Types of Brain Herniation Syndromes

SyndromeMechanismImaging FindingsClinical Presentation
Uncal

Downward displacement of medial temporal lobe into the posterior fossa through the incisural opening

Seen in patients with unilateral hemispheric mass lesions

Contralateral temporal horn widening

Ipsilateral ambient and prepontine cistern widening

Uncus extending into the suprasellar cistern

Ipsilateral pupil dilation and ophthalmoplegia

Contralateral or ipsilateral hemiparesis

Decerebrate posturing

Central [transtentorial]

Downward displacement of cerebral hemispheres and basal nuclei compressing and displacing diencephalon and midbrain rostrocaudally through the tentorial notch

Effacement of the sulci

Obliteration of the suprasellar cistern

Compression and posterior displacement of the quadrigeminal cistern

Medium-sized, fixed pupils

Early coma

Decorticate posturing

Cheyne-Stokes respiration

Diabetes insipidus

Cingulate [subfalcine]

Lateral displacement of the cingulate gyrus under the anterior falx

Attenuation of ipsilateral aspect of frontal horn

Asymmetric anterior falx

Obliteration of ipsilateral atrium of lateral ventricle

Septum pellucidum shift

Small reactive pupils

Headache

Contralateral leg paralysis

Ascending

Infratentorial mass effect protruding through the tentorial opening compressing the midbrain and cerebellar structures at the tentorial edges

Spinning top appearance of midbrain

Narrowing of bilateral ambient and quadrigeminal cisterns

Progressive stupor

Nausea and vomiting

Tonsillar

Cerebellar tonsils protruding into the foramen magnum compressing adjacent medulla and upper cervical cord

Cerebellar tonsils at the level of the dens on axial view and 5 mm below foramen magnum on sagittal view [7 mm in children]

Cushing triad

Coma

Bilateral arm dysesthesia

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

TABLE 16. Neuroimaging and Electrophysiologic Techniques and Findings in Disorders of Consciousness

TechniqueMeasurementStrengthsLimitationsVegetative StateMinimally Conscious StateComatose
FDG-PET Metabolic Relatively direct measure of neuronal energy use [glucose uptake] Ionizing [limited repeated measures] Voxel-based: Hypometabolism in lateral and medial frontoparietal cortices Metabolic dysfunction in left hemisphere
Functional MRI CBF High-resolution structural imaging of grey-white matter [DTI] and functional imaging [spectroscopy, resting, passive, and active CBF paradigms]

Sensitive to movement artifacts requiring sedation/anesthesia

Incompatible with ferromagnetic material [deprivation, pumps, electrodes]

Activation fMRI:
Low-level cortical activation
DMN—partially preserved
Activation fMRI: Near-normal high-level cortical activation
EEG/ERPs Electrical Repeatable, portable, and inexpensive Muscle, eye, and dysautonomia artifacts
Challenging source reconstruction
EEG: Slow-wave activity through night and periods of REM sleep ERP-poor outcome with absence of a cortical response to electrical stimulation of median nerves
EEG-TMS Electrical Stereotaxic stimulation connectivity studies Stimulation areas are limited by muscle artifacts TMS triggers a simple, local EEG response similar to deep sleep/anesthesia Complex activations in distant cortical areas

CBF, Cerebral blood flow;DMN, default model network;DTI, diffuse tensor imaging;EEG, electroencephalogram;ERPs, event-related potentials;FDG,18F-fluorodeoxyglucose;fMRI, functional magnetic resonance imaging;PET, positron emission tomography;REM, rapid eye movement;TMS, transcranial magnetic stimulation.

From Parrillo JE, Dellinger RP:Critical care medicine, principles of diagnosis and management in the adult, ed 5, Philadelphia, 2019, Elsevier.

Pain and Somatoform Disorders

TONYA M. PALERMO, ... LONNIE K. ZELTZER, in Developmental-Behavioral Pediatrics, 2008

CONVERSION DISORDER

Conversion disorder is characterized by medically unexplained deficits or alterations of voluntary motor or sensory function that is suggestive of a neurological or medical illness. These symptoms are judged to have either been initiated or perpetuated by psychological factors and are preceded by conflicts or other stressors. The symptom or deficit may not include pain, may be under voluntary control, may be intentionally produced or feigned, or may be a culturally sanctioned experience. The symptom or deficit cannot, after appropriate medical investigation, be entirely explained by a neurological or general medical condition or be substance induced. Documented conversion disorder is rare and is reported in fewer than 1% of individuals in community settings. Conversion disorder has been described in children and adolescents as involving a variety of motor and sensory symptoms.114–116

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Somatoform Disorders

Betty Ann Tzeng, Stuart Eisendrath, in Encyclopedia of the Neurological Sciences, 2003

Conversion Disorder

Conversion disorder is a condition in which the presenting symptom is a loss or alteration of physical function. The symptom usually mimics a neurological condition. It may look like motor symptoms, such as focal weakness, dysarthria, or paralysis. It may also mimic sensory deficits, such as numbness or blindness. Finally, the disorder may present as seizure-like symptoms or a cognitive disorder such as amnesia.

The onset of conversion disorder is acute and usually associated with a stressor. A classic example is a man who has an internal conflict about his feelings of aggression. He gets into an argument with his wife one day and suddenly his arm becomes “paralyzed.” According to psychodynamic theory, this symptom resolves his conflicted feelings between wanting to strike his wife but not wanting to harm her. The resulting disability both relieves anxiety over the conflict and punishes the man for having the unacceptable wish to hit his wife. Patients with conversion disorder have a prognosis for the symptoms to resolve within weeks if they had good premorbid functioning and their conflict is resolvable. However, recurrences within the patients' lifetimes are common.

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Pain Patients

Shamim H. Nejad M.D., Menekse Alpay M.D., in Massachusetts General Hospital Handbook of General Hospital Psychiatry [Sixth Edition], 2010

Conversion Disorder

Conversion disorder may be manifested as a pain syndrome with a significant loss or alteration in physical function that mimics a physical disorder. Conversion symptoms can include paresthesia, numbness, dysphonia, dizziness, seizures, globus hystericus, limb weakness, sexual dysfunction, or pain. If pain or sexual symptoms are the sole complaints, the diagnosis is pain disorder or sexual pain disorder rather than conversion disorder. Pain, numbness, and weakness often form a conversion triad in the pain clinic.

Psychological factors are judged to be etiologic for the pain when a temporal relationship between the symptoms and a psychosocial stressor exists—the person must not be intentionally producing the symptom. A mechanism of primary or secondary gain needs to be evident before the diagnosis can be confirmed. La belle indifférence and histrionic personality traits have little value in making or excluding the diagnosis of conversion. A conversion V on the MMPI denotes the hypochondriacal traits and relative absence of depression that accompany conversion. Evoked responses, an electromyogram [EMG], an electroencephalogram [EEG], MRI and PET scans, and repeated physical examinations are useful for identifying patients with misdiagnoses of hysteria.46

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Psychiatric Emergencies

Steven W. Salyer PA‐C, ... Brooke Ashley Veale, in Essential Emergency Medicine, 2007

Diagnosis

Conversion disorder is diagnosed based on DSM‐IV criteria. The criteria are as follows:

1

At least one symptom, either motor or sensory, suggests a neurological deficit or other medical condition.

2

Symptoms are initiated or exacerbated by stressors, including conflict.

3

Symptoms are not intentionally produced by the patient.

4

After investigation, the symptom cannot be explained by a medical condition, ingestion of a substance, or a culturally based experience.

5

Symptoms cause clinically significant distress or impairment.

6

Symptoms are not limited to pain or sexual dysfunction, do not occur only during somatization disorder, and are not better explained by another psychiatric illness.

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Somatoform Disorders

Ann Kerr Morrison, in Encyclopedia of Psychotherapy, 2002

I.B. Conversion Disorder

Conversion disorder is characterized usually by only one symptom at a time, and this symptom, by definition, mimics neurologic disease. Historically, the type of symptoms has extended beyond those that mimic neurologic disease but neurologic-like symptoms [seizures, paralysis, numbness, deafness, or blindness] have always also been the most prominent. Commonly, the patient has both underlying diseases as well as conversion symptoms. Conversion disorder also is more common in women than in men and is found in both chronic [greater than 6 months] and acute [less than 6 months] forms. Due to the relatively high rate at which individuals either are later diagnosed with neurologic disease or have concurrent neurologic disease, the recommendation to minimize workups to exclude organic causes, generally made for somatoform disorders, is not applicable to conversion disorder. However once this workup is completed, the same principles of supportive, benign management prevails. Most authors advocate a nonconfrontative yet authoritative explanation that recovery is expected over a relatively brief period of time. An explanation that medical tests do not show signs of any serious progressive disease should be provided without confrontation or argument and without suggesting that the problems are “all in your head.” These straightforward prescriptions for recovery allow most individuals to return to normal function. In cases in which suggestions and reassurance alone do not result in recovery, physical rehabilitation and other behavioral techniques such as relaxation and rest may be added. If the stressors presumed to be responsible for the conversion symptom in the first place cannot be ascertained from a standard history, then interviewing techniques such as narcotherapy or hypnosis may be used. The primary purpose of identifying the stressors is to be able to modify them through therapy. Narcotherapy and hypnosis may also be used to enhance the suggestion and expectation of recovery from the conversion symptom. Longer-term psychodynamic therapy is advocated by some for those individuals with chronic or recurrent conversion symptoms. Given that the stressor may well include marital or family issues therapy aimed at these areas may also be necessary.

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What is the underlying cause of conversion disorder?

Conversion disorder is thought to be caused by the body's reaction to a stressful physical or emotional event. Some research has identified potential neurological changes that may be related to symptoms of the disorder.

Who is most likely to develop conversion disorder?

Among adults, women diagnosed with conversion disorder outnumber men by a 2:1 to 10:1 ratio; less educated people and those of lower socioeconomic status are more likely to develop conversion disorder; race by itself does not appear to be a factor.

What is the main feature of conversion disorder?

Conversion disorder is a mental condition in which a person has blindness, paralysis, or other nervous system [neurologic] symptoms that cannot be explained by medical evaluation.

How do you get conversion disorder?

What causes conversion disorder?.
A history of childhood abuse..
Having other mental health conditions, especially depression or anxiety..
A recent stressful or traumatic event..
A recent health condition or event acting as a trigger for conversion disorder..

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