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Distinguishing conversion disorder from neurologic impairment.


Could neurology and psychiatry be two sides of the same coin? The many close links between the two disciplines have long been appreciated. Historically, neurology grew out of neuropsychiatry, a well-established discipline by the 19th century.[1,2] The syndrome long referred to as hysteria has been studied by both; the first formal documentation can be traced back to the time of Hippocrates.[1,10] What was this perplexing condition that caused an individual to lose their sight or the use of a limb without apparent organic justification? Was it mere psychiatric sequelae or could there be a physiologic basis for the symptomatology? Hysteria became the focal point for the great debate between psychogenic and biogenic origins of psychiatric dysfunction. The divergence between neurology and neuropsychiatry took part mainly during the 20th century after the advent of Freud's psychoanalytic theories took root.[1,4,5]

During the past three decades, psychiatry has reclaimed its biological underpinnings with renewed appreciation from other disciplines. Biogenic explanations have been uncovered for many psychiatric illnesses. There is growing speculation that a substantial portion of patients with hysteria, now referred to as conversion disorder (CD), are in fact, organic brain disorders in the early stages where they are most difficult to detect.[2,4,10] Thus, the twain do meet: a syndrome that was originally believed to hail from the body and then later deemed to hail from the mind, has returned to its biological ties. Hysteria or conversion disorder has come full circle. The purpose of this article is to describe the evolution of CD from its initial decree as a hysterical disorder to the more modern schools of thought including its epidemiology, diagnostic guidelines and nursing implications.

History of Conversion Disorder

The symptomatology of hysteria has been described since antiquity. The term "hysteria" derives from the Greek which means "uterus." The ancient Egyptians attributed hysteria to a malpositioned or wandering uterus; hence, all victims of hysteria were presumably female. Galen, in 130 AD, believed hysteria was due to an engorged uterus.[3,11] Hysteria as evidenced by mysteriously paralyzed limbs, inexplicable fainting spells and sudden bouts of blindness was a common occurrence in 18th century Victorian literature. Renowned playwright Arthur Miller penned a drama set during the second world war with the main character suffering from hysteria as a result of the extreme psychological stress produced by wartime.[1,5]

The first formal documented study on hysteria was done by Sydenham in the 1560s who was the first to declare that hysteria can simulate almost all forms of organic disease and deemed that hysteria originated not in the uterus, but the mind. He stated: "Paralysis of one limb or one side of the body may be due to apoplexy (stroke) or may proceed from some violent commotion of the mind."[1]

Two hundred years after Sydenham, hysteria was studied by leading French neurologist Charcot, who dubbed the puzzling syndrome as "neurological nonsense."[1,3,10] He was fascinated by the group of patients who could not be classified into traditional clinical categories and theorized that hysteria was an organic weakness of the nervous system. Sigmund Freud, the famed neurologist best known for his theory of psychoanalysis, became fascinated with Charcot's work on hysteria and went to Paris to study with him and translate his works into English. Freud eventually published Studies in Hysteria, and was responsible for replacing the term hysteria with "conversion" as he believed hysterical symptoms were intrapsychic conflicts that were "converted" into a physical symptom.[1,5] Simply put, CD is a disorder characterized by the presence of one or more neurological symptoms, for example, paralysis, blindness or paresthesias that cannot be explained by a known neurological or medical disorder.[3] When modern psychotherapy was ushered in during the 19th century, it was the patient with conversion disorder who became the focal point for the debate between psychogenic and biogenic theories.

Classification of Conversion Disorder

Medical classification of conversion disorder as we know it today has undergone several revisions in the official statistical labeling reference of the American Psychiatric Association, The Diagnostic and Statistical Manual of Mental Disorders (DSM)[3,14] Historically there has been confusion with usage of the terms hysteria and conversion. Hysteria of itself is a confusing term with its present-day connotation of extreme, uncontrolled emotional distress. In the original DSM in 1952, conversion disorder was known as conversion reaction. In the 1968 revision of DSM-II, conversion reaction was renamed hysterical neurosis: conversion type. In 1980, the term conversion was dropped altogether in DSM-III because some practitioners were errantly using "conversion hysteria" and "hysterical neurosis" interchangeably. Between 1980 and 1994, much debate took place on where to "place" conversion disorder in the upcoming DSM-IV: should it be grouped with the dissociative or the somato-form disorders? In 1994, it was decided to retain conversion disorder with the somatoform disorders due to the perceived advantage of facilitating the critical differential diagnosis, recognizing that patients usually see physicians other than psychiatrists initially before subsequent referral to a neurologist (Table 1).[10]
Table 1. Diagnostic Criteria for Conversion Disorder

A. One or more symptoms or deficits affecting voluntary motor or sensory
function that suggest at neurologic or other general medical condition.

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

C. The symptom or deficit is not intentionally produced or feigned (as in
fictitious disorder or malingering).

D. 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.

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

F. 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.

From: Diagnostic and Statistical Manual of Mental Disorders, 4th ed.
Copyright American Psychiatric Association, Washington, 1994. USed
with permission.

Somatizing patients reside in a strange limbo between psychiatry and medicine. Conversion symptoms are thought to be the result of a collaboration between the mind and nervous system although the exact nature of this relationship is not fully understood; what results is a Tower of Babel that obscures accurate identification and nomenclature.

Clinical Presentation

Conversion disorder is a syndrome where the patient exhibits some type of physiological loss of function without organic explanation. DSM-IV limits conversion symptoms to either voluntary or motor functions which are, of course, neurologic functions.[3,6,10] Thus, the symptoms of CD are uncannily similar to those of neurologic dysfunction. The hallmark of CD, according to DSM-IV, and the most important diagnostic consideration is a pseudoneurological symptom which cannot be fully explained on a physiological basis. Motor symptoms can include paralysis, weakness, aphonia, impaired balance and even urinary retention. Sensory symptoms include paresthesias, blindness, deafness, hallucinations and seizures.[3,4,10,16] Different references cite a variety of symptoms to be the most common; blindness and paralysis seem to be cited the most often by a majority of sources.

Symptoms of CD classically have a rapid onset with the patient exhibiting "la belle indifference," a peculiar state where the patient appears strangely calm and unconcerned in light of the troubling circumstances. The la belle indifference could also be viewed as stoicism or denial in general medical conditions as well, a consideration to always be aware of when undertaking the differential diagnosis. In Freud's day, conversion symptoms were believed to arise from an unconscious psychic conflict so unacceptable to the individual that it could not be confronted and was thus "converted" into a physical deficit, allowing partial expiation of the forbidden conflict. The conversion symptoms were thought to bring both primary gain (blocking their awareness of the conflict) and secondary gain (winning sympathy or attention from others).[5] Theories of symbolism are now thought to be invalid, a holdover from the 19th century, especially since new evidence for a biological origin for CD gains increased attention.[10]


Conversion disorder can occur in both sexes, all age groups, races and ethnic and social backgrounds.[4,5,10,15] Anyone can experience CD, however some generalizations have been found. There is a markedly higher incidence in females, especially in childhood cases. Onset of CD usually begins in late childhood to the early adult years and seldom presents after age 35 years. If onset occurs in middle age or senescence, the probability of underlying neurological disease is greatly enhanced.[10] CD has a long association with enlisted men, especially those who suffer from posttraumatic stress disorder (PTSD). In fact, any extreme emotional duress has been found to be a significant preexisting factor. Persons with emotional disturbances such as histrionic, passive-aggressive or borderline personalities may also have a predisposition to develop CD. Some researchers have noted a correlation between CD and persons of lower educational and psychological sophistication.[10,16]

To further confuse the picture, a person with any medical illness can have CD as well as any person with preexisting neurological disease. In fact, medical illness is frequently cited as a preexisting factor.[10,16] Thus, the patient with epileptic seizures can also suffer with pseudoseizures. CD and physical illness are not mutually exclusive by any means and the possibility for overlap between the two is infinite.

Differential Diagnosis

To determine whether the patient presenting with conversion symptomatology is afflicted with CD versus neurological dysfunction, an exhaustive differential diagnostic effort must be undertaken (Table 2). CD should always be kept as a tentative diagnosis until all else is ruled out. The diagnostic difficulty is not that conversion symptoms suggest neurological disease, but that symptoms of neurological disease are often misdiagnosed as CD; thus the differential diagnosis is very important and can be tricky. In its early stages, multiple sclerosis (MS) may present with paramount psychiatric stigmata and has been misdiagnosed as CD or mere emotional disturbance. Fortunately, the advent of magnetic resonance imaging (MRI) has enabled the detection of demyelinating plaque, thus decreasing the incidence of misdiagnosis.[16] Medical disorders which present with nonspecific transient abnormalities such as systemic lupus erythematosis (SLE) or porphyria, pose the greatest difficulty in differential diagnosis.[3] Occasionally, patients with Guillain-Barre syndrome are misdiagnosed with conversion disorder, especially those with a previous psychiatric history or concurrent psychiatric condition. The early symptoms of weakness, clumsiness or falling, with associated subjective paresthesias can resemble a conversion disorder. Post-encephalitis syndrome, with its residual deficits such as motor weakness, dysphagia and cognitive changes, may also be misdiagnosed as CD. The diagnosis can be made by repeated neurologic examinations to watch for progression of the symptoms, obtaining a thorough medical and psychosocial history from the patient, as well as details about the onset of the symptom(s). The Minnesota Multiphasic Personality Inventory (MMPI), although rarely diagnostic, may also help investigate conversion.[10]

Table 2. Features Useful in Discriminating Between Conversion Disorder and Neurological
Coma 1. Etiology of coma difficult to determine
 2. Eye movements may present as horizontal,
 saccadic jerking movements
 3. Exhibits forceful eyed closing
 4. Oculovestibular testing may produce spontaneous
 vomiting, grimacing or symptoms of discomfort
 5. EEG normal unless there is preexisting disease

Lower 1. May exhibit "la belle indifference"
Extremity 2. Reflexes will be normal, fasiculations absent
 3. Drags affected limb behind body when ambulating
 4. Paralyzed limb may move normally during sleep
 5. May exhibit normal postural trunk adjustments
 to maintain balance
 6. Absence of flexion of upper extremity on
 affected side

Blindness 1. May exhibit "la belle indifference"
 2. Pupillary reaction normal bilaterally
 unless there is preexisting abnormally
 3. Blindness may be selective and does
 not bump into objects or harm
 self; is usually able to feed self

Seizures 1. May have seizure activity only when "audience"
 is present
 2. May scream throughout the entire seizure
 3. Usually not incontinent of urine
 4. Does not bite tongue or injure self
 5. Lack of post-ictal state

 Neurological Impairment

Coma 1. Etiology of coma usually quickly discerned
 2. Eye movements often present as roving nystagmus
 3. Eyelids close (if at all) with a slow, gradual
 4. Oculovestibular testing produces a sustained
 deviation away from tested ear (or absence of
 reaction with brain death)
 5. EEG will usually exhibit abnormally

Lower 1. Usually exhibits signs of distress or fear
Extremity 2. Reflexes may be hyperactive or absent;
Paralysis fasiculations often seen in affected limb
 3. Circumducts weak leg for support with ambulation
 4. Paralyzed limb will not move during sleep
 5. Often not able to adjust posture and may
 slump to one side
 6. Often exhibits flexion of upper extremities
 on affected side

 1. Is often distressed and fearful
 2. Blind eye may have abnormal or absent pupillary
 response or react only with consensual pupil testing
 3. Requires assistance with mobility
 and safety issues

Seizures 1. Seizure activity occurs both in the
 presence of other and when unattended
 2. Screams only at onset of seizure
 3. May have urinary incontinence
 4. May bite tongue and injure self
 5. Post-ictal state usually present

In many cases, clues to assist in ruling out neurological disease may be evident from the onset. From a strictly anatomical standpoint, conversion symptoms fail to respond to known patterns of nerve distribution or function. For example, a paralyzed limb may retain normal reflexes, fasciculations will be absent and electromyelography (EMG) studies may be normal. In cases of CD hemisensory deficit, there may be no overlap at the midline which violates all established anatomical rules. In cases of glove anesthesia (numbness of the hands), the insensitivity of the hands often stops abruptly at the wrists, an obviously too-clear demarcation. Other suspicious diagnostic signs may include paralyzed limbs that move during sleep; paralyzed arms with shoulder muscles that behave normally in general postural adjustments of the trunk which directly contradict what we know about the nervous system. Acknowledging the diagnostic challenge that CD presented, Stoudemire, author of Improving the Formulation of Neurologic Differential Diagnosis, cited Shraberg and D'Souza's case study of 1982 where a young woman in an opiate-induced comatose state was misdiagnosed with CD because she was noted to exhibit forcible eye closure and had periods of intermittent alertness. Subsequent electroencephalographic (EEG) studies of the patient revealed diffuse abnormalities and a computed tomography (CT scan) of the brain was significant for cerebral edema.[16] Hence, the need for accurate diagnosis, including the use of imaging studies, cannot be overemphasized.

Several clues to help differentiate CD from neurological dysfunction are outlined in Merritt's Textbook of Neurology.[15] To differentiate hysterical paralysis from organic paralysis, Merritt's suggests testing deep tendon reflexes (DTR) which will be absent in the latter and present in the former. In cases of paralyzed lower limbs, the absence of Hoover's sign (the downward pressure of the opposite heel when attempting to lift the affected limb off of the bed) can be noted. With hysterical paralysis the affected limbs offer no resistance to passive movement yet demonstrate normal tone and reflexes.[15]

To differentiate hysterical gait disorders from neurological ataxia, Merritt's suggests that the patient with CD will drag the paralyzed limb behind the body, not circumvented nor used for support as seen in the patient with an organic lesion. Also, the arm on the affected side will not develop the flexed posture commonly seen in organic disease. Hyperactive reflexes and the Babinski reflex with conversion hemiplegia will be absent.[15]

To rule out organic versus hysterical coma, EEG is the most helpful tool. In hysterical coma, the EEG will be normal unless the patient has preexisting organic disease or is under pharmacological influence. Eye and eyelid clues are probably the most helpful. In hysterical coma, the eyes will often remain forcibly closed and when opened for examination, will close abruptly versus the slow smooth lid descent seen in organic coma. Nystagmus, in conversion coma, will be absent; instead the eyes may move back and forth in saccadic jerks. Oculovestibular testing will reveal nystagmus and possible spontaneous vomiting in the conversion coma versus a sustained deviation away from the tested side is seen in true coma.[15]

Treatment of CD

While the focus of this text does not concentrate on the treatment of CD, it will be mentioned briefly. Certain factors in the patient with CD are thought to be prognosticators for recovery. Positive prognosticators include the absence of preexisting psychological or medical illness, including PTSD. A rapid onset of symptoms is also thought to be a positive prognosticator whereas the patient with longstanding psychiatric history, repeated episodes of conversion or those who stand to secondarily gain, are thought to be poor prognosticators.[3,6,10,16]

Present treatment no longer revolves around psychiatric intervention which has usually been met with resistance from the conversion patient who finds it hard to believe that his symptoms are "imaginary" or "mental.." Most sources feel that symptomatology can decrease with suggestion but do stress that the health care worker must "allow" the patient to have their symptom(s) while encouraging them to ventilate their feelings and concerns since informing the patient that their symptoms are imaginary often worsens the symptom.[10,14] The rehabilitation for conversion paralysis is nonconfrontational; the patient is not made aware that the disability is thought to be psychological. Confronting the patient with the information that the cause of the symptom is psychological is rarely helpful and may adversely affect the patient's relationship with the therapeutic team. The patient's symptoms are treated as if the weakness were organic and no attempt is made to treat the patient by using traditional psychotherapeutic techniques.[14]

During the acute phase of CD, parenteral amobarbital or lorazepam may be helpful especially if a traumatic event was recently experienced. Psychopharmacological treatment may be necessary, especially if there is a coexisting psychiatric disorder. Medications must be monitored because many patients with psychiatric disturbances tend to use medications erratically or unreliably. In patients with coexisting psychiatric disease, available data indicate that pharmacologic treatment is inconsistently effective.[3,6,10] According to most sources, resolution of the conversion symptom is usually spontaneous, often occurring in less than a month from onset, disappearing as quickly as it appeared.[3,5,6] Unless secondary complications occur as a result of the conversion symptom, such as muscle contractures or skin breakdown, the patient usually recovers to his or her baseline status.

The discussion of prognosticators and treatment for conversion disorder may soon be a moot point for some cases The following section delves into the possibility that what is now believed to be CD may actually be an early indication of neurological disease.

New Theories on Conversion Disorder

Perhaps Sydenham was not completely errant in thinking "hysteria was the result of a nervous commotion." New research suggests that conversion disorder may actually be an early disruption in the functioning of the nervous system.[3,10,16] Some studies suggest that a substantial portion of CD patients are in fact, exhibiting signs of organic brain disorders in the early stages when they are most difficult to detect.[4] Two of the more prominent theories to explain the biological basis for conversion disorder involve the possibility of a disturbance in arousal mechanism or cerebral asymmetry, the theory that one of the cerebral hemispheres is larger in size and more developed than the other, causing an unequal awareness and interaction with each other.[8,14]

The theory of disturbed CNS arousal suggests that patients diagnosed with CD have a disturbance in cortical arousal which sets off negative feedback loops between the cerebral cortex and brainstem reticular formation. These increased levels of corticofugal output, where messages are directed away from the cerebral cortex, may inhibit afferent sensorimotor impulses leading to a diminished awareness of bodily sensation and could account for the manifested sensory deficits and la belle indifference.[3]

The theory of cerebral asymmetry in CD has gained more favor. In this theory, the pseudoneurological symptom has been conceptualized to arise from stressful environmental events acting on the affective right hemisphere of the cerebral cortex in predisposed individuals. Neuropsychiatric testing in these individuals has shown to reveal subtle cerebral impairments in verbal communication, memory, affect, incongruence and suggestibility.[3] Could cerebral asymmetry play a role in the way somatosensory stimuli is processed and interpreted? Could dominant and nondominant hemispheres also play a role in CD? In the theory of hemispheric asymmetry, the predominant role of the right hemisphere is emphasized. This is supported by the fact that when unilateral, conversion symptoms are more frequently manifested on the left side of the body versus the right side.[2,3,10,16]

Could the right hemisphere be disorganized in certain predisposed individuals? Could portions of the right hemisphere responsible for maintaining the somesthetic body image "malfunction?" Studies in Sweden have supported the hypothesis of right hemispheric dysfunction evidenced by laterality of movements during sleep and waking. These studies suggest that there is some type of cognitive inversion that may signal increased activation of right hemisphere motor programs with spatial versus sequential coding of movement information.[10,12]

Many practitioners go as far as to declare the diagnosis of hysteria to be "myth" due to the findings of various follow up studies with patients diagnosed as CD who later develop organic disease that can account for the original conversion symptom. A study by Whitlock concluded that 63% of conversion patients later developed some form of organic brain disease.[2,17] Another 3-11 year follow-up study revealed 13-60% of all hospitalized patients with conversion disorder later developed an organic illness that could account for the original symptom.[2,17] In 1984, Ford and Folks noted that 20% of 50 documented cases of conversion disorder had a co-existing neurological disease.[2,8]

Due to findings such as these, many clinicians now feel that conversion symptoms that present as paresthesias on the left side of the body should be assumed to be neuropathologic despite paresthesias which may not correlate with normal neuroanatomical boundaries; these may be underlying neurophysiological changes in process. Aminoff feels that a too-hasty pronouncement of hysteria/conversion disorder is diagnostically unstable and a fertile source of clinical error as it can mask underlying medical and neurologic conditions; the conversion disorder label obscures true organic pathologies.[2]

Nursing Implications

Nursing measures for the patient with conversion disorder center on both psychological and physiological needs. The nurse must be aware that the diagnosis of CD should remain initially tentative until the differential diagnosis is completed, heeding the adage that "the diagnostic difficulty is not that conversion disorder mimics neurologic dysfunction but that neurological dysfunction mimics conversion disorder." The neuroscience nurse must be aware of the newer theories that suggest an organic basis for CD and thus, to treat all conversion symptoms as "real" (organic) in nature; to remember that conversion symptoms are genuinely felt and are not consciously willed. When the possibility of CD is raised, a nurse's negative response to the patient can be harmful especially if the patient does not seem to respond to treatment. The nurse may unconsciously allow the diagnosis of CD to skew perceptions during the assessment and evaluation phases; it may affect sensitivity to data and after analysis of findings, dismiss some observations as simply hysterical responses.[9]

The patient with CD must be "allowed" to have the symptom. Psychiatric consultation may be ordered but in any event, the nurse must engage in nonthreatening, nonconfrontational therapeutic dialogue. Adequate teaching and preparation for the various tests associated with the differential diagnosis must be done throughout this phase of hospitalization; encourage ventilation of feelings and concerns while providing reassurance.[14]

As for the physiological needs of the patient with CD, mobility and skin care usually need to be addressed first. With prolonged loss of motor or sensory function as in weakness or paralysis, secondary complications can occur. Contractures or disuse atrophy can lead to irretrievable loss of function if prompt interventions are not undertaken. To diminish the chances of this occurring, encourage the patient's independence with activities of daily living (ADL) to not only promote mobility but to enhance self esteem as well. If there is significant impairment with gait or balance, consultations with the physical or occupational therapy departments may be necessary. The safety needs of the patient must be addressed to prevent untoward injury. Encourage the patient's diversion from the symptom(s) and personal circumstances through therapeutic recreation. Consultation with a psychiatric nurse liaison may also be helpful. Assist the patient to develop a sense of accomplishment by establishing goals early on along with realistic measures to meet these goals.


The human psyche is a complex entity. The perplexing machinations of the mind are capable of simulating a multiplicity of organic diseases, thus confusing many healthcare practitioners. Controversy exists as to whether conversion disorder is an accurate diagnosis for some patients, especially those with symptoms involving the left side of the body. Some studies suggest that early organic brain disease is the underlying culprit responsible for the pseudoneurological conversion symptom. This text provides an overview for neuroscience nurses to a confusing malady noted since antiquity, especially important in the light of the hypotheses that suggest organic causation for the disorder previously believed to be solely psychiatric in origin.


[1.] Alexander FG, Selesnick ST: Pages 94-96, 170-173 in: The History of Psychiatry. Harper & Row, 1966.

[2.] Aminoff MJ: Pages 422-425 in: Neurology and General Medicine. Churchill Livingstone, 1989.

[3.] Barsky A: Somatoform Disorders. Pages 1251-1258 in: Kaplan HI, Sadock BJ (editors). Comprehensive Textbook Of Psychiatry, 6th ed. Williams & Wilkins, 1995.

[4.] Bootzin RR, Acocella JR: Pages 148-151 in: Abnormal Psychology: Current Perspectives, 3rd ed. Random House, 1980.

[5.] Cameron N: Personality Development and Psychopathology. Houghton-Mifflin, 1963.

[6.] Cassem NH: Handbook of General Hospital Psychiatry, 3rd ed. Mosby Year Book, 1991.

[7.] Diagnostic and Statistical Manual of Mental Disorders, 4th ed. American Psychiatric Association, 1994.

[8.] Ford CV, Folks, DG: Conversion disorders: An overview. Psychosomatics 1985; 26:371-383.

[9.] Haber J, Hoskins P, Leach A: Comprehensive Psychiatric Nursing, 3rd ed. McGraw-Hill, 1987.

[10.] Hales RE, Yudofsky SC, Talbott JA: Pages 591-603 in: Textbook of Psychiatry, 2nd ed. American Psychiatric Press, 1994.

[11.] Kent DA, Tomasson K, Coryell W: Course and outcome of conversion and somatization disorders: A four-year follow-up. Psychosomatics 1995; 36(2):138-144.

[12.] Lauerma H: Nocturnal limb movements in conversion paralysis. J New Ment Dis 1993; 181(11):707-709.

[13.] Nicolson R, Feinstein A: Conversion dissociation and multiple sclerosis. J Nerv Ment Dis 1994; 182(11):668-669.

[14.] Roberts RA: A closer look at conversion paralysis. Rehab Nurs 1994, 19(4):241-243.

[15.] Rowland LP: Pages 25-26, 56-57, 437 in: Merritt's Textbook of Neurology. Lea & Febiger, 1989.

[16.] Stoudemire A, Fogel B: Psychiatric Care of the Medical Patient. Oxford University Press, 1993.

[17.] Whitlock FA: Pages 185-209 in: Hysteria. John Wiley & Sons, Inc., 1982
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Author:Parobek, Virginia M.
Publication:Journal of Neuroscience Nursing
Date:Apr 1, 1997
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