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Conversion Disorders Clinical Presentation

  • Author: Scott A Marshall, MD; Chief Editor: David Bienenfeld, MD  more...
 
Updated: Nov 09, 2015
 

History

Conversion symptoms are those that suggest neurologic disease, but no explanation of these symptoms is found following physical examination and diagnostic testing. The presentation is acute in onset and may follow a psychologically conflictual situation. Conversion symptoms are seen in various clinical settings and include conversion disorder; somatization disorder; affective disorders; antisocial personality disorder; alcohol or drug abuse; or organic, neurologic, or medical illnesses.

In some situations, an immediate precipitating source of stress may be disclosed, such as a loss of employment or divorce. The patient may have a discordant home life. A history of sexual or physical abuse is not uncommon and can be seen in as many as one third to one half of patients with dissociative disorder, respectively. Therefore, a complete and comprehensive psychosocial history is of vital importance. Patients with conversion disorder are said to have a relative lack of concern about the nature or implications of the symptoms; Freud described this as la belle indifference. This is not a helpful diagnostic characteristic because it is not specific or sensitive for conversion and should have no isolated role in separating organic from psychiatric disease.[12] Systematic reviews on this subject found the frequency of this finding at 21% among those with a conversion disorder and 29% among those with organic disease.[19]

Diagnostic criteria (DSM-5)

Diagnostic criteria for conversion disorder as per the DSM-5 are as follows:[1]

  • One or more symptoms of altered voluntary motor or sensory function.
  • Physical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions.
  • The symptom or deficit is not better explained by another medical or mental disorder.
  • The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.

Possibilities to consider when a patient presents with symptoms of probable psychogenic origin include the following:

  • Symptoms are exclusively a function of somatoform disorder, factitious disorder, or malingering.
  • Symptoms are secondary to other psychiatric etiologies such as depressive disorder or anxiety disorders.
  • Symptoms coexist with a physical disorder.
  • The symptoms are an unusual manifestation of a physical disorder.

The DSM-5 lists strict criteria for diagnosing conversion disorder. However, 2 of the listed conditions may be determined only by a person with expertise in neurologic conditions, neuroanatomy, and the recognized clinical patterns of disease in correlation with the lesion location. This is usually a neurologist. The psychiatric assessment can differentiate conversion disorder from other somatoform disorders, factitious disorder, and malingering and can elucidate the psychodynamics that are very important in treatment. The neurologist must recognize the nonorganic process and rule out imitators while avoiding potentially dangerous diagnostic or therapeutic interventions. The neurologist and psychiatrist are thus prepared to diagnose conversion disorder best when working in concert.[12]

Patients with conversion disorder may present with hemiparesis, paraparesis, monoparesis, alteration of consciousness, visual loss, seizure like activity, pseudocoma, abnormal gait disturbance, aphonia or dysphonia, lack of coordination, or a bizarre movement disorder. Patients who are more medically naïve typically have more implausible presenting symptoms and vice versa. The presenting symptoms depend on the cultural milieu, the degree of medical sophistication, and the underlying psychiatric issue.

Patients with conversion disorder may deny any emotional problem and quite commonly resist consultation with psychiatry. Therefore, responsibility lies with other medical personnel to perform the initial management prior to conveying the diagnosis.

Next

Physical

A full physical examination with attention to the mental status and neurologic examination should be performed. Certain principles are used during the neurologic examination to distinguish psychogenic deficits from neurologic ones. The pattern of deficits usually does not conform to known anatomic pathways. For example, patients who present with monoparesis do not have weakness in a corticospinal tract or neuropathic or myopathic distribution. In addition, no changes may be seen in reflexes or tone that typically would be expected.

The physician should contrast formal examination from functional observations. Patients who do not move a limb when asked on examination may be observed to use that limb inadvertently while dressing or talking. Importantly, one should differentiate inability to move a limb on command from spontaneous movements. This may imply a receptive aphasia rather than a conversion disorder. Patients who do not dorsiflex the foot while seated may walk on the heels when asked to do so. Another example might be a patient who cannot stand on one leg who may be observed to do so while putting on pants.

Observations when the patient is unaware of being examined are helpful. Patients with psychogenic movements may have no such movements when observed in the waiting room. Multiple examinations by one or more practitioners may disclose variable results. However, caution is necessary when applying these rules. No single feature is absolute. The knowledge pertaining to neuroanatomy and the clinical deficits that arise from certain abnormalities is not completely known, thus resulting in limitations of the neurologic examination. In addition, patients can embellish on organic deficits, thereby making clinical assessment difficult and further introduction of variability between examiners.

Of concern, older data, most notably by Eliot Slater in 1965, published rates of 33% for patients with conversion disorder ultimately developing a physical illness that may account for their symptoms.[20] Patients with conversion disorder not uncommonly have a comorbid medical or neurologic illness. An example is the patient who exhibits both epileptic seizures and psychogenic nonepileptic seizures, a clinical situation accounting for up to 10-20% of referrals to epilepsy referral centers.[21, 22] Although current rates of misdiagnosis are low, this remains a valid concern among practitioners.[11]

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

Mental status examination

See the list below:

  • Appearance - Normal dress; appropriate eye contact; normal hygiene
  • Gait/station - Normal or ataxia, some type of psychogenic paresis, pseudochorea, astasia-abasia pattern of gait (ie, inability to walk due to weakness or balance deficits but can hop on 1 leg back and forth to the bathroom)
  • Attitude - Appropriate
  • Behavior - Could be preoccupied with symptoms or indifferent
  • Speech - May be normal or have evidence of the conversion disorder such as aphonia, dysphonia, verbal tics, stuttering
  • Attention/concentration - May be decreased due to preoccupation with symptoms or may be normal
  • Memory - Normal or impaired [23]
  • Orientation - Likely oriented to person, place, and time
  • Mood - Perhaps anxious about condition; perhaps indifferent
  • Affect - May be restricted; labile or mood incongruent
  • Thought process - Could also vary from concrete and perseverative to normal; obsessive component also possible
  • Thought content - Not likely suicidal or homicidal unless comorbid conditions present
  • Hallucinations - Possible hallucinations present (The patient usually retains some insight that these are not real. The conversion hallucinations often involve multiple modalities [verbal, tactile, visual]. Compared with hallucinations in psychosis that usually involve a single modality, these hallucinations are often psychologically significant [ie, "I heard my ex-boyfriend's voice telling me that he had made a big mistake."]. Often they are imaginative and childish in nature and often presented as a story. [15] Please note that if the hallucinations are better accounted for by post traumatic stress disorder or dissociative identity disorder, a diagnosis of conversion disorder should not be made.) [15]
  • Insight - Limited to poor
  • Judgment - Varies from case to case

Other specific details to help diagnose 3 different common conversion symptoms include the following:

  • Psychogenic hemiparesis
    • Unilateral weakness or hemiparesis is one manner in which the patient with conversion disorder may present.
      • Classic hemiparesis represents a deficit of the corticospinal tract. In an acute lesion of the corticospinal tract, a patient may demonstrate flaccidity of the weak limbs, which is associated with decreased reflexes. In more chronic lesions, the patient may develop spasticity of the affected limbs, hyperreflexia, and an extensor toe sign (positive Babinski). The patient with hemiparesis from a corticospinal tract lesion may demonstrate weakness of the extensor muscles to a greater extent than the flexor muscles and may show greater weakness distally than proximally.
      • None of these findings would likely be seen in the patient with conversion disorder. In psychogenic hemiparesis, the muscle contractions are poorly sustained and may weaken abruptly as the patient resists the force exerted by the examiner. This is felt clinically as a "give-way" or ratchet-like weakness, unlike the fluid weakness throughout the range of motion usually felt by the examiner in an upper or lower motor neuron lesion. Note that many of these type of signs have been shown to not be specific for conversion, including give-way weakness.[24]
    • The Hoover sign may also be elicited. When a patient in the recumbent position flexes the thigh and lifts the leg, the downward movement of the contralateral leg is automatic. The examiner places a hand beneath the heel and asks the patient to raise the paretic leg. In feigned weakness, no appreciable downward movement is evident. In addition, when the patient is asked to raise the normal leg, the downward movement is appreciated from the paretic leg. This is felt to be a reasonably reliable indication of a possible conversion disorder.[12]
    • Another helpful tool is examining the sternocleidomastoid muscle. Normal contraction of this muscle results in the face rotating in the opposite direction. Therefore, the patient with psychogenic weakness may display weakness of the contralateral sternocleidomastoid (ie, weakness in turning the face towards the hemiparetic side).
    • Recognizing the patient with psychogenic hemiparesis includes observing the following:
      • No side-to-side changes in reflexes or tone
      • Give-way quality of weakness[24]
      • Extensor and flexor muscles equally weak
      • Contralateral sternocleidomastoid weakness
      • Positive Hoover sign[25]
      • Difference between formal examination and general observations (ie inconsistency)[12]
  • Psychogenic nonepileptic seizures
    • Distinguishing between a psychogenic nonepileptic seizure, or pseudoseizure, and an epileptic seizure is challenging. The manifestations of each are diverse, and the clinical diagnosis rests on historical information from witnesses with varying observational skills. Simultaneous video electroencephalogram (EEG) monitoring has significantly improved the accuracy of diagnosis, but this technique is expensive and not routinely available. Psychogenic seizures may constitute up to 20% of all patients in an epilepsy referral center.[26] Please refer to the article on Psychogenic Seizures in the eMedicine Neurology section for more details.
    • Classic clues that may be suggestive of a psychogenic nonepileptic seizure include the following:
      • Ineffectiveness of multiple antiepileptic drugs
      • Induced by stress or emotional upset
      • Lack of physical injury
      • Lack of headache or myalgias following convulsions
      • Lack of incontinence
      • Biting the tip of the tongue as opposed to the side or the lip
      • History of sexual or physical abuse[17]
      • Signs or symptoms suggestive of another conversion
      • Memory of a generalized ictal event
    • Ictal characteristics that suggest nonepileptic seizure include the following:[12]
      • Gradual onset of ictus
      • Prolonged duration (>4 min)
      • Atypical or excessive motor activity such as thrashing, rolling from one side to the other, pelvic thrusting, or arrhythmic (out-of-phase) jerking such as alternating side flexion and extension of the arms
      • Waxing and waning amplitude
      • Intelligible speech
      • Bilateral motor activity with preserved consciousness
      • Clinical features that change from one spell to the next (ie, nonstereotyped)
      • Lack of postictal confusion
      • Postictal crying or cursing
      • Directed violent acts
      • Eyes closed during the ictus[27]
      • Resistance to eye opening
      • Purposeful resistance to passive movements
  • Psychogenic movement disorders
    • Conversion disorder can imitate the entire spectrum of movement disorders and include tremor, chorea, myoclonus, dystonia, tics, parkinsonism, knee buckling, and a host of other bizarre gait disturbances. A commonly used term for a type of this last phenomenon is an astasia-abasia gait pattern, in which the patient makes wild movements of the trunk and arms during a gait evaluation but does not fall or err from a stressed gait such as a tandem or toe gait.[28]
    • Variations of astasia-abasia have been described. Psychogenic camptocormia is a conversion reaction manifest by patients ambulating with a severe forward flexion posture at the waist. This was originally described with military personnel during the early 20th century.[6] A recumbent-type gait has also been reported in which a patient was found to walk normally with her eyes open; however, when her eyes were closed, she would continue to walk while falling backward into the arms of examiners. Interestingly, the patient would continue to exhibit a steppage gait as an attempt at walking. When her eyes were opened, she would appear bewildered to be lying on the floor.[5]
    • The clenched fist syndrome has been described as a classic conversion reaction. This is manifested by patients who exhibit a tightly closed fist posture with resistance to all distal hand movement due to severe pain. A finding to alert the clinician to this is paradoxical stiffness, in which a change in finger flexion with motion of the wrist does not occur. Clenched fist syndrome is seen after minor trauma with associated pain and swelling.[7]
    • Clinical symptoms or signs that may help distinguish psychogenic movements from organic ones include the following:
      • Abrupt onset of symptoms
      • Character of movements atypical of recognized patterns and have inconsistent amplitude, frequency, and distribution
      • Characteristics of movements change over time
      • Entrainment of the tremor to the rate requested by the examiner
      • Spontaneous remissions
      • Movements disappear with distractions
      • Movements increase with attention
      • Response to placebo, psychotherapy, or suggestion
      • Paroxysmal symptoms
      • Nonobjective weakness or sensory changes also present
      • Obvious secondary gain (eg, litigation, health insurance claim, military service)
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Causes

Neuroimaging studies of conversion disorders indicate hypofunction of the dominant hemisphere and a consequent overactivity in the non-dominant side. Other neuroanatomic findings have been seen with conversion disorder. Marshall et al reported changes in regional cerebral blood flow (rCBF) in a female patient with a left leg paralysis and intact sensory modalities for which no anatomic cause of her weakness could be found. Attempting to move her paralyzed leg did not show activation of contra lateral motor cortex, but rather contra lateral orbit-frontal and anterior cingulated cortex were activated. This implied an anatomic inhibition of primary motor cortex in one case of hysterical paralysis.[29]

Others have shown via rCBF analysis that the left temporal region has decreased rCBF. rCBF studies have also implicated the thalamus, putamen, and caudate on the side opposite the motor and sensory conversion symptoms. Published reports show improved rCBF with resolution of the conversion symptoms.[9]

Functional MRI studies have implicated the orbitofrontal cortex and the anterior cingulate gyrus as active in mediating an inhibitory effect on movement and sensation in patients with psychogenic motor and sensory complaints.[30]

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

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

Learning theorists believe that such symptoms develop from classical conditioning that occurs during childhood and that these learned behaviors arise again as coping mechanisms when the person is subjected to overwhelming stress later in life.

Such symptoms also can be viewed as a form of physical communication of an emotionally charged idea or feeling when one is unable to verbalize the conflict because of personal or social taboos.

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Contributor Information and Disclosures
Author

Scott A Marshall, MD Major, Medical Corps, US Army; Assistant Professor of Neurology, Uniformed Services University of the Health Sciences; Staff Neurologist, Staff Intensivist, Brooke Army Medical Center

Scott A Marshall, MD is a member of the following medical societies: American Academy of Neurology, Wilderness Medical Society, Neurocritical Care Society

Disclosure: Nothing to disclose.

Coauthor(s)

Mark E Landau, MD Associate Professor of Neurology, Uniformed Services University of the Health Sciences; Consulting Staff, Assistant Chief, Section of Neurophysiology, Department of Neurology, Walter Reed Army Medical Center

Mark E Landau, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Craig G Carroll, DO Staff Neurologist, Head of Clinical Neurophysiology Section, Naval Medical Center Portsmouth

Craig G Carroll, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Bryan Schwieters, MD Consulting Physician, Schwieters Medical PLLC and VirtualPsych, LLC

Bryan Schwieters, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association

Disclosure: Received consulting fee from pfizer for speaking and teaching.

Alexis Llewellyn, PhD Licensed Psychologist and Owner, Katy Center for Psychology and Counseling Services

Alexis Llewellyn, PhD is a member of the following medical societies: American Psychological Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

David Bienenfeld, MD Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

Additional Contributors

Barry I Liskow, MD Professor of Psychiatry, Vice Chairman, Psychiatry Department, Director, Psychiatric Outpatient Clinic, The University of Kansas Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

The opinions expressed in this work belong solely to those of the authors. They should not be interpreted as necessarily representative or endorsed by the Uniformed Services University, The United States Army, The Department of Defense, or any other agency of the federal government.

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