15 APPROACH TO CONVERSION DISORDER Table 15.1 Disorder Common Symptoms Diagnostic Test Transient ischemic attack Temporary loss of motor or sensory function, intermittent limb shaking, clonic jerking, tonic posturing Neuroimaging Cerebral angiography Carotid ultrasound Coagulopathy screening Frontal lobe epilepsy Bilateral motor activity with preservation of consciousness, lack of postictal confusion; may have “soft signs” of pelvic thrusting, crying Video EEG Addition of sphenoidal electrodes SPECT Hypokalemic periodic paralysis (thyrotoxic periodic paralysis is subtype) Muscle paralysis, acute hypokalemia, hyperthyroidism, commonly precipitated by heavy carbohydrate loads or after exercise Potassium levels Thyroid function tests Syncope (cardiac arrhythmia, long QT syndrome, vasovagal response, orthostatic hypotension) Convulsions, myoclonus, loss of consciousness, auditory and visual hallucinations Electrocardiography Arrhythmia monitoring Tilt-table testing Autoimmune encephalitis (ie, limbic encephalitis, paraneoplastic encephalitis) Dyskinesias, dystonic posturing, seizures, choreoathetoid movements CSF/serum antibody testing Rule out neoplasm Creutzfeldt-Jakob disease Ataxia, neglect, apraxia, aphasia, hemiparesis, myoclonus, mutism, cognitive decline EEG MRI Brain biopsy CSF 14-3-3 protein Abbreviations: CSF, cerebrospinal fluid; EEG, electroencephalography; SPECT, single photon emission computed tomography. Source: Adapted from Refs. 13–16. Table 15.2 Validated Not Validated Hoover sign Nonpyramidal weakness Abductor sign Absent pronator drift Abductor finger sign Arm drop test Spinal injury test Barré test Collapsing/give-away weakness Wrong-way tongue deviation Co-contraction Platysma sign Motor inconsistency Babinski trunk–thigh test Midline splitting Supine catch sign Splitting of vibration Sternocleidomastoid test Nonanatomical sensory loss Bowlus-Currier test Inconsistency/changing pattern of sensory loss Yes–no test Systematic failure Gait fluctuation Dragging, monoplegic gait Excessive slowness Chair test Psychogenic Romberg test Walking on ice Noneconomic posture Sudden knee buckling Staggering to obtain support from opposite walls Exaggerated swaying without falling Astasia–abasia Opposite of astasia–abasia Sudden side steps Cross legs Expressive behavior Source: Adapted from Ref. 17: Daum C, Hubschmid M, Aybek S. The value of ‘positive’ clinical signs for weakness, sensory and gait disorders in conversion disorder: a systematic and narrative review. Neurol Neurosurg Psychiatry. 2014; 85(2):180–190.
APPROACH TO THE PATIENT WITH CONVERSION DISORDER
Patients with medically unexplained symptoms account for a significant proportion of neurological consultations.1
Such symptoms may include abnormal movements, seizure-like episodes, paralysis, sensory loss, and blindness. Unfortunately, there is no common language to describe such phenomena, with many different terms used by neurologists and psychiatrists alike.2 The term conversion disorder (CD), or functional neurological symptom disorder, is a unifying diagnosis that can be used to describe neurologically unexplained symptoms.
Terms used to describe neurologically unexplained symptoms
Psychogenic
Functional
Stress-induced
Hysterical
EPIDEMIOLOGY OF CONVERSION DISORDER
Incidence: CD occurs in 4 to 12 per 100,000 population per year3 and may be seen in both children and adults.
In children, the prevalence is equal among boys and girls; however, in adults, CD is seen 2 to 5 times more often in women than in men.4
Frequent psychiatric comorbidities include depression, anxiety disorders, post-traumatic stress disorder (PTSD), dissociative disorders, and borderline personality disorder.5
HISTORICAL PERSPECTIVE
Jean-Martin Charcot, a French neurologist, was the first to use the term functional to describe symptoms that did not have an organic basis.
Sigmund Freud was the first to use the term conversion to describe a mechanism whereby unwanted experiences, such as trauma, are repressed in the subconscious but then become “converted” to physical symptoms.
In 1980, the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III), required that for the diagnosis of CD psychological factors must be associated with the etiology of symptoms, evidenced by the following: there exists a temporal relationship with an environmental stimulus related to a psychological conflict, the symptom enables the patient to avoid a noxious stimulus, or the symptom allows the patient to get support from the environment that might otherwise not be forthcoming.6
In 2000, the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), retained the criterion of “associated psychological factors” but removed specifiers.7
Presently, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), does not note a requirement for any association with psychological factors.8
NEUROBIOPSYCHOSOCIAL MODEL
Neuroimaging studies in patients with CD suggest the following:
Increased limbic activity in response to stressful/traumatic stimuli
Disruption of prefrontal circuits, including premotor areas
Greater connectivity between the amygdala and motor preparatory areas during states of arousal, suggesting a possible mechanism of abnormal emotional processing interfering with normal motor planning9
Limited studies with voxel-based morphometry (VBM) demonstrated increased thickness of the premotor cortex in patients with hemiparetic CD compared with normal controls,10 whereas cortical thinning in the motor and premotor regions was observed in patients with nonepileptic seizures compared with normal controls.11
DIAGNOSIS
It remains well accepted that psychological factors play a role in CD; however, such factors may not always be identified or apparent at the time of the initial evaluation or even well into the course of treatment.
To reflect this, in 2013 DSM-5 removed the criterion for the presence of known psychological factors and provided the alternative name of functional neurological symptom disorder.8
The diagnosis of CD may be challenging, depending on the type of presenting symptom. Whereas nonepileptic seizures may be easily diagnosed by the absence of video electroencephalographic (EEG) findings, the diagnosis of conversion in a patient presenting with a movement disorder (eg, tremor, myoclonus, dystonia) is more difficult.
When a patient presents with symptoms that do not fit with a known neurological disorder, it is imperative that all possible medical conditions be ruled out before CD is diagnosed. This may involve collaboration with the patient’s primary care physician, internist, or specialist.
Historical publications have suggested that the incidence of the eventual diagnosis of an actual medical or neurological condition in a patient being treated for CD is quite high, between 30% and 60%.12 The medical conditions often misdiagnosed as CD are listed in Table 15.1.
More recent studies, however, have demonstrated a rate of CD misdiagnosis of only 3% to 7%. It is therefore important that physicians be thorough yet do not become preoccupied with the fear of misdiagnosing CD, which risks delay of treatment.13
To complicate the matter, 5% to 15% of patients with CD will have a comorbid organic neurological disorder.1
The Use of “Positive Clinical Signs” in the Diagnosis of Conversion Disorder
Historically, neurologists have used a set of “positive signs” specific to functional disorders to identify patients with CD; however, very few of these commonly used signs have been validated.12 Results of a recent systematic review of the validity of “positive signs” are shown in Table 15.2.
Historical Approach to the Diagnosis of Psychogenic Movement Disorders
In 1988, Fahn and Williams developed a set of diagnostic criteria for psychogenic movement disorders (PMDs) to be used in patients with equivocal or uncertain diagnoses. These criteria have been widely applied by neurologists and movement disorder specialists, although they have not been validated.18,19
Medical Conditions Often Misdiagnosed as Conversion Disorder
In 2006, Shill and Gerber20 reorganized the criteria of Fahn and Williams and proposed additional criteria based on disease modeling; however, these too have significant limitations, including the suggestion that a PMD can be diagnosed without a consideration of neurological phenomenology (Table 15.3).19,20
Validated and Nonvalidated “Positive” Clinical Signs in Conversion Disorder
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Approach to Conversion Disorder
