Treatment of Psychogenic Movement Disorder: Psychotropic Medications

Valerie Voon

ABSTRACT

Psychogenic movement disorder (PMD) is a subtype of conversion disorder (CD) characterized by symptoms of tremor, dystonia, myoclonus, and gait disorders.

The treatment literature is sparse with multiple methodological flaws. There are no psychotropic treatment studies specific to PMD. The limited literature on psychotropic treatment studies (dopamine receptor antagonists and antidepressants) in CD and other functional disorders is reviewed, focusing on potential pathophysiologic mechanisms. A hypothesis on the mechanism of action of antidepressants on psychogenic movement symptoms is proposed. General recommendations for psychotropic treatments are suggested and common patient questions raised in the prescribing of psychotropic medications in this population are addressed. Finally, recommendations for treatment studies in PMD are discussed. Our observations suggest that the efficacy of antidepressants on psychogenic movement symptoms can be dissociated from cross-sectional psychiatric diagnoses and measurements of depression or anxiety, consistent with the literature on antidepressants and other functional disorders. The presence of any depressive or anxiety symptoms, regardless of severity, should be actively treated, given the otherwise poor prognosis of the chronic PMD population. There may also be a rationale for a trial of antidepressants in PMD patients without overt comorbid psychiatric diagnoses, although further studies are necessary to support this observation. The preliminary evidence suggests that active intervention with antidepressants can alter the prognosis of patients with chronic PMD.

INTRODUCTION

Psychogenic movement disorder (PMD) is a subtype of conversion disorder (CD) characterized by symptoms of tremor, dystonia, myoclonus, and gait disorders. CD, a broader term focusing on unexplained neurologic symptoms, is classified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) (1), as a somatoform disorder—a type of disorder with unexplained physical symptoms related to underlying psychological factors.

The community point prevalence of CD is reported at 50 per 100,000 with the prevalence over a period of a year
at approximately twice this rate (2). PMD itself is diagnosed in approximately 2% to 3% of patients in subspecialized movement disorder clinics (3). The differences between prognostic outcomes in acute versus chronic CD patients are profound, with recovery rates of 90% versus 45%, respectively (4). Yet, despite the high rates of disability, the financial burden, and the poor prognosis in patients with chronic symptoms, these patients are often underrecognized and undertreated (5).

The literature on the treatment of CD mirrors this clinical reality. The treatment literature is sparse and focuses on behavior therapy, rehabilitation, hypnosis, and psychotherapeutic techniques (6). Existing studies have multiple methodological flaws including small sample sizes, lack of controls, and heterogeneous populations (6). The mix of acute and chronic patients and the presence of different conversion subtypes in study populations confound the results of most studies.

The limited literature on psychotropic treatment studies (dopamine receptor antagonists and antidepressants) will be reviewed, focusing on potential pathophysiologic mechanisms. There are no psychotropic treatment studies specific to PMD; as such, this chapter focuses on psychotropic studies of CD and other specific somatoform disorders. A hypothesis on the mechanism of action of antidepressants on psychogenic movement symptoms will be proposed. General recommendations for psychotropic treatments will be suggested according to published guidelines and literature on the treatment of the comorbid psychiatric disorders. Common patient questions raised in the prescribing of psychotropic medications in this population will also be addressed. Finally, recommendations for treatment studies in PMD and issues in design and implementation will be discussed.

DOPAMINE RECEPTOR ANTAGONISTS

Rampello et al. (7) report on a two-month open-label trial in 18 patients with mixed CD symptoms of paralysis, anesthesia, and pseudoseizures, comparing haloperidol, 6 mg (n = 6), and sulpiride, 800 mg (n = 12). The sulpiride 800 mg group had a statistically significant improvement (p <0.002) in comparison to the haloperidol group on the Middlesex Health Questionnaire (hysterical traits and symptoms). The sulpiride arm was extended a further 2 months at a lower dose of 400 mg with a subsequent loss in the improvement of symptoms. The authors conclude that a hyperdopaminergic state may play a pathophysiologic role in the CD symptoms.

The study can be further reinterpreted in light of recent PET imaging studies by Kapur and Seeman (8). Antipsychotic occupancy of the D2 receptor between 65% and 80% has been demonstrated to correlate with efficacy on the psychotic symptoms of schizophrenia, whereas occupancy of greater than 80% correlates with the emergence of extrapyramidal symptoms (EPS).

Haloperidol is a D2 receptor antagonist with a slow dissociation constant, which at 6 mg occupies greater than 80% of D2 receptors. The results for the haloperidol arm in the study by Rampello et al. may thus be confounded by EPS side effects, which were not reported. Sulpiride, an atypical antipsychotic, is a D2 and D3 receptor antagonist with a rapid dissociation constant. At a dose of 800 mg, sulpiride occupies less than 80% of D2 receptors. In the study by Rampello et al., sulpiride 800 mg was effective on CD symptoms; at 400 mg, the efficacy was lost. In this light, Rampello et al. suggest that antipsychotic agents targeting CD symptoms may be efficacious at doses similar to those required for antipsychotic effects, and that higher doses that may result in EPS symptoms should be avoided. Functional neuroimaging studies focusing on dopaminergic activity may be potentially useful, and the role of the D3 receptor remains to be clarified.

In addition to the small sample size, the open-label nature of the study, and the need for replication of findings, significant design issues limit the generalizability of the Rampello et al. study to the PMD population. The study population was a heterogeneous group of patients experiencing a range of CD symptoms which did not include PMDs. Different pathophysiologic mechanisms may mediate the production of these differing symptoms. The duration of symptoms was also not reported, creating potential confounders given the differences in prognoses between acute and chronic symptoms. Finally, the outcome measure of the study focused only on the CD symptoms, whereas clinically relevant outcome measures should focus more broadly on functional status, quality of life, and psychiatric symptoms in addition to the motor symptoms.

ANTIDEPRESSANTS

The evidence for the efficacy of antidepressants in PMD comes from the literature on overlapping functional disorders demonstrated to respond to antidepressants and our own clinical experience with the PMD population. In a cohort of 24 PMD patients reviewed by Williams et al. (9), 70% of these patients either had been treated or were currently being treated with antidepressants.

Antidepressants and Functional Disorders

A range of functional disorders including functional somatic syndromes, somatization disorder and globus hystericus have been demonstrated to respond to antidepressants. These functional disorders may have overlaps with PMD, thus indirectly supporting the role for antidepressants in PMD.

Functional somatic syndromes, previously recognized in the medical literature as discrete clinical entities, have recently been theorized to have a common underlying pathophysiology, and similar responses to treatment (10, 11). The most common of these medically unexplained syndromes include chronic pain, irritable bowel syndrome, chronic fatigue syndrome, and fibromyalgia. The functional somatic syndromes notably do not include CD, although there may indeed be some degree of pathophysiologic overlap. A metaanalysis of 94 randomized controlled trial (RCT) studies of a variety of functional somatic syndromes demonstrated that these syndromes can respond to antidepressants (12). The response was dissociated from the presence of depression although the exact relationship between these syndromes and depression and anxiety remains to be clarified. The concept of the “affective spectrum disorders” with disorders of similar comorbidities, heritability, and response to treatment has also been proposed. Such a scheme classifies the functional somatic syndromes as a form of an affective disorder (13).

An overlapping relationship may also exist between somatization disorder and CD. In one longitudinal study, 65% of patients initially diagnosed with CD were subsequently rediagnosed with somatization disorder in a 10-year follow-up (14). Similarly, in one cross-sectional study, 20% of patients admitted to a conversion disorder ward had diagnoses of somatization disorder (15).

An 8-week open-label trial of nefazodone in patients with somatization disorder (n = 15) resulted in a 75% improvement in global outcome (Clinical Global Improvement), functioning (Medical Outcome Study Short Form—36), and somatic symptoms (visual analog scale) (16). Notably, neither depression (Hamilton Depression Rating Scale) nor anxiety (Hamilton Anxiety Rating Scale) measures were predictive of outcome, suggesting that the improvement of somatization disorder with antidepressants was independent of comorbid depressive or anxiety symptoms.

Globus hystericus, a CD symptom also known as functional dysphonia, has been reported in case reports to respond to antidepressants and to ECT prompting a suggestion of this symptom to be a manifestation of depression (17).

Antidepressants and Psychogenic Movement Disorder: Clinical Experience

A review of the clinical psychiatric experience of the Movement Disorders Centre at the Toronto Western Hospital (TWH) supports the utility of antidepressants in the treatment of PMD.

From January 2003 to July 2004, 23 patients with diagnoses of PMD underwent psychiatric assessment. Fifteen patients were treated with antidepressants and followed in a nonblinded prospective manner. Eight patients were not followed due to distance (n = 2), follow-up with the patient’s psychiatrist (n = 2), and patient refusal (n = 4). The diagnosis was made by a movement disorders neurologist utilizing Fahn and Williams’s definite and probable criteria for the diagnosis of PMD (9). Patients in whom the diagnosis of factitious symptoms, or malingering, could not be definitively made were included within the cohort. Four patients with suspected neurologic disorders at the time of assessment were not included in the analysis. The symptoms were of chronic duration (longer than 3 months). Treatment visits occurred on average every 2 weeks, ranging from weekly to monthly.

The patients were assessed for psychiatric diagnoses with the Mini International Neuropsychiatric Inventory (MINI) (18), a shortened version of the Structured Clinical Interview for the Diagnosis of DSM-IV disorders. The diagnoses of panic attacks, chronic pain, somatization disorder, hypochondriasis, factitious symptoms, or malingering are not coded in the MINI and were made using DSM-IV criteria. The previous and current use of antidepressants (type, dose, and duration) was reviewed through patient interview, collateral information, and pharmacy record review.

A history of physical and sexual abuse was ascertained using the following questions: Have you ever experienced physical or sexual abuse? Has anyone ever touched you in a way that made you uncomfortable? Were you disciplined excessively as a child?

The severity of depressive symptoms was assessed using the clinician-rated Montgomery-Asberg Depression Rating Scale (MADRS) (19), and the patient-rated Beck Depression Inventory (20). Anxiety symptoms were assessed using the patient-rated Beck Anxiety Inventory (21). The Clinical Global Impression of Severity and Change of overall (nonmotor symptoms and function) and motor symptoms was documented.

The outcomes are summarized here and reported in greater detail elsewhere (22). The characteristics of the group were as follows: 18 women and five men; 16 married; mean age 43.5 (standard deviation 13.5); mean duration illness 73.0 (standard deviation 65.1); and 40% previously on antidepressants. Somatization disorder was identified in three (13%); stressors at onset in 12 (52%); previous models in eight (35%); abuse history in two (9%); and “la belle indifférence” in five (22%). There were no significant differences between the treated and untreated groups.

The group’s MADRS improved following antidepressant treatment (p <0.01) assessed at a mean of 3 months. Supportive psychotherapy was provided concurrently for three and family intervention in one. Ten of the 15 patients treated with antidepressants maintained a PMD diagnosis, with five diagnosed with primary hypochondriasis, somatization disorder, or likely factitious symptoms or malingering. Eight of the ten PMD patients had marked improvements, with one having mild improvement. Seven patients attained complete resolution of motor symptoms. Three of these patients did not have a current depression or
anxiety diagnosis and had low baseline depression and anxiety scores, with one patient having anxiety disorder diagnoses but low measurement scores. The patient who did not improve did not have a current psychiatric diagnosis and had low measurement scores. The other PMD patients had diagnoses of major depression, generalized anxiety, panic disorder, and/or agoraphobia.

The five patients with alternate primary diagnoses did not improve with antidepressant treatment alone.

Antidepressants and Psychogenic Movement Disorders: Discussion of Clinical Experience

The patient population was a group with psychogenic movement symptoms of chronic duration, although the final diagnoses revealed greater diagnostic heterogeneity. The patients with likely factitious symptoms or malingering did not improve; given the inherent difficulties in the diagnosis of these patients, inclusion of these patients represents a potentially significant confounder. Somatization disorder was likely underdiagnosed as extensive collateral or medical records were not obtained.

Nine percent of patients had a history of physical or sexual abuse. The evaluation was limited in that only three screening questions were asked, and that emotional abuse or neglect was not screened. However, the results stand in contrast to that of the literature on pseudoseizures demonstrating a high association with a history of trauma (23,24). Although trauma has been suggested as a potential precursor for the mechanism of dissociation in pseudoseizures (23,25), it appears not to be as relevant in the PMD population. Furthermore, this difference also suggests that the populations may have differing underlying personality traits and prognoses.

Forty percent of patients were either previously or currently on antidepressants, keeping with the known literature (9). However, closer review of the antidepressant history reveals that only 17% of the patients had an adequate trial (an adequate dose for at least 6 weeks’ duration) of antidepressants, and that only 13% of these patients were currently using antidepressants of an adequate dose. Optimal doses were thus likely not achieved during any of these previous trials. Despite the high association of PMD with antidepressant use, the patients were still undertreated.

The range of antidepressants utilized in our treatment trials included the specific serotonin reuptake inhibitors (SSRI), paroxetine and citalopram, and venlafaxine, a dual serotonin and norepinephrine reuptake inhibitor (SNRI). The dose ranges were in the upper range of normal.

Forty percent of patients with clinician-rated and patient-rated depression and anxiety scores of normal severity had marked improvements on antidepressants. Detailed psychiatric assessment of these three patients revealed diagnoses ranging from previous major depression (likely in partial remission), previous posttraumatic stress disorder (likely in partial remission), and generalized anxiety disorder, panic attacks, and agoraphobia. These results suggest that the efficacy of antidepressants on global and motor outcomes may be dissociated from current cross-sectional psychiatric diagnoses and measurements of depression or anxiety.

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