Psychogenic Movement Disorders Amitabh Gupta and Anthony E

Psychogenic movement disorders Amitabh Gupta and Anthony E. Lang

Movement Disorders Unit, Toronto Western Hospital, Purpose of review University of Toronto, Ontario, Canada This review summarizes the progress made in the area of psychogenic movement Correspondence to Dr Anthony E. Lang, MD, FRCPC, disorders (PMDs) over the past 2 years, and a simplified classification of diagnostic Director, Movement Disorders Unit, Toronto Western Hospital, 399 Bathurst Street, McLaughlin 7-418, certainty is proposed that incorporates electrophysiological assessment. Toronto M5T 2S8, Ontario, Canada Recent findings Tel: +1 416 603 6422; fax: +1 416 603 5004; e-mail: [email protected] Functional magnetic resonance imaging studies have demonstrated altered blood flow in conversion disorders that may reflect changes in synaptic activity. Current Opinion in Neurology 2009, 22:430–436 Electrophysiological testing shows limitations in distinguishing between psychogenic and organic propriospinal myoclonus and dystonia. Recent evidence cautions against the uncritical acceptance of all cases of posttraumatic myoclonus and ‘jumpy stump’ as being organic in nature. ‘Essential palatal tremor’ is recognized as a rather heterogeneous group of tremors that includes psychogenic tremor. Two recent studies evaluating the long-term prognosis of psychogenic tremor differ in the degree of unfavorable outcome. Different groups of PMDs might have distinctive gait characteristics with prognostic, diagnostic, or therapeutic value. Two recent reviews provide comprehensive information on the understudied area of PMDs in children. Summary The diagnosis of PMDs should not be regarded as a diagnosis of exclusion. Careful clinical assessment is critical, and imaging or electrophysiological studies may provide important insights and confirmation of the diagnosis though some cases remain challenging and current assessments fail to provide needed clarification. Treatment is often delayed, contributing to a largely unfavorable long-term outcome. Well designed randomized control trials that validate and compare therapeutic options are urgently required.

Keywords children, diagnosis, investigations, movement disorders, psychogenic, treatment

Curr Opin Neurol 22:430–436 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins 1350-7540

the literature of the past 2 years and summarize how Introduction PMDs are currently diagnosed, investigated, and treated. Psychogenic movement disorders (PMDs) are movement disorders that result from a psychological or psychiatric rather than neurological disturbance. The primary psy- Diagnosis chiatric diagnosis varies; most cases are considered to be Although no single clinical finding is pathognomonic for conversion disorders, in which the problem is caused by PMDs, several features are quite helpful. The clinical an unconscious mechanism, but infrequently some are aspects of specific types of PMDs (i.e. tremors, myoclo- factitious disorders or malingering, in which the abnormal nus, dystonia, Parkinsonism, gait disorders) have been movements are purposefully feigned. Traditionally, reviewed at length elsewhere [6–8]. Table 1 [8,9] pro- PMDs represented a diagnosis of exclusion. This percep- vides a list of typical historical and clinical clues to the tion was fuelled by the observation that PMDs can mimic diagnosis. various organic diseases, sometimes with confounding test results [1], and by studies and experiences of high Over a decade ago, criteria were proposed for various false positive rates [2–4]. Over the years, stricter clinical levels of diagnostic certainty of PMDs [10]. With the criteria, improved imaging, and investigational advances subsequent progress made in establishing clinical charac- have allowed the diagnosis of PMDs to be made more teristics and investigational methods, it appears timely comfortably [5], and organic movements are far less to propose modifications to the diagnostic classifica- often misdiagnosed as psychogenic. Here, we review tion, including the incorporation of electrophysiological

1350-7540 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI:10.1097/WCO.0b013e32832dc169

Table 1 Clues suggesting psychogenic cause Historical General examination Abrupt onset (symptoms often maximal at that time) Movement inconsistent Static course Variability over time (frequency, amplitude, direction/distribution of movement) Spontaneous remissions/cures Distractibility reduces or resolvesa, attention increases movement Paroxysmal symptoms (generally nonkinesigenic)b Selective disability Psychiatric comorbiditiesc Entrainment (especially with tremor) Secondary gain (often not apparent) Movement incongruous with organic movement disorders Risk factors for conversion disorderd Mixed (often bizarre) movement disorders Psychological stressorse Paroxysmal attacks (including pseudoseizures) Multiple somatizations/undiagnosed conditions Precipitated paroxysms (often suggestible/startle) Employed in allied health professions (infrequent) Suggestibilityf Effortful production or deliberate slowness (without fatiguing) of movement Self-inflicted injury (caution: tic disorders) Delayed and excessive startle response to a stimulus Burst of verbal gibberish or stuttering speechg False (give-away) weakness Nonanatomical sensory loss or spread of movement Certain types of abnormal movements common in individuals with PMDsh Functional disability out of proportion to examination findings a Distractibility should be tested both with mental and motor tasks. Although most often organic movement disorders are not suppressed, organic tics or akathisia can be suppressible, and recently it was shown that diaphragmatic tremor was suppressed by simple motor tasks, perhaps by interference with central nervous system circuitry [9]. b Separation from organic paroxysmal dyskinesias can be challenging, particularly if they occur infrequently with prolonged symptom-free periods. c Psychiatric diseases can also coincide with organic illness or present as part of the organic movement disorder. d Sexual and physical abuse, trauma. e Often initiated by injury (often minor) or motor vehicle accident associated with litigation or compensation. f Application of pressure with finger or tuning fork may reduce symptom. With paroxysmal symptom, suggestibility and placebo trial may not be helpful, unless repeated reversals with placebo are documented when symptom otherwise is frequent and attacks are prolonged. g Particularly if the entire word is repeated (typically broken up into syllables, each repeated), rather than the initial syllable. h Such movements include dystonia that begins as a fixed posture (particularly if abrupt onset, painful, and early contractures are seen); bizarre gait; twisting facial movements that move mouth to one side or the other (organic dystonia of the facial muscles usually does not pull the mouth sidewise). Adapted from [8].

techniques (Table 2) [10–12]. The remainder of this Patients with motor conversion disorders (MCDs) have review will discuss recent diagnostic and therapeutic been shown to activate the motor cortex in a pattern that approaches, with an emphasis on developments in the differs from controls simulating weakness [17]. areas of investigational methods, posttraumatic move- Although this suggests that cerebral activity is changed ment disorders, psychogenic tremor, psychogenic gait in MCD, comparison to organic weakness requires elu- disorders, and PMDs in children. cidation. Similarly, in patients with a sensory conversion disorder, fMRI has demonstrated that vibratory stimu- Investigations lation of the affected limb fails to activate the contra- Nuclear imaging, in contrast to magnetic resonance ima- lateral cortical sensory area. This result supports the ging (MRI), has proven quite helpful in distinguishing notion that clinical deficits in this psychiatric condition psychogenic Parkinsonism from Parkinson’s disease. are associated with real changes in blood flow that Well established methods include fluorodopa positron indicate reduced cortical responsiveness. The mechan- emission tomography (FDOPA-PET), bCIT single ism underlying these changes is not well understood, but photon emission computed tomography (SPECT) cortical activation was shown to be restored with bilateral [13,14], and, recently also, 123I-Isoflupane SPECT stimulation [18], possibly acting as a ‘distractor’ to [15]. As these methods detect the degree of viable reverse inhibition. dopaminergic neurons of the substantia nigra (PET) or their respective synaptic termini in the striatum Previous studies have established the utility of specialized (SPECT), scan results are normal in psychogenic cases electrophysiological techniques in aiding or confirming the but show diminished signal in Parkinson’s disease. diagnosis of certain PMDs, particularly psychogenic tre- Although it has been suggested that nuclear imaging mor and psychogenic myoclonus. These studies have been may be normal in some early cases of Parkinson’s disease, reviewed elsewhere [11,19,20]. Recent electrophysiologi- recent evidence suggests that most of these cases are cal studies have better delineated PMDs. Compared with likely falsely classified [16]. Therefore, nuclear imaging controls, PMD patients exhibited an excessive affective may be extremely useful in distinguishing psychogenic response to the startle eye blink reflex [21]. When pictures Parkinsonism from Parkinson’s disease. invoking either positive or negative affective states were shown at the time of eliciting the eye blink startle, reflex Functional MRI (fMRI) imaging of conversion disorders potentiation was seen in both conditions, in contrast to the has provided interesting insights into the condition. normal inhibition with the negative affective state seen in

Table 2 Diagnostic classiﬁcation of psychogenic movement disorders Traditional Proposed revision

Classification of degrees of certainty in diagnosisa Classification of degrees of certainty in diagnosis 1. Documentedb 1. Documented (as in original) Remittance with suggestion, physiotherapy, 2a. Clinically established plus other features (as in original) psychotherapy, placebos, ‘while unobserved’ 2b. Clinically established minus other features 2. Clinically establishedb Unequivocal clinical features incompatible with organic Inconsistent over time/incongruent with clinical disease with no features suggesting another underlying condition R other manifestations: other ‘false’ neurological or psychiatric problem signs, multiple somatizations, obvious psychiatric disturbance 1 þ 2a þ 2b ¼ Clinically Definite 3. Probable Inconsistent/incongruent no other features 3. Laboratory-supported definite Consistent/congruent þ ‘false’ neurological signsc Electrophysiological evidence proving a psychogenic Consistent/congruent þ multiple somatizationsc movement disorder (primarily in cases of psychogenic 4. Possibled tremor and psychogenic myoclonus) Consistent/congruent þ obvious emotional disturbancec a Adapted from [12]. b Subsequently, Fahn and his coauthors [10] proposed combining categories 1 þ 2 under ‘Clinically Definite’. c We proposed to reclassify these patients under ‘Possible’. d We also questioned the utility of retaining the ‘Possible’ category as this generally represents patients with organic movement disorders with additional psychiatric problems rather than a true ‘Possible psychogenic movement disorder’ [11].

controls. It remains to be seen whether this result can PMDs and the organic counterpart may not be differ- separate PMDs from organic disease, particularly in entiated with electrophysiological studies is dystonia. patients with underlying concurrent psychopathology. TMS has shown increased cortical excitability (decreased Central motor conduction is typically normal in patients SICI, LICI, ICF) in both groups [25], suggesting that this with MCD. Using transcranial magnetic stimulation abnormality can occur as a consequence of the dystonic (TMS) in such patients, Liepert et al. [22] found that postures or, alternatively, it may be an ‘endophenotype’ motor threshold, short and long interval intracortical inhi- that predisposes to the dystonia in both organic and bition (SICI and LICI), and intracortical facilitation (ICF) psychogenic cases. A distinction between these two were similar to that in controls, indicating unchanged possibilities was not possible, as the unaffected side baseline cortical excitability. When movements were ima- was not investigated. Avanzino et al. [26] analyzed both gined, however, cortical excitability was decreased in the sides with TMS and obtained similar results, supporting affected limb of MCD patients but increased in the the conclusion that the cortical hyperexcitability may unaffected limb as it was in the limbs of healthy individ- reflect a predisposing ‘endophenotypic trait’ for dystonia uals. Further confirmatory studies are required. Theoreti- in either condition [27], although transcallosal or ipsilat- cally, this decreased cortical excitability with motor ima- eral descending influences from the involved hemisphere gery might be able to separate conversion disorder from could still result in these changes being secondary to the factitious disorder or malingering. postures. Future investigation searching for improved electrophysiological approaches could provide great Some electrophysiological testing fails to distinguish value, as clinical distinction between organic and psycho- PMDs from organic movement disorders, indicating com- genic dystonia can be extremely challenging [28,29]. plex overlapping neuronal mechanisms and the importance of careful clinical assessment. Electrophysiological Posttraumatic movement disorders findings are very similar between simulated propriospinal Posttraumatic movement disorders are a source of con- myoclonus (PSM) and the organic counterpart [23]. Aside siderable controversy. Complex regional pain syndrome from a generally longer electromyographic burst duration (CRPS) type I typically following minor injury may be observed in controls purposefully simulating PSM, a associated with fixed dystonia, myoclonus, and tremor. fixed pattern of muscle recruitment, synchronous acti- Some authors have provided considerable evidence in vation of agonist and antagonist, electromyographic burst favor of a psychogenic cause [30,31], whereas others favor duration less than 1000 ms, and slow conduction in the an ‘organic’ explanation [32]. Munts et al. [33] recently spinal cord (5–15 m/s) have been shown in both groups. presented the electrophysiological characterization of In a recent case of confirmed psychogenic PSM following myoclonus associated with CRPS. However, it was sub- eye surgery [24], electrophysiological analysis demon- sequently argued that their findings of burst duration strated slow conduction, short burst duration, consistent length of more than 70 ms, variability in burst character- caudal muscle activation, and absence of premovement istics, side-to-side coherence, and entrainment were potentials, with only some variability in muscle activation strongly supportive of a psychogenic cause of the move- possibly suggesting a PMD. Another example in which ments [34]. The ‘jumpy stump’ (an uncommon but widely

acknowledged ‘peripheral’ movement disorder develop- psychogenic tremor were diagnosed prior to assessment ing in an amputated limb) has been considered another of distinctive parameters, and sample size was small. In example of an organic posttraumatic movement disorder. addition, the method of evaluating entrainment (10 s of Zadikoff et al. [35] recently presented a case of psycho- wrist extension and flexion in the unaffected arm) is genic ‘jumpy stump’, in which paroxysmal rhythmical probably not an adequate assessment of this feature. jerking movements of the stump were associated with Kumru et al. [42] assessed whether dual task interference palpable muscle activation in the proximal limb. Electro- (difficulties with carrying out tasks simultaneously with physiological analysis confirmed reciprocal contraction both arms) could distinguish psychogenic tremor from of hamstrings and quadriceps at 8 Hz, increased EMG Parkinsonian rest tremor and essential tremor. Only psy- activity with stump restraint (indicating voluntary effort chogenic tremor patients showed delayed reaction time against resistance), variability, and distractibility with when they performed a simple reaction time task to a visual coherence. This case cautions against the uncritical appli- stimulus with their nontremulous side when tremor was cation of the diagnosis of ‘jumpy stump’ as organic, but present compared with when it was not. It is unclear the true prevalence of psychogenic movements in such whether this method is superior to classic distraction patients remains unclear without further systematic paradigms (with respect to ease of testing, reliability, study. sensitivity, and specificity) and it requires that the tremor be intermittent rather than persistent. Psychogenic tremors Psychogenic tremor can be remarkably variable in its Evaluation of long-term prognosis of psychogenic tremor presentation, as supported by recent case reports [19], has proven difficult, as underscored by two recent studies as well as severe and disabling. Recent experience with a similar follow-up period (3 years). Earlier inves- suggests that the diagnosis should be considered in tigations have reported tremor remission rates of only patients failing deep brain stimulation surgery for tremor 20%. McKeon et al. [43] arrived at a similar pessimistic [36]. In recent years, it has become clear that some patients outlook, finding a 65% disability rate on patient-reported who would have been previously diagnosed as ‘essential disability scales. In contrast, Jankovic et al. [44] reported a palatal tremor’ have a psychogenic cause. Recognizing the better prognosis with a 60% improvement rate. However, heterogeneous nature of ‘essential palatal tremor’, includ- they included any degree of improvement, as measured ing a PMD, a learned movement, and tics, Zadikoff et al. on a global rating scale, their patients had a shorter [37] proposed the term ‘isolated palatal tremor’ to avoid duration of symptoms at the time of diagnosis (0.9 years confusion with other more homogeneous disorders such as versus 1.5 years in the McKeon study), and they had a essential tremor and essential myoclonus (now myoclonus greater proportion of patients enrolled in treatment. This dystonia). Psychogenic palatal tremor may or may not have study also lacked a prospective follow-up design and extrapalatal movements. As in other forms of psychogenic confirmatory electrophysiological assessment of psycho- tremor, psychogenic palatal tremor is typically variable in genic tremor used in the McKeon report. Nonetheless, frequency (often changes in response to challenging motor favorable prognostic signs were determined, which tasks), and it may be entrained and suppressed by dis- included the patient’s perception of effective treatment tracting maneuvers. By definition, the MRI is always by the physician, elimination of stressors, and compliance normal [38]. One patient with a 2 Hz palatal tremor with the treatment regimen. No statistical difference in restricted to the posterior soft palate determined to be long-term outcome was found between patients involved psychogenic even had a sensory trick that suppressed the and not involved in litigation. tremor [39]. Finally, psychogenic suprahyoid neck tremor was recently reported; this appeared suddenly, was irre- Psychogenic gait disorders gular, disappeared with open mouth or with distraction, Given the variable presentation of psychogenic gait [45], and resolved with placebo injection [40]. formal tests definitively identifying this condition would be very helpful but have yet to be developed. On the Investigations of how to better identify psychogenic tre- basis of Paul Blocq’s original description of an astasia– mor are ongoing. Kenney et al. [41] studied what features abasia patient who effectively propelled a chair while might distinguish psychogenic tremor from essential tre- being seated, Okun et al. [46] assessed whether this ‘chair mor, given that sensitivity and specificity of psychogenic test’ could distinguish psychogenic from organic gait. clues generally lack systematic evaluation in this context. Eight of nine patients with psychogenic gait moved much Psychogenic tremor was differentiated by negative family better sitting in a chair than when walking in the upright history, sudden onset, spontaneous remission, shorter position, whereas nine organic gait disorder patients duration of tremor, suggestibility, and distractibility. Cur- performed similarly in both conditions. Although prom- iously, entrainment was not seen often in either tremor ising, test sensitivity and specificity need to be assessed type. The authors’ claim that the results have predictive with a larger sample size and a more diversified control value is limited by the fact that essential tremor and group (the control group had seven Parkinson’s disease

patients); for example, patients with lower body dystonia might show false positive results if they were able to use Treatment the chair as a geste antagoniste, and patients with ‘gait A delay in diagnosing PMDs should be avoided at all apraxia’ who can perform normal bicycling leg move- costs. Failure to do so often results in multiple referrals, ments might also fair better in the chair than on standing. repeated unnecessary diagnostic tests, unjustified and potentially harmful treatments including medication Baik and Lang [47] assessed gait abnormalities in a large trials and even surgeries, and the perpetuation of the group of patients with PMDs. When patients were belief of underlying organic illness. This also delays the subdivided into those with more generalized PMDs initiation of appropriate treatment (though, as discussed that also compromised the gait and those with a pure below, treatment is often very different), which reduces psychogenic gait disorder, the mixed PMD group efficacy, particularly if treatment is started 6–12 months most frequently showed slowness of gait (followed by after onset of the movement disorder. To maximize dystonic gait), whereas the pure gait group most com- treatment compliance, it should be acknowledged that monly displayed buckling of knees (followed by astasia– the patient has a movement disorder (i.e. a form of abasia). This study provides an incentive to assess tremor, myoclonus, or dystonia) and a biological expla- whether gait differences among PMD subpopulations nation provided. Lastly, despite the various treatments have diagnostic, predictive, or therapeutic value and applied, evidence-based data are limited, and prospective whether these differences reflect distinct pathophysio- double-blinded studies are urgently required. logical processes. Therapy is best administered in multimodal fashion. Psychogenic movement disorders in children Psychotherapy [50], cognitive behavioral therapy, reha- PMDs in children have been addressed by recent reviews bilitation [51,52], antidepressants [53], and hypnosis [54] [48,49]. Uncommon before the age of 10 years, clinical have had variable success. Monthly sessions of acupunc- clues in children are derived from the adult literature. As in ture produced normalization for only 4–5 days in a adults, there is female sex predominance, they comprise patient with psychogenic jerking movements [55]. She approximately 3% of children visiting movement disorders was wheelchair bound, with symptoms present for over a clinics, and the distribution of psychiatric diagnosis shows decade. This effect may have simply been because of a conversion disorder in up to 80%, followed by somatization reduction of anxiety or some other form of placebo effect. disorders (10–20%) and factitious disorders (<5%). Quite Recently, a 17-year-old boy with psychogenic aphonia for in contrast to the adults, malingering was not reported. 20 months who had failed speech therapy recovered Similar to adults [10], dystonia and tremor were the most completely following two sessions of repetitive TMS common clinical phenotypes, followed remotely by gait [56 ]. Low-frequency stimulation was used, rather than disorders. In addition, dystonia was fixed in most cases and the high-frequency pulses usually applied to psychogenic usually preceded by minor physical trauma. limb paralysis intended to directly activate the primary motor areas. Functional imaging data in psychogenic Some differences are noteworthy. Although in adults the paralysis have shown decreased activity in the primary nondominant limb may be most often affected (except for motor cortex and increased activity in prefrontal cortex. tremor in psychogenic Parkinsonism), children more Thus, low-frequency stimulation may have inhibited the frequently have PMDs in their dominant limb. It has overactive prefrontal areas resulting in disinhibition of been suggested that this may reflect incomplete hemi- the primary motor cortex. Target choice might be critical; spheral lateralization [49]. Although coexisting organic low-frequency stimulation resulted in rapid recovery, neurological disease is well recognized in patients with whereas high-frequency treatment takes many weeks psychogenic neurological complaints, associated organic and produces variable success. In light of the strong movement disorders are rare in children with PMDs [49] potential for a placebo effect, a controlled trial is clearly in contrast to estimates in adults, which range between 10 needed to demonstrate reproducibility, taking into and 25%. Similarly, psychiatric diseases in children account the well established effect of patient anticipation appear to be less common, as most studies report 10% on treatment outcomes [57]. comorbidity, compared with the 40% rate quoted for adults with PMDs. However, Ferrara and Jankovic Data on long-term prognosis are scarce, but most studies [48] reported a 50% comorbidity rate (anxiety, depres- point to significant impact on quality of life. Anderson sion, irritability) and a 40% rate of perfectionistic person- et al. [58] compared 66 patients with PMDs to 704 with ality, a common trait in patients with conversion dis- Parkinson’s disease and found increased psychiatric orders. Lastly, psychogenic dystonia is less easily and comorbidity, more severe mental health disturbances, comfortably diagnosed in children, given the spectrum and very similar levels of disability and physical quality of organic dystonia that results from genetic mutations, of life, despite the fact that patients with PMDs were neurometabolic diseases, and other causes. 20 years younger, had shorter disease duration (4 versus

7 years), and were compared to a Parkinson’s disease 5 Voon V, Lang AE, Hallett M. Diagnosing psychogenic movement disorders: which criteria should be used in clinical practice? Nat Clin Pract Neurol 2007; population with a 30% prevalence of motor fluctuators. 3:134–135. Prognosis appears to be better in children with PMDs. In 6 Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neurol one study [49], 50% of children remitted, 40% returned 2006; 5:695–700. to normal school life, whereas 20% experienced only 7 Sa DS, Galvez-Jimenez N, Lang AE. Psychogenic movement disorders. In: Watts RL, Koller WC, editors. Movement disorders: neurologic principles and partial improvement or remained disabled. As with practice. New York: McGraw Hill; 2004. pp. 891–914. adults, children who remitted were treated in their first 8 Pringsheim T, Chen R, Lang AE. Psychogenic movement disorders. 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