Search

OBJECTIVES The objective of this study was to compare the effect on functional tremor of active versus sham repetitive transcranial magnetic stimulation and investigate whether the addition of hypnosis might help to prolong any repetitive transcranial magnetic stimulation-induced therapeutic effect. METHODS We compared the effect of 5 consecutive daily sessions of active/sham repetitive transcranial magnetic stimulation on functional tremor, at 1 and 2 months, in a randomized, double-blind, 2-arm, parallel-controlled study. In a second open-label phase, all patients underwent 3 weekly sessions of hypnosis combined with single sessions of real repetitive transcranial magnetic stimulation. The primary outcome was a change in the Psychogenic Movement Disorder Rating Scale at month 1 when compared with baseline. Secondary outcomes were changes in the Psychogenic Movement Disorder Rating Scale and Tremor subscores, the 36-item Short Form Health Survey, the Self-Report Hospital Anxiety and Depression Scale, the Hamilton Depression Rating Scale, and the Clinical Global Impression Scale assessed at months 1, 2, 6, and 12. RESULTS A total of 33 outpatients affected by functional tremor were screened, and 18 outpatients fulfilling the inclusion criteria (8 men, 10 women) were randomized. One month after the intervention, the mean Psychogenic Movement Disorder Rating Scale score had decreased in both groups, but the differences from baseline were only significant in the active repetitive transcranial magnetic stimulation group (P < .001). This remained significant at month 2 (P < .001). The significant decrease of the Psychogenic Movement Disorder Rating Scale and Tremor subscores were maintained at months 6 and 12 for the active repetitive transcranial magnetic stimulation group. For the control group, the Psychogenic Movement Disorder Rating Scale score had returned almost to its baseline value by month 2 and remained unchanged at months 6 and 12. CONCLUSION Repetitive transcranial magnetic stimulation could represent a valuable therapeutic option in the management of functional tremor. © 2019 International Parkinson and Movement Disorder Society.

Objective We sought to determine whether abnormalities in emotion processing underlie functional (psychogenic) dystonia, one of the most common functional movement disorders. Methods Motor and emotion circuits were examined in 12 participants with functional dystonia, 12 with primary organic dystonia, and 25 healthy controls using functional magnetic resonance imaging at 4T and a finger-tapping task (motor task), a basic emotion-recognition task (emotional faces task), and an intense-emotion stimuli task. Results There were no differences in motor task activation between groups. In the faces task, when compared with the other groups, functional dystonia patients showed areas of decreased activation in the right middle temporal gyrus and bilateral precuneus and increased activation in the right inferior frontal gyrus, bilateral occipital cortex and fusiform gyrus, and bilateral cerebellum. In the intense-emotion task, when compared with the other groups, functional dystonia patients showed decreased activation in the left insular and left motor cortices (compared to organic dystonia, they showed an additional decrease in activation in the right opercular cortex and right motor cortex) and increased activation in the left fusiform gyrus. Conclusions Functional dystonia patients exhibited stimulus-dependent altered activation in networks involved in motor preparation and execution, spatial cognition, and attentional control. These results support the presence of network dysfunction in functional dystonia. © 2017 International Parkinson and Movement Disorder Society.

Background Movement disorders associated with complex regional pain syndrome type I have been a subject of controversy over the last 10 years regarding their nature and pathophysiology, with an intense debate about the functional (psychogenic) nature of this disorder. The aim of this study was to test sensorimotor plasticity and cortical excitability in patients with complex regional pain syndrome type I who developed a fixed posture of the hand. Methods Ten patients with complex regional pain syndrome type I in the right upper limb and a fixed posture of the hand (disease duration less than 24 months) and 10 age-matched healthy subjects were enrolled. The following parameters of corticospinal excitability were recorded from the abductor pollicis brevis muscle of both hands by transcranial magnetic stimulation: resting and active motor thresholds, short-interval intracortical inhibition and facilitation, cortical silent period, and short- and long-latency afferent inhibition. Sensorimotor plasticity was tested using the paired associative stimulation protocol. Results Short-interval intracortical inhibition and long-latency afferent inhibition were reduced only in the affected right hand of patients compared with control subjects. Sensorimotor plasticity was comparable to normal subjects, with a preserved topographic specificity. Conclusions Our data support the view that motor disorder in complex regional pain syndrome type I is not associated with abnormal sensorimotor plasticity, and it shares pathophysiological abnormalities with functional (psychogenic) dystonia rather than with idiopathic dystonia. © 2016 International Parkinson and Movement Disorder Society

Mind-brain dualism has dominated historical commentary on dystonia, a dichotomous approach that has left our conceptual grasp of it stubbornly incomplete. This is particularly true of functional dystonia, most diagnostically challenging of all functional movement disorders, in which the question of inherent psychogenicity remains a focus of debate. Phenomenological signs considered in isolation lack the specificity to distinguish organic and nonorganic forms, and dystonia's variability has frustrated attempts to develop objective laboratory-supported standards. Diagnostic criteria for functional dystonia that place emphasis on psychiatric symptoms perform poorly in studies of reliability, partly explained by the high frequency of psychopathology in organic dystonia. Novel approaches from the cognitive neurosciences may offer a way forward. Theory on Bayesian statistical prediction in cognitive processing is supported by sufficient experimental evidence for this model to be taken seriously as a way of reconciling contradictory notions about voluntary and unconscious motor control in functional movement disorders. In a Bayesian formulation of functional dystonia, misallocation of attention and abnormal predictive beliefs generate movements that are executed without a sense of agency. Building on this framework, there is a consensus that a biopsychosocial approach is required and that a unified philosophy of brain and mind is the best way to locate dystonia in the neurology-psychiatry borderland. At a practical level, movement disorder neurologists are best placed to differentiate organic from functional dystonia. The main role of psychiatrists is in the diagnosis and management of the primarily psychiatric disorders that often accompany dystonia. © 2016 International Parkinson and Movement Disorder Society.

BACKGROUND: In a small group of patients, we have previously shown that a combination of electrophysiological tests was able to distinguish functional (psychogenic) tremor and organic tremor with excellent sensitivity and specificity. OBJECTIVES: This study aims to validate an electrophysiological test battery as a tool to diagnose patients with functional tremor with a "laboratory-supported" level of certainty. METHODS: For this prospective data collection study, we recruited 38 new patients with functional tremor (mean age 37.9 ± 24.5 years; mean disease duration 5.9 ± 9.0 years) and 73 new patients with organic tremor (mean age 55.4 ± 25.4 years; mean disease duration 15.8 ± 17.7 years). Tremor was recorded at rest, posture (with and without loading), action, while performing tapping tasks (1, 3, and 5 Hz), and while performing ballistic movements with the less-affected hand. Electrophysiological tests were performed by raters blinded to the clinical diagnosis. We calculated a sum score for all performed tests (maximum of 10 points) and used a previously suggested cut-off score of 3 points for a diagnosis of laboratory-supported functional tremor. RESULTS: We demonstrated good interrater reliability and test-retest reliability. Patients with functional tremor had a higher average score on the test battery when compared with patients with organic tremor (3.6 ± 1.4 points vs 1.0 ± 0.8 points; P

Background Ten to fifteen percent of Parkinson's disease (PD) patients recruited to clinical trials have scans without evidence of dopaminergic deficit, whose presence represents a heterogeneous patient population. Methods A cohort of 41 patients with parkinsonism and scans without evidence of dopaminergic deficit at baseline, were subdivided into groups according to their final clinical diagnoses and nigrostriatal dopamine function assessed after 2 years of study. At follow up, 23 patients had clinically probable PD or unclassified parkinsonism with normal nigrostriatal dopamine imaging (“true” scans without evidence of dopaminergic deficit), nine were diagnosed with another tremulous condition, five had psychogenic parkinsonism, and four had phenoconverted to PD with reduced nigrostriatal dopamine function. We analyzed nonmotor symptoms at baseline and follow-up in subgroups of patients with scans without evidence of dopaminergic deficit in comparison with a random sample of 62 PD patients and 195 healthy controls (HCs). All patients were enrolled in the Parkinson's Progressive Marker's Initiative. Results Patients who had true scans without evidence of dopaminergic deficit had more severe rapid eye movement sleep disorder, depression, anxiety, and autonomic dysfunction than HCs in addition to more frequent depressive symptoms and worse cardiovascular dysfunction than patients with PD (P = 0.038, P = 0.047, respectively). Patients with true scans without evidence of dopaminergic deficit had normal olfaction that was significantly better than that of patients with PD (P

Some patients diagnosed with Parkinson’s disease (PD) have intact dopaminergic function by PET or single-photon emission computed tomography (SPECT) imaging, most notably in four large trials using PET with 6-[18F]-fluoro-L-dopa (18F-dopa)1 or SPECT with [123I] β-CIT,2–4 where it occurred in 5% to 15% of studied patients; this phenomenon has been called scans without evidence of dopaminergic deficit (SWEDD). The basis for SWEDD is controversial and could in theory be the result of imaging error, clinical (diagnostic) error, or occurrence of a different process clinically similar to PD; true PD presenting without dopaminergic deficit has not been favored as an explanation, given that symptoms of disease generally emerge only after substantial loss of nigral dopamine neurons and striatal dopamine.5,6 Longitudinal studies of patients with SWEDD have shown that the majority of these patients do not develop a dopaminergic deficit7,8; final diagnoses include other tremor syndromes (essential tremor, dystonic tremor, and fragile X tremor ataxia syndrome) and other causes of parkinsonism (other degenerative causes, vascular, medication induced, and psychogenic).9 However, a minority of patients with SWEDD subsequently do develop dopaminergic deficits—2 of 16 patients in one report,8 4 of 30 in another,9 and 6 of 72 in the PRECEPT study.7 In 248 patients with unclassified parkinsonism studied with [123I] β-CIT scans at baseline and followed for a mean 18 months, 22 of 112 eventually diagnosed with PD had SWEDD.10 Furthermore, SWEDD has been associated with a higher than expected frequency of nonmotor features of PD, including depression, sleep disorders, autonomic dysfunction, and hyposmia.11 The basis for SWEDD is therefore varied, with most representing PD mimics, but rare cases may, for unclear reasons, represent early PD.

Deep brain stimulation (DBS) may improve disabling tics in severely affected medication and behaviorally resistant Tourette syndrome (TS). Here we review all reported cases of TS DBS and provide updated recommendations for selection, assessment, and management of potential TS DBS cases based on the literature and implantation experience. Candidates should have a Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM V) diagnosis of TS with severe motor and vocal tics, which despite exhaustive medical and behavioral treatment trials result in significant impairment. Deep brain stimulation should be offered to patients only by experienced DBS centers after evaluation by a multidisciplinary team. Rigorous preoperative and postoperative outcome measures of tics and associated comorbidities should be used. Tics and comorbid neuropsychiatric conditions should be optimally treated per current expert standards, and tics should be the major cause of disability. Psychogenic tics, embellishment, and malingering should be recognized and addressed. We have removed the previously suggested 25-year-old age limit, with the specification that a multidisciplinary team approach for screening is employed. A local ethics committee or institutional review board should be consulted for consideration of cases involving persons younger than 18 years of age, as well as in cases with urgent indications. Tourette syndrome patients represent a unique and complex population, and studies reveal a higher risk for post-DBS complications. Successes and failures have been reported for multiple brain targets; however, the optimal surgical approach remains unknown. Tourette syndrome DBS, though still evolving, is a promising approach for a subset of medication refractory and severely affected patients.

Propriospinal myoclonus is a rare movement disorder that is hypothesized to arise from a spinal generator that transmits activity up and down the spinal cord via long propriospinal pathways. Polymyography is mandatory for the diagnosis, but the typical electrophysiological pattern described for propriospinal myoclonus has been also found in patients with psychogenic axial jerks, supported by the presence of a Bereitschaftspotential (BP; from German, "readiness potential," also called the premotor potential). We evaluated polymyographic findings in 65 patients referred to us with a clinical diagnosis of propriospinal myoclonus and also looked for the presence of the BP, as detected by jerk-locked back-averaging. At clinical reassessment by a movement disorder specialist, nearly one-half of the patients had clinical clues suggestive of a psychogenic cause of the jerks. Electrophysiological studies were carried out on all 65 patients. Polymyography findings revealed an incongruent electromyographic pattern for propriospinal myoclonus in 84.6% of patients and the presence of the BP in 86.1% of the entire cohort. When taking into account either the presence of BP and/or incongruence of polymyographic features, all patients, including the approximately 50% clinically diagnosed as organic propriospinal myoclonus by a movement disorder expert, had strong neurophysiological evidence for a psychogenic origin of their jerks. The clinical distinction of propriospinal myoclonus from psychogenic axial jerks is unreliable. This is the largest cohort of patients with axial jerks reported so far and we suggest that most of the patients with a clinical picture that clinically resembles propriospinal myoclonus are likely to be psychogenic.

Successive attempts at rebranding may be behind at least some of the proliferation of terms we have at our disposal when describing patients with what are now most often referred to as “psychogenic,” “conversion,” or “somatoform” symptoms. The most popular term in the movement disorder literature, “psychogenic,” provides the aetiology of the disorder within the name, indicating that the symptoms are “born of the mind.” Here we argue that it is logical to stop using a term that defines the disorder with regard to a poorly defined aetiology that is not supported by current evidence, and, instead, to use a broad term—functional—not as a “polite eponym” but as a term that is freer from such assumptions and does not reinforce dualistic thinking. The main argument for change is not political or even practical, but scientific. © 2013 International Parkinson and Movement Disorder Society

It has been reported that patients who have Parkinson's disease have a high prevalence of somatisation (functional neurological symptoms) compared with patients who have other neurodegenerative conditions. Numerous explanations have been advanced for this phenomenon. Here, with illustrative cases, we discuss this topic, including its clinical importance, and suggest a link between the pathophysiology of Parkinson's disease and the proposed propensity to develop functional symptoms.

Background: Psychogenic (or functional) movement disorders (PMDs) are considered sporadic. Despite the growing literature describing the clinical features and the natural history of sporadic cases with PMDs, their occurrence in familial clusters is not reported. Methods: We identified 10 patients from 5 families affected by PMDs. In this report, we describe the clinical characteristics along with videos and long-term follow-up of these patients. Results: Clinical clues from the history and signs suggesting a functional origin of the symptoms in these patients with familial PMD were similar to those identified in sporadic cases. The phenomenology of the PMD was similar in the affected members of the same family. Conclusions: We wish to highlight that a positive family history does not necessarily imply an organic disorder. When a positive family history for a condition is reported by a patient with PMD, examination of these further affected members may be needed and may identify further family members suffering from PMDs. A positive family history of PMDs may be an additional risk factor for developing PMDs. V C 2013 Movement

Background Functional movement disorders (FMDs) are thought to be rare in the elderly. Clinical characteristics of the elderly people who develop FMDs are rarely reported. The objective of this study was to highlight the clinical characteristics of FMD in the elderly and compared these with a cohort of patients with a younger age of onset. Methods The authors performed a retrospective review of the clinical records of patients with FMD who were seen at their center in the last 5 years and had consented to be included in research studies. Patients fulfilling currently accepted diagnostic criteria for FMD as documented, clinically established, or probable were included. Results Of 151 patients with FMD who were identified and had sufficient information, 21.0% (n=33) had an onset after age 60 years (elderly group). The mean age of onset of FMD was 63.5 years (standard deviation, 5.2 years) in the elderly group and 35.5 years (standard deviation, 12.6 years) in the younger group. Tremor was the most common movement disorder in both groups (elderly group, 33.3%; younger group: 38.9%). Fixed dystonia was not observed in any patient who had an FMD onset after age 60 years. Gait abnormalities were significantly more common in the elderly group (69.7%) than in younger patients (23.5%; P

Functional neurological symptoms are one of the most common conditions observed in neurological practice, but understanding of their underlying neurobiology is poor. Historic psychological models, based on the concept of conversion of emotional trauma into physical symptoms, have not been implemented neurobiologically, and are not generally supported by epidemiological studies. In contrast, there are robust clinical procedures that positively distinguish between organic and functional motor signs that rely primarily on distracting attention away from movement or accessing it covertly. We aimed to investigate the neurobiological principles underpinning these techniques and implications for understanding functional symptoms. We assessed 11 patients with functional motor symptoms and 11 healthy controls in three experimental set-ups, where voluntary movements were made either with full explicit control or could additionally be influenced automatically by factors of which participants were much less aware (one-back reaching, visuomotor transformation, and precued reaction time with variable predictive value of the precue). Patients specifically failed in those tasks where preplanning of movement could occur and under conditions of increasing certainty regarding the movement to be performed. However, they implicitly learned to adapt to a visuomotor transformation as well as healthy controls. We propose that when the movement to be performed can be preplanned or is highly predicted, patients with functional motor symptoms shift to an explicit attentive mode of processing that impairs kinematics of movement control, but movement becomes normal when such processes cannot be employed (e.g., during unexpected movement or implicit motor adaptation). © 2013 Movement Disorders Society.

The facial phenotype of psychogenic movement disorders has not been fully characterized. Seven tertiary-referral movement disorders centers using a standardized data collection on a computerized database performed a retrospective chart review of psychogenic movement disorders involving the face. Patients with organic forms of facial dystonia or any medical or neurological disorder known to affect facial muscles were excluded. Sixty-one patients fulfilled the inclusion criteria for psychogenic facial movement disorders (91.8% females; age: 37.0 ± 11.3 years). Phasic or tonic muscular spasms resembling dystonia were documented in all patients most commonly involving the lips (60.7%), followed by eyelids (50.8%), perinasal region (16.4%), and forehead (9.8%). The most common pattern consisted of tonic, sustained, lateral, and/or downward protrusion of one side of the lower lip with ipsilateral jaw deviation (84.3%). Ipsi- or contralateral blepharospasm and excessive platysma contraction occurred in isolation or combined with fixed lip dystonia (60.7%). Spasms were reported as painful in 24.6% of cases. Symptom onset was abrupt in most cases (80.3%), with at least 1 precipitating psychological stress or trauma identified in 57.4%. Associated body regions involved included upper limbs (29.5%), neck (16.4%), lower limbs (16.4%), and trunk (4.9%). There were fluctuations in severity and spontaneous exacerbations and remissions (60%). Prevalent comorbidities included depression (38.0%) and tension headache (26.4%). Fixed jaw and/or lip deviation is a characteristic pattern of psychogenic facial movement disorders, occurring in isolation or in combination with other psychogenic movement disorders or other psychogenic features. © 2012 Movement Disorder Society

The diagnosis of psychogenic movement disorders (PMDs) may be challenging, given the lack of accurate and reliable tests.1 Two sets of clinical criteria, the Fahn-Williams (FW)2 and Shill-Gerber (SG)3 criteria, have been developed to assist in the diagnostic process and avoid the diagnosis-by-exclusion approach to PMD. Reliability and applicability of these criteria are essential because misdiagnosis may delay the initiation of appropriate treatment, leading to poor outcomes.4 We measured interobserver diagnostic agreement and clinical certainty judgment (according to FW and SG criteria) of PMD among movement disorder specialists (MDS) and general neurologists (non-MDS). We also examined whether diagnostic agreement based exclusively on motor phenomenology was satisfactory.

Psychogenic movement disorder is defined as abnormal movements unrelated to a medical cause and presumed related to underlying psychological factors. Although psychological factors are of both clinical and pathophysiological relevance, very few studies to date have systematically assessed their role in psychogenic movement disorder. We sought to assess the role of previous life stress using validated quantitative measures in patients with psychogenic movement disorder compared with age- and sex-matched healthy volunteers as well as a convenience sample of patients with focal hand dystonia. Sixty-four patients with psychogenic movement disorder (72% female; mean age, 45.2 years [standard deviation, 15.2 years]), 38 healthy volunteers (74% female; mean age, 49 years [standard deviation, 13.7 years]), and 39 patients with focal hand dystonia (37% female; mean age, 48.7 years [standard deviation, 11.7 years]) were evaluated using a standardized psychological interview as well as validated quantitative scales to assess trauma and previous stressors, depression, anxiety, and personality traits. Patients with psychogenic movement disorder reported higher rates of childhood trauma, specifically greater emotional abuse and physical neglect, greater fear associated with traumatic events, and a greater number of traumatic episodes compared with healthy volunteers and patients with focal hand dystonia controlled for depressive symptoms and sex (Bonferroni corrected P < .005). There were no differences in categorical psychiatric diagnoses or scores on childhood physical or sexual abuse subscales, personality traits, or the dissociative experience scale. Our findings highlight a biopsychosocial approach toward the pathophysiology of psychogenic movement disorder, although the association with psychological issues is much less prominent than expected compared with the nonepileptic seizure population. A careful psychological assessment is indicated to optimize therapeutic modalities.

Over the last 25 years, clinical neurophysiology has made many advances in the understanding, diagnosis, and even treatment of different movement disorders. Transcranial magnetic stimulation has been the biggest technical advance. Progress in pathophysiology includes improved knowledge about bradykinesia in Parkinson's disease, loss of inhibition and increased plasticity in dystonia, abnormal startle in hyperekplexia, and various features of psychogenic movement disorders that can aid diagnosis. Studies have been done looking at the use of noninvasive brain stimulation for therapy, but effects are generally small.

As the field of movement disorders has developed and matured over the past 25 years, psychogenic movement disorders have become increasingly recognized in subspecialty clinics. The diagnosis can be challenging and should be based on positive features rather than a purely exclusionary approach. The clinical phenotype can be quite varied, although certain categories of abnormal movement are more common than others. Electrophysiological studies may be particularly useful in establishing the diagnosis, especially with respect to tremor and myoclonus, and an argument can be made for adding a "laboratory-supported definite" category to earlier classification schemes. The diagnosis of psychogenic dystonia remains a major challenge, although there are some recent promising developments with respect to the evaluation of cortical plasticity that require further study. The pathogenesis of psychogenic movement disorders is poorly understood; insights may be provided from the study of other neurological conversion disorders such as psychogenic hemiparesis. Psychogenic movement disorders typically result in considerable disability and negatively impact quality of life to the same or greater extent than do many organic movement disorders. Treatment is extremely challenging, and many patients experience chronic disability despite various therapeutic interventions. Given the personal and societal impact of these problems, further advances in our understanding of their pathogenesis and the subsequent development of effective therapies are sorely needed.

Background: This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. Results: The signal-to-noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal-to-noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. Conclusions: These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal-to-noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society

Background: We report 4 patients with young-onset monogenetic parkinsonism, each of whom was misdiagnosed with either a psychogenic movement disorder or chronic fatigue syndrome for 10 to 23 years after the onset of their first symptoms. Results: Once the diagnosis was eventually made, they all had a rapid and excellent response to levodopa, albeit with the early appearance of interdose dyskinesias in 3. Conclusions: We discuss possible reasons for the missed diagnosis despite the relentless progression of their motor handicap. DAT scanning supported the revised clinical diagnosis of parkinsonism. V C 2011 Movement Disorder Society

Psychogenic paralysis presents a real treatment challenge. Despite psychotherapy, physiotherapy, antidepressants, acupuncture, or hypnosis, the outcome is not always satisfactory with persistent symptoms after long-term follow-up. We conducted a retrospective study to assess clinical features and to propose an alternative treatment based on repetitive transcranial magnetic stimulation (rTMS). Seventy patients (44 F/26 M, mean age: 24.7 +/- 16.6 years) experienced paraparesis (57%), monoparesis (37%), tetraparesis (3%), or hemiparesis (3%). A precipitating event was observed in 42 patients, primarily as a psychosocial event or a physical injury. An average of 30 stimuli over the motor cortex contralateral to the corresponding paralysis was delivered at low frequency with a circular coil. The rTMS was effective in 89% of cases, with a significantly better outcome for acute rather than chronic symptoms. In conclusion, motor cortex rTMS seem to be very effective in patients with psychogenic paralysis and could be considered a useful therapeutic option.

Although the understanding of dystonia has improved in recent years, primary dystonia is still insufficiently recognized and patients may not receive the correct diagnosis, leading to transient or permanent misclassification of their symptoms. We reviewed cases of primary dystonia who were at first misdiagnosed and analyzed the reasons why the correct diagnosis was first missed and later retained. Primary dystonia is misdiagnosed mainly, but not exclusively, in favor of other movement disorders: Parkinson's disease (PD), essential tremor, myoclonus, tics, psychogenic movement disorder (PMD), and even headache or scoliosis. Accounts are more numerous for PD and PMD, where diagnostic tests, such as DAT scan and psychological assessment, support clinical orientation. The correct diagnosis was achieved in all cases following the recognition of inconsistencies in the first judgment and of distinctive clinical features of dystonia. These clues have been collected here and assembled into a diagnostic epitome.

Recent developments in our understanding of psy- chogenic movement disorders have not yet led to advances in treatment. A potentially beneficial treatment strategy is sug- gestion, the voluntary use by the physicians of techniques that introduce into the patient's mind a belief that he or she will be healed. Principalism, the dominant school of contem- porary medical ethics, holds that the use of suggestion is not ethically justifiable because it undermines patient autonomy and degrades the doctor-patient relationship. However, evi- dence from a variety of sources (neuroimaging, anecdote, expert opinion, randomized controlled trials, and meta-analy- sis) supports the efficacy of suggestion as a treatment for psychogenic movement disorders. When issues of choice, consent, deceit, disclosure, and decision-making are analyzed from the perspective of an ethics of care, we see that sugges- tion may enhance patient autonomy and does not violate the trust between doctors and their patients. I conclude that sug- gestion is therefore an ethically justifiable treatment for patients with psychogenic movement disorders. 2010 Movement Disorder Society

Spinal Myoclonus (SM) is characterized by brief and sudden movements caused by the activation of muscles belonging to adjacent spinal myotomes. Recent reports have indicated that "typical" clinical and electrophysiological features of SM can be mimicked voluntarily. A useful tool that can distinguish between organic and psychogenic jerks is the detection of a Bereitschaftspotential (BP). In this study, we looked for evidence of a BP in a cohort of patients with idiopathic SM. A clinical and neurophysiological assessment of 20 patients affected by idiopathic SM was performed. A video EEG-EMG multichannel recording was performed in each patient to detect BP. An expert neurophysiologist (PB) reviewed the BP recordings and divided them into those showing a definite, possible, and no BP. A clinical assessment of the videoed movements was performed by two neurologists expert in movement disorders (KB and MJE) who indicated if the movements were compatible with organic or psychogenic myoclonus. A definite or possible BP was recorded in 15 out of 20 patients. Clinical raters agreed in their clinical opinion on 15 patients (75%). All patients where both raters agreed the movements appeared to be organic had definite or possible BP. BP are commonly seen in patients with idiopathic SM. There is discordance between clinicians in their clinical rating of SM as organic or psychogenic, but even in those patients where movements appear clinically to be organic, a BP is commonly detected, indicating that the aetiology is psychogenic. This suggests that BP recordings are a useful adjunct to clinical assessment in the accurate diagnosis of patients with idiopathic SM.

Five hundred and nineteen members of the Movement Disorder Society completed a 22-item questionnaire probing diagnostic and management issues in psychogenic movement disorders (PMD). When patients showed definite evidence of PMD with no other unexplained clinical features, approximately 20% said they informed patients of the diagnosis and requested no further neurological testing. The 51% who reported conducting standard neurological investigations to rule out organic causes before presenting the diagnosis to such patients had fewer years of fellowship training and fewer PMD patients seen per month. A non-PMD diagnosis was correlated with patients' normal social or personal functioning, little or no employment disruption, lack of non-physiologic findings, and lack of psychiatric history. Ongoing litigation was more predictive of the PMD diagnosis for US compared to non-US respondents. Two thirds of respondents, more commonly younger and academic clinician researchers, refer PMD patients to a psychiatrist or mental health specialist while also providing personal follow up. Physician reimbursement, insurability of PMD patients, and ongoing litigation interfered with managing PMD patients to a greater extent in the US compared to non-US countries. Acceptance of the diagnosis by the patient and identification and management of psychological stressors and concurrent psychiatric disorders were considered most important for predicting a favorable prognosis. These findings suggest that expert opinions and practices related to diagnosing and managing PMD patients differ among movement disorders neurologists. Some of the discrepancies may be accounted for by factors such as training, type of practice, volume of patients, and country of practice, but may also reflect absence of practice guidelines.

Inadequate coping strategies may cause some patients to develop psychogenic symptoms in periods of stress. This may be more prominent in patients with lower intelligence levels. Twenty-six patients with psychogenic neurological disorders (PND) were tested for coping abilities and intelligence and compared with 18 healthy controls and 26 patients with various nonpsychogenic disorders. Patients with PND have slightly lower IQ levels and active coping skills compared with healthy controls but not to nonpsychogenic patients. Low IQ was not associated with low active coping skills in either of the groups. Low active coping is not the result of low IQ and is not specific for psychogenic symptoms. At least part of the lower coping skills reported in patients with psychogenic symptoms may be the result of having an illness in general. (C) 2009 Movement Disorder Society

Patients admitted to movement disorders outpatient unit at a university hospital between January 2002 and June 2007 were screened for psychogenic movement disorders (PMDs). Out of 1,743 patients, 49 patients (2.8%), including four children, were diagnosed to have PMDs. Women to men ratio was 34/15. The mean age and the age-at-onset were 41 +/- 17 years and 36 +/- 15 years in the adult group, and 10 +/- 2 and 9 +/- 2 years in children. Among the whole group, 44% had tremor, 24% dystonia, 12% pure gait disorders, 8% parkinsonism, 6% chorea-ballism, and 4% tic disorder. PMD developed acutely in 85% of patients, and distractibility was observed in 83%. Of the patients, 81% met the criteria for clinically established PMD, whereas 16% for documented and 2% for probable PMD. Although our data was obtained from a different culture, our results showed that hospital-based frequency and phenomenological features between our PMD group and previously reported ones are similar.

Psychogenic movement disorders (PMDs) are well characterized in adults, but childhood-onset PMDs have not been extensively studied. We reviewed the medical records of children who were diagnosed in our clinic with PMDs since 1988 and identified 54 patients with PMDs, representing 3.1% of our pediatric movement disorder population and 5.7% of all PMD cases. The mean age at symptom onset was 14.2 years (+/-2.11, range 7.6-17.7). Similar to published data in adults, two-thirds of children exhibited multiple PMD phenotypes, the most common being tremor followed by dystonia and myoclonus. Most PMDs were abrupt in onset, paroxysmal and triggered by identifiable physical or psychological trauma. As in adults, childhood PMDs were more likely to affect females, but there was no female predominance in children less than 13 years old. Although prior studies suggest that medically unexplained symptoms beginning in childhood often follow a benign course, this cohort of children experienced marked disability and morbidity related to PMDs, including prolonged school absences and unnecessary surgical procedures in more than one-fifth of patients.

We describe the presenting features and long-term outcomes of patients with electrophysiologically-confirmed psychogenic tremor. Clinical information for all patients with psychogenic tremor confirmed by our Movement Disorders Neurophysiology Laboratory (2003-2004) was reviewed. A follow-up questionnaire was administered to all included patients in 2007. Psychogenic tremor was documented in 62 patients; 33 responded to the questionnaire (53%). Median onset-age was 50 years (range, 15-71); 23 were female (70%). Clinical certainty of psychogenic etiology was: definite, 8 (24%); probable, 16 (49%), and possible, 9 (27%). Characteristic electrodiagnostic features of psychogenic tremor were documented in all. All but two patients were ultimately given a definite diagnosis of psychogenic tremor; recommended psychiatric consultation was only done by 12 (36%). Twenty-one patients (64%) rated tremor disability as moderate or severe after a median follow-up of 5.1 years (range, 3.3-19). Improvement occurred spontaneously in 5 (15%), and after a specific intervention in 4 (12%), whereas 3 (9%) had mild but unchanged symptoms. The mean duration of symptoms, prior to diagnosis with psychogenic tremor, was significantly shorter for patients with mild or no tremor at follow-up (P = 0.037). Physiologically-confirmed psychogenic tremor carries a poor prognosis, with unremitting or worse tremor persisting 3-years after diagnosis in most.

The Greek term astasia-abasia literally translates to mean inability to stand and to walk. Although today we would classify the syndrome as a conversion disorder, it was considered a separate disease by Paul Blocq (1860-1896), who described this phenomenon as the inability to maintain an upright posture, despite normal function of the legs in the bed. Paul Blocq's original 1888 articles on astasia abasia were read, partly translated from French to English, and the cases were summarized. A review of a selection of the literature following Blocq's description on astasia abasia was performed. Present day literature was consulted as well. Blocq reviewed what was known about astasia abasia in two papers. Although he was the first to use the combined term astasia abasia, he referred to similar descriptions of Charcot, Richer, Mitchell, Jaccoud, Roméi, and Erlenmeyer. Blocq's contribution was in compiling the experiences and observations of preeminent 19th century neurologists. He recognized that paralysis, jumping, fits, tremor, and bizarre behavior could all be associated with the syndrome. He distinguished the disorder from hysteria. Moreover, he presented a formal delineation of the gait disorder and provided a pathophysiologic concept. Prognosis was considered favorable. Paul Blocq directed attention to psychogenic gait disorders by publishing a small case series on astasia abasia. Today, these case descriptions would be likely considered cases of conversion or psychogenic gait disorder, with or without other conversion/psychogenic movement disorders.

Despite recent advances, psychogenic movement disorder (PMD) remains a poorly understood phenomenon. Emotional functioning and responsiveness to stress are believed to play a role in the development of psychogenic symptoms, but empirical studies examining emotional responsiveness in PMD and other conversion disorders are lacking. We investigated modulation of the startle eyeblink reflex by affective pictures in 12 patients with PMD and 12 age- and education-matched control participants. Participants viewed positive, neutral, and negative pictures, while eyeblink responses to white noise bursts were recorded. Control participants showed the expected pattern of startle modulation, with significant potentiation by negative pictures and slight (nonsignificant) inhibition by positive pictures. In the PMD group, however, both positive and negative pictures yielded significantly greater startle responses than neutral pictures. Depression and anxiety symptomatology did not correlate with startle modulation, and the two groups did not differ in self-reported emotional reactions to the pictures. Our findings suggest that individuals with PMD show aversive physiological reactions to positive as well as negative stimuli. Abnormal affective startle modulation may be used to help distinguish between malingering and PMD. Future studies using larger samples are needed to better understand the role of emotions in conversion disorder. © 2007 Movement Disorder Society

Patients with psychogenic movement disorders (PMD) often report severe impairment, yet the impact of PMD on disability and quality of life has not been examined. We compared 66 patients with PMD and 704 patients with Parkinson's disease (PD) on measures of disability (Older Americans Resources and Services Scale, OARS); quality of life (QOL; SF-12v2 Health Survey) and psychiatric symptomatology (Brief Symptom Inventory 18, BSI-18). On the total OARS, PMD and PD patients reported similar levels of disability (17.6 +/- 6.6, 19.8 +/- 10.9, P = 0.490 at "best" function and 24.1 +/- 11.2, 26.2 +/- 14.3, P = 0.497 at their "worst" function). PMD patients reported similar Physical Health QOL to PD patients (38.9 +/- 14.5, 39.8 +/- 11.6, P = 0.652) but worse mental health QOL (41.6 +/- 13.4 vs. 48.9 +/- 11.0, P < 0.001). On the BSI-18, PMD patients reported higher levels of distress on the Global Symptom Index (62.03 +/- 9.6 vs. 53.7 +/- 9.9, P < 0.001) and on Anxiety, Depression and Somatization subscales (PMD vs. PD scores: Anxiety 58.9 +/- 12.0 vs. 52.3 +/- 10.1, P < 0.001; Depression 58.8 +/- 11.9 vs. 51.3 +/- 10.3, P < 0.001; Somatization 60.5 +/- 11.0 vs. 54.7 +/- 8.7, P < 0.001). Thus, severity of disability reported by the PMD group was equal to that seen in a progressive neurodegenerative condition. Quality of life and mental health implications of PMD were also evident. PMD impacts several aspects of patient function and daily life.

Psychogenic Parkinsonism (PsyP) can be clinically difficult to differentiate from Parkinson's disease (PD). Striatal dopamine transporter (DAT) imaging could be helpful in differentiating them. We performed 123I-Ioflupane single-photon emission computed tomography (SPECT) in 9 patients with suspected PsyP. In 1 patient, 123I-Ioflupane SPECT disclosed bilateral decrease of striatal tracer uptake that indicated nigrostriatal degeneration. In this patient, a parkin gene mutation was detected. In the other 8 patients, 123I-Ioflupane SPECT was normal and supported the initial suspicion of PsyP. Normal DAT imaging supports the diagnosis of PsyP, whereas reduced striatal tracer uptake suggests an underlying neurodegenerative Parkinsonism and should encourage the search for additional causes for the syndrome. © 2006 Movement Disorder Society

We evaluated the concordance between independent clinical, electrophysiological, and [123I]-FP-CIT SPECT scan explorations as a staged procedure for an accurate diagnosis in 9 patients referred with a diagnosis of suspected psychogenic parkinsonism. Three patients were reclassified as pure psychogenic parkinsonism (PP), 6 with a form of combined psychogenic parkinsonism and Parkinson's disease (PP + PD), and none with pure Parkinson's disease (PD). Electrophysiological recordings showed the characteristics of psychogenic tremor in 5 of 7 patients with tremor. In two of these 5, PD tremor was also recorded. SPECT scan results were abnormal in five of 9 patients. In one case of clinically suspected PP + PD, SPECT scan results were normal. Long-term follow-up supported the final diagnosis of PP (initial clinical misdiagnosis). Electrophysiology contributes to the clinical diagnosis of psychogenic tremor and may help confirm associated organic PD tremor. [123I]-FP-CIT SPECT is a robust test to ascertain dopaminergic denervation and increase the confidence of the clinical and electrophysiological diagnosis of associated PD. A combination of clinical, electrophysiological, and [123I]-FP-CIT SPECT scan explorations improves diagnostic accuracy in order to distinguish PP from PP + PD. © 2005 Movement Disorder Society

Dyskinesias are known to occur in many patients with Parkinson's disease treated with dopaminergic drugs but to date, drug-induced dyskinesias have not been observed in humans with no underlying basal ganglia disorder. We describe a patient with psychogenic parkinsonism and intravenous apomorphine abuse leading to subsequent choreatiform dyskinesias.

The differentiation of psychogenic from organic tremors, particularly those of a dystonic nature, can be difficult on clinical grounds. Entrainment of tremulous movements of different body parts into a single rhythm has been used clinically as a means of distinguishing these tremor forms, based on the inability of a patient with hysterical tremor to generate voluntary tapping oscillations independent of their ongoing tremor oscillation. The coherence entrainment test is a quantified electrophysiological entrainment test performed on accelerometer or surface EMG tremor signals. This test was carried out on 25 patients referred with suspected psychogenic tremor or dystonic tremor and on 10 normal subjects attempting to tap two independent voluntary oscillations. Using established and new clinical diagnostic criteria, patients were assigned the following final clinical diagnoses: 6 cases of clinically definite dystonic tremor, 5 cases of probable dystonic tremor, 2 cases of classic essential tremor, 5 cases of clinically definite psychogenic tremor, 3 cases of probable psychogenic tremor and 4 uncertain cases. On comparing these clinical diagnoses with those reached by a coherence entrainment test subsequently carried out on each patient, there was 100% concordance in both clinically definite and clinically probable patients. In uncertain cases, when later clinical information came to light, this also corroborated with the coherence entrainment diagnosis. No normal subjects were able to "mimic" organic tremor. The coherence entrainment test appears to be a sensitive and specific means of distinguishing psychogenic tremor from dystonic and other organic tremors.

The development of abnormal posturing of the neck or shoulder after local injury has been termed posttraumatic cervical dystonia (PTCD). Certain features seem to distinguish a unique subgroup of patients with this disorder from those with features more akin to typical idiopathic cervical dystonia, such as onset and maximum disability that occurs very quickly after injury, severe pain and a fixed abnormal posture. In an attempt to clarify the nature of this syndrome further, we evaluated 16 such patients (8 men, 8 women). Motor vehicle accident and work-related injuries were common precipitants, with posturing usually developing shortly after trauma, and little progression occurring after the first week. A characteristic, painful, fixed head tilt and shoulder elevation were present in all but one patient, who had a painless elevated shoulder and painful contralateral shoulder depression, as well as nondermatomal sensory loss in 14 patients. Additional abnormalities included dystonic posturing in a limb (2 patients) or jaw (1 patient), limb tremor (3 patients) and "give-way" limb weakness (8 patients). The tremor and the jaw dystonia demonstrated features suggestive of a psychogenic movement disorder, most commonly distractibility. Litigation or compensation was present in all 16 patients. Intravenous sodium amytal improved the posture, pain or both in 13 of 13 patients; in 7 of 13 the sensory deficit either markedly improved or normalized. General anesthesia demonstrated full range of motion in all 5 patients assessed. Psychological evaluations suggested that psychological conflict, stress, or both were being expressed via somatic channels in 11 of 12 tested patients. Our results suggest an important role of psychological factors in the etiology or maintenance of abnormal posture, pain and associated disability of these patients. The role of central factors triggered in psychologically vulnerable individuals after physical trauma is discussed. We propose that the disorder be referred to as "posttraumatic painful torticollis" rather than characterize it as a form of dystonia until further information on its pathogenesis is forthcoming.

Parkinson's syndrome (PS) is frequently encountered in disorders associated with prominent degeneration of the nigrostriatal pathway as in Parkinson's disease, multisystem atrophy, and progressive supranuclear palsy (presynaptic PS). Drug-induced parkinsonism, a common, underdiagnosed health problem and psychogenic parkinsonism are causes of Parkinson's syndrome which, evidence suggests, occurs without degeneration of nigrostriatal structures. We review clinical features and results of DAT imaging in drug-induced parkinsonism and psychogenic parkinsonism. These two conditions normally give normal striatal DAT imaging results; an abnormal result in either case could exclude both conditions, corroborating a diagnosis of organic parkinsonism in uncertain cases.

We describe three patients who presented with 4 to 5 Hz tremors of the suprahyoid region of the neck. Two developed their tremors in association with levosulpiride treatment. When they opened their mouths, the neck tremors disappeared; no tongue tremors were observed. However, a videofluoroscopic examination showed the presence of tongue tremors at rest. The remaining patient had a psychogenic tremor.

Contains fulltext : 53696.pdf (Publisher’s version ) (Closed access) Psychogenic movement disorders are common in everyday neurological practice, comprising up to 25% of the patient population in movement disorders clinics. The diagnosis is often difficult, as is illustrated by the high proportion of patients with an organic neurological disease whose movement disorder is misdiagnosed as psychogenic. Here, we describe a woman with a longstanding and treatment-resistant psychogenic movement disorder that responded dramatically to acupuncture. The diagnostic and therapeutic merits of acupuncture are discussed.

Psychogenic tremor has become a rare movement disorder. Twenty-five patients from our movement disorder unit presented either with obviously nonorganic body shaking during stance or with extremity tremors. A sudden onset and a variable but rarely remitting course of the condition was common. The "coactivation sign of psychogenic tremor" and absent finger tremor were the most consistent criteria to separate them from organic tremors. Quantitative analysis of tremor shows decreasing amplitudes in most organic tremors when the extremity is loaded with additional weights. In contrast, we found an increase of tremor amplitude for most of the cases with psychogenic tremor. This might be caused by increased coactivation to maintain the oscillation. These clinical and electrophysiological features suggest a clonus mechanism induced by coactivation as the pathophysiological basis of psychogenic extremity tremor. Psychiatric evaluation did not show overt signs of hysteria for the majority of the patients. However, we found depression and functional somatic or psychosomatic conditions to be frequent among the patients. A reduced ability to cope with stressful situations may play a significant role. The clinical course of the condition is usually far from benign. We conclude that psychogenic tremor can be positively diagnosed by means of neurologic signs in the majority of patients and is not only a diagnosis of exclusion. The poor outcome makes early and serious neuropsychiatric attempts at therapy necessary.

We report on a 45-year-old man with a history of multiple psychiatric admissions for a gait disorder and episodic weakness thought to be psychogenic who was subsequently diagnosed with status cataplecticus due to narcolepsy. The gait difficulties resolved with venlafaxine. This case demonstrates that status cataplecticus can be misdiagnosed as a psychogenic gait disorder.

Recent criteria for the classification of palatal tremor use clinical, imaging, and electrophysiological features to differentiate essential and symptomatic forms. A case of probable psychogenic palatal tremor (PPT) is described within the context of these criteria, which lack clear guidelines for diagnosing PPT. The heterogenous nature of essential palatal tremor and its relationship with PPT, voluntary palatal movements, and tics is discussed.

Two schoolboys with diagnostic criteria for psychogenic movement disorder (PMD) are described: one with bizarre tremor of the right hand and a very slow and cautious gait, another with exaggerated trunk sway and collapses during standing and walking.