Movement disorders : official journal of the Movement Disorder Society
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Rapid eye movement sleep behavior disorder is characterized by dream enactment and complex motor behaviors during rapid eye movement sleep and rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia) during polysomnography. Rapid eye movement sleep behavior disorder may be idiopathic or symptomatic and in both settings is highly associated with synucleinopathy neurodegeneration, especially Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. Rapid eye movement sleep behavior disorder frequently manifests years to decades prior to overt motor, cognitive, or autonomic impairments as the presenting manifestation of synucleinopathy, along with other subtler prodromal "soft" signs of hyposmia, constipation, and orthostatic hypotension. ⋯ Patients with rapid eye movement sleep behavior disorder are frequently prone to sleep-related injuries and should be treated to prevent injury with either melatonin 3-12 mg or clonazepam 0.5-2.0 mg to limit injury potential. Further evidence-based studies about rapid eye movement sleep behavior disorder are greatly needed, both to enable accurate prognostic prediction of end synucleinopathy phenotypes for individual patients and to support the application of symptomatic and neuroprotective therapies. Rapid eye movement sleep behavior disorder as a prodromal synucleinopathy represents a defined time point at which neuroprotective therapies could potentially be applied for the prevention of Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. © 2017 International Parkinson and Movement Disorder Society.
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Alterations of circadian rhythms are among the most debilitating non-motor symptoms in Parkinson's Disease (PD). Although a growing awareness towards these symptoms has occurred during the last decade, their underlying neuropathophysiology remains poorly understood and consequently no effective therapeutic strategies are available to alleviate these problems. ⋯ Here I dissect, over disease progression, the relative causal contribution to health impairments in PD patients of dysfunctions in the different components of the neural network governing circadian rhythms. A deeper understanding of these mechanisms will provide not only a greater understanding of disease neuropathology, but also hold the promise for effective therapies. © 2016 International Parkinson and Movement Disorder Society.
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Disruption in cerebellar and basal ganglia networks during a visuospatial task in cervical dystonia.
Although dystonia is traditionally conceptualized as a basal ganglia disorder, increasing interest has been directed at a different neural network node, the cerebellum, which may play a significant role in the pathophysiology of dystonia. Abnormal sensorimotor processing and disturbed motor schemes, possibly attributable to cerebellar changes, remain unclear. ⋯ This promotes the view that dystonia results from miscommunication between the basal ganglia and cerebellar loops, thus providing new insights into the brain regions essential for the development of cervical dystonia. © 2017 International Parkinson and Movement Disorder Society.
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Essential Tremor (ET) is a common movement disorder that can be disabling. Initial treatment is in the form of medical therapies. Patients with medically refractory ET seek surgical intervention which include radiofrequency thalamotomy, deep brain stimulation, and radiosurgical thalamotomy. Radiosurgical thalamotomy is a minimally invasive surgical option which is especially valuable for elderly and high surgical risk patients. ⋯ Radiosurgery is a safe and valuable treatment option for medically refractory essential tremor, especially for the elderly or those with high surgical risk for DBS or radiofrequency thalamotomy. © 2017 International Parkinson and Movement Disorder Society.
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Executive functions including behavioral adaptation and impulse control are commonly impaired in movement disorders caused by striatal pathology. However, as yet it is unclear what aspects of behavioral abnormalities are related to pathology in which striatal subcomponent, that is, the matrix and the striosomes. We therefore studied cognitive control in X-linked dystonia-parkinsonism, a model disease of striosomal degeneration, using behavioral paradigms and EEG. ⋯ This dissociable pattern of cognitive deficits most likely reflects predominant dysfunction of the striosomal compartment and its connections to the anterior cingulate cortex in X-linked dystonia-parkinsonism. The results underscore the importance of striosomes for cognitive function in humans and suggest that striosomes are relays of error-related behavioral adaptation but not inhibitory control. © 2017 International Parkinson and Movement Disorder Society.