Movement disorders : official journal of the Movement Disorder Society
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Randomized Controlled Trial Comparative Study Clinical Trial
Long-term benefits of rivastigmine in dementia associated with Parkinson's disease: an active treatment extension study.
In patients with dementia associated with Parkinson's disease (PD), the efficacy and safety of rivastigmine, an inhibitor of acetylcholinesterase and butyrylcholinesterase, were previously demonstrated in a 24-week double-blind placebo-controlled trial. Our objective was to determine whether benefits were sustained over the long term. Following the double-blind trial, all patients were permitted to enter an active treatment extension study, during which they received rivastigmine 3-12 mg/day. ⋯ Placebo patients switching to rivastigmine for the active treatment extension experienced a mean cognitive improvement similar to that of the original rivastigmine group during the double-blind trial. The adverse event profile was comparable to that seen in the double-blind trial. Long-term rivastigmine treatment appeared well tolerated and may provide sustained benefits in dementia associated with PD patients who remain on treatment for up to 48 weeks.
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The disease-specific Unified Multiple System Atrophy Rating Scale (UMSARS) has been developed recently and validated for assessing disease severity in multiple system atrophy (MSA). Here, we aimed at (1) assessing rates of disease progression in MSA and (2) validating UMSARS for sensitivity to change over time. Impairment was assessed at two time points 12 months apart using UMSARS Part I (historical review), UMSARS Part II (motor examination), as well as measures of global disease severity, including UMSARS Part IV, Hoehn and Yahr (HY) Parkinson's disease staging, Schwab England Activities of Daily Living (SE ADL), and a three-point global Severity Scale (SS3). ⋯ Furthermore, the increases in HY staging, SE ADL and SS3 correlated significantly with UMSARS I, UMSARS II, and UMSARS IV progression. This report is the first prospective study showing rapid annual UMSARS rates of decline in MSA. Our data contribute to the ongoing validation process of UMSARS, and they facilitate the planning and implementation of future neuroprotective intervention trials.
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Comparative Study
Cortical atrophy in the cerebellar variant of multiple system atrophy: a voxel-based morphometry study.
This study aimed to determine in vivo the atrophy patterns in clinically established cerebellar variant of multiple-system atrophy (MSA-C) using voxel-based morphometry (VBM). Thirteen patients with MSA-C (12 probable, 1 possible) and 13 healthy controls matched for age and sex were included. High-resolution MR images were acquired with a 1.5 T scanner. ⋯ A negative correlation was observed between a cerebellar ataxia score and the volume of cerebellar hemispheres, peduncles, and pons. To compare this atrophy pattern to that of spinocerebellar ataxia (SCA2), which was previously reported by our group, a conjunction analysis was assessed. We observed a volume loss shared by both disorders comprising the cerebellum, vermis, pons, mesencephalon, orbitofrontal, mid-frontal, and temporomesial cortex of both hemispheres as well as the left insular cortex.
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Comment Letter Comparative Study
Glucocerebrosidase mutations are also found in subjects with early-onset parkinsonism from Venezuela.
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To test the hypothesis that reduced reactions to proprioceptive input signals contribute to postural instability in Parkinson's disease (PD), pulses of mechanical vibration were applied to the neck muscles of PD patients and healthy controls. This stimulus elicits postural reactions in standing subjects. Participating were 13 moderately affected PD patients, 13 severely affected PD patients, and 13 age-matched healthy subjects. ⋯ Comparison of the measures during on and off testing revealed no significant differences. These results indicate that neither afferent proprioceptive deficits nor central integrative functions but rather scaling and habituation of erroneous proprioceptive information are disturbed in the postural control of advanced PD. Nondopaminergic structures seem to be responsible for this impairment.