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121.
Probable RBD and association with neurodegenerative disease markers: A population‐based study
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Philipp Mahlknecht MD PhD Klaus Seppi MD Birgit Frauscher MD Stefan Kiechl MD Johann Willeit MD Heike Stockner MD Atbin Djamshidian MD PhD Michael Nocker MD Verena Rastner MD Michaela Defrancesco MD PhD Gregor Rungger MD Arno Gasperi MD Werner Poewe MD Birgit Högl MD 《Movement disorders》2015,30(10):1417-1421
122.
Johannes?LevinEmail author Sylvia?Maa? Madeleine?Schuberth Gesine?Respondek Friedemann?Paul Ullrich?Mansmann Wolfgang?H.?Oertel Stefan?Lorenzl Florian?Krismer Klaus?Seppi Werner?Poewe Gregor?Wenning The PROMESA study group Armin?Giese Kai?B?tzel Günter?H?glinger 《Journal of neural transmission (Vienna, Austria : 1996)》2016,123(4):439-445
Formation of toxic α-synuclein oligomers appears to be a key underlying pathological mechanism of synucleinopathies such as Parkinson’s disease or multiple system atrophy (MSA). Given that Epigallocatechin-gallate has been shown to inhibit α-synuclein aggregation, it might represent a causal treatment option. Therefore, we set out to evaluate the safety, tolerability and a potential disease-modifying effect of Epigallocatechin-gallate in patients with MSA after 48 weeks of treatment. Power calculation was performed on existing natural history data on the progression of the Unified MSA Rating Scale as primary readout parameter. To assess the efficacy of Epigallocatechin-gallate versus placebo regarding the reduction of disease progression measured during the study period (80 % power, 5 % p level, 50 % effect size) 36 patients per group are needed. Considering a drop-out rate of 20 % a total of 86 patients will be recruited in this multicentre study. These data provide a solid rationale to investigate whether supplementation of Epigallocatechin-gallate can delay the progression of the MSA-related disability. 相似文献
123.
124.
Rissling I Frauscher B Kronenberg F Tafti M Stiasny-Kolster K Robyr AC Körner Y Oertel WH Poewe W Högl B Möller JC 《Sleep》2006,29(1):108-111
STUDY OBJECTIVE: A preliminary study by our group suggested an association between daytime sleepiness and the catechol-O-methyltransferase (COMT) val158met polymorphism (rs4680) in patients with Parkinson disease (PD). We sought to confirm this association in a large group of patients with PD. DESIGN: Genetic association study in patients with PD. SETTING: Movement disorder sections at 2 university hospitals. PARTICIPANTS: PD patients with and without episodes of suddenly falling asleep matched for antiparkinsonian medication, disease duration, sex, and age, who participated in a previous genetic study on dopamine-receptor polymorphisms. INTERVENTIONS: Not applicable. MEASUREMENTS AND RESULTS: In this study, 240 patients with PD (154 men; age 65.1 +/- 6.1 years; disease duration 9.4 +/- 6.0 years) were included. Seventy had the met-met (LL), 116 the met-val (LH), and 54 the val-val (HH) genotype. In the combined LL+LH group (featuring reduced COMT activity), the mean Epworth Sleepiness Scale (ESS) score was 9.0 +/- 5.9 versus 11.0 +/- 6.1 in the HH (high COMT activity) group (P = .047). Forty-seven percent of the LL and LH patients had sudden sleep onset compared with 61% of the HH patients (P = .07). Logistic regression, however, showed that both pathologic ESS scores (i.e., > 10) and sudden sleep onset were predicted by subjective disease severity (P < .001 each) but not by the COMT genotype. CONCLUSIONS: Our previous finding that the L-allele may be associated with daytime sleepiness could not be confirmed in the present study. Altogether, our data do not support a clinically relevant effect of the COMT genotype on daytime sleepiness in PD. 相似文献
125.
The present review shows that vascular parkinsonian syndrome (VPS) fulfilling stringent diagnostic criteria for parkinsonism is a rare disease that cannot always be distinguished from neurodegenerative parkinsonism on clinical grounds. Thus VPS needs to be differentiated from other disturbances, which have distinct phenomenological and therapeutical features including isolated gait disturbances associated with subcortical arteriosclerotic encephalopathy and neurodegenerative parkinsonism complicated by comorbid vascular encephalopathy. Acute or subacute VPS is usually caused by contralateral infarctions involving the external globus pallidus, ventrolateral thalamus, and, less often, the substantia nigra. Chronic VPS with insidious onset is related to bilateral subcortical infarctions affecting thalamocortical projections. Differentiation from degenerative parkinsonism is difficult in cases of VPS that display a progressive course and response to levodopa. 相似文献
126.
Giladi N Fichtner A Poewe W Boroojerdi B 《Journal of neural transmission (Vienna, Austria : 1996)》2010,117(12):1395-1399
This open-label study (NCT00243945) investigated the efficacy of rotigotine transdermal system in 54 Parkinson’s disease (PD)
patients with unsatisfactory control of early morning motor impairment and sleep disturbances. Rotigotine dose was up titrated
for 8 weeks and maintained for 4 weeks. Mean rotigotine dose at end of maintenance was 11.83 mg/24 h (SD 3.86). Patients had
two overnight hospital stays at baseline and end of treatment during which early morning motor performance was assessed, prior
to first morning dose of regular oral antiparkinsonian medication. Rotigotine improved mean Unified Parkinson’s Disease Rating
Scale (UPDRS) part III score by −9.3 points, mean Timed Up and Go test duration by −1.4 s and mean morning finger tapping
by 26.5 taps/min; 46% of patients were considered responders (≥30% improvement of UPDRS III). Mean Nocturnal Akinesia, Dystonia
and Cramps Sum Score was reduced by 61%; mean number of nocturias decreased by 32%. Rotigotine also improved sleep quality.
These results suggest a role for rotigotine in treatment of nocturnal and early morning motor disabilities in PD patients. 相似文献
127.
Karla Eggert MD David Squillacote MD Paolo Barone MD Richard Dodel MD Regina Katzenschlager MD Murat Emre MD Andrew J. Lees MD Olivier Rascol MD PhD Werner Poewe MD Eduardo Tolosa MD Claudia Trenkwalder MD Marco Onofrj MD Fabrizio Stocchi MD PhD Giuseppe Nappi MD Vladimir Kostic MD Jagoda Potic MD Evzen Ruzicka MD DSc Wolfgang Oertel MD and in cooperation with the German Competence Network on Parkinson's Disease 《Movement disorders》2010,25(7):896-905
Perampanel, a novel, noncompetitive, selective AMPA‐receptor antagonist demonstrated evidence of efficacy in reducing motor symptoms in animal models of Parkinson's disease (PD). We assessed the safety and efficacy of perampanel for treatment of “wearing off” motor fluctuations in patients with PD. Patients (N = 263) were randomly assigned to once‐daily add‐on 0.5, 1, or 2 mg of perampanel or placebo. The primary objective was to determine whether there was a dose‐response relationship for efficacy among the 3 perampanel doses and placebo. The primary efficacy endpoint for each treatment was measured as the least‐squares (LS) mean change from baseline to week 12 in percent “off” time reduction during the waking day, as recorded by patient diaries. The primary efficacy analysis was a 1‐sided Williams test for dose‐response trend at the 0.025 level of significance. At week 12, dose‐response trends, as determined by the Williams test, were not statistically significant for LS mean reduction in percent “off” time during the waking day (P = 0.061, with significance defined as P ≤ 0.025). The 2 higher perampanel doses (ITT population; n = 258) produced nonsignificant reductions from baseline to week 12 in percent “off” time during the waking day versus placebo (7.59%, P= 0.421 [1 mg], 8.60%, P = 0.257 [2 mg] versus 5.05% [placebo]; significance for pairwise comparisons defined as P ≤ 0.05). There were no significant changes in dyskinesia or cognitive function in any perampanel group versus placebo. Adverse events were similar across treatment groups. Perampanel treatment was well tolerated and safe, but failed to achieve statistical significance in primary and secondary endpoints. © 2010 Movement Disorder Society 相似文献
128.
Elisabeth Wolf MD Klaus Seppi MD Regina Katzenschlager MD Guenter Hochschorner MD Gerhard Ransmayr MD Petra Schwingenschuh MD Erwin Ott MD Iris Kloiber MD Dietrich Haubenberger MD Eduard Auff MD Werner Poewe MD 《Movement disorders》2010,25(10):1357-1363
Several randomized placebo‐controlled trials have consistently shown antidyskinetic effects of amantadine in levodopa treated patients with advanced Parkinson's disease (PD). However, all of these were of short duration and there have been claims that the effect of amantadine on levodopa induced dyskinesias (LID's) wear off after about 9 months of treatment. This randomized placebo‐controlled parallel‐group study was performed to assess the long‐term antidyskinetic effect of amantadine in 32 PD patients, who after having been on stable amantadine therapy for LID over at least one year‐ were switched in a double blind manner to amantadine or placebo and followed for 3 weeks. Dyskinesia duration and intensity were assessed by UPDRS IV items 32 and 33 as well as by patient's diaries. The primary outcome was the score change of UPDRS IV items 32 + 33 between baseline and 3 weeks after treatment as well as the between treatment group comparison of the score change of UPDRS IV items 32 + 33. There was a significant increase of UPDRS IV items 32 + 33 in patients treated with placebo from 3.06 (95% CI, 2.1–4.03) at baseline to 4.28 (95% CI, 3.1–5.4) at three‐week follow‐up (P = 0.02) compared with no significant change between baseline 3.2 (95% CI, 2.1–4.4) to follow‐up 3.6 (95% CI, 2.3–4.8) in patients staying on amantadine. These findings argue for long‐term antidyskinetic efficacy of amantadine in PD patients with LID's. © 2010 Movement Disorder Society 相似文献
129.
Wenning GK Stefanova N Jellinger KA Poewe W Schlossmacher MG 《Annals of neurology》2008,64(3):239-246
To this day, the cause of multiple system atrophy (MSA) remains stubbornly enigmatic. A growing body of observations regarding the clinical, morphological, and biochemical phenotypes of MSA has been published, but the interested student is still left without a clue as to its underlying cause. MSA has long been considered a rare cousin of Parkinson's disease and cerebellar degeneration; it is rich in acronyms but poor in genetic and environmental leads. Because of the worldwide research efforts conducted over the last two decades and the discovery of the alpha-synuclein-encoding SNCA gene as a cause of rare familial Parkinson's disease, the MSA field has seen advances on three fronts: the identification of its principal cellular target, that is, oligodendrocytes; the characterization of alpha-synuclein-rich glial cytoplasmic inclusions as a suitable marker at autopsy; and improved diagnostic accuracy in living patients resulting from detailed clinicopathological studies. The working model of MSA as a primary glial disorder was recently strengthened by the finding of dysregulation in the metabolism of myelin basic protein and p25alpha, a central nervous system-specific phosphoprotein (also called tubulin polymerization promoting protein, TPPP). Intriguingly, in early cases of MSA, the oligodendrocytic changes in myelin basic protein and p25alpha processing were recorded even before formation of glial cytoplasmic inclusions became detectable. Here, we review the evolving concept that MSA may not just be related to Parkinson's disease but also share traits with the family of demyelinating disorders. Although these syndromes vary in their respective cause of oligodendrogliopathy, they have in common myelin disruption that is often followed by axonal dysfunction. 相似文献
130.
Peralta C Stampfer-Kountchev M Karner E Köllensperger M Geser F Wolf E Seppi K Benke T Poewe W Wenning GK 《Journal of neural transmission (Vienna, Austria : 1996)》2007,114(5):585-588
Summary. To compare frequency and degree of orthostatic hypotension (OH) in Parkinson’s disease (PD) and Parkinson’s disease with dementia
(PDD) and its effect on attention and word fluency, blood pressure (BP) and heart rate changes during tilt were determined
in 10 PD and 8 PDD patients. Attention and word fluency were evaluated in supine and tilted position using standard neuropsychological
tests.
OH defined as systolic BP (SBP) drop of ≥20 mmHg and/or diastolic BP (DBP) drop of ≥10 mmHg was present in 5 PDD patients
and in 2 PD patients. SBP drop was significantly greater in PDD than in PD patients (P < 0.05). Whereas word fluency was unaffected by tilt in both patient groups, attention as assessed with the Test of Everyday
Attention (TEA) deteriorated significantly in the PDD group, correlating with blood pressure response (ΔSBP and TEA-2, r = 0.828, P < 0.05; ΔDBP and TEA-2, r = 0.828, P < 0.05).
We conclude that OH is frequent in PDD and should be addressed therapeutically since it may exacerbate attentional dysfunction. 相似文献