Publications by authors named "Martin Wilhelm Kurz"

Background: Endovascular thrombectomy, the preferred treatment for acute large-vessel occlusion stroke, is highly time-dependent. Many patients live far from thrombectomy centers due to large geographical variations in stroke services. This study aimed to explore the consequences of long transport distance on the proportion of thrombectomy-eligible patients who underwent thrombectomy, the clinical outcomes with or without thrombectomy, the timelines for patients transported, and the diagnostic accuracy of large-vessel occlusion in primary stroke centers.

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Background: Virtual reality simulation training may improve the technical skills of interventional radiologists when establishing endovascular thrombectomy at limited-volume stroke centers. The aim of this study was to investigate whether the technical thrombectomy performance of interventional radiologists improved after a defined virtual reality simulator training period. As part of the quality surveillance of clinical practice, we also assessed patient outcomes and thrombectomy quality indicators at the participating centers.

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Objective: Computed tomography (CT) scan is a fast and widely used modality for early assessment in patients with symptoms of a cerebral ischemic stroke. CT perfusion (CTP) is often added to the protocol and is used by radiologists for assessing the severity of the stroke. Standard parametric maps are calculated from the CTP datasets.

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Background and Purpose- Tenecteplase represents a promising alternative to alteplase as thrombolytic treatment in acute ischemic stroke. There are limited data on tenecteplase 0.4 mg/kg in patients with increased stroke severity.

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Background: Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD.

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Parkinson's disease (PD) is the second most common neurodegenerative illness after Alzheimer's disease (AD). Cognitive impairment and dementia are common features in PD and characterized by a wide range of cognitive deficits distinct from those seen in AD. Mild cognitive impairment occurs even early in PD and is associated with shorter time to dementia.

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Several recent studies have shown that dementia is common in Parkinson's disease (PD), and that in some patients, cognitive impairment occurs even at the time of diagnosis. The point prevalence of dementia in PD is close to 30% and the incidence rate is increased 4-6 times as compared to controls. The cumulative prevalence is very high, at least 75% of PD patients who survive for more than 10 years will develop dementia.

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Apolipoprotein E gene alleles have been linked to various cardiovascular and neurodegenerative disorders. There have been conflicting reports of associations between Apolipoprotein E alleles and Parkinson disease and Parkinson disease dementia. To investigate the role of Apolipoprotein E alleles in Parkinson disease and Parkinson disease dementia, we have determined Apolipoprotein E genotypes in a group of patients with Parkinson disease (n = 95) and compared them with those of healthy control participants (n = 73).

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Familial amyloid polyneuropathy (FAP) is rare and most commonly caused by the Val30Met mutation of the transthyretin (TTR) gene. Beside polyneuropathy, other complications due to amyloid deposits occur, but may vary in phenotype. The mutation tends to occur in endemic clusters.

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Carriers of expanded alleles of the fragile X mental retardation (FMR1) gene may display parkinsonism, cognitive decline, and behavioral changes. The authors screened 2 male groups of patients affected with Parkinson's disease (PD) (n = 137). One group (n = 56) was followed longitudinally for up to 12 years.

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Dementia is common in patients with Parkinson's disease (PDD). The etiology of PDD is still unclear, but exciting advances have been made in discovering pathogenetic components in Parkinson's disease (PD), implicating the role of genetic factors. It is, however, still controversial whether genetic factors also contribute to the development of dementia in PD.

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Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB) are common clinical dementias characterized neuropathologically by the presence of cortical Lewy body pathology and with distinct clinical and neurobiological similarities. Importantly, genetic factors seem to play a key role in the pathogenesis of Parkinson's disease. In the current article, we examine the evidence for a genetic component to DLB and PDD by reviewing studies of familial PDD and DLB as well as familial coincidental PDD and DLB, and report the genes involved.

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