Search

Your search keyword '"van Eimeren, T"' showing total 328 results
Start Over Author "van Eimeren, T"
328 results on '"van Eimeren, T"'

51. Characterization of disease-specific covariance patterns of neurodegeneration in FTLD-variants

Author

Hammes, J., Bischof, G., Anderl-Straub, S., Barthel, H., Beer, A. J., Danek, A., Eickhoff, S., Fassbender, K., Fliessbach, K., Landwehrmeyer, B., Lauer, M., Ludolph, A. C., Prudlo, J., Schroeter, M. L., Sabri, O., Schmidt-Diehl, J., Schneider, A., Semler, E., Wiltfang, J., Drzezga, A., Otto, M., van Eimeren, T., Hammes, J., Bischof, G., Anderl-Straub, S., Barthel, H., Beer, A. J., Danek, A., Eickhoff, S., Fassbender, K., Fliessbach, K., Landwehrmeyer, B., Lauer, M., Ludolph, A. C., Prudlo, J., Schroeter, M. L., Sabri, O., Schmidt-Diehl, J., Schneider, A., Semler, E., Wiltfang, J., Drzezga, A., Otto, M., and van Eimeren, T.

Published
2018

52. Radiological biomarkers for diagnosis in PSP: Where are we and where do we need to be?

Author

Whitwell, J.L. Höglinger, G.U. Antonini, A. Bordelon, Y. Boxer, A.L. Colosimo, C. van Eimeren, T. Golbe, L.I. Kassubek, J. Kurz, C. Litvan, I. Pantelyat, A. Rabinovici, G. Respondek, G. Rominger, A. Rowe, J.B. Stamelou, M. Josephs, K.A. for the Movement Disorder Society-endorsed PSP Study Group

Subjects
eye diseases
Abstract

PSP is a pathologically defined neurodegenerative tauopathy with a variety of clinical presentations including typical Richardson's syndrome and other variant PSP syndromes. A large body of neuroimaging research has been conducted over the past two decades, with many studies proposing different structural MRI and molecular PET/SPECT biomarkers for PSP. These include measures of brainstem, cortical and striatal atrophy, diffusion weighted and diffusion tensor imaging abnormalities, [18F] fluorodeoxyglucose PET hypometabolism, reductions in striatal dopamine imaging and, most recently, PET imaging with ligands that bind to tau. Our aim was to critically evaluate the degree to which structural and molecular neuroimaging metrics fulfill criteria for diagnostic biomarkers of PSP. We queried the PubMed, Cochrane, Medline, and PSYCInfo databases for original research articles published in English over the past 20 years using postmortem diagnosis or the NINDS-SPSP criteria as the diagnostic standard from 1996 to 2016. We define a five-level theoretical construct for the utility of neuroimaging biomarkers in PSP, with level 1 representing group-level findings, level 2 representing biomarkers with demonstrable individual-level diagnostic utility, level 3 representing biomarkers for early disease, level 4 representing surrogate biomarkers of PSP pathology, and level 5 representing definitive PSP biomarkers of PSP pathology. We discuss the degree to which each of the currently available biomarkers fit into this theoretical construct, consider the role of biomarkers in the diagnosis of Richardson's syndrome, variant PSP syndromes and autopsy confirmed PSP, and emphasize current shortfalls in the field. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Published
2017

54. Which ante mortem clinical features predict progressive supranuclear palsy pathology?

Author

Respondek, G. Kurz, C. Arzberger, T. Compta, Y. Englund, E. Ferguson, L.W. Gelpi, E. Giese, A. Irwin, D.J. Meissner, W.G. Nilsson, C. Pantelyat, A. Rajput, A. van Swieten, J.C. Troakes, C. Josephs, K.A. Lang, A.E. Mollenhauer, B. Müller, U. Whitwell, J.L. Antonini, A. Bhatia, K.P. Bordelon, Y. Corvol, J.-C. Colosimo, C. Dodel, R. Grossman, M. Kassubek, J. Krismer, F. Levin, J. Lorenzl, S. Morris, H. Nestor, P. Oertel, W.H. Rabinovici, G.D. Rowe, J.B. van Eimeren, T. Wenning, G.K. Boxer, A. Golbe, L.I. Litvan, I. Stamelou, M. Höglinger, G.U. for the Movement Disorder Society-Endorsed PSP Study Group

Subjects
eye diseases
Abstract

Background: Progressive supranuclear palsy (PSP) is a neuropathologically defined disease presenting with a broad spectrum of clinical phenotypes. Objective: To identify clinical features and investigations that predict or exclude PSP pathology during life, aiming at an optimization of the clinical diagnostic criteria for PSP. Methods: We performed a systematic review of the literature published since 1996 to identify clinical features and investigations that may predict or exclude PSP pathology. We then extracted standardized data from clinical charts of patients with pathologically diagnosed PSP and relevant disease controls and calculated the sensitivity, specificity, and positive predictive value of key clinical features for PSP in this cohort. Results: Of 4166 articles identified by the database inquiry, 269 met predefined standards. The literature review identified clinical features predictive of PSP, including features of the following 4 functional domains: ocular motor dysfunction, postural instability, akinesia, and cognitive dysfunction. No biomarker or genetic feature was found reliably validated to predict definite PSP. High-quality original natural history data were available from 206 patients with pathologically diagnosed PSP and from 231 pathologically diagnosed disease controls (54 corticobasal degeneration, 51 multiple system atrophy with predominant parkinsonism, 53 Parkinson's disease, 73 behavioral variant frontotemporal dementia). We identified clinical features that predicted PSP pathology, including phenotypes other than Richardson's syndrome, with varying sensitivity and specificity. Conclusions: Our results highlight the clinical variability of PSP and the high prevalence of phenotypes other than Richardson's syndrome. The features of variant phenotypes with high specificity and sensitivity should serve to optimize clinical diagnosis of PSP. © 2017 International Parkinson and Movement Disorder Society. © 2017 International Parkinson and Movement Disorder Society

Published
2017

55. Tauopathien

Author

Kovacs, G. G., primary, Respondek, G., additional, van Eimeren, T., additional, Höller, E., additional, Levin, J., additional, Müller, U., additional, Schwarz, S., additional, Rösler, T. W., additional, Schweyer, K., additional, and Höglinger, G. U., additional

Published
2018
Full Text
View/download PDF

64. Hemichorea with Contralateral High Signal Intensity Putaminal Lesion on T1-Weighted Images in Non-Ketotic Hyperglycemia

Author

Achilles, E. I. S., Maus, V., Fink, G. R., Maintz, D., van Eimeren, T., Mpotsaris, A., Achilles, E. I. S., Maus, V., Fink, G. R., Maintz, D., van Eimeren, T., and Mpotsaris, A.

Abstract

A 64-year-old diabetic female patient presented with involuntary unilateral hyperkinetic movements of the left limbs. Cranial MRI showed a contralateral high signal intensity putaminal lesion on T1-weighted images without any signal changes in the T2-weighted images. This finding is characteristic for hemichorea-hemiballism associated with insufficiently treated diabetes mellitus. Additionally, proton MR spectroscopy was performed and revealed a decreased N-acetylaspartate/creatine and N-acetylaspartate/choline ratio, indicating neuronal damage of the contralateral putamen.

Published
2016

65. Revised clinical diagnostic criteria for progressive supranuclear palsy (PSP)

Author

Hoeglinger, G., Respondek, G., Stamelou, M., Kurz, C., Josephs, K., Lang, A., Mollenhauer, B., Mueller, U., Nilsson, C., Whitwell, J., Arzberger, T., Gelpi, E., Giese, A., Irwin, D., Meissner, W., Pantelyat, A., van Swieten, J., Troakes, C., Antonini, A., Bhatia, K., Bordelon, Y., Corvol, J. C., Colosimo, C., Dodel, R., Grossman, M., Kassubek, J., Krismer, F., Levin, J., Morris, H., Nestor, P., Oertel, W., Rabinovici, G., Rowe, J., van Eimeren, T., Wenning, G., Yu, J. -T., Golbe, L. I., Litvan, I., Boxer, A., Hoeglinger, G., Respondek, G., Stamelou, M., Kurz, C., Josephs, K., Lang, A., Mollenhauer, B., Mueller, U., Nilsson, C., Whitwell, J., Arzberger, T., Gelpi, E., Giese, A., Irwin, D., Meissner, W., Pantelyat, A., van Swieten, J., Troakes, C., Antonini, A., Bhatia, K., Bordelon, Y., Corvol, J. C., Colosimo, C., Dodel, R., Grossman, M., Kassubek, J., Krismer, F., Levin, J., Morris, H., Nestor, P., Oertel, W., Rabinovici, G., Rowe, J., van Eimeren, T., Wenning, G., Yu, J. -T., Golbe, L. I., Litvan, I., and Boxer, A.

Published
2016

71. Human face processing is tuned to sexual age preferences

Author

Ponseti, J, Granert, O, van Eimeren, T, Jansen, O, Wolff, S, Beier, K, Deuschl, G, Bosinski, H, Siebner, H, Ponseti, J, Granert, O, van Eimeren, T, Jansen, O, Wolff, S, Beier, K, Deuschl, G, Bosinski, H, and Siebner, H

Abstract

Human faces can motivate nurturing behaviour or sexual behaviour when adults see a child or an adult face, respectively. This suggests that face processing is tuned to detecting age cues of sexual maturity to stimulate the appropriate reproductive behaviour: either caretaking or mating. In paedophilia, sexual attraction is directed to sexually immature children. Therefore, we hypothesized that brain networks that normally are tuned to mature faces of the preferred gender show an abnormal tuning to sexual immature faces in paedophilia. Here, we use functional magnetic resonance imaging (fMRI) to test directly for the existence of a network which is tuned to face cues of sexual maturity. During fMRI, participants sexually attracted to either adults or children were exposed to various face images. In individuals attracted to adults, adult faces activated several brain regions significantly more than child faces. These brain regions comprised areas known to be implicated in face processing, and sexual processing, including occipital areas, the ventrolateral prefrontal cortex and, subcortically, the putamen and nucleus caudatus. The same regions were activated in paedophiles, but with a reversed preferential response pattern.

Published
2014

94. Imaging movement-related activity in medicated Parkin-associated and sporadic Parkinson's disease.

Author

van Eimeren T, Binkofski F, Buhmann C, Hagenah J, Strafella AP, Pramstaller PP, Siebner HR, Klein C, van Eimeren, Thilo, Binkofski, Ferdinand, Buhmann, Carsten, Hagenah, Johann, Strafella, Antonio P, Pramstaller, Peter P, Siebner, Hartwig R, and Klein, Christine

Abstract

Treatment-related motor complications such as dyskinesias are a major problem in the long-term management of Parkinson's disease (PD). In sporadic PD, a relatively early onset of the disease is known to be associated with an early development of dyskinesias. Although linked with early onset, patients with Parkin-associated PD often show a stable long-term response to dopaminergic therapy without developing treatment-induced motor complications. Therefore, we reasoned that this difference in vulnerability to develop dyskinesias under long-term dopaminergic therapy may be associated with differences in movement-related activation patterns in Parkin-associated compared to sporadic PD. To test this hypothesis, medicated non-dyskinetic patients with either Parkin-associated or sporadic PD underwent functional magnetic resonance imaging (fMRI) while performing externally specified or internally selected movements. Patients with Parkin-associated and sporadic PD showed no difference in movement-related activation patterns. Moreover, the covariates 'age' and 'disease duration' similarly influenced brain activation in both patient groups. The present finding suggests that a stable long-term motor response in some patients with Parkin-associated PD may not be related to differences in cortical recruitment. In conclusion, our findings corroborate a substantial pathophysiologic overlap between Parkin-associated and sporadic PD and lend further support to the notion that Parkin-associated PD is a suitable genetic model for sporadic PD. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

95. Increased striatal dopamine release in Parkinsonian patients with pathological gambling: a [11C] raclopride PET study.

Author

Steeves, T. D. L., Miyasaki, J., Zurowski, M., Lang, A. E., Pellecchia, G., Van Eimeren, T., Rusjan, P., Houle, S., and Strafella, A. P.

Subjects
DRUG therapy for Parkinson's disease, PARKINSON'S disease patients, IMPULSE control disorders, DOPAMINE, DOPAMINERGIC mechanisms, POSITRON emission tomography, NEUROBIOLOGY, PATHOLOGICAL physiology
Abstract

Pathological gambling is an impulse control disorder reported in association with dopamine agonists used to treat Parkinsons disease. Although impulse control disorders are conceptualized as lying within the spectrum of addictions, little neurobiological evidence exists to support this belief. Functional imaging studies have consistently demonstrated abnormalities of dopaminergic function in patients with drug addictions, but to date no study has specifically evaluated dopaminergic function in Parkinsons disease patients with impulse control disorders. We describe results of a [11C] raclopride positron emission tomography (PET) study comparing dopaminergic function during gambling in Parkinsons disease patients, with and without pathological gambling, following dopamine agonists. Patients with pathological gambling demonstrated greater decreases in binding potential in the ventral striatum during gambling (13.9%) than control patients (8.1%), likely reflecting greater dopaminergic release. Ventral striatal bindings at baseline during control task were also lower in patients with pathological gambling. Although prior imaging studies suggest that abnormality in dopaminergic binding and dopamine release may be markers of vulnerability to addiction, this study presents the first evidence of these phenomena in pathological gambling. The emergence of pathological gambling in a number of Parkinsons disease patients may provide a model into the pathophysiology of this disorder. [ABSTRACT FROM AUTHOR]

Published
2009
Full Text
View/download PDF

99. Heterozygous carriers of a Parkinor PINK1mutation share a common functional endophenotypeSYMBOL

Author

Nuenen, B F.L. van, Weiss, M M., Bloem, B R., Reetz, K, van Eimeren, T, Lohmann, K, Hagenah, J, Pramstaller, P P., Binkofski, F, Klein, C, and Siebner, H R.

Abstract

To use a combined neurogenetic-neuroimaging approach to examine the functional consequences of preclinical dopaminergic nigrostriatal dysfunction in the human motor system. Specifically, we examined how a single heterozygous mutation in different genes associated with recessively inherited Parkinson disease alters the cortical control of sequential finger movements.

Published
2009
Full Text
View/download PDF

100. Morphometric fingerprint of asymptomatic Parkinand PINK1mutation carriers in the basal ganglia

Author

Binkofski, F, Reetz, K, Gaser, C, Hilker, R, Hagenah, J, Hedrich, K, van Eimeren, T, Thiel, A, Büchel, C, Pramstaller, P P., Siebner, H R., and Klein, C

Abstract

Mutations in the Parkinand PINK1genes can cause parkinsonism. Since asymptomatic carriers of a single mutant allele of the Parkinor PINK1gene display a presynaptic dopaminergic dysfunction in the striatum, they provide a unique in vivo model to study structural and functional reorganization in response to latent nigrostriatal dysfunction. We hypothesized that subclinical nigrostriatal neurodegeneration caused by these mutations would induce morphologic changes in the dysfunctional striatal gray matter.

Published
2007
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results