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Parkinson Disease: HELP
Articles by Florian Holtbernd
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, Florian Holtbernd wrote the following 4 articles about Parkinson Disease.
+ Citations + Abstracts
1 Review Brain imaging findings in idiopathic REM sleep behavior disorder (RBD) - A systematic review on potential biomarkers for neurodegeneration. 2017

Heller, Julia / Brcina, Nikolina / Dogan, Imis / Holtbernd, Florian / Romanzetti, Sandro / Schulz, Jörg B / Schiefer, Johannes / Reetz, Kathrin. ·Department of Neurology, RWTH Aachen University, Pauwelsstraße 30, Aachen, Germany; JARA - Institute Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH, Jülich and RWTH Aachen University, Aachen, Germany. · Department of Neurology, RWTH Aachen University, Pauwelsstraße 30, Aachen, Germany. · Department of Neurology, RWTH Aachen University, Pauwelsstraße 30, Aachen, Germany; JARA - Institute Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH, Jülich and RWTH Aachen University, Aachen, Germany. Electronic address: kreetz@ukaachen.de. ·Sleep Med Rev · Pubmed #27542516.

ABSTRACT: Idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of physiological atonia of skeletal muscles with abnormal behavior during dream sleep. RBD may be the initial manifestation of neurodegenerative diseases, particularly of α-synucleinopathies such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). However, gauging the individual risk of subsequent phenoconversion and making assumptions on the type of disease that may subsequently follow RBD is challenging. Over the past years, a growing number of studies have sought to establish reliable neuroimaging markers to detect neurodegenerative brain changes in RBD subjects at the earliest possible stage. The present review summarizes recent advances in brain imaging in RBD and provides recommendations for the application of currently available structural and functional neuroimaging modalities to monitor disease progression and risk of subsequent phenoconversion. Further imaging research applying multimodal approaches is encouraged to enhance accuracy of prognoses. Additionally, more longitudinal studies are warranted to validate findings from cross-sectional studies on RBD progression and risk of subsequent phenoconversion. Aside from enabling reliable prognoses on a single-subject-level in the near future, this might give further insight into RBD pathophysiology, and finally augment the development of intervention strategies and disease-modifying therapies.

2 Article Flow-metabolism dissociation in the pathogenesis of levodopa-induced dyskinesia. 2016

Jourdain, Vincent A / Tang, Chris C / Holtbernd, Florian / Dresel, Christian / Choi, Yoon Young / Ma, Yilong / Dhawan, Vijay / Eidelberg, David. · ·JCI Insight · Pubmed #27699242.

ABSTRACT: Levodopa-induced dyskinesia (LID) is the most common, disruptive complication of Parkinson's disease (PD) pharmacotherapy, yet despite decades of research, the changes in regional brain function underlying LID remain largely unknown. We previously found that the cerebral vasomotor and metabolic responses to levodopa are dissociated in PD subjects. Nonetheless, it is unclear whether levodopa-mediated dissociation is exaggerated in LID or distinguishes LID from non-LID subjects. To explore this possibility, we used dual-tracer positron emission tomography to quantify regional cerebral blood flow and metabolic activity in 28 PD subjects (14 LID, 14 non-LID), scanned before and during intravenous levodopa infusion. Levodopa-mediated dissociation was most prominent in the posterior putamen (

3 Article Dopaminergic correlates of metabolic network activity in Parkinson's disease. 2015

Holtbernd, Florian / Ma, Yilong / Peng, Shichun / Schwartz, Frank / Timmermann, Lars / Kracht, Lutz / Fink, Gereon R / Tang, Chris C / Eidelberg, David / Eggers, Carsten. ·Center for Neurosciences, The Feinstein Institute for Medical Research, Manhasset, New York, 11030. · Department of Neurology, University of Cologne, Cologne, Germany. · Max-Planck Institute for Neurological Research, Cologne, Germany. · Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Jülich Research Center, Jülich, Germany. ·Hum Brain Mapp · Pubmed #26037537.

ABSTRACT: Parkinson's disease (PD) is associated with distinct metabolic covariance patterns that relate to the motor and cognitive manifestations of the disorder. It is not known, however, how the expression of these patterns relates to measurements of nigrostriatal dopaminergic activity from the same individuals. To explore these associations, we studied 106 PD subjects who underwent cerebral PET with both (18) F-fluorodeoxyglucose (FDG) and (18) F-fluoro-L-dopa (FDOPA). Expression values for the PD motor- and cognition-related metabolic patterns (PDRP and PDCP, respectively) were computed for each subject; these measures were correlated with FDOPA uptake on a voxel-by-voxel basis. To explore the relationship between dopaminergic function and local metabolic activity, caudate and putamen FDOPA PET signal was correlated voxel-wise with FDG uptake over the entire brain. PDRP expression correlated with FDOPA uptake in caudate and putamen (P < 0.001), while PDCP expression correlated with uptake in the anterior striatum (P < 0.001). While statistically significant, the correlations were only of modest size, accounting for less than 20% of the overall variation in these measures. After controlling for PDCP expression, PDRP correlations were significant only in the posterior putamen. Of note, voxel-wise correlations between caudate/putamen FDOPA uptake and whole-brain FDG uptake were significant almost exclusively in PDRP regions. Overall, the data indicate that PDRP and PDCP expression correlates significantly with PET indices of presynaptic dopaminergic functioning obtained in the same individuals. Even so, the modest size of these correlations suggests that in PD patients, individual differences in network activity cannot be explained solely by nigrostriatal dopamine loss.

4 Article Abnormal metabolic network activity in REM sleep behavior disorder. 2014

Holtbernd, Florian / Gagnon, Jean-François / Postuma, Ron B / Ma, Yilong / Tang, Chris C / Feigin, Andrew / Dhawan, Vijay / Vendette, Mélanie / Soucy, Jean-Paul / Eidelberg, David / Montplaisir, Jacques. ·From the Center for Neurosciences (F.H., Y.M., C.C.T., A.F., V.D., D.E.), The Feinstein Institute for Medical Research, Manhasset, NY · Center for Advanced Research in Sleep Medicine (J.-F.G., R.B.P., M.V., J.M.), Hôpital du Sacré-Coeur de Montréal · Department of Psychology (J.-F.G., M.V.), Université du Québec à Montréal · Department of Neurology (R.B.P.), Montreal General Hospital · Montreal Neurological Institute (J.-P.S.), McGill University · and Department of Psychiatry (J.M.), University of Montreal, Montréal, Canada. ·Neurology · Pubmed #24453082.

ABSTRACT: OBJECTIVE: To determine whether the Parkinson disease-related covariance pattern (PDRP) expression is abnormally increased in idiopathic REM sleep behavior disorder (RBD) and whether increased baseline activity is associated with greater individual risk of subsequent phenoconversion. METHODS: For this cohort study, we recruited 2 groups of RBD and control subjects. Cohort 1 comprised 10 subjects with RBD (63.5 ± 9.4 years old) and 10 healthy volunteers (62.7 ± 8.6 years old) who underwent resting-state metabolic brain imaging with (18)F-fluorodeoxyglucose PET. Cohort 2 comprised 17 subjects with RBD (68.9 ± 4.8 years old) and 17 healthy volunteers (66.6 ± 6.0 years old) who underwent resting brain perfusion imaging with ethylcysteinate dimer SPECT. The latter group was followed clinically for 4.6 ± 2.5 years by investigators blinded to the imaging results. PDRP expression was measured in both RBD groups and compared with corresponding control values. RESULTS: PDRP expression was elevated in both groups of subjects with RBD (cohort 1: p < 0.04; cohort 2: p < 0.005). Of the 17 subjects with long-term follow-up, 8 were diagnosed with Parkinson disease or dementia with Lewy bodies; the others did not phenoconvert. For individual subjects with RBD, final phenoconversion status was predicted using a logistical regression model based on PDRP expression and subject age at the time of imaging (r(2) = 0.64, p < 0.0001). CONCLUSIONS: Latent network abnormalities in subjects with idiopathic RBD are associated with a greater likelihood of subsequent phenoconversion to a progressive neurodegenerative syndrome.