scholarly journals Altered Activation in Cerebellum Contralateral to Unilateral Thalamotomy May Mediate Tremor Suppression in Parkinson’s Disease: A Short-Term Regional Homogeneity fMRI Study

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0157562 ◽  
Author(s):  
Zhi Wen ◽  
Jie Zhang ◽  
Jielan Li ◽  
Jiankun Dai ◽  
Fuchun Lin ◽  
...  
2020 ◽  
Vol 274 ◽  
pp. 792-798
Author(s):  
Hai-Hua Sun ◽  
Ping-Lei Pan ◽  
Jian-Bin Hu ◽  
Jing Chen ◽  
Xue-Yang Wang ◽  
...  

2021 ◽  
Vol 11 (8) ◽  
pp. 959
Author(s):  
Konstantin G. Heimrich ◽  
Thomas Lehmann ◽  
Peter Schlattmann ◽  
Tino Prell

Recent evidence suggests that the vagus nerve and autonomic dysfunction play an important role in the pathogenesis of Parkinson’s disease. Using heart rate variability analysis, the autonomic modulation of cardiac activity can be investigated. This meta-analysis aims to assess if analysis of heart rate variability may indicate decreased parasympathetic tone in patients with Parkinson’s disease. The MEDLINE, EMBASE and Cochrane Central databases were searched on 31 December 2020. Studies were included if they: (1) were published in English, (2) analyzed idiopathic Parkinson’s disease and healthy adult controls, and (3) reported at least one frequency- or time-domain heart rate variability analysis parameter, which represents parasympathetic regulation. We included 47 studies with 2772 subjects. Random-effects meta-analyses revealed significantly decreased effect sizes in Parkinson patients for the high-frequency spectral component (HFms2) and the short-term measurement of the root mean square of successive normal-to-normal interval differences (RMSSD). However, heterogeneity was high, and there was evidence for publication bias regarding HFms2. There is some evidence that a more advanced disease leads to an impaired parasympathetic regulation. In conclusion, short-term measurement of RMSSD is a reliable parameter to assess parasympathetically impaired cardiac modulation in Parkinson patients. The measurement should be performed with a predefined respiratory rate.


1997 ◽  
Vol 12 (3) ◽  
pp. 306-314 ◽  
Author(s):  
Viktor Müller ◽  
Bettina Mohr ◽  
Regina Rosin ◽  
Friedemann Pulvermüller ◽  
Friedemann Müller ◽  
...  

Brain ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 137-154 ◽  
Author(s):  
J. R. BAKER ◽  
N. J. DAVEY ◽  
P. H. ELLAWAY ◽  
C. L. FRIEDILAND

2018 ◽  
Vol 11 (4) ◽  
pp. 867-874 ◽  
Author(s):  
Haidar Salimi Dafsari ◽  
Luisa Weiß ◽  
Monty Silverdale ◽  
Alexandra Rizos ◽  
Prashanth Reddy ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Silvia P. Caminiti ◽  
Chiara Siri ◽  
Lucia Guidi ◽  
Angelo Antonini ◽  
Daniela Perani

This fMRI study deals with the neural correlates of spatial and objects working memory (SWM and OWM) in elderly subjects (ESs) and idiopathic Parkinson’s disease (IPD). Normal aging and IPD can be associated with a WM decline. In IPD population, some studies reported similar SWM and OWM deficits; others reported a greater SWM than OWM impairment. In the present fMRI research, we investigated whether compensated IPD patients and elderly subjects with comparable performance during the execution of SWM and OWM tasks would present differences in WM-related brain activations. We found that the two groups recruited a prevalent left frontoparietal network when performing the SWM task and a bilateral network during OWM task execution. More specifically, the ESs showed bilateral frontal and subcortical activations in SWM, at difference with the IPD patients who showed a strict left lateralized network, consistent with frontostriatal degeneration in IPD. The overall brain activation in the IPD group was more extended as number of voxels with respect to ESs, suggesting underlying compensatory mechanisms. In conclusion, notwithstanding comparable WM performance, the two groups showed consistencies and differences in the WM activated networks. The latter underline the compensatory processes of normal typical and pathological aging.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7957
Author(s):  
Lina Wang ◽  
Yongsheng Yuan ◽  
Jianwei Wang ◽  
Yuting Shen ◽  
Yan Zhi ◽  
...  

Aims We sought to explore the role of the SLC6A3 rs393795 allelic variant in cerebral spontaneous activity and clinical features in Parkinson’s disease (PD) via imaging genetic approach. Methods Our study recruited 50 PD and 45 healthy control (HC) participants to provide clinical, genetic, and resting state functional magnetic resonance imaging (rs-fMRI) data. All subjects were separated into 16 PD-AA, 34 PD-CA/CC, 14 HC-AA, and 31 HC-CA/CC four subgroups according to SLC6A3 rs393795 genotyping. Afterwards, main effects and interactions of groups (PD versus HC) and genotypes (AA versus CA/CC) on cerebral function reflected by regional homogeneity (ReHo) were explored using two-way analysis of covariance (ANCOVA) after controlling age and gender. Finally, Spearman’ s correlations were employed to investigate the relationships between significantly interactive brain regions and clinical manifestations in PD subgroups. Results Compared with HC subjects, PD patients exhibited increased ReHo signals in left middle temporal gyrus and decreased ReHo signals in left pallidum. Compared with CA/CC carriers, AA genotype individuals showed abnormal increased ReHo signals in right inferior frontal gyrus (IFG) and supplementary motor area (SMA). Moreover, significant interactions (affected by both disease factor and allelic variation) were detected in right inferior temporal gyrus (ITG). Furthermore, aberrant increased ReHo signals in right ITG were observed in PD-AA in comparison with PD-CA/CC. Notably, ReHo values in right ITG were negatively associated with Tinetti Mobility Test (TMT) gait subscale scores and positively related to Freezing of Gait Questionnaire (FOG-Q) scores in PD-AA subgroup. Conclusions Our findings suggested that SLC6A3 rs393795 allelic variation might have a trend to aggravate the severity of gait disorders in PD patients by altering right SMA and IFG function, and ultimately result in compensatory activation of right ITG. It could provide us with a new perspective for exploring deeply genetic mechanisms of gait disturbances in PD.


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