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000137841 0247_ $$2doi$$a10.1093/brain/awu380
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000137841 0247_ $$2ISSN$$a1460-2156
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000137841 041__ $$aEnglish
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000137841 1001_ $$0P:(DE-2719)9000341$$aWeiss, Daniel$$b0$$eFirst author$$udzne
000137841 245__ $$aSubthalamic stimulation modulates cortical motor network activity and synchronization in Parkinson's disease.
000137841 260__ $$aOxford$$bOxford Univ. Press$$c2015
000137841 264_1 $$2Crossref$$3online$$bOxford University Press (OUP)$$c2015-01-02
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000137841 520__ $$aDynamic modulations of large-scale network activity and synchronization are inherent to a broad spectrum of cognitive processes and are disturbed in neuropsychiatric conditions including Parkinson's disease. Here, we set out to address the motor network activity and synchronization in Parkinson's disease and its modulation with subthalamic stimulation. To this end, 20 patients with idiopathic Parkinson's disease with subthalamic nucleus stimulation were analysed on externally cued right hand finger movements with 1.5-s interstimulus interval. Simultaneous recordings were obtained from electromyography on antagonistic muscles (right flexor digitorum and extensor digitorum) together with 64-channel electroencephalography. Time-frequency event-related spectral perturbations were assessed to determine cortical and muscular activity. Next, cross-spectra in the time-frequency domain were analysed to explore the cortico-cortical synchronization. The time-frequency modulations enabled us to select a time-frequency range relevant for motor processing. On these time-frequency windows, we developed an extension of the phase synchronization index to quantify the global cortico-cortical synchronization and to obtain topographic differentiations of distinct electrode sites with respect to their contributions to the global phase synchronization index. The spectral measures were used to predict clinical and reaction time outcome using regression analysis. We found that movement-related desynchronization of cortical activity in the upper alpha and beta range was significantly facilitated with 'stimulation on' compared to 'stimulation off' on electrodes over the bilateral parietal, sensorimotor, premotor, supplementary-motor, and prefrontal areas, including the bilateral inferior prefrontal areas. These spectral modulations enabled us to predict both clinical and reaction time improvement from subthalamic stimulation. With 'stimulation on', interhemispheric cortico-cortical coherence in the beta band was significantly attenuated over the bilateral sensorimotor areas. Similarly, the global cortico-cortical phase synchronization was attenuated, and the topographic differentiation revealed stronger desynchronization over the (ipsilateral) right-hemispheric prefrontal, premotor and sensorimotor areas compared to 'stimulation off'. We further demonstrated that the cortico-cortical phase synchronization was largely dominated by genuine neuronal coupling. The clinical improvement with 'stimulation on' compared to 'stimulation off' could be predicted from this cortical decoupling with multiple regressions, and the reduction of synchronization over the right prefrontal area showed a linear univariate correlation with clinical improvement. Our study demonstrates wide-spread activity and synchronization modulations of the cortical motor network, and highlights subthalamic stimulation as a network-modulating therapy. Accordingly, subthalamic stimulation may release bilateral cortical computational resources by facilitating movement-related desynchronization. Moreover, the subthalamic nucleus is critical to balance inhibitory and facilitatory cortical players within the motor program.
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000137841 650_7 $$2NLM Chemicals$$aAntiparkinson Agents
000137841 650_7 $$046627O600J$$2NLM Chemicals$$aLevodopa
000137841 650_2 $$2MeSH$$aAdult
000137841 650_2 $$2MeSH$$aAged
000137841 650_2 $$2MeSH$$aAntiparkinson Agents: therapeutic use
000137841 650_2 $$2MeSH$$aCortical Synchronization: drug effects
000137841 650_2 $$2MeSH$$aCortical Synchronization: physiology
000137841 650_2 $$2MeSH$$aDeep Brain Stimulation: methods
000137841 650_2 $$2MeSH$$aEvoked Potentials, Motor: physiology
000137841 650_2 $$2MeSH$$aFemale
000137841 650_2 $$2MeSH$$aHumans
000137841 650_2 $$2MeSH$$aLevodopa: therapeutic use
000137841 650_2 $$2MeSH$$aLongitudinal Studies
000137841 650_2 $$2MeSH$$aMale
000137841 650_2 $$2MeSH$$aMiddle Aged
000137841 650_2 $$2MeSH$$aMotor Cortex: physiopathology
000137841 650_2 $$2MeSH$$aNerve Net: physiopathology
000137841 650_2 $$2MeSH$$aNeural Pathways: physiopathology
000137841 650_2 $$2MeSH$$aParkinson Disease: pathology
000137841 650_2 $$2MeSH$$aParkinson Disease: therapy
000137841 650_2 $$2MeSH$$aPsychomotor Performance: drug effects
000137841 650_2 $$2MeSH$$aSubthalamus: physiology
000137841 650_2 $$2MeSH$$aTime Factors
000137841 650_2 $$2MeSH$$aTreatment Outcome
000137841 7001_ $$0P:(DE-2719)9000158$$aKlotz, Rosa$$b1$$udzne
000137841 7001_ $$0P:(DE-HGF)0$$aGovindan, Rathinaswamy B$$b2
000137841 7001_ $$0P:(DE-2719)9000291$$aScholten, Marlieke$$b3$$udzne
000137841 7001_ $$aNaros, Georgios$$b4
000137841 7001_ $$aRamos-Murguialday, Ander$$b5
000137841 7001_ $$0P:(DE-2719)9000039$$aBunjes, Friedemann$$b6$$udzne
000137841 7001_ $$aMeisner, Christoph$$b7
000137841 7001_ $$aPlewnia, Christian$$b8
000137841 7001_ $$0P:(DE-2719)2811170$$aKrüger, Rejko$$b9$$udzne
000137841 7001_ $$aGharabaghi, Alireza$$b10
000137841 77318 $$2Crossref$$3journal-article$$a10.1093/brain/awu380$$b : Oxford University Press (OUP), 2015-01-02$$n3$$p679-693$$tBrain$$v138$$x1460-2156$$y2015
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000137841 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4408429
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