The impact of cortical lesions on thalamo-cortical network dynamics after acute ischaemic stroke: a combined experimental and theoretical study

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• dc.contributor.author Van Wijngaarden, Joeri B. G.ca
• dc.contributor.author Zucca, Riccardoca
• dc.contributor.author Finnigan, Simonca
• dc.contributor.author Verschure, Paul F. M. J.ca
• dc.date.accessioned 2016-09-06T14:06:29Z
• dc.date.available 2016-09-06T14:06:29Z
• dc.date.issued 2016
• dc.description.abstract The neocortex and thalamus provide a core substrate for perception, cognition, and action, and are interconnected through different direct and indirect pathways that maintain specific dynamics associated with functional states including wakefulness and sleep. It has been shown that a lack of excitation, or enhanced subcortical inhibition, can disrupt this system and drive thalamic nuclei into an attractor state of low-frequency bursting and further entrainment of thalamo-cortical circuits, also called thalamo-cortical dysrhythmia (TCD). The question remains however whether similar TCD-like phenomena can arise with a cortical origin. For instance, in stroke, a cortical lesion could disrupt thalamo-cortical interactions through an attenuation of the excitatory drive onto the thalamus, creating an imbalance between excitation and inhibition that can lead to a state of TCD. Here we tested this hypothesis by comparing the resting-state EEG recordings of acute ischaemic stroke patients (N = 21) with those of healthy, age-matched control-subjects (N = 17). We observed that these patients displayed the hallmarks of TCD: a characteristic downward shift of dominant α-peaks in the EEG power spectra, together with increased power over the lower frequencies (δ and θ-range). Contrary to general observations in TCD, the patients also displayed a broad reduction in β-band activity. In order to explain the genesis of this stroke-induced TCD, we developed a biologically constrained model of a general thalamocortical module, allowing us to identify the specific cellular and network mechanisms involved. Our model showed that a lesion in the cortical component leads to sustained cell membrane hyperpolarization in the corresponding thalamic relay neurons, that in turn leads to the de-inactivation of voltage-gated T-type Ca2+-channels, switching neurons from tonic spiking to a pathological bursting regime. This thalamic bursting synchronises activity on a population level through divergent intrathalamic circuits, and entrains thalamo-cortical pathways by means of propagating low-frequency oscillations beyond the restricted region of the lesion. Hence, pathological stroke-induced thalamo-cortical dynamics can be the source of diaschisis, and account for the dissociation between lesion location and non-specific symptoms of stroke such as neuropathic pain and hemispatial neglect.en
• dc.description.sponsorship This work was supported by the European Research Council under the European Union's Seventh Framework Programme FP7/2007-2013/ERC grant agreement n. 341196 [CDAC], and the Research and Technological Development Programme FP7-ICT-612139 in the WYSIWYD project to PFMJV. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en
• dc.format.mimetype application/pdfca
• dc.identifier.citation Van Wijngaarden JBG, Zucca R, Finnigan S, Verschure PFMJ. The impact of cortical lesions on thalamo-cortical network dynamics after acute ischaemic stroke: a combined experimental and theoretical study. PLoS Comput. Biol. 2016 Aug 10;12(8):e1005048. DOI: 10.1371/journal.pcbi.1005048
• dc.identifier.doi http://dx.doi.org/10.1371/journal.pcbi.1005048
• dc.identifier.issn 1553-734X
• dc.identifier.uri http://hdl.handle.net/10230/27277
• dc.language.iso engen
• dc.publisher Public Library of Science (PLoS)ca
• dc.relation.ispartof PLoS Computational Biology. 2016 Aug 10; 12(8): e1005048
• dc.relation.projectID info:eu-repo/grantAgreement/EC/FP7/341196
• dc.relation.projectID info:eu-repo/grantAgreement/EC/FP7/612139
• dc.rights © 2016 van Wijngaarden et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri https://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword Neuronsen
• dc.subject.keyword Electroencephalographyen
• dc.subject.keyword Ischemic strokeen
• dc.subject.keyword Thalamic nucleien
• dc.subject.keyword Strokeen
• dc.subject.keyword Lesionsen
• dc.subject.keyword Action potentialsen
• dc.subject.keyword Thalamusen
• dc.title The impact of cortical lesions on thalamo-cortical network dynamics after acute ischaemic stroke: a combined experimental and theoretical studyen
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion