Paper Info
Title
The Impact of Cortical Lesions on Thalamo-Cortical Network Dynamics after Acute Ischaemic Stroke: A Combined Experimental and Theoretical Study.
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 alpha-peaks in the EEG power spectra, together with increased power over the lower frequencies (delta and theta-range). Contrary to general observations in TCD, the patients also displayed a broad reduction in beta-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.
Year
DOI
Venue
2016
10.1371/journal.pcbi.1005048
PLOS COMPUTATIONAL BIOLOGY
Field
DocType
Volume
Thalamus,Population,Neocortex,Bursting,Neuroscience,Lesion,Biology,Diaschisis,Wakefulness,Bioinformatics,Electroencephalography
Journal
12
Issue
ISSN
Citations 
8
1553-7358
0
PageRank 
References 
Authors
0.34
0
4
Name
Order
Citations
PageRank
Joeri B. G. van Wijngaarden100.34
Riccardo Zucca27011.03
Simon Finnigan300.34
Paul F. M. J. Verschure4677116.64