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Focal lesions induce large-scale percolation of sleep-like intracerebral activity in awake humans
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Focal lesions induce large-scale percolation of sleep-like intracerebral activity in awake humans
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Focal lesions induce large-scale percolation of sleep-like intracerebral activity in awake humans
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Journal Article
Focal lesions induce large-scale percolation of sleep-like intracerebral activity in awake humans
2021
Overview
•Focal lesions can lead to network effects whose neuronal mechanisms are elusive.•We contrast intracranial EEG recorded before and after surgical lesions in humans.•Full-fledged, sleep-like slow waves appear in the perilesional area.•Slow waves also percolate through long-range existing patterns of connectivity.•The intrusion of sleep-like activity may underlie the network effect of focal lesions.
Focal cortical lesions are known to result in large-scale functional alterations involving distant areas; however, little is known about the electrophysiological mechanisms underlying these network effects. Here, we addressed this issue by analysing the short and long distance intracranial effects of controlled structural lesions in humans. The changes in Stereo-Electroencephalographic (SEEG) activity after Radiofrequency-Thermocoagulation (RFTC) recorded in 21 epileptic subjects were assessed with respect to baseline resting wakefulness and sleep activity. In addition, Cortico-Cortical Evoked Potentials (CCEPs) recorded before the lesion were employed to interpret these changes with respect to individual long-range connectivity patterns. We found that small structural ablations lead to the generation and large-scale propagation of sleep-like slow waves within the awake brain. These slow waves match those recorded in the same subjects during sleep, are prevalent in perilesional areas, but can percolate up to distances of 60 mm through specific long-range connections, as predicted by CCEPs. Given the known impact of slow waves on information processing and cortical plasticity, demonstrating their intrusion and percolation within the awake brain add key elements to our understanding of network dysfunction after cortical injuries.
