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Increases in high-amplitude, low-frequency EEG oscillations during non-rapid eye movement (NREM) sleep serve as markers of neuronal silencing, which disrupts functional connectivity and is associated with a loss of awareness and responsiveness. Cortical slowing likewise occurs during wakefulness, upon sleep deprivation, and accompanies performance deterioration. Recent work has revealed similar oscillations (termed 'sleep-like slow waves') following stroke in brain regions close or connected to a brain lesion, offering a plausible but untested mechanism for stroke-related behavioural impairment. Here, we simultaneously recorded EEG and behavioural performance while 30 unilateral stroke patients (12 left hemisphere, 18 right hemisphere) and 27 age-matched healthy adults completed a computerised perceptual decision-making task. Stroke patients had predominantly middle cerebral artery strokes (n=25), with a small subset of posterior cerebral artery (n=4), and anterior cerebral artery/middle cerebral artery (n=1) lesions. Sleep-like slow waves occurred more frequently in stroke patients relative to healthy controls, with limited spatial specificity when comparing patients with left and right lesion sites (more slow waves ipsilateral of the lesion). Furthermore, there was a significant correlation between slow wave occurrence and the accuracy and speed of perceptual reports in stroke patients, suggesting that variations in the occurrence of slow waves may contribute to cognitive heterogeneity post-stroke. As sleep-like slow waves predict deficits in perceptual decision-making following stroke, they represent a plausible mechanism of post-lesion functional network dysfunction extending beyond the damaged regions, thereby contributing to broader cognitive impairments.
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Pearce et al. (2026) studied this question.
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