Slow waves generation and propagation in a model of brain lesions

• A brain model links local disconnection to sleep-like slow waves after lesions. • Virtual lesions in brain networks generate perilesional sleep-like slow waves. • Network hierarchy constrains slow wave propagation across the connectome. • Topology and synchronous slow waves drive stronger propagation to distant areas. • Post-lesional slow waves provide a dynamic mechanism for diaschisis. Slow waves (SWs), the hallmark of non-rapid eye movement (NREM) sleep, reflect the periodic occurrence of transient silent periods in cortical neurons (Down states). During NREM, SWs and Down states physiologically disrupt large-scale network interactions. Since early EEG studies, SWs have also been observed in awake patients after brain injury. Emerging evidence indicates that these intrusions of sleep-like activity interfere with ongoing network activity and contribute to motor and cognitive deficits; yet, the mechanisms governing the generation and spread of post-lesional SWs remain unclear. Here, we extend a neural mass model of EEG to capture transitions between wake-like and sleep-like dynamics and embed it in connectome-based networks with virtual lesions. This model supports that local disfacilitation, topology-dependent propagation, and synchrony-dependent amplification throughout the connectome are sufficient to produce post-lesional SWs. These mechanisms reproduce the spatial gradients of post-lesional SWs previously reported in patient studies, and identify actionable targets for neuromodulation and rehabilitation.