Slow Oscillations Track Acute Stroke Injury but Not Functional Recovery

A central goal in translational stroke research is to identify neurophysiological biomarkers that index injury severity and provide information about subsequent functional outcome. Cortical slow oscillations (SOs; 0.1–1.0 Hz) are suppressed after ischemic stroke and recover over the following days to weeks. Whether SO recovery actually tracks behavioral recovery, and whether pre-stroke network organization relates to outcome, has not been tested within individual animals. Using longitudinal wide-field calcium imaging in Thy1-GCaMP6f mice (n = 25), we tracked ipsilateral and contralateral SO power across baseline, 24 hours, and one week after photothrombotic stroke of the left somatosensory forepaw cortex, classifying animals by the presence (STI+; n = 14) or absence (STI−; n = 11) of secondary thalamic injury. Acute ipsilateral SO power was suppressed and tracked concurrent behavioral deficit (ρ = −0.718, p < 0.001), remaining associated with deficit after adjustment for infarct volume (partial ρ = −0.448, p = 0.025). By one week SO power had partially recovered, yet its recovery was dissociated from forelimb use. Week 1 SO power showed no association with behavior in any region or hemisphere (all |ρ| ≤ 0.074, all p > 0.5), and SO recovery did not differ significantly between STI groups despite STI+ animals remaining more impaired (p = 0.011). Pre-stroke SO laterality was associated with week 1 behavioral outcome, independent of infarct size (ρ = −0.518, p = 0.008; partial ρ = −0.446, p = 0.026). Acute SO suppression therefore indexes injury severity beyond infarct volume, whereas spontaneous recovery of SO power is not a reliable surrogate biomarker of week 1 functional outcome. Pre-stroke interhemispheric SO balance emerged as an exploratory candidate source of prognostic information, identifying pre-injury brain state as a dimension that warrants prospective validation.