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Cerebrovascular dynamics and pathomechanisms that evolve in the minutes andhours following traumatic vascular injury in the brain remain largely unknown.We investigated the pathophysiology evolution within the first three hoursafter closed-head traumatic brain injury (TBI) and subarachnoid hemorrhage(SAH), two common traumatic vascular injuries, in mice. We took a multi-modalimaging approach using photoacoustic, color Doppler, and magnetic resonanceimaging (MRI) in mice. Brain oxygenation (%sO2) and velocity-weighted volume ofblood flow (VVF) values significantly decreased from baseline to fifteenminutes after both TBI and SAH. TBI resulted in 19.2% and 41.0% ipsilateral%sO2 and VVF reductions 15 minutes post injury while SAH resulted in 43.9% %sO2and 85.0% VVF reduction ipsilaterally (p<0.001). We found partial recovery of%sO2 from 15 minutes to 3-hours after injury for TBI but not SAH. Hemorrhage,edema, reduced perfusion, and altered diffusivity were evident from MRI scansacquired 90-150 minutes after injury in both models although the spatialdistribution was mostly focal for TBI and diffuse for SAH. The results revealthat the cerebral %sO2 deficits immediately following injuries are reversiblefor TBI and irreversible for SAH. Our findings can inform future studies onmitigating these early responses to improve long-term recovery.

Hyperacute pathophysiology of traumatic and vascular brain injury captured by ultrasound, photoacoustic, and magnetic resonance imaging