4.2 Article

Ultrasound, photoacoustic, and magnetic resonance imaging to study hyperacute pathophysiology of traumatic and vascular brain injury

Journal

JOURNAL OF NEUROIMAGING
Volume 33, Issue 4, Pages 534-546

Publisher

WILEY
DOI: 10.1111/jon.13115

Keywords

medical image analysis; multimodal imaging; traumatic brain injury

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The study investigates the pathophysiological changes in mice's brain within the first 3 hours after traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) using multimodal imaging. The results show that both TBI and SAH result in decreased brain oxygenation and blood flow, but TBI can recover while SAH cannot. MRI scans also reveal hemorrhage, edema, reduced perfusion, and altered diffusivity in both injury models. These findings can inform future studies on improving long-term recovery.
Background and PurposeCerebrovascular dynamics and pathomechanisms that evolve in the minutes and hours following traumatic vascular injury in the brain remain largely unknown. We investigated the pathophysiology evolution in mice within the first 3 hours after closed-head traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH), two significant traumatic vascular injuries. MethodsWe took a multimodal imaging approach using photoacoustic imaging, color Doppler ultrasound, and MRI to track injury outcomes using a variety of metrics. ResultsBrain oxygenation and velocity-weighted volume of blood flow (VVF) values significantly decreased from baseline to 15 minutes after both TBI and SAH. TBI resulted in 19.2% and 41.0% ipsilateral oxygenation and VVF reductions 15 minutes postinjury, while SAH resulted in 43.9% and 85.0% ipsilateral oxygenation and VVF reduction (p < .001). We found partial recovery of oxygenation from 15 minutes to 3 hours after injury for TBI but not SAH. Hemorrhage, edema, reduced perfusion, and altered diffusivity were evident from MRI scans acquired 90-150 minutes after injury in both injury models, although the spatial distribution was mostly focal for TBI and diffuse for SAH. ConclusionsThe results reveal that the cerebral oxygenation deficits immediately following injuries are reversible for TBI and irreversible for SAH. Our findings can inform future studies on mitigating these early responses to improve long-term recovery.

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