Dissociation of Diffusion and Perfusion Responses After Intracerebral Hemorrhage

Background and PurposeIntracerebral hemorrhage (ICH) triggers complex secondary injury processes that extend beyond hematoma formation. While structural and diffusion MRI are widely used to characterize tissue injury, the spatiotemporal evolution of cerebral perfusion after ICH, particularly in small-animal models, remains poorly defined. Here, we performed a longitudinal multiparametric MRI study to delineate the relationship between microstructural injury and cerebral perfusion following experimental ICH. MethodsA collagenase-induced mouse model of ICH was studied longitudinally from baseline to 21 days post-stroke. Hematoma volume, tissue microstructure, and cerebral blood perfusion (CBP) were quantified using T2*-weighted MRI, diffusion-weighted imaging, and pseudo-continuous arterial spin labeling (pCASL) MRI, respectively. Apparent diffusion coefficient (ADC) and CBP were quantified in multiple brain regions from both ipsilateral and contralateral hemispheres and analyzed using linear mixed-effects models. ResultsHematoma volume peaked acutely and gradually attenuated over time. ADC exhibited an early reduction largely confined to the striatum, followed by progressive recovery, consistent with localized cytotoxic edema and subsequent attenuation. In contrast, CBP showed a marked bilateral hypoperfusion during the acute phase, followed by a delayed perfusion increase that was spatially restricted to the ipsilateral striatum. Notably, significant contralateral perfusion alterations were observed despite minimal contralateral diffusion changes, indicating a dissociation between microstructural injury and vascular regulation. ConclusionsMicrostructural and perfusion responses after ICH follow distinct spatiotemporal trajectories. Whereas diffusion abnormalities are largely localized to the hemorrhagic core, perfusion disturbances extend bilaterally beyond the lesion site. These findings challenge the common assumption of contralateral physiological stability after focal hemorrhage and highlight the value of quantitative perfusion MRI for capturing systemic cerebrovascular responses that are not reflected by diffusion or anatomical measures alone.