Perihemorrhagic pathophysiology of spontaneous intracerebral hemorrhages (ICH) remains unclear. Recently, ischemic changes in the perihemorrhagic zone (PHZ) have been discussed as a potential source of secondary damage. In this study, we focussed on diffusion and perfusion characteristics of experimental ICH.Methods
Experimental ICH was induced with a double injection model in rats. In total, 49 animals were examined at three timepoints within 3.5 h after ICH with a 2.35T animal scanner. We investigated perihemorrhagic relative apparent diffusion coefficients (rADC) and relative mean transit time (rMTT). Animals were divided into 2 groups; controls (gr1, n = 27) and facilitated hematoma evacuation with recombinant tissue plasminogen activator (rt-PA) after the first of 3 imaging time points (gr2, n = 22). Diffusion (rADC) and perfusion (rMTT) characteristics were analyzed in 3 regions of interest surrounding the hematoma (ROI1–3).Results
Overall rADC and rMTT values in ROI3 (normal tissue) did not show any changes. There was mild edema—not ischemia—in ROIs1 and 2 at TP1 with rADC of 1.05–1.18 in both groups indicating vasogenic edema (not ischemia). This did not change with hematoma evacuation. There was mild (non-critical) perfusion reduction in ROIs1 and 2 at TP1, which disappeared after clot evacuation in group 2 (P < 0.05 for TP3). Multifactorial ANOVA showed a solid trend (0.06 < P < 0.1) for clot evacuation associated normalization of perfusion in ROIs 1 and 2 within and in between groups 1 and 2.Conclusions
We demonstrated vasogenic edema and mild perfusion reduction in the PHZ above the ischemic threshold. The existence of a perihemorrhagic “penumbra” indicating critically ischemic tissue analogous to ischemic stroke is unlikely.