ADC and T2 signal intensity changes in perihematomal, cortical, and intrahematomal regions of interest in a rat intracerebral hemorrhage model with and without decompressive craniectomy

Objective: Intracerebral hemorrhage (ICH) is associated with high mortality and morbidity rates. The pathologic contribution of secondary ischemia in perihematomal tissues is controversial. No acute treatment of ICH is available, apart from the supportive care. Decompressive craniectomy (DC), however, is a promising treatment modality, and we recently showed that DC improved neurological outcome and mortality in experimental ICH. To further explore the effects of DC on the brain tissue after ICH, we decided to evaluate magnetic resonance imaging (MRI) changes in and around hematoma following DC.

Methods: We used autologous blood injection model to produce ICH in basal ganglia in Wistar rats. We randomly allocated the rats into five groups as: ICH-only (without DC) and three groups of ICH with DC performed at 1, 6, or 24 h, and DC-only group (without ICH). After a baseline MRI on day 0, re-imagings followed on days 3 and 7. We assessed cytotoxic and vasogenic edema. For this, we collected relative apparent diffusion coefficient (rADC) and relative T2 signal intensity (rT2-SI) values. Regions of interest (ROIs) included: inner parts of the hematoma, tissues surrounding the hematoma (perihematomal inner and outer layers), and the ipsilateral cortex.

Results: In the ICH-only group, no decreased rADC values were observed in the perihematomal ROIs. In this group, rADC and rT2-SI values of the cortex showed no changes during the follow-up. rADC was increased in earlier DC groups (1 and 6 h) on day 3 compared to ICH-only group. No increase in rT2-SI accompanied this finding. Intrahematomal ROI’s showed no differences on MRI related to the timing of the DC. Increased rT2-SI in perihematomal outer ROI was a consistent finding during the follow-up, starting from the baseline imaging and it was further increased on day 3 when DC was performed at 6 h.

Conclusions: We found no evidence of perihematomal ischemic penumbra in the hyperacute phase (day 0) in ICH model. We also suggest that hematoma leads to no secondary injury in the cortex. DC performed earlier than 24 h induced MRI changes suggesting tissue expansion both in perihematomal tissues and the cortex. DC generates no effect on inner hematomal MRI parameters, thus the composition of the hematoma remains same despite DC.