Article
Perfusion-dependent impairment of cerebral autoregulation in malignant hemispheric stroke
Perfusionsabhängige Einschränkung der zerebralen Autoregulation bei malignem Media Infarkt
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Published: | May 8, 2019 |
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Objective: Regional loss of cerebral autoregulation (CA) has been shown to play a key role in secondary brain damage attributable to edema formation and infarct progression in malignant hemispheric stroke (MHS). However, it remains unclear to what extent CA impairment depends on the regional perfusion level within the affected hemisphere. Therefore, in the present study we performed a spatial-temporal assessment of CA in patients undergoing decompressive hemicraniectomy (DC) for treatment of MHS.
Methods: In 24 patients undergoing DC, autoregulation over the affected hemisphere was intraoperatively assessed by continuous cortical perfusion mapping by Laser Speckle Imaging (LSI) and mean arterial blood pressure (MAP) monitoring. Regions of interest (ROIs) were positioned within the color-coded LSI perfusion map and LSI-specific cortical perfusion was calculated within the infarcted and non-infarcted cortex. Cortical perfusion was normalized to 100% and six levels of cortical perfusion were defined (0–20%, 20–40%, 40–60%, 60–80%, 80–100% and >100%). Means, standard deviations and confidence intervals (CI) of the cortical perfusion level, MAP and the interaction of both variables during a 20-minute monitoring period were estimated with a linear random slope model and Pearson correlation analysis.
Results: For each perfusion level, n=578 ROIs were analyzed across all hemispheres. Pearson correlation analysis showed significantly less autoregulation impairment in non-infarcted tissue (>100%: r=0.36) than in tissue with critically reduced cortical perfusion (20–40%: r=0.67; 40–60%: r=0.68; 60–80%: r=0.68; *p<0.05). Further, linear cortical perfusion changes per mmHg MAP were significantly greater in areas with critically reduced perfusion (40–60%: 0.42% per mmHg and 60–80%: 0.46% per mmHg) compared to non-infarcted (>100%: 0.22% per mmHg) or infarcted (0–20%: 0.29% per mmHg) areas (*p<0.001).
Conclusion: Spatial identification of regions with penumbral perfusion patterns may be critical for effectively targeting CA as a strategy to prevent secondary neurologic injury in patients suffering MHS.