Subjects with hemodynamic failure stage 2 (i.e. misery-perfusion) have heightened risk of acute and chronic brain tissue damage. One of the most important signs of misery-perfusion is a negative cerebrovascular reactivity (CVR). CVR is defined as a blood flow response to a vasoactive stimulus. Recently blood-oxygenation-level-dependent (BOLD) CVR was proposed to detect misery-perfusion. However, BOLD-CVR MRI signal does not reflect CBF changes directly and discrepancies between negative BOLD-CVR and negative CBF changes have been reported. To better assess these discrepancies, we performed a multimodal clinical misery-perfusion assessment with perfusion-weighted-MRI and transcranial-Doppler complimentary to BOLD-CVR in patients with symptomatic steno-occlusive disease.
Here we have shown that brain regions with negative BOLD-CVR present within the ipsilateral symptomatic hemisphere exhibit classical hemodynamic sign of misery perfusion and increasing need for compensatory leptomeningeal collateralisation. Specifically, regions with negative BOLD-CVR show an increase in CBV, as well as a prolonged MTT and TTP.3-5 The only parameter not showing classical signs of misery perfusion is CBF, where one would expect . Here CBF did not show a significant difference between ipsi- and contralateral hemisphere. Regarding collateralisation, the diastolic and systolic PCA-P2 flow velocity was significantly increased towards the ipsilateral hemisphere indication a need for compensatory collateral pathways to preserve perfusion.6 This can also be seen with the strong correlation between volume of the region of negative BOLD-CVR, the average CVR within the region of negative BOLD-CVR and the systolic PCA-P2 flow. With increasing volumes and decreasing quantitative negative CVR, the need for compensatory flow over the PCA-P2 will increasing.
Brain regions with negative BOLD-CVR present within the ipsilateral symptomatic hemisphere exhibit classical hemodynamic sign of misery perfusion and increasing need for compensatory leptomeningeal collateralisation, increasing the evidence of a true vascular phenomenon.
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