Résumé
Delayed cerebral ischemia is a dramatic and yet poorly understood complication of aneurysmal subarachnoid hemorrhage. To these days, most effort has focused on macrovasospasm, a phenomenon occurring together with secondary neurological deterioration. However, emerging evidence from animal models and physiological clinical studies point towards an underestimated but fundamental role for early microvascular defects in the pathogenesis of delayed ischemia.Hypothesis: we suspect that early brain injuries inflicted to microvascular components, in particular capillary pericytes, lead to long-lasting microcirculatory defects and eventually to delayed cerebral ischemia. We suppose that macrovasospasm acts as a secondary element further hindering microperfusion in precociously affected areas.Method: we proposed a monocentric, prospective, interventional pilot trial for assessing the link between early microvascular alterations after aneurysmal subarachnoid hemorrhage using early dynamic 18F-fluorodesoxyglucose Positron Emission Tomography/Computer Tomography (dynamic 18F-FDG PET/CT) and delayed complications. Subjects with high-risk for delayed ischemia were included.Results: among high risk for DCI patients, 77% of them presented at least one vasospasm of a large vessel and 63% of them were concerned by a severe vasospasm phenomenon. We noted a significant inter-individual variability in K1 microparameter quantification but a strong reduction of CMRglu in the subgroup of patients under GA. According to paired analysis there was no statistically significant association between global K1, neither global CMRglu and delayed severity of patients.Discussion: we showed that the K1 parameter, reflecting the cerebral blood flow, and the cerebral metabolic rate of glucose varied greatly between individuals. We confirmed the strong impact of general anesthesia on cerebral metabolic rate of glucose. This study does not position the dynamic 18F-FDG PET/CT as a tool for predicting progression to delayed cerebral ischemia, it provides someinteresting insights into possible pathophysiological signatures of delayed cerebral ischemia after SAH.