| Delayed cerebral ischemia (DCI) is the major complication after subarachnoid hemorrhage (SAH) increasing morbidity and mortality by 3 times. DCI is an ideal model to study cerebral ischemia as, in contrast with thrombo-embolic stroke, patients are in the hospital when ischemia develops. The pathogenesis of DCI is still unclear and a diagnostic test is lacking. Vasospasm was traditionally thought to be causative for DCI. However, since vasospasm has a positive predictive value of only 60%, additional factors must play a role. Treatment for DCI exist, but efficacy has not been proven with randomized clinical trials. One important hindrance for performing trials is the lack of a reliable test for DCI. We aim to investigate the pathogenesis of DCI and develop a diagnostic test. In progressing DCI, a cerebral perfusion deficit is preceding the final infarction. Whether a perfusion deficit is reversible (penumbra) or becomes infarction (DCI) depends on the equilibrium between perfusion deficits and autoregulation capability. To elucidate the pathogenesis of DCI we will study this equilibrium on three levels: 1. vasospasm of the major brain vessels, 2. vasospasm on microvasculatory level and 3. ischemic changes on brain tissue level. For this purpose serial measurements with both CT and MRI are performed. First we will optimize CT and MRI protocols for follow up of SAH patients. Second we will investigate the pathogenesis of DCI by relating the time-course of 1) vasospasm, 2) cerebral perfusion and vasoreactivity and 3) early ischemic changes on tissue level to the development of DCI. Also the diffusion-perfusion mismatch and vasoreactivity on MRI is related to the penumbra-infarct map on CTP. Third, depending on these results we will develop a diagnostic test for DCI either with CT or MRI. And fourth we will study response on treatment and relate this to the development of DCI. |
