Beyond delayed cerebral vasospasm: infarct patterns in patients with subarachnoid hemorrhage

Angiographic vasospasm (CVS) has been accused to be the main cause of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH). However, treatment success including endovascular treatment remains to be improved. We performed a pattern analysis of ischemic lesions in SAH patients in the absence of angiographic cerebral vasospasm to generate further hypotheses concerning etiology and risk factors of DCI apart from vasospastic narrowing.

We retrospectively included 309 patients with cerebral infarcts after SAH. Vasospasm was assessed by means of CT or MR angiography and perfusion measurement or digital subtraction angiography. All clinical and radiological data were used to determine the most probable etiology for new infarcts.

Twenty-seven percent of patients showed infarcts without presence of angiographic vasospasm. Seventy-three percent of these "atypical infarcts" were induced by complications of aneurysm therapy, 7 % by hypoxia, 2 % by ICP-related herniation. In 17 %, the etiology remained unclear; however, disturbances of the microcirculation for different reasons were the most likely cause in these patients.

Beyond CVS and treatment complications, a not insignificant number of SAH patients suffered from infarcts of other etiology probably due to disturbance of the microcirculation. Therapeutic approaches for vasodilation of angiographic vasospasm alone should be reconsidered.