Abstract

Introduction: Cerebral vasospasm with a raised risk for secondary ischemia is a frequent complication after subarachnoid hemorrhage (SAH). The early diagnosis of focal or global cerebral hypoperfusion is important in order to allow treatment before irreversible ischemic damage occurs (intensive care and/or neurointervention). We tested, whether the implementation of “whole brain” volume Perfusion CT (VPCT) for the examination of patients with suspected cerebral vasospasm delivers relevant information about the localization and characteristics of arterial vasospasm and the volume at risk of secondary infarction. Patients and Methods: Patients were eligible for this study, if they had been admitted to our department with suspicion of cerebral vasospasm due to SAH. Patients first received a non-contrast CT of the brain to exclude acute hydrocephalus. After that, VPCT was performed. CT angiographic axial and coronal maximum-intensity projections (MIP) were generated from thin slice recons of the VPCT dataset at peak arterial time. Images were assessed for presence of arterial vasospasm or occlusion and compared with conventional CTA or DSA. The distribution of ischemic lesions was analyzed on 3D perfusion parameter maps of cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT) and time to drain (TTD). Results: 11 patients with SAH were examined with VPCT. In all patients, focal areas of cerebral hypoperfusion were detected on the color coded VPCT parameter maps. The highest sensitivity was found for MTT and TTD. Focal reductions of CBV strongly correlated with infarction on follow-up CT. 8 patients (73%) had focal stenotic lesions of intracranial artery segments due to vasospasm visible on the thin MIP reconstructions of the 4D CTA arterial phase. All of these stenotic lesions were also visible on conventional CTA or DSA, resulting in 100% sensitivity of the 4D CTA reconstructions. In 2 patients, balloon angioplasty of the vasospastic segments was performed subsequently; in both patients, VPCT showed normalization of both the perfusion maps and the vessel diameter afterwards. Conclusion: VPCT is a non-invasive method that allows detecting cerebral vasospasm in patients suffering from SAH. It has the potential to demonstrate brain areas with a focal perfusion deficit as well as vasospastic arterial segments. DSA will remain the gold standard for detection of cerebral vasospasm, but VPCT has the potential to improve diagnosis and treatment decisions in patients suffering from vasospasm due to SAH.

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