C erebral infarction with permanent vasospasminduced delayed ischemic neurological deficits (DIND) after aneurysmal subarachnoid hemorrhage (aSAH) is a feared and unfortunately frequent complication, responsible for poor functional and overall outcome. 2 The pathophysiology of DIND and vasospasminduced delayed cerebral infarction (DCI) after aSAH is multifactorial and still not fully understood. It is well accepted that vasospasm is a major contributor to DIND and DCI, but it is also assumed that processes already initiated shortly after aSAH render some brain areas more vulnerable for vasospasm than others. 20,27,33 In up to 15% of patients, cerebral infarction and a fixed neurological deficit (including death) are irreversible end points of a dynamic process starting with tissue predisposition and asymptomatic vasospasm, followed by symptomatic vasospasm and transient DIND. For the successful prevention of infarction by antivasospastic therapy, timely recognition of abbreviatioNs aSAH = aneurysmal subarachnoid hemorrhage; BFV = blood flow velocity; CBF = cerebral blood flow; CBV = cerebral blood volume; CTA = CT angiography; CTP = CT perfusion; DCI = delayed cerebral infarction; DIND = delayed ischemic neurological deficits; DSA = digital subtraction angiography; MIP = maximum-intensity projection; MTT = mean transit time; NPV = negative predictive value; PPV = positive predictive value; ROI = region of interest; TCD = transcranial Doppler sonography; TTP = time to peak; TTS = time to start. obJective This prospective study investigated the role of whole-brain CT perfusion (CTP) studies in the identification of patients at risk for delayed ischemic neurological deficits (DIND) and of tissue at risk for delayed cerebral infarction (DCI). methods Forty-three patients with aneurysmal subarachnoid hemorrhage (aSAH) were included in this study. A CTP study was routinely performed in the early phase (Day 3). The CTP study was repeated in cases of transcranial Doppler sonography (TCD)-measured blood flow velocity (BFV) increase of > 50 cm/sec within 24 hours and/or on Day 7 in patients who were intubated/sedated. results Early CTP studies revealed perfusion deficits in 14 patients, of whom 10 patients (72%) developed DIND, and 6 of these 10 patients (60%) had DCI. Three of the 14 patients (21%) with early perfusion deficits developed DCI without having had DIND, and the remaining patient (7%) had neither DIND nor DCI. There was a statistically significant correlation between early perfusion deficits and occurrence of DIND and DCI (p < 0.0001). A repeated CTP was performed in 8 patients with a TCD-measured BFV increase > 50 cm/sec within 24 hours, revealing a perfusion deficit in 3 of them (38%). Two of the 3 patients (67%) developed DCI without preceding DIND and 1 patient (33%) had DIND without DCI. In 4 of the 7 patients (57%) who were sedated and/or comatose, additional CTP studies on Day 7 showed perfusion deficits. All 4 patients developed DCI. coNclusioNs Whole-brain CTP on Day 3 after aSAH allows early and rel...
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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