Relationship between vasospasm, cerebral perfusion, and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

Abstract

Introduction Vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is thought to cause ischemia. To evaluate the contribution of vasospasm to delayed cerebral ischemia (DCI), we investigated the effect of vasospasm on cerebral perfusion and the relationship of vasospasm with DCI. Methods We studied 37 consecutive SAH patients with CT angiography (CTA) and CT perfusion (CTP) on admission and within 14 days after admission or at time of clinical deterioration. CTP values (cerebral blood volume, cerebral blood flow (CBF) and mean transit time), degree of vasospasm on CTA, and occurrence of DCI were recorded. Vasospasm was categorized as follows: no spasm (0-25% decrease in vessel diameter), moderate spasm (25-50% decrease), and severe spasm (>50% decrease). The correspondence of the flow territory of the most spastic vessel with the least perfused region was evaluated, and differences in perfusion values and occurrence of DCI between degrees of vasospasm were calculated with 95% confidence intervals (95% CI). Results Fourteen patients had no vasospasm, 16 were moderate, and seven were severe. In 65% of patients with spasm, the flow territory of the most spastic vessel corresponded with the least perfused region. There was significant CBF (milliliters per 100 g per minute) difference (−21.3; 95% CI, −37↔−5.3) between flow territories of severe and no vasospasm. Four of seven patients with severe, six of 16 with moderate, and three of 14 patients with no vasospasm had DCI. Conclusion Vasospasm decreases cerebral perfusion, but corresponds with the least perfused region in only two thirds of our patients. Furthermore, almost half of patients with severe vasospasm do not have DCI. Thus, although severe vasospasm can decrease perfusion, it may not result in DCI.

Cerebral Autoregulation after Subarachnoid Hemorrhage: Comparison of Three Methods

“…The two modalities measure different anatomic regions of the brain as well as different vascular beds. It is conceivable that focal disturbances of cerebral blood flow, which are known to occur after SAH, 38 may influence the two modalities differently. Furthermore, current understanding of the development of DCI suggests a multifactorial process with microemboli, microthrombosis, macrovascular spasm, and cortical spreading depolarization all playing a part.…”

A Phase I proof-of-concept and safety trial of sildenafil to treat cerebral vasospasm following subarachnoid hemorrhage

“…4,6,7,11 In those patients, 50% will develop DCI. 7,8,17,61 With this strong correlation, it is recommended that CVS be used as an initial outcome measure when assessing potential treatments for DCI. 13,78 However, as research continues to elucidate the multifactorial nature of DCI, future interventions will need to attack not only CVS, but other contributors to DCI as well.…”

Can CT Perfusion Guide Patient Selection for Treatment of Delayed Cerebral Ischemia?

“…In recent years, CTP has also been used as a complimentary diagnostic tool for evaluation of DCI related to vasospasm. Specifically, qualitative CTP deficits have a high sensitivity and specificity [1-3,5, [13][14][15] for vasospasm reported in 97% of patients with vasospasm compared to 24% without vasospasm [5]. Furthermore, Aralasmak et al correlated CTP deficits and the degree of vessel narrowing with CTP deficits occurring in 83% of patients with severe vasospasm compared to 26% with mild-moderate and 15% without vasospasm [2].…”