Purpose To evaluate the correlation between angiographic measures of Moyamoya disease and tissue-level impairment from measurements of tissue perfusion and cerebrovascular reactivity (CVR). Materials and Methods The relationship between perfusion-weighted arterial spin labeling (ASL) and hypercarbic blood oxygenation-level dependent (BOLD) CVR and time-to-peak (TTP) were compared with angiographically measured risk factors including arterial circulation time (ACT) and modified Suzuki Score (mSS) in patients (n=15) with Moyamoya disease. Results Hemodynamic contrasts provided information not apparent from structural or angiographic imaging. Mean z-statistics demonstrate that BOLD is significantly (P=0.017) higher in low mSS hemispheres (z-statistic=5.0±2.5) compared to high mSS hemispheres (z-statistic=3.7±1.7), implying that regions with less advanced stages of Moyamoya disease have higher reactivity. After correcting for multiple comparisons, a strong trend for a direct relationship (R=0.38; P=0.03) between BOLD TTP and ACT was observed, and a significant inverse relationship between CBF and ACT (R=−0.47; P=0.01) was found, demonstrating that BOLD and ASL contrasts reflect DSA measures of vascular compromise in Moyamoya disease, albeit with different sensitivity. Conclusion Correlative measures between angiography and hemodynamic methods suggest that BOLD and ASL could be used for expanding the diagnostic imaging infrastructure in Moyamoya patients and potentially tracking tissue response to revascularization.
Rupture of a cerebral arteriovenous malformation can result in devastating hemorrhage with a possibility of serious neurological injury or death. Endovascular embolization is an important adjunct in the treatment of cerebral arteriovenous malformations, and in a small number of cases may provide definitive treatment. Currently available embolic agents have several shortcomings, including the possibility of recanalization, adhesiveness to the endovascular microcatheter and suboptimal handling at the time of surgical resection. Onyx is an ethylene vinyl alcohol copolymer dissolved in dimethyl sulfoxide that was approved by the US FDA in July 2005 as an embolic agent for brain arteriovenous malformations. Although long-term follow-up is limited, this agent appears to offer several advantages over the other available embolic agents for the endovascular management of arteriovenous malformations and other vascular lesions.
'Vascular steal' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n ¼ 40) underwent a multimodal 3.0T MRI protocol including structural (T 1 -weighted and T 2 -weighted fluidattenuated inversion recovery) and hemodynamic (BOLD and CBF-weighted arterial spin labeling) functional MRI during room air and hypercarbic gas administration. CBF changes in regions demonstrating negative BOLD reactivity were recorded, as well as clinical correlates including symptomatic hemisphere by infarct and lateralizing symptoms. Fifteen out of forty participants exhibited negative BOLD reactivity. Of these, a positive relationship was found between BOLD and CBF reactivity in unaffected (stenosis degreeo50%) cortex. In negative BOLD cerebrovascular reactivity regions, three patients exhibited significant (Po0.01) reductions in CBF consistent with vascular steal; six exhibited increases in CBF; and the remaining exhibited no statistical change in CBF. Secondary findings were that negative BOLD reactivity correlated with symptomatic hemisphere by lateralizing clinical symptoms and prior infarcts(s). These data support the conclusion that negative hypercarbia-induced BOLD responses, frequently assigned to vascular steal, are heterogeneous in origin with possible contributions from autoregulation and/or metabolism.
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