Assessment of cerebrovascular insufficiency with MR-ASL perfusion in patients with moyamoya angiopathy

Purpose. To develop a methodology for assessing the degree of cerebrovascular insufficiency in patients with moyamoya angiopathy (AMM) based on measurement of cerebral blood flow (CBF) and determination the presence of arterial transit artifact (ATA) using MR method of arterial spin labeling (ASL).

Materials and methods. The study included 47 patients with AMM who underwent 148 MR studies in PCASL mode (296 hemispheres), of which 47 (94 hemispheres) were done before surgical treatment. On received perfusion maps 7 areas of interest (ROI) were manually set in the gray and white matter of the brain using “Fusion” technique outside the ATA zones. The CBF values at the central point of the ATA were estimated. In the preoperative stage, 47 patients underwent direct angiography to assess the stage of the disease according to Suzuki, the presence and severity of leptomeningeal and transdural collaterals and MR angiography to assess the stage of the disease according to Houkin and the level of ICA stenosis. Statistical processing included univariate analysis of variance (ANOVA) and chi-square test (IBM SPSS Statistics 23).

Results. ATA was detected in 77% of studies (69% of hemispheres). The average minimum CBF in ATA was 120.2 ± 21.1 ml/min/ 100 g at the lower bound of the confidence interval of 117.43 ml/min / 100 g. The average maximum CBF in ATA was 234.9. Depending on the CBF values in the MCA territory and the presence of ATA, 4 degrees of perfusion deficiency were identified: degree 0 (CBF = 64.5 ± 16.2 ml/min / 100 g, without ATA) corresponded to the stage of “compensation” of cerebral blood flow, degree 1 (CBF = 61.5 ± 16.6 ml/min/ 100 g, with ATA) – “subcompensation”, degree 2 (CBF = 26.5 ± 7.2 ml/min/100 g, with ATA) – “initial decompensation”, degree 3 (CBF = 16.0 ± 4.7 ml/min / 100 g, without ATA) – “decompensation”. The highlighted degrees statistically significantly differed among themselves in all ROIs (p < 0.0001). More severe perfusion deficiency corresponded to the more developed stages of AMM according to Suzuki and Houkin, proximal stenosis of the ICA (p < 0.0001), and more severe neurological deficit (p < 0.02). The occurrence of ATA reliably reflected the presence of leptomeningeal collaterals (p < 0.001).

Conclusions. The proposed method for assessing patterns of ASL perfusion has a good agreement with the stage of the disease, the presence of sources of collateral circulation, the severity of neurological deficit and can be used to assess cerebrovascular insufficiency in patients with AMM.

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