The Possible Difference of Underlying Pathophysiologies between “Ivy Sign” on Contrast-Enhanced MRI and FLAIR

We read with interest the article by Wang et al titled “Ivy Sign in Moyamoya Disease: A Comparative Study of the FLAIR Vascular Hyperintensity Sign Against Contrast-Enhanced MR Imaging.” The results of the study carried out by Wang et al are agreeable, which show that the ivy sign score on contrastenhanced MR imaging was statistically significantly correlated with the amount of leptomeningeal collateral from the posterior cerebral artery on digital subtraction angiography, while the ivy sign score on FLAIR was not. A previous report also speculated that the ivy sign score on contrast-enhanced MR imaging may correspond to angiographic cortical microvascularization via leptomeningeal collaterals. Although the authors did not clearly mention it, their results revealed different underlying pathophysiologies between the ivy sign on contrast-enhanced MR imaging and FLAIR. Moreover, the ivy sign on contrast-enhanced MR imaging may not be an alternative to that on FLAIR, based on the following opinions derived from their results. First, the ivy sign score on contrast-enhanced MR imaging before surgery was significantly correlated with the postoperative revascularization grade. The study speculated that the more leptomeningeal collaterals present before surgery, the better the outcome of the revascularization operation would be. The ivy sign on contrastenhancedMR imaging may be angiographic cortical microvascularization via leptomeningeal collaterals. However, the ivy sign on FLAIR before surgery was not significantly correlated with the postoperative revascularization grade. This result indicates that the ivy sign on FLAIR may not reflect leptomeningeal collaterals, but the slow flow of maximally dilated pial vasculature (microscopic cortical microvascularization) compensates for the decreased perfusion. The ivy sign may be observed in the posterior MCA region on FLAIR if the ivy sign on FLAIR reflects leptomeningeal collaterals from the posterior cerebral artery similar to the ivy sign on contrast-enhanced MR imaging. However, it was more frequently observed in the anterior MCA region than in the posterior MCA region on FLAIR in our previous study. Did the distribution of ivy signs in the study population ofWang et al differ between contrast-enhanced MR imaging and FLAIR? The ivy sign on FLAIR was significantly correlated with the cerebrovascular reserve on SPECT, suggesting that it may reflect the slow flow of maximally dilated pial vasculature. The postoperative decrease in ivy signs on FLAIR in the operative side with an increase in cerebrovascular reserve on SPECT supports the current hypothesis. Second, they showed that the ivy sign score on contrastenhanced MR imaging was negatively correlated with CBF in the MCA region in the late Suzuki stage. Their speculation was that it was because of the imbalance between leptomeningeal collaterals and abnormal ICA and Moyamoya vessels; however, posterior circulation (posterior cerebral artery stenosis or occlusion) was often involved in this phase, and various amounts of leptomeningeal collaterals may be present on a case-by-case basis. Therefore, the ivy sign on contrast-enhanced MR imaging in the late Suzuki stage may be attributable to maximally dilated pial vasculature, as well as leptomeningeal collaterals. Further study with the ivy sign distribution and cerebrovascular reserve assessment will be needed to confirm the different underlying pathophysiologies between the ivy sign on contrast-enhanced MR imaging and FLAIR.