We thank Zhang and colleagues for their comments. While potential mechanisms were not addressed in detail in our article,1 we and others have previously proposed that RCVS-associated brain hemorrhage results from dynamic arterial caliber changes that cause postischemic reperfusion injury or abrupt vasodilatation and rupture of small arteries.1-3 Several observations support this hypothesis. First, RCVS-associated lobar hemorrhages are usually located in arterial watershed regions and often coexist with ischemic lesions, suggesting that ischemia-reperfusion injury is an important mechanism. Second, reversible brain edema can precede RCVS-associated brain hemorrhage, suggesting that the vascular process initially involves small vessels that are beyond the resolution of angiography. Indeed, Ducros et al4 have shown that RCVS is a dynamic arteriopathy, with the more proximal arteries becoming affected later. Hence, it is not a prerequisite, as suggested by Zhang and colleagues, to document vasoconstriction prior to brain hemorrhage in order to prove our hypothesis.
Singhal AB. Reversible Cerebral Vasoconstriction Syndrome and Hemorrhagic Events: Who Precedes Whom?—Reply. Arch Neurol. 2011;68(12):1614–1615. doi:10.1001/archneur.68.12.1615-a
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