Author Affiliation: Department of Neurology, Massachusetts General Hospital, Boston.
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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