Abstract
Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by severe headaches, with or without other acute neurological symptoms, and diffuse segmental constriction of cerebral arteries that resolves spontaneously within 3 months.[1] It can occur spontaneously, especially in middle-aged women[1]; at least half the cases occur after exposure to vasoactive drugs or post-partum. This syndrome is often associated with a favorable outcome in 95% of cases.[1] However, the prognosis of RCVS is especially determined by stroke occurrence. Its management is inspired by what is applied in aneurysmal subarachnoid hemorrhage (aSAH), whose main complication is vasospasm and delayed cerebral ischemia (DCI). Although the physiopathology of RCVS is unclear, it appears to be distinct from aSAH. Indeed, the vasoconstriction in RCVS may be dependent on the activity and sensitivity of vascular receptors, which can lead to a more systemic effect on all brain vessels, as opposed to being dependent on the vasospasm induced by local clot lysis, as has been suggested in aSAH.[2] As cerebral arteries are densely innervated, the release of norepinephrine or neuropeptide Y from the sympathetic nerve endings may cause vasoconstrictions.[3] Angiographically, SAH-induced vasospasm is more commonly long-segmental and mainly around the bleeding focus, compared with the multiple, short-segmental, and diffuse changes seen in RCVS.[4] However, by analogy, RCVS is treated by nimodipine, and in some rare cases, the use of milrinone might be considered.[3]
Published Version
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