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We thank Drs. De Simone and Ranieri for their comments and interest in our article.1 Our hypothesis does not support a dysfunction of aquaporin (AQP) 4 in idiopathic intracranial hypertension (IIH); rather, an unknown type of AQP (e.g., aquaglyceroporin) may be involved at the venodural junction and may trigger the hydrodynamic cascade of IIH. We agree that a direct discharge of glymphatic fluid into the venous blood has not been documented in studies of CSF hydrodynamics2; however, the techniques used to demonstrate the existence of the glymphatic and lymphatic systems of the brain were not able to detect any venous CSF outflow, leading some to question even the existence of a venous CSF outflow pathway in the brain.3 Based on our clinical experience (i.e., cerebral venous thrombosis) and on previous experimental studies, we feel that a direct discharge of glymphatic fluid into venous blood seems highly likely.4
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Author disclosures are available upon request (journal{at}neurology.org).
- © 2019 American Academy of Neurology
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