Journal
SCIENCE
Volume 367, Issue 6483, Pages 1211-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax7171
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Funding
- National Institute of Neurological Disorders and Stroke
- National Institute on Aging (U.S. National Institutes of Health) [R01NS100366, RF1AG057575, K08NS089830]
- NIH-NINDS [R35 NS097265]
- U.S. Army Research Office [MURI W911NF1910280]
- Fondation Leducq Transatlantic Networks of Excellence Program
- Novo Nordisk Foundation
- Lundbeck Foundation
- EU Horizon 2020 research and innovation program [666881]
- H2020 Societal Challenges Programme [666881] Funding Source: H2020 Societal Challenges Programme
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Stroke affects millions each year. Poststroke brain edema predicts the severity of eventual stroke damage, yet our concept of how edema develops is incomplete and treatment options remain limited. In early stages, fluid accumulation occurs owing to a net gain of ions, widely thought to enter from the vascular compartment. Here, we used magnetic resonance imaging, radiolabeled tracers, and multiphoton imaging in rodents to show instead that cerebrospinal fluid surrounding the brain enters the tissue within minutes of an ischemic insult along perivascular flow channels. This process was initiated by ischemic spreading depolarizations along with subsequent vasoconstriction, which in turn enlarged the perivascular spaces and doubled glymphatic inflow speeds. Thus, our understanding of poststroke edema needs to be revised, and these findings could provide a conceptual basis for development of alternative treatment strategies.
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