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Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Review criteriaWe searched PubMed for articles in all year ranges with multiple combinations of search terms including, "post-haemorrhagic hydrocephalus", "post-infectious hydrocephalus", "worldwide", "epidemiology", "ETV/CPC", "VP Shunt", "NKCC1", "SPAK", "Toll-like receptors" "inflammation", "obstruction", "impaired reabsorption", "CSF hypersecretion", "cerebrospinal fluid". There were no language exclusions and articles chosen were based on relevance to topics covered in this Review. Peer review information Nature Reviews Neurology thanks [Referee# 1 name], [Referee#2 name] and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

Prolonged intake of excessive amounts of ethanol is known to have adverse effects on the central nervous system (CNS). Here we investigated the effects of acute and chronic ethanol exposure and withdrawal from chronic ethanol exposure on glymphatic function, which is a brain-wide metabolite clearance system connected to the peripheral lymphatic system. Acute and chronic exposure to 1.5 g/kg (binge level) ethanol dramatically suppressed glymphatic function in awake mice. Chronic exposure to 1.5 g/kg ethanol increased GFAP expression and induced mislocation of the astrocyte-specific water channel aquaporin 4 (AQP4), but decreased the levels of several cytokines. Surprisingly, glymphatic function increased in mice treated with 0.5 g/kg (low dose) ethanol following acute exposure, as well as after one month of chronic exposure. Low doses of chronic ethanol intake were associated with a significant decrease in GFAP expression, with little change in the cytokine profile compared with the saline group. These observations suggest that ethanol has a J-shaped effect on the glymphatic system whereby low doses of ethanol increase glymphatic function. Conversely, chronic 1.5 g/kg ethanol intake induced reactive gliosis and perturbed glymphatic function, which possibly may contribute to the higher risk of dementia observed in heavy drinkers.

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