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. 2024 Mar 11;25(1):34. doi: 10.1186/s10194-024-01741-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Possible pathogenetic mechanisms of migraine involving the glymphatic system dysfunction. CSD can be responsible for a transient PVS closure causing a GS impairment. The GS dysfunction can lead to the accumulation of excitatory, pro-inflammatory and vasodilator molecules involved in the development and the exacerbation of migraine. CSD: cortical spreading depression; PVS: perivascular space; ROS: reactive oxygen species; CGRP: calcitonin gene-related peptide; ATP: adenosine triphosphate; TNF-α: tumor necrosis factor alpha; IL-1β: interleukin 1-beta; HIF-1α: hypoxia-inducible factor 1-alpha