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. 2021 Jul 18;10(2):927–939. doi: 10.1007/s40122-021-00288-3

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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-nc/4.0/.

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Fig. 1 — Microglial activation plays an important role in pain post hemorrhagic stroke and interactions with other cells. After a stroke, inflammation can cause pain, and pain can also aggravate the inflammatory response. When microglia and macrophages are activated, they can differentiate into two subtypes, M1 (which increase inflammation and pain) and M2 (protective), under the influences of different chemokines. However, the specific functions of the two subtypes of microglia in post-stroke pain have not yet been clarified. At the same time, microglia may have an impact on astrocytes during the ongoing inflammation, thereby changing the functional state of the blood–brain barrier (BBB)