• Kaibin Shi, De-Cai Tian, Zhi-Guo Li, Andrew F Ducruet, Michael T Lawton, and Fu-Dong Shi.
• Tianjin Medical University General Hospital, Tianjin, China; Department of Neurology, and Department of Neurosurgery, Barrow Neurological Institute, St Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
• Lancet Neurol. 2019 Nov 1; 18 (11): 1058-1066.

AbstractStroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell death and the release of factors such as damage-associated molecular patterns (DAMPs) that elicit localised inflammation in the injured brain region. Such focal brain inflammation aggravates secondary brain injury by exacerbating blood-brain barrier damage, microvascular failure, brain oedema, oxidative stress, and by directly inducing neuronal cell death. In addition to inflammation localised to the injured brain region, a growing body of evidence suggests that inflammatory responses after a stroke occur and persist throughout the entire brain. Global brain inflammation might continuously shape the evolving pathology after a stroke and affect the patients' long-term neurological outcome. Future efforts towards understanding the mechanisms governing the emergence of so-called global brain inflammation would facilitate modulation of this inflammation as a potential therapeutic strategy for stroke.Copyright © 2019 Elsevier Ltd. All rights reserved.

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