Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Aug;23(8):407-431.
doi: 10.1007/s11910-023-01282-2. Epub 2023 Jul 3.

Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke

Diana L Alsbrook  1 , Mario Di Napoli  2 , Kunal Bhatia  3 , José Biller  4 , Sasan Andalib  5 , Archana Hinduja  6 , Roysten Rodrigues  7 , Miguel Rodriguez  8 , Sara Y Sabbagh  9 , Magdy Selim  10 , Maryam Hosseini Farahabadi  9 , Alibay Jafarli  11 , Afshin A Divani  12
Affiliations
Review

Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke

Diana L Alsbrook et al. Curr Neurol Neurosci Rep. 2023 Aug.

Abstract

Purpose of review: This review aims to provide an overview of neuroinflammation in ischemic and hemorrhagic stroke, including recent findings on the mechanisms and cellular players involved in the inflammatory response to brain injury.

Recent findings: Neuroinflammation is a crucial process following acute ischemic stroke (AIS) and hemorrhagic stroke (HS). In AIS, neuroinflammation is initiated within minutes of the ischemia onset and continues for several days. In HS, neuroinflammation is initiated by blood byproducts in the subarachnoid space and/or brain parenchyma. In both cases, neuroinflammation is characterized by the activation of resident immune cells, such as microglia and astrocytes, and infiltration of peripheral immune cells, leading to the release of pro-inflammatory cytokines, chemokines, and reactive oxygen species. These inflammatory mediators contribute to blood-brain barrier disruption, neuronal damage, and cerebral edema, promoting neuronal apoptosis and impairing neuroplasticity, ultimately exacerbating the neurologic deficit. However, neuroinflammation can also have beneficial effects by clearing cellular debris and promoting tissue repair. The role of neuroinflammation in AIS and ICH is complex and multifaceted, and further research is necessary to develop effective therapies that target this process. Intracerebral hemorrhage (ICH) will be the HS subtype addressed in this review. Neuroinflammation is a significant contributor to brain tissue damage following AIS and HS. Understanding the mechanisms and cellular players involved in neuroinflammation is essential for developing effective therapies to reduce secondary injury and improve stroke outcomes. Recent findings have provided new insights into the pathophysiology of neuroinflammation, highlighting the potential for targeting specific cytokines, chemokines, and glial cells as therapeutic strategies.

Keywords: Astrocytes; Brain damage; Chemokines; Cytokines; Edema; Glial cells; Hemorrhagic stroke; Immune cells; Inflammatory response; Intracerebral hemorrhage; Ischemic stroke; Microglia; Neuroinflammation; Pathophysiology; Secondary injury; Therapeutic targets.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Schematic representation of neuroinflammation after stroke. Following stroke, activated microglia and astrocytes release proinflammatory cytokines and chemokines, leading to the recruitment and activation of immune cells such as monocytes and T cells from the periphery. This leads to further production of proinflammatory cytokines, perpetuating the inflammatory response. The inflammatory response contributes to the progression of brain damage, but also plays a role in tissue repair and neuroplasticity. Blood-brain barrier (BBB), matrix metalloproteinases (MMPs), nitric oxide (NO), danger-associated molecular patterns (DAMPs), high mobility group box-1 (HMGB1), interleukin (IL), and tumor necrosis factor (TNF). This figure is not exhaustive and only includes some of the main contributors and pathophysiological processes involved in neuroinflammation in stroke
See this image and copyright information in PMC

References

    1. Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, et al. 2021 Guideline for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline from the American Heart Association/American Stroke Association. Stroke. 2021;52(7):e364–467. 10.1161/STR.0000000000000375. - DOI - PubMed
    1. Jung S, Gilgen M, Slotboom J, El-Koussy M, Zubler C, Kiefer C, et al. Factors that determine penumbral tissue loss in acute ischaemic stroke. Brain. 2013;136(Pt 12):3554–60. 10.1093/brain/awt246. - DOI - PubMed

    2. This article examines the factors that contribute to the loss of penumbral tissue in cases of acute ischemic stroke. The study identifies variables such as time to treatment, collateral circulation, and infarct core size as critical determinants of penumbral tissue loss.

    1. Jurcau A, Simion A. Neuroinflammation in cerebral ischemia and ischemia/reperfusion injuries: from pathophysiology to therapeutic strategies. Int J Mol Sci. 2021;23(1):14. 10.3390/ijms23010014. - DOI - PMC - PubMed
    1. DiSabato DJ, Quan N, Godbout JP. Neuroinflammation: the devil is in the details. Journal of neurochemistry. 2016;139(Suppl 2):136–53. 10.1111/jnc.13607. - DOI - PMC - PubMed
    1. Schaeffer S, Iadecola C. Revisiting the neurovascular unit. Nat Neurosci. 2021;24(9):1198–209. 10.1038/s41593-021-00904-7. - DOI - PMC - PubMed

    2. This article revisits the concept of the neurovascular unit, emphasizing its crucial role in maintaining brain function and highlighting its relevance in neurological disorders. The review provides insights into the molecular and cellular mechanisms underlying neurovascular unit dysfunction and highlights its potential as a therapeutic target for various neurological conditions.