Year: 2024
Type: editorial
Abstract: In the days to weeks following spontaneous subarachnoid hemorrhage (SAH) up to 30% of patients develop brain infarcts, the imaging correlate of delayed cerebral ischemia (DCI). 1 DCI is of clinical relevance due to its high incidence, its demonstrated negative impact on outcome, and its delayed occurrence relative to the index SAH.The latter suggests a therapeutic window of opportunity.1,2 However, DCI cannot be predicted due to a lack of reliable biomarkers, and prevention is centered on the use of the oral calcium antagonist nimodipine which reduces the risk of DCI and poor outcome.Other more effective treatments are unavailable because DCI's pathophysiology is not understood.3 Anatomically, vasospasm of the larger brain vessels, and on a cellular level neutrophilmediated inflammation have been linked to secondary injury processes and DCI.4,5 However, large-vessel vasospasm and DCI are correlated poorly, 6 and neutrophils have complex and essential roles in immunity, tissue repair, and resolution of inflammation.Thus, interventions targeting large vessel vasospasm or broad blockade of neutrophil recruitment or function are not suitable treatment strategies.In this issue of Stroke, Nakagawa et al. present a study that follows both conceptual frameworks of DCI pathophysiology, vasospasm and neutrophils, further downstream by investigating a potential association between microvasospasm and neutrophil extracellular traps (NETs) in a mouse model of SAH. 7 NETs are DNA filaments decorated with cytotoxic and proinflammatory proteins, secreted by neutrophils into the extracellular space
Source: Stroke
Authors: Jens Witsch, Thilo Witsch, Kimberly Martinod
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4403901155