15.09.2020 | Invited Commentary
Commentary on TNF-R1 Correlates with Cerebral Perfusion and Acute Ischemia Following Subarachnoid Hemorrhage
verfasst von:
H. E. Hinson
Erschienen in:
Neurocritical Care
|
Ausgabe 3/2020
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Excerpt
The quest to identify accurate biomarkers of delayed ischemic neurologic deficit (DIND) after aneurysmal subarachnoid hemorrhage (aSAH) has been both daunting and, at times, bewildering due our incomplete understanding of the underlying mechanism of DIND. Historically, DIND, and thus poor outcome after aSAH, was thought to be due to large vessel vasospasm. This view evolved as treatment trials addressing vasospasm failed to completely prevent DIND. In recent years, clinicians and investigators have recognized that large vessel spasm is likely only one of several pathways resulting in DIND [
1]. It is widely believed that inflammation plays at least a partial role in the pathophysiology that results in DIND, which has resulted in intense study of inflammatory proteins as candidate predictive biomarkers. Produced by monocytes and macrophages, the inflammatory cytokine tumor necrosis factor alpha (TNF-a) is one such candidate. Levels of TNF-a in the blood [
2] and in the cerebrospinal fluid [
3] have been associated with poor outcome after aSAH, but not with angiographic vasospasm [
2]. These observations provide one of many examples of the apparent disconnect between DIND and imaging findings. …