Abstract
Aneurysmal subarachnoid hemorrhage (aSAH) represents only a small portion of all strokes, but accounts for almost half of the deaths caused by stroke worldwide. Neurosurgical clipping and endovascular coiling can successfully obliterate the bleeding aneurysms, but ensuing complications such as cerebral vasospasm, acute and chronic hydrocephalus, seizures, cortical spreading depression, delayed ischemic neurological deficits, and delayed cerebral ischemia lead to poor clinical outcomes. The mechanisms leading to these complications are complex and poorly understood. Early brain injury resulting from transient global ischemia can release molecules that may be critical to initiate and sustain inflammatory response. Hence, the events during early brain injury can influence the occurrence of delayed brain injury. Since the damage associated molecular pattern molecules (DAMPs) might be the initiators of inflammation in the pathophysiology of aSAH, so the aim of this review is to highlight their role in the context of aSAH from diagnostic, prognostic, therapeutic, and drug therapy monitoring perspectives. DAMPs represent a diverse and a heterogenous group of molecules derived from different compartments of cells upon injury. Here, we have reviewed the most important DAMPs molecules including high mobility group box-1 (HMGB1), S100B, hemoglobin and its derivatives, extracellular matrix components, IL-1α, IL-33, and mitochondrial DNA in the context of aSAH and their role in post-aSAH complications and clinical outcome after aSAH.
Highlights
Aneurysms are the weak bulging lesions or abnormal dilatations present in 1–5% of the adult population [1]
The elevated high mobility group box-1 (HMGB1) levels were higher in the cerebrospinal fluid (CSF) of patients with a poor clinical outcome after aSAH and HMGB1 levels correlated with Tumor necrosis factor (TNF)-α, IL-6, and IL-8, suggesting an indispensable role of HMGB1 in ongoing inflammation [22]
damage associated molecular pattern molecules (DAMPs) have been shown to be implicated in various CNS disorders, for instance, it has been demonstrated that HMGB1 is involved in ischemic/hypoxic and microhemorrhagic events occurring in the course of spontaneous seizures [146,147]
Summary
Aneurysms are the weak bulging lesions or abnormal dilatations present in 1–5% of the adult population [1]. Aneurysms are formed due to the hemodynamic shear stress in the arterial wall at the bifurcation of arteries and are marked by chronic inflammation and degeneration in the arterial wall [2,3]. The rupture of an intracranial aneurysm leads to subarachnoid hemorrhage that accounts for only 5% of all the stroke events, but the mortality inflicted by it is around 50% (32 to 67%) and affects a relatively younger age group compared to ischemic stroke [4,5,6]. The fatality of the disease is reflected by 20% deaths occurring before any medical attention, 30% within 24 h of onset, and 40–60% within a month after subarachnoid hemorrhage [4,8]. One third remains lifelong dependent and those who have a good recovery still have neurological and/or cognitive deficits [9,10]
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