Abstract
Intracerebral hemorrhage (ICH) is a subtype of stroke which is associated with the highest mortality and morbidity rates of all strokes. Although it is a major public health problem, there is no effective treatment for ICH. As a consequence of ICH, various blood components accumulate in the brain parenchyma and are responsible for much of the secondary brain damage and ICH-induced neurological deficits. Therefore, the strategies that could attenuate the blood component-induced neurotoxicity and improve hematoma resolution are highly needed. The present article provides an overview of blood-induced brain injury after ICH and emphasizes the need to conduct further studies elucidating the mechanisms of hematoma resolution after ICH.
Highlights
Intracerebral Hemorrhage (ICH) is a devastating sub-type of stroke caused by blood vessel rupture in the brain and the subsequent bleeding into the surrounding tissue [1]
The key factors that contribute to secondary brain injury after ICH are thrombin, hemoglobin, hemin, and iron—the blood components that are known to activate cytotoxic, excitotoxic, oxidative, and inflammatory pathways [7]
Hb released after intraventricular hemorrhage is taken up into neurons via CD163, causing increased cellular iron leading to neuronal death [73,74]
Summary
Intracerebral Hemorrhage (ICH) is a devastating sub-type of stroke caused by blood vessel rupture in the brain and the subsequent bleeding into the surrounding tissue [1]. The worldwide incidence of ICH has risen by ~47% over the last 20 years [2], and hospital admissions have increased by 18% in the past ten years [19]. Hypertension increases the risk of ICH approximately two-fold [23] and is associated with 83% of ICH patients [24] Another risk factor that accounts for ~20% of ICH is cerebral amyloid angiopathy, which is characterized by the deposition of amyloid-β plaques in capillaries, arterioles, and small arteries within the brain. White-matter abnormalities seem to increase the risk of both sporadic and familial intracerebral hemorrhage, implicating a prominent role of vascular deformities in the onset of ICH. Age increases the risk of comorbidities, including hypertension, vascular deformities, and cerebral amyloid angiopathy, that contribute to the pathology of ICH [2,22]. The data pertinent to the present article was collected by the PubMed database search with no time limitation and using the search terms intracerebral hemorrhage, thrombin, hemoglobin, hemin, and iron
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