Neuroinflammation after intracerebral hemorrhage

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Neuroinflammation after intracerebral hemorrhage

Spontaneous intracerebral hemorrhage (ICH) is a particularly severe type of stroke for which no specific treatment has been established yet. Although preclinical models of ICH have substantial methodological limitations, important insight into the pathophysiology has been gained. Mounting evidence suggests an important contribution of inflammatory mechanisms to brain damage and potential repair...

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Brain Injury After Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) is a subtype of stroke with high morbidity and mortality. The mechanisms underlying ICH-induced brain injury have become better understood during the past decade. Experimental investigations have indicated that thrombin formation, red blood cell lysis, and iron toxicity play a major role in ICH-induced injury and that these mechanisms may provide new therapeutic t...

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Seizures after Spontaneous Intracerebral Hemorrhage

OBJECTIVE In patients with spontaneous intracerebral hemorrhage (ICH), the risk factors for seizure and the effect of prophylactic anticonvulsants are not well known. This study aimed to determine the risk factor for seizures and the role for prophylactic anticonvulsants after spontaneous ICH. METHODS Between 2005 and 2010, 263 consecutive patients with spontaneous ICH were retrospectively as...

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Hemorrhage burden predicts recurrent intracerebral hemorrhage after lobar hemorrhage.

BACKGROUND AND PURPOSE Small asymptomatic cerebral hemorrhages detectable by gradient-echo MRI are common in patients with intracerebral hemorrhage (ICH), particularly lobar ICH related to cerebral amyloid angiopathy (CAA). We sought to determine whether hemorrhages detected at the time of lobar ICH predict the major clinical complications of CAA: recurrent ICH or decline in cognition and funct...

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Targeting heme oxygenase after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is the primary event in approximately 10% of strokes, and has higher rates of morbidity and mortality than ischemic stroke. Experimental evidence suggests that the toxicity of hemoglobin and its degradation products contributes to secondary injury that may be amenable to therapeutic intervention. Hemin, the oxidized form of heme, accumulates in intracranial hemato...

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ژورنال

عنوان ژورنال: Frontiers in Cellular Neuroscience

سال: 2014

ISSN: 1662-5102

DOI: 10.3389/fncel.2014.00388