Abstract
Intracerebral hemorrhage (ICH), defined as bleeding into the brain parenchyma, is a significant public health issue. Although it accounts for only 10 to 15% of strokes, it is associated with the highest morbidity and mortality rates. Despite advances in the field of stroke and neurocritical care, the principles of acute management have fundamentally remained the same over many years. The main treatment strategies include aggressive blood pressure control, early hemostasis, reversal of coagulopathies, clot evacuation through open surgical or minimally invasive surgical techniques, and the management of raised intracranial pressure.
Highlights
A PubMed search for articles published up to June 2019 was performed using the terms “intracerebral hemorrhage” [Title] and (“spontaneous” [Title/Abstract]), which turned out 1,102 articles
The presence of diffusion-weighted imaging (DWI) lesions in the perihematomal region is associated with higher hematoma volumes, whereas remote lesions are associated with lobar hemorrhages, leukoaraiosis, higher rates of anti-platelet medication, amyloid angiopathy, previous Intracerebral hemorrhage (ICH), and atrial fibrillation[32,33,34,35,36,37,38]
Another possible explanation for this phenomenon is the occurrence of hyperacute and spontaneous hemorrhage following an ischemic stroke of embolic etiology with recanalization[39]
Summary
A PubMed search for articles published up to June 2019 was performed using the terms “intracerebral hemorrhage” [Title] and (“spontaneous” [Title/Abstract]), which turned out 1,102 articles. Intracerebral hemorrhage (ICH) is defined as bleeding into the brain parenchyma that may extend into the ventricles and, less frequently, the subarachnoid and subdural spaces[1] It accounts for 10 to 15% of all causes of stroke and is associated with the highest mortality rates (around 35% at 7 days and 59% at 1 year)[1,2,3]. Primary ICH represents 78 to 88% of cases and originates from spontaneous rupture of small vessels, usually from chronic hypertension and cerebral amyloid angiopathy (CAA)[1,6]. Progressive deposition of beta-amyloid peptide on the wall of leptomeningeal and cortical vessels reduces their complacency, leading to a spectrum of hemorrhagic manifestations including cerebral microbleeds (CMB), cortical superficial siderosis (cSS), and intracerebral hemorrhage. The main characteristics of CAA are the presence of lobar, cortical or cortical-subcortical
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