This article reviews the epidemiology, pathophysiology and management of primary intracerebral hemorrhage. In North American and European populations, 15% of strokes are due to intracerebral hemorrhage. Pathologically in hypertension, early arteriolar proliferation of smooth muscle is followed later by smooth muscle cell death and collagen deposition. This eventually leads to occlusion or ectasia of arterioles. The latter leads to Charcot-Bouchard aneurysm formation and possible intracerebral hemorrhage. Amyloid deposition in the tunica media causes similar brittle arterioles. Fibrin globes in concentric spheres attempt to seal off the site of bleeding. But vasculopathy (either amyloid or hypertensive) inhibits the contractile capability of arterioles. The size of the final sphere of blood at cessation of bleeding determines the clinical spectrum, from asymptomatic to fatal. Since arteriolar bleeding is slower than arterial bleeding, several hours exist where intervention may be useful. While medical intervention is controversial, guidelines for blood pressure, intracranial pressure, glucose and seizure management exist. Surgical trials have tended to show no benefit. Recombinant factor VIIa is undergoing investigation as hemostatic therapy for intracerebral hemorrhage, to limit clot expansion and possibly also as a hemostatic adjunct to surgery.
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