Intracerebral haemorrhage

Introduction Spontaneous intracerebral haemorrhage (ICH) is the most devastating type of stroke, and is a leading cause of disability among adults. Primary ICH originates from the spontaneous rupture of small arterioles damaged by chronic hypertension or cerebral amyloid angiopathy (CAA). Secondary ICH is the result of bleeding from vascular malformations, haemorrhagic transformation of an ischaemic stroke, tumours, abnormal coagulation or vasculitis. Spontaneous ICH begins with rupture of a small, chronically damaged and fragmented artery or arteriole. Rapid extravasation of blood into the parenchyma leads to the formation of a space-occupying haematoma, which in turn results in oedema and swelling of the surrounding brain tissue. Chronic hypertension leads to pathological changes within the tunica media of small- and medium-sized arterioles of 100–600 µm in diameter. This vasculopathy is characterized by: (i) degeneration of medial smooth muscle cells; (ii) small miliary aneurysms associated with thrombosis and microhaemorrhages; (iii) accumulation of non-fatty deposits between the intima and media; and (iv) fibrinoid necrosis and hyalinization of the intima, preferentially at bifurcation points and distal portions of the vessel. Primary affected structures include the thalamus, basal ganglia, deep periventricular grey matter, pons and cerebellum. Cerebral amyloid angiopathy leads to spontaneous ICH in elderly people and results from amyloid protein being deposited within the media and adventitia of small- to medium-sized vessels. Cerebral amyloid angiopathy has a predilection for leptomeningeal and penetrating vessels of the cortex, which may undergo fibrinoid necrosis as seen in chronic hypertension. The apolipoprotein E gene is polymorphic, and apolipoprotein Eε2 (ApoE2) and apolipoprotein Eε4 (ApoE4) genotypes (cognate proteins shown in parentheses) are risk factors for CAA-associated ICH.