Expansion
Ischaemic in about 85 per cent, haemorrhagic in 15 per cent
Expansion
Ischaemic (about 85 per cent)
- Thrombotic: on atherosclerosis, typically at the carotid bifurcation or intracranially
- Embolic: from the heart in atrial fibrillation, from a mural thrombus after infarction, or from carotid plaque. Often haemorrhagic transformation on reperfusion
- Lacunar: small perforating vessels affected by lipohyalinosis in chronic hypertension, giving pure motor, pure sensory or ataxic hemiparesis syndromes
- Watershed: between arterial territories, after global hypoperfusion
Haemorrhagic (about 15 per cent)
- Intracerebral: hypertension causing Charcot-Bouchard microaneurysm rupture in basal ganglia, thalamus, pons and cerebellum; cerebral amyloid angiopathy causing lobar haemorrhage in the elderly
- Subarachnoid: berry aneurysm rupture
Histological evolution: red neurones at 12 to 24 hours, neutrophils then macrophages over days, liquefactive necrosis with cavitation and surrounding gliosis over weeks to months. The brain is unique in liquefying rather than showing coagulative necrosis.
The ischaemic penumbra, viable but non-functioning tissue around the infarct core, is the target of thrombolysis and thrombectomy, which is why time to treatment is critical.