Cerebrovascular Disease Pathology
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Direct answer
Infarction in the territory of a cerebral artery — pale and anaemic when thrombotic, haemorrhagic when an embolus lyses and reperfuses necrotic capillaries — and spontaneous intracerebral haemorrhage are the twin pillars of cerebrovascular disease. The middle cerebral artery is the most commonly affected vessel; hypertensive haemorrhage favours the putamen and external capsule from Charcot-Bouchard microaneurysms of lenticulostriate perforators, while subarachnoid haemorrhage belongs to ruptured berry aneurysms of the circle of Willis, the anterior communicating artery leading. Microscopically, red (eosinophilic) neurons appear by 12-24 hours, neutrophils follow, and months later a cystic gliosed cavity remains. In India, rheumatic mitral stenosis with atrial fibrillation remains a distinctive cause of stroke in the young.
What you must remember
- Infarct evolution: red neurons at 12-24 hours; neutrophil peak at 24-72 hours; macrophages from day 3; reactive astrocytosis over weeks; end stage a cystic cavity lined by gliosis.
- Thrombotic versus embolic: atherothrombosis over a ruptured carotid plaque occludes in situ (pale infarct); cardiac emboli — atrial fibrillation, mitral stenosis, recent infarct, endocarditis — lodge in the middle cerebral artery and produce haemorrhagic transformation on reperfusion.
- Lacunar infarcts: small (under about 1.5 cm) deep infarcts in basal ganglia, internal capsule and basis pontis, from lipohyalinosis of penetrating arteries in hypertension; pure motor hemiparesis is the classic syndrome.
- Hypertensive haemorrhage map: putamen-external capsule commonest, then thalamus, pons and cerebellar dentate; Charcot-Bouchard microaneurysms plus lipohyalinotic fibrinoid necrosis of lenticulostriates.
- Berry aneurysm: congenital media defect at arterial branch points of the circle of Willis, hypertensive and smoking amplified; associations — autosomal dominant polycystic kidney disease, Ehlers-Danlos type IV, coarctation; anterior communicating artery is the commonest site.
- Subarachnoid haemorrhage: thunderclap worst headache of my life; sentinel bleeds; vasospasm days 3-14 (nimodipine prophylaxis); communicating hydrocephalus from blocked arachnoid granulations.
- Borderzone (watershed) infarcts: ACA-MCA boundary and deep white matter borderzones, from systemic hypoperfusion — cardiac arrest, profound hypotension; laminar cortical necrosis follows global ischaemia.
Sudden hemiparesis: the first hour
A 62-year-old diabetic develops right weakness and dysarthria at breakfast; the clock, not the differential, decides management first. Non-contrast computed tomography separates the two universes: hyperdense white basal ganglia blood means hypertensive haemorrhage — blood pressure titration and reversal of coagulopathy — while a normal or subtly hypodense MCA-territory study means ischaemia, and the thrombolysis window (four and a half hours from onset) governs everything. Only afterwards does the aetiological hunt begin: carotid imaging for a plaque, electrocardiography and echocardiography for atrial fibrillation or a mural thrombus. When the same catastrophe strikes a 28-year-old Indian, the list lengthens in a country-specific way: rheumatic mitral stenosis with atrial fibrillation throwing an embolus, patent foramen ovale with venous thrombus, premature atherosclerosis, tuberculous vasculitis, antiphospholipid syndrome and sickle cell vasculopathy in central India. Age reranks the same pathology.
Small vessels, berry sacs
Two named vascular lesions carry disproportionate viva weight. Charcot-Bouchard microaneurysms — fusiform dilatations of lipohyalinotic lenticulostriate perforators — explain why hypertensive bleeding lands in the putamen and pons; treating hypertension empties them of significance. Berry aneurysms sit at bifurcations where the media is developmentally deficient; they rupture without warning, and a substantial share announce themselves earlier with a sentinel "warning leak" that is misdiagnosed as migraine at peril of the patient.
Frequently asked questions
Which artery is most often involved in cerebral infarction?
The middle cerebral artery, whether by carotid embolus or in-situ thrombosis — producing contralateral face and arm weakness with aphasia or neglect.
What are Charcot-Bouchard aneurysms?
Microaneurysms on lipohyalinotic lenticulostriate perforators in chronic hypertension, the source of putaminal and pontine haemorrhage.
Why do embolic infarcts become haemorrhagic?
The embolus fragments and reperfuses necrotic capillaries, which rupture into the infarcted tissue — the same physiology that makes haemorrhagic transformation a recognised risk of thrombolysis.
Where do berry aneurysms most commonly arise?
At branch points of the circle of Willis, most often the anterior communicating artery; associated with polycystic kidney disease, Ehlers-Danlos type IV and coarctation.
What causes a lacunar infarct?
Lipohyalinosis of deep penetrating arteries in hypertension, producing small cystic infarcts of the internal capsule or pons with pure motor hemiparesis.