Cerebral infarction
- Lesion
When one brain artery is blocked, the tissue it feeds dies and liquefies; the age of the infarct can be read from the cells present.
What it is
Focal ischemia follows occlusion of a single artery by a thrombus on atherosclerotic plaque or by an embolus, most often from the heart or carotid bifurcation. The brain dies by liquefactive necrosis, and over weeks the dead tissue is cleared to leave a cavity lined by gliosis. Embolic infarcts are often hemorrhagic because the clot moves and blood re-enters damaged vessels. Collateral flow (circle of Willis, leptomeningeal anastomoses) sets how large the infarct becomes.
Structure
- Hemorrhagic (red) infarct: multiple petechial bleeds, typical of emboli and of venous sinus thrombosis.
- Venous infarcts are hemorrhagic and often bilateral and parasagittal when the superior sagittal sinus clots.
- Inflammatory vasculitides (primary CNS angiitis, giant cell arteritis, infections such as syphilis or tuberculosis) can also cause infarcts.
Step by step
- A thrombus or embolus blocks an artery and flow falls below what neurons need.
- Within minutes ATP fails; ion pumps stop and neurons depolarise.
- Excess glutamate opens calcium channels (excitotoxicity) and free radicals form.
- Core neurons die; the penumbra survives for a while on collateral flow.
- Without reperfusion the infarct grows into the penumbra and liquefies.
- Microglia and blood macrophages clear the debris; astrocytes wall off a cavity.
How a brain infarct changes with time
| Time | Gross | Microscope |
|---|---|---|
| First 6 hours | No visible change | Little to see; early edema |
| 12 to 48 hours | Pale, soft, swollen; grey-white border blurred | Red neurons, edema, neutrophils arrive |
| 2 to 10 days | Gelatinous, friable tissue | Macrophages (gitter cells) take over; vessels proliferate |
| 3 weeks to months | Liquefied, then a cavity | Cavity lined by reactive astrocytes and macrophages laden with lipid and hemosiderin |
Clinical notes
- Sudden focal deficit mapped to an arterial territory: the middle cerebral artery gives contralateral face and arm weakness and, on the dominant side, aphasia.
- Transient ischemic attack: symptoms resolve without infarct on imaging; a warning of stroke.
Test yourself
Think of the answer, then tap the question to see it.
What type of necrosis does a brain infarct show?
Liquefactive necrosis: the dead tissue softens and is removed, leaving a cavity.
Why are embolic infarcts often hemorrhagic?
The embolus fragments or moves on, and blood re-enters capillaries whose walls were damaged by ischemia.
Which cells dominate an infarct about one to two weeks old?
Macrophages (gitter cells) filled with lipid from broken-down myelin.
Elsewhere in DurgiPedia
- Cerebral blood flow, brain metabolism and intracranial pressure
- Recognising a stroke: BE-FAST and the NIH Stroke Scale
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Ischemic Stroke (StatPearls (NCBI Bookshelf), 2026); Transient Ischemic Attack (StatPearls (NCBI Bookshelf), 2026).
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Representative model, for educational purposes only.
