[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Central nervous system](https://durgical.com/en/general-pathology/areas/cns/) › Cerebral infarction

# 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.

Updated Nov 12, 2026

## Key points

- Brain infarcts undergo liquefactive necrosis, unlike the coagulative necrosis of other solid organs.
- Embolism (atrial fibrillation, carotid plaque, endocarditis, paradoxical emboli) favours the middle cerebral artery territory and often gives hemorrhagic infarcts.
- Thrombosis on atheroma favours the carotid bifurcation, the origin of the middle cerebral artery and the basilar artery.
- Timeline: red neurons by 12 to 24 hours, neutrophils days 1 to 3, macrophages from day 3 for weeks, then a cavity rimmed by gliosis.
- The penumbra is the threatened rim that can be saved if flow returns quickly.

## 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.

## Memory aid

The brain melts instead of setting: liquefactive necrosis, cleared by foamy macrophages, ending as a hole with a glial wall.

## 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.

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## Elsewhere in DurgiPedia

- [Cerebral blood flow, brain metabolism and intracranial pressure](https://durgical.com/en/physiology/cerebral-blood-flow-brain-metabolism-and-intracranial-pressure/)
- [Recognising a stroke: BE-FAST and the NIH Stroke Scale](https://durgical.com/en/clinical-exam/recognising-a-stroke-be-fast-and-the-nih-stroke-scale/)

## Connections

## Related 10

- [Global hypoxic-ischemic brain injury](https://durgical.com/en/general-pathology/global-hypoxic-ischemic-brain-injury/)
- [Small vessel disease: hypertensive and amyloid hemorrhage](https://durgical.com/en/general-pathology/small-vessel-disease-hypertensive-and-amyloid-hemorrhage/)
- [How brain cells react to injury](https://durgical.com/en/general-pathology/how-brain-cells-react-to-injury/)
- [Infarction: red vs white, and what decides the damage](https://durgical.com/en/general-pathology/infarction-red-vs-white-and-what-decides-the-damage/)
- [Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous](https://durgical.com/en/general-pathology/patterns-of-necrosis-coagulative-liquefactive-caseous-fat-fibrinoid-gangrenous/)
- [Systemic (arterial) thromboembolism](https://durgical.com/en/general-pathology/systemic-thromboembolism/)
- [Thrombosis and Virchow's triad](https://durgical.com/en/general-pathology/thrombosis-and-virchow-s-triad/)
- [Hypoxia, ischemia and reperfusion injury](https://durgical.com/en/general-pathology/hypoxia-ischemia-and-reperfusion-injury/)
- [Consequences of atherosclerosis](https://durgical.com/en/general-pathology/consequences-of-atherosclerosis/)
- [Large-vessel vasculitis: giant cell vs Takayasu](https://durgical.com/en/general-pathology/large-vessel-vasculitis-giant-cell-vs-takayasu/)

## Related conditions 8

- [Ischaemic stroke](https://durgical.com/en/conditions/ischaemic-stroke/)
- [Transient ischaemic attack](https://durgical.com/en/conditions/transient-ischaemic-attack/)
- [Brainstem stroke syndromes (Wallenberg and others)](https://durgical.com/en/conditions/brainstem-stroke-syndromes/)
- [Carotid artery stenosis](https://durgical.com/en/conditions/carotid-artery-stenosis/)
- [Cerebral venous sinus thrombosis](https://durgical.com/en/conditions/cerebral-venous-sinus-thrombosis/)
- [Primary angiitis of the central nervous system](https://durgical.com/en/conditions/primary-angiitis-of-the-central-nervous-system/)
- [Atrial fibrillation](https://durgical.com/en/conditions/atrial-fibrillation/)
- [Antiphospholipid syndrome](https://durgical.com/en/conditions/antiphospholipid-syndrome/)

[← All of general pathology](https://durgical.com/en/general-pathology/)

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](https://www.ncbi.nlm.nih.gov/books/NBK499997/) (StatPearls (NCBI Bookshelf), 2026); [Transient Ischemic Attack](https://www.ncbi.nlm.nih.gov/books/NBK459143/) (StatPearls (NCBI Bookshelf), 2026).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/cerebral-infarction/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/cerebral-infarction/