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Pathology - Cerebral Infarction
I. Definition & Epidemiology
VI. Histopathology (Microscopic Changes)
I. Definition & Epidemiology
- Definition: Cerebral infarction is ischemic (lack of blood flow) necrosis (tissue death) of a brain region. This is crucial to understand
- the fundamental nature of the condition.
- Epidemiology: It's the most common type of stroke (~80%), predominantly affecting the elderly. Remember this high prevalence and its association with age.
- Thromboembolism: The majority of cases result from blood clots (thromboemboli) originating in the internal carotid artery or the left side of the heart. These clots travel to and block a cerebral artery. Understand the source of the emboli is key here.
- In situ thrombosis: A smaller percentage arises from clots forming directly within a cerebral artery, often due to atherosclerosis (hardening of the arteries). Distinguish between emboli and in situ thrombosis.
- Artery Occlusion: Sustained blockage of a cerebral artery leads to ischemia and subsequent necrosis in the brain area supplied by that artery. The longer the occlusion, the greater the damage.
- Rapid Onset: Cerebral infarction presents with a sudden onset of neurological symptoms specific to the affected artery's distribution. This is a hallmark of stroke.
- Middle Cerebral Artery Involvement: Most infarctions affect the middle cerebral artery, resulting in contralateral (opposite side) hemiplegia (paralysis) or hemiparesis (weakness), homonymous hemianopia (loss of half of the visual field in both eyes), and dysphasia (language impairment). Memorize these common symptoms and their locations.
- Transient Ischemic Attacks (TIAs): TIAs are brief episodes of focal neurological symptoms (less than 24 hours) that serve as significant warning signs for future infarction. Recognize TIAs as crucial predictors.
- 24 hours: The infarcted area softens, and the grey-white matter boundary becomes indistinct. Cerebral edema (brain swelling) and midline shift may occur.
- 48 hours - 10 days: The infarct becomes gelatinous, and the distinction between infarct and normal tissue clarifies.
- 10 days - 3 weeks: Liquefaction (conversion to liquid) and cystic changes (cavity formation) develop.
- Hemorrhagic Infarct: Reperfusion (restoration of blood flow) can sometimes lead to bleeding into the infarcted area.
VI. Histopathology (Microscopic Changes)
- First 48 hours: Ischemic neuronal changes (shrunken, eosinophilic neurons) and neutrophil (white blood cell) infiltration are observed.
- Later Stages: Mononuclear cells (other white blood cells) remove myelin debris, and astrocytes (glial cells) proliferate as the infarct heals.
- Mortality: High initial mortality (20% at 1 month), followed by a 10% annual mortality rate.
- Complications: Pneumonia, depression, contractures (muscle shortening), constipation, bedsores, and significant emotional impact on the family are common. Remember the range of potential complications.
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