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We examined the brains of 14 patients (four men and 10 women, mean age 68.9 years) who died from brain herniation after cardioembolic stroke with persistent occlusion of the internal carotid-middle cerebral arterial axis. Our examination showed hemorrhagic infarct in seven patients and pale infarct in the other seven, contradicting the commonly proposed pathophysiologic mechanism for the development of hemorrhagic infarct that the opening of previously occluded vessels makes an infarct hemorrhagic. Analysis of blood pressure after stroke revealed one or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic infarct without a reopening of the occluded artery. Such arterial hypertension was not always present in patients with pale infarct. Hemorrhage into an infarct with persisting occlusion of the proximal artery is assumed to occur when the involved blood vessels are exposed to the force of arterial blood pressure from the leptomeningeal collaterals. This occurs when arterial blood pressure rises after stroke in the presence of efficient leptomeningeal collaterals and before occlusion of these collaterals by a swollen cerebral hemisphere containing a large infarct.

Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke.