The progression of motor deficits is associated with a relatively poor functional outcome. Diabetes mellitus and the severity of motor deficit on admission may predict progression of motor deficits.

No abstract

Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.

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. (Stroke 1989;20:876-883)