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Whether watershed infarcts and internal junctional infarcts have different mechanisms remains unknown. Of 493 consecutive patients with ischemic stroke or transient ischemic attack, 26 had 1 watershed infarct or more (8 anterior and 21 posterior) and 18 had 1 internal junctional infarct or more. Patients with watershed infarcts were more likely to have arterial hypertension [95% confidence intervals of odds ratio (CIOR): 1.04-6.15] and internal carotid artery stenosis >50% (95% CIOR: 1.03-7.12) than patients without borderzone infarcts. Patients with internal junctional infarcts were more likely to have heart diseases than patients without borderzone infarcts (95% CIOR: 1.46-10.52). This preliminary study suggests that both subtypes of borderzone infarcts probably have different mechanisms.

It has recently been suggested that most small (<15 mm) subcortical infarcts (SSI) of the centrum ovale (CO) are of lacunar type. We investigated this hypothesis in 255 consecutive patients with a first-ever ischemic stroke who were examined within 24 h after stroke onset and survived on day 10. Fifty-seven patients had CO-SSI: they were older and more likely to have a silent infarct, a lacunar syndrome, arterial hypertension, leuko-araiosis and SSI localized in the basal ganglia or internal capsule and less likely to have a nonlacunar syndrome. On multiple linear regression analysis, independent factors correlated with CO-SSI were the leuko-araiosis score and the presence of a silent infarct, diabetes mellitus and arterial hypertension. However, the presumed cause of the index stroke was large-vessel disease in 7 patients and heart disease in 16. Though we confirm that patients with CO-SSI are more likely to have risk factors for small-vessel disease, a complete diagnostic workup remains necessary in patients with such infarcts because other mechanisms account for one third of them.

Atrial septal aneurysms (ASA) are frequent findings on transesophageal echocardiographies. Whether they are more frequent in patients with cerebral ischemia of unknown cause remains unclear. We investigated this question in 154 consecutive patients with an ischemic stroke or transient ischemic attack. The 16 patients with ASA were younger, less likely to have arterial hypertension and more likely to have a patent foramen ovale (PFO) or an unknown cause of stroke, but they did not differ for number and side of infarcts, other demographic data and vascular risk factors. Patients with ASA unassociated to PFO were also more likely to have an unknown cause of stroke. These findings lead to the hypothesis that ASA might be sources of cerebral emboli.

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