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SUMMARY We report two patients with large subcortical hemispheric infarctions, located in areas prone to the development of lacunes, who had occlusion of the middle cerebral artery demonstrated by arteriography. The cortical vessels were perfused by leptomeningeal collaterals. We suggest that large vessel arterial disease should be considered as a possible etiology of large subcortical infarctions and propose that the term lacune should not be used in cases in which neither the size nor the pathophysiologic mechanism of the lesion conform to C. M. Fisher's description. Stroke Vol 14, No 6, 1983AS DESCRIBED BY C. M. Fisher, lacunar infarc tions are small vascular lesions 0.5-1.5 mm in diame ter encountered at autopsy in deep gray structures of the brain, adjacent white matter, or brainstem, in pa tients with a history of chronic hypertension.1 " 5All of the arterial beds in which lacunes can be found are distinguished by a pattern of terminal perfusion with out collaterals. These small infarctions are the result of small atherosclerotic plaques, fibrinoid necrosis or lipohyalinosis of small arterioles (e.g., lenticulostriate or thalamoperforating arteries, paramedian branches of the basilar artery), rather than a consequence of cerebral embolism, internal carotid artery disease or diabetes mellitus. 5-7As an example, Capsular lacunes are considered to result from blockage of penetrating deep branches of the middle cerebral artery, rather than from occlusion of the middle cerebral artery itself or of the internal carotid artery. 7In patients with presumed lacunar infarction com puted tomography (CT) may be normal or show a small deep lesion. [8][9][10][11][12][13] But recently, relatively large le sions of the basal ganglia, internal capsule and thala mus, in patients with unquestionable vascular disease have also been designated as "lacunar" infarctions, or distinguished by such terms as "super" lacunes or "giant" lacunes."-14 It appears to us that these large infarctions may be consequent to pathologic processes different from those described by C. M. Fisher for lacunes and that the use of the now classical term may be questionable. 7For instance, preexisting hyperten sion is no longer an invariable finding. 15In addition, large vessel arterial stenosis and occlusion or cardiac sources of arterial embolism, are being increasingly described in patients with these larger infarctions. [10][11][12] To underline the importance of major vessel arterial occlusion as a cause of such alleged "lacunar" infarc tions, we report two patients who sustained subcortical infarction involving the putamen, the anterior limb of the internal capsule and the caudate nucleus, as a result of middle cerebral artery occlusion at its stem. Case Reports Case 1A 24 year old right-handed woman was admitted with progressive left-sided weakness of 12 hours dura tion. She did not have a history of hypertension, heart disease or diabetes mellitus. For a two year period she had used oral contraceptive pills but had stopped the drug three months ...

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Fifty-nine patients had arteriography because of episodes of amaurosis fugax. Only one third of them had atherosclerotic lesions potentially treatable by carotid endarterectomy. Another third had normal arteriograms, some of these had migraine, heart disease or platelet disorders presumed to be the cause of their symptoms. Patients with amaurosis fugax are a heterogeneous group, and their visual symptoms should not be considered a specific indicator of stenosis of the internal carotid artery.