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Neurology. 2008 Jun 10;70(24 Pt 2):2386-93. doi: 10.1212/01.wnl.0000314686.94007.d0.

Anterior cerebral artery infarction: stroke mechanism and clinical-imaging study in 100 patients.

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Stroke Center and Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, Korea.



Stroke mechanisms and clinical features of anterior cerebral artery (ACA) territory infarction have rarely been investigated using MRI.


To verify stroke mechanisms and to make clinical imaging correlation.


Clinical, MRI, and angiographic findings of 100 consecutive patients with ACA infarction were studied.


Motor dysfunction (n = 91) was the most common symptom, and severe motor dysfunction was related to supplementary motor area/paracentral lobule involvement (p = 0.016). Hypobulia/apathy (n = 43) was related to involvement of frontal pole (p = 0.002), corpus callosum/cingulate gyrus (p = 0.003), and superior frontal gyrus (p < 0.001), and occurred more frequently in patients with bilateral lesions followed by left lesions. Urinary incontinence (n = 30) was not related to any specific lesion locations. Grasp reflex (n = 25) was related to corpus callosum involvement (p = 0.035). Angiographic (mostly MR angiography) results showed that 68 patients had local ACA atherosclerosis, most often at A2 segment. The stroke mechanisms included cardiogenic embolism in 10, internal carotid artery-ACA embolism in 6, and ACA atherosclerosis in 61 patients. In the latter group, detailed stroke mechanisms included local branch occlusion (n = 20), in situ thrombotic occlusion (n = 20), artery-to-artery embolism (n = 12), and a combination (n = 9). Patients with intrinsic ACA disease more often had hypobulia (p = 0.077) and corpus callosal involvement (p = 0.016) than those with embolism either from the internal carotid artery or the heart.


Anterior cerebral artery (ACA) atherosclerosis is the most important stroke etiology in our population, causing infarction with various mechanisms. Topographic lesion patterns and consequent clinical features of ACA infarction are determined by diverse pathogenic mechanisms and the status of collateral circulation.

[Indexed for MEDLINE]

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