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From the Stroke Center and Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, Korea.
Address correspondence and reprint requests to Dr. Jong S. Kim, Stroke Center and Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, Korea jongskim{at}amc.seoul.kr
Background: Stroke mechanisms and clinical features of anterior cerebral artery (ACA) territory infarction have rarely been investigated using MRI.
Objectives: To verify stroke mechanisms and to make clinical imaging correlation.
Methods: Clinical, MRI, and angiographic findings of 100 consecutive patients with ACA infarction were studied.
Results: 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 fontal 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.
Conclusion: 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.
Abbreviations: A-com = anterior communicating artery; AAE = artery-to-artery embolism; ACA = anterior cerebral artery; AIF = anterior internal frontal artery; CM = callosomarginal artery; DWI = diffusion-weighted imaging; FP = frontal pole; FrP = frontopolar artery; GR = gyrus rectus; ICA = internal carotid artery; ITO = in situ thrombotic occlusion; LBO = local branch occlusion; MIF = middle internal frontal artery; MRA = MR angiogram; Orf = orbitofrontal artery; PC = precuneus; PCA = paracentral artery; PIF = posterior internal frontal artery; PL = paracentral lobule; SFG = superior frontal gyrus; SMA = supplementary motor area; SP = superior parietal artery; TE = echo time; TOAST = Trial of Org 10172 in Acute Stroke Treatment; TR = repetition time.
Supported by a grant from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology of Korea (M103KV010010 06K2201 01010).
Disclosure: The authors report no disclosures.
Received September 28, 2007. Accepted in final form February 20, 2008.
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  Anterior Cerebral Artery Territory Infarction Journal Watch Neurology, August 19, 2008; 2008(819): 2 - 2. [Full Text]
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