Infarcts involving the territory of the anterior cerebral artery (ACA) are uncommon, accounting for a considerably small share of the total number of ischemic infarcts. The risk factors and etiology of strokes in this vascular territory are largely the same as for the other principal cerebral arteries including hypertension, dyslipidemias, diabetes mellitus, smoking, atherosclerosis, and cardioembolism. However, it is possible that the peculiar manifestations of its clinical syndromes and the suspicion that many infarcts in this arterial territory are silent could result in the underdiagnosis of strokes involving the ACA or its branches.
The ACA emerges from the anterior clinoid segment of the internal carotid artery. It then continues anteromedially towards the longitudinal fissure. Near this point, the anterior communicating artery (ACoA) forms, creating an anastomosis between both ACA’s. Each ACA then advances between the two cerebral hemispheres and over the callosal sulcus in a posterior direction towards the parieto-occipital sulcus. Superficial and deep branches emerge along its course. These include Heubner’s, orbitofrontal, frontopolar, anterior internal frontal, middle internal frontal, posterior internal frontal, paracentral, superior parietal, inferior parietal, pericallosal, and callosomarginal arteries. The ACA itself often divides into five segments, usually labeled as A1 through A5, or as proximal (A1), ascending (A2, A3), and horizontal segments. A significant feature of the ACA is its robust anastomotic complex; this may account for the low rate of infarcts in this vascular distribution. Notably, infarctions simultaneously affecting both cerebral hemispheres may also be present among ACA stroke cases. These are rare and characteristically occur because of clinically significant anatomical variations affecting both ACA's at any point along its course. The most recognizable patterns are the azygos, bihemispheric, and ACA with hypoplastic or absent A1 segment.
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