Anterior Cerebral Artery Stroke: Role of Collateral Systems on Infarct Topography

Abstract

Background and Purpose: The circle of Willis (CoW) and leptomeningeal anastomoses play an important role in transforming infarct topography following middle cerebral artery occlusion. Their role in infarct topography following anterior cerebral artery occlusion is not well understood. The aim of this study was to evaluate the role of the CoW and leptomeningeal anastomoses in modifying regional variation in infarct topography following occlusion of the anterior cerebral artery and its branches. Methods: Perfusion and magnetic resonance imaging of patients with anterior cerebral artery stroke and evidence of vessel occlusion were segmented and manually registered to standard brain template for voxel-wise comparison. Next, a computer model of the cerebral arteries was formulated as network of nodes connected by cylindrical pipes. The experiments included occlusion of successive branches of the anterior cerebral artery while the configurations of the CoW were varied. Results: Forty-seven patients with a median age of 77.5 years (interquartile range, 68.0–84.5 years) were studied. The regions with the highest probabilities of infarction were the superior frontal gyrus (probability =0.26) and anterior cingulate gyrus (probability =0.24). The regions around the posterior cingulate gyrus (probability =0.08), paracentral lobule (probability =0.05), precuneus and superior parietal lobule (probability =0.03) had a low probability of infarction. Following occlusions distal to the anterior communicating artery, the computer model demonstrated an increase in flow (>30%) in neighboring cortical arteries with leptomeningeal anastomoses. Conclusions: Traditionally the CoW has been regarded as the primary collateral system. However, our computer model shows that the CoW is only helpful in redirecting flow following proximal vessel occlusions (pre-anterior communicating artery). More important are leptomeningeal anastomoses, which play an essential role in distal vessel occlusions, influencing motor outcome by modifying the posterolateral extent of infarct topography.

Injury of the Corticofugal Tract from the Secondary Motor Area in Middle Cerebral Territory Infarction: A DTI Study

“…The MCA perfused various brain regions, including subcortical regions (e.g., corona radiata, internal capsule, globus pallidus, caudate nucleus, thalamus) and the cerebral cortex (e.g., primary motor cortex and premotor cortex). [33][34][35][36] According to fMRI studies, subcortical infarction in the corona radiata and internal capsule is confirmed following MCA territory infarction. [37][38][39] Given that the CST and CFT axons project to the corona radiata and internal capsule, 34,35 we thought that degeneration of the CST and CFT could be attributed to damage in the subcortical white matter by MCA territory infarction.…”

Topographic Evolution of Anterior Cerebral Artery Infarction and Its Impact on Motor Impairment

“…The probability of an infarct in the paracentral lobule in our study was low (0.05) which would lead us to conclude that the paracentral lobule is less likely to be involved in motor deficit (see Table 1). The low probability of infarction of the paracentral lobule can be explained by the compensatory capacity of leptomeningeal anastomoses which exist between cortical branches of the ACA (posterior inferior frontal, paracentral, and superior parietal arteries) and MCA (central, precentral, and anterior parietal arteries) [7].…”

“…The M1, premotor cortices, and SMA are supplied by branches of the middle cerebral artery (MCA) and anterior cerebral artery (ACA). Following vessel occlusion, the compensatory capacity of collateral systems, the Circle of Willis, and interterritorial leptomeningeal anastomoses will attempt to maintain cerebral perfusion and, in the process, modify infarct topography [4][5][6][7].…”

Corin is regulated by circ-0012397/miR-200a-3p and inhibits the oxygen-glucose deprivation-induced apoptosis of SHSY5Y neuroblastoma cells

“…As a major neurological disease, ischemic stroke is mainly caused by atherosclerosis, cardiac embolism, and cerebral small-vessel occlusion ( 1 ). Cerebral artery occlusion can cause cerebral ischemia and hypoxia, leading to neuronal apoptosis and brain parenchyma necrosis ( 2 ). These pathological changes may lead to neurological dysfunction, disability, or even death.…”

“…Neuronal apoptosis after ischemic stroke has been widely studied to salvage dysfunctional neurons ( 2 ). Generally, apoptosis caused by stroke is mediated through numerous pathways, such as the mitochondrial pathway and the protein 53 (p53)-mediated apoptosis pathway ( 4 ).…”