PubMed · 9218252
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K Houkin. 1997. [IC-IC bypass].. https://pubmed.ncbi.nlm.nih.gov/9218252/
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We simulated parent artery occlusion therapy for basilar head aneurysms to elucidate the hemodynamic changes induced by different occlusion sites and diameters of the posterior communicating arteries (PCom) as collateral pathways. A vascular model of the vertebrobasilar system with a basilar head aneurysm was constructed. Four types of occlusion were simulated: Basilar artery occlusion distal to (Type A), between (Type B) and proximal to (Type C) the superior cerebellar arteries, and bilateral vertebral artery occlusion (Type D). Glycerol solution was perfused into the model, and the half-life of the dye injected into the aneurysm was calculated and regarded as an index of stagnant flow in the aneurysm. The half-life was increased significantly and nonlinearly after parent artery occlusion, depending on the occlusion site and the ratio of two PCom diameters (diameter ratio). Intra-aneurysmal stagnation developed markedly in Type A and Type B in the diameter ratio higher than 0.70 and considerably in Type C in the ratio higher than 0.80. Additional P1 occlusion of the posterior cerebral artery enhanced the stagnation in Type A and B. Since the results are consistent with the published clinical data, the simulation study will be useful for speculating the efficacy of the therapeutic occlusion.
Persistent embryological carotid-basilar anastomoses are rare. There has been no report on persistent anastomosis between the accessory meningeal artery and the antero-superior cerebellar artery. We describe a 3-year-old boy with moyamoya disease manifesting such a congenital vascular anomaly, namely, a large anastomosis between the accessory meningeal artery and the antero-superior cerebellar artery associated with marked hypoplasia of the basilar artery. This persistent vascular anomaly is considered embryologically as an additional variant of the persistent primitive trigeminal artery, i.e., a "stapedo-trigemino-cerebellar" variant.
We present a patient with unusual cerebrovasculature due to the absence of anastomosis between anterior and posterior circulations and bilateral fetal posterior cerebral arteries. This resulted in an atypical 'cerebellar' top-of-the-basilar syndrome, with bilateral superior cerebellar artery infarctions. We review the clinical presentation and radiologic findings and explain the embryologic origin of this vascular anatomy.