中大脳動脈M1部塞栓症に対する局所線溶療法施行後のレンズ核線条体動脈領域病巣の検討

抄録

Middle cerebral artery (MCA) occlusion can be treated successfully with local intraarterial infusion of tissue-type plasminogen activator (t-PA). If the M1 segment of MCA is occluded, the ischemia of lenticulostriate territory occurs. The lenticulostriate arteries are end-arteries, whereas the cortical branches of MCA have leptomeningeal anastomoses. The pathophysiological effect on the lentriculostriate arterial territory after quick reperfusion of the M1 by fibrinolytic therapy is, however, not yet well understood. We investigated changes in neuroradiological findings for the lenticulostriate arterial territory following fibrinolytic therapy for embolic M1 occlusion.
The clinical and neuroradiological findings in nine patients treated with intra-arterial infusion of t-PA were reviewed. All patients had had computerized tomographic (CT) scans before and after fibrinolysis. Six (66.7%) had areas of increased attenuation on immediate postperfusion CT scans in the lenticulostriate arterial territory. Three patterns were categorized according to the changes in neuroradiological findings in the lenticulostriate arterial territory following sequential CT scans. In three cases (Group 1), the high density lesions as seen in the immediate postperfusion CT scans disappeared within 24 hours; they subsequently became low density areas. In three cases (Group 2), the high density lesions as seen in the immediate postperfusion CT scans persisted for several days. Only one of them was symptomatic. Three cases (Group 3) had normal findings on immediate postperfusion CT scans; all showed low density areas on the next day. All patients were observed to show hemorrhagic transformation within seven days.
In Group 1, the rapid clearance of the high attenuation represented contrast that had entered into the disrupted blood-brain barrier (BBB). In Group 2, hemorrhagic extravasation had occurred in the lenticulostriate arterial territory since the vessel walls were damaged so badly that they no longer could resist the pressure of reperfusion. In Group 3, recirculation caused oligemia due to the no-reflow phenomenon.