论文部分内容阅读
Objective: To determine the course of vascular changes in childhood post-vari cella arteriopathy (PVA) and its relationship to recurrent arterial ischemic str oke or TIA (AIS/TIA).Methods: Subjects were children with AIS/TIA occurring <1 y ear after varicella, ischemic localization consistent with unilateral disease af fecting the supraclinoid internal carotid arteryor proximal anterior or middle c erebral arteries, and no identified AIS/TIA etiology other than PVA. Charts, bra in MRI, and sequential cerebral vessel imaging (selective cerebral angiography o r MR angiography [SCA/MRA]) were retrospectively reviewed. Results: Twenty-thre e children had varicella at age 1.0 to 10.4 years and had single or multiple AIS /TIAs 4 to 47 weeks later. Initial SCA/MRA was performed within 1 month of prese ntation, and each child had one to five repeat SCA/MRAs during a 4-to 87-month period. There was vascular stenosis in 19 children, maximal on initial studies in 15 of these. Subsequent stenosis regression occurred in 17 children.In 11 of these, one or two additional SCA/MRAs showed further regression as long as 48 mo nths after presentation; there was no restenosis. Eight of 23 children had recur rent AIS/TIA with antithrombotic therapy within 33 weeks of presentation, includ ing 1 of 17 children with documented stenosis regression. Conclusion:Vascular st enosis of childhood post-varicella arteriopathy takes a monophasic course, gene rally with subsequent stenosis regression and only occasional stenosis progressi on after arterialischemic stroke/TIA. Arterial ischemic stroke/TIA rarely recurs with antithrombotic prophylaxis after stenosis regression occurs.
Objective: To determine the course of vascular changes in childhood post-vari cella arteriopathy (PVA) and its relationship to recurrent arterial ischemic str oke or TIA (AIS / TIA). Methods: Subjects were children with AIS / TIA occurring <1 y ear after varicella, ischemic localization consistent with unilateral disease af fecting the supraclinoid internal carotid arteryor proximal anterior or middle c erebral arteries, and no identified AIS / TIA etiology other than PVA. Charts, bra in MRI, and sequential cerebral vessel imaging (selective cerebral angiography Results: Twenty-thre e children had varicella at age 1.0 to 10.4 years and had single or multiple AIS / TIAs 4 to 47 weeks later. Initial SCA / MRA was performed within 1 month of prese ntation, and each child had one to five repeat SCA / MRAs during a 4-to 87-month period. There was vascular stenosis in 19 children, maximal on initial studies in 15 of these. Subsequent stenosis 11 of these, one or two additional SCA / MRAs showed further regression as long as 48 mo nths after presentation; there was no restenosis. Eight of 23 children had recur rent AIS / TIA with antithrombotic therapy within 33 weeks of presentation, includ ing 1 of 17 children with documented stenosis regression. Conclusion: Vascular st enosis of childhood post-varicella arteriopathy takes a monophasic course, gene rally with subsequent stenosis regression and only occasional stenosis progressi on after arterialischemic stroke / TIA. Arterial ischemic stroke / TIA rarely recurs with antithrombotic prophylaxis after stenosis regression occurs.