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Abstract

Impaired cerebral vasoreactivity after embolization of arteriovenous malformations: assessment with serial acetazolamide challenge xenon CT.

R W Tarr, D W Johnson, J A Horton, H Yonas, S Pentheny, S Durham, C A Jungreis and S T Hecht
American Journal of Neuroradiology May 1991, 12 (3) 417-423;
R W Tarr
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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D W Johnson
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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J A Horton
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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H Yonas
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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S Pentheny
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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S Durham
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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C A Jungreis
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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S T Hecht
Department of Radiology, University of Pittsburgh School of Medicine, Presbyterian-University Hospital, PA 15213.
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Abstract

Embolization of a portion of the nidus of an arteriovenous malformation not only may alter hemodynamics within the nidus, but also may change blood flow dynamics in adjacent normal vessels. Sequential acetazolamide-challenge xenon CT cerebral blood flow studies were performed in eight patients before and after embolization of arteriovenous malformations to assess the hemodynamic effects on the major vascular territories supplying the malformation. Acetazolamide is a potent cerebral vasodilator, and its administration combined with cerebral blood flow studies allows assessment of cerebral vasoreactivity. In seven of the eight patients, one or more parenchymal areas exhibited a normal cerebral blood flow augmentation response to acetazolamide before embolization, but diminished acetazolamide flow augmentation was seen after embolization, indicating abnormal vasoreactivity. We found that the decrease in vasoreactivity peaked 6-10 days after embolization. In one of the eight patients, a temporary delayed neurologic deficit developed during a period of impaired cerebral vasoreactivity following embolization. Our results suggest that embolization of an arteriovenous malformation can induce vasoreactivity changes in adjacent normal vessels. Because these changes appear to be somewhat time-dependent, an appropriate interval should be observed between embolization stages or before surgical resection of an arteriovenous malformation following embolization to allow hemodynamic equilibration to occur. Acetazolamide challenge combined with serial cerebral blood flow studies following embolization enables determination of this hemodynamic equilibration.

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American Journal of Neuroradiology
Vol. 12, Issue 3
1 May 1991
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Impaired cerebral vasoreactivity after embolization of arteriovenous malformations: assessment with serial acetazolamide challenge xenon CT.
R W Tarr, D W Johnson, J A Horton, H Yonas, S Pentheny, S Durham, C A Jungreis, S T Hecht
American Journal of Neuroradiology May 1991, 12 (3) 417-423;

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Impaired cerebral vasoreactivity after embolization of arteriovenous malformations: assessment with serial acetazolamide challenge xenon CT.
R W Tarr, D W Johnson, J A Horton, H Yonas, S Pentheny, S Durham, C A Jungreis, S T Hecht
American Journal of Neuroradiology May 1991, 12 (3) 417-423;
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