Brain arteriovenous malformation

, by  Atos Alves de Sousa, Lucas Alverne Freitas de Albuquerque, Marcos Dellaretti , popularity : 10%
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*2. Occlusive Hyperemia

In 1993, Al-Rodhan et al. [1] proposed this alternative explanation for postoperative hemorrhage and edema following AVM resection and gave some evidence against the NPPB hypothesis. They conclude that “ the complications of hemorrhage and edema associated with the resection of high-flow AVM’s are the result of two separate but interrelated mechanisms involving both the arterial feeders and the venous drainage systems. 1) Stagnant arterial flow in former AVM feeders and their parenchymal branches with subsequent worsening of the existing hypoperfusion and ischemia and subsequent hemorrhage and/or edema into these areas, and; 2) obstruction of the venous outflow system of the brain adjacent to the AVM with subsequent passive hyperemia, engorgement, and further arterial stagnation. In addition, disturbed autoregulation at the microcirculation level may play a role.”

The precise pathophysiology mechanism of the hemorrhage and edema that can manifest after AVM resection is not completely understood. In literature there is a lot of evidence in favor of and against these two hypotheses. As Zacharia et al. [115] we believe that ultimately these hypotheses are not mutually exclusive and perhaps exist in a spectrum of hemodynamic alteration following AVM resection.