Radiation treatment of arteriovenous malformations (AVMs) has a slow and progressive vaso-occlusive effect. Some studies suggested the possible role of vascular structure in this process. An AVM is a network of abnormal vessels with different sizes and morphologies and the final goal of any treatment is to cause complete AVM obliteration or in other words to close the arterial-veinous connection by closing all the possible blood pathways through the AVM nidus.

     Our purpose was to test the models of obliteration response.

     A detailed biomathematical model has been used, where the morphological, biophysical, and hemodynamic characteristics of intracranial AVM vessels are faithfully reproduced.

     The effect of radiation on plexiform and fistulous AVM nidus vessels was simulated using this theoretical model.The similarities of vascular and electrical networks were used to construct this biomathematical AVM model and provide an accurate rendering of transnidal and intranidal hemodynamics. The response of different vessels to radiation and their obliteration probability as a function of different angiostructure were simulated and total obliteration was defined as the probability of obliteration of all possible vascular pathways.

     The dose-response of the whole AVM is observed to depend on the vascular structure of the intra-nidus AVM. Furthermore, a plexiform AVM appears to be more prone to obliteration compared with an AVM of the same size but having more arteriovenous fistulas. Finally, a binomial model was introduced, which considers the number of crucial vessels and is able to predict the dose-response behavior of AVMs with complex vascular structure.

     This study used a model.

     For patients with AVMs of nonplexiform angioarchitecture, radiosurgery seems to be less effective.

     A plexiform AVM appears to be more prone to obliteration compared with an AVM of the same size but having more arteriovenous fistulas.