Abstract

INTRODUCTION

THEORETICAL MODELS OF BRAIN AVMs

APPLICATIONS OF BRAIN AVM MODELS

FUTURE OF THEORETICAL BRAIN AVM MODELS

REFERENCES

Discussion
Board

Brain arteriovenous malformation (AVMs) are congenital vascular lesions that can occur anywhere in the central nervous system and consist primarily of three distinct components: (1) arterial feeders, (2) a conglomerate of enlarged abnormal vessels (nidus), and (3) draining veins. The abnormal low-resistance, high-flow shunting of blood within the AVM without an intervening capillary bed causes additional structural fatigue, further enlargement, and possible rupture. Hemorrhage is the most serious sequela of AVMs, accounting for 50% of their clinical presentation, a 10% to 17% death rate, and a severe disability rate of 20% to 29%. The in vivo identification of a cause or mechanism of hemorrhage has remained elusive due to the delicate nature of the AVM nidus vessels and the resultant inaccessibility of catheters intranidally. Given these limitations, the primary mechanism of hemorrhage is believed to be hemodynamic in nature. The flow of blood and the resultant forces exert a large shear stress on the walls of the abnormal nidus vessels causing additional structural fatigue and eventual rupture. Knowledge of the biophysical and hemodynamic interactions and their role in the development and rupture of brain AVMs has significantly advanced current understanding in the management of AVMs. The purpose of this paper is to review: (1) the types of models applicable to AVM physiology; (2) advantages, disadvantages, and limitations of each of these models; and (3) future developments of modeling techniques to improve the applicability of models in the identification of underlying mechanisms of AVM rupture.

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Presentation Number SAhademenos0839
Keywords: AVM, model, hemorrhage, stroke