(Stroke. 2000;31:2466.)
© 2000 American Heart Association, Inc.
Original Contributions |
Experimental Radiosurgery Simulations Using a Theoretical Model of Cerebral Arteriovenous Malformations
From the Department of Radiological Sciences (T.F.M., G.J.H.), Division of Neurosurgery (A.A.F. De S.), and Department of Radiation Oncology (T.D.S.), University of California at Los Angeles, School of Medicine and Medical Center.
Correspondence to Tarik F. Massoud, MD, Section of Neuroradiology, Department of Radiology, University of Cambridge School of Clinical Medicine, Addenbrooke’s Hospital, Hills Rd, Box 219, Cambridge CB2 2QQ, UK. E-mail tfm23{at}cam.ac.uk
Background and Purpose—A novel biomathematical arteriovenous malformation (AVM) model based on electric network analysis was used to investigate theoretically the potential role of intranidal hemodynamic perturbations in elevating the risk of rupture after simulated brain AVM radiosurgery.
Methods—The effects of radiation on 28 interconnected
plexiform and fistulous AVM nidus vessels were simulated by predefined
random or stepwise occlusion. Electric circuit analysis
revealed the changes in intranidal flow, pressure, and risk of rupture
at intervals of 3 months during a 3-year latency period after simulated
partial/complete irradiation of the nidus using doses <25 and 
25 Gy.
An expression for risk of rupture was derived on the basis of the
functional distribution of the critical radii of component vessels. The
theoretical effects of radiation were also tested on AVM nidus vessels
with progressively increasing elastic modulus (E) and
wall thickness during the latency period, simulating their eventual
fibrosis.
Results—In an AVM with E=5.0x104
dyne/cm2, 4 (14.3%) of a total 28 sets of AVM radiosurgery
simulations revealed theoretical nidus rupture (risk of rupture
100%). Three of these were associated with partial nidus coverage
and 1 with complete treatment. All ruptures occurred after random
occlusion of nidus vessels in AVMs receiving low-dose radiosurgery.
Intranidal hemodynamic perturbations were observed in
all cases of AVM rupture; the occlusion of a fistulous component
resulted in intranidal rerouting of flow and escalation of the
intravascular pressure in adjacent plexiform components. Risk of
rupture was found to correlate with nidus vessel wall strength: a low
E of 1.9x104 dyne/cm2 resulted
in a 92.8% incidence of AVM rupture, whereas a higher E
of 7.0x104 dyne/cm2 resulted in only a 3.6%
incidence of AVM rupture. A dramatic reduction in rupture incidence was
observed when increasing fibrosis of the nidus was modeled during the
latency period.
Conclusions—It was found that the theoretical occurrence of AVM hemorrhage after radiosurgery was low, particularly when radiation-induced fibrosis of nidus vessels was considered. When rupture does occur, it would appear from a theoretical standpoint that the occlusion of intranidal fistulas or larger-caliber plexiform vessels could be a significant culprit in the generation of critical intranidal hemodynamic surges resulting in nidus rupture. The described AVM model should serve as a useful research tool for further theoretical investigations of cerebral AVM radiosurgery and its hemodynamic sequelae.
Editorial Comment
Department of Neurological Surgery, University of California, Davis, Sacramento, California