ABSTRACT
Intracranial arterial aneurysms historically have been thought to result from a developmental abnormality in vasculogenesis or angiogenesis, resulting in an error in the normal cycle of cell birth, apoptosis, and maintenance of the normal extracellular matrix (1) and ultimately leading to fatigue of the viscoelastic elements of the vessel wall and outward ballooning of the affected vascular segment with an increasing propensity to rupture as they enlarge. Although computer models have recently been used to elucidate the growth and rupture mechanism of aneurysms (2,3), it remains an area of active investigation.
