Pathological and hemodynamic concepts regarding the origin, growth, and rupture of intracranial saccular aneurysms are reviewed. Aneurysms form as a result of an interplay between hemodynamic factors, such as axial stream impingement and the water hammer effect, and structural weaknesses at apices of arterial bifurcations, such as congenital and acquired medial defects, funnel-shaped dilatations, and areas of thinning. Hypertension and time aid the formation of aneurysms. Unknown factors in women and in some families also play a role. Enlargement of aneurysms results from an interplay between mechanical factors, such as self-excitation and resonance, that produce structural fatigue and pathological processes of repair of the aneurysmal wall. Rupture of aneurysms is caused by the same hemodynamic factors that effect growth and is also influenced by extramural pressure. Pathologically, a major rupture may be preceded by fibrinous and leukocytic infiltration of the wall, bleb formation, and a minor hemorrhage. Such minor leaks can be followed by healing and growth. Aneurysms that escape major hemorrhage or heal successfully after a hemorrhage can grow to giant proportions, but remain susceptible to rupture despite their size, unless they become completely thrombosed. Intramural thrombosis may be stimulated by minor leaks and is dependent upon the physical characteristics of aneurysms. Experimental, angiographic, and clinical studies that pertain to the origin, growth, and rupture of aneurysms are also reviewed.