Pathobiology of human intracranial saccular aneurysms
Mária Tóth, György L. Nádasy, Tibor Kerényi, István Nyáry, and Emil Monos (Hungary)
Intracranial saccular aneurysms develop in the course of life in a few percent of the total population. Usually they grow slowly, remain unnoticed, but their rupture induces subarachnoid bleeding with fatal or devastating consequences. Several theories have been constructed to explain the pathomechanism of aneurysm development and rupture. Here these theories will be re viewed. The very complicated blood flow pattern in arteries at the human cerebral base, instability of collateral circulation as well as blood pressure changes can disturb normal, laminar blood flow at bifurcations. With endothelial damage, integrity of basal lamina and internal elastic lamina will also be affected. Evagination of the thin wall occurs with increasing stresses on medial elements. Any pathological factor affecting molecular structures joining connective tissue components with each other, or with the cellular structures, will promote the evagination process. With further enlargement of the sack, increasing mechanical forces make the presence of smooth muscle cells impossible in the wall. When this happens, the ability to rearrange, reorientate connective tissue fibers with the aid of active forces will be lost. Passive rearrangement of fiber structure governed by distending forces, thinning of the wall will be the result, unavoidably leading to the fatal outcome. We can conclude that current hypotheses of human intracranial saccular aneurysm development are not necessarily contradictory. Probably, they describe different fac tors promoting separate phases in the aneurysm development.
Biomed Rev 2000; 11: 53-61.
Received 5 January 1999 and accepted 15 April 1999.
Correspondence and reprint requests to Dr Mária Tóth, Clinical Research Department, 2nd Institute of Physiology, Semmelweis University of Medicine, Üllöi út 78/a (POBox 448, H-1446 Budapest), H-1082 Budapest, Hungary. Tel.: 36 1 3343 162, 36 1 2100 306, Fax: 36 1 3343 162, E-mail: email@example.com