Besides apical medial gaps, lateral and circular medial gaps can be found occasionally at the branching sites of human intracranial arteries, supporting Forbus's idea (1930) of their mechanism of formation and contradicting those put forward by later workers. The large medial gaps situated just distal to the branching sites, considered by Stehbens (1963) to be degenerative in origin, may result from enlargement of congenital multiple apical gaps. Degeneration of the internal elastic layer in the area of medial gaps consists in enlargement and partial fusion of its "physiologic" windows. In contrast to the prevailing opinion, human intracranial arteries do have a well-developed external elastic layer whose density gradually decreases with increasing lengths of the medial gaps. The fundus of a mature aneurysm generally contains no continuous elastic membrane or fiber and relatively little granular elastic material. The equilibrium between partial degeneration and steady reformation of adventitial collagen fibers makes possible the growth of an aneurysm. The thickening of the aneurysmal intima appears to be in causal relationship with the stagnation zones existing in larger aneurysms. In special cases small islets of the arterial media can get into the fundus of an aneurysm, whose spindle-like smooth muscle cells, arranged in a parallel manner, may dissociate themselves from each other and be transformed into spider-like cells.