Dilatative arteriopathy (dolichoectasia) involves preferentially the intracranial vertebral and basilar arteries. Rarely, the dilated arteries can compress the third ventricle, contributing to hydrocephalus. There are also reports that describe compression of the pons and the medulla by dilated and tortuous vertebral and basilar arteries. Genetic, infectious, inflammatory, immunological, and degenerative factors all may cause or contribute to the formation and progression of dolichoectasia. Patients with dolichoectasia have also been found to have lacunar infarcts, severe leukoaraiosis, and severe etat crible (dilated Virchow-Robin spaces around penetrating arteries). White matter lesions and lacunar infarcts are generally attributed to disease of small penetrating intracranial arteries. Penetrating arterial pathology involves thickening of the arterial media that contains abnormal amounts of fibrinoid material and lipids. Abnormal connective tissue within the arterial wall affects biochemical constituents such as matrix metalloproteinases. Increased activity of matrix metalloproteinases makes small arteries more permeable and loosens the blood-brain barrier.