Unlike SDH, EDH is caused by local impact loading of the head and is, thus, nearly always associated with contact injury. EDH arises from injury of the middle
meningeal artery and its branches near the impact site. In a typical case, EDH occurs when a fracture crosses the middle meningeal artery, which adheres tightly to the inner surface of the temporal bone. About 24% of all instances of skull fracture are associated with EDH (Edna 1983); only about 1% of EDH are not associated with a fracture (Galbraith 1973). Edges of fractured bone can cause laceration of underlying dural arteries and, less frequently, veins. In rare cases, EDH is caused by lacerations of one or more branches of the venous sinuses or emissary veins. EDH rarely occurs spontaneously. Bilateral EDH is uncommon. Bilateral EDH in the absence of fracture has been reported in a few children under 10 years of age (Cooper 1987). Deformation of the elastic skull in children can strip the dura from the inner table and lacerate the adherent vessels (Mealey 1960; Freytag 1963).
Fracturing of the skull absorbs much of the impact energy itself. Consequently, EDH is less likely to produce cerebral contusion injuries than SDH. Only 25% of patients suffering EDH exhibit associated parenchymal lesions of the brain (Bricolo and Pa-sut 1984; Guillermain 1986). If a parenchymal lesion does occur, it may produce a concomitant SDH.
Was this article helpful?