Abstract
There appear to be 3 factors in the development of papilloedema - an arterial shunt to the prelaminar tissue and a raised venous pressure in the absence of a raised intraocular pressure, which are passive effects, and an overspill of pial autoregulative vasodilatation which is not passive. In addition the arterial shunt may lead to excessive local autoregulative effects. The engorgement of the fine vessels of the prelaminar tissue, the loss of the spontaneous venous pulse on the disc and the venous overfilling are thought to indicate increased supply and blood flow rather than the reverse. The other general causes of papilloedema can also be explained by the autoregulative mechanism or its breakdown as they involve hypercapnia, tissue anoxia or severe hypertension.