Few problems in ophthalmology have provoked more speculation than the pathogenesis of papilledema. Though extensive investigations have been carried out over a period of almost a hundred years, many gaps remain in our knowledge of this subject. Most of the existing information about papilledema has been provided by clinical and pathologic studies rather than by experimental investigation. These studies and the various mechanisms of the pathogenesis of papilledema hypothesized by their authors have been reviewed adequately by Brégeat,1 Duke-Elder,2 and Walsh.3 The majority of published experimental studies of papilledema fall into three categories: (1) attempts to simulate expanding intracranial lesions, (2) elevations of intracranial pressure for short periods, and (3) the production of internal hydrocephalus. Though reports of many of these experiments have asserted the production of papilledema in animals, the methods employed have not yielded consistently reproducible results. Unfortunately, reports of the production of papilledema were