The pathogenesis of the transient obscurations of vision that occur with papilledema is a subject of speculation and debate. We present four examples of transient obscurations of vision that were clinically indistinguishable from those of papilledema; they occurred in patients with elevated optic discs from causes not related to increased intracranial pressure. The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes. We postulate that such mechanisms may apply in all cases of optic disc elevation, including papilledema.