damage to the optic nerve caused by chronic papillede-ma.
If elevated intracranial pressure goes undetected, bilateral loss of vision can develop, because chronic papilledema often leads to gliosis and atrophy of the optic nerve. The same problem can develop if the cause of the elevated pressure cannot be corrected. The pathogenic mechanism is not well understood, but ischemia is thought to play an important role. The time needed to develop this complication is variable and is not predictable in individual cases. The transient obscurations of vision often associated with papilledema seem to be unrelated to the risk of atrophy. The visual impairment can begin acutely or subacutely, often with arcuate visual field defects that are very similar to those in patients with chronic open-angle glaucoma, and as is the case with glaucoma, the central-most portions of the visual field are initially spared. The process, once begun, can seem impossible to stop, resulting in total optic atrophy and blindness. Patients with chronic papilledema need to be monitored by an experienced ophthalmologist. Papillede-ma that threatens in this manner (i.e., moderate to marked levels of papilledema that last longer than a few weeks) must be brought under control, either by shunting procedures or high-dose acetazolamide therapy. Serial lumbar punctures are not usually a satisfactory method of control. While a lumbar puncture is essential to establish the initial diagnosis, it rarely needs to be repeated. Patients under this type of threat to their vision can also benefit from optic nerve sheath fenestration. This type of procedure is not effective for control of headache, but can reverse the disc swelling and protect the optic nerve.
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