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Nine patients with maculopathy (macular holes, macular cysts, and lamellar holes) and ten patients with optic neuritis were examined in order to determine changes in the visual evoked potential (VEP) in response to pattern-reversal stimulation. Eyes with lamellar holes had normal P100 latency, but eyes with macular cysts and macular holes had prolonged P100 latency. Eyes with optic neuritis exhibited greater prolongation of the P100 latency than eyes with macular holes. In contrast, eyes with macular holes had a greater reduction in the steady-state VEP amplitude than eyes with optic neuritis. The prolonged latency occurring in maculopathy may be due to a peculiar amplitude summation noted with half-field VEP, rather than to a true conduction delay like that seen in eyes with optic neuritis. The amplitude slope, which is usually positive in normal controls, was negative for 85.7% of eyes with macular holes and 69.2% of eyes with optic neuritis. The negative amplitude slope may represent a subtle defect in retinal ganglion X cells. Eyes with significantly lower values for four or more of the nine central test points on quantitative automated perimetry had negative amplitude slopes and prolonged P100 latency.

Two patients (two men, 56 and 59 years old) had sphenoid sinus mucocele originating in the anterior clinoid process. In one case the mucocele initially mimicked diabetic ophthalmoplegia with pupil-sparing palsy of the oculomotor (third) nerve. After resolution of the palsy, severe visual loss developed with minimal recovery of vision after surgery. The second patient had recurrent episodes of retrobulbar optic neuropathy with optic atrophy and decreased vision. Visual loss from sphenoid sinus mucoceles is usually associated with a poor prognosis if surgical treatment is delayed more than seven to ten days.

To improve understanding and effectiveness of therapy in optic nerve disease, various causes of so-called optic neuritis should be identified when possible. The clinical characteristics of demyelinating optic neuropathy can be contrasted with those of ischemic optic neuropathy, nutritional optic neuropathy, true optic nerve inflammation (e.g., luetic), optic nerve infiltration with tumor, and compression neuropathy caused by adjacent tumor. Radiologic studies and other means of investigating patients with optic neuritis are reviewed. Arguments in favor of, and against, treatment of presumed demyelinating optic neuritis are presented along with representative corticosteroid treatment regimens. The natural tendency toward spontaneous improvement of optic neuritis makes the effect of treatment difficult to assess.