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Steven R. Heidemann, PhD; David Kaufman, DO
East Lansing, Mich

Arch Ophthalmol. 1991;109(7):916.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We read with interest the article by Sergott et al¹ and the ensuing correspondence.² In view of the poor state of understanding of axonal transport, we urge that the role of axoplasmic transport, if any, be deemphasized in further discussions of the efficacy of optic nerve sheath fenestration (ONSF) in the treatment of nonarteritic anterior ischemic optic neuropathy. In our view, this important discussion asks the following four questions. Does ONSF ameliorate nonarteritic anterior ischemic optic neuropathy? If so, is this related to edema, intraoptic nerve sheath pressure, or compression of the optic nerve? Does the edematous condition inhibit axoplasmic transport that, in turn, causes an electrophysiologic deficit responsible for visual loss? The first two issues are crucial, particularly in view of the opening of a surgical "Pandora's box" eloquently outlined by Hayreh,² a misgiving shared by us. However, any focus on the third . . . [Full Text PDF of this Article]

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