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Editors Selection IGR 11-2

Basic science: Scleral edge

Comment by Claude Burgoyne on:

14745 Scleral edge, not optic disc or retina, is the primary site of injury in chronic glaucoma, Hasnain SS, Medical Hypotheses, 2006; 67: 1320-1325

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The idea described by Hasnain (1039) that retinal ganglion cell axons appear vulnerable to physical compression as they turn around Bruch's membrane to enter the neural canal is not new - having been discussed in the axonal transport papers by Anderson, Minckler and Quigley. These are the classic papers (not cited in this article) that demonstrated obstruction to flow within the lamina cribrosa at normal levels of IOP which was profoundly worsened following acute and chronic IOP elevation. The controversy that arose from these studies was about the mechanism of this obstruction (mechanical compression versus ischemia). Since that time our notions of the neuropathy have broadened. The pathophysiologies within the optic nerve head are recognized to be not just axonal, but connective tissue and cellular in origin and it is assumed that they are multifactorial. Seperate but related pathophysiologies within the RGC stroma, photoreceptors and lateral geniculate body are now proposed. The central premise of this report is that an ischemic insult in glaucoma causes the Border Tissues of Elschnig to atrophy leading to progressive collapse of the axons against the scleral edge. A new look at this hypothesis would be interesting if it was based on a serious review of the existing literature and a solid knowledge of optic nerve head anatomy. Unfortunately this article does not achieve those standards and no anatomic evidence of Border tissue atrophy from the author's own work or that of others is offered.

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