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Douglas R. Anderson, MD; Mont Cartwright, MD
Miami

Arch Ophthalmol. 1989;107(2):168.

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

In Reply.

—Dr Choplin is, of course, exactly right. When we find statistical correlation between severity of damage and height of IOP, we cannot conclude (but can only suspect) cause-and-effect relationships. Most of us would be willing to discard intuitively the possibility that damage to the nerve would cause elevation of IOP, and so we are left with two alternatives: that a higher pressure participates in the process of optic nerve damage or that both optic nerve damage and higher pressure have resulted from some common basis. Dr Choplin, for example, cites an old theory of glaucoma, recently resurrected with regard to low-tension glaucoma, that perhaps a change in the blood vessels or collagen occurs both in the trabecular meshwork and in the lamina cribrosa, thereby accounting for simultaneous appearance of nerve damage and a rise in IOP.

Nearly all of us presently believe that IOP is a causative factor . . . [Full Text PDF of this Article]

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