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June 16, 1999

New Perspectives in Glaucoma

Author Affiliations

Margaret A.WinkerMD, Deputy EditorIndividualAuthorPhil B.FontanarosaMD, Interim CoeditorIndividualAuthor

JAMA. 1999;281(23):2186-2187. doi:10-1001/pubs.JAMA-ISSN-0098-7484-281-23-jac90005

To the Editor: Drs Dreyer and Lipton1 review a number of pathophysiological theories and potential therapeutic strategies for treating glaucoma that exploit recent advances in our understanding of glaucoma's cellular pathology. While the possible interventions they describe show great promise, the authors neglect to discuss another approach to the treatment of glaucoma that is of great potential importance—an approach that can achieve reversal of ocular vasospasm as well as improvement of ocular circulation. In the last 30 years many publications have attested that (a) ocular blood flow is compromised by glaucoma; (b) the insult responsible can be vasospastic, and therefore reversible2; and (c) the extent of vasospasm can be correlated with degree of visual defect.3 It is irrelevant whether ischemia is the primary insult or a result of increased pressure, since improvement of circulation by treatment with vasodilators such as calcium channel blockers has been shown to benefit glaucoma patients.4 In addition, reversal of vasospasm using carbon dioxide has also been shown to be effective in a study of low-tension glaucoma patients.5 We therefore believe that in the future, the most effective glaucoma drug will not only reduce intraocular pressure and inhibit the cascade of events leading to apoptosis but also will ensure adequate circulation in the optic nerve head and reverse ischemia and vasospasm in those locations.

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