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Kiuchi et al. (522) have previously demonstrated that the magnitude of the supine rise in intraocular pressure in eyes with normal tension glaucoma correlates with visual field progression. Does medical therapy blunt this supine rise? To address this important question, the investigators have conducted a well-designed crossover study evaluating the supine rise in intraocular pressure before and after a one-month treatment with timolol, latanoprost, and brinzolamide in 24 subjects with newly-diagnosed normal tension glaucoma. Interestingly, they found no appreciable blunting of the supine IOP rise with any of the medications: the supine IOP rise was approximately 3 mmHg before treatment and after a one-month course of each medication. Postural changes in intraocular pressure have been recognized for decades. Growing interest in circadian intraocular pressure variation requires recognition that we all spend approximately eight hours per day in the supine position, which causes our intraocular pressure to rise substantially. While healthy optic nerves can apparently tolerate this posture-driven rise, glaucomatous optic nerves may not.
Medications may not protect the optic nerve from supine IOP elevations in eyes with NTG
The pathophysiology of normal tension glaucoma is intriguing and elusive, but a role for intraocular pressure reduction has been established by the Collaborative Normal-Tension Glaucoma Study. And while the clinical implications of postural intraocular pressure elevations in eyes with normal tension glaucoma have not been established, it is troubling that medications may not protect the optic nerve from supine IOP elevations in these eyes. We hope that future research will help elucidate the clinical consequences, if any, of postural intraocular pressure elevations in eyes with glaucoma. And we wonder if, by bypassing the natural outflow pathways, surgical interventions such as trabeculectomy and glaucoma drainage devices suppress the supine rise.