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John C. Morrison, M.D. [NEI Strategic Planning]

John C. Morrison, M.D.

Dr. Morrison received his M.D. from the Oregon Health and Science University and did an ophthalmology residency at the same institution. Prior to residency, he worked for approximately 3 years with Dr. Ken Swan and Dr. E. Michael Van Buskirk, performing research on various anatomic and experimental pathology problems. Following residency, Dr. Morrison did a one-year glaucoma fellowship with Dr. Van Buskirk, continuing my anatomic studies on the ciliary body and questions of aqueous production. After that, he did a 2-year fellowship with Dr. Harry Quigley at the Wilmer Eye Institute. He has been on the faculty at the Casey Eye Institute since 1988.

It was during his fellowship at Johns Hopkins that he began to concentrate on understanding the mechanisms of glaucomatous optic nerve damage. Dr. Morrison’s research dealt with the composition of the normal and glaucomatous optic nerve head, working mostly with primate tissues and the laser-induced model of elevated IOP. At the end of his fellowship, he became increasingly interested in understanding the cellular aspects of optic nerve damage, as induced by chronically elevated IOP. He also determined that developing a cost-effective model of this process using laboratory rats would be an important advance. Although the anatomy of the rat optic nerve head differs from that of the primate, Dr. Morrison believes that events occurring at the cellular level could still be determined, and would likely be similar to those occurring in primates. Throughout this work, Dr. Morrison’s premise has been that basic mechanisms could be determined using this less expensive model, and later confirmed using the more costly primate models in well-focused experiments.

Although recent clinical studies have supported the value of aggressive management of intraocular pressure in glaucoma, many patients with severe glaucomatous visual loss will continue to lose vision in spite of apparent good IOP control. Dr. Morrison believes that much of this difficulty likely stems from the peculiar nature of glaucomatous optic nerve damage. Numerous clinical studies, including several multicenter clinical trials, now support the observation that advanced optic nerve damage alters the susceptibility of remaining optic nerve fibers and that eyes with advanced optic nerve damage require lower IOP in order to prevent further loss. A better understanding of the mechanisms of pressure-induced optic neuropathy may lead us to treatments that would be effective when used in conjunction with maximal pressure lowering strategies.

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