July 25, 2012
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The pathway to ‘curing’ glaucoma
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Nearly 20 years ago, when I was a first-year resident, we approached glaucoma almost exactly the same way we do today. Sure, today we have better imaging modalities for the optic nerve and more sophisticated visual field strategies. But fundamentally we still visually inspect the optic nerve and give eye drops to lower pressure. To “cure” glaucoma, I think we need to make three fundamental changes in our approach.
- Earlier definitive diagnosis. Currently, rendering a diagnosis of glaucoma depends upon the presence of glaucomatous optic atrophy. That’s a lot like diagnosing diabetes only when microaneurysms are first detected in the retina, which we now know comes many years after the first hints at insulin resistance. In glaucoma, we have to look past the optic nerve to other structural and chemical changes in the central nervous system that underlie this disease. We are just now learning this biochemistry, and until we know more, our diagnosis is limited to early detection of the final common pathway — optic nerve damage.
- Stop talking about IOP. Clearly, there is a mechanical and pressure-related component to glaucoma, but we know there is much, much more. As we gain better understanding of the cellular processes that govern apoptosis and cell death, we must better recognize the triggers (and potential targets for therapy) that lead to optic atrophy in this condition.
- Stop giving eye drops. Topical therapy has already been largely supplanted by early surgical intervention in Europe, where the ophthalmic community clearly recognized the limitations of patient compliance, the burden of cost and the risk to the ocular surface of chronic instillation of topical medications. There must be a better approach, and early surgery must not be the whole answer. As we develop better methods of sustained drug delivery and a better understanding of glaucoma as a systemic disease, these alternative approaches will certainly come to light.