Evolving definition of glaucoma will alter treatment patterns, too

Key Points

Hong Kong-Glaucoma has long been thought of as a disease with one component: elevated IOP. That definition, however, is changing to identify the disease as an optic neuropathy characterized by a specific pattern of optic nerve head and visual field damage. That's the word from Theodore Krupin, MD, Department of Ophthalmology, Sorrel Rosin Eye Center, Northwestern University, Chicago. He was speaking here at the World Ophthalmology Congress.

"We can go way back in time when glaucoma was described as being characterized just by elevated IOP and ophthalmologists used the so-called '22 Rule of Thumb' to define glaucoma," Dr. Krupin said. "But over the years there has been a change in that definition that reflects a more accurate way of thinking about the disease and thus affects the preferred practice patterns for ophthalmologists."

Optic neuropathy

"Glaucoma is a progressive neurodegenerative disorder," Dr. Krupin said. "Elevated IOP is only a risk factor, not the disease per se." Structural damage precedes functional change in glaucoma, and retinal nerve fiber layer [RNFL] injury can be observed up to 6 years before visual field defects are detected, he said. Between 25% and 40% of optic nerve fibers can be lost from an eye that retains a normal visual field, Dr. Krupin added.

The association between glaucoma and elevated IOP is still valid, but it is not absolute.

More than IOP control

"Glaucoma is more than just an increase in IOP, and treatment is more than just lowering IOP," Dr. Krupin said. "Most patients who have an elevated IOP don't have an optic neuropathy-the so-called ocular hypertensive patients, and the progression of that glaucomatous neuropathy is not always prevented or even slowed by reducing IOP. On the other hand, in low-pressure or normal-tension glaucoma, the glaucomatous optic neuropathy is not always associated with an elevated IOP."

Still, IOP currently is the only risk factor of the disease amenable to modification by the clinician, and controlling IOP is still a valid course of action, he said.

"The aim of our treatment, however, should not be simply to reduce IOP but to halt the neurodegeneration of the retinal ganglion cells and their axons," Dr. Krupin said. "The ultimate aim is to halt progression before the stage of severe damage."

Along with the deaths of neurons in the retina, evidence also exists that glaucoma is associated with damage to the lateral geniculate nucleus and the visual cortex, he said.

"The most important concept is that structural damage occurs before the ability to detect visual field damage," Dr. Krupin said. "So when monitoring patients who have elevated pressure and ocular hypertension or glaucoma with visual field loss, it's more important to examine and evaluate the optic nerve than just to rely on visual field changes."

This concept puts the onus on clinicians to pay more attention to structural abnormalities, he said. "We have new tools available now, such as scanning devices of the optic nerve, that enable us to discover RNFL defects or changes in the cupping of the optic nerve at levels before there's any damage in the psychophysical or visual field function," he said.

"The goal of management is to detect glaucoma damage at earlier stages," Dr. Krupin added. "By the time you see a defect on standard automated perimetry, it's not really early glaucoma; it's moderate glaucoma. The earlier we detect glaucomatous damage, the greater the opportunity to reduce the occurrence of functional and quality of life loss by the patient."

What does the future of glaucoma therapy hold? According to Dr. Krupin, the ultimate staging method would be an in vitro determination or detection of an accelerated rate of retinal ganglion cell death. "I think this is the future of glaucoma staging and detection, and, therefore, management. But it's still the future," he said.