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    Glaucoma may not be the disease you think it is

    Growing evidence supports IOP, CSF pressure differential

     

    Exploring the concept

    The idea that CSF pressure contributes to glaucoma was first presented in 2008. Eight years later, a growing body of retrospective and prospective data support the two-pressure model, Dr. Berdahl noted.

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    Intracranial pressure (ICP) is already recognized as a factor in optic nerve dysfunction. Intracranial hypertension causes the optic nerve to bow outward. The pressure differential impedes axonal transport at the lamina cribrosa, depriving the optic nerve of nutrition. If the metabolic needs of the optic nerve are not met for a sufficiently long period, the nerve withers and vision suffers.

    Dr. Berdahl suggested that glaucoma is the end result of the same situation in reverse. Pressure inside the eye is higher than intracranial pressure, which results in the posterior cupping that is seen in glaucoma. Axonal transport is impeded at the lamina cribrosa and the optic nerve, its metabolic needs unmet, eventually withers and vision is lost.

    “This represents a potential redefinition of glaucoma,” he said. “This concept opens up entirely new therapeutic modalities and options for patients and physicians. And it explains physiology and pathophysiology that don’t fit the traditional one-pressure model.”

    Elevated IOP might explain primary open-angle glaucoma, he continued.

    But elevated IOP cannot account for normotension glaucoma. Nor can clinicians explain why elevated IOP may not lead to glaucoma in ocular hypertensives. The two-pressure model does.

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    In individuals without glaucoma, the pressure differential between IOP and intracranial pressure is about four mm Hg. In individuals with glaucoma, the pressure gradient across the lamina cribrosa in greater, in the range of 13 mm Hg and higher.

    “What causes cupping visual field loss in glaucoma? I believe the cupping is caused by the posteriorly directed forces generated when the IOP is greater than the ICP,” Dr. Berdahl said. “The visual field loss is caused by axonal death as the nutrient and waste transport needs of the optic nerve are not met because transport cannot get into the higher pressure environment beyond the lamina cribrosa.”

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    He sees the same mechanism at work in normotension glaucoma. These individuals have normal IOP but a low ICP. The pressure gradient across the lamina cribrosa is high enough to impede axonal transport and eventually cause damage to the ocular nerve and increasing loss of vision.

    Ocular hypertension

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