Eyeworld

79 EW GLAUCOMA February 2016 IOP, blood pressure, and CSF pressure: an integrated model In fact, glaucoma may be a 3-pres- sure disease because blood pressure and CSF pressure are not indepen- dent of one another. "At low blood pressure," Dr. Harris said, "CSF pressure is also low to facilitate central nervous system perfusion. At high blood pressure, CSF pressure is high to prevent cere- bral hemorrhage. If blood pressure is reduced by medical therapy, CSF pressure is also reduced, and IOP remains stable, which lowers ocular perfusion pressure and puts the optic nerve at risk." Clinical implications These data are intriguing and the hypotheses are attractive to help make sense of glaucoma. But much more research is necessary to estab- lish these relationships and to shed insight on blood pressure and/or CSF pressure as potential therapeutic targets for glaucoma. In the meantime, it is not unrea- sonable to measure blood pressure in the office when confronted with a progressing patient whose IOP seems adequately controlled and who is on systemic therapy for hypertension. If blood pressure is low in the office, a 24-hour blood pressure assessment may reveal significant nocturnal dips in blood pressure. If so, a conversation with the internist may allow an adjustment in systemic hy- pertension therapy—either a lower dose, a different agent, or avoidance of nighttime dosing. EW Editors' note: The physicians have no financial interests related to this article. Contact information Harris: alharris@indiana.edu Lee: opticdisc@gmail.com Medeiros: fmedeiros@glaucoma.ucsd.edu barrier between the intraocular and retrobulbar spaces." The intraocular portion of the optic nerve head is acted upon by the IOP. The retrobulbar portion of the optic nerve head is acted on by the cerebrospinal fluid (CSF) pres- sure within the retrobulbar optic nerve sheath, he added. "The translaminar pressure difference is the IOP minus the pressure in the retrobulbar CSF space and determines the stresses and strains of the optic nerve head," Dr. Harris said. Could CSF pressure play a role in glaucoma? "In fact, low CSF pressure has been associated with glaucomatous optic neuropathy as far back as the 1970s," he said. More recently, 2 studies have provided additional support for this hypothesis. In a retrospective review of lumbar punctures in patients with and without glaucoma, CSF pressure was significantly lower (9.2 mm Hg) in glaucoma patients versus non-glaucomatous control subjects (13.2 mm Hg). There was a dose-response relationship between CSF pressure and cup-disc ratio, Dr. Harris added. "This was confirmed in a pro- spective study, in which CSF pres- sure was lower in both high tension and low tension glaucoma (11.7 and 9.5 mm Hg, respectively) compared to controls (12.9 mm Hg)," he said. Interestingly, CSF pressure declines with age, which may help explain glaucoma's increasing preva- lence with age. The interaction between IOP and CSF pressure and their effects on the configuration of the lamina cribrosa may provide a theoretical mechanism for the mechanical theory of glaucoma. High IOP causes backbowing of the lamina, with kinking and distortion of the axons that can block axoplasmic flow, according to Eun Ji Lee, MD, South Korea. In this model, IOP reduction would allow the lamina to shift back forward, resulting in therapeutic benefit. "Laminar thickness is import- ant," she said. "It is a measure of how well the lamina can resist the pressure difference across it. In glau- coma, the lamina thins, which may explain progression even at lower IOP."

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