Ocular Perfusion Pressure vs Estimated Trans-Lamina Cribrosa Pressure Difference in Glaucoma: The Central India Eye and Medical Study (An American Ophthalmological Society Thesis).

PURPOSE To test the hypothesis that taking translamina pressure difference into consideration changes associations between ocular perfusion pressure and glaucomatous optic neuropathy. METHODS The population-based Central India Eye and Medical Study included 4711 subjects. Ocular perfusion pressure was calculated as follows: ⅔ [diastolic blood pressure + ⅓ × (systolic blood pressure - diastolic blood pressure)] - IOP. Cerebrospinal fluid pressure (mm Hg) was estimated as follows: 0.44 body mass index (kg/m(2)) + 0.16 diastolic blood pressure (mm Hg) - 0.18 × age (years) - 1.91. Translamina pressure difference was IOP minus cerebrospinal fluid pressure. RESULTS In multivariate analysis, higher open-angle glaucoma prevalence was associaed with higher IOP (P<.001; odds ratio [OR], 1.19; 95% CI, 1.15, 1.24) or with higher translamina pressure difference (P<.001; OR, 1.15; 95% CI, 1.10, 1.19), but not with ocular perfusion pressure (P<.37). A smaller neuroretinal rim area was correlated with higher IOP (P<.001; standardized coefficient beta -0.09) or larger translamina pressure difference (P<.001; β -0.10), but not with ocular perfusion pressure (P=.26). Greater prevalence of angle-closure glaucoma was associated with higher IOP (P<.001; OR, 1.22; 95% CI, 1.15, 1.28) or higher translamina pressure difference (P<.001; OR, 1.19; 95% CI, 1.13, 1.25) or lower ocular perfusion pressure (P<.04; OR, 0.95; 95% CI, 0.90, 0.996). Correlation coefficients were highest for the association with IOP and lowest for ocular perfusion pressure. A smaller rim area was correlated with higher IOP (P<.001; beta -0.08) and higher translamina pressure difference (P<.001; beta -0.08); rim area and ocular perfusion pressure were not significantly associated (P=.25). CONCLUSIONS The present study provides information on the relationship of translamina pressure difference to the development of optic nerve damage in what is presently called glaucoma. It does not provide support of the idea that ocular perfusion pressure plays a major role in the pathogenesis of optic neuropathy.