Purpose
To test whether the minimum rim area assessed by spectral domain optical coherence tomography (SD-OCT), based on the shortest distance from Bruch's Membrane Opening (BMO) to the inner limiting membrane, corresponds more closely to retinal nerve fiber layer (RNFL) thickness and visual field mean deviation (MD) than current rim measures in early glaucoma.
Design
Prospective cross-sectional study.
Methods
221 participants with non-endstage glaucoma or high-risk ocular hypertension performed standard automated perimetry, and received SD-OCT and confocal scanning laser ophthalmoscopy (CSLO) scans, on the same day. Rim area measured by CSLO was compared with three SD-OCT rim measures from radial B-scans: horizontal rim area between BMO and ILM within the BMO plane; mean minimum rim width (BMO-MRW); and minimum rim area (BMO-MRA) optimized within sectors and then summed. Correlations between these measures and either MD from perimetry or RNFL thickness from SD-OCT were compared using Steiger's test.
Results
RNFL thickness was better correlated with BMO-MRA (r=0.676) or BMO-MRW (r=0.680) than with either CSLO Rim Area (r=0.330, p<0.001) or Horizontal Rim Area (r=0.482, p<0.001). MD was better correlated with BMO-MRA (r=0.534) or BMO-MRW (r=0.546) than with either CSLO Rim Area (r=0.321, p<0.001) or Horizontal Rim Area (0.403, p<0.001). The correlation between MD and RNFL thickness was r=0.646.
Conclusions
Minimum rim measurements from SD-OCT are significantly better correlated to both RNFL thickness and MD than rim measurements within the BMO plane, or based on the clinical disc margin. They provide new structural parameters for both diagnostic and research purposes in glaucoma.
ABSTRACT.Background: To assess the lumbar cerebrospinal fluid pressure (CSF-P) in ocular hypertensive subjects with elevated intraocular pressure (IOP) but without development of glaucomatous optic nerve damage.
Methods:The prospective interventional study included 17 patients with ocular hypertension and 71 subjects of a nonglaucomatous control group. All patients underwent a standardized ophthalmologic and neurological examination including measurement of lumbar CSF-P. In the ocular hypertensive group, the IOP was corrected for its dependence on central corneal thickness (IOP corrected ). The trans-lamina cribrosa pressure difference (Trans-LCPD) was calculated as IOP corrected ) CSF-P.Results: CSF-P was significantly (p < 0.001) higher in the ocular hypertensive group (16.0 ± 2.5 mmHg) than in the control group (12.9 ± 1.9 mmHg). CSF-P was significantly associated with IOP corrected (p < 0.001; r = 0.82). In multivariate analysis, CSF-P was significantly correlated with IOP corrected (p < 0.001) and marginally significantly with mean blood pressure (p = 0.05). Trans-LCPD was not associated significantly with blood pressure (p = 0.69).Conclusion: Some ocular hypertensive subjects with increased intraocular pressure measurements (after correction for their dependence on central corneal thickness) had an abnormally high lumbar cerebrospinal fluid pressure. Assuming that lumbar cerebrospinal fluid pressure correlated with orbital cerebrospinal fluid pressure, one may postulate that the elevated retro-lamina cribrosa pressure compensated for an increased intraocular pressure. The elevated retro-lamina cribrosa pressure may have led to a normal trans-laminar pressure difference in the eyes with elevated intraocular pressure, so that glaucomatous optic nerve damage did not develop. Intraocular pressure, cerebrospinal fluid pressure and arterial blood pressure were correlated with each other.
Lamina cribrosa thickness and peripapillary sclera thickness decreased significantly with axial length, in addition to a glaucoma-related thinning of the lamina cribrosa. In non-axially elongated eyes, the peripapillary sclera thickness did not vary significantly between glaucomatous eyes and normal eyes.
The trans-lamina cribrosa pressure difference as the difference of intraocular pressure minus the lumbar CSF pressure was the main pressure parameter associated with the amount of glaucomatous optic nerve damage. This may suggest that the CSF pressure as trans-lamina cribrosa counter pressure against the intraocular pressure may play some role in the pathogenesis of glaucomatous optic neuropathy.
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