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Original Investigation
February 7, 2019

Association Between Lamina Cribrosa Defects and Progressive Retinal Nerve Fiber Layer Loss in Glaucoma

Author Affiliations
  • 1Hamilton Glaucoma Center, Shiley Eye Institute, Viterbi Family Department of Ophthalmology, University of California, San Diego
  • 2Tehran University of Medical Sciences, Tehran, Iran
JAMA Ophthalmol. Published online February 7, 2019. doi:10.1001/jamaophthalmol.2018.6941
Key Points

Question  Does an association exist between lamina cribrosa defects and local or global retinal nerve fiber layer thinning over time among patients with open-angle glaucoma?

Findings  In this longitudinal cohort study of 51 eyes in 43 patients, lamina cribrosa defects were an independent risk factor for retinal nerve fiber layer thinning, and glaucoma progression was topographically associated with lamina cribrosa defect location. Different factors were associated with the rate of retinal nerve fiber layer thinning in eyes with or without lamina cribrosa defects.

Meaning  Assessment of lamina cribrosa focal defects may inform the evaluation of glaucoma progression risk, and eyes with lamina cribrosa defects should undergo frequent monitoring.


Importance  Certain features of the lamina cribrosa may be associated with increased risk of glaucoma progression.

Objectives  To compare the rates of retinal nerve fiber layer (RNFL) thinning in patients with open-angle glaucoma with or without lamina cribrosa (LC) defects and to evaluate factors associated with the rate of glaucoma progression in eyes with LC defects.

Design, Setting, and Participants  This longitudinal cohort study designed in September 2017 and conducted at a tertiary glaucoma center in California included 51 eyes of 43 patients with LC defects and 83 eyes of 68 patients without LC defects followed up for a mean (SD) of 3.5 (0.8) years from April 2012 to May 2017.

Main Outcomes and Measures  Focal LC defects were detected using swept-source optical coherence tomographic images. All participants underwent visual field testing and spectral-domain optical coherence tomography for RNFL thickness measurements every 6 months. Univariate and multivariable random-effects models were used to compare the rate of local and global RNFL loss.

Results  The mean (95% CI) age at baseline for individuals with LC defects was 69.5 (65.4 to 73.6) years, and for those without LC defects, it was 69.6 (67.2-72.0) years; 18 individuals (41%) with LC defects and 35 individuals (51%) without LC defects were men; 6 individuals (14%) with LC defects and 17 individuals (25%) without were African American. The mean (95% CI) rate of global RNFL loss in eyes with LC defects was 2-fold faster than that in eyes without LC defects (−0.91 [−1.20 to −0.62] vs −0.48 [−0.65 to −0.31] μm/y; difference, −0.43 [−0.76 to −0.09] μm/y; P = .01). The rate of RNFL thinning was faster in the LC defect sectors than that in the unaffected sectors (difference, −0.90 [95% CI, −1.68 to −0.12] μm/y, P = .02). Thinner corneal thickness was the only factor that was associated with a faster rate of RNFL loss in eyes with LC defects (β2 = −0.09 [95% CI, −0.14 to −0.04], P = .001). No association was found between mean intraocular pressure during follow-up and the mean rate of RNFL thinning in eyes with LC defects (β2, −0.05 [95% CI, −0.17 to 0.06], P = .36).

Conclusions and Relevance  These data suggest that LC defects are an independent risk factor for RNFL thinning and that glaucoma progression may correspond topographically to the LC defect location. Thinner corneal thickness in eyes with LC defects was associated with faster further glaucoma progression. In the management of open-angle glaucoma, LC findings may inform the likelihood and rate of glaucoma progression.