Lamina cribrosa defects linked to accelerated retinal nerve fibre layer thinning
medwireNews: Retinal nerve fibre layer (RNFL) thinning progresses faster in eyes with lamina cribrosa (LC) defects than it does in eyes without such defects, shows an analysis of patients enrolled in the Diagnostic Innovations in Glaucoma Study.
“These findings suggest that assessment of LC focal defects adds information to the evaluation of the risk and rate of glaucoma progression”, say Robert Weinreb (University of California, San Diego, USA) and co-investigators.
Using swept-source and spectral-domain optical coherence tomography, the researchers found that, during a mean 3.5-year follow-up, the rate of global RNFL loss was more than twice as fast among the 51 eyes with LC defects as among the 83 without, at 0.91 versus 0.48 μm/year.
LC defects were located in the inferotemporal sector in 20 eyes, in the supratemporal sector in 19 eyes and in both sectors in 12 eyes, and further analysis showed that the localised rate of RNFL thinning in the sector with the LC defect was significantly faster than that in the unaffected sector, at 1.60 versus 0.70 μm/year.
“This finding supports previous reports that showed regional differences in the LC properties may make specific portions of the optic nerve particularly susceptible to neural loss”, Weinreb et al remark.
And they note that the presence of an LC defect remained significantly associated with faster RNFL thinning after adjustments for potential confounders.
In a written comment that accompanies the study, both of which appear in JAMA Ophthalmology, Joel Schuman (New York University School of Medicine, USA) and co-authors say that the results suggest that “when detected, LC defects may provide valuable information that can inform treatment” of glaucoma.
They caution, however, that the study had “[s]everal methodologic limitations”, including the use of suboptimal imaging acquisition and assessment techniques for the detection of LC abnormalities and a “[r]eliance on expert classification of defects rather than on automated methods of LC assessment.”
They add: “More accurate and detailed data on LC microstructural abnormalities could have enabled stronger or different associations with glaucomatous RNFL progression.”
In spite of this, Schuman et al say that the study “provides compelling evidence for the future inclusion of LC defects in the routine assessment of patients with glaucoma.”
They conclude: “Moving forward, more sensitive approaches to detection of LC defects should enable a fuller understanding of the potential for abnormalities of this tissue to predict progression and inform treatment.”
By Laura Cowen
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