Elsevier

Ophthalmology

Volume 115, Issue 9, September 2008, Pages 1480-1488.e2
Ophthalmology

Original article
Low Luminance Visual Dysfunction as a Predictor of Subsequent Visual Acuity Loss from Geographic Atrophy in Age-Related Macular Degeneration

Presented in part at: American Academy of Ophthalmology Annual Meeting, November 2006, Las Vegas, Nevada.
https://doi.org/10.1016/j.ophtha.2008.03.009Get rights and content

Objective

To show that low luminance visual dysfunction is predictive of subsequent visual acuity (VA) loss in eyes with geographic atrophy (GA) resulting from age-related macular degeneration (AMD).

Design

Cohort study examining the prospective natural history study of GA from 1992 through 2000 at the Wilmer Eye Institute.

Participants

Ninety-one participants with GA resulting from AMD without choroidal neovascularization in at least 1 eye who completed a 2-year study examination.

Methods

Annual examinations included measurement of best-corrected VA, low luminance VA, Pelli-Robson contrast sensitivity, reading speed, examination, and fundus photography. The total GA area was quantified, as was the GA within a 10.2-mm2 circle centered on the fovea.

Main Outcome Measures

Visual acuity loss at 2 years and risk factors for visual loss.

Results

Participants with baseline VA of 20/50 or more had a 40% 2-year rate of VA loss of 3 lines or more, compared with 13% for the participants with worse baseline acuities. The baseline low-luminance deficit (LLD) in VA was a strong predictor of subsequent VA loss for all levels of baseline VA. Within the good baseline VA group, the relative risk (RR) of 3-line loss for the worse LLD group compared with the better LLD group was 2.88 (95% confidence interval [CI], 1.13–7.35). The LLD is a stable and reproducible measure. Other significant visual function predictors of subsequent VA loss in eyes with good baseline VA included foveal dark-adapted sensitivity (RR, 4.20; 95% CI, 1.39–12.71) and reduced reading rate (RR, 2.43; 95% CI, 1.11–5.31). The rate of VA loss within the good acuity group was higher when the GA included 25% to 75% of the central 10.2 mm2 than in eyes with GA including less than 25% or more than 75% of the central 10.2 mm2. The following were not significant predictors of subsequent VA loss among these participants: age, gender, fellow eye diagnosis, fellow eye VA, baseline GA area, and GA enlargement rate.

Conclusions

Visual function measures can predict the risk of future VA loss in subjects with GA and good baseline VA. They may allow identification of the highest risk group for VA loss, enabling more efficient design of clinical trials. They also may be appropriate surrogate measures of foveal health in short-term treatment trials.

Financial Disclosure(s)

The authors have no proprietary or commercial interest in any materials discussed in this article.

Section snippets

Patients and Methods

A National Institutes of Health-funded prospective natural history study of GA resulting from AMD was conducted at the Wilmer Eye Institute between 1992 and 2000. The study was approved by the Johns Hopkins University School of Medicine's Institutional Review Board, and written informed consent was obtained from all study participants. This study adhered to the Declaration of Helsinki. One hundred fifty-eight subjects enrolled. The primary entry criterion was having GA as a result of AMD,

Results

Table 1 gives the baseline characteristics for the 91 participants with 2-year data.

Low Luminance Visual Dysfunction

These prospective natural history data show that the LLD, a simple, inexpensive, and rapid measure of visual function, was a strong predictor of the subsequent risk for losing VA in eyes with GA. This measure was studied because of the clear difficulties experienced by participants with GA in dim illumination and the body of research showing reductions in dark-adapted function in patients with AMD. The authors previously showed, in a small pilot study, that in eyes with drusen with reduced

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Manuscript no. 2007-977.

Financial Disclosure(s): The authors have no proprietary or commercial interest in any materials discussed in this article.

Supported by the National Institutes of Health, Bethesda, Maryland (grant nos.: EY08552 and EY14148).

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