Abstract
Purpose :
Idiopathic macular telangiectasia type 2 (MacTel 2) is associated with both choroidal thickening and outer retinal disruption, but it is unclear if there is a correlation between the extent of these two clinical features. In this retrospective, observational clinical study, we investigate the relationship between choroidal thickness and area of ellipsoid zone defect in MacTel 2 using enhanced-depth imaging (EDI) spectral-domain topical coherence tomography (SD-OCT).
Methods :
We examined 20 eyes from 10 patients who underwent EDI SD-OCT imaging for MacTel Type 2 between 2012 and 2014 at Herzig Eye Institute, Toronto, Canada. Choroidal thickness measurements were made at the fovea and at 5 points within an interval of 500µm in both directions, nasal and temporal from the fovea, by semi-automated segmentation of B-scan EDI SD-OCT images. Ellipsoid zone defect was defined as diffuse and focal disruptions occurring in the photoreceptor inner segment/outer segment (IS/OS) junction, which appeared as hyporeflective grey shades on C-scan ("en-face") SD-OCT images. The total area of defect was manually measured by a single observer using built-in software tool. Univariate analysis was used to determine the mean and spread of collected anatomical values. Bivariate linear regression was used to evaluate the association between subfoveal choroidal thickness or average choroidal thickness across the central 1-mm segment and the area of ellipsoid zone defect.
Results :
Both subfoveal and average central choroidal thicknesses were positively associated with area of ellipsoid zone defect (p < 0.00001). Subfoveal choroidal thickness (µm) ranged from 118 to 523 (mean 319.4 ± SD 91.3), average choroidal thickness (µm) ranged from 122 to 474 (mean 286.2 ± SD 85.3), and area of ellipsoid zone defect (mm2) ranged from 1.53 to 6.53 (mean 3.71 ± SD 1.43).
Conclusions :
Choroidal thickness correlates with area of ellipsoid zone defect in patients with macular telangiectasia type 2. This information provides another clinical perspective on the pathophysiology of MacTel, and can be considered in new models of its pathogenesis. This study also introduces the value of EDI SD-OCT in assessing quantifiable parameters of MacTel, which may guide future research for a better understanding of this currently idiopathic disease.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.