March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Focal Lamina Cribrosa Defects and Glaucomatous Visual Field Progression
Author Affiliations & Notes
  • Omar S. Faridi
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
  • Sung Chul Park
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, New York Medical College, Valhalla, New York
  • Daniel Su
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Mount Sinai School of Medicine, New York, New York
  • Joseph Simonson
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
  • Anthony T. Hsu
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
  • Carlos G. De Moreas
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, NYU School of Medicine, New York, New York
  • Christopher Teng
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, New York Medical College, Valhalla, New York
  • Celso Tello
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, New York Medical College, Valhalla, New York
  • Jeffrey M. Liebmann
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, NYU School of Medicine, New York, New York
  • Robert Ritch
    Einhorn Clinical Research Center, New York Eye and Ear Infirmary, New York, New York
    Ophthalmology, New York Medical College, Valhalla, New York
  • Footnotes
    Commercial Relationships  Omar S. Faridi, None; Sung Chul Park, None; Daniel Su, None; Joseph Simonson, None; Anthony T. Hsu, None; Carlos G. De Moreas, None; Christopher Teng, None; Celso Tello, None; Jeffrey M. Liebmann, Carl Zeiss Meditec, Inc (F), Carl Zeiss Meditec, Inc. (C), Heidelberg Engineering, GmbH. (F), Optovue, Inc. (C), Topcon, Inc. (C); Robert Ritch, None
  • Footnotes
    Support  Ettinger Foundation Research Fund of the New York Glaucoma Research Institute, New York, NY. Dr. Park is the Peter Crowley Research Scientist at the New York Eye and Ear Infirmary.
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 3694. doi:
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      Omar S. Faridi, Sung Chul Park, Daniel Su, Joseph Simonson, Anthony T. Hsu, Carlos G. De Moreas, Christopher Teng, Celso Tello, Jeffrey M. Liebmann, Robert Ritch; Focal Lamina Cribrosa Defects and Glaucomatous Visual Field Progression. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3694.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To compare glaucomatous visual field (VF) progression between eyes with and without focal lamina cribrosa (LC) defects.

Methods: : Serial horizontal and vertical enhanced depth imaging optical coherence tomography (EDI OCT) B-scans of the optic nerve head (interval between scans: approximately 30 µm) were obtained prospectively from glaucoma patients with 5 or more prior 24-2 VF tests. EDI OCT scans were reviewed for the presence of focal LC defects (focal LC disinsertion or full-thickness LC defect) that violated the smooth curvilinear contour of the normal anterior laminar surface. The maximum width of each focal LC defect was required to be ≥100 µm. Progression rates were calculated using pointwise linear regression (PLR) analysis and averaged to generate the global progression rate (dB/yr) for each eye. VF progression was defined as having ≥1 significantly progressing point(s) (slope <-1.0 dB /yr at P<0.01). The rates at these points were averaged to generate the localized progression rate (dB/yr) for each eye. Age, intraocular pressure [IOP], baseline visual field [VF] mean deviation [MD], a detected disc hemorrhage, and central corneal thickness [CCT] were recorded.

Results: : A total of 104 eyes were included (104 patients; mean age, 66±13 yr; mean baseline VF MD, -10.2±7.6 dB): 45 eyes had focal LC defects and 59 did not (control group). The mean number of VF tests (9.2 vs. 8.8) and follow-up period (6.7 vs. 7.1 yrs) were similar between the two groups (all P>0.2). Significantly more eyes had progressed in the LC defect group than in the control group (27 eyes [61%] vs. 16 eyes [27%]; P<0.001). Mean global (-0.61 vs. -0.22 dB/yr) and localized progression rates (-3.51 vs. -1.96 dB/yr) were significantly greater in eyes with focal LC defects than in those without (P=0.015 and 0.010, respectively), whereas the mean number of progressing points were similar between the two groups (5.4 vs. 5.1; P=0.5). After adjusting for age, mean follow-up IOP, baseline VF MD, disc hemorrhage detection, and CCT, however, there was a borderline, but non-significant difference between groups regarding global (P=0.08) and localized (P=0.16) progression rates. Among the evaluated parameters, the presence of focal LC defect and number of VF tests were significantly associated with VF progression in both univariate (OR, 4.27; P<0.001 and OR, 1.19; P=0.0027, respectively) and multivariate (OR, 4.87; P<0.001 and OR, 1.20; P=0.002, respectively) logistic regression analyses.

Conclusions: : Focal LC defect is highly associated with glaucomatous VF progression.

Keywords: lamina cribrosa • imaging/image analysis: clinical • visual fields 
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