Combined Use of Retinal Nerve Fiber Layer and Ganglion Cell-Inner Plexiform Layer Event-based Progression Analysis.

PURPOSE: To evaluate patterns of glaucomatous structural progression using the combined retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GCIPL) event-based progression analysis feature provided by spectral-domain optical coherence tomography (SD-OCT)'s - (GPA) software. DESIGN: Retrospective observational case series. METHODS: Seventy-nine (79) patients were identified with open-angle glaucoma (OAG) showing clinically confirmed structural progression within a minimum 3-year follow-up period. For each eye, RNFL and GCIPL GPA data were obtained from serial SD-OCT data from 2012 to 2017. An integrated GPA map thereafter was merged by vascular landmark-guided superimposition of RNFL and GCIPL GPA event-based progression maps onto the RNFL imagery (resulting in what we call the GPA PanoMap). The GPA PanoMap progression patterns were classified as (1) RNFL-only, (2) GCIPL-only, (3) concurrent (both RNFL and GCIPL), (4) GCIPL after RNFL, and (5) RNFL after GCIPL. The locations of structural progression were classified, based on an earlier schematic model, as (1) superior vulnerability zone (SVZ), (2) papillomacular bundle (PM), (3) macular vulnerability zone (MVZ), and (4) inferoinferior portion. Structural progression patterns on the GPA PanoMap were evaluated according to the location of progression. Among the eyes with progression in the inferior hemiretina, structural progression patterns on the GPA PanoMap were evaluated according to the baseline structural damage. RESULTS: On the GPA PanoMap, when structural progression was located in the SVZ or inferoinferior portion, it was detected only in the RNFL area; when progression was located in the PM or MVZ, various patterns were observed, among which the concurrent pattern was the majority in both areas (43.8% and 45.6% in the PM and MVZ, respectively). Among the eyes with progression in the inferior hemiretina (n = 66), the location of progression varied but did not differ significantly according to the baseline deviation map (P = .440). The progression patterns of MVZ were significantly different among the baseline deviation map patterns (P = .023); however, all of the progression patterns of the inferoinferior portion were RNFL-only. CONCLUSION: The various progression patterns were confirmed according to the locations and baseline patterns of glaucomatous structural change on the integrated GPA map (GPA PanoMap). Combined use of RNFL and GCIPL GPA or the GPA PanoMap could be useful for determination of structural progression and understanding of its patterns in patients with glaucoma.

Temporal Relation between Macular Ganglion Cell-Inner Plexiform Layer Loss and Peripapillary Retinal Nerve Fiber Layer Loss in Glaucoma.

PURPOSE: To investigate the temporal relationship between inferior macular ganglion cell-inner plexiform layer (mGCIPL) loss and corresponding peripapillary retinal nerve fiber layer (pRNFL) defect on the optical coherence tomography (OCT) deviation map in glaucoma. DESIGN: Retrospective, observational study. PARTICIPANTS: A total of 151 patients with early-stage glaucoma (visual field [VF] mean deviation between -1.5 and -5.5 decibels [dB]). METHODS: Spectral-domain OCT mGCIPL and pRNFL deviation maps were obtained for the baseline (from January 2012 to August 2012) and again for the follow-up (from January 2015 to August 2015). An integrated deviation map thereafter was merged by vascular landmark-guided superimposition of mGCIPL and pRNFL deviation maps onto RNFL imagery. On the basis of an earlier schematic model, the inferotemporal peripapillary area was divided into (1) the macular vulnerability zone (MVZ) and (2) the inferoinferior portion. MAIN OUTCOME MEASURES: Temporal sequence of inferior mGCIPL loss and corresponding pRNFL (i.e., pRNFL in MVZ) defect on integrated deviation map. RESULTS: At baseline, 99 (65.6%) of the 151 eyes showed inferior mGCIPL loss. In addition, 112 eyes (74.2%) and 5 eyes (3.3%) showed inferoinferior pRNFL defect and pRNFL defect in the MVZ, respectively. At the 3-year follow-up, 112 (74.2%) of the eyes showed inferior mGCIPL loss, whereas 123 eyes (81.5%) and 25 eyes (16.6%) showed inferoinferior pRNFL defect and pRNFL defect in the MVZ, respectively. Ninety-four eyes initially showed inferior mGCIPL loss without pRNFL defect in the MVZ; among them, 19 (20.2%) subsequently showed defect during the 3-year follow-up interval. Meanwhile, among the 52 eyes without preexisting inferior mGCIPL loss, only 1 (1.9%; P < 0.001) developed a pRNFL defect in the MVZ during the 3-year follow-up interval. CONCLUSIONS: In eyes with early glaucoma, mGCIPL change is frequently detected before corresponding pRNFL change. This could be the result of a superior sensitivity of mGCIPL deviation map that allows detection of an abnormality in the mGCIPL thickness earlier. In this light, OCT pRNFL analysis alone likely would overlook macular damage. Macular OCT imaging should be included in the imaging algorithm for the serial observation of patients with glaucoma.