Ganglion Cell-inner Plexiform Layer Thinning Research Articles

Predictors of retinal atrophy in multiple sclerosis: A longitudinal study using spectral domain optical coherence tomography with segmentation analysis

BackgroundMultiple sclerosis is an inflammatory demyelinating disease characterized by progressive axonal loss affecting mainly the inner retinal layers. Optical coherence tomography (OCT) provides in-vivo quantification of the retinal layers and allows measuring progressive retinal changes. Our objective was to assess the longitudinal changes in the retina using spectral domain OCT (SDOCT) and to identify independent predictors affecting retinal thinning in MS patients. MethodsA prospective study in a tertiary care MS center was conducted to study the longitudinal retinal changes in MS patients. All subjects underwent baseline and follow up OCT assessment with segmentation analysis. Regression analysis was performed to assess clinical factors (age, sex, disease duration, history of optic neuritis before baseline, non-ocular clinical relapses) and MRI disease activity during the follow-up period. ResultsThe study included 102 MS patients with a mean follow-up duration of 3.9 ± SD years. At the last follow-up assessments, there were significant thinning of the average macular thickness (AMT) (p < .001), macular nerve fiber layer (MRNFL) (p < .001), ganglion cell-inner plexiform layer (GCIPL) (p < .001), and the peripapillary nerve fiber layer (PRNFL) (p < .001), compared to baseline. Early disease duration up to 10 years was associated with thinning of AMT, PRNFL, and GCIPL, while longer disease duration (> 15 years) was associated with only GCIPL thinning. Prior optic neuritis was predictive of more thinning of PRNFL (p = < .01), while MRI activity and female gender were significantly associated with more MRNFL thinning (p = < .01). ConclusionMS is associated with longitudinal thinning affecting AMT inner retinal layers (MRNFL, GCIPL, PRNFL). Early disease duration, female gender, MRI activity, and prior optic neuritis were predictive of faster rate of neuro-axonal loss. This may have implications in the design of future therapeutic trials.

Integrating Macular Ganglion Cell Inner Plexiform Layer and Parapapillary Retinal Nerve Fiber Layer Measurements to Detect Glaucoma Progression

To investigate the temporal relationship among progressive macular ganglion cell inner plexiform layer (GCIPL) thinning, progressive parapapillary retinal nerve fiber layer (RNFL) thinning, and visual field (VF) progression in patients with primary open-angle glaucoma (POAG). Prospective study. One hundred thirty-six POAG patients (231 eyes) followed up for ≥5 years. OCT imaging of the macular GCIPL and parapapillary RNFL and perimetry were performed at ∼ 4-month intervals. Progressive GCIPL and RNFL thinning were determined by Guided Progression Analysis (GPA) of serial GCIPL and RNFL thickness maps. The specificities of GPA were calculated from the proportions of eyes with progressive GCIPL or RNFL thinning in 67 eyes of 36 healthy individuals followed up for ≥5 years. Visual field progression (likely or possible) was determined by the Early Manifest Glaucoma Trial criteria. Hazard ratios for VF progression, progressive RNFL thinning, and progressive GCIPL thinning, as determined by time-varying Cox models. GPA detected 57 eyes (24.7%) with progressive GCIPL thinning and 66 eyes (28.6%) with progressive RNFL thinning at a specificity of 95.5% and 91.0%, respectively. Thirty-five eyes (15.2%) demonstrated progressive RNFL and GCIPL thinning, whereas 53 eyes (22.9%) demonstrated progressive RNFL or GCIPL thinning. Eyes with progressive GCIPL thinning had a higher risk for progressive RNFL thinning (HR, 5.27; 95% confidence interval [CI], 2.89-9.62), whereas eyes with progressive RNFL thinning were also at a higher risk for progressive GCIPL thinning (HR, 2.99; 95% CI, 1.48-6.02), after adjusting for baseline covariates. The HRs for likely and possible VF progression were 3.48 (95% CI, 1.51-8.01) and 2.74 (95% CI, 1.26-5.98), respectively, on detection of progressive GCIPL thinning and 3.66 (95% CI, 1.68-7.97) and 2.54 (95% CI, 1.23-5.21), respectively, on detection of progressive RNFL thinning after adjusting for baseline covariates. Eyes with VF progression were not at risk of progressive RNFL or GCIPL thinning (P ≥ 0.493). Progressive macular GCIPL thinning and progressive parapapillary RNFL thinning are mutually predictive. Because progressive RNFL thinning and progressive GCIPL thinning are both indicative of VF progression, integrating macular GCIPL and parapapillary RNFL measurements is relevant to facilitate early detection of disease deterioration in glaucoma patients.

Evaluation of Ganglion Cell-Inner Plexiform Layer Thinning in Eyes With Optic Disc Hemorrhage: A Trend-Based Progression Analysis.

To evaluate the rate of change in ganglion cell-inner plexiform layer (GCIPL) thickness measured by optical coherence tomography (OCT) using a trend-based approach in early-stage glaucomatous eyes with disc hemorrhage (DH) and to compare the GCIPL thinning rate with that in glaucomatous eyes without DH. This prospective observational study included 46 patients with early-stage open-angle glaucoma and DH who underwent serial spectral-domain OCT measurements for at least 30 months. The GCIPL thinning rate was determined in the global, superior, or inferior hemiretinas and in six macular sectors by linear regression and was compared between glaucomatous eyes with DH and fellow glaucomatous eyes without DH and between glaucomatous eyes with DH and non-DH glaucomatous control eyes. The GCIPL thinning rate (mean ± standard deviation) was significantly more rapid in glaucomatous eyes with DH than in fellow eyes without DH in the inferior hemiretina (-1.07 ± 0.75 vs. -0.44 ± 0.54 μm/y, P = 0.001), inferotemporal sector (-1.13 ± 1.00 vs. -0.61 ± 0.66 μm/y, P = 0.028), and inferior sector (-1.33 ± 0.79 vs. -0.42 ± 0.78 μm/y, P < 0.001). The GCIPL thinning rate was significantly more rapid in glaucomatous eyes with DH than in glaucomatous controls without DH in the global area (-0.78 ± 0.85 vs. -0.32 ± 0.48 μm/y, P = 0.002), the inferior hemiretina (-1.00 ± 0.94 vs. -0.37 ± 0.67 μm/y, P < 0.001), and the inferotemporal sector (-1.31 ± 1.07 vs. -0.34 ± 0.75 μm/y, P < 0.001). The GCIPL thinning rate on OCT was significantly more rapid in glaucomatous eyes with DH than in fellow glaucomatous eyes without DH or glaucomatous control eyes without DH. DH could be associated with progression of glaucoma in terms of GCIPL thinning.

Usefulness of 10-2 Matrix Frequency Doubling Technology Perimetry for Detecting Central Visual Field Defects in Preperimetric Glaucoma Patients

It is generally acknowledged that structural loss can precede functional loss in some patients with early glaucoma. However, conventional standard automated perimetry (SAP) has limitations in the detection of functional loss, especially in the macular area. This study explores visual field loss in the macular areas of patients with preperimetric glaucoma exhibiting structural thinning in the area by examining the correlations between the ganglion cell-inner plexiform layer (GCIPL) and the results of matrix frequency-doubling technology (FDT) 10-2 tests. The structure-function relationships between the GCIPL thicknesses and the mean sensitivities (MSs) of the corresponding areas based on conventional SAP 24-2, FDT 10-2, and FDT 24-2 were examined in 62 patients. The highest correlation was found for FDT 10-2 (r = 0.544, P < 0.001) followed by FDT 24-2 (r = 0.433, P = 0.002) and SAP (r = 0.346, P = 0.007). The correlation coefficients between each GCIPL sector and the corresponding central MS according to FDT 24-2 and 10-2 were all statistically significant, and the correlations were significantly stronger for FDT 10-2 than 24-2 in the inferior and inferonasal sectors. In conclusion, preperimetric glaucoma patients with structural loss in the macula as indicated by GCIPL thinning also exhibited functional loss as revealed by FDT 10-2, and the functional loss was less evident with conventional SAP.

Rate of Macular Ganglion Cell-inner Plexiform Layer Thinning in Glaucomatous Eyes With Vascular Endothelial Growth Factor Inhibition.

To evaluate the rate of progressive macular ganglion cell-inner plexiform layer (GCIPL) thinning in patients with open-angle glaucoma (OAG) who had been treated with intravitreal antivascular endothelial growth factor (VEGF) injection for wet age-related macular degeneration (AMD). This study was a retrospective modified case control study with fellow eye comparison. We enrolled bilateral OAG patients who had been treated with repeated anti-VEGF injections for unilateral wet AMD and followed-up on for a minimum of 24 months by Cirrus high-definition optical coherence tomography. The rate of macular GCIPL thinning was determined by linear regression of serial optical coherence tomography GCIPL thickness measurements over time. We compared the rate of macular GCIPL thinning between anti-VEGF-treated eyes and fellow untreated dry AMD eyes. This study involved 32 OAG eyes of 16 subjects. The total follow-up period was 58.4±25.5 (24 to 98) months, and the mean number of anti-VEGF injections was 10.6±10.4 (3 to 40). The eyes with repeated anti-VEGF treatment differed significantly from their fellow eyes in the rate of GCIPL thinning (-2.95±3.58 vs. -0.77±0.95 µm/y, P=0.015). Also, multivariable regression analyses showed that anti-VEGF injection was significantly associated with the rate of GCIPL thinning (P=0.025). In subjects with bilateral OAG, the rate of GCIPL thinning is significantly faster in eyes treated with anti-VEGF injection for wet AMD than in untreated dry AMD fellow eyes. This finding suggests that in glaucomatous eyes, VEGF inhibition could play a role, at least in part, in progressive change of inner retinal layers.

S.18.01 - Brain imaging studies in pathological gamblers: are the underlying neural mechanisms similar to those of drug abusers?

To evaluate the association between genetic risk for cardiovascular disease and retinal thinning in early glaucoma.Prospective, observational genetic association studyMulticohort study combining a cohort of patients with suspect and early manifest primary open-angle glaucoma (POAG), a cohort of patients with perimetric POAG, and an external normative control cohort.A cardiovascular disease genetic risk score was calculated for 828 participants from the Progression Risk of Glaucoma: Relevant SNPs [single nucleotide polymorphisms] with Significant Association (PROGRESSA) study. Participants were characterized as showing either predominantly macular ganglion cell–inner plexiform layer (GCIPL), predominantly peripapillary retinal nerve fiber layer (pRNFL) or equivalent macular GCIPL and pRNFL spectral-domain OCT thinning. The cardiovascular disease genetic risk scores for these groups were compared to an internal reference group of stable suspected glaucoma and of an external normative population. Replication was undertaken by comparing the phenotypes of participants from the Australia New Zealand Registry of Advanced Glaucoma (ANZRAG) with the normative control group.Spectral-domain OCT and Humphrey Visual Field (HVF) change.After accounting for age, sex, and intraocular pressure (IOP), participants with predominantly macular GCIPL thinning showed a higher cardiovascular disease genetic risk score than reference participants (odds ratio [OR], 1.76/standard deviation [SD]; 95% confidence interval [CI], 1.18–2.62; P = 0.005) and than normative participants (OR, 1.32/SD; 95% CI, 1.12–1.54; P = 0.002). This finding was replicated by comparing ANZRAG participants with predominantly macular GCIPL change with the normative population (OR, 1.39/SD; 95% CI, 1.05–1.83; P = 0.022). Review of HVF data identified that participants with paracentral visual field defects also demonstrated a higher cardiovascular disease genetic risk score than reference participants (OR, 1.85/SD; 95% CI, 1.16–2.97; P = 0.010). Participants with predominantly macular GCIPL thinning exhibited a higher vertical cup-to-disc ratio genetic risk score (OR, 1.48/SD; 95% CI, 1.24–1.76; P < 0.001), but an IOP genetic risk score (OR, 1.12/SD; 95% CI, 0.95–1.33; P = 0.179) comparable with that of the normative population.This study highlighted the relationship between cardiovascular disease and retinal thinning in suspect and manifest glaucoma cases.

Macular ganglion cell-inner plexiform layer thickness for detection of early retinal toxicity of hydroxychloroquine.

This study evaluated the macular ganglion cell-inner plexiform layer (GC-IPL) thickness using spectral-domain (SD) optical coherence tomography (OCT) in patients with chronic exposure to hydroxychloroquine (HCQ). A total of 90 patients (90 eyes) treated with HCQ for at least 5years and normal controls were included in the study. A fundus examination, automated threshold perimetry, and GC-IPL thickness measurements using the Cirrus high-definition OCT ganglion cell analysis algorithm were performed in all patients treated with HCQ. Average, minimum, and sectorial macular GC-IPL thicknesses were compared between the patients and controls. There was no statistically significant difference in age or sex between the groups. The anterior segment and fundoscopy were normal in all patients and controls. Visual field (VF) testing was normal in all patients. The average, minimum, and sectorial macular GC-IPL thicknesses were significantly lower in patients than those in control subjects. There was significant thinning of the macular GC-IPL in the absence of clinically evident HCQ-related retinopathy and VF abnormalities. Measurements of the macular GC-IPL thickness using SD-OCT may therefore be useful in the early diagnosis and in monitoring the progression of retinal changes in patients receiving long-term HCQ therapy.

Evaluation of Ganglion Cell-Inner Plexiform Layer Thickness after Vitreoretinal Surgery with Internal Limiting Membrane Peeling in Cases with Idiopathic Macular Hole.

Objectives:To evaluate macular retinal ganglion cell-inner plexiform layer (GCIPL) thickness after vitrectomy with internal limiting membrane (ILM) peeling for idiopathic macular holes using spectral domain optical coherence tomography (SD-OCT).Materials and Methods:Eighteen eyes of 18 patients with unilateral idiopathic macular hole who underwent vitrectomy with ILM peeling were retrospectively analyzed. Healthy fellow eyes of the patients and 18 eyes of 18 age-matched healthy individuals constituted the control group. The patients were evaluated at 1 day, 1 week, 1 month, and 3 months after surgery. The best corrected visual acuity (BCVA) measurements, biomicroscopic examination findings and SD-OCT measurements were recorded. Ganglion cell-inner plexiform layer thickness was evaluated with ganglion cell analysis software of Cirrus HD-OCT before surgery and at 1 month and 3 months after surgery and compared with control groups. Presence of dissociated optic nerve fiber layer (DONFL) was evaluated with C-scan mode.Results:Of the 18 patients, 9 were male and 9 were female with a mean age of 65.6±5.6 (55-77) years. Preoperative BCVA was 0.75±0.19 logMAR, while it was 0.44±0.17 logMAR and 0.36±0.15 logMAR at postoperative 1 and 3 months, respectively (p<0.001). Postoperative mean GCIPL thickness was 66.33±17.28 µm. There was a correlation between mean GCIPL thickness and BCVA at postoperative 3 months (p<0.01). When compared with the control group, GCIPL thickness was significantly thinner in all quadrants of all patients at postoperative 3 months. Dissociated optic nerve fiber layer appearance was observed on C-scan in 13 of 18 eyes postoperatively. There was no correlation between the presence of DONFL and BCVA (p>0.05).Conclusion:Internal limiting membrane peeling during macular hole surgery may cause functional and/or structural changes that may be associated with visual acuity. Significant GCIPL thinning and DONLF appearance may occur postoperatively.

Ganglion Cell–Inner Plexiform Layer Change Detected by Optical Coherence Tomography Indicates Progression in Advanced Glaucoma

To examine the performance of Guided Progression Analysis (GPA; Carl Zeiss Meditec, Dublin, CA) in spectral-domain optical coherence tomography (OCT) in detecting progressive thinning of ganglion cell-inner plexiform layer (GCIPL) and retinal nerve fiber layer (RNFL) in glaucoma. Longitudinal, observational study. A total of 196 eyes of 123 primary open-angle glaucoma patients (mean follow-up, 5.0 years). Macular GCIPL and peripapillary RNFL thicknesses were measured by Cirrus HD-OCT (Zeiss, Dublin, CA), and progressive GCIPL and RNFL thinning were assessed by GPA. The reference standard of glaucoma progression was determined by visual field (VF) progression. Glaucomatous eyes were classified into mild (117 eyes) or moderate to advanced (79 eyes) groups based on VF defects. Ganglion cell-inner plexiform layer and RNFL thinning rates were compared between progressors and nonprogressors. Visual field survival estimates in eyes with and without progressive GCIPL and RNFL thinning were evaluated by Kaplan-Meier survival analysis and compared with the log-rank test. Progressive GCIPL and RNFL thinning assessed by OCT GPA. Seventy-six eyes (38.8%) and 43 eyes (21.9%) demonstrated progressive GCIPL and RNFL thinning, respectively, and 48 eyes (24.5%) were classified as progressors by reference standard. The rate of change in the average GCIPL thickness was significantly higher in progressors (-1.05±0.98 μm/year for mild glaucoma and-0.66±0.30 μm/year for moderate to advanced glaucoma) than in nonprogressors (-0.47±0.54 μm/year for mild glaucoma and-0.31±0.50 μm/year for moderate to advanced glaucoma), regardless of glaucoma severity (P < 0.05). Eyes with progressive GCIPL thinning had lower VF survival estimates than eyes without, regardless of glaucoma severity. However, the rate of change in the average RNFL thickness did not differ significantly in moderate to advanced glaucoma (P= 0.765; -0.26±0.55 μm/year for progressors and-0.33±0.92 μm/year for nonprogressors), and VF survival estimates did not differ significantly between eyes with and without progressive RNFL thinning in moderate to advanced glaucoma (P= 0.781). Ganglion cell-inner plexiform layer GPA provides a new approach for evaluating glaucoma progression. It may be more useful for detecting progression in the advanced stages of glaucoma than RNFL GPA.

Trend-based Analysis of Ganglion Cell–Inner Plexiform Layer Thickness Changes on Optical Coherence Tomography in Glaucoma Progression

To evaluate the rate of thinning in ganglion cell-inner plexiform layer (GCIPL) thickness by optical coherence tomography (OCT) in glaucomatous eyes and to use a trend-based approach to determine its diagnostic ability for detecting glaucoma progression. Prospective, observational study. Sixty-five patients with primary open-angle glaucoma with a minimum 3-year follow-up involving serial spectral-domain OCT measurement of GCIPL thickness. Patients were divided into a nonprogressor group (n= 38) and a progressor group (n= 27) on the basis of serial red-free photography or visual field tests. The rates of GCIPL thinning in the global region, affected hemifield, and 6 macular sectors, and the minimum thickness, were determined by linear regression and compared between groups. The area under the receiver operating characteristic curves (AUCs) were calculated for each parameter. The GCIPL thinning rates were compared between affected hemifields and unaffected hemifields. The macular GCIPL thinning rates in the progressor and nonprogressor groups and the ability of the GCIPL thinning rate to diagnose glaucoma progression. The GCIPL thinning rate was significantly faster in progressors than in nonprogressors in the global area (P < 0.001); in the affected hemifield (P= 0.001); in the temporal, vertical, and nasal sectors of the affected hemifield (P= 0.017, 0.032, and 0.030, respectively); and in the minimum GCIPL thickness (P < 0.001). In the temporal sectors, the GCIPL thinning rates were significantly faster in the affected than in the unaffected hemifield (P= 0.013). The best GCIPL parameters were the global (AUC= 0.791), minimum (AUC= 0.755), inferior hemifield (AUC= 0.708), and affected hemifield (AUC= 0.702) thinning rates. The global circumpapillary retinal nerve fiber layer thinning rate correlated significantly with the global and inferotemporal sector GCIPL thinning rates (rho= 0.259 and 0.366, respectively). The GCIPL thinning rate on OCT was significantly faster for patients with glaucoma with progression than for those without progression. The GCIPL thinning rate of the temporal sector was faster in the affected than in the unaffected hemifield, suggesting that the glaucomatous damage may progress locally in a specific sequence. Trend-based analysis of GCIPL thickness on OCT may be useful for assessing glaucoma progression objectively and quantitatively.

Retinal ganglion cell and axonal loss in optic neuritis: risk factors and visual functions.

PurposeThe peripapillary retinal nerve fiber layer (pRNFL) and the macular ganglion cell-inner plexiform layer (GCIPL) are important predictive factors for the prognosis of optic neuritis (ON). We investigated the risk factors for pRNFL and GCIPL thinning in ON and its relationship with visual function.Patients and methodsWe analyzed 33 eyes of 33 patients with a first attack of unilateral ON. Patients were divided into two groups according to pRNFL and GCIPL thinning, using spectral-domain optical coherence tomography. We evaluated patients' age, sex, color vision, visual acuity (VA), optic nerve findings on MRI, elapsed period from onset of visual symptoms to steroid treatment, visual field (VF) mean deviation (MD), average pRNFL thickness, and GCIPL thickness.ResultsThere was no patient with residual VF defect in the groups without pRNFL or GCIPL thinning. Significant correlations were found between pRNFL (some sectors) and GCIPL (all sectors) thickness and BCVA and VF MD (P<0.03 for all). Multivariate logistic regression analysis revealed that only worse initial VF MD was a significant risk factor of pRFNL and GCIPL thinning after ON (OR, 0.841; 95% CI, 0.730-0.970; P=0.017 and OR, 0.871; 95% CI, 0.761-0.998; P=0.046, respectively).ConclusionRetinal ganglion cell and axonal losses occurred in ON cases showing severe initial VF loss. Therefore, it is necessary to pay more attention to the degree of initial VF loss in ON while considering the possibility of residual VF loss accompanying pRNFL and GCIPL thinning.

The Association Between Retinal Neuronal Layer and Brain Structure is Disrupted inPatients with Cognitive Impairment andAlzheimer's Disease.

Both healthy and pathological aging due to Alzheimer's disease (AD) are associated with decreased brain grey matter volume (GMV) and disrupted white matter (WM) microstructure. Thinner macular ganglion cell-inner plexiform layer (GC-IPL) measured by spectral-domain optical coherence tomography has been reported in patients with AD and mild cognitive impairment. Emerging evidence suggested a link between thinner GC-IPL and lower GMV in subjects with no dementia using region-of-interest-based approach. However, it remains unknown whether GC-IPL thickness is associated with brain WM microstructure and how such association differed between normal and cognitively impaired subjects. Here, for subjects with no cognitive impairment (NCI), thinner GC-IPL was associated with lower WM microstructure integrity in the superior longitudinal fasciculus, inferior fronto-occipital fasciculus, corticospinal tracts, anterior thalamic radiation, and cingulum regions, while it was weakly associated with lower GMV in visual cortex and cerebellum. Nevertheless, these retina-brain associations were disrupted in the presence of cognitive impairment. Correlations between GMV and GC-IPL were lost in patients with cognitive impairment but no dementia (CIND) and AD patients. GC-IPL was related to WM microstructural disruption in similar regions with decreased significance. In contrast, lower WM microstructure integrity in the fornix showed a trend of correlation with thinner GC-IPL in both CIND and AD but not NCI. Collectively, our findings suggest the possible physiological retina-brain relationship in healthy aging, which might be disrupted by disease-induced changes in patients with cognitive impairment. Longitudinal study with larger patient sample should follow to confirm the disease mechanism behind these retina-brain relationship changes.

Ganglion cell analysis at acute episode of nonarteritic anterior ischemic optic neuropathy to predict irreversible damage. A prospective study.

To assess the capability of ganglion cell-inner plexiform layer (GCIPL) thickness analysis by optical coherence tomography (OCT) to detect early neuronal loss in nonarteritic anterior ischemic optic neuropathy (NAION). Sixteen patients with unilateral NAION participated in this prospective study. Complete ophthalmologic evaluation including visual acuity, visual field (VF) test, and spectral domain optical coherence tomography (SD-OCT) of peripapillary retinal nerve fiber layer (pRNFL) and GCIPL thickness were performed in the acute phase (within 1week: 2.7 ± 2.1days) and at 2weeks, 1month, 3 and 6months after diagnosis. The mean time elapsed from acute episode to irreversible damage detection by GCIPL and pRNFL analysis was registered. Correlations between the GCIPL thinning and functional parameters such as best-corrected visual acuity (BCVA) and visual field indices [mean deviation (MD) and visual field index (VFI)] in acute and chronic phase were also analyzed. NAION eyes showed a significant thinning of the mean GCIPLminimum (min) compared to the unaffected eyes as early as 2.2days after symptoms onset (p = 0.017) and at each follow-up visit. (p ≤ 0.003). The mean GCIPL average (av) was also thinner in NAION eyes compared to uninvolved eyes at 1 (p = 0.003), 3 (p = 0.002) and 6months (p < 0.001). At the acute phase, 100% of NAION eyes showed significant pRNFL thickening, while abnormal thinning was evident in GCIPLav, GCIPLmin, and GCIPL deviation map analysis in 31.3, 56.3, and 62.5% of NAION eyes. The abnormal thinning rates increased to 43.8, 75, and 81.3% at 2weeks and to 62.5, 100, and 100% at 1month, respectively. At 2weeks, GCIPLmin thickness significantly correlated with both acute and chronic BCVA, MD, and VFI. Furthermore, the mean superior and inferior GCIPL thicknesses at 2weeks associated with corresponding mean inferior and superior hemifield MD at 6months. GCIPL analysis by SD-OCT can be considered as a useful biomarker to establish ganglion cell damage. GCIPL min and GCIPL deviation map are abnormally thinner in 56.3 % and 62.5 % of eyes at presentation, respectively. Therefore, both parameters are abnormally thinned in more than 50 % of eyes at presentation. At 2 weeks, GCIPL min thickness significantly correlated with chronic BCVA, MD and VFI; therefore, GCIPL min thickness can predict final visual dysfunction.

Correlation Between En Face Optical Coherence Tomography Defects of the Inner Retinal Layers and Ganglion Cell Inner Plexiform Layer Analysis After Internal Limiting Membrane Peeling for Idiopathic Full-Thickness Macular Hole

The purpose of this study was to report en face optical coherence tomography (OCT) inner retinal changes after internal limiting membrane (ILM) peeling for idiopathic full-thickness macular hole (IFTMH) and to correlate these findings with macular ganglion cell inner plexiform layer (GC-IPL) analysis. This prospective study included 20 patients with IFTMH treated using pars plana vitrectomy with ILM peeling. All patients were analyzed using en face OCT at 6 months after surgery to determinate the effect of ILM peeling on the inner retinal layers. Correlation between the GC-IPL en face OCT findings and that obtained by three-dimensional volumetric OCT scanning also was performed. Seven patients (35%) showed defects in the retinal nerve fiber layer (RNFL) that appeared as multiple dark dots with no visible defects at the GC-IPL, either with en face OCT or 3D volumetric OCT scanning. Thirteen patients (65%) showed a similar combination of RNFL defects and well-circumscribed defects in the underlying GC-IPL. These defects could be visualized on en face OCT display, and they correlated with areas of GC-IPL thinning detected in the 3D volumetric OCT scanning. With ILM peeling, en face OCT scanning showed two forms of inner retinal layers changes. The first form was the concentric macular dark spots (CMDS) with intact GC-IPL. The second form appeared in the CMDS with evident localized defects in the underlying GC-IPL. These defects correlate with the areas of GC-IPL thinning detected using 3D volumetric OCT scanning.

Retinal degeneration in primary-progressive multiple sclerosis: A role for cortical lesions?

Background: Retinal atrophy in multiple sclerosis (MS) is secondary to optic nerve focal inflammation and to injury of the posterior visual pathway. Objectives: To investigate the contribution of cortical lesions (CLs) to retinal pathology in primary-progressive multiple sclerosis (PPMS). Methods: We performed a cross-sectional evaluation of 25 patients and 20 controls, relating magnetic resonance imaging (MRI) metrics of visual pathway integrity with parameters derived from spectral-domain optical coherence tomography (peripapillary retinal nerve fiber layer (RNFL) thickness, ganglion cell + inner plexiform layer (GCIPL) thickness, and macular volume (MV)). Results: Mean RNFL, GCIPL thickness, and MV were significantly reduced in patients compared to controls. MV and GCIPL thickness were significantly correlated with visual acuity. RNFL thinning was associated with thalamus and visual cortex volume (respectively, p = 0.01 and p < 0.05). In addition to thalamic volume, GCIPL thinning was associated with CLs and intracortical lesion number and volume, leucocortical lesion volume (all p ⩽ 0.05) while MV decrease was associated with CLs volume (p = 0.05) and intracortical lesion number and volume (p < 0.05). Conclusion: Our results suggest that RNFL thinning and GCIPL thinning/MV decrease may be explained by alternative mechanisms including retrograde trans-synaptic degeneration and/or a common pathophysiologic process affecting both the brain with CLs and the retina with neuronal loss.

Retinal ganglion cell neuronal damage in diabetes and diabetic retinopathy.

To examine the association of diabetes and diabetic retinopathy (DR) with retinal ganglion cell (RGC) loss. Observational case-control study. Type 2 diabetes cases and age-gender matched controls without diabetes. Spectral-domain optical coherence tomography (OCT) parameters of RGCs were calculated after automated segmentation of macular scans. DR severity was graded on fundus photographs using the modified Airlie House Classification system. Generalized estimating equation was used to compare OCT parameters between cases and controls, adjusted for covariates. Average ganglion cell-inner plexiform layer (GC-IPL) and average retinal nerve fibre layer (RNFL) thicknesses. We analyzed 227 cases and 227 controls. The mean age (years) of cases was 58.3 and controls was 58.1 (P = 0.13). Among cases, 101 had none, 25 had mild and 101 had moderate or severe DR. Compared with controls, GC-IPL and RNFL were thinner in all cases [mean difference (95% confidence interval [CI]): GC-IPL -4.49 µm (-2.92; -6.06), RNFL -0.93 µm (-0.09; -1.85)], including cases with no DR [mean difference (95% CI), GC-IPL -4.37 µm (-2.72; -6.02), RNFL -1.06 µm (-0.10; -2.02)]. Cases with any DR had thinner GC-IPL than controls [mean difference (95% CI): GC-IPL -4.81 µm (-2.12; -7.50)]. Among cases, subjects with moderate or severe DR had thinner GC-IPL than subjects with no DR [mean difference (95% CI): GC-IPL -2.07 µm (-0.08; -4.07)]. RGC loss is present in subjects with diabetes and no DR, and is progressive in moderate or severe DR. RGC neuronal damage in diabetes and DR can be clinically detected using OCT.

The Ability of 10-2 Short-Wavelength Perimetry in Detecting Functional Loss of the Macular Area in Preperimetric Glaucoma Patients.

To better understand functional loss in the macular area of preperimetric glaucoma patients exhibiting structural loss by exploring correlations between parameters of the ganglion cell-inner plexiform layer (GCIPL) and 10-2 short-wavelength perimetry (SWAP). One hundred thirty-four patients underwent 10-2 SWAP and conventional 24-2 visual field (VF) testing using a Humphrey field analyzer and macular scanning via Cirrus optical coherence tomography (OCT). Correlations between GCIPL thickness (GCIPLT) and the mean sensitivity (MS) of topographically corresponding areas explored in various VF tests were calculated. Correlations between GCIPL parameters and MS of the VF, in terms of the asymmetries of various VF sectors, were also determined. Glaucoma patients, preperimetric by standard 24-2 VF analysis but exhibiting GCIPL thinning, had lower MS in 10-2 SWAP and central 24-2 VF analyses. The correlations between average GCIPLT and the corresponding MS were significant for both 10-2 SWAP (r = 0.291, P = 0.018) and 24-2 standard automated perimetry (r = 0.235, P = 0.029). The associations between sectoral GCIPLT and the corresponding 10-2 SWAP MS were significant for all sectors, with the highest correlation evident in the inferotemporal (r = 0.324, P = 0.009) and the lowest in the superonasal GCIPL sectors (r = 0.214, P = 0.043). Asymmetric relationships between GCIPLT and 10-2 SWAP MS exhibited similar yet stronger correlations. Preperimetric glaucoma patients exhibiting structural loss in the macula also had functional loss revealed by 10-2 SWAP, which was less prominent in conventional 24-2 VF. Therefore, if structural abnormality is evident in the macular area, the central VF areas should be further examined even if the standard 24-2 data appear to be normal.

Macular nerve fibre and ganglion cell layer changes in acute Leber's hereditary optic neuropathy

AimsTo evaluate longitudinal retinal ganglion cell inner plexiform layer (GC-IPL) and macular retinal nerve fibre layer (mRNFL) thickness changes in acute Leber's hereditary optic neuropathy (LHON).MethodsSix eyes of four patients...

Clinical Clues to Predict the Presence of Parafoveal Scotoma on Humphrey 10-2 Visual Field Using a Humphrey 24-2 Visual Field

To investigate characteristics related to the presence of parafoveal scotoma on Humphrey 10-2 visual field (VF) in early glaucoma patients. Prospective, cross-sectional study. participants: Ninety-one eyes from 91 patients with glaucomatous optic neuropathy were prospectively tested with a 10-2 VF test. Glaucoma patients were classified into eyes with or without parafoveal scotoma on 10-2 VF based on pattern deviation plot. The central 10 degree region of Humphrey 24-2 VF test comprised 12 points and any abnormal VF points depressed <5%, <2%, <1%, or <0.5% from the normal database on pattern deviation plot were analyzed. Various factors related to the presence of parafoveal scotoma on 10-2 VF were analyzed. Abnormal 24-2 VF points, macular ganglion cell-inner plexiform layer thickness. The presence of abnormal 24-2 VF points <0.5% was significantly different between eyes with and without parafoveal scotoma on 10-2 VF (P < .01). The minimum macular ganglion cell-inner plexiform layer thickness (P = .04), any central 12 points depressed <0.5% on 24-2 VF (P < .01), and any central 12 points depressed <5% on 24-2 VF that spatially corresponds to macular ganglion cell-inner plexiform layer thinning (P < 0.01) were related factors to the presence of parafoveal scotoma on 10-2 VF. Glaucomatous eyes with any abnormal 24-2 VF points on the central 10 degree region that are depressed <0.5% or <5% that correlates to macular ganglion cell-inner plexiform layer thinning should receive attention and be further evaluated with a 10-2 VF test.

Longitudinal analysis of retinal nerve fiber layer and ganglion cell-inner plexiform layer thickness in ethambutol-induced optic neuropathy.

The aim of the study was to evaluate longitudinal analysis of peripapillary retinal nerve fiber layer (RNFL) and perifoveal ganglion cell-inner plexiform layer (GCIPL) thickness in patients being treated with ethambutol (EMB). This prospective longitudinal cohort study enrolled 37 patients who were treated with EMB for pulmonary tuberculosis. Best-corrected visual acuity, color vision test, automated perimetry, fundus photography, and RNFL and GCIPL thickness were measured at baseline and at 4and 6months after the start of EMB treatment, using Cirrus optical coherence tomography. Among 37 patients, EMB-induced optic neuropathy occurred in one patient (2.7%). In this patient, thickening of the RFNL and thinning of the GCIPL were noted at the onset of symptoms. After discontinuation of EMB, RNFL and GCIPL thickness progressively normalized. Changes in RNFL and GCIPL thickness were not statistically significant in the 36 patients who did not exhibit EMB-induced optic neuropathy-related symptoms during follow-up (all P values > 0.05). Thickening of the peripapillary RNFL and thinning of the perifoveal GCIPL is an effective quantitative and early marker for diagnosis of EMB-induced optic neuropathy.