Vitrectomy Improves Contrast Sensitivity in Multifocal Pseudophakia With Vision Degrading Myodesopsia.

PURPOSE: Multifocal intraocular lenses (MFIOL) are associated with degradation in contrast sensitivity function (CSF); yet the contribution of vitreous is not known, nor is the benefit of vitrectomy. DESIGN: Prospective, nonrandomized clinical study. METHODS: A total of 180 eyes of 180 patients (55 MFIOL, 60 monofocal intraocular lenses [MIOL], 65 phakic) with symptomatic vitreous opacities were enrolled. Vitreous structure was assessed with quantitative ultrasonography (QUS). Vision was evaluated with visual acuity and CSF measurements. RESULTS: Vitreous echodensity was the same in all lens cohorts, yet CSF was worse in MFIOL eyes (P < .001). In 86 patients who elected vitrectomy, there was 68% greater vitreous echodensity and 31% worse CSF than in observation controls (P < .0001 for each). Preoperatively, CSF was 25% worse in MFIOL than in MIOL (P = .014). Postoperatively, vitreous echodensity decreased by 55%, 51%, and 52%, whereas CSF improved by 37% 48% in and 43% in MFIOL, MIOL, and phakic eyes, respectively (P < .0001 for each). NEI Visual Function Questionnaire analyses showed improved visual well-being. CONCLUSIONS: Patients with vision degrading myodesopsia who elected vitrectomy had greater vitreous echodensity and worse CSF than controls, but no other differences in age, sex, or myopia. MFIOL eyes had worse CSF than MIOL and phakic eyes, very possibly due to combined effects of the MFIOL and vitreous opacification. Limited vitrectomy reduced vitreous echodensity and improved CSF in all eyes. All patients with CSF-degrading vitreous opacities benefited from limited vitrectomy, including those with MFIOL. As MFIOL eyes had 37% improvement in CSF, patients with MFIOL and vision degrading myodesopsia merit consideration of vitrectomy.

Vitreous Structure and Visual Function in Myopic Vitreopathy Causing Vision-Degrading Myodesopsia.

PURPOSE: Myopic vitreopathy features precocious fibrous vitreous liquefaction and early posterior vitreous detachment (PVD). It is unclear whether visual function is affected by myopic vitreopathy and PVD. This study assessed the relationships among axial length, structural vitreous density, PVD, and visual function. DESIGN: Retrospective case-control study. METHODS: Ultrasonography measurements were made of axial length, logMAR VA, contrast sensitivity function (CSF [Freiburg acuity contrast test]), and quantitative B-scan ultrasonography. RESULTS: Seventy-nine subjects (45 men and 34 women; mean age: 49 ± 14 years) were analyzed. Axial lengths ranged from 22 to 29.2 mm (mean: 24.9 ± 1.8 mm; myopic eyes: 26.35 ± 1.35 mm; and nonmyopic eyes: 23.45 ± 0.75 mm; P < .001). With increasing axial length there was greater vitreous echodensity (R: 0.573; P < .01) and degradation in CSF (R: 0.611; P < .01). Subgroup analyses found that myopic eyes (>- 3 diopters) had 37% more vitreous echodensity than nonmyopic eyes (762 ± 198 arbitrary units [AU] vs. 557 ± 171 AU, respectively; P < .001) and that CSF was 53% worse in myopic eyes (3.30 ± 1.24 Weber index [%W]) than in nonmyopic eyes (2.16 ± .59 %W; P < .001). Myopic eyes with PVD had 33% greater vitreous echodensity (815 ± 217 AU; P < .001) and 62% degradation in CSF (3.63 ± 2.99 %W) compared to nonmyopic eyes with PVD (613 ± 159 AU; 2.24 ± 0.69 %W; P < .001, each). Limited vitrectomy was performed in 11 of 40 cases (27.5%), normalizing vitreous echodensity and CSF in each case. CONCLUSIONS: Axial myopia is associated with increased fibrous vitreous liquefaction and echodensity, as well as profound degradation of CSF. PVD in myopic eyes is associated with even more structural and functional abnormalities, normalized by limited vitrectomy. These findings may explain some common complaints of myopic patients with respect to vision and quality of life.

Assessment of Vitreous Structure and Visual Function after Neodymium:Yttrium-Aluminum-Garnet Laser Vitreolysis.

PURPOSE: Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser treatment is performed on vitreous floaters, but studies of structural and functional effects with objective outcome measures are lacking. This study evaluated Nd:YAG laser effects by comparing participants with vitreous floaters who previously underwent laser treatment with untreated control participants and healthy persons without vitreous floaters using quantitative ultrasonography to evaluate vitreous structure and by measuring visual acuity and contrast sensitivity function to assess vision. DESIGN: Retrospective, comparative study. PARTICIPANTS: One eye was enrolled for each of 132 participants: 35 control participants without vitreous floaters, 59 participants with untreated vitreous floaters, and 38 participants with vitreous floaters previously Nd:YAG-treated. Of these, 25 were dissatisfied and sought vitrectomy; 13 were satisfied with observation. METHODS: The 39-item National Eye Institute Visual Function Questionnaire (NEI-VFQ-39) to assess participant visual well-being, quantitative ultrasonography (QUS) to measure vitreous echodensity, and best-corrected visual acuity (BCVA) and contrast sensitivity function (CSF) to evaluate vision. MAIN OUTCOME MEASURES: Results of NEI-VFQ-39, QUS, BCVA, and CSF. RESULTS: Compared with control participants without vitreous floaters, participants with untreated vitreous floaters showed worse NEI-VFQ-39 results, 57% greater vitreous echodensity, and significant (130%) CSF degradation (P < 0.001 for each). Compared with untreated eyes with vitreous floaters, Nd:YAG-treated eyes had 23% less vitreous echodensity (P < 0.001), but no differences in NEI-VFQ-39 (P = 0.51), BCVA (P = 0.42), and CSF (P = 0.17) results. Of 38 participants with vitreous floaters who previously were treated with Nd:YAG, 25 were dissatisfied and seeking vitrectomy, whereas 13 were satisfied with observation. Participants seeking vitrectomy showed 24% greater vitreous echodensity (P = 0.018) and 52% worse CSF (P = 0.006). Multivariate linear regression models confirmed these findings. CONCLUSIONS: As a group, participants previously treated with Nd:YAG laser for bothersome vitreous floaters showed less dense vitreous, but similar visual function as untreated control participants with vitreous floaters. Because some treated eyes showed less dense vitreous and better visual function than those of untreated control participants, a prospective randomized study of Nd:YAG laser treatment of vitreous is warranted, using uniform laser treatment parameters and objective quantitative outcome measures.

STRUCTURAL AND FUNCTIONAL CHARACTERISTICS OF LAMELLAR MACULAR HOLES.

PURPOSE: Lamellar macular holes (LMHs) can been subdivided into tractional and degenerative subtypes. This cross-sectional cohort study compared structural and functional characteristics in these subtypes hypothesizing that tractional LMH has a higher prevalence of vitreopapillary adhesion and tangential traction (macular pucker), whereas degenerative LMH has more ellipsoid zone disruption and worse vision, measured three different ways. METHODS: Tractional LMH (n = 22) and degenerative LMH (n = 15) were distinguished by optical coherence tomography criteria. Separate spectral domain optical coherence tomography scanning of the macula and optic disk was performed. Visual acuity, contrast sensitivity function (Weber Index, %W), and the degree of visual distortions (3-dimensional threshold Amsler grid; % volume lost [%VL]) were quantified. RESULTS: Vitreopapillary adhesion was present in 14/22 (64%) tractional, but in only 3/15 (20%) degenerative LMH (P = 0.006). Macular pucker was present in 19/22 (86%) tractional, but in only 8/15 (53%) degenerative LMH (P = 0.011). Ellipsoid zone disruption was present in 13/15 (87%) degenerative, but in only 2/22 (9%) tractional LMH (P = 0.0001). Visual acuity was better in tractional than degenerative LMH (P = 0.006), as was contrast sensitivity function (tractional = 3.44 ± 1.07 %W, degenerative = 4.66 ± 1.73 %W; P = 0.015). Visual distortions were less in tractional (0.33 ± 0.61 %VL) than in degenerative (0.85 ± 0.68 %VL) LMH (P = 0.014). CONCLUSION: Structure and visual function differ significantly in subtypes of LMH. Tractional LMH has 3-fold higher prevalence of vitreopapillary adhesion and 2-fold higher prevalence of macular pucker. Degenerative LMH has 9-fold more ellipsoid zone disruption, worse visual acuity and contrast sensitivity function, and 3-fold more distortions. Thus, outer retinal integrity seems more closely correlated with vision than anterior structural abnormalities in LMH.

The effects of aging vitreous on contrast sensitivity function.

PURPOSE: Contrast sensitivity function (CSF) declines with age. When unassociated with cataracts, this is hypothesized to be due to macular ganglion cell complex (GCC) thinning. However, other studies found associations with increased vitreous echodensity and posterior vitreous detachment (PVD). We investigate the relationship between CSF, vitreous echodensity, PVD, and GCC thickness as related to age in the same subjects. METHODS: Age, CSF (Weber index: %W), vitreous echodensity (quantitative ultrasonography [QUS]), lens status (phakia or pseudophakia), best-corrected visual acuity (BCVA), and GCC thickness (SD-OCT) were evaluated in 57 eyes of 57 subjects with (n = 32, mean age = 62 years) and without (n = 25, mean age = 44 years) PVD (P < 0.001). A multivariate linear regression analysis was performed to assess the effects of independent variables on CSF. RESULTS: CSF was 51.2% worse in eyes with PVD (2.98 ± 0.31 %W) compared to no PVD (1.97 ± 0.24 %W; P < 0.001). QUS was 55.8% greater in eyes with PVD than those without (P < 0.001). Among all subjects, PVD status, vitreous echodensity, and age were the only independent variables demonstrating significant effects on CSF. Lens status, BCVA, and GCC thickness did not demonstrate association with CSF. CONCLUSIONS: PVD, vitreous echodensity, and age are determinants of CSF. PVD and increased vitreous echodensity are each associated with diminished CSF, independent of age. Thus, in the absence of GCC thinning and cataracts, vitreous changes may be a cause of decreased CSF with age.

Long-Term Safety and Efficacy of Limited Vitrectomy for Vision Degrading Vitreopathy Resulting from Vitreous Floaters.

PURPOSE: Vitreous floaters can lower visual acuity (VA) and degrade contrast sensitivity function (CSF). Limited vitrectomy improves VA and normalizes CSF, but long-term results in a large series with objective quantitative outcome measures are lacking. DESIGN: Case series. PARTICIPANTS: One hundred ninety-five eyes of 145 patients (87 men, age = 57.6 ± 4.3 years; 58 women, age = 61.5 ± 12.0 years) reporting bothersome vitreous floaters were compared to 70 age-matched controls. Posterior vitreous detachment (PVD) alone was the cause in 96/195 (49.2%), myopic vitreopathy alone was the cause in 30/195 (15.4%), PVD with myopic vitreopathy was the cause in 56/195 (28.7%), and asteroid hyalosis was the cause in 13/195 eyes (6.7%). METHODS: Limited vitrectomy with 25-gauge instruments was performed without surgical PVD induction, preserving 3 to 4 mm of retrolental vitreous in phakic eyes. Follow-up averaged 32.6 ± 23.5 months (range, 3-115 months), with 2 years or more in 144 eyes, 3 years or more in 69 eyes, 4 years or more in 51 eyes, and 5 years or more in 24 eyes. MAIN OUTCOME MEASURES: Visual acuity, 39-item National Eye Institute Visual Function Questionnaire (VFQ) results, CSF (Weber index), and quantitative ultrasonography results. RESULTS: After surgery, vitreous echodensity decreased by 94.1% (P < 0.0001) and VFQ results improved by 19.3% (P < 0.0001). Preoperative VA was 0.68 ± 0.21, improving to 0.77 ± 0.19 after surgery (P < 0.0001). Preoperative CSF was degraded by 91.3% compared with controls (P < 0.0001), normalizing at 1, 3, 6, 12, 24, 36, and 48 months after surgery (P < 0.00005 for each). There were no cases of endophthalmitis. There were 3 retinal tears and 3 retinal detachments that underwent successful repair. Clinically significant vitreous hemorrhage developed in 2 patients, clearing spontaneously. Two macular puckers and 4 recurrent floaters from new PVD were cured by re-operation. Cataract surgery occurred in 21 of 124 patients (16.9%; mean age, 64 ± 7 years; none younger than 53 years), an average of 13.1 ± 6.8 months after vitrectomy. CONCLUSIONS: Limited vitrectomy for Vision Degrading Vitreopathy decreases vitreous echodensity, improves patient well-being, improves VA, and normalizes CSF. The long-term efficacy and safety profiles suggest this may be a safe and effective treatment for clinically significant vitreous floaters, warranting a prospective randomized trial.

Incidence of Cataract Surgery after Vitrectomy for Vitreous Opacities.

PURPOSE: A computational model of vitreous oxygen consumption and transport predicts that limited vitrectomy will result in lower retrolental oxygen levels than extensive vitrectomy, and that higher retrolental oxygen would promote cataractogenesis. This study compared the incidence and timing of cataract surgery after limited versus extensive vitrectomy for vitreous opacities. METHODS: Ninety-six phakic eyes in 75 patients (aged 55±14 years) underwent limited 25 G vitrectomy with preservation of 3 to 4 mm of retrolental vitreous and without surgical posterior vitreous detachment induction. Of these 96 eyes, 48 eyes in 37 patients (aged 56±14 years) had a minimum of 24 months' follow-up and were compared with 23 eyes from 18 patients (aged 63±8 years) who underwent extensive vitrectomy. RESULTS: Limited vitrectomy patients were older than extensive vitrectomy patients (P < 0.015), yet only 17 of 96 eyes (18%) required cataract surgery after limited vitrectomy (mean follow-up = 20±17 months). In eyes with a minimum follow-up of 24 months, 17 of 48 eyes (35%; age = 53-81 years) with limited vitrectomy required cataract surgery, versus 20 of 23 eyes (87%; age = 50-75 years) with extensive vitrectomy (P < 0.0001). Just before cataract surgery, visual acuity was comparable in each group (0.47±0.18 in the limited vitrectomy group vs. 0.54±0.30 in the extensive vitrectomy group; P = 0.23). Cataract surgery occurred an average of 12.4±5.1 months after limited vitrectomy, compared with 7.3±3.9 months after extensive vitrectomy (P < 0.002). CONCLUSIONS: The incidence of cataract surgery was lower after limited vitrectomy, which had a longer interval until cataract surgery compared with extensive vitrectomy. These findings are consistent with the computational model of oxygen consumption and transport and suggest clinical strategies to mitigate postvitrectomy cataractogenesis.

Degradation of Contrast Sensitivity Function Following Posterior Vitreous Detachment.

PURPOSE: To evaluate the effect of posterior vitreous detachment (PVD) on contrast sensitivity function (CSF) in previously normal eyes, with the hypothesis that PVD reduces CSF. DESIGN: Prospective observational case series. METHODS: At a single clinical practice 28 eyes were evaluated: 8 eyes of 8 adults (mean age 54.4 ± 10.1 years; range 39-68 years) with normal CSF documented by Freiburg Acuity Contrast Testing (Weber index: %W) who subsequently experienced PVD, as confirmed by ultrasonography and optical coherence tomography; 8 fellow eyes without PVD; and 12 control eyes: 9 eyes with PVD in patients who chose observation and 3 fellow eyes without PVD. RESULTS: At study entry there was no significant difference in CSF of fellow eye controls (mean 1.44 ± 0.27 %W; range 1.06-2.00 %W) and eyes that subsequently developed PVD (1.81 ± 0.61 %W; P = .146; range 1.01-2.69 %W). Following PVD there was a 52.5% reduction in CSF (2.76 ± 0.30 %W; P = .001; range 2.25-3.14 %W). CSF in the patients who chose limited vitrectomy (2.51 ± 0.46 %W; range 2.03-3.06 %W) was 41.8% worse than in the eyes with PVD of patients who chose observation (1.46 ± 0.21 %W; P = .001; range 1.08-1.87 %W). After vitrectomy, CSF improved by an average of 43.2%, normalizing in each case at 1 month (CSF 1.51 ± 0.28 %W; P = .001; range 1.14-2.00 %W), 3 months (1.38 ± 0.10 %W; P = .0002; range 1.28-1.51 %W), and 12 months (1.34 ± 0.34 %W; P = .0001; range 1.01-1.89 %W, n = 5) postoperatively, attaining the same CSF as the control fellow eyes (1.34 ± 0.20 %W; range 1.06-1.56 %W). CONCLUSION: PVD is associated with significant reduction in CSF of previously normal eyes. This quantifiable negative impact on visual function can distinguish patients who are not significantly bothered by vitreous floaters from those with clinically significant symptoms.

Quantifying Visual Dysfunction and the Response to Surgery in Macular Pucker.

PURPOSE: To measure the effects of macular pucker (MP) on macular structure and quantify function by measuring visual acuity (VA), contrast sensitivity (CS), and distortions. The effects of surgery were quantitatively evaluated using these measures. DESIGN: Prospective, comparative case series. PARTICIPANTS: Fifty-three patients with unilateral MP and normal fellow eyes: 24 operated MP subjects, 17 unoperated controls, and 12 reproducibility subjects. METHODS: Posterior vitreous detachment was diagnosed by ultrasound and ellipsoid zone disruption (EZD) was determined by OCT, which also measured macular thickness and volume. Vision was assessed, by measuring VA (logMAR) and CS (Freiburg acuity contrast testing: Weber index, %W). A visual distortions index (%DI) was calculated using 3-dimensional threshold Amsler grid testing. Comparisons to controls were performed before surgery and at 1, 3, 6, and 12 months after vitrectomy/membrane peel without chromodissection. MAIN OUTCOME MEASURES: Posterior vitreous detachment (ultrasound), EZD (OCT), macular thickness and volume (OCT), VA (logMAR), CS (%W), distortions (%DI). RESULTS: Posterior vitreous detachment was present in 90% of MP eyes, but only 50% of fellow eyes (P < 0.001). All structural and functional indices were worse (28% to 5-fold) in the 24 operated MP eyes than the 17 unoperated MP eyes (P < 0.001). Before surgery, EZD was present in 33% of operated MP eyes but none of the unoperated MP eyes (P < 0.02). The macula was thicker (514±85 µm vs. 257±59 µm; P < 0.001) with greater volume (3.22±0.56 µl vs. 2.14±0.22 µl; P < 0.001) in operated MP eyes than normal fellow eyes. Before surgery, MP eyes had VA = 0.53 logMAR (Snellen equivalent, 20/67) vs. controls = 0.21 (20/32); P < 0.001; CS was 8.61±5.36 %W vs. controls = 3.71±1.47 %W (P < 0.001); and distortions were 7.61±12.6 %DI vs. controls = 0.13±0.61 %DI (P < 0.001). EZD was associated with worse VA (P < 0.01) and CS (P < 0.03) before and after surgery. Each outcome measure improved progressively at 1, 3, 6, and 12 months after surgery, but only %DI and macular volume normalized. CONCLUSIONS: These quantitative measures characterize the impact of MP on macular structure and function. All indices improved after surgery, but only distortions and macular volume normalized. Contrast sensitivity measurements and quantification of distortions can objectively assess visual dysfunction in MP and may be useful outcome measures of therapy.

Proteomic Analysis of Embryonic and Young Human Vitreous.

PURPOSE: The proteomic profile of vitreous from second-trimester human embryos and young adults was characterized using mass spectrometry and analyzed for changes in protein levels that may relate to structural changes occurring during this time. This vitreous proteome was compared to previous reports to confirm proteins already identified and reveal novel ones. METHODS: Vitreous from 17 human embryos aged 14 to 20 weeks gestation (WG) and from a 12-, a 14-, a 15-, and a 28-year-old was individually analyzed using tandem mass spectrometry-based proteomics. Peptide spectral count associations with embryonic age were assessed using a general linear model of fold changes and Spearman's rank correlation. Differences between embryonic and young adult vitreous proteomes were also compared. Immunohistochemistry was used to evaluate three proteins in five additional fetal (10-18 WG) human eyes. RESULTS: There were 1217 proteins identified in fetal and young adult human vitreous, 206 after quantile normalization and variance filtering. In embryos, the peptide counts of 37 proteins changed significantly from 14 to 20 WG: 75.7% increased, 24.3% decreased. Immunohistochemistry confirmed the absence of clusterin and cadherin in 10 and 14 WG eyes and their presence at 18 WG. Comparing embryonic to young adult vitreous, 47 proteins were significantly higher or lower. A total of 768 proteins not previously identified in the literature are presented. CONCLUSIONS: Proteins previously unreported in the human vitreous were identified. The human vitreous proteome undergoes significant changes during embryogenesis and young adulthood. A number of protein levels change considerably during the second trimester, with the majority decreasing.

Ultrasound-based quantification of vitreous floaters correlates with contrast sensitivity and quality of life.

PURPOSE: Clinical evaluation of floaters lacks quantitative assessment of vitreous structure. This study used quantitative ultrasound (QUS) to measure vitreous opacities. Since floaters reduce contrast sensitivity (CS) and quality of life (Visual Function Questionnaire [VFQ]), it is hypothesized that QUS will correlate with CS and VFQ in patients with floaters. METHODS: Twenty-two eyes (22 subjects; age = 57 ± 19 years) with floaters were evaluated with Freiburg acuity contrast testing (FrACT; %Weber) and VFQ. Ultrasonography used a customized probe (15-MHz center frequency, 20-mm focal length, 7-mm aperture) with longitudinal and transverse scans taken in primary gaze and a horizontal longitudinal scan through premacular vitreous in temporal gaze. Each scan set had 100 frames of log-compressed envelope data. Within each frame, two regions of interest (ROIs) were analyzed (whole-central and posterior vitreous) to yield three parameters (energy, E; mean amplitude, M; and percentage of vitreous filled by echodensities, P50) averaged over the entire 100-frame dataset. Statistical analyses evaluated E, M, and P50 correlations with CS and VFQ. RESULTS: Contrast sensitivity ranged from 1.19%W (normal) to 5.59%W. All QUS parameters in two scan positions within the whole-central ROI correlated with CS (R > 0.67, P < 0.001). P50 in the nasal longitudinal position had R = 0.867 (P < 0.001). Correlations with VFQ ranged from R = 0.52 (P < 0.013) to R = 0.65 (P < 0.001). CONCLUSIONS: Quantitative ultrasound provides quantitative measures of vitreous echodensity that correlate with CS and VFQ, providing objective assessment of vitreous structure underlying the functional disturbances induced by floaters, useful to quantify vitreous disease severity and the response to therapy.

Inner retinal optic neuropathy: vitreomacular surgery-associated disruption of the inner retina.

PURPOSE: Macular pucker (MP) and macular hole (MH) are vitreomaculopathies treated by vitrectomy and membrane peel. The complication of postoperative central scotoma can be associated with significant reduction in visual acuity (VA). We seek to determine whether retinal nerve fiber layer (RNFL) disruption is the pathophysiologic basis of this defect. Mitigating clinical circumstances also were sought. METHODS: Eleven eyes from 10 pseudophakic patients who had undergone vitrectomy with peeling for either MH or MP were studied with clinical measures, including optical coherence tomography (OCT). Membrane specimens were evaluated by immunohistochemistry for neurofilament, a marker for the inner retina. Ten eyes from 10 pseudophakic patients who underwent repeat surgery for persistent or recurrent pathology were evaluated to determine the relationship between the timing of reoperation and clinical outcome. RESULTS: Cases with a postoperative central scotoma (N=4) had worse VA (~20/600) compared to those without (N=7, ~20/30, P=0.01). Eyes with a central scotoma had significantly reduced RNFL thickness in the temporal quadrant (53.67 vs. 72.33 µm, P=0.05) by OCT. A central scotoma was associated with more disruption of the inner retina on immunohistochemistry (P=0.03). In patients with persistent or recurrent pathology, waiting six months before reoperation resulted in better functional outcomes (P=0.03). CONCLUSIONS: Central scotomata and poor VA were associated with disruption of the RNFL during membrane peeling. Affected patients have RNFL thinning and signs of optic neuropathy, for which we propose the term inner retinal optic neuropathy (IRON). In patients requiring reoperation, waiting six months between surgeries may reduce the risk of IRON.

Vitrectomy for floaters: prospective efficacy analyses and retrospective safety profile.

PURPOSE: Floaters impact vision but the mechanism is unknown. We hypothesize that floaters reduce contrast sensitivity function, which can be normalized by vitrectomy, and that minimally invasive vitrectomy will have lower incidences of retinal tears (reported at 30%) and cataracts (50-76%). METHODS: Seventy-six eyes (34 phakic) with floaters were evaluated in 2 separate studies. Floater etiologies were primarily posterior vitreous detachment in 61 of 76 eyes (80%) and myopic vitreopathy in 24 of 76 eyes (32%). Minimally invasive 25G vitrectomy was performed without posterior vitreous detachment induction, leaving anterior vitreous, and using nonhollow probes for cannula extraction. Efficacy was studied prospectively (up to 9 months) in 16 floater cases with Freiburg Acuity Contrast Testing (Weber index [%W] reproducibility = 92.1%) and the National Eye Institute Visual Function Questionnaire. Safety was separately evaluated in 60 other cases followed up on an average of 17.5 months (range, 3-51 months). RESULTS: Floater eyes had 67% contrast sensitivity function attenuation (4.0 ± 2.3 %W; control subjects = 2.4 ± 0.9 %W, P < 0.013). After vitrectomy, contrast sensitivity function normalized in each case at 1 week (2.0 ± 1.4 %W, P < 0.01) and remained normal at 1 month (2.0 ± 1.0 %W, P < 0.003) and 3 months to 9 months (2.2 ± 1.5 %W, P < 0.018). Visual Function Questionnaire was 28.3% lower in floater patients (73.2 ± 15.6, N = 16) than in age-matched control subjects (93.9 ± 8.0, N = 12, P < 0.001), and postoperatively improved by 29.2% (P < 0.001). In the safety study of 60 floater cases treated with vitrectomy, none developed retinal breaks, infection, or glaucoma after a mean follow-up of 17.5 months. Only 8 of 34 cases (23.5%) required cataract surgery (none younger than 53 years) at an average of 15 months postvitrectomy. CONCLUSION: Floaters lower contrast sensitivity function, which normalizes after vitrectomy. Visual Function Questionnaire quantified improvement in satisfaction. Not inducing posterior vitreous detachment reduced retinal tear incidence from 30% to 0% (P < 0.007). Postvitrectomy cataract incidence was reduced from 50% to 23.5% (P < 0.02). This approach thus seems effective and safe in alleviating the visual dysfunction induced by floaters.

Neuron-specific enolase is elevated in asymptomatic carriers of Leber's hereditary optic neuropathy.

PURPOSE: Neuron-specific enolase (NSE) is a biomarker for neuronal stress. Leber's hereditary optic neuropathy (LHON) is a mitochondrial disease affecting retinal ganglion cells (RGC). These RGCs and their axons in the retinal nerve fiber layer (RNFL) and optic nerve head may show subclinical pathology in unaffected mutation carriers, or undergo cell death in affected patients. We hypothesize that increased levels of blood NSE may characterize LHON carriers as a biomarker of ongoing RGC stress. METHODS: Serum was obtained from 74 members of a Brazilian pedigree with LHON carrying the homoplasmic 11778/ND4 mitochondrial DNA mutation. Classified by symptoms and psychophysical metrics, 46/74 patients were unaffected mutation "carriers," 14/74 were "affected," and 14/74 were "off-pedigree" controls. Serum NSE levels were determined by ELISA specific for the γ subunit of NSE. RESULTS: Serum NSE concentrations in carriers (27.17 ± 39.82 µg/L) were significantly higher than affected (5.66 ± 4.19 µg/L; P = 0.050) and off-pedigree controls (6.20 ± 2.35 µg/L; P = 0.047). Of the 14/46 (30.4 %) carriers with significantly elevated NSE levels (mean = 75.8 ± 42.3 µg/L), 9/14 (64.3%) were male. Furthermore, NSE levels were nearly three times greater in asymptomatic male carriers (40.65 ± 51.21 µg/L) than in asymptomatic female carriers (15.85 ± 22.27 µg/L; P = 0.034). CONCLUSIONS: Serum NSE levels are higher in LHON carriers compared with affected and off-pedigree individuals. A subgroup of mostly male carriers had significantly elevated serum NSE levels. Thus, male carriers are at higher risk for LHON-related neuronal stress.

Long-term results of office-based pneumatic retinopexy using pure air.

AIMS: The long-term results of office-based pneumatic retinopexy (PR) using only filtered air were evaluated in a case series of rhegmatogenous retinal detachments with more than 3 years of follow-up, on average. METHODS: 77 cases of primary rhegmatogenous retinal detachments arising from superior tears (mean=1.6 tears) were treated with cryopexy (n=61) or laser (next day, n=16) and intravitreal injection of pure air in an office setting. The macula was detached preoperatively in 37 eyes (48.1%). Outcome measures were single-operation success, final reattachment rates and visual acuity (VA). RESULTS: Subjects were followed for 6-186 months (mean follow-up = 40.7 months, 46.8% ≥ 2 years, 25% ≥ 5 years). In all cases, the air bubble was gone within 5 days. Single-operation success was achieved in 62/77 (80.5%) eyes. Repeat PR was successful in four cases, increasing the PR reattachment rate to 85.7%. Scleral buckle was performed on the remaining 11 eyes (14.3%), 1 with vitrectomy. The final reattachment rate was 100%. VA improved ≥ 2 Snellen lines in 53.2% of patients, with 50/77 (64.9%) attaining VA ≥ 20/40. Following PR, 87% of subjects had the same or better VA. CONCLUSIONS: Office-based pure-air PR achieves acceptable reattachment rates with good visual outcomes and long-term efficacy. Eliminating the need for expansile gases makes this approach more widely available, decreases recovery time and lowers healthcare costs.

Low-density lipoprotein receptor-related protein is decreased in optic neuropathy of Alzheimer disease.

BACKGROUND: Alzheimer disease (AD) is associated with optic nerve degeneration, yet the underlying pathophysiology of this disease and the optic nerve disorder remain poorly understood. Low-density lipoprotein receptor-related protein (LRP) is implicated in the pathogenesis of AD by mediating the transport of amyloid-ß (Aß) out of the brain into the systemic circulation. As a key player in the reaction to central nervous system injury, astrocytes associate with LRP in AD. This study investigates the role of LRP and astrocytes in the pathogenesis of AD optic neuropathy. METHODS: To investigate the role of LRP and astrocytes in the pathogenesis of AD optic neuropathy, we conducted immunohistochemical studies on postmortem optic nerves in AD patients (n = 11) and age-matched controls (n = 10) to examine the presence of LRP. Quantitative analyses using imaging software were used to document the extent of LRP in neural tissues. Axonal integrity was assessed by performing immunohistochemistry on the subjects' optic nerves with an antibody to neurofilament (NF) protein. Double-immunofluorescence labeling was performed to investigate whether LRP colocalized with astrocytes, expressing glial fibrillary acidic protein. RESULTS: LRP expression was decreased in AD optic nerves compared to that in controls (P < 0.001). LRP immunoreactivity was observed in the microvasculature and perivascularly in close proximity to the astrocytic processes. Colocalization of LRP in the astrocytes of optic nerves was also demonstrated. The presence of optic neuropathy was confirmed in the AD optic nerves by demonstrating greatly reduced immunostaining for NF protein as compared to controls. CONCLUSIONS: The reduction of LRP in the AD degenerative optic nerves supports the hypothesis that LRP may play a role in the pathophysiology of AD optic neuropathy.

Vitreoschisis in macular diseases.

OBJECTIVES: Vitreoschisis is a possible pathogenic mechanism in macular diseases. Thus, the vitreoretinal interface was evaluated in monkey eyes and patients with various macular diseases in search of vitreoschisis. It is hypothesised that vitreoschisis is present in macular holes (MH) and macular pucker (MP), but not in other maculopathies. METHODS: Histopathology was studied in 14 monkey eyes and a vitrectomy specimen of a patient with macular pucker. Optical coherence tomography/scanning laser ophthalmoscopy (OCT/SLO) was performed in 239 eyes: 45 MH, 45 MP, 51 dry age-related macular degeneration (AMD), 53 non-proliferative diabetic retinopathy (NPDR) and 45 controls. RESULTS: Immunohistochemistry demonstrated lamellae in the posterior vitreous cortex of 12/14 (86%) monkey eyes. With OCT/SLO, vitreoschisis was detected in 24/45 (53%) MH and 19/45 (42%) MP eyes, but in only 7/53 (13%) NPDR, 3/51 (6%) AMD and 3/45 (7%) control eyes (p<0.001 for all comparisons). Rejoining of the inner and outer walls of the split posterior vitreous cortex was visible in 16/45 (36%) MH eyes and 15/45 (33%) MP eyes. Histopathology of the MP specimen confirmed a split with rejoining in the posterior vitreous cortex. CONCLUSIONS: Vitreoschisis was detected in half of eyes with MH and MP, but much less frequently in controls, AMD and NPDR patients. These findings suggest that anomalous PVD with vitreoschisis may be pathogenic in MH and MP.