Choroidal thickness does not differ among normal, NTG, and POAG subjects, suggesting a lack of relationship between choroidal thickness and glaucoma based on EDI OCT measurements.

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PURPOSE. We determined the time lag between loss of retinal ganglion cell function and retinal nerve fiber layer (RNFL) thickness.METHODS. Glaucoma suspects were followed for at least four years. Patients underwent pattern electroretinography (PERG), optical coherence tomography (OCT) of the RNFL, and standard automated perimetry testing at 6-month intervals. Comparisons were made between changes in all testing modalities. To compare PERG and OCT measurements on a normalized scale, we calculated the dynamic range of PERG amplitude and RNFL thickness. The time lag between function and structure was defined as the difference in time-to-criterion loss between PERG amplitude and RNFL thickness.RESULTS. For PERG (P < 0.001) and RNFL (P ¼ 0.030), there was a statistically significant difference between the slopes corresponding to the lowest baseline PERG amplitude stratum ( 50%) and the reference stratum (>90%). Post hoc comparisons demonstrated highly significant differences between RNFL thicknesses of eyes in the stratum with most severely affected PERG ( 50%) and the two strata with least affected PERG (>70%). Estimates suggested that the PERG amplitude takes 1.9 to 2.5 years to lose 10% of its initial amplitude, whereas the RNFL thickness takes 9.9 to 10.4 years to lose 10% of its initial thickness. Thus, the time lag between PERG amplitude and RNFL thickness to lose 10% of their initial values is on the order of 8 years.CONCLUSIONS. In patients who are glaucoma suspects, PERG signal anticipates an equivalent loss of OCT signal by several years. (Invest Ophthalmol Vis Sci. 2013;54:2346-2352 DOI: 10.1167/iovs.12-11026 A n issue central to the treatment of glaucoma is determining the onset of the disease. The current understanding is that early signs of glaucoma often manifest as permanent atrophic changes in the optic nerve, which are detected by characteristic visual field defects. Structural changes can be observed directly by examining the optic nerve, but also by measuring the optic nerve and retinal nerve fiber layer (RNFL) thickness with imaging devices. It is likely that these clinically manifest structural-functional changes are preceded by subclinical stages, at which retinal ganglion cells (RGC) have lost their autoregulatory ability in response to a chronically stressful biomechanical, vascular, or molecular environment, and become increasingly dysfunctional over time until they die and are eliminated from the neuronal pool.1 The transition between normal and abnormal homeostasis may be considered the true time of disease onset, whereas the stage of RGC dysfunction preceding death represents the ideal stage during which therapeutic strategies to prevent cell death and visual loss should be initiated.The electrical responsiveness of RGC to contrast-reversing visual stimuli can be monitored noninvasively in human and experimental models of glaucoma with the pattern electroretinogram (PERG).2-7 Recent studies in human and mouse models of glaucoma have shown that in the early stages of the disease the m...

Glaucoma is a common and permanent blinding sequelae of K-pro surgery. In K-pro patients, elevated IOP and changes in the optic nerve head should result in a high index of suspicion for glaucoma. Management is frequently surgical and typically entails placement of a GDD.

Penetrating keratoplasty (PKP) is associated with an increased risk of secondary glaucoma. The development of glaucoma after PKP is an important risk factor for decreased corneal graft survival. The incidence of glaucoma after corneal transplant as well as the mechanism of developing increased intraocular pressure is reviewed in this paper. Treatments for post-PKP glaucoma include medications, laser, and surgery. The most frequent surgical glaucoma intervention is implantation of a glaucomadrainage device. Recent advances in corneal transplantation surgery may help to decrease corneal failure and the risk of developing post-keratoplasty glaucoma.

Purpose To compare the safety and efficacy of Baerveldt implantation and trabeculectomy with mitomycin C (MMC) in patients who have not had prior incisional glaucoma surgery. Design Retrospective comparative case series Patients A total of 125 patients with low risk glaucoma undergoing primary glaucoma surgery, including 55 patients who received a 350-mm2 Baerveldt glaucoma implant and 70 patients who had a trabeculectomy with mitomycin C Methods Eligible patients were identified using current procedural terminology codes, and their medical records were retrospectively reviewed. Main Outcome Measures The primary outcome measure was surgical success (IOP ≤ 21 mm Hg and reduced ≥ 20% from baseline, IOP > 5 mm Hg, no reoperation for glaucoma, no loss of light perception vision). Secondary outcome measures included visual acuity, intraocular pressure (IOP), number of glaucoma medications, and complications. Results The cumulative probability of success at 3 years with or without medical therapy was 87% in the Baerveldt group and 76% in the trabeculectomy group (p = 0.23). Postoperative complications occurred in 11 (20%) patients in the Baerveldt group and 20 (29%) patients in the trabeculectomy group (p = 0.27). Follow-up (mean ± SD) was 27 ± 19 months in the Baerveldt group and 34 ± 20 in the trabeculectomy group (p = 0.053). Conclusions Similar rates of surgical success and postoperative complications were observed with trabeculectomy with mitomycin C and Baerveldt implantation during 3 years of follow-up. Both are viable primary glaucoma procedures in patients without prior ocular surgery.

Recurrent ectasia was diagnosed on average two decades after PK. Ectatic changes were often bilateral and occasionally recurred after regrafting, suggesting that host cellular and/or biochemical factors may be responsible. Repeat PK for recurrent ectasia is successful in the intermediate term.