Clinical results of ab interno trabeculotomy using the trabectome for open-angle glaucoma: the Mayo Clinic series in Rochester, Minnesota.

PURPOSE: To determine outcomes of ab interno trabeculotomy for treatment of open-angle glaucoma (OAG). DESIGN: Retrospective interventional single-surgeon, single-center case series. METHODS: Data were collected from 246 patients undergoing ab interno trabeculotomy between September 1, 2006, and December 1, 2010, with 3 months' follow-up or longer. Kaplan-Meier analysis was performed using Criteria A (postoperative intraocular pressure [IOP] ≤21 mm Hg or ≥20% reduction from preoperative IOP) and Criteria B (IOP ≤18 mm Hg and ≥20% reduction in IOP). Failure included increased glaucoma medications or subsequent surgery. Failure risk factors were identified using Cox proportional hazards ratio (HR). RESULTS: Of 88 cases of ab interno trabeculotomy-only and 158 cases of ab interno trabeculotomy with cataract extraction, the retention rate was 70% for 1 year and 62% for 2 years. Preoperative mean IOP was 21.6 ± 8.6 mm Hg; the number of glaucoma medications was 3.1 ± 1.1. At 24 months postoperatively, mean IOP was reduced 29% to 15.3 ± 4.6 mm Hg (P < 0.001) and the number of glaucoma medications was reduced 38% to 1.9 ± 1.3 (P < 0.001) with a success rate of 62% (95% CI, 56%-68%) using Criteria A and 22% (95% CI, 16%-29%) using Criteria B. Failure risk factors using Criteria A included primary OAG (HR 3.14, P < 0.01, 95% CI, 1.91-5.17) and past argon laser trabeculoplasty (HR 1.81, P < 0.01, 95% CI, 1.18-2.77). Using Criteria B, the HR for pseudoexfoliative glaucoma was 0.43 (P < 0.01, 95% CI 0.27-0.67). Of the cases, 66 (26.8%) required subsequent surgery on an average of 10 months (2 days to 3.2 years) after ab interno trabeculotomy. CONCLUSIONS: For criteria involving IOP ≤18 mm Hg, the 24-month survival of ab interno trabeculotomy is low. This surgery is appropriate for patients requiring a target IOP of 21 mm Hg or above.

Delayed-onset symptomatic hyphema after ab interno trabeculotomy surgery.

PURPOSE: To describe patients who have experienced delayed-onset hyphema after ab interno trabeculotomy surgery with the Trabectome (Neomedix Corp) for open-angle glaucoma. DESIGN: Retrospective case series. METHODS: study population: Patients at Mayo Clinic, Rochester, Minnesota, who underwent Trabectome surgery between September 1, 2006, and December 31, 2010, and who had symptomatic hyphema at least 2 months after surgery. observation procedure: Patients with blurred vision at least 2 months after Trabectome surgery were examined for the presence of hyphema using a slit lamp and gonioscopy. main outcome measures: Proportion of patients experiencing delayed-onset symptomatic hyphema after Trabectome surgery. Associated factors and clinical course for these patients. RESULTS: Of 262 cases of Trabectome surgery, there were 12 cases of delayed-onset symptomatic hyphema (4.6%). The average age was 74.3 years (range, 66 to 82 years). Median time to onset of hyphema was 8.6 months (range, 2 to 31 months) after surgery. Symptom onset commonly occurred on awakening. The most common characteristic was maintaining a sleep position on the surgical side. Most hyphemas resolved within 1 to 2 weeks, except in 1 patient, who required trabeculectomy for a refractory intraocular pressure spike. CONCLUSIONS: This is a series of patients with symptomatic delayed-onset hyphema after Trabectome surgery in the absence of further surgeries or trauma. Likely mechanisms are exertion-related increase in episcleral venous pressure or ocular compression from sleeping on the surgical side, followed by sudden decompression and blood reflux. Symptomatic patients should identify and avoid associated triggers because delayed-onset hyphema may be associated with intermittent intraocular pressure spikes that may require medical or surgical treatment.

Decreased corneal sensitivity and abnormal corneal nerves in Fuchs endothelial dystrophy.

PURPOSE: To determine corneal sensitivity and evaluate corneal nerves before and after keratoplasty for Fuchs endothelial dystrophy. METHODS: Central corneal sensitivity, measured by using a Cochet-Bonnet esthesiometer in 69 eyes before and after different keratoplasty procedures for Fuchs dystrophy, was compared with that of 35 age-matched normal corneas. Corneal nerves were qualitatively examined by confocal microscopy in 42 eyes before and after Descemet stripping endothelial keratoplasty (DSEK). RESULTS: Corneal sensitivity in Fuchs dystrophy (4.61 ± 1.42 cm) was lower than that of age-matched controls (5.74 ± 0.48 cm, P < 0.001). Sensitivity decreased by 1 month after DSEK (2.98 ± 2.01 cm, P < 0.001), returned to preoperative sensitivity by 24 months (4.50 ± 1.63 cm, n = 33, P = 0.99), but remained lower than controls at 36 months (4.50 ± 1.48 cm, n = 15, P < 0.001). Sensitivity at 36 months after penetrating keratoplasty (1.46 ± 1.98 cm) remained decreased compared with preoperative sensitivity (P < 0.001). Subbasal nerves appeared sparse with abnormal branching before and through 36 months after DSEK. Sensitivity was lower in corneas without visible subbasal nerves by confocal microscopy at 12 months after DSEK (P < 0.005) than in corneas with visible nerves. Stromal nerves were frequently tortuous and formed loops in Fuchs dystrophy, and this appearance persisted in some eyes at 36 months after DSEK. CONCLUSION: Corneal sensitivity is decreased in Fuchs dystrophy compared with normal and remains subnormal even at 3 years after endothelial keratoplasty. Decreased sensitivity is likely to be related to loss of subbasal nerves and abnormal nerve morphology, which persist after endothelial keratoplasty.

Posterior vitreous detachment and retinal tear after repetitive transcranial magnetic stimulation.

This case report describes a 60-year-old woman who experienced a posterior vitreous detachment (PVD) and retinal tear after her 11th session of 1 Hz repetitive transcranial magnetic stimulation (rTMS) for the treatment of major depression. Although we cannot conclude that rTMS caused her PVD and retinal tear, the temporal association is strong, and we hypothesize a possible pathophysiology of the event. As part of the routine clinical monitoring of rTMS side effects, we encourage attention toward ophthalmologic symptoms, especially in older patients.

Potentially deadly carcinogenic chromium redox cycle involving peroxochromium(IV) and glutathione.

Peroxochromium(IV) complexes are putative DNA-damaging and mutagenic agents in chromium(VI)-mediated carcinogenesis. The reaction between aquaethylenediaminebis(peroxo)chromium(IV) and glutathione at neutral pH exhibits a cyclic redox process displaying a persistent recycling of Cr(IV) and Cr(VI) with the intervention of chromium(V) intermediates. The coordination by a glutathione molecule triggers an autooxidation of the Cr(IV)-peroxo complex to Cr(VI) via an internal electron-transfer process followed by reduction to Cr(IV) via metastable chromium(V) intermediates. The cycle is repeated by the second peroxo species. The Cr(V) and -(IV) intermediates have been characterized as mono- and bisglutathionato complexes with or without a coordinated peroxo moiety. These intermediates are capable of damaging DNA, as evidenced by single strand breaks and DNA oxidation. The implication here is that the potential for a persistent, if not perpetual, deadly chromium carcinogenic cycle exists in the cellular milieu through the assistance of molecular oxygen and glutathione.

Unilateral megalopapilla and contralateral optic nerve hypoplasia: a case report and review of the literature.

We report the incidental finding of megalopapilla in the contralateral eye of a 10-year-old black child with optic nerve hypoplasia. Megalopapilla is a rare entity characterized by an enlarged optic disk without other morphologic abnormalities except for an enlarged cup/disk ratio. To the best of our knowledge, the concurrence of megalopapilla and optic nerve hypoplasia in the same individual has not been reported previously.

CNGA3 mutations in two United Arab Emirates families with achromatopsia.

PURPOSE: ACHROMATOPSIA RESULTS FROM MUTATIONS IN ONE OF THREE GENES: cyclic nucleotide-gated channel, alpha-3 (CNGA3); cyclic nucleotide-gated channel, beta-3 (CNGB3); and guanine nucleotide-binding protein, alpha-transducing activity polypeptide 2 (GNAT2). We report the responsible mutations in two United Arab Emirates families who have this autosomal recessive disease. METHODS: Clinical examinations were performed in seven patients from three nuclear families. Molecular genetic testing for common CNGA3 and CNGB3 mutations was undertaken using standard protocols. RESULTS: All patients were extremely light sensitive and had reduced visual acuity and no color perception. Fundus examinations did not show any visible abnormalities. After further pedigree analysis, two of the families were found to be linked through the paternal line. Two mutations in CNGA3 were identified: Arg283Trp and Gly397Val. Family A, the larger pedigree, had one branch in which two sisters and one brother were homozygous for the Gly397Val mutation and another branch in which a brother and sister were compound heterozygous for both aforenamed mutations. Family B, however, only had two brothers who were homozygous for the Arg283Trp mutation. CONCLUSIONS: Achromatopsia in these two United Arab Emirates families results from two different mutations in CNGA3. Two branches of the same pedigree had individuals with both homozygous and compound heterozygous disease, demonstrating a complex molecular pathology in this large family.