Pigment dispersion syndrome (PDS) is an interesting condition that can lead to secondary open angle glaucoma. Pigmentary glaucoma is primarily a disease of young people, myopes and men. PDS is characterized by the presence of Krukenberg spindles, iris trans-illumination defects, trabecular meshwork pigmentation and backward bowing of the iris. Posterior bowing of the iris causes rubbing of the pigmented iris epithelium against lens structures, liberation of pigment and trabecular meshwork changes that result in reduced aqueous outflow with the risk of glaucoma. Peripheral laser iridotomy can reverse backward bowing of the iris and may prevent progression of pigmentary glaucoma.

These studies demonstrated that stimulation of the P2X7R can mediate RGC death and that this mechanism plays a role in ischemia-induced neurodegeneration in the human retina.

Aims To develop human organotypic retinal cultures (HORCs) to study retinal ganglion cell (RGC) death in response to ischaemic and excitotoxic insults, both known to cause loss of RGCs and proposed as mechanisms involved in glaucomatous retinal neurodegeneration. Methods Human donor eyes were obtained within 24 h post mortem. The retina was isolated and explants cultured using two techniques. THY-1 mRNA (assessed by real-time quantitative PCR) and neuronal nuclei (NeuN) (assessed by immunohistochemistry) were used as markers of RGCs. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL). Results The distribution of THY-1 mRNA and NeuN-labelling within the human retina was consistent with the expected distribution of RGCs. Gross morphology and retinal architecture remained stable over a 96 h culture period. THY-1 mRNA and NeuN-labelled RGC layer cells decreased over the culture period, and there was an increase in TUNEL-labelling with time, but HORCs cultured in serum-free DMEM/HamF12 medium were useful for up to 48 h in culture. N-methyl-d-aspartate (10 µM) caused a reduction in THY-1 mRNA by 24 h and decreased the numbers of NeuN-labelled RGC layer neurons by 48 h, suggesting that the loss of THY-1 mRNA was a marker of RGC stress prior to death. Simulated ischaemia (60 min oxygen/glucose deprivation) caused a reduction at 24 h in both THY-1 mRNA and the numbers of NeuN-labelled neurons of HORCs. Conclusion HORCs provide a useful model to investigate RGC insult by neurodegenerative mechanisms that may lead to glaucoma in human eyes

PURPOSE. The aim of our study was to determine whether IOP lowering in glaucomatous and ocular hypertensive (OHT) eyes leads to an improvement in the full-field photopic negative response (PhNR) of the electroretinogram. METHODS.A prospective nonrandomized interventional cohort study was conducted. Patients with OHT or glaucomatous optic neuropathy were recruited, and photopic full-field electroretinograms (ERG) were performed at baseline and then repeated 1 to 2 months later. The change in PhNR amplitude was compared between those eyes that had a significant lowering in IOP (defined as >25% decrease from baseline or to a predetermined target IOP) during follow-up and those that did not. RESULTS.From a cohort of 30 eyes, 18 eyes had a significant reduction in IOP during follow-up (n ¼ 18) and 12 eyes had no significant change in IOP (<25% reduction in IOP, n ¼ 12). A significant increase in PhNR amplitude and the PhNR/b-wave amplitude ratios was observed in the reduced IOP group, but not in the IOP stable group for the two flash intensities used (2.25 and 3.00 cd.s/m 2 ).CONCLUSIONS. The full-field PhNR amplitude provides a potentially reversible measure of inner retinal function that improves after IOP lowering. Further study now is required to assess its use as a measure of optic nerve health in glaucoma patients.(Invest Ophthalmol Vis Sci.

Background: To determine whether postoperative subconjunctival bevacizumab significantly alters bleb vascularity.

Phacoemulsification performed after trabeculectomy significantly increased rates of bleb failure in the following 12 months but not at 24 months.

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The purpose of this study was to present the management of a series of patients referred with infraorbital nerve paraesthesia that developed after insignificant orbital floor fracture without diplopia or exophthalmos, and that did not require initial surgical repair. This is a retrospective interventional case series. The main outcome and measures were assessment of preoperative symptoms including neuralgia and sensory symptoms; review of periorbital computed tomography (CT) scans; and assessment of postoperative effects of surgery for infraorbital nerve decompression. Nine patients were identified who developed neuralgia affecting the infraorbital nerve distribution from a cohort of 79 patients who presented with orbital floor fracture. Six were female and three were male. Age range was 22 to 73 years with a mean of 48 years. Six patients were clinically depressed due to the chronic pain. In addition, two patients had dizziness on upgaze; one patient had blurring of central vision on eye movements; and one patient had mood swings. Reviews of CT scans revealed subtle disruption of the infraorbital canal in all cases. All nine patients underwent infraorbital nerve decompression. Abnormal adhesions between the nerve and its bony canal were found in five of nine cases. Follow-up ranged from 3 to 37 months (mean: 18 months). Following surgery, after a variable period of time ranging from 1 day to 3 months, all patients had resolution of their symptoms. Mean follow-up was 18 months. Reconstructive surgeons should be aware that infraorbital nerve neuralgia, secondary to disruption of the nerve in the distorted bony canal, may be another indication for surgical intervention following orbital floor trauma in selected cases, in addition to more traditionally accepted indications. Neuralgia and causalgia are probably more common than previously thought and symptoms should be actively sought in the patient's history or else risk being overlooked and inappropriately managed. Long-term follow-up of such patients is unlikely to be practical. Patient and/or family practitioner education of possible sequelae may be one possible solution to detect this type of problem early. Nerve decompression, where indicated, may improve the patient's neuralgia and associated behavioral changes and quality of life. An optimal diagnostic and management algorithm is yet to be established.