To examine the safety and efficacy of selective laser trabeculoplasty as primary treatment for patients with open-angle glaucoma. Methods: Forty-five eyes of 31 patients with openangle glaucoma or ocular hypertension (intraocular pressure [IOP] Ն23 mm Hg on 2 consecutive measurements) underwent selective laser trabeculoplasty as primary treatment. All patients underwent complete ophthalmic evaluation before and at intervals after treatment. This evaluation included visual acuity, slitlamp examination, ophthalmoscopy, gonioscopy, and visual field analysis. The IOP was measured 1 hour, 1 day, 1 week, and 1, 3, 6, 12, 15, and 18 months postoperatively. During the follow-up period, patients were treated with topical antiglaucoma medications as required. Results: Mean ± SD decreased by 7.7±3.5 mm Hg (30%), from 25.5±2.5 mm Hg to 17.9±2.8 mm Hg (PϽ.001). Only 2 eyes (4%) did not respond to selective laser trabeculoplasty, and 3 eyes (7%) required topical medications to control their IOP at the end of the follow-up period. Forty eyes (89%) had a decrease of 5 mm Hg or more. Visual acuity, visual fields, and gonioscopic findings remained unchanged. Complications included conjunctival redness and injection within 1 day postoperatively in 30 eyes (67%). One hour after selective laser trabeculoplasty, an increase in IOP of more than 5 mm Hg was detected in 5 eyes (11%), while an increase in IOP between 2 and 5 mm Hg was measured in 3 eyes (7%). Conclusion: Selective laser trabeculoplasty is effective and safe as a primary treatment for patients with ocular hypertension and open-angle glaucoma.

Damage to the optic nerve in mammals induces retrograde degeneration and apoptosis of the retinal ganglion cell (RGC) bodies. The mechanisms that mediate the response of the neuronal cells to the axonal injury are still unknown. We have previously shown that semaphorins, axon guidance molecules with repulsive cues, are capable of mediating apoptosis in cultured neuronal cells (Shirvan, A., Ziv, I., Fleminger, G., Shina, R., He, Z., Brudo, I., Melamed, E., and Brazilai, A. (1999) J. Neurochem. 73, 961-971). In this study, we examined the involvement of semaphorins in an in vivo experimental animal model of complete axotomy of the rat optic nerve. We demonstrate that a marked induction of type III semaphorin proteins takes place in ipsilateral retinas at early stages following axotomy, well before any morphological signs of RGC apoptosis can be detected. Time course analysis revealed that a peak of expression occurred after 2-3 days and then declined. A small conserved peptide derived from semaphorin 3A that was previously shown to induce neuronal death in culture was capable of inducing RGC loss upon its intravitreous injection into the rat eye. Moreover, we demonstrate a marked inhibition of RGC loss when axotomized eyes were co-treated by intravitreous injection of functionblocking antibodies against the semaphorin 3A-derived peptide. Marked neuronal protection from degeneration was also observed when the antibodies were applied 24 h post-injury. We therefore suggest that semaphorins are key proteins that modulate the cell fate of axotomized RGC. Neutralization of the semaphorin repulsive function may serve as a promising new approach for treatment of traumatic injury in the adult mammalian central nervous system or of ophthalmologic diseases such as glaucoma and ischemic optic neuropathy that induce apoptotic RGC death.

Bone marrow-derived MSCs can deliver NTFs by intravitreal injection and can be neuroprotective after ONT. This approach might be further studied to deliver NTFs by autotransplantation in glaucomatous eyes.

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