To describe the optic neuropathy associated with the genetic defect in Friedreich ataxia and suggest a pathophysiologic mechanism. Methods: An experimental model of retinal ganglion cell death in the presence of metal chelation was used to test a hypothetical mechanism for the optic neuropathy of Friedreich ataxia. Results: Study of cultured rat retinal ganglion cells suggests that abnormal regulation of intracellular iron levels could increase sensitivity to reactive oxygen species and lead to cell death in these metabolically active tissues. Conclusion: We hypothesize that decreased expression of frataxin, the mutated gene in Friedreich ataxia, could cause an optic neuropathy by increasing the sensitivity of retinal ganglion cells to oxidative stress.

Retinal detachments following modern cataract surgery in high myopia are much less common than previously reported. We attribute this to small incision size, continued maintenance of the anterior chamber, posterior chamber IOL implantation, and lack of intraoperative complications.

Acute visual decrease after PDT for AMD is uncommon. Visual recovery may occur in some patients, but a precise estimate is difficult to determine given the small sample size.