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Purpose: To determine whether repeated intravitreal triamcinolone (IVTA) injections in patients with Behçet disease that is resistant to conventional therapy will prevent recurrences of uveitis., Design: Prospective preliminary clinical trial., Methods: Nine eyes of five patients with Behçet disease with sight-threatening uveitis that was resistant to conventional therapy received repeated IVTA injections. Each patient was examined monthly, and IVTA was given when the TA particles that remained in the vitreous were judged to be gone before the next visit., Results: Repeated IVTA completely prevented the recurrence of uveitis in eight eyes, and the one eye that had an attack experienced the uveitis when the TA particles disappeared quicker than expected. It was possible to stop systemic corticosteroid and/or immunosuppressive agents within 1 year after IVTA in three patients., Conclusion: These results indicate that repeated IVTA will prevent the recurrence of uveitis in patients with Behçet disease with frequent ocular attacks that is resistant to conventional therapy.

Purpose: To compare a macular hole from accidental Nd:YAG laser injury with idiopathic macular holes., Methods: Case report. In a 24-year-old man with accidental Nd:YAG laser injury, right eye, Amsler grid testing and optical coherence tomography were performed., Results: Nd:YAG laser injury was responsible for a macular hole about 700 microm in diameter. The visual acuity was 20/100. Amsler grid testing displayed a central scotoma with no surrounding distortion. Optical coherence tomography showed a defect in all retinal layers at the macula., Conclusion: The scotoma caused by Nd:YAG laser injury is not surrounded by distortion; the hole is produced by the defect of all retinal layers. In contrast, idiopathic macular holes generally produce a pincushion pattern on Amsler grid testing and have no tissue loss.

The expression of the proto-oncogenes c-fos and c-jun was examined by in situ hybridization at various timepoints following transient retinal ischemia by means of ligation of the retinal central artery in the rat. Ischemia of 90-minute duration resulted in the degeneration of neurons in both the ganglion cell layer and the inner nuclear layer at 48 hours after reperfusion. The expression of c-fos and c-jun messenger RNA throughout the entire inner nuclear layer was transiently coinduced following 90-minute retinal ischemia with a peak at 1 hour after reperfusion. This expression was also found in the ganglion cell layer at 3 hours after reperfusion. Weak signals for c-fos and c-jun mRNA were observed at 24 hours after reperfusion and returned to near control levels by 48 hours. c-jun protein expression was detected in the ganglion cell layer, the middle of the inner nuclear layer, and optic nerve head at 3 hours, but not 1 hour, after lethal ischemia/reperfusion; however, c-fos protein expression was not detected after reperfusion. Whereas no neuronal degenerative changes were found at 7 days after 30-minute ischemic retina, c-fos and c-jun messenger RNA were also induced at 1 hour postreperfusion. To our knowledge, this study is the first report to show expression patterns of immediate-early genes after retinal ischemia/reperfusion. These results suggest that changes in expression of c-fos and c-jun after transient retinal ischemia are similar to those after transient brain ischemia, and the selective occlusion of the central retinal artery will provide a useful model for studying ischemic neuronal degeneration in vivo in the rat retina.

Entrainment of the circadian pacemaker in the suprachiasmatic nucleus is accomplished by two neural pathways, the retinohypothalamic and geniculohypothalamic tracts. The geniculohypothalamic tract, which originates from the intergeniculate leaflet and a portion of the ventral lateral geniculate nucleus, is composed of fibers immunoreactive to neuropeptide Y. To assess the processing of photic information by the geniculohypothalamic tract, neuropeptide Y immunoreactivity in the suprachiasmatic nucleus of rats kept under various external lighting conditions was determined by enzyme immunoassay of micropunched tissues. Neuropeptide Y levels in the suprachiasmatic nucleus steadily increased when rats were exposed to continuous light and reached a peak in 2 h before returning to basal level. The amount of increase did not depend on intensity and duration of light exposure. A light pulse as short as 5 min elicited a similar rise in neuropeptide Y, indicating that the response is due to the sudden transition from dark to light. This response, however, was only observed when the dark to light transition occurred at circadian time 0 (subjective dawn) of the pacemaker. A light pulse at circadian time 0, which effectively induces the increase in neuropeptide Y level, does not significantly shift the phase of the circadian rhythm. This observation indicates that the photic pathway utilizing neuropeptide Y may be functional only when the endogenous circadian rhythm is synchronized to external light and dark cycles. Administration of an excitatory amino acid antagonist (MK-801) blocked the increase of neuropeptide Y by light, while an agonist (N-methyl-D-aspartate) induced similar facilitatory effects to that of light on the neuropeptide Y level in the rat suprachiasmatic nucleus. These results suggest that the geniculohypothalamic tract processes photic information so as to facilitate distinction of the transition between light and darkness that occurs either at subjective dawn or dusk.