Optic nerve injury induces optic nerve degeneration and retinal ganglion cell (RGC) death that lead to visual disturbance. In this study, we examined if topical ripasudil has therapeutic potential in adult mice after optic nerve crush (ONC). Topical ripasudil suppressed ONC-induced phosphorylation of p38 mitogen-activated protein kinase and ameliorated RGC death. In addition, topical ripasudil significantly suppressed the phosphorylation of collapsin response mediator protein 2 and cofilin, and promoted optic nerve regeneration. These results suggest that topical ripasudil promotes RGC protection and optic nerve regeneration by modulating multiple signaling pathways associated with neural cell death, microtubule assembly and actin polymerization.
Purpose
We conducted cross-sectional examinations to determine the frequency of peripapillary retinoschisis (PRS) in eyes with glaucoma and suspected glaucoma and analyzed the pathogenesis of PRS by using spectral-domain optical coherence tomography (SD-OCT).
Patients and Methods
In 1516 cases involving glaucoma and suspected glaucoma, we retrospectively reviewed the disc and macular volume scans obtained by SD-OCT and categorized PRS into two groups based on whether the retinoschisis was closer to the optic nerve over the Bruch’s membrane opening (BMO) (ahead group) or did not go past the BMO (behind group) and then compared the characteristics between both groups.
Results
The total frequency of PRS was 1.49% (20/1342 eyes) in primary open-angle glaucoma (POAG) eyes and 0.59% (10/1687 eyes) in glaucoma suspects. In the behind group, PRS was mostly detected in the inner layers of the retina (retinal nerve fiber layer: 30.9%, ganglion cell layer: 21.8%, inner plexiform layer: 7.3%). However, in the ahead group, PRS was detected in the outer layers (inner nuclear layer: 10%, outer plexiform layer: 20%, outer nuclear layer: 50%). In addition, the eyes in the ahead group had significantly greater axial lengths and significantly smaller spherical equivalent values. These two differences suggest that the pulling force of the vitreous traction may play an important role in PRS only in the behind group and that the scleral stretching force may play a role in the development of PRS in the ahead group.
Conclusion
The frequency of PRS in patients with POAG is higher than that in patients with suspected glaucoma. Both forms of PRS are affected by posterior vitreous detachment and axial length elongation. Careful follow-up is required to assess the development of PRS in glaucoma suspects. The pathogenesis of PRS has been elucidated to some degree by classifying the morphological condition of the PRS and BMO.
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