Recent Research Ruminations

Previous findings suggested that elevated trans-laminar cribrosa pressure difference (TLCPD), instead of IOP itself, is a vital factor for the development of glaucoma (1). Further investigating the effect of focal lamina cribrosa (LC) defect on glaucoma progression, we explored the binocular comparison of LC defect within 93 NTG patients with asymmetric visual field loss. LC defects were found to be more common in eyes with better visual fields and exhibited lower peak IOP. Then, evaluating ocular parameters in patients (one eye with LC defect and the other without), we found eyes with LC defect to exhibit significantly better mean deviation, lower IOP, but longer axial length and larger tilt ratio. The rebalance of TLCPD mediated by focal LC defect may be the reason for the delay of glaucoma progression. These results were confirmed in rhesus monkeys. We therefore hypothesize that the spontaneous channel may connect the intraocular cavity and subarachnoid space, leading to fluid diffusion and reduced IOP. As a result, TLCPD is rebalanced in a lower level, potentially inhibiting glaucomatous optic neuropathy progress.

The American Academy of Ophthalmology’s Preferred Practice Patterns highlights low cerebrospinal fluid pressure (CSFP) as a risk factor for primary open angle glaucoma. However, retinal vasculature changes following CSFP reduction have not previously been studied. Recently, we performed OCT-A scans in patients undergoing diagnostic lumbar puncture and showed a CSFP reduction (2). Vessel density in the macular region decreased significantly after CSFP reduction. We also identified a significant relationship between CSFP reduction and macular parainferior vessel density decrease. However, the optic nerve head vessel density did not change after CSFP reduction. Additionally, choroidal thickness significantly decreased in the subfoveal and peripapillary region after CSFP reduction and a significant association between CSFP and the ratio of small to medium vessel layer to total choroidal thickness was found. This is the first demonstration of dynamic vascular changes after CSFP reduction in humans and provides more clinical evidence on the diagnostic paradigms for glaucoma. 

Finally, transscleral cyclophotocoagulation (TSCP) has been described as a safe and effective treatment, providing excellent IOP control in malignant glaucoma and acute primary angle closure (APAC) patients. Our previous studies provided clinical signs that TSCP induced damage or inflammation may change the structure of the anterior vitreous (3), lowering posterior pressure and causing a backward movement of the lens-iris diaphragm. This leads to anterior chamber deepening and reopening of angle in prolonged APAC and younger patients with chronic angle closure glaucoma (CACG). Recently, we found further evidence of vitreous modification caused by a fixed dosage of TSCP in three young patients with CACG, and some porcine eyes and rabbit eyes in vitro (4). This suggests that low dose TSCP with an audible “burst” could be used as an anterior vitreous modification procedure, having a significant effect on the management of young CACG patients.