Purpose: To investigate the effect of a prostaglandin (PG) analogue with or without preservative benzalkonium chloride (BAK) on corneal sensitivity.Methods: Central corneal sensitivity was measured prospectively with a Cochet–Bonnet esthesiometer in patients with normal tension glaucoma (NTG) or primary open angle glaucoma (POAG) before and 1 and 3 months after treatment. All patients began treatment with PG monotherapy with or without BAK preservative.Results: The study enrolled 84 patients: 52 NTG and 32 POAG. The treatment was PG with BAK preservative in 45 eyes and without BAK preservative in 39 eyes. Without BAK, the mean corneal sensitivity was 58.22 ± 3.56, 57.77 ± 4.59, and 56.33 ± 5.47 mm before and after 1 and 3 months, respectively; with BAK the mean corneal sensitivity was 58.20 ± 4.51, 56.31 ± 6.22, and 55.52 ± 6.23 mm. Corneal sensitivity was reduced significantly in patients using PG with the preservative BAK after 3 months (p = 0.033). Co-administration of artificial tears did not affect this reduction in corneal sensitivity.Conclusions: PG with the preservative BAK reduced corneal sensitivity and artificial tears did not improve this reduction. Reduced corneal sensitivity and accompanying side effects should be considered in the long-term use of PG with the preservative BAK.

Purpose: In retinal endothelial cells, homocysteine (Hcy) activates matrix metalloproteinase (MMP)-9, which results in apoptosis. This study investigated these effects of Hcy in human trabecular meshwork cells (HTMC).Methods: HTMC cultures using 5 mM low or 20 mM high glucose (HG)-containing media were exposed to 100 μM Hcy for 3 days. Cell viability was assessed with the MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide) assay. The MMP-9 and tissue inhibitor of MMP (TIMP)-1 levels were measured by western blotting and the degree of apoptosis was analyzed with flow cytometry using Annexin-propidium iodide double staining.Results: Exposure to Hcy in HG decreased cell viability compared to HG alone (<i>p</i> = 0.036). Compared to HG alone, co-exposure to Hcy with HG decreased the TIMP-1 levels, albeit not significantly (<i>p</i> = 0.094), and did not affect the MMP-9 levels (<i>p</i> = 0.413). In addition, co-exposure to Hcy with HG produced no difference in the degree of apoptosis compared to HG alone (<i>p</i> = 0.437).Conclusions: Unlike in retinal endothelial cells, Hcy did not affect the activities of TIMP-1, MMP-9, or the degrees of apoptosis significantly in HTMC. Thus, the effects Hcy may be limited in HTMC.

To investigate the effects of prostaglandin E2 agonist omidenepag (OMD) on the expression of matrix metalloproteinase (MMP) in human trabecular meshwork (TM) cells. Methods:Primarily cultured human TM cells were exposed to 0, 1, 10 or 40 µmol/L OMD for 3 days.The permeability through the TM cell monolayer was assessed using carboxyfluorescein. Expressions of mRNA and protein levels of MMP-1, -3, -9 were measured by RT-PCR and western blotting, respectively. Also the permeability, expression of mRNA and protein levels of MMPs was measured after exposure to 1 µmol/L latanoprost free acid (LAT).Results: OMD and LAT did not affect the cellular survival (all p>0.05). Each concentration of OMD and LAT did not affect the permeability of carboxyfluorescein significantly (all p>0.05). LAT increased the level of MMP-1 protein but did not increase the levels of MMP-3 and MMP-9 proteins. Each concentration of OMD did not affect the levels of MMP-1, -3, -9 proteins (all p>0.05) Conclusions: In TM cells, prostaglandin E2 agonist OMD did not increase the permeability through the TM cell monolayer, and the protein levels of MMPs. These suggest that the direct effect on the trabecular outflow by OMD may be limited.

Purpose: We report a patient with bilateral dural arteriovenous fistulae (DAVF) who initially presented with unilateral, isolated trochlear nerve palsy; and later with contralateral, oculomotor nerve palsy.Case summary: A 72-year-old male without any underlying disease or a trauma history visited with sudden vertical diplopia in both eyes that had developed 5 days prior. Brain magnetic resonance imaging (MRI) performed before his first visit was unremarkable. The eye movement test revealed hyperdeviation and limitation of downgaze in the left eye; we thus suspected unilateral, ischemic trochlear nerve palsy and this was indeed observed. However, the diplopia did not improve and limitations of the upper, medial gaze of the right eye developed after 3 months. Follow-up examinations (orbital computed tomography, brain MRI, and cerebral angiography) revealed bilateral DAVF running from the left to the right. He underwent gamma-knife radiosurgery; then the eye movement limitations and diplopia improved.Conclusions: Diplopia manifesting as paralysis in an elderly patient may be caused by DAVF; the diplopia may not always be the common ischemic paralytic strabismus. DAVF should be considered during differential diagnosis and further radiological examinations may be needed.