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Delayed recognition of Horner syndrome secondary to internal carotid artery dissection after scuba diving

mechanism that increases uveoscleral outflow. However, PG agents have several adverse effects, including induction of increased inflammatory cytokines, which results in intraocular inflammation. Cystoid macular edema, which is caused by a disruption of the blood-retinal barrier or by a disruption of the blood-aqueous barrier, has also been associated with the use of PG agents. We speculate that these actions of PG agents may be associated with increased VEGF levels. And many studies have reported that inflammation increases VEGF levels in systemic diseases. In the eye, although there have been studies reporting an association between VEGF and uveitis and that systemic immune suppressive agents resulted in decreased VEGF levels in the aqueous humor. However, few studies have characterized possible associations between ocular inflammation and levels of VEGF. Some previous studies have reported that VEGF plays a physiological role in neuroprotection and survival. Several studies reported increased blood flow and neuroprotection of retinal ganglion cells in animal models, and in an in vivo study of PG use, either alone or in combination with other drugs. More studies are therefore needed to further investigate the possible associations of PG agent use and neuroprotection conferred by VEGF or other factors. In summary, we showed increased VEGF concentrations in the aqueous humor of DM patients and glaucoma patients who used PG agents. However, it was unclear whether they played positive or negative roles in these patients. This will need to be decided by additional studies with larger cohorts.