There is an accumulating body of evidence that immunological mechanisms play a prominent role in the pathogenesis of diabetic retinopathy (DR), which is characterized by many features typical of inflammation. The upregulation of cytokines and other inflammatory mediators leading to persistent low-grade inflammation and an influx of leukocytes, is believed to contribute actively to DR-associated damage to the retinal vasculature and retinal neovascularization. This review will describe preclinical and clinical studies that document an inflammatory basis for DR and that support the use of nonsteroidal anti-inflammatory drugs, corticosteroids, and anti-vascular endothelial growth factor agents in its treatment. In addition, emerging therapeutic approaches based on ongoing investigations will be discussed, including those involving blockade of angiotensin receptors and other molecular targets such as tumor necrosis factor-alpha.
To report a series of patients manifesting ulnar neuropathy as an extraocular complication following macular hole surgery and facedown positioning. Methods: Retrospective chart review of 7 patients identified by the operating surgeon as developing ulnar neuropathy during the immediate postoperative period after undergoing vitrectomy surgery with fluid-gas exchange for macular hole followed by at least 1 week of strict facedown positioning. Results: All 7 patients developed symptoms of ulnar neuropathy, including paresthesias, dysesthesias, pain, weakness, and muscle atrophy. Signs included abnormal electromyogram, prolonged nerve conduction velocities, and impaired neurologic clinical test results in patients ex
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