Intraocular pressure, a major modifiable risk factor for glaucoma, has been shown to fluctuate throughout the day in patients with glaucoma. The detection and measurement of this fluctuation may help guide the clinical management of glaucomatous individuals. The Sensimed Triggerfish contact lens sensor (CLS), which has recently gained approval for marketing in the USA, is designed to detect intraocular pressure-related changes in an eye over a 24-hour period. This review will provide an overview of the Triggerfish CLS, as well as summarize current clinical data pertaining to the device. Overall, the current evidence suggests that the Triggerfish CLS is safe and well tolerated, and provides reproducible results. One challenge of using the Triggerfish CLS is that it may only provide data on relative changes in intraocular pressure rather than absolute intraocular pressure. In addition, its validity at estimating intraocular pressure compared to other methods is still controversial. Despite these limitations, recent studies suggest a myriad of potential indications for the Triggerfish CLS, including predicting glaucomatous progression and predicting efficacy of glaucoma treatment. With further research, the Triggerfish CLS may become a useful tool for eye care practitioners.

Diabetes mellitus is a disease with considerable morbidity and mortality worldwide. Breakdown of the blood-retinal barrier and leakage from the retinal vasculature leads to diabetic macular edema, an important cause of vision loss in patients with diabetes. Although epidemiologic studies and randomized clinical trials suggest that glycemic control plays a major role in the development of vascular complications of diabetes, insulin therapies for control of glucose metabolism cannot prevent long-term retinal complications. The phenomenon of temporary paradoxical worsening of diabetic macular edema after insulin treatment has been observed in a number of studies. In prospective studies on non-insulin-dependent (type 2) diabetes mellitus patients, a change in treatment from oral drugs to insulin was often associated with a significant increased risk of retinopathy progression and visual impairment. Although insulin therapies are critical for regulation of the metabolic disease, their role in the retina is controversial. In this study with diabetic mice, insulin treatment resulted in increased vascular leakage apparently mediated by betacellulin and signaling via the epidermal growth factor (EGF) receptor. In addition, treatment with EGF receptor inhibitors reduced retinal vascular leakage in diabetic mice on insulin. These findings provide unique insight into the role of insulin signaling in mediating retinal effects in diabetes and open new avenues for therapeutics to treat the retinal complications of diabetes mellitus.

In diabetes, there are two major physiological aberrations: (i) Loss of insulin signaling due to absence of insulin (type 1 diabetes) or insulin resistance (type 2 diabetes) and (ii) increased blood glucose levels. The retina has a high proclivity to damage following diabetes, and much of the pathology seen in diabetic retinopathy has been ascribed to hyperglycemia and downstream cascades activated by increased blood glucose. However, less attention has been focused on the direct role of insulin on retinal physiology, likely due to the fact that uptake of glucose in retinal cells is not insulin-dependent. The retinal pigment epithelium (RPE) is instrumental in maintaining the structural and functional integrity of the retina. Recent studies have suggested that RPE dysfunction is a precursor of, and contributes to, the development of diabetic retinopathy. To evaluate the role of insulin on RPE cell function directly, we generated a RPE specific insulin receptor (IR) knockout (RPEIRKO) mouse using the Cre-loxP system. Using this mouse, we sought to determine the impact of insulin-mediated signaling in the RPE on retinal function under physiological control conditions as well as in streptozotocin (STZ)induced diabetes. We demonstrate that loss of RPE-specific IR expression resulted in lower a-and bwave electroretinogram amplitudes in diabetic mice as compared to diabetic mice that expressed IR on the RPE. Interestingly, RPEIRKO mice did not exhibit significant differences in the amplitude of the RPEdependent electroretinogram c-wave as compared to diabetic controls. However, loss of

Purpose. Nonmydriatic fundus cameras allow retinal photography without pharmacologic dilation of the pupil. However, currently available nonmydriatic fundus cameras are bulky, not portable, and expensive. Taking advantage of recent advances in mobile technology, we sought to create a nonmydriatic fundus camera that was affordable and could be carried in a white coat pocket. Methods. We built a point-and-shoot prototype camera using a Raspberry Pi computer, an infrared-sensitive camera board, a dual infrared and white light light-emitting diode, a battery, a 5-inch touchscreen liquid crystal display, and a disposable 20-diopter condensing lens. Our prototype camera was based on indirect ophthalmoscopy with both infrared and white lights. Results. The prototype camera measured 133mm × 91mm × 45mm and weighed 386 grams. The total cost of the components, including the disposable lens, was $185.20. The camera was able to obtain good-quality fundus images without pharmacologic dilation of the pupils. Conclusion. A fully functional, inexpensive, handheld, nonmydriatic fundus camera can be easily assembled from a relatively small number of components. With modest improvements, such a camera could be useful for a variety of healthcare professionals, particularly those who work in settings where a traditional table-mounted nonmydriatic fundus camera would be inconvenient.

It has been hypothesised that non-arteritic ischaemic optic neuropathy is caused by vitreous traction on the optic nerve. The authors recently took care of a patient who developed a posterior vitreous detachment shortly after she was diagnosed with non-arteritic ischaemic optic neuropathy. Her visual field spontaneously improved after the posterior vitreous detachment. This case report provides some evidence that non-arteritic ischaemic optic neuropathy, vitreous traction, and posterior vitreous detachment may be related.

Fluocinolone implantation is associated with a significant reduction in macular edema as measured by spectral domain optical coherence tomography in the early postoperative period, a result that is consistent with the proposed mechanism of the drug.

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