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Objective To review progress toward an electronic retinal prosthesis for outerretinal degeneration. Method Literature review. Results Retinal degenerations such as retinitis pigmentosa result in a lossof photoreceptors. There is a secondary loss of inner retinal cells, but significantnumbers of bipolar and ganglion cells remain for many years. Electrical stimulationcan produce phosphenes in the eyes of individuals who are blind as a resultof retinitis pigmentosa. Several research groups are trying to exploit thisphenomenon to produce artificial vision with electronic retinal prostheses.Two groups, with private company sponsorship, have recently implanted first-generationdevices in subjects with advanced retinitis pigmentosa. They have reportedlimited preliminary results. This article seeks to put these results in abroader context and review potential obstacles to successful prosthesis development.These include inner retinal cell viability, high thresholds, signal encoding,power requirements, biocompatibility, and device encapsulation. Conclusion There has been substantial progress toward an electronic retinal prosthesis,but fully functional, long-lasting devices are not on the immediate horizon.

A highly myopic patient had surgery for retinal detachment in both eyes. After 3 procedures, the left eye developed phthisis bulbi. After multiple procedures, the right eye underwent a vitrectomy for proliferative vitreoretinopathy. A plaque of preretinal tissue was removed. We found bone on pathologic examination. The retina remains attached, and visual acuity is 20/200. Ultrasonography showed additional evidence of calcification of both eyes, presumably metaplastic bone.

von Hippel-Lindau disease is a member of the group of phakomatoses. It is characterized by formation of angiomas or hemangioblastomas in the retina, cerebellum, and occasionally in other tissues. Pheochromocytoma and renal cell carcinoma may also occur. Polycythemia can be seen, usually with cerebellar hemangioblastomas, renal cell carcinomas, or pheochromocytomas.1 The retinal tumors usually enlarge, and exudation from these lesions may lead to retinal detachment. Less commonly, peripheral retinal breaks may occur, leading to rhegmatogenous detachment.2This may occur after treatment of an angioma. I have observed a case with several unusual features. Preretinal membranes were present in both eyes, with spontaneous peeling in one eye and peeling after treatment of a peripheral angioma in the other eye. In both eyes, macular breaks resulted. In the treated eye, rhegmatogenous detachment occurred as a result of the macular break, along with traction originating from the treated lesion. The patient

The Vogt-Koyanagi-Harada syndrome includes inflammation of the uveal tract, retina, and meninges. Integumentary and auditory signs are common. Neurologic involvement has been reported. We studied two patients who manifested many of the varied clinical signs of Vogt-Koyanagi-Harada syndrome, but who also showed focal neurologic involvement, including acute transverse myelitis and ciliary ganglionitis. Both patients responded well to corticosteroid therapy. The findings in these patients and the results of previous studies suggest that Vogt-Koyanagi-Harada syndrome is a cell-mediated autoimmune disorder in which a component of myelin acts as an inciting antigen.

The right optic nerves of three cynomolgus monkeys were frozen under direct visualization after a modified Kröhnlein operation. Left optic nerves were subjected to an identical procedure without freezing. Postoperatively, visual evoked responses (VERs) could not be obtained by stimulating right eyes, while electroretinograms from both eyes and VERs obtained by stimulating left eyes were normal. Extensive lesions which were found in the right optic nerves of all animals were histologically similar to those obtained by freezing in the brain.

• We evaluated the condition of a patient with chronic papilledema due to pseudotumor cerebri in whom a permanent, monocular, inferior, altitudinal, visual field defect suddenly developed. Clinical and fluorescein angiographic findings indicated that the loss of visual field was due to ischemic optic neuropathy. Ischemic optic neuropathy might occur in papilledema if the tissue pressure in the optic disc becomes sufficiently elevated to occlude the pressure-sensitive prelaminar arterioles.

• Visual acuity screening was performed in the home in an adult population, using a standardized, retroilluminated chart. A pinhole disk was utilized to retest those subjects who initially failed the screening. All subjects failing the screening with the pinholes, and an equal number of age-matched subjects passing the screening (controls), were asked to have a complete ophthalmologic examination, including a protocol refraction in an eye clinic (clinic examination). Without use of the pinhole disk, 14.4% of subjects failed to read a 20/40 line. Use of the pinholes reduced the failure rate to 6.9%. Fifty-seven percent of those failing and 55% of controls had the clinic examination. Determination of best-corrected visual acuity after protocol refraction in the clinic indicated that the false-positive rate (the percentage of subjects who failed the screening but had visual acuity of 20/40 or better on the clinic examination) for the screening was 26%, and the false-negative rate (the percentage of subjects who passed the screening but had visual acuity of worse than 20/40 on the clinic examination) was 1.5%. Use of a pinhole disk is highly effective for visual acuity screening, reducing the false-positive rate by more than half.

Every compulsive ophthalmologist (and certainly every ophthalmology resident) has wished for a single reference source so complete that it may be consulted with no fear of omitting a condition from the differential diagnosis or of overlooking a significant finding when the diagnosis is known. I suspect that such fear is the motivating force behind Ocular Syndromes and Systemic Diseases . The book is divided into two sections. The first and main section lists syndromes and systemic diseases that may have ocular involvement. Under each heading, a general description of the entity, ocular findings, and nonocular findings are found. A few references are provided for each entity. The second section lists ocular signs and symptoms; under each heading, the conditions in which the symptoms or finding may occur are grouped. The primary limitations of the first section are the brevity and resultant lack of depth of each description; only a thumbnail sketch