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Natalie Borodoker, BA; Lucian V. Del Priore, MD PhD; Cynthia de A. Carvalho, MD; Lawrence A. Yannuzzi, MD
New York, NY

Arch Ophthalmol. 2002;120:994-995.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A 51-YEAR-OLD white woman with a long history of psychiatric problems and no family history of hereditary retinal degeneration experienced decreased vision in both eyes for several years. She had received thioridazine hydrochloride (Mellaril; Sandoz Pharmaceutical Co, Hanover, NJ) 300 mg daily from 1978 through 1997 and chlorpromazine hydrochloride (Thorazine; SmithKline Beecham, Philadelphia, Pa) 600 mg daily from 1986 through 1998.

Best-corrected visual acuity was 20/60 OD and 20/100 OS with markedly constricted visual fields and central scotomas in both eyes. Anterior segment and vitreous were normal, but both eyes had large patches of atrophy outside the arcades and within the macula with sparing of foveal pigmentation. Diffuse increases in hyperpigmentation were located in the periphery of both eyes (Figure 1). Geographic areas of hyperfluorescence corresponding to hypopigmented or absent . . . [Full Text of this Article]

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