March 1973, when she developed a left pleural effusion. She was subsequently treated with a variety of chemotherapeutic agents which included cytoxan, methotrexate, 5-fluorouracil, prednisone, diethylstilboestrol, and a short trial of L-PAM. In May 1975 she was started on tamoxifen, 90 mg (60 mg/M2) twice daily, and halotestin, 10 mg (7 mg/M2) twice daily as a participant in a randomised trial to study the effect of increasing doses of tamoxifen with or without halotestin. Currently accepted tamoxifen doses vary from 10 to 20 mg twice daily.The patient noted the onset of decreasing vision in about October 1976 after 17 months of treatment with tamoxifen and halotestin. The total dose of tamoxifen at that time was slightly greater than 90 g. A previous ocular examination in May 1976 showed a visual acuity of RE 6/9 (20/30) and LE 6/7 5 (20/25). The fundus examination was recorded as normal. Ophthalmological examination in October 1977 revealed a best corrected visual acuity of 6/15 (20/50) in each eye. Visual field testing with the IV4e and 14e white targets on the Goldmann perimeter showed peripheral constriction and central scotomas. The conjunctivae, corneae, and intraocular pressures were normal. Mild nuclear sclerosis and a few cortical spoke-like opacities were present on both lenses. Fundus examination (Fig. 1) revealed a myriad of tiny, refractile, intraretinal lesions at all levels of the sensory retina. These lesions were concentrated in both maculae but extended to the ora serrata. At the level of the retinal pigment epithelium there were 250 to 400 ,m diameter yellow-white granular areas which were most prominent posterior to the equator but were noted in the far peripheral retina as well. Cystoid macular oedema was present bilaterally. The optic discs were normal and the retinal arterioles appeared 177 on 11 May 2018 by guest. Protected by copyright.