Tamoxifen side effects, age-related macular degeneration (AMD) or cancer associated retinopathy (CAR)?

PURPOSE: Differential diagnosis of maculopathies can be difficult but is important if patients also suffer from other diseases such as breast cancer treated with antiestrogens. The main possible diagnoses, especially in the elderly, are age-related macular degeneration, tamoxifen and cancer-associated retinopathy (CAR). METHODS: We describe an 84-year-old patient with breast and colon cancer, who complained of a decrease in visual acuity after treatment with low-dose antiestrogens. She underwent a general ophthalmological investigation, perimetry and electroretinographic examination with multifocal (m-ERG) and flash-electroretinogram (flash-ERG). RESULTS: Visual acuity was reduced to 1/50 and 0.3. The ophthalmological examination was normal, except for extensive bilateral maculopathy with shining crystalline deposits, central and peripheral visual field defects, slightly affected scotopic and photopic potentials in the flash-ERG, and an abnormal m-ERG. CONCLUSIONS: The findings are expected with age-related macular degeneration with crystalline drusen, but also with CAR. Even if the single and total dosage of antiestrogens given to the patient is sufficient to cause tamoxifen retinopathy, this diagnosis can be excluded because, in tamoxifen retinopathy unlike in the case presented here, the deposits are not distributed in all retinal layers.

Pupillary light reflexes in patients with Leber's hereditary optic neuropathy.

BACKGROUND: According to a recent pupillographic study, patients with Leber's hereditary optic neuropathy (LHON) show the same pupillary behaviour as normals. Because this raises many questions concerning the real nature of LHON and challenges our concept of the afferent pupillary system, we tried to verify the results of this study. METHODS: Pupillary function was assessed in 34 normal subjects and 40 patients with LHON. Pupillary light reflexes were recorded by means of the Compact Integrated Pupillograph (CIP, AMTech). Under mesopic conditions 200-ms stimuli were presented at two different stimulus intensities. Latency, constriction amplitude and baseline diameter were defined automatically. Pupil light reflexes were compared between LHON patients and normals and between the better and the worse eye in 20 LHON patients with different visual acuities. RESULTS: For both stimuli there were significant differences in latency between LHON patients and controls. The latency of the pupil light reflex proved to be about 20 ms longer for LHON patients, and the amplitude was significantly smaller for the bright stimulus. Within LHON patients, the eyes with the worse visual acuity had a significantly smaller constriction amplitude than the eyes with the better visual acuity. CONCLUSION: The results of our study confirm that LHON really is an optic nerve disease and that the pupillary light reflexes are not normal.

Interaction of the indirectly acting topical sympathomimetics cocaine and pholedrine.

In suspected Horner's syndrome, cocaine eye drops are applied to verify the diagnosis. Subsequent application of hydroxyamphetamine or pholedrine eye drops allows localization of the site of the interruption in the oculosympathetic pathway. In the present study the influence of cocaine on subsequent pholedrine testing was examined. Cocaine 5% and pholedrine 5% eye drops were applied to eight (72-h interval only six) normal volunteers with light-colored irides. The ages of the subjects ranged from 23 to 40 years. Eye drops were applied to the same eye at varying intervals of up to 72 h, with the cocaine being given between 8:30 and 9:30 a.m. Pupil diameters were recorded by means of a frame-grabber card in a personal computer and were subsequently measured before and at 50-60 min after each drug application in 1.7 cd/m2 ambient light. In the absence of pretreatment with cocaine, pholedrine changed the mean pupil diameter from 6.89 to 8.57 mm. At 12 h after cocaine pretreatment the pupil remained dilated. Pholedrine dilated the pupil further, from 7.69 to 8.61 mm. When cocaine was given 24 h before pholedrine, the pupil dilated from 6.75 to 8.25 mm; at 48 h after cocaine application, pholedrine dilated the pupil from 6.14 to 8.20 mm; and at 72 h after cocaine pretreatment, pholedrine dilated the pupil from 5.74 to 8.00 mm. As compared with the mean diameter of the untreated contralateral pupil, the pholedrine-induced dilation amounted to 2.32 mm in the absence of cocaine pretreatment, 1.04 mm at 12 h after cocaine application, 1.29 mm at 24 h after cocaine administration, 1.89 mm at 48 h after cocaine pretreatment, and 2.18 mm at 72 h after cocaine application. The residual cocaine effect interfered with the mean pupil dilation produced by pholedrin for at least 48 h. To ensure that the sensitivity of the pholedrine test is maximal, the examiner should delay its use for more than 48 h after the cocaine test.