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January 1992

Retinocalcarine Function in Alzheimer's Disease: A Clinical and Electrophysiological Study

Author Affiliations

From the Department of Ophthalmology, Harvard Medical School, and the Massachusetts Eye and Ear Infirmary (Drs Rizzo, Sandberg, and Lessell), the Department of Psychology, Boston University (Dr Cronin-Golomb), the Department of Neurology, Massachusetts General Hospital (Drs Growdon and Chiappa), and the Department of Neurology, Boston University School of Medicine (Dr Rosen), Boston; and the Department of Brain and Cognitive Sciences and the Clinical Research Center, Massachusetts Institute of Technology, Cambridge (Dr Corkin).

Arch Neurol. 1992;49(1):93-101. doi:10.1001/archneur.1992.00530250097023

• Impaired visual function in Alzheimer's disease (AD) could result from either precortical or cortical lesions, or both. In a parallel psychophysical study of visual function in AD, we found that contrast sensitivity function, color vision, stereoacuity, and back-ward masking were impaired relative to the performance of age-matched control subjects, whereas performance on a critical flicker fusion test was normal. The intent of the present study was to determine whether abnormalities of the retinocalcarine pathway contribute to visual dysfunction. We performed neuro-ophthalmological examinations on 38 patients with AD; from this group, 25 received additional psychophysical testing and 13 underwent electrophysiological testing. Clinical neuro-ophthalmological examinations, full-field electroretinograms, focal electroretinograms, and pattern visual evoked potentials were normal in all patients tested. There was no evidence of retinocalcarine abnormality specific to AD. We conclude that the visual impairment experienced by some patients with AD primarily results from involvement of the visual association cortices rather than from precortical damage, at least before the end stage of the disease.

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