Retinocalcarine function in Alzheimer's disease. A clinical and electrophysiological study
J. F. Rizzo 3rd, A. Cronin-Golomb, J. H. Growdon, S. Corkin, T. J. Rosen, M. A. Sandberg, K. H. Chiappa and S. Lessell
Department of Ophthalmology, Harvard Medical School, Boston, MA.
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 backward 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.
