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Visual dysfunction in Alzheimer's disease: Relation to normal aging
Author(s) -
CroninGolomb Alice,
Corkin Suzanne,
Rizzo Joseph F.,
Cohen Jennifer,
Growdon John H.,
Banks Kathleen S.
Publication year - 1991
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410290110
Subject(s) - flicker fusion threshold , audiology , stereoscopic acuity , alzheimer's disease , degenerative disease , contrast (vision) , dementia , psychology , spatial frequency , color vision , ageing , medicine , central nervous system disease , flicker , ophthalmology , neuroscience , disease , visual acuity , pathology , optics , physics , electrical engineering , engineering
In patients with Alzheimer's disease (AD), compared with age‐matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). Critical flicker fusion thresholds were normal, relative to age‐matched healthy subjects. For color, the majority of the errors were tritanomalous (blue axis). Color and stereoacuity deficits were unrelated to severity of dementia, in accordance with models of vision that describe these functions as modular rather than diffuse for cortical localization. Although contrast sensitivity was depressed throughout the frequency range in AD, more patients were impaired at low than at high spatial frequencies, contrasting with the observed normal aging pattern of high‐frequency loss. Healthy elderly subjects showed depressed critical flicker fusion thresholds and reduced contrast sensitivity at high frequencies, relative to the young group; differences between these groups were not found for the other vision tests. A subset of the AD group received detailed neuro‐ophthalmological examination, and no abnormalities were found. This finding, taken together with normal thresholds for critical flicker fusion, suggests that the widespread visual dysfunction reported here is more likely to be related to known pathological changes in primary visual and association cortex in AD than to changes in the retina or optic nerve.