Visual Processing in Alzheimer’s Disease

Abstract

Four percent of 88 Alzheimer’s patients seen in 1992–93 at the Memory Disorders and Alzheimer’s Disease Center at Loyola University of Chicago had as the presenting symptom difficulty in processing visual information. Complex visual disturbances have been described in Alzheimer’s disease (AD), including constructional and visuoperceptual disorientation, spatial agnosia, facial identification problems, Balint’s syndrome, and impairment of contrast sensitivity functions (Adelstein et al. 1992, Mendez et al. 1992, Rizzo et al. 1992, Hof and Bouras 1991, Cronin-Golomb et al. 1991, Mendez et al. 1990 a,b, Flicker et al. 1990). This widespread visual dysfunction may reflect known pathological changes in the primary visual pathways or in the association cortex, or both. Pathological changes have been described in the optic nerve (Hinton et al. 1986, Sadun 1989), the primary and the association visual cortices (Lewis et al. 1987, Armstrong et al. 1990, Bell and Ball 1990, Levine et al. 1992). Trick et al (1989) and Katz et al (1989) have reported changes in the pattern electroretinograms suggesting that there is a quantifiable retinal ganglion cell dysfunction in Alzheimer’s disease. However, Katz et al. (1989) also found that pattern VEPs and flash VEPs had normal P100 responses but had a delayed second positive component suggesting a dysfunction of visual association cortex. In a prospective study (Mendez et al., 1990) found that all 30 patients studied had some disturbances in figure analysis, and 57% of these patients had some form of visual agnosia. These authors concluded that complex visual disturbances are more frequent than previously realized.KeywordsPrimary Visual CortexBrodmann AreaChAT ActivityContrast Sensitivity FunctionVisual AgnosiaThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.