Vision and cognition in Alzheimer’s disease
Introduction
Alzheimer’s disease (AD) is the most common cause of abnormal cognitive decline in older adults [89], and neuropathological changes underlying AD involve visual pathways [61], [63], [111]. As sight is “the first door of the intellect” (Paccioli, ca 1445–ca 1514 [11]), it is reasonable to suspect that visual decline may contribute to intellectual deterioration in AD. AD is now reported to impair visual sensory functions including spatial contrast sensitivity [32], [43], [49], color, stereopsis, temporal resolution [23], [25] and motion [33], [103]. AD can also affect visual attention [68], [74] and “higher” visual functions such as reading, route finding, object localization and recognition [24], [48], [60], [73], [101]. Better understanding of these vision-related deficits could aid diagnosis, interpretation of cognitive scores, and interventions to improve functional capacity in patients with AD [22].
The selectivity of visual deficits and relation to disease stage and locus of CNS impairment in AD remain uncertain. Recent polemic concerns selectivity of “ventral” (“what” or “temporal”) vs “dorsal” (“where” or “parietal”) visual pathway deficits in AD [40], [48] including movement perception deficits [6], [46], [83], [91], [95], [96]. Moreover, Kurylo et al. [48] suggested that visual dysfunction does not follow overall disease progression in AD but rather reflects sporadic involvement in certain cases. Visual function in AD is an issue of theoretical and practical importance that requires further investigation.
The purpose of this study was to investigate visual and cognitive abilities in older individuals with and without AD. We tested the hypotheses that AD produces both ventral and dorsal visual pathway deficits while sparing basic sensory functions, and that these visual function deficits correlate with overall severity of AD.
Section snippets
Subjects
Forty-three volunteers with AD (mean age 71.9 years, SD=8.3 years; mean education 13.2 years, SD=3.2 years) were recruited from the Alzheimer’s Disease Research Center in the Department of Neurology. The diagnosis of probable AD was based on standard criteria (NINCDS-ADRDA [58]). All participants with AD were living at home, able to attend to personal needs and were still driving or had recently quit. Group mean Clinical Dementia Rating (CDR) score was 0.69, indicating mild dementia.
Static visual functions
There were no significant differences (Wilcoxon 2-Sample Test) between participants with AD and control subjects in static visual acuity measured at near (20/27.3 [11.7] vs 20/26.6 [8.4], P=0.69) and at far (20/27.7 [16.7] vs 20/26.1 [10.3], P=0.91). CS was slightly lower in the AD group (1.75 [0.22] vs 1.84 [0.21], P=0.04). There was also no significant difference in stereoacuity between the AD and control groups (150.2 [230.4] vs 71.4 [78.0], P=0.31). Individuals with AD performed worse than
Discussion
In line with our hypothesis, the findings indicate that AD affects visual functions while sparing several basic visual sensory functions. Compared to controls, participants with mild AD showed significant impairments of visuospatial construction, higher visual perception and memory (WAIS-R Block Design, CFT-copy, FRT, VRT, TMT) and processing of complex motion (SFM). They also showed significant reductions on multiple measures of attention. On measures of static visual acuity, stereoacuity or
Conclusions
Vision impairment is the presenting complaint in a small minority of patients who later manifest neurodegenerative disease [8], [78], [82], [93]. A “visual variant” of AD [51] is reported in a small proportion of cases and is well known since its description in the late 1980s [8]. This uncommon subtype of AD (aka posterior cortical atrophy) presents with severe visuoperceptual and visuomotor impairments [35], [40], [59] resembling the “minor forms of Bálint syndrome” described by Hécaen and
Acknowledgements
This work was supported by NIH PO NS19632 and CDC R49/CCR710136.
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