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Neurophysiologic analyses of low- and high-level visual processing in Alzheimer disease

From the Departments of Neurology, Brain and Cognitive Sciences, Neurobiology and Anatomy, and Ophthalmology and the Center for Visual Science, University of Rochester Medical Center, NY.

Address correspondence and reprint requests to Dr Duffy, Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642-0673 cjd{at}cvs.rochester.edu

Objective: We developed visual motion evoked potential (EP) measures related to navigational impairment in Alzheimer disease (AD) and have now applied these methods to explore the role of elementary perceptual and attentional mechanisms mediating these effects.

Methods: Older adult (OA) control subjects and AD patients underwent visual motion perceptual testing, attentional performance monitoring, and basic neuropsychological and visual assessments. We recorded stationary pattern onset and visual motion onset EPs as well as behavioral event–related potentials during centered visual fixation.

Results: Psychophysical assessment demonstrated visual motion perceptual impairments in patients with AD, half of whom also showed low sensitivity in the attentional task. The low sensitivity AD patients had small pattern onset and absent motion onset EPs, whereas the high sensitivity AD patients had large pattern onset EPs and normal motion onset EPs.

Conclusions: We conclude that visual evoked potentials (EPs) are abnormal in all patients with Alzheimer disease (AD): Those with small pattern and motion onset EPs may have greater AD pathology in visual cortex, whereas those with larger pattern onset EPs may have greater AD pathology in higher centers. These findings highlight the utility of visual EPs in distinguishing between syndromic variants of AD associated with particular patterns of functional decline.

Supported by grants from NIA (AG17596) and NEI (EY10287).

Disclosure: The authors report no conflicts of interest.

Received June 19, 2006. Accepted in final form February 5, 2007.

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