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Anti-Saccade Performance Predicts Executive Function and Brain Structure in Normal Elders

Mirsky, Jacob B. MA; Heuer, Hilary W. PhD; Jafari, Aria BS; Kramer, Joel H. PsyD; Schenk, Ana K. PhD; Viskontas, Indre V. PhD; Miller, Bruce L. MD; Boxer, Adam L. MD, PhD

Cognitive and Behavioral Neurology: June 2011 - Volume 24 - Issue 2 - p 50–58
doi: 10.1097/WNN.0b013e318223f6c6
Original Studies

Objective To assess the neuropsychological and anatomical correlates of anti-saccade (AS) task performance in normal elders.

Background The AS task correlates with neuropsychological measures of executive function and frontal lobe volume in neurological diseases, but has not been studied in a well-characterized normal elderly population. Because executive dysfunction can indicate an increased risk for cognitive decline in cognitively normal elders, we hypothesized that AS performance might be a sensitive test of age-related processes that impair cognition.

Method The percentage of correct AS responses was evaluated in 48 normal elderly subjects and associated with neuropsychological test performance using linear regression analysis and gray matter volume measured on magnetic resonance imaging scans using voxel-based morphometry.

Results The percentage of correct AS responses was associated with measures of executive function, including modified trails, design fluency, Stroop inhibition, abstraction, and backward digit span, and correlated with gray matter volume in 2 brain regions involved in inhibitory control: the left inferior frontal junction and the right supplementary eye field. The association of AS correct responses with neuropsychological measures of executive function was strongest in individuals with fewer years of education.

Conclusions The AS task is sensitive to executive dysfunction and frontal lobe structural alterations in normal elders.

Supplemental Digital Content is available in the text.

Department of Neurology, Memory and Aging Center, University of California, San Francisco, CA

Supported by the National Institutes of Health (K23NS48855, R01AG031278, and R01AG038791 to Adam L. Boxer; P01AG019724 and P50AG0300601 to Bruce L. Miller); the John Douglas French Foundation (Adam L. Boxer); the Hellman Family Foundation (Adam L. Boxer); and the L. Hillblom Foundation (Bruce L. Miller).

Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website,

Disclosure Statement: There are no actual or potential conflicts of interest.

Reprints: Adam L. Boxer, MD, PhD, Memory and Aging Center, Department of Neurology, University of California, San Francisco, Box 1207, San Francisco, CA 94143 (e-mail:

Received June 2, 2010

Accepted May 7, 2011

© 2011 Lippincott Williams & Wilkins, Inc.