Journal of the International Neuropsychological Society

Research Articles

Cognitive reserve moderates decline in information processing speed in multiple sclerosis patients

RALPH H.B. BENEDICTa1a2 c1, SARAH A. MORROWa1a2, BIANCA WEINSTOCK GUTTMANa1a2, DIANE COOKFAIRa1a2 and DAVID J. SCHRETLENa3

a1 Department of Neurology, Division of Cognitive and Behavioral Neurosciences, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York

a2 Jacobs Neurological Institute, Buffalo, New York

a3 Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland

Abstract

Cognitive reserve is widely recognized as a moderator of cognitive decline in patients with senile dementias such as Alzheimer’s disease. The same effect may occur in multiple sclerosis (MS), an immunologic disorder affecting the central nervous system. While MS is traditionally considered an inflammatory, white matter disease, degeneration of gray matter is increasingly recognized as the primary contributor to progressive cognitive decline. Our aim was to determine if individual differences in estimated cognitive reserve protect against the progression of cognitive dysfunction in MS. Ninety-one patients assessed twice roughly 5 years apart were identified retrospectively. Cognitive testing emphasized mental processing speed. Cognitive reserve was estimated by years of education and by performance on the North American Adult Reading Test (NAART). After controlling for baseline characteristics, both years of education (p = .013) and NAART scores (p = .049) significantly improved regression models predicting cognitive decline. Symbol Digit Modalities Test (SDMT) performance showed no significant change in patients with > 14 years of education, whereas it declined significantly in patients with ≤ 14 years of education. We conclude that greater cognitive reserve as indexed by either higher premorbid intelligence or more years of education protects against the progression of cognitive dysfunction in MS. (JINS, 2010, 16, 829–835.)

(Received January 19 2010)

(Reviewed June 02 2010)

(Accepted June 02 2010)

Correspondence:

c1 Correspondence and reprint requests to: Ralph H.B. Benedict, Department of Neurology, 100 High Street (D-6), Buffalo, New York 14203. E-mail: benedict@buffalo.edu

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