Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Int Neuropsychol Soc. 2010 Sep;16(5):829-35. doi: 10.1017/S1355617710000688. Epub 2010 Jul 8.

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

Author information

  • 1Department of Neurology, Division of Cognitive and Behavioral Neurosciences, State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York, USA. benedict@buffalo.edu

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.

PMID:
20609273
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Cambridge University Press
    Loading ...
    Write to the Help Desk