Processing Speed Delays Contribute to Executive Function Deficits in Individuals with Agenesis of the Corpus Callosum
Abstract
Corpus callosum malformation and dysfunction are increasingly recognized causes of cognitive and behavioral disability. Individuals with agenesis of the corpus callosum (AgCC) offer unique insights regarding the cognitive skills that depend specifically upon callosal connectivity. We examined the impact of AgCC on cognitive inhibition, flexibility, and processing speed using the Color-Word Interference Test (CWIT) and Trail Making Test (TMT) from the Delis-Kaplan Executive Function System. We compared 36 individuals with AgCC and IQs within the normal range to 56 matched controls. The AgCC cohort was impaired on timed measures of inhibition and flexibility; however, group differences on CWIT Inhibition, CWIT Inhibition/Switching and TMT Number-Letter Switching appear to be largely explained by slow performance in basic operations such as color naming and letter sequencing. On CWIT Inhibition/Switching, the AgCC group was found to commit significantly more errors which suggests that slow performance is not secondary to a cautious strategy. Therefore, while individuals with agenesis of the corpus callosum show real deficits on tasks of executive function, this impairment appears to be primarily a consequence of slow cognitive processing. Additional studies are needed to investigate the impact of AgCC on other aspects of higher order cortical function.
Additional Information
© 2012 International Neuropsychological Society (INS). Published by Cambridge University Press. Received: September 15, 2011; final revision: January 6, 2012; accepted January 6 , 2012. We thank the participants and their families for making this study possible and the D-KEFS team for the generous contribution of their data. Portions of this study served as the Master's Thesis of the co-first author, Kathryn Harrell, at the Fuller Graduate School of Psychology. This work was supported by the Simons Foundation (L.K.P. on grant held by Ralph Adolphs at Caltech). National Institutes of Health (E.H.S., K-02 NS052192, R01 NS058721; E.J.M., K12 NS01692, 1K23MH083890-01; E.H.S, E.J .M. and R.J.J., KL2 RR024130), and the UCSF Program for Breakthrough Biomedical Research (E.H.S.); and R.J.J .. NIHINCRR UCSF-CfSI Grant Number ULI RR024131. No conflicts of interest exist. Drs. Marco and Harrell contributed equally to this manuscript.Attached Files
Accepted Version - nihms444760.pdf
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Additional details
- PMCID
- PMC3605885
- Eprint ID
- 31784
- DOI
- 10.1017/S1355617712000045
- Resolver ID
- CaltechAUTHORS:20120601-162937886
- Simons Foundation
- NIH
- K-02 NS052192
- NIH
- R01 NS058721
- NIH
- K12 NS01692
- NIH
- 1K23MH083890-01
- NIH
- KL2 RR024130
- University of California, San Francisco
- NIH
- UL1 RR024131
- Created
-
2012-06-04Created from EPrint's datestamp field
- Updated
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2021-11-09Created from EPrint's last_modified field