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Altered effective connectivity during performance of an information processing speed task in multiple sclerosis.

Victoria M Leavitt1, Glenn Wylie, Helen M Genova

  • 1Neuropsychology & Neuroscience, Kessler Foundation Research Center, West Orange, NJ 07052, USA. vleavitt@kesslerfoundation.org

Multiple Sclerosis (Houndmills, Basingstoke, England)
|October 4, 2011
PubMed
Summary

Individuals with multiple sclerosis (MS) show altered brain connectivity during a processing speed task compared to healthy controls (HC). The MS group exhibited increased connections to frontal regions, suggesting greater neural recruitment to maintain task performance despite slower speeds.

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Area of Science:

  • Neuroscience
  • Neuroimaging
  • Clinical Neurology

Background:

  • Functional magnetic resonance imaging (fMRI) studies in multiple sclerosis (MS) show varied activation patterns.
  • Investigating effective connectivity using Granger causality analysis (GCA) can reveal distinct neural network differences.

Purpose of the Study:

  • To characterize directed neural connections in individuals with MS during a processing speed task.
  • To compare brain connectivity patterns between MS patients and healthy controls (HC).

Main Methods:

  • fMRI and GCA were employed to analyze effective connectivity during a modified Symbol Digit Modality Task (mSDMT).
  • 16 individuals with MS and 17 HC participated, performing the mSDMT within an MRI scanner.
  • Eight seed regions, identified from prior HC studies, were selected for analysis.

Main Results:

  • The MS group achieved similar accuracy to HC but were significantly slower on the mSDMT.
  • While both groups shared overlapping brain connections, the MS group displayed significant differences in connectivity.
  • Specifically, individuals with MS showed increased connectivity from multiple regions to bilateral frontal cortices compared to HC.

Conclusions:

  • The findings support the neural efficiency hypothesis in MS.
  • Increased neural recruitment in the MS group suggests a compensatory mechanism to maintain cognitive function amidst neurological pathology.