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Microstructural Gray Matter Integrity Deteriorates After an Ischemic Stroke and Is Associated with Processing Speed.

Sharmila Sagnier1,2,3, Gwenaëlle Catheline4, Bixente Dilharreguy4

  • 1UMR-5287, CNRS, Université de Bordeaux, EPHE PSL Research University, Bordeaux, France. sharmila.sagnier@chu-bordeaux.fr.

Translational Stroke Research
|April 19, 2022
PubMed
Summary

Gray matter (GM) integrity declines after ischemic stroke (IS), evidenced by increased mean diffusivity (MD). This GM microstructural change correlates with slower processing speed, indicating a potential biomarker for cognitive decline post-stroke.

Keywords:
Diffusion tensor imagingGray matterLongitudinalProcessing speedStroke

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Area of Science:

  • Neurology
  • Neuroimaging
  • Cognitive Science

Background:

  • Microstructural changes post-ischemic stroke (IS) are primarily documented in white matter.
  • Limited data exists on gray matter (GM) microstructural alterations and their cognitive impact following IS.

Purpose of the Study:

  • To assess longitudinal changes in GM integrity using mean diffusivity (MD) after IS.
  • To investigate the relationship between GM microstructural changes and cognitive performance one year post-stroke.

Main Methods:

  • Prospective study of 104 IS patients without pre-stroke disability.
  • 3-T brain MRI with diffusion tensor imaging to measure GM MD and volume at baseline and 1 year.
  • Cognitive assessments including Montreal Cognitive Assessment, Isaacs set test, and Zazzo cancellation task (ZCT).

Main Results:

  • No significant GM volume loss was observed.
  • GM MD increased significantly between baseline and 1 year post-IS.
  • Increased GM MD in left fronto-temporal regions correlated with increased ZCT completion time.

Conclusions:

  • Deterioration of GM integrity, indicated by increased MD, is associated with slowed processing speed after IS.
  • GM microstructural changes may serve as a biomarker for cognitive frailty following ischemic stroke.
  • This study enhances understanding of the mechanisms underlying cognitive impairment after IS.