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Lesion network mapping for post-stroke cognitive impairment.

Yijun Zhou1, Yue Wang2, Jing Jing2

  • 1Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing, China.

International Journal of Stroke : Official Journal of the International Stroke Society
|February 5, 2026
PubMed
Summary
This summary is machine-generated.

This study reveals how brain lesions from strokes and white matter changes disrupt neural networks, causing cognitive impairment. White matter changes significantly mediate stroke-related cognitive deficits, highlighting potential targets for brain stimulation.

Keywords:
Post-stroke cognitive impairmentacute infarctlesion network mappingneuromodulation targetswhite matter hyperintensity

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Area of Science:

  • Neuroscience
  • Neurology
  • Medical Imaging

Background:

  • Post-stroke cognitive impairment (PSCI) is linked to infarcts and white matter hyperintensities (WMH).
  • The network disconnection mechanisms underlying PSCI are not fully understood.

Purpose of the Study:

  • To map functional and structural network disconnections in PSCI.
  • To examine the mediating role of WMH in the relationship between lesions and cognitive status.
  • To identify potential neuromodulation targets for PSCI.

Main Methods:

  • Connectome-based lesion-symptom mapping (CLSM) was used in 376 acute ischemic stroke patients.
  • Disconnection maps were generated from infarct and WMH lesions.
  • Regression and mediation models analyzed cognitive relationships and WMH effects. Validation was done in 78 cerebral small vessel disease patients.

Main Results:

  • Infarcts and WMH create coherent network disconnection patterns, most affecting attention and processing speed (APS).
  • Lesion impact scores predicted 3-month cognitive outcomes better than volumetric measures.
  • WMH significantly mediated the link between infarcts and PSCI/APS deficits.

Conclusions:

  • A network-level framework for PSCI is established.
  • Acute (infarcts) and chronic (WMH) vascular lesions play distinct but synergistic roles.
  • The left temporo-parieto-occipital junction is a potential neuromodulation target.