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Reward Decision Network Disconnection in Poststroke Apathy: A Prospective Multimodality Imaging Study.

Yirong Fang1, Xian Chao1, Jinjing Wang1

  • 1Department of Neurology, Centre for Leading Medicine and Advanced Technologies of IHM, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.

Human Brain Mapping
|January 21, 2025
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Summary

Post-stroke apathy (PSA) has distinct subtypes linked to reward decision network (RDN) damage. Specific white matter disconnections in the RDN predict apathy biotypes, highlighting RDN

Keywords:
apathydiffusion tensor imagingneuroimagingresting‐state fMRIreward decision networkstrokewhite matter disconnection

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Area of Science:

  • Neuroscience
  • Neurology
  • Psychiatry

Background:

  • Apathy is a common neuropsychiatric symptom after stroke, affecting goal-directed behavior.
  • The reward decision network (RDN) is implicated in apathy, but its dysfunction in post-stroke apathy (PSA) is not fully understood due to heterogeneity and confounding factors.
  • Understanding PSA heterogeneity and its link to RDN damage is crucial for targeted interventions.

Purpose of the Study:

  • To dissect the heterogeneity of post-stroke apathy (PSA) by identifying distinct patient biotypes.
  • To explore the relationship between lesion-induced damage to the reward decision network (RDN) and PSA.
  • To investigate the predictive power of RDN-specific white matter (WM) disconnections on PSA biotypes.

Main Methods:

  • Prospective recruitment of 207 acute ischemic stroke patients and 60 healthy controls.
  • Neuroimaging and longitudinal neuropsychiatric assessments.
  • Multivariate analysis and clustering to define PSA biotypes based on functional connectivity and clinical data.
  • Lesion embedding into a connectome atlas to generate WM disconnection maps and quantify regional damage.
  • XGBoost modeling to predict PSA biotypes using RDN-specific versus whole-brain WM disconnection scores.

Main Results:

  • Four distinct PSA biotypes were identified: persistent apathy with depression (Biotype 4), persistent apathy (Biotype 2), non-apathetic (Biotype 3), and delayed-onset apathy (Biotype 1).
  • RDN-specific WM disconnection models significantly outperformed whole-brain models in predicting PSA biotypes (p < 0.001).
  • Specific WM disconnection patterns were associated with biotypes: extensive RDN damage in Biotype 4, anterior cingulate cortex damage in Biotype 1, and orbitofrontal cortex damage in Biotype 2.

Conclusions:

  • PSA exhibits significant heterogeneity with distinct clinical and neurobiological underpinnings.
  • RDN damage, particularly white matter disconnections in specific regions like the anterior cingulate cortex and orbitofrontal cortex, is a critical factor in PSA variability and onset.
  • Apathy pathogenesis involves distinct mechanisms and shares neurobiological substrates with depression.