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Cortical network characteristics in post-stroke anxiety: an fNIRS-based study
Xue Qian1,2, Qinglei Wang3, Jie Wang1,2
1Changzhou Dean Hospital, Changzhou, Jiangsu, China.
Frontiers in Neuroscience
|February 2, 2026
Summary
Post-stroke anxiety (PSA) is linked to reduced prefrontal cortex activation during cognitive tasks. Comorbid depression further alters activation in these brain regions, suggesting potential therapeutic targets.
Area of Science:
- Neuroscience
- Clinical Neurology
- Psychiatry
Background:
- Post-stroke anxiety (PSA) is a common complication affecting patient recovery.
- The neural mechanisms underlying PSA remain incompletely understood.
- Prefrontal cortex dysfunction is implicated in various neuropsychiatric disorders.
Purpose of the Study:
- To investigate prefrontal hemodynamic activity in patients with PSA at rest and during cognitive tasks.
- To identify neural correlates of PSA for potential clinical applications.
- To explore the influence of comorbid depression on neural alterations in PSA.
Main Methods:
- Functional near-infrared spectroscopy (fNIRS) was used to measure brain activity.
- Fifty patients with PSA and 45 controls were recruited.
- Participants underwent resting-state and verbal fluency task (VFT) assessments.
Main Results:
- Patients with PSA showed significantly reduced bilateral frontopolar cortex (FPC) activation during the VFT compared to controls.
- Comorbid depression in PSA patients was associated with further reduced activation in the bilateral FPC and left dorsolateral prefrontal cortex (DLPFC).
- No significant differences in resting-state functional connectivity were found between groups.
Conclusions:
- Reduced bilateral FPC activation may be a key neural substrate for PSA.
- Altered FPC and DLPFC activation patterns in PSA patients with depression may indicate neural correlates of depressive symptoms.
- These findings offer potential targets for future research and clinical interventions in PSA.
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