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Neuroplasticity Following Stroke from a Functional Laterality Perspective: A fNIRS Study.
Ying Song1, ZhiFang Sun1, WeiZhen Sun1
1Rehabilitation Center, Qilu Hospital of Shandong University, No. 107 Wenhua West Road, Lixia District, Jinan, 250012, Shandong, China.
Stroke-induced hemiplegia disrupts the brain's typical hemispheric dominance in motor control. Neuroplasticity in right-hemiplegia patients may compensate for motor deficits by strengthening sensorimotor cortex connectivity.
Area of Science:
- Neuroscience
- Neurology
- Biomedical Engineering
Background:
- Resting-state functional connectivity (rsFC) alterations in sensorimotor cortex are key to understanding stroke recovery.
- Hemiplegia, resulting from stroke, affects motor function and brain lateralization.
- Neuroplasticity plays a crucial role in the brain's adaptation to injury.
Purpose of the Study:
- To investigate changes in rsFC within the sensorimotor cortex of patients with left or right hemiplegia.
- To explore the role of lateralization and neuroplasticity in post-stroke motor recovery.
- To identify potential biomarkers for motor function impairment and recovery.
Main Methods:
- Utilized resting-state functional near-infrared spectroscopy (fNIRS) on 73 participants (26 left hemiplegia, 21 right hemiplegia, 26 controls).
- Employed whole-brain analysis with Pearson correlation for rsFC calculations.
- Correlated rsFC findings with motor function assessments.
Main Results:
- Normal controls exhibit stronger left-hemisphere motor component rsFC, a pattern absent in stroke groups.
- Right-hemiplegia patients showed increased rsFC between left S1 and M1 compared to controls, inversely correlating with motor function.
- rsFC within the ipsilesional M1 negatively correlated with motor function in both hemiplegia groups.
- rsFC within the contralesional M1 was weakened in stroke patients compared to controls.
Conclusions:
- Stroke-induced hemiplegia disrupts sensorimotor cortex lateralization.
- Strengthened rsFC in right-hemiplegia may represent a compensatory mechanism for motor impairment.
- Findings have implications for brain-computer interfaces and neuromodulation therapies to enhance cortical plasticity and motor function.
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