Altered brain-behavior coupling during inhibitory control in ankylosing spondylitis: ERP evidence from NoGo-P3
Lei Zhang1,2, Fang Lu3, Yuxin He4
1Department of Rheumatology and Immunology, Jinling, Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Ankylosing Spondylitis patients show altered brain-behavior coupling during inhibitory tasks, suggesting increased effortful neural recruitment. This may serve as an electrophysiological marker for executive dysfunction in Ankylosing Spondylitis.
Area of Science:
- Neuroscience
- Cognitive Psychology
- Rheumatology
Background:
- Cognitive dysfunction is increasingly recognized in Ankylosing Spondylitis (AS).
- Neural mechanisms of inhibitory control in AS are not well understood.
- Altered cognitive function in AS may involve task-dependent brain-behavior coupling.
Purpose of the Study:
- To investigate executive control in AS using a Go/NoGo task.
- To examine brain-behavior coupling during inhibitory processing in AS patients.
- To identify potential electrophysiological markers of altered executive function in AS.
Main Methods:
- 16 male AS patients and 23 healthy controls performed a Go/NoGo task with 32-channel EEG.
- Event-related potential (ERP) analysis focused on N2 and NoGo-P3 components.
- Linear regression models tested ERP × Group interactions for brain-behavior coupling; theta-band power was also analyzed.
Main Results:
- AS patients exhibited lower Go accuracy and longer Go reaction times.
- In AS patients, NoGo accuracy positively correlated with NoGo-P3 amplitude (FCz, Cz).
- A significant ERP × Group interaction for NoGo-P3 at FCz indicated differing brain-behavior coupling between groups; enhanced theta power was observed in AS during NoGo processing.
Conclusions:
- Findings suggest altered brain-behavior coupling during inhibitory control in AS, particularly the NoGo-P3 component.
- This pattern indicates greater reliance on effortful neural recruitment for successful inhibition in AS.
- Altered executive processing in AS may be identifiable via electrophysiological markers.
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