Cognitive processes in goal-directed attentional system dysfunction of generalized anxiety disorder

Background Attentional control theory proposes that anxiety impairs the goal-directed attentional system, which has been well-documented in subclinical populations. However, the underlying cognitive mechanisms of generalized anxiety disorder (GAD) remain poorly understood. A thorough investigation of the goal-directed attentional system in GAD may clarify its etiological and pathophysiological roles and offer insights for developing targeted interventions. Method This study investigated two key subcomponents of the goal-directed attentional system in GAD: inhibition and shifting functions. Twenty-four GAD patients and twenty-eight healthy controls (HC) were recruited and completed the Attentional Control Scale. Behavioral performance and 64-channel EEG data were collected during the Go/No-Go and more-odd shifting tasks. Results Self-reported questionnaire and behavioral performance indicated that GAD patients had significantly lower total and subscale scores ( p  < 0.001) and higher inverse efficiency ( p  < 0.01), reflecting subjective attentional control deficits and reduced processing efficiency. EEG results revealed reduced NoGo-N2 ( p  < 0.01) and NoGo-P3 ( p  < 0.001) peak amplitudes in GAD, indicating impaired subprocesses of response inhibition. Furthermore, GAD patients exhibited decreased theta power ( p  < 0.05) and theta-phase/gamma-amplitude coupling (TGC, p  < 0.05) during the more-odd shifting task, suggesting deficits in attentional processing and impaired neural communication related to cognitive flexibility. HAMA scores were significantly correlated with behavioral performance, NoGo-N2 and NoGo-P3 amplitudes in the Go/No-Go task, and TGC in the more-odd shifting task (all p  < 0.01). These results suggest that higher levels of anxiety are associated with deficits in inhibitory control, cognitive resources, and neural oscillatory dysfunction. Conclusion These findings provide neurophysiological insights into attentional deficits in GAD, highlighting impairments in inhibitory control and cognitive flexibility. Understanding these deficits can offer guidance for developing targeted interventions to enhance cognitive control in GAD. Trial registration: The trial is registered on ClinicalTrials.gov (ChiCTR2400079676, January 9, 2024).