A neurocognitive account of attentional control theory: how does trait anxiety affect the brain's attentional networks?

Eysenck, Michael W · 2022 · Taylor and Francis

DOI: 10.1080/02699931.2022.2159936

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Summary

This review paper provides a neurocognitive account of Attentional Control Theory (ACT), aiming to explain how trait anxiety affects the brain’s attentional networks. ACT posits that high trait anxiety impairs processing efficiency through inefficient executive processes, even if performance effectiveness is maintained via compensatory strategies. The authors integrate ACT with recent neuroimaging evidence to map these cognitive processes onto specific neural mechanisms, focusing on the interactions between the fronto-parietal network (FPN), the cingular-opercula network (CON), and the default mode network (DMN). This synthesis seeks to clarify the neural substrates of anxiety-induced cognitive deficits and identify potential targets for neurocognitive interventions. The authors analyze existing empirical data from functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) studies to test ACT’s predictions within this network framework. They examine how trait anxiety perturbs the normative anti-correlation between the DMN, associated with worry and mind-wandering, and the FPN, responsible for goal-directed attention. The review also investigates the role of the CON, particularly the dorsal anterior cingulate cortex (dACC), in mediating compensatory control and error monitoring when goal-directed processes fail. Specific evidence includes ERP components like the N2 and Error-Related Negativity (ERN), as well as fMRI measures of activation and connectivity in the dorsolateral prefrontal cortex (DLPFC) and ACC during tasks requiring inhibition, shifting, and updating. The findings indicate that trait anxiety increases susceptibility to distraction, evidenced by enhanced N2pc components in high-anxious individuals, reflecting misallocated attention to distractors. This is linked to increased or poorly deactivated DMN activity, which disrupts efficient switching to the FPN. Consequently, high-anxious individuals exhibit impaired goal-directed control, often showing reduced sustained FPN activation. To maintain performance, they rely on compensatory mechanisms mediated by the CON. This is demonstrated by greater dACC activity during conflict tasks, larger ERN amplitudes, and increased frontal effort markers like the Contingent Negative Variation. However, functional connectivity between the dACC and DLPFC is often reduced in anxious individuals, suggesting disrupted communication between conflict detection and control implementation hubs. The significance of this work lies in refining ACT by defining processing efficiency in terms of optimal, task-dependent interactions between the FPN, CON, and DMN, rather than isolated regional activation. The authors conclude that anxiety competes for limited resources, perturbing network dynamics and forcing reliance on inefficient compensatory control. This neurofunctional model offers a more holistic evidential basis for evaluating anxiety theories and suggests that interventions targeting these specific network interactions could improve processing efficiency in anxious individuals.

Key finding

Trait anxiety impairs processing efficiency by perturbing the anti-correlation between the fronto-parietal and default mode networks, necessitating increased compensatory activity in the cingular-opercula network to maintain task performance.

Methodology

review

Provenance

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StageOutcomeToolModelPromptAttemptsCompleted
discover success 1 2026-05-06
archive success core_acuk 7 2026-06-02
extract success cached 2 2026-06-10
clean success 1 2026-06-01
chunk success 1 2026-06-01
embed success 1 2026-06-02
enrich success 1 2026-05-06
promote success 2 2026-06-06
summarize success llm qwen3.6-27b-prismaquant summ-v5 3 2026-06-10
tag success vector_similarity 23 2026-06-11
verify success 2 2026-06-10

Summary generated by qwen3.6-27b-prismaquant on 2026-06-10; verification: verified.

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