Abstract
Purpose: Anxiety disorders are a major global issue. Diagnosis via symptoms, not biological causes, delivers poor treatment outcomes. Our frontal EEG biomarker, Goal Conflict Specific Rhythmicity (GCSR; 4-12 Hz), developed from our long-standing detailed neuropsychological theory of anxiety processes, is reduced by all chemical types of selective anxiolytic and is high in cases across a range of currently diagnosed anxiety disorders.
Methods: We assessed frontal sources of GCSR, recording scalp EEG at either low resolution (Experiment 1, 32 channels, University of Otago, ♀:33, ♂:16) or high resolution (Experiment 2, 128 channels, University of Auckland, ♀:10, ♂:8) in healthy participants performing a Stop Signal Task to generate GCSR as previously.
Principal results: sLORETA demonstrated GCSR sources consistently in the right inferior frontal gyrus and, more strongly but less consistently, medial frontal gyrus. Variation was consistent with that of stopping in the same Stop Signal Task, depending on task demands.
Major conclusions: The sources of GCSR are consistent with our theory that hippocampal output receives goal information, detects conflict, and returns a negative biasing signal to the areas encoding goals in the current task. They match the variation in the control of stopping when response urgency changes. GCSR appears to index a biological type of anxiety unlike any current diagnosis and should help improve accuracy of diagnosis - anchored to actions of selective anxiolytic drugs. This task-related frontal "theta" rhythmicity provides proof-of-concept for further development of our theory of the neuropsychology of anxiety in direct human tests.