Anxious/depressed individuals exhibit disrupted frontotemporal synchrony during cognitive conflict encoding.

Anxiety and depressive disorders are associated with cognitive control deficits, yet their underlying neural mechanisms remain poorly understood. Here, we used high-resolution stereotactic EEG (sEEG) to determine how anxiety and/or depression modulates neural and behavioral responses when cognitive control is engaged in individuals with medically refractory epilepsy undergoing sEEG monitoring for surgical evaluation. We analyzed sEEG data recorded from frontotemporal regions of 29 participants (age range: 19-55, mean age: 35.5, female: 16/29) while they performed a Multi-Source Interference Task (MSIT) designed to elicit cognitive conflict. Neurobehavioral interviews, symptom rating scales, and clinical documentation were used to categorize participants as demonstrating anxiety and/or depression symptoms (A/D, n=13) or as epilepsy controls (EC, n=16). Generalized linear mixed-effects (GLME) models were used to analyze behavioral and neural data. Models of oscillatory power were used to identify brain regions within conflict-encoding networks in which coherence and phase locking values (PLV) were examined in A/D and EC. A/D participants demonstrated a greater conflict effect (response time slowing with higher cognitive load), without impairment in response time (RT) or accuracy compared to EC. A/D participants also showed significantly enhanced conflict-evoked theta (4-8Hz) and alpha (8-15Hz) power in the dorsolateral prefrontal cortex (dlPFC) and amygdala as well as widespread broadband activity in the lateral temporal lobe (LTL) compared to EC. Additionally, theta coherence and PLV between dlPFC-LTL and dlPFC-amygdala were reduced by conflict in A/D. Our findings suggest individuals with anxiety/depression symptoms exhibit heightened frontotemporal oscillatory activity and disrupted frontotemporal synchrony during cognitive conflict encoding, which may indicate a greater need for cognitive resources due to ineffective cognitive processing. These results highlight a potential role of frontotemporal circuits in conflict encoding that are altered in anxiety/depression, and may further inform future therapeutic interventions aimed at enhancing cognitive control in these populations.