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Anxiety Alters Neural Pathways for Emotional Control, Highlighting Compensatory Mechanisms
Anxious individuals rely less on the dorsolateral prefrontal cortex (FPl) for controlling emotional actions, according to a recent study published in Nature Communications. The study compared a high-anxiety group (n=52) with a non-anxious control group (n=41) to assess emotional action control.
“This study uses neurochemical, structural, and functional measures to characterize neural circuits supporting control of emotional action tendencies in individuals with high anxiety,” authors said in the study.
Participants engaged in a social approach-avoidance task, pulling, or pushing a joystick to approach or avoid happy and angry faces. Behavioral analysis revealed that both groups exhibited similar congruency effects, with no significant group differences in controlling automatic emotional action tendencies. However, functional MRI scans showed that while both groups activated FPl during emotion control, the high-anxiety group did not exhibit the same neural congruency effect in FPl. Bayesian analysis confirmed that the absence of this effect in the high-anxiety group was statistically significant.
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To investigate FPl excitability, authors used magnetic resonance spectroscopy (MRS) and structural connectivity via diffusion-weighted imaging (DWI). High-anxiety participants displayed higher FPl excitability and stronger amygdalofugal projections to FPl compared to non-anxious individuals. Notably, in the high-anxiety group, amygdalofugal-FPl connectivity was not linked to behavioral congruency, suggesting a distinct neural mechanism for emotion control in these individuals.
The results imply that anxious individuals might rely more on compensatory mechanisms involving other prefrontal regions like the dorsolateral prefrontal cortex.
“We provide evidence for a functional anatomical shift in the implementation of emotional control in anxious individuals, from FPl to [dorsolateral prefrontal cortex] (dlPFC). This functional anatomical shift is linked to changes in the strength of amygdalofugal projections to FPl and complemented by FPl overexcitability,” authors concluded. “This shift might explain why highly anxious individuals struggle to implement flexible emotional action selection during challenging emotional situations, and it suggests interventions to normalize FPl activity in anxiety disorders.”
Further research is needed to better understand the underlying mechanisms and potential therapeutic applications of these findings, authors noted.
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