Toward a mechanistic understanding of the role of error monitoring and memory in social anxiety.

Cognitive models state that social anxiety (SA) involves biased cognitive processing that impacts what is learned and remembered within social situations, leading to the maintenance of SA. Neuroscience work links SA to enhanced error monitoring, reflected in error-related neural responses arising from mediofrontal cortex (MFC). Yet, the role of error monitoring in SA remains unclear, as it is unknown whether error monitoring can drive changes in memory, biasing what is learned or remembered about social situations. Motivated by the longer-term goal of identifying mechanisms implicated in SA, in the current study we developed and validated a novel paradigm for probing the role of error-related MFC theta oscillations (associated with error monitoring) and incidental memory biases in SA. Electroencephalography (EEG) data were collected while participants completed a novel Face-Flanker task, involving presentation of task-unrelated, trial-unique faces behind target/flanker arrows on each trial. A subsequent incidental memory assessment evaluated memory biases for error events. Severity of SA symptoms were associated with greater error-related theta synchrony over MFC, as well as between MFC and sensory cortex. Social anxiety also was positively associated with incidental memory biases for error events. Moreover, greater error-related MFC-sensory theta synchrony during the Face-Flanker predicted subsequent incidental memory biases for error events. Collectively, the results demonstrate the potential of a novel paradigm to elucidate mechanisms underlying relations between error monitoring and SA.

Towards a mechanistic understanding of the role of error monitoring and memory in social anxiety.

Cognitive models state social anxiety (SA) involves biased cognitive processing that impacts what is learned and remembered within social situations, leading to the maintenance of SA. Neuroscience work links SA to enhanced error monitoring, reflected in error-related neural responses arising from mediofrontal cortex (MFC). Yet, the role of error monitoring in SA remains unclear, as it is unknown whether error monitoring can drive changes in memory, biasing what is learned or remembered about social situations. Thus, we developed a novel paradigm to investigate the role of error-related MFC theta oscillations (associated with error monitoring) and memory biases in SA. EEG was collected while participants completed a novel Face-Flanker task, involving presentation of task-unrelated, trial-unique faces behind target/flanker arrows on each trial. A subsequent incidental memory assessment evaluated memory biases for error events. Severity of SA symptoms were associated with greater error-related theta synchrony over MFC, as well as between MFC and sensory cortex. SA was positively associated with memory biases for error events. Consistent with a mechanistic role in biased cognitive processing, greater error-related MFC-sensory theta synchrony during the Face-Flanker predicted subsequent memory biases for error events. Our findings suggest high SA individuals exhibit memory biases for error events, and that this behavioral phenomenon may be driven by error-related MFC-sensory theta synchrony associated with error monitoring. Moreover, results demonstrate the potential of a novel paradigm to elucidate mechanisms underlying relations between error monitoring and SA.

Effects of olfactory training on resting­state effective connectivity in patients with posttraumatic olfactory dysfunction.

The present study investigated if and how the smell training scheme affects resting­state effective connectivity. We focused on connectivity among brain regions that participate in olfactory­related processes, including the piriform cortex, amygdala, orbitofrontal cortex (OFC), insula, and cingulate cortex. Sixteen patients with posttraumatic olfactory dysfunctions between the ages of 18 and 36 years participated in this study. Olfactory performance of subjects was evaluated using the Sniffin' Sticks test kit and then, resting­state functional magnetic resonance imaging (fMRI) was performed. Of the 16 participants, 8 underwent olfactory training for 16 weeks and the remaining 8 did not receive the treatment (the control group). After 16 weeks, participants in both groups underwent the same procedure (smell testing and the MRI examination). Olfactory performance scores were compared between groups using an independent samples t­test. Spectral dynamic causal modeling was applied to resting­state fMRI data to identify alterations in effective connectivity due to the smell training. We found that patients in the treatment group improved in the odor discrimination task and overall olfactory function as compared to the control group. Compared to the control group, patients in the treatment group had increased self­inhibitory connectivity of the OFC and increased excitatory connectivity from the cingulate cortex to the insula. Moreover, the excitatory connectivity from the OFC to the cingulate cortex was found to be weaker following the olfactory training scheme. This study shows that a smell training scheme can cause changes in resting­state effective connectivity parameters that can be attributed to improvements in the odor discrimination task.