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Exploring the correlation between frequency-dependent brain activity and cognitive function in social anxiety
Junbing He1, Nadire Aximu2, Tokiko Yoshida3
1Research Center for Child Mental Development, Chiba University, Chiba, Japan; United Graduate School of Child Development, Osaka University, Suita, Japan.
Background:
Social anxiety disorder (SAD) is a prevalent psychiatric disorder, yet its underlying neural mechanisms remain unclear. Patients with SAD often show cognitive impairments associated with brain dysfunction. However, no study has examined the relationship between frequency-dependent brain activity and cognitive performance in SAD using resting-state functional magnetic resonance imaging (rs-fMRI) and neuropsychological assessments. In this study, we examined this association in patients with SAD using rs-fMRI.
Methods:
rs-fMRI data were collected from 27 patients with SAD and 40 healthy controls (HCs). Frequency-dependent alterations in fractional amplitude of low-frequency fluctuations (fALFF) were examined across typical (0.01-0.08 Hz), slow-5 (0.01-0.027 Hz), and slow-4 (0.027-0.073 Hz) bands to identify regions with abnormal spontaneous brain activity. Cognitive function was assessed using the Cambridge Neuropsychological Test Automated Battery. Correlations among abnormal brain activity, clinical symptoms, and cognitive functions were analyzed.
Results:
Compared with HCs, patients with SAD showed lower mean fALFF (mfALFF) in the bilateral postcentral gyrus across the typical and slow-5 bands, but only in the left postcentral gyrus for the slow-4 band. While mfALFF was not significantly associated with clinical symptom severity, significant correlations were observed between mfALFF and cognitive functioning.
Conclusions:
Our findings indicate that cognitive function in patients with SAD is associated with frequency-dependent abnormalities in spontaneous brain activity, particularly reduced mfALFF in the postcentral gyrus. Additionally, frequency-dependent neural markers may help identify and target cognitive dysfunction in SAD, with abnormal postcentral gyrus activity potentially contributing to understanding of its underlying neural mechanisms.
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