Yuna Jang, EKyong Yoon, Arum Hong, Hye Youn Park
SSD involves a multilayered neurobiological architecture, where persistent network-level limitations coexist with longitudinal subcortical and cortical changes. While broader functional deficits endure, clinical recovery is accompanied by longitudinal thalamic changes and is more directly associated with localized sensorimotor reorganization. These findings suggest that addressing both persistent network differences and longitudinal recovery-related changes is essential for effective SSD management.
AIM: Somatic symptom disorder (SSD) is a functional disorder characterized by dysregulated neural processing of bodily signals. However, the neural mechanisms underlying recovery versus chronicity in SSD remain unclear. We investigated hierarchical neurophysiological features associated with symptom persistence and improvement using longitudinal source-localized electroencephalography (EEG).
METHODS: Resting-state EEG was analyzed in 83 patients with SSD and 80 matched healthy controls, with 76 participants completing a 6-month follow-up. We examined longitudinal changes in source-localized spectral power and network efficiency in relation to somatic and affective symptom trajectories.
RESULTS: Patients showed a significant reduction in somatic symptoms (P < 0.001) over time. SSD featured a persistent deficit in Gamma-band global efficiency (P = 0.035) that remained lower than healthy levels (P = 0.972 for interaction), representing residual neurobiological vulnerability. Conversely, thalamic spectral power exhibited significant group × time interactions (P < 0.05), reflecting longitudinal subcortical changes. Symptomatic relief was specifically associated with nodal efficiency reorganization within the left central sensorimotor region (Beta band, r = -0.54, P < 0.001). These associations remained robust after controlling for depression and anxiety, with mediation analyses indicating that these associations were largely independent of affective fluctuations.
CONCLUSIONS: SSD involves a multilayered neurobiological architecture, where persistent network-level limitations coexist with longitudinal subcortical and cortical changes. While broader functional deficits endure, clinical recovery is accompanied by longitudinal thalamic changes and is more directly associated with localized sensorimotor reorganization. These findings suggest that addressing both persistent network differences and longitudinal recovery-related changes is essential for effective SSD management.