Neurophysiological mechanisms underlying interoceptive hypersensitivity in somatic symptom disorder: a mediation...

Somatic Symptom Disorder (SSD) is defined by distressing physical symptoms and exaggerated psychological responses, and interoceptive hypersensitivity is widely regarded as a central feature, but the neuro-psychological pathway from neural interoceptive processing to clinical symptoms is not well elucidated. Hence, the present study sought to investigate the neurophysiological basis of interoceptive hypersensitivity in SSD and the mediating role of alexithymia.

Fifty-two medication-naive patients with SSD and 52 age- and sex-matched healthy controls (HC) underwent clinical assessment with PHQ-15 and TAS-20, as well as high-resolution EEG recording, and interoceptive hypersensitivity was quantified via heartbeat-evoked potential (HEP) amplitudes obtained during a heartbeat tracking task and resting-state Phase Lag Index (PLI). A structural equation model (SEM) was then used to formally test the proposed parallel multiple mediation pathway.

SSD patients exhibited significantly higher somatic distress, alexithymia, and interoceptive accuracy compared to HCs (p< 0.001). Neurophysiologically, the SSD group demonstrated significantly increased resting-state PLI and higher HEP amplitudes (2.20 ± 1.10 vs. 1.20 ± 0.80 μV, p< 0.001), presenting a robust and clinically realistic effect size (Cohen's d = 1.04). Mediation analysis confirmed that alexithymia significantly and specifically mediated the relationship between HEP amplitude and somatic symptom severity (specific indirect effect = 0.820, p = 0.025). A combined diagnostic model using HEP and TAS-20 scores achieved an Area Under the Curve (AUC) of 0.866.

SSD is characterized by amplified cortical processing within the interoceptive network, and this neural hypersensitivity to visceral signals is strongly associated with clinical somatic distress, a process partially mediated by impaired emotional identification. Therefore, HEP amplitude and alexithymia are exploratory candidate indicators that directly support the use of neurophysiological and emotional regulation interventions in the treatment of SSD.