ArticleFrontiers in psychiatry2026
Neurophysiological mechanisms underlying interoceptive hypersensitivity in somatic symptom disorder: a mediation analysis of alexithymia.
Article in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Background: 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. Methods: 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. Results: 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. Conclusion: 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.