Right Hemispheric Broca's Homologue Mediates Pain-Depression Loop: fNIRS Evidence of Language Network Remodeling in Comorbid Chronic Pain and Depression

Background Chronic somatic pain (CSP) modulates the neuropathological mechanisms of depression, but how it reshapes neural circuits remains unclear. This study investigated CSP-specific prefrontal dynamic changes and their mediating role in pain-depression comorbidity. Methods 129 participants were recruited (43 each in Major Depressive Disorder with Chronic Somatic Pain group (MDD + CSP), MDD without Chronic Somatic Pain group (MDD-CSP), and Healthy Control group (HC)). Hemodynamic responses during a Verbal Fluency Task (VFT) and resting state were measured using functional near-infrared spectroscopy (fNIRS). Intergroup comparisons (Kruskal-Wallis/Mann-Whitney U tests), mediation analysis (FDR-corrected), and Spearman correlation analysis were used to dissect interactions between neural and clinical indices. Results 1. Frontopolar (FP) Functional Abnormalities: Task-state hypofunction: Bilateral FP activation was reduced in all MDD groups (Channels Ch16/22/23/35/36, χ² >7.287, p < 0.002). Resting-state hyperfunction: Right FP (Ch35/36) activation was higher in MDD + CSP than HC (p < 0.012). 2. CSP-Specific Language Network Suppression: Compared to MDD-CSP, MDD + CSP showed reduced activation in the right hemispheric Broca's homologue (RH-Broca, Ch51, U = 577.5). Visual Analog Scale (VAS) scores negatively correlated with suppression in Broca's area/RH-Broca (Ch2/49/50/51/53, ρ < -0.5, p < 0.001). 3. Bidirectional Mediation Effect: RH-Broca (Ch53) mediated both the VAS→SDS path (β = 1.17, 95% CI: 0.66–1.71) and SDS→VAS path (β = 0.13, 95% CI: 0.08–0.18). 4. Brain Network Reorganization: During task, MDD groups showed increased Connection Density (CP, χ²=12.268) and Local Efficiency (Gamma, χ²=9.314). During rest, higher Small-Worldness (Sigma, U = 633) in MDD-CSP predicted treatment resistance. Conclusion CSP exacerbates depression via: ① Selective suppression of the language network (Broca's area/RH-Broca), ② Establishing a bidirectional pain-depression loop via RH-Broca (Ch53), and ③ Driving maladaptive neuroplasticity in prefrontal networks. RH-Broca activation is a potential biomarker for neuromodulation therapy in comorbid depression.