ArticleBMC psychiatry2026
Right broca homologue mediates the pain-depression circuit: a case-control Functional Near-Infrared Spectroscopy (fNIRS) study on language network remodeling in chronic pain-depression comorbidity.
Article in BMC 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.
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Abstract
backgroundChronic somatic pain (CSP) and major depressive disorder (MDD) frequently co-occur and are associated with poor prognosis. However, the neural circuit mechanisms underlying the modulation of MDD pathology by CSP remain unclear.
methodsThis case-control study included 129 participants who underwent fNIRS during a verbal fluency task (VFT) and at rest. Participants were divided into three groups (n = 43 each): MDD patients with comorbid CSP (MDD + CSP), MDD patients without CSP (MDD-CSP), and healthy controls (HC). This study aimed to identify CSP-specific neural signatures and examine their mediating role between pain and depression.
resultsCompared with HC, all MDD patients exhibited reduced activation in the bilateral frontopolar cortex during the task. A key finding was that, relative to both HC and the MDD-only group, the comorbid group showed selectively lower activation in the right-hemispheric Broca's homologue (RH-Broca) (p = 0.003). Pain intensity was negatively correlated with RH-Broca activation (p < 0.001). Mediation analysis revealed a bidirectional mediating effect of RH-Broca activation on the pain-depression relationship: it mediated both the pathway from pain to depression (indirect effect β = 1.17, 95% CI: 0.66-1.71) and the pathway from depression to pain (indirect effect β = 0.13, 95% CI: 0.08-0.18). At rest, the comorbid group displayed hyperactivation in the right frontopolar cortex, whereas the MDD-only group showed alterations in small-world network properties.
conclusionSelective hypoactivation in the right-hemispheric language network, particularly in the RH-Broca, is closely associated with the comorbidity of chronic somatic pain and major depressive disorder and may contribute to their mutual exacerbation. These findings support the view that the RH-Broca serves as a putative neural node connecting pain and depressive symptoms, potentially forming a bidirectional loop in comorbid patients. This neural circuit may represent a promising target for neuromodulation therapy in patients with MDD comorbid with CSP.
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