Abstract
<p>Background Pain catastrophizing is a cognitive–affective trait associated with heightened pain experience. Within the fear-avoidance model, it promotes fear, hypervigilance, and avoidance. Although neuroimaging studies have implicated sensory–affective and default mode networks in catastrophizing, existing evidence is limited by heterogeneity across clinical pain populations, making it difficult to isolate the intrinsic neural correlates of catastrophizing as a trait.Methods Sixty healthy adults underwent resting-state fMRI during capsaicin-induced sustained pain. Seed-to-voxel functional connectivity was analyzed using four seeds: primary somatosensory cortex (S1), secondary somatosensory cortex (S2), posterior insula, and posterior cingulate cortex (PCC). Group-level effects of the Pain Catastrophizing Scale (PCS) and its interaction with subjective pain intensity on whole-brain connectivity were examined using voxel-wise multiple regression.Results Higher PCS was associated with increased S2–anterior cingulate cortex/medial prefrontal cortex (ACC/mPFC) connectivity and reduced PCC–visual association cortex (BA19) connectivity. A significant PCS × pain intensity interaction emerged in PCC–supplementary motor area (SMA) connectivity, with reduced coupling at higher pain intensity in high catastrophizers but increased coupling in low catastrophizers.Conclusions Our findings indicate that pain catastrophizing is not a unitary affective amplification but rather a multidimensional cognitive–affective configuration distributed across multiple intrinsic networks, corresponding to three functional levels: sensory–affective appraisal, self-referential processing, and context-dependent behavioral regulation. By isolating these patterns from the qualitative heterogeneity of prior clinical pain samples, our findings delineate a neural configuration more likely to reflect trait-like features of catastrophizing itself rather than confounds of specific pain conditions. Significance Statement To clarify the intrinsic neural mechanisms of pain catastrophizing in a controlled experimental setting, we examined resting-state functional connectivity in healthy individuals under a standardized pain model. The analysis revealed three connectivity pathways: increased S2–ACC/mPFC coupling, reduced PCC–visual association cortex coupling, and a pain-dependent reversal of PCC–SMA coupling between high and low catastrophizers. These pathways converge onto the core components of the fear-avoidance model, offering neural correlates for a framework previously characterized at the cognitive–behavioral level.</p>