Pain Catastrophising Amplifies Parietal Responses to Painful Laser Stimulation in Healthy Controls.

Background: Pain catastrophising is a maladaptive cognitive-emotional trait linked to greater pain severity and poorer outcomes, yet its neurophysiological correlates remain unclear.

Objectives: We tested whether pain catastrophising amplifies cortical responses to nociceptive input, independent of subjective pain intensity.

Methods: Fifty-two healthy adults underwent EEG during painful laser stimulation (n = 29; mean age 24.3 ± 10.9 years; 55.2% female) or non-painful electrical stimulation (n = 23; mean age 23.3 ± 8.5 years; 56.5% female). Each trial comprised a triplet of stimuli (S1, S2, S3) with a 1.5-s interstimulus interval; 30 triplets were delivered per modality. Associations between Pain Catastrophising Scale (PCS) scores and amplitudes of laser-evoked potentials (LEP-N2P2) and somatosensory-evoked potentials (SEP-N1P2) were tested using mixed-effects models, with trial-level pain ratings as a covariate.

Results: Higher PCS scores were associated with greater LEP-N2P2 amplitude for the first stimulus (S1) in the painful condition, independent of pain ratings, at the parietal midline electrode (Pz). No associations were observed between PCS and SEP-N1P2 in the non-painful condition, or between PCS and early N1 components of LEP or SEP.

Conclusions: Pain catastrophising selectively amplifies later-stage cortical responses to painful stimuli, strongest at first presentation (S1) and localised to parietal Pz channel, with no effects in non-painful controls stimulation modality. These findings support LEPs as mechanistic biomarkers of catastrophising-related vulnerability. Combined with psychological assessment, such markers could improve early screening, risk stratification, and personalised interventions targeting maladaptive salience and attentional processes in pain.

Significance Statement: Pain catastrophising was associated with amplified laser-evoked potential (LEP-N2P2) responses during painful, but not non-painful, stimulation in healthy adults. The effect was localised to the parietal midline, strongest for the first stimulus in a sequence, and diminished with repetition. These findings suggest modality-dependent cortical modulation and highlight LEP-N2P2 as a potential neural marker of maladaptive pain processing.