TY - JOUR PY - 2022// TI - Augmented pain inhibition and higher integration of pain modulatory brain networks in women with self-injury behavior JO - Molecular psychiatry A1 - Lalouni, Maria A1 - Fust, Jens A1 - Bjureberg, Johan A1 - Kastrati, Granit A1 - Fondberg, Robin A1 - Fransson, Peter A1 - Jayaram-Lindström, Nitya A1 - Kosek, Eva A1 - Hellner, Clara A1 - Jensen, Karin B. SP - ePub EP - ePub VL - ePub IS - ePub N2 - Individuals who engage in nonsuicidal self-injury (NSSI) have demonstrated insensitivity to pain compared with individuals without NSSI. Yet, the neural mechanisms behind this difference are unknown. The objective of the present study was to determine which aspects of the pain regulatory system that account for this decreased sensitivity to pain. In a case-control design, 81 women, aged 18-35 (mean [SD] age, 23.4 [3.9]), were included (41 with NSSI and 40 healthy controls). A quantitative sensory testing protocol, including heat pain thresholds, heat pain tolerance, pressure pain thresholds, conditioned pain modulation (assessing central down-regulation of pain), and temporal summation (assessing facilitation of pain signals) was used. Pain-evoked brain responses were assessed by means of fMRI scanning during thermal pain. NSSI participants showed a more effective central down-regulation of pain, compared to controls, assessed with conditioned pain modulation. The neural responses to painful stimulation revealed a stronger relation between nociceptive and pain modulatory brain regions in NSSI compared to controls. In line with previous studies, pressure and heat pain thresholds were higher in participants with NSSI, however, there were no correlations between pain outcomes and NSSI clinical characteristics. The augmented pain inhibition and higher involvement of pain modulatory brain networks in NSSI may represent a pain insensitive endophenotype associated with a greater risk for developing self-injurious behavior.

Language: en

LA - en SN - 1359-4184 UR - http://dx.doi.org/10.1038/s41380-022-01639-y ID - ref1 ER -