Non-Suicidal Self-Injury: Pain Addiction Mechanisms, Neurophysiological Signatures, and Therapeutic Advances
Abstract
The aim of this study was to review the neurobiological mechanisms, epidemiology, and therapeutic interventions for non-suicidal self-injury (NSSI), emphasizing the pain addiction model and electroencephalographic biomarkers as frameworks for precision intervention. A narrative review of the literature was conducted using PubMed, Web of Science, CNKI, and Wanfang Data up to October 2025. Search strategy employed the terms "non-suicidal self-injury," "pain addiction," "electroencephalography," "endogenous opioid system," and "HPA axis." Selection criteria prioritized original human studies, high-quality systematic reviews, and mechanistic investigations. Pain addiction and electroencephalography (EEG) were selected as focal variables based on their explanatory power: pain addiction elucidates NSSI perpetuation through endogenous opioid-mediated reward sensitization and dopaminergic reinforcement, while event-related potentials (ERPs) provide temporal precision in mapping cognitive-affective dysregulation underlying emotional impulsivity and regulatory deficits. Global adolescent NSSI prevalence averages 17.2%, with Chinese rates reaching 24.7% and trends toward earlier onset. Neurobiological substrates include fronto-limbic dysregulation, hypoactive hypothalamic-pituitary-adrenal (HPA) axis function with blunted cortisol reactivity, and endogenous opioid system alterations producing widespread hypoalgesia. EEG/ERP studies demonstrate increased N2 amplitude with decreased P3…
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