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Abstract

Nonsuicidal self-injury (NSSI) is a complex phenomenon, particularly common in adolescence, with severe psychiatric sequelae. NSSI is most often used to regulate emotions and alleviate distress and aversive inner tension. Emotion dysregulation and low distress tolerance are common symptoms observed in most psychiatric disorders, potentially explaining the overlapping comorbidity with NSSI. Consistently, recent research indicates that increasing NSSI severity (e.g., frequency of NSSI) is associated with more severe emotion dysregulation and comorbid psychopathology. More transdiagnostic and dimensional approaches are imperative, to disentangle and clarify the existing literature on NSSI.

Moreover, further research investigating neurobiological systems that may underlie the psychosocial risk factors of NSSI as well as the engagement and maintenance of NSSI is warranted. Previous research indicates that individuals with NSSI perceive limited or no pain during NSSI episodes. Moreover, fronto-limbic neural systems (e.g., prefrontal cortex (PFC), amygdala, hypothalamus), neuroendocrinological systems such as the endogenous opioid system, the hypothalamic-pituitary-adrenal (HPA) axis, and the hypothalamic-pituitary-thyroid (HPT) axis, as well as physiological systems such as the autonomic nervous system (ANS) play a central role in pain perception as well as emotion and stress regulation. However, systematic research in the context of adolescent NSSI is still scarce. Therefore, the aim of this work is to extend theoretical and empirical knowledge on neurobiological correlates of NSSI while further examining the influence of dimensional NSSI severity and comorbid psychopathology.

Study I examined associations of altered basal beta-endorphin (BE) and pain sensitivity (PS) with experimental heat pain in female adolescents with NSSI compared to healthy controls (HC). Results indicated reduced PS and lower BE levels in adolescents with NSSI. Moreover, additional effects of comorbid psychopathology on BE and PS were observed. Study II investigated the effect of NSSI severity on the HPA axis and ANS response to experimental pain. Results revealed an increasing HPA axis response (e.g., cortisol) following pain with increasing NSSI frequency. Moreover, after adjusting for comorbid psychopathology, greater NSSI severity was associated with a decreased heart rate during pain and an increased heart rate variability following pain. Findings indicate an increased pain-related compensatory mechanism of NSSI on the HPA axis and ANS in individuals with NSSI, independent of comorbid psychopathology. Study III investigated resting-state PFC activity in adolescents with NSSI compared to HC. Results revealed a reduced PFC activity in adolescents with NSSI. Further, increased PFC connectivity was associated with greater severity of comorbid psychopathology but not with NSSI-specific behaviors (e.g., NSSI frequency). Study IV examined HPT axis functioning in adolescents with NSSI compared to HC. Results indicated a blunted HPT axis functioning in adolescents with NSSI, strongly associated with more severe borderline personality disorder symptoms, depressive symptoms, and symptomatic distress.