关键词: 非自杀性自伤, 神经生理机制, 共病障碍

Abstract:

Non-suicidal self-injury (NSSI) is a major mental disorder whereby one deliberately and rapidly hurts himself/herself without a clear suicidal intent, but which may lead to severe damage to one’s body and mind. This review researched studies from the last ten years to examine the mechanism underlying NSSI from the perspectives of neuropsychology as well as for comparative study. Based on this research, we attempted to build an integrated model of the cognitive and neural mechanisms of NSSI.
Neural studies have shown that the emotion system of NSSI patients may not function well (e.g., over-activation of the amygdala), causing emotional dysregulation in patients, which in turn is a major cause of NSSI. Thus, damage to the control system, such as the abnormal activation of prefrontal cortex, may also play an important role in NSSI and may lead to the loss of inhibitory control, making it hard for NSSI patients to resist the impulse to hurt themselves. Meanwhile, dysfunctional reward systems, such as the orbitofrontal cortex, may attach NSSI behavior to relief or something good. As such, patients fail to understand that hurting themselves is a bad ideal, thus causing the recrudescence of NSSI. In addition, abnormal pain perception, which is related to the HPA axis, may also contribute to NSSI behavior by reducing the level of pain felt, thereby increasing eagerness for pain. We also discussed the role of possible neurotransmitters or genetic shortages in NSSI. For example, the short alleles of the 5-HTT gene-linked polymorphic region weaken the regulatory function of the transmitter and induce emotional regulation disorders in the individual. Another example shows that endogenous opioid peptides, which are involved in the process of pain and mood regulation (and whose levels may be reduced due to individuals’ frustrating early-life experiences and genetic factors), can promote the act of NSSI. Similarly, after the opioid receptor is stimulated, the level of dopamine in NSSI patients increases, and one may obtain a sense of pleasure from self-harming behavior.
With regard to comorbidities, NSSI had some partially overlapping mechanisms compared with suicide, addiction, eating disorders, and mood disorders. Self-injury and suicide attempts showed different performances on EEG indicators, but they also showed some similarities from the perspective of behavioral research and functional imaging. In addition, NSSI behavior is significantly related to substance addiction, and both are accompanied by impairment of inhibition control as well as the desire for certain substances or behaviors caused by abnormalities in the opioid and dopamine systems. Meanwhile, eating disorders and self-harm behaviors have high comorbidity rate. Eating disorders can be seen as indirect self-harm, and the EEG and functional imaging indicators of both are similar in part. Finally, depressive disorder is also a disorder that has a high comorbidity rate with NSSI. Patients with depressive disorder may regulate their emotions through self-harm, and the two have common risk factors and partially overlapping neural mechanisms. Studying the similarities and differences between the above-mentioned comorbid conditions and NSSI behavior can help us understand self-injury from different angles and implement early warning and intervention in multiple directions.
Therefore, we built a model that explained the cognitive process combined with the neural mechanism of NSSI, matching every step of NSSI with its neural bases, as well as presenting the neural correlations between NSSI and comorbidities. Further research may focus on longitudinal studies, such as building models that describe the development of NSSI; explore gender differences from a prospective of neuroscience (whether and why more women hurt themselves than men); discuss treatments for NSSI (whether there are any more effective treatment methods); and examine whether there’s a correlation between the dysfunctional attention system and NSSI behavior.

Key words: NSSI, neural mechanism, comorbidity