169 Psychopathological and neurobiological overlap between anorexia nervosa and self-injurious behavior The opioid system modulates the dopaminergic (DA) system (42), which is also hypothesized to be involved in NSSI. In animal models with reduced DA neurons, self-biting behavior was observed when DA-agonists were administered, whereas DA-antagonists had a reversing effect on this behavior. Self-injury in animals was mainly observed when the animal was in isolation or physically restricted (43). As DA is the major neurotransmitter involved in reward processing (44), and reward is crucial in engagement and reinforcement of NSSI, altered DA levels in the reward circuit seem to be involved in NSSI. However, humane data on the role of DA in NSSI are lacking. Another neurotransmitter that might be implicated in NSSI is the serotonergic (5-HT) system (40). Associations have been made between 5-HT and impaired emotion regulation and impulsivity (17), which are both psychological risk factors for NSSI. Also, 5-HT dysfunction has been linked to several psychiatric disorders associated with NSSI, such as depression, anxiety, BPD and eating disorders (17, 42). Genetic studies have found a correlation between polymorphisms in 5-HT transporters and increased probability of NSSI, particularly when mediated by stress exposure (34). However, other studies found no relation between NSSI and 5-HT levels (45). Neuroimaging studies in patients with NSSI (with or without a specific psychiatric condition) suggest involvement of brain circuits related to negative valence, reward and habit formation, and cognitive control (36). For example, NSSI-expressing individuals seem to have more inhibitory control towards NSSI-related pictures than controls. Plener e.a (2012) (46) found increased activation in the limbic system (amygdala, anterior cingulate cortex) in response towards these pictures, which was related to increased levels of arousal. They also found increased activation in the prefrontal cortex, which was related to a controlling response towards the observed limbic over-activation. This could suggest that the initial arousing response towards NSSI was neutralized, probably because of the final rewarding experience of NSSI. Kraus e.a. (2010) (47) and Reitz e.a. (2015) (48) found similar imaging results related to NSSI-triggering acts and while experiencing physical pain. Ammerman et al. (2018) (36) stated that these findings support the regulative effects of NSSI on emotional processing. Liu (2017) (41) proposes a habit model to explain NSSI. The author describes a shift from voluntary behavior (instrumental learning) to repetitive habitual behavior (stimulus-response learning) occurring over time. Similar to addiction, when the self-injury becomes a habit, it loses the sensitivity to the positive outcome. This shift is paralleled by a shift from the ventral to the dorsal striatum, as observed in addiction. Other research showed that NSSI decreased arousal mostly in individuals infrequently engaging in the behavior, which suggests that the reinforcing and rewarding effects are the strongest during the onset of the behavior. The positive effects of pain relief after NSSI were lower in frequent NSSI-patients, supporting NSSI as a habitual ‘rewarding’ experience (36). This implicates that risk factors for NSSI possibly change over time, just as NSSI and its neurobiological correlates might become more habitual over time (41).
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