Serotonin
Coccaro and colleagues have done much to advance the hypothesis that a deficit in the serotonin system is implicated in self-injurious behavior. They found (1997c) that irritability is the core behavioral correlate of serotonin function, and the exact type of aggressive behavior shown in response to irritation seems to be dependent on levels of serotonin - if they are normal, irritability may be expressed by screaming, throwing things, etc. If serotonin levels are low, aggression increases and responses to irritation escalate into self-injury, suicide, and/or attacks on others.
Simeon et al. (1992) found that self-injurious behavior was significantly negatively correlated with number of platelet imipramine binding sites (self-injurers have fewer platelet imipramine binding sites, a level of serotonin activity) and note that this "may reflect central serotonergic dysfunction with reduced presynaptic serotonin release. . . . Serotonergic dysfunction may facilitate self-mutilation."
When these results are considered in light of work such as that by Stoff et al. (1987) and Birmaher et al. (1990), which links reduced numbers of platelet imipramine binding sites to impulsivity and aggression, it appears that the most appropriate classification for self-injurious behavior might be as an impulse-control disorder similar to trichotillomania, kleptomania, or compulsive gambling.
Herpertz (Herpertz et al, 1995; Herpertz and Favazza, 1997) has investigated how blood levels of prolactin respond to doses of d-fenfluramine in self-injuring and control subjects. The prolactin response in self-injuring subjects was blunted, which is "suggestive of a deficit in overall and primarily pre-synaptic central 5-HT (serotonin) function." Stein et al. (1996) found a similar blunting of prolactin response on fenfluramine challenge in subjects with compulsive personality disorder, and Coccaro et al. (1997c) found prolactin response varied inversely with scores on the Life History of Aggression scale.
It is not clear whether these abnormalities are caused by the trauma/abuse/invalidating experiences or whether some individuals with these kinds of brain abnormalities have traumatic life experiences that prevent their learning effective ways to cope with distress and that cause them to feel they have little control over what happens in their lives and subsequently resort to self-injury as a way of coping.
Knowing when to stop - pain doesn't seem to be a factor. Most of those who self-mutilate can't quite explain it, but they know when to stop a session. After a certain amount of injury, the need is somehow satisfied and the abuser feels peaceful, calm, soothed. Only 10% of respondents to Conterio and Favazza's 1986 survey reported feeling "great pain"; 23 percent reported moderate pain and 67% reported feeling little or no pain at all. Naloxone, a drug that reverses the effects of opiods (including endorphins, the body's natural painkillers), was given to self-mutilators in one study but did not prove effective (see Richardson and Zaleski, 1986). These findings are intriguing in light of Haines et al. (1995), a study that found that reduction of psychophysiological tension may be the primary purpose of self-injury. It may be that when a certain level of physiological calm is reached, the self-injurer no longer feels an urgent need to inflict harm on his/her body. The lack of pain may be due to dissociation in some self-injurers, and to the way in which self-injury serves as a focusing behavior for others.
