Abstract
Abstract
Intimate partner violence (IPV) is an important criminal justice and public health problem that negatively affects quality of life and health. Research is needed to better understand IPV perpetration to generate more targeted interventions and prevent victimization. There is a vast literature supporting the role of various psychosocial factors that influence IPV perpetration, and interest is growing in research contributions from the biological sciences. One topic that is oft missing from the discussion of biological drivers of IPV perpetration is the reward systems of the brain and how they might influence patterns of violent behavior in intimate relationships. Although preliminary data from both animal and human research suggest that there are perturbations in the reward circuitry of the brain associated with aggressive behavior, these findings have the potential to inform IPV research and integrate theories of IPV perpetration in a biopsychosocial model.
Introduction
I
In recent years, there has been an increased interest in constructing a biopsychosocial model of IPV, representing the set of biological, psychological, and social or environmental factors that increase risk for aggression and violence in intimate relationships. Feminist theories of IPV perpetration posit that IPV is a product of men's efforts to control women in a patriarchal society (Stark 2007), noting that despite potentially contributing psychosocial factors that affect both men and women, IPV is mainly perpetrated against women (Truman and Morgan 2014). Furthermore, there is extensive research documenting the effect of psychosocial factors, such as childhood violence exposure (Ehrensaft et al. 2003), emotional dysregulation (Nedegaard and Sbrocco 2014; Persampiere et al. 2014), and neurocognitive deficits (Cohen et al. 1999, 2003) in promoting maladaptive strategies for conflict resolution that increase IPV risk. Together with neuropsychological research, however, there is increasing evidence from the biological sciences that suggests that IPV is a maladaptive social behavior that should be more broadly viewed as a brain health problem enabled by the presence of a diverse set of biopsychosocial factors.
Research examining biological correlates of IPV advances our understanding of partner abuse as more than a problem in conflict resolution related to various neuropsychological deficits. Although deficits in executive function undoubtedly contribute to the manifestation of IPV, there are still those who batter without the presence of any such risk, suggesting that there are other factors driving IPV behavior. Other research examining the biological correlates of IPV implicates head injury and genetics as well as perturbations in physiological arousal, neurotransmission, and endocrine function as potential risk factors for IPV (Pinto et al. 2010). These factors highlight differences in behavioral reactivity and how an individual might be biologically primed to engage in violence. One notable omission, however, is the discussion of the neural reward systems and how they may influence IPV behavior.
In general, IPV can be viewed as a goal-directed behavioral strategy to maintain status and power in a relationship. For example, an abusive partner may feel threatened during an argument or wish to control a relationship and use force to elicit compliance from an intimate. This explanation frames IPV as a motivated behavior with rewarding properties that can be reinforced over repeated events. Animal, or preclinical, research suggests that there are indeed rewarding aspects to successful aggression that drive behavioral choice to increase the likelihood of future aggression. Importantly, this motivation for aggression is controlled by the reward circuitry in the brain. This research, although in its early stages, has implications for the study of IPV, especially in light of recent findings in human research that show changes in the reward circuitry of generally violent individuals. As such, the rewarding properties of aggressive behavior and future directions are discussed.
Aggression and Reward
Preclinical investigations reveal that aggressive behavior is rewarding for successful aggressors, rendering participation in aggressive social encounters desirable. Using the social defeat stress model wherein territorial mice are given the opportunity to attack smaller intruder mice, Golden et al. (2016) found that aggressive, but not nonaggressive, territorial mice demonstrated a preference for environments associated with the aggressive encounters, suggesting that they found the aggression rewarding. Furthermore, manipulation of the basal forebrain, circuitry critical for reward, could cause the aggressive encounters to become rewarding for previously nonaggressive mice. Critically, manipulation of the same brain regions in the opposite direction caused mice that previously found the attack rewarding to behave as if aggressive social encounters were now aversive, suggesting that aberrant processing of violence might be treatable (Golden et al. 2016).
In a follow-up study, the same group demonstrated that repeated opportunities for aggression could transform previously nonaggressive mice into mice that find aggressive encounters rewarding (Golden et al. 2017). These animals subsequently developed persistent preference for environments associated with aggressive encounters. Taken together, the authors concluded that this group of animals demonstrated the “winner effect,” such that aggressive behavior became desirable after successful aggressive social encounters, and that this effect is driven in part by co-opting the reward circuitry of the brain (Golden et al. 2017). Moreover, it has also been shown that aggressive mice will work to receive the opportunity for aggressive encounters (Golden et al. 2017), and that exposure to these encounters engages some of the same molecular pathways in the brain's reward circuitry engaged by chronic exposure to addictive drugs (Aleyasin et al. 2017). These exciting new data suggest that violent encounters may actually be addictive in a manner similar to cocaine or heroin, engaging reward circuitry that drives repeated violent behavior even when the individual does not consciously desire it.
Taken together, these studies suggest that there are neurobiologically rewarding aspects to successful aggression that increase the likelihood of future aggression. One major limitation of the aforementioned preclinical work in relation to IPV is that these studies describe intermale violence: the model is limited by the fact that even the most aggressive male mice will not attack females. However, there is evidence for the role of the reward systems in aggressive behavior in humans that could inform IPV research. Multiple human imaging studies of antisocial and psychopathic individuals with and without comorbid psychiatric disorders show changes in the structure and function of the striatum, a region of the brain involved in reinforced learning, the selection of behavioral responses, and reward. Antisocial and psychopathic individuals have increased striatal volume and impaired reward processing, leading to maladaptive changes in behavioral responses, including approach behavior and appraisal of stimuli (Glenn and Yang 2012). Such impaired reward processing could alter the evaluation of social stimuli and social engagement such that behavior is biased toward riskier action. Accordingly, one recent study of adolescent twins found structural changes in the frontal cortex and striatal regions that were associated with psychopathic traits in both males and females. Specifically, findings indicated a positive relationship between psychopathic traits and striatal volume. Given its general role in behavior, researchers concluded that altered striatal morphology in individuals with psychopathic traits may direct behavior toward risky behavioral strategies for immediate reward, sensation seeking, and impulsivity (Yang et al. 2015).
Implications for IPV Research
The finding that successful aggression is rewarding at the neurobiological level, leading to the selection of aggressive behavioral strategies during subsequent social interactions, could make an important contribution to IPV research. In the context of IPV, the rewarding properties of aggression would increase the likelihood of future violence if the abuser continuously obtains positive outcomes for internal goals, such as neutralization of a perceived threat or social dominance. Importantly, initial partner aggression may have been driven by the presence of a multitude of well-known IPV risk factors that act in a society in which male dominance is promoted (Stark 2007). For example, the abusive partner may have poor conflict resolution skills in the presence or absence of neurocognitive deficits, hostile cognitive bias, or have problems of emotional control that facilitate violent action (Persampiere et al. 2014; Pinto et al. 2010). Together with the rewarding aspects of aggression, these factors could generate a pattern of violence in relationships. Indeed, reward systems provide a potential piece of the puzzle that could explain persistent IPV behavior. Future research is needed to determine how neural reward circuitry and its interaction with other IPV risk factors drive partner violence.
Conclusion
In an effort to incorporate neural reward systems into the discussion of IPV risk, it is best to reframe IPV within the biopsychosocial paradigm as a maladaptive social behavior that depends on brain health in multiple neural systems (e.g., reward, executive function). This moves our understanding beyond unitary explanations that view IPV simply as an inability to resolve conflict or a symptom of biological dysfunction. IPV is a goal-directed behavioral strategy employed during social interactions that depend on the combinatorial effect of biological, psychological, and social risk factors. A batterer's psychosocial exposures condition both biological processes and behavior such that an individual arrives at a social encounter predisposed to violent action. In other words, neurobiological responses exist in the context of psychosocial exposures. With this understanding, risk factors can be integrated in a comprehensive explanation of violent behavior in intimate relationships that is consistent with maladaptive social information processing and other more complete explanations of IPV.
Footnotes
Author Disclosure Statement
No competing financial interests exist for any author.
