Figure 11.1

Maladaptations of the reward pathway can shift behavior from normal to impulsive to compulsive. Under normal conditions, if a salient stimulus causes a favorable outcome, this behavior will be encoded as a pleasurable reward. The learning of this pleasurable reward is called “liking,” and is an opioid-dependent process. The knowledge and anticipation of this pleasurable reward is called “wanting,” and is a dopamine-dependent process. An increase in “wanting” is said to underlie impulsivity, such that the drive for the pleasurable reward outweighs the outcome and the behavior is repeated without forethought. In some individuals, there is a higher probability that “wanting” behavior will develop into impulsive behavior due to an underlying environmental or genetic risk. This increased risk is deemed an “impulsivity trait” and can lead to the development of impulsive disorders such as binge eating, drug addiction, and, perhaps, impulsive violence. Repetition of the impulsive behavior, or binging, does not happen all the time; the absence of behavior, however, can lead to a stronger desire, or anticipation, for the reward. It is this cycle of binge–abstinence–anticipation that can lead to compulsivity. When a behavior becomes compulsive, the reward no longer matters and the behavior is strictly driven by stimulus. It is through this mechanism that habits develop.

An increase in “wanting” is said to underlie impulsivity, such that the drive for the pleasurable reward outweighs the outcome and the behavior is repeated without forethought or weighing the favorableness of the outcome (progression of the process from Figure 11.1, left, to Figure 11.1, middle) [14–16]. In some individuals, there is a higher probability that “wanting” behavior will develop into impulsive behavior due to an underlying environmental or genetic risk.

This increased risk is deemed an “impulsivity trait,” and can lead to the development of impulsive disorders such as drug addiction, binge eating, gambling, or, as hypothesized here, impulsive violence when impulsivity leads to habit, or compulsivity (progression of Figure 11.1, middle, to Figure 11.1, right) [8–17]. Repetition of the impulsive behavior, called binging, does not happen all the time; the absence of behavior, however, can lead to a stronger desire, or anticipation, for the reward. It is this cycle of binge–abstinence–anticipation that can lead to compulsivity [14–16]. When a behavior becomes compulsive, the reward no longer matters, and the behavior is strictly driven by stimulus. It is through this mechanism that habits develop, just as in the classical conditioning of Pavlovian dogs. In the case of impulsive violence, hypothetically the stimulus is an environmental provocation, and the compulsive habit is retaliatory impulsive violence.

How Do Reward Pathways Regulate the Maladaptive Shift of Normal to Impulsive to Compulsive?

In a basal, unstimulated state, in a normal individual the subcortical reward center is inhibited by inputs from the prefrontal cortex leading to an inhibition of behavior (Figure 11.2A) [14–16]. When a salient stimulus is presented, via activation of dopaminergic neurons in the midbrain, the ventral striatum becomes activated, which overrides the inhibition from the cortex and elicits goal-directed behavior (Figure 11.2B).

Figure 11.2

Reward-seeking behavior in response to salient stimuli. (A) In a basal, unstimulated state, the subcortical reward center is normally inhibited by inputs from the prefrontal cortex leading to an inhibition of behavior. (B) When a salient stimulus is presented, via activation of dopaminergic neurons in the midbrain, the striatum becomes activated, which overrides the inhibition from the cortex and elicits goal-directed behavior. (C) However, in individuals prone to impulsive behaviors, the subcortical reward center, in an unstimulated state, hypothetically receives less inhibitory input from the cortex, leaving these individuals more sensitive, or primed, to engage in reward-seeking behavior. In response to a salient stimulus, these individuals have a greater influx of dopamine to the striatum, which elicits a greater drive for goal-directed behavior. (D) If this goal-directed behavior is repeated enough times, the locus of control shifts, such that dopaminergic inputs to the reward center target the area of the striatum important for stimulus-directed behavior. Since the behavior is now being controlled by habit (i.e., stimulus-directed) instead of reward (i.e., goal-directed), the stimulus loses its salience and drives the behavior automatically and impulsive violence results over and again from the provocative stimulus.

However, in individuals who are prone to impulsive behaviors, the subcortical reward center, in a unstimulated state, hypothetically receives less inhibitory input from the cortex, leaving these individuals more sensitive, or primed, to engage in reward-seeking behavior (Figure 11.2C) [8–16]. In response to a salient stimulus, these individuals have a greater influx of dopamine first to the ventral striatum, which elicits a greater drive for goal-directed behavior (Figure 11.2C). If this behavior is repeated enough times, the locus of control shifts, such that dopaminergic inputs to the reward center target the area of the dorsal striatum that is important for stimulus-directed behavior (Figure 11.2D) [15]. Since the behavior is now being controlled by habit (i.e., stimulus-directed) instead of reward (i.e., goal-directed), the stimulus loses its salience and drives the behavior automatically; impulsive violence results over and again from the provocative stimulus [8–17].

Can Impulsive Violence Potentially Be Modified by Treatment?

Is there any treatment that can control impulsive violence in institutional settings across the wide range of psychiatric disorders in which it is observed? The literature suggests that treating the underlying psychiatric disorder is the first order of business, and in some cases, control of mood and psychosis may mitigate impulsive violence [3–9]. Psychotherapeutic interventions such as cognitive behavioral therapy (CBT) or dialectical behavioral therapy (DBT) for individuals or groups may also be effective [5]. However, in practice, such interventions have not reduced impulsive violence adequately in institutional settings.

Should control of impulsive violence be possible by “unlearning” or normalization of maladaptive behavior? Although theoretically possible with the interventions mentioned above, or empirically observed in those, for example, who are addicted to drugs following a long period of enforced abstinence, the success rate is disappointingly low and the recidivism rate disappointingly high. Perhaps it is time to direct psychotherapeutic and psychopharmacologic interventions to restoring the balance between top-down control and bottom-up drives, so that impulses that are triggered by conditioned stimuli no longer trigger habitual behavior in patients with impulsive violence. Thus, novel psychotherapeutic interventions, such as cognitive remediation, could theoretically help to restore top-down inhibitory controls [20,21]. Pro-cognitive psychopharmacologic agents may also help in this regard [22]. Aggressive antipsychotic treatment can also reduce bottom-up emotional drive [3–5], but is not commonly implemented in many institutional settings [3–5]. An optimistic note has recently been sounded by the approval of lisdexamfetamine for one of the impulsive–compulsive disorders, binge-eating disorder, in which theoretical modulation of dopaminergic neurons that feed into the reward center reset the balance of too much bottom-up drive and insufficient top-down inhibition [23]. This is consistent with shifting control away from stimulus-directed behavior, regulated by the dorsal striatum, and back toward goal-directed behavior, regulated by the ventral striatum, while also restoring adequate cortical inhibitory control. Lessons learned from emerging new targets for treatment of drug addiction may also provide leads for how to treat impulsive violence as a behavioral addiction.