Our combined findings show that even short-term exposure to violent media has specific effects on cortical functioning, and that these include diminished activation within a network that regulates behaviors such as reactive aggression.
Although the lateral orbitofrontal cortex has so far been discussed with regard to reactive aggression, there is evidence that this region, especially on the right side, has a more general role in the context-dependent regulation of behavior. Right ltOFC shows robust activation, for example, during tasks of response inhibition where subjects must periodically suppress or change behaviors based on changing external cues 
. Additional works have shown that these behavior-relevant cues can be social: ltOFC has been observed to become active, for example, when a subject processes second-person accounts of embarrassing actions or violations of social norms 
. Indeed, those with ltOFC lesions fail to even detect violations of social norms 
. Right ltOFC has also been shown to be responsive to angry faces 
, which are common indicators that a violation of social norms has occurred 
, and some individuals with ltOFC lesions are unable to detect anger in facial expressions 
. These combined findings suggest that ltOFC is generally active during situations in which external cues demand that behaviors be changed or suppressed.
The involvement of ltOFC in the regulation of reactive aggression is not surprising if one considers how dependent this behavior is on external contexts. When danger is sensed, for example, one must consider several different factors before deciding how to respond. Is the threat real? Would the environment tolerate aggressive behavior? Is the other individual stronger? Only by integrating these contextual details can one achieve an adequate sense of the situation and respond (or not) accordingly.
In many individuals with ltOFC deficits, the foregoing considerations appear to be either absent or disconnected from the behavioral outcome, with the overall result that minor provocations can trigger inappropriate aggressive responses. In one experiment that divided murderers into predatory and affective groups, affective murderers had less glucose metabolism in lateral prefrontal regions than both predatory murderers and normal controls, who did not differ 
. Another study found reductions in ltOFC glucose metabolism within subjects that had histories of reactive aggression and impulsive outbursts 
. A constellation of these ltOFC-related deficits appears in a case report 
of a patient with damage to this region who, in addition to being hyperaggressive, failed to detect violations of social norms and could not recognize anger in facial expressions. Although each of these symptoms alone could derive from a wide variety of other deficits, their combined presence in this case is consistent with a common involvement of ltOFC.
The above studies indicate that ltOFC integrates contextual information to regulate reactive aggression, as others have proposed 
. The data from the aggression questionnaire support this interpretation. Our results, however, extend these findings and indicate that repeated exposure to violent media leads to diminished response in this region and functional disconnection from the amygdala, as well as increased response in motor planning areas.
Although these results are suggestive, further data will be required to assess the specific effects of these functional changes on behavior. Because numerous studies have already linked exposure to violent media with an increase in aggressive behavior 
, it seems reasonable to consider the effect observed here as a plausible component of a mechanism; however, it is important to note that in an otherwise pacific individual, it is very unlikely that these exposure-related changes are a sufficient catalyst for the emergence of criminal aggression. The strongest evidence for this claim is the fact that, although many individuals watch violent media, relatively few go on to commit criminally violent acts.
Aggression is a complex phenomenon, encompassing numerous distinct behaviors that must derive from a wide range of neural networks. Thus, although we examined short-term changes in the cortical response of adults watching violent stimuli, exposure occurring at different frequencies or at different stages of development may induce other cortical changes that affect aggressive behavior. Certainly, the involvement of other networks in the regulation of reactive aggression and other behaviors is well known. As early as the mid-nineteenth century, for example, it was observed that damage to the ventromedial prefrontal cortex could induce “animal passions” in a patient, manifest as a flagrant disregard for social norms and the welfare of others 
. Additional studies have demonstrated that these frontal deficits may also render one more prone to commit aggressive acts 
. Because some studies have suggested that ventromedial areas monitor stimulus-outcome-reward associations 
, behavioral disorders related to lesions in this area have been proposed to reflect a diminished awareness of social rules and frameworks 
. Lateral lesions, in contrast, appear to cause violations
of these rules to go unnoticed. In both cases, increases in violent behavior have been reported. Although changes in ventromedial response were not observed in the present work, this should not be taken as evidence that these regions are not involved in these or other exposure-related effects.
The present results indicate that violent media exert a unique effect on a cortical network that is associated with the regulation of reactive aggression and other context-dependent behaviors. This effect may be part of a broad mechanism that can link exposure to violent media with the emergence or increased likelihood of aggressive behavior. Given the complex nature of aggression, however, it should not be taken as the complete mechanism itself. Further studies should determine the role of other aggression-related networks and examine how and when these changes interact with behavioral phenotypes.