The aim of the present study is to test hypotheses related to information processing differences pertaining to prefrontal functioning between impulsive- aggressive and premeditated-aggressive individuals. According to the clinical literature, damage to the prefrontal cortex results in poor impulse control and explosive, aggressive outbursts (Duffy & Campbell, 1994). However, although problems of disinhibition are implicated, there are many ways in which prefrontal dysfunction may heighten the risk for aggressive behaviour.
Perhaps most salient are defects in executive functions. Such functions involve the ability to plan and problem-solve, deficits in which may lead to careless or
inappropriate behaviours, interpersonal inappropriateness, as well as rigidity or difficulty modifying behaviour. A lessened capacity to self-correct, learn, and think flexibly, will have a particularly salient effect in situations which lack clear rules and structure as an inability to generate a suitable response may exacerbate frustration and thus the tendency to reflexive emotional responding.
A reliance on reflexive responding suggests a certain degree of behavioural rigidity. The behavioural rigidity which is often associated with frontal lobe damage manifests in overly persistent or perseverative responding (Lezak, Howieson &
Loring, 2004). Such perseveration can be understood as the continuation of a response after it is no longer appropriate. An inability to adjust inappropriate behaviours in social situations may lead to heightened interpersonal conflict. Related to this notion is the ability to correctly interpret the emotion of others, that is, deficits in such abilities will also result in inappropriate responding in social interactions. The
inability to inhibit inappropriate behavioural responses may also have a particularly salient influence in propelling one toward aggressive responding. Prefrontal deficits may result in an inability to control the behavioural expression of mood changes, and thus the usual capacity to inhibit inappropriate emotional responses may break down.
Studies of patients with neurological disorders have provided provocative insights into which structural brain mechanisms, when damaged, may predispose some persons to antisocial and aggressive behaviour. However, while such individuals indicate a link between brain damage and the onset of antisocial behaviour, it could be argued that these findings have little relevance to those individuals in the community who have consistent aggressive behaviour throughout their lives, yet have not suffered gross brain damage. It has been speculated that such individuals possess more subtle prefrontal dysfunction than the blunt damage in acquired sociopaths, but there have been few tests of this hypothesis. Specifically, it is not known whether aggressive individuals in the community have subtle structural deficits in the prefrontal cortex in the absence of discernable lesions.
With the exception of Stanford et al. (1997), most neuropsychological research on aggression have investigated possible deficits in either incarcerated prison inmates or psychiatric patients, ignoring the large number of individuals in the general
population who commit aggressive acts yet have not come into contact with the criminal justice or mental health systems. Such sampling biases inhibit the usefulness of such results in the development of interventions and treatments for reducing specific forms of aggression.
The current review has also emphasised the importance of distinguishing between predominantly impulsive-aggressive behaviour and predominantly premeditated-aggressive behaviour. While distinguishing between aggressive
subtypes is clearly important for understanding the causal features of such behaviour, it has also been shown to be crucial in relation to proper intervention and treatment (Pulkkinen, 1996; Vitaro et al., 1998). Furthermore, the results of Barratt et al. (1997a) and Malone et al. (1998) clearly suggest that the extent to which biological variables influence impulsive- and premeditated-aggressive behaviour differs. The problem is, however, as Scarpa and Raine (2000) highlighted, “few studies of the biological bases of antisocial behaviour in humans have categorised aggression or violence according to these subtypes” (p. 321). Rather, most have used heterogeneous groups of aggressive individuals comparing them to non-aggressive controls. This has led to equivocal and sometimes misleading results throughout the literature. In
attempting to overcome these problems, the current study attempts to delineate the neurobiology of aggression through an investigation of the neuropsychological differences between predominantly impulsive- and predominantly premeditated- aggressive individuals.
Studies of subjects with acquired frontal lobe injury support the association between increased aggression and focal orbitofrontal, or ventromedial frontal injury, or both. The neuropsychological literature, however, tends to find increased
aggressive behaviour associated with deficits in executive function, which correlate with dorsolateral prefrontal dysfunction (Dolan & Anderson, 2002; Stanford et al., 1997). The dorsolateral and orbitofrontal prefrontal cortex are parts of an integrative functional system and they typically work together, even in a single situation. Thus, one hypothesis to account for discrepant data is that orbitofrontal and dorsolateral prefrontal dysfunction contribute to aggressive dyscontrol in different ways.
Dorsolateral dysfunction may become evident through its impact on executive functions. Such executive deficits, as investigated in Study 1, may increase the risk of
aggression through its direct effects on impulse control, planning, self-monitoring, and cognitive flexibility. Individuals who have dysfunction involving the orbitofrontal cortex comprise a different group. Retrospective data strongly support a link between the disinhibited type of frontal network syndrome and aggressive dyscontrol. Thus, dysfunction in the orbitofrontal cortex may lead to aggression through impaired emotion recognition, as examined in Study 2, as well as through inhibitory, response reversal, and decision-making deficits investigated in Study 3 (Brower & Price, 2001).
Chapter 5