La reformulación de la teoría de la imagen espacial

Despite increasing support for the impulsive-premeditated aggression distinction as outlined in the previous chapter, surprisingly little is known about the neurophysiological and neuroanatomical factors that characterise these subtypes of aggression in humans. Indications can nevertheless be gained from the literature on the cortical and subcortical mechanisms thought to be involved in aggression and violence per se.

At a cortical level, it has been proposed that abnormalities of the anterior cingulate cortex and orbitofrontal cortex, regions of the ventromedial prefrontal cortex, alone or in combination with abnormalities of the amygdala, underlie the hyperarousal and dyscontrol states seen in impulsive aggressors (Best, Williams & Coccaro, 2002; Blair, 2004; Davidson et al., 2000b; New et al., 2002, 2004). Blair and Davidson et al. proposed that the anterior cingulate cortex and orbitofrontal cortex are normally activated during anger arousal via serotonergic mechanisms and exert inhibitory influence over aggressive emotional responding via mechanisms including inhibition of the amygdala, hypothalamus, and brainstem periaqueductal gray.

Certainly, damage to medial frontal and orbitofrontal cortex is associated with increased risk for the display of impulsive-aggression in humans whether the lesion occurs in childhood (Anderson et al., 1999; Pennington & Bennetto, 1993), or

adulthood (Grafman et al., 1996). In addition, neuroimaging data have revealed reduced frontal functioning in patients presenting with reactive aggression

(Søderstrom et al., 2000; Volkow & Tancredi, 1987; Volkow et al., 1995). Further studies of impulsive-aggression have found hypoactivation of the anterior cingulate cortex and orbitofrontal regions of the prefrontal cortex (Best et al., 2002; New et al., 2002). Interestingly, this reduced frontal functioning is not observed in patients presenting with predominantly premeditated-aggression (Raine et al., 1998). This is consistent with neuropsychological data that indicate that psychopathic individuals, individuals who present with marked instrumental aggression, do not present with poor performance on general measures of frontal lobe functioning (LaPierre, Braun, & Hodgins, 1995; Mitchell et al., 2002).

It has been suggested that regions of the orbitofrontal cortex are involved in a system that is crucial for social cognition and the modulation of impulsive-aggression (Blair, 2004; Blair & Cipolotti, 2000). The orbitofrontal cortex receives highly

processed sensory information concerning an individual‟s environmental experience (Mesulam, 1986) and is hypothesised to play a role in the perception of social signals, in particular, facial expressions of anger (Blair et al., 1999). Rolls (2000) suggested that the orbitofrontal cortex modulates the subcortical systems mediating impulsive- aggression through the expectations of reward and identifying if these expectations have been violated. He argued that frustration, which has been linked to the display of impulsive-aggression, occurs following the initiation of a specific behaviour to

achieve an expected reward and the subsequent absence of this reward. It can

therefore be suggested that orbitofrontal cortex may increase neuronal activity in the subcortical systems mediating impulsive-aggression when an expected reward has not been achieved and suppress neuronal activity when the expected reward is achieved.

Blair and Cipolotti (2000) proposed a further process termed Social Response Reversal (SRR). The position stresses the role of social cues in modulating social behaviour (Blair, 2001; Blair & Cipolotti, 2000). The SRR is thought to be activated by another individual‟s angry expression, other negative valenced expressions and situations associated with social disapproval. In line with this, the orbitofrontal cortex is activated by negative emotional expressions including anger, fear and disgust (Blair et al., 1999; Kesler-West et al., 2001; Sprengelmeyer, Rausch, Eysel & Przuntek, 1998). Moreover, patients with orbitofrontal lesions are impaired in their ability to recognise facial expressions, particularly anger (Blair & Cipolotti, 2000; Hornak et al., 1996).

In a discussion of the literature, Davidson et al. (2000b) suggested that individuals can typically regulate their negative affect and can also profit from

restraint-producing cues in their environment, such as others‟ facial expression of fear or anger. Information about behaviours that indiciate threat (e.g., hostile stares,

threatening words) is conveyed to the amygdala, which then projects to other limbic structures, and it is there that information about social context derived from the orbitofrontal projections is integrated with one‟s current perceptions. The

orbitofrontal cortex, through its connections with other prefrontal sectors and with the amygdala, thus plays an important role in inhibiting impulsive-aggressive outbursts because prefrontal activations that occur during anger arousal constrain the impulsive expression of emotional behaviour.

Davidson et al. (2000b) further proposed that dysfunctions in one or more of these regions and/or in the interconnections among them may be associated with faulty regulation of negative emotion and an increased propensity for impulsive- aggression. Firstly, people with prefrontal and/or amygdala dysfunction might

misinterpret environmental cues, such as facial expressions of others, and react impulsively to a misperceived threat. According to Albert, Walsh and Jonik (1993), most acts of human aggression are a reaction toward a threat, be it real or imagined. Therefore, the perception of whether a stimulus is threatening is vital in the cognitive processing leading to aggressive behaviour. Secondly, evidence suggests that

individuals vary considerably in their ability to suppress negative emotion. Therefore, individuals with decreased prefrontal activity may have greater difficulty suppressing negative emotions than those individuals who have greater prefrontal activation.

3.6 Subcortical Structures

Subcortically, four structures are viewed as important in mediating aggressive behaviour: the amygdala, hippocampus, midbrain area, and thalamus. The amygdala, hippocampus and prefrontal cortex make up part of the limbic system governing the expression of emotion, while the thalamus relays inputs from subcortical limbic structures to the prefrontal cortex (Mirsky & Siegel, 1994). Traditionally, subcortical and limbic regions of the brain have been viewed as involved in the generation of aggressive feelings and behaviours, while the prefrontal cortex is viewed as inhibiting and modulating these basic emotions (Weiger & Bear, 1988). Consequently, it could be argued that it is the relative balance of activity between the prefrontal and

subcortical brain regions which may be critically important in predisposing one to aggressive behaviour. If prefrontal functioning is reduced relative to subcortical structures, the individual may be more prone to aggression in general and perhaps impulsive-aggression in particular. Raine et al.‟s (1998) results support this argument, finding lower prefrontal activity in affective (impulsive) murderers and higher

3.7 Conclusion

The consistency across studies suggests that prefrontal dysfunction may underlie a predisposition to aggressive behaviour. Evidence is strongest for an association between prefrontal dysfunction and an impulsive subtype of aggressive behaviour (e.g., Bassarath, 2001b; Brower & Price, 2001; Raine et al., 1998). However, given the lack of specificity in research in aggression regarding the subtypes of impulsive- and premeditated-aggression, the mediating role of the prefrontal cortex in premeditated-aggression cannot be ruled out.

Chapter 4