Neurocognitive models of aggression, the antisocial personality disorders, and psychopathy. (Advances in Neuropsychiatry).

Abstract

This paper considers neurocognitive models of aggression and relates them to explanations of the antisocial personality disorders. Two forms of aggression are distinguished: reactive aggression elicited in response to frustration/threat and goal directed, instrumental aggression. It is argued that different forms of neurocognitive model are necessary to explain the emergence of these different forms of aggression. Impairments in executive emotional systems (the somatic marker system or the social response reversal system) are related to reactive aggression shown by patients with "acquired sociopathy" due to orbitofrontal cortex lesions. Impairment in the capacity to form associations between emotional unconditioned stimuli, particularly distress cues, and conditioned stimuli (the violence inhibition mechanism model) is related to the instrumental aggression shown by persons with developmental psychopathy. (J Neurol Neurosurg Psychiatry 2001;71:727-731)

Keywords: aggression; amygdala; orbitofrontal cortex

The goal of this paper is to consider neurocognitive models of aggression and relate these accounts to explanations of the antisocial personality disorders. However, firstly it is necessary to differentiate between the disorders conduct disorder (CD), antisocial personality disorder (APD), "acquired sociopathy" and psychopathy, and reactive and instrumental aggression.

Both CD and APD are DSM-IV diagnoses. Conduct disorder, effectively the child form of APD, and APD are both diagnosed on the basis of behaviour; thus, it is necessary to show at least three different forms of antisocial behaviour for at least 6 months to be diagnosed with CD. Those considered to have APD must present with a pervasive pattern of antisocial behaviour that begins in childhood or early adolescence and continues into adulthood. (1) "Acquired sociopathy" was a term introduced to characterise persons who, after acquired lesions of the orbitofrontal cortex, fulfil the DSM-III diagnostic criteria for "sociopathic disorder", an antecedent of APD. (2) The term was introduced after the study of a patient who presented with profound emotional and behavioural changes after lesions to the ventromedial cortex. (2)

Classifications of psychopathy are not synonymous with diagnoses of CD or APD but represent an extension. Psychopathy, in both childhood and adulthood, is currently defined with high scores on clinically based rating scales: for children, the psychopathy screening device (PSD) (3) and for adults, the revised psychopathy checklist (PCL) (4) Factor analyses of behaviours rated on both the PSD and PCL disclose two independent factors: (1) an emotion dysfunction factor defined largely by emotional shallowness and lack of guilt and (2) an antisocial behaviour factor defined largely by instrumental aggression and the commission of a wide variety of offence types. (5 6) High scores on the antisocial behaviour factor of the PSD and PCL are closely associated with the diagnosis of CD and APD respectively. (5) However, high scores on the emotion dysfunction factor, although highly correlated with scores on the antisocial behaviour factor, are less closely associated with the DSM diagnoses. More interestingly, scores on the emotion dysfunction factor seem to be determined, to a certain extent, by different influences from scores on the antisocial behaviour factor. Thus, both socioeconomic status and IQ are correlated with scores on the antisocial factor, but neither are associated with scores on the emotion dysfunction factor. (6) Moreover, whereas scores on the antisocial behaviour factor decline with age, scores on the emotion dysfunction factor remain constant. (7) This persistence suggests that the emotion dysfunction factor may more closely reflect the neurocognitive impairment(s) that are thought to result in the development of psychopathy.

The main reason for distinguishing these disorders is the high likelihood that there is no single explanation for all of them. Indeed, as regards CD and APD, there are strong suggestions that the diagnosed populations are highly heterogeneous. Thus, different risk factors are associated with life course persistent CD (appearing before the age of 10 years) and adolescence limited CD (appearing after 10 years). (8) In addition, there are considerable differences in the constellation of symptoms that different cases of CD …