ABSTRACT
The short answer is yes. But what is its nature? Is it largely a perceived/attributed relationship? Is it an association? Is it causal? And in which direction does the relationship primarily fl ow? Moreover, if there is a relationship, is intervening in one side of that relationship, possibly with treatment for mental disorder, likely to reduce the incidence of the other, namely criminal behaviour? However, the key questions, adverted to earlier, are why should mental disorder make a difference to the probability of criminal activity, and in what ways; that is, either to increase or decrease its likelihood? Three illustrations will serve as a reminder of how complicated all this is likely to be. First a report of an exceptional case in which a brain tumour ‘caused’ a man to engage in paedophilia (BBC News, 2002). The report dealt with a man with no previous history of sex offending who began to show an obsessive interest in child pornography; he also solicited prostitutes at massage parlours. After conviction for molesting children and further persistent inappropriate sexual behaviour he was found to have a brain tumour the size of an egg. The tumour was removed; the man’s behaviour improved. At some later point his interest in pornography returned and it was found that the tumour had re-grown; it was removed and the behaviour disappeared. Notably, the two neurologists dealing with the case found the tumour to be located in the right lobe of the orbifrontal cortex, an area of the brain believed to be tied to ‘judgment, impulse control and social behaviour’ (Choi, 2002). The compromised functioning of this area has also been characterised, somewhat more dramatically, as causing people to be ‘biologically disadvantaged in developing a conscience’ (see generally Raine, 1993). Of course, the validity of such an explanation is highly vulnerable, as indicated by the comments of a behavioural neurologist, also cited in Choi’s article in the New Scientist, who questioned whether there may have been hormonal changes due to the tumour. What is exceptional about the report is the chronology of the changes: normal behaviour – tumour – abnormal
behaviour – tumour removal – normal behaviour; and then the pattern repeated. The second illustration concerns dopamine agonists.1 These are administered to treat Parkinson’s disease and have been found to have, in rare cases, the curious side effect of producing compulsive behaviour in people who had no history of the relevant behaviours; typically gambling, excessive alcohol and food consumption, and hypersexuality. Taking patients off the medication led to an abatement in the behaviours. Warnings about the drugs are now included in the accompanying information leafl ets. Both of these illustrate the potential for changes in the brain to be associated with changes in behaviour: these can in turn be deemed criminal according to the nature of the behaviour expressed. Yet even demonstrable changes in the brain, not in themselves mental disorders but physical changes, do not necessarily cause changes in behaviour. And here the third illustration is helpful. Evidence from positron emission tomography (PET scanning) suggests that the kinds of neurological changes in the brain associated with the development of dementia in older people can be shown amongst much younger people who have none of the relevant behaviours: testament either to considerable plasticity in the brains of younger people or to more complex explanations of the relationship between cause and effect. Or both. It is appropriate to remain cautious about any suggested associations between brain pathology and criminal behaviour.
