A ‘techno-somatic’ (Pickersgill, forthcoming) ethic is today widespread, though not hegemonic, within much of contemporary ‘Western’ psychiatry. Such an approach entails an epistemological emphasis on technoscientific methodologies and knowledges, and an ontological preoccupation with the body as the locus of psychopathology. A techno-somatic ethic thus engenders, for instance, a perspective on psychiatric research that privileges studies into neurotransmitters and genes over epidemiological and sociological investigations into the social determinants of psychopathology. Such an orientation both legitimates, and is legitimated by, an understanding of psychiatric disorder as being in some way localizable within the body (including the brain). Nowhere is a techno-somatic approach more apparent than in neuroscientific research into psychiatric disorders. Although the relationship between neuroscience and clinical practice is ‘uncertain’ (Cullen and Cohn, Reference Cullen, Cohn and Webster2006: 117), it is clear that neurologic approaches to the study of conditions like schizophrenia and depression are increasingly common and the idiom of these researches resonates through psychiatry (Rose, Reference Rose2007).

Imaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have significant scientific, clinical and cultural authority (Beaulieu, Reference Beaulieu2001, Reference Beaulieu2002; Dumit, Reference Dumit2004; Joyce, Reference Joyce2008), and, like genetic tools and methods (Rosenberg, Reference Rosenberg2007), are imbued with the hopes of funders, researchers, practitioners and publics (Borck, Reference Borck2008; Hagner and Borck, Reference Hagner and Borck2001). As with genetics, neuroscience may also be a focus of concern to many. Psychiatrists, for instance, can be critical of what they construe as determinism and therapeutic nihilism within neuroscientific research (e.g. Benning, Reference Benning2003; Lewis, Reference Lewis2006). Sociologists too are not unaware of the degree to which neuroscience potentially renders problematic certain of their assumptions and theoretical positions. Neurologic attempts to ‘explain’ behaviour may thus be taken to be part of the broader ‘reductionist challenge’ (Duster, Reference Duster2006) presented by biomedical science.

Yet, totalizing critiques of somatic reductionism stand in marked contrast to some of the claims of scientists themselves. For instance, in the introduction to a 2008 special issue of the journal Science on the ‘Genetics of behavior’, the editors opened with the following assertion:

Sociologists have long been aware of the disjuctures between what scientists say and what they do. Nevertheless, it does seem that there are significant differences between the simplistic determinism occasionally ascribed to scientific research, and the more sophisticated ontologies performed (Mol, Reference Mol2002) through such investigation (Barnes and Dupré, Reference Barnes and Dupré2008). Behavioural genetics, as well as epigenetics and, in particular, neuroscience, may work within a reductionist epistemological rubric, but the ontological assumptions of such research are often far from crude. Instead, the development of behaviour and personality is cast as a complex, multimodal process involving reciprocal interactions between different realms of biology and ‘environment’ (e.g. Caspi et al., Reference Caspi, McClay, Moffitt, Mill, Martin and Craig2002; Foley et al., Reference Foley, Eaves, Wormley, Silberg, Maes and Kuhn2004; Kendler, Reference Kendler2005; Turner, Reference Turner2001). Understandings of ‘the environment’ operationalized by many scientists are expansive, ranging from the cellular environment to socio-economic status. They may also, in some instances, be crudely formulated, particularly when compared to sociological and anthropological conceptualizations of the social world (Dingwall et al., Reference Dingwall, Nerlich and Hillyard2003). However, it is clear that even the most ‘biological’ of psychiatric research apportions at least some kind of causal role for the development of psychopathology to ‘factors’ that lie outside the material limits of the body.

Totalizing critiques of biological determinism thus seem inadequate for the multiple reductions performed through contemporary neuroscience. Nevertheless, the ways in which soma and society are articulated with one another within research and discourse demands attention. To what extent are everyday, mundane understandings about ‘the’ social world assimilated into the developmental pathways assumed for different behaviours and personality traits? Do reconfigurations in the relationships between soma, psyche and society challenge and reshape dominant understandings of these ontological realms? What implications do these multimodal models have for the entities under study: in the case of psychopathologies, to what extent are the disease concepts (Canguilhem, Reference Canguilhem1998 [1966]) through which they are structured reshaped? What opportunities are there for category expansion and the creation of new ‘kinds’ (Hacking, Reference Hacking2002) of ‘deviant’? These are complex questions that necessitate an engagement with neuroscience which moves away from simple criticism but which nonetheless attends to its ethical and political valence.

In this article, the significance of these questions will be illustrated through an analysis of scientists’ accounts of the development and expression of personality disorders associated with antisocial behaviour. These accounts were elicited from professionals employing a wide range of methods, technologies and techniques in their research to elucidate how structural and functional differences in the brains of individuals classified with personality disorder correlate with the personality traits and behaviours constitutive of these conditions. First, an overview of personality disorders associated with antisocial behaviour is given, before, second, a review of some of the neuroscientific literature on personality disorder. From there, the narrative shifts to discuss the accounts of professionals working in this area on the aetiology and expression of this set of conditions. A description of the methods of the larger study from which the analysis is drawn is also given. The article concludes with thoughts on the degree to which ‘the environment’ is configured as playing a role in personality disorder, the way that this has shaped the ontologies of these conditions presented by the scientists, and their normative implications.

Antisocial personality disorders

Personality disorders, especially those associated with antisocial behaviour, exemplify the enduring difficulty of biomedical adjudication between normality and pathology (Canguilhem, Reference Canguilhem1998 [1966]). With a long and turbulent history (Berrios, Reference Berrios1993), these conditions have long been part of the work of psychiatrists in Europe and North America. Today, they are officially defined as clusters of ‘personality traits [that] are inflexible and maladaptive and cause either significant functional impairment or subjective distress’ (APA, 1987: 335). Being ‘whole person disorders’ (Eastman and Starling, Reference Eastman and Starling2006), the ethical and clinical basis for their position as objects of psychiatric concern has been repeatedly considered and negotiated.

Personality disorders associated with antisocial behaviour are particularly controversial (Manning, Reference Manning2002), not least because of the debate animated by recent (2007) changes to the Mental Health Act of England and Wales (Pilgrim, Reference Pilgrim2007). The primary categorizations employed to characterize individuals considered to be extremely antisocial are antisocial personality disorder (ASPD) and psychopathic personality disorder (psychopathy). While these terms are, on occasion, used synonymously (Reid, Reference Reid2001), the latter is commonly considered a more severe pathology.

The ‘official’ terminological standard (Timmermans and Berg, Reference Timmermans and Berg2003) for ASPD is located in the American Psychiatric Association (APA) Diagnostic and statistical manual of mental disorders (DSM). The criteria were first introduced in 1980 in the third edition of this text, though there were, and continue to be, similarities with earlier categories pertaining to antisocial individuals, such as sociopathic personality disorder (Pickersgill, forthcoming). Psychopathy is a far older category, dating back to nineteenth-century Europe (Berrios, Reference Berrios1993; Werlinder, Reference Werlinder1978). Never a recognized APA diagnostic, this culturally resonant category has nevertheless endured within clinical and scientific discourse, helping to structure broader understandings of antisociality. Today, it is most closely associated with the work of Robert Hare, who developed a psychological tool called the ‘Psychopathy Checklist’ to characterize this condition. Hare has also developed a version for the measurement of ‘callous unemotional traits’ in 12–18-year-olds called the ‘Psychopathy Checklist—Youth Version’ (PCL-YV), and the ‘Antisocial Process Screening Device’ for younger children. The term callous unemotional (CU) traits is used to emphasize the scientific and clinical consensus that psychopathy is an adult disorder, and that a child with CU traits is not necessarily predestined to develop the condition later in life.

Both ASPD and psychopathy continue to command the attention of a variety of mental health professionals and researchers, including psychoanalysts, clinical psychologists and epidemiologists. Today, as part of the broader techno-somatic imperative within psychiatry, neuroscience is an increasingly significant stakeholder in these conditions, though—as Berrios (Reference Berrios1993) has pointed out—personality disorders have long been the focus of neurologic research and theorization.

Neuroscience and personality disorder

What kinds of neurobiological research exist for personality disorder? As with the study of other forms of psychopathology, such as schizophrenia, there is no one focus for such work, in spite of a far smaller number of active investigators.Footnote ¹ One of the leading researchers on ASPD is Adrian Raine, Richard Perry University Professor of Criminology and Psychiatry at the University of Pennsylvania. Trained in experimental psychology at Oxford, with a PhD in psychology from York, Raine has been researching antisocial behaviour since the 1980s and many of his studies have focused on the neurobiological correlates of ASPD. Raine is perhaps most widely known for his structural MRI studies examining the volume of ‘grey matter’ in the prefrontal cortex of individuals categorized with ASPD. This area of the brain is associated with ‘executive function’, which includes the ability to discriminate between conflicting thoughts, suppress urges and work towards a goal. Raine and colleagues (Reference Raine, Lencz, Bihrle, Lacasse and Colletti2000) maintain that individuals with ASPD have a reduced volume of grey matter (compared to those who do not meet diagnostic criteria for ASPD), and suggest that this might underlie some of the characteristics associated with the disorder. Work such as Raine's, examining the prefrontal cortex of individuals with ASPD, is a common strand of neurobiological research relating to antisocial personality disorders, and violent and antisocial behaviour more generally.

Another key research track examines the amygdala. Found deep within the brain, the amygdala is considered to play an important role in the processing of emotion. James Blair of the US National Institute of Mental Health is one of the more prominent researchers working in this area. Like other researchers influenced by the work of Robert Hare, it is Blair's contention that psychopathy is an emotional disorder, and a dysfunctioning amygdala is at its root (Blair et al., Reference Blair2005). Blair employs molecular genetics, functional imaging and neuropsychological tests to elucidate the nature and extent of this dysfunction. More specifically, Blair believes that a key feature of individuals with psychopathy is that they have markedly low anxiety; Blair's thesis is that the amygdala, which is associated with anxiety, is dysfunctional in individuals categorized as psychopathic. It is this dysfunction, possibly confounded by impairment to another brain region (the orbitofrontal cortex) that results in the particular personality traits ascribed to psychopathy (Blair, Reference Blair2003).

Molecular genetics, especially ‘neurogenetics’ (the study of the role of genes in the nervous system, including the brain), is another growing area of study in personality disorders associated with antisocial behaviour. Of particular prominence here is Essi Viding, Reader in Developmental Psychopathology at University College London, and Research Associate in the Institute of Psychiatry (Fontaine and Viding, Reference Fontaine and Viding2008; Viding and Jones, Reference Viding and Jones2008). Work exploring the effects of the neurotransmitter serotonin in the brain (Dolan and Anderson, Reference Dolan and Anderson2003; Soderstrom et al., Reference Soderstrom, Blennow, Manhem and Forsman2001) is also being undertaken.

The different theories underlying neurobiological research into personality disorder are not mutually exclusive; a conviction of the salience of one of these cerebral structures or functions in the development of ASPD or psychopathy does not preclude a belief that one or several others are also important. Indeed, it is conventional to regard personality disorder as having correlates in different regions of the brain, and some investigators, like well-known British psychiatrist Mairead Dolan of Monash University, study two or more of them (Dolan, Reference Dolan2002; Dolan and Park, Reference Dolan and Park2002).

Neuroscientific research into ASPD and psychopathy is thus a diverse field, characterized by a relatively small number of high-profile researchers, and with no clear consensus regarding what ‘causes’ these conditions. What is nevertheless common to all the researchers is a degree of holism in their articulations of personality disorder. In their published work, neuroscientists do not necessarily exclude so-called ‘environmental factors’ in the accounts of ASPD and psychopathy they advance (e.g. Blair et al., Reference Blair, Mitchell and Blair2005; Dolan, Reference Dolan1994; Volkow and Tancredi, Reference Volkow and Tancredi1987). Simplistic cerebral reductionism and determinism of the sort seen in nineteenth-century phrenology (Rafter, Reference Rafter1997) are therefore not always evident within this research, though they may be taken to be implicit in scientists' claims as they ‘travel’ (Latour, Reference Latour1987) into discursive arenas beyond those through which they were assembled, and are stripped of the assertions of contingency attached by their creators. In light of the apparent lack of overt determinism in what neuroscientists write, it might reasonably be asked what they say about the ontology of personality disorder. It is perhaps through vocal discourse that neuroscientific claims are felt most powerfully beyond the laboratory: the verbal contributions of researchers in university and hospital seminars, in multidisciplinary workshops and conferences, and in documentaries and other television appearances. It is thus to verbal accounts of neuroscientists on the aetiology and expression of personality disorder that this article now turns.

Methods

This article is part of a larger study concerning the relationship between neuroscience and clinical practice with regard to personality disorders associated with antisocial behaviour. The analysis which follows draws on interviews with nine neuroscientists studying some aspect of personality disorder. Neuroscience is a broad term, including, among others, genetic, structural, functional and chemical studies of the brain. Here, ‘neuroscientist’ refers to any investigator whose research focuses primarily on the brain. As described above, the volume of neuroscientific research into personality disorder in general and psychopathy and ASPD in particular is slim, particularly compared to other psychiatric categories such as schizophrenia. Accordingly, there are few neuroscientists in this area with voices prominent within British clinical and policy spheres. The nine scientists interviewed represent a significant proportion of these individuals, the majority of whom are also recognized internationally for their work. One of the interviewees is located in Canada, four work in the United States, and four are based in England. While this is not a large sample, the purposive sampling strategy and small number of investigators actively researching the neuroscience of personality disorder means that while general claims about neuroscience cannot be made, the analysis nevertheless provides a high degree of moderatum generalizability sufficient for the aims of this article (Payne and Williams, Reference Payne and Williams2005).

During recruitment, the research was introduced to potential participants in terms similar to those outlined above; i.e. social scientific research concerned with the relationship between neuroscience and clinical practice, and, in particular, the degree to which neuroscientific ideas were interacting with and, perhaps, reshaping clinical opinion. Questions were asked regarding the respondents' research, and their views on the aetiology, diagnosis and treatment of personality disorder. The research was concerned with the ways in which ASPD and psychopathy were framed (Rosenberg, Reference Rosenberg, Rosenberg and Golden1992) in relation to these issues. Accordingly, the respondents were allowed to speak freely, and while they were gently queried about some of their responses, they were never criticized. As has been noted, some of these researchers held positions of authority and influence; issues of power were therefore germane to the encounter, as with any so-called ‘elite’ interview (Richards, Reference Richards1996). However, the nature of the questions and the study aims ensured that power asymmetries were not as salient as they might have been in other forms of interviewing, such as where researchers directly challenge respondents on their opinions. Taking place over 2006 and 2007, the individual interview encounters lasted between 45 minutes and several hours, and in some cases included attendance at a talk, or lunch or coffee (allowing continued informal discussion). Responses to formal interview questions were recorded, transcribed and coded deductively and inductively; close attention was paid to the research themes, as well as any other relevant topics that emerged across all the interviews. The interview data were not considered to give an insight into what the respondents ‘really’ felt about personality disorder (Gilbert and Mulkay, Reference Gilber and Mulkay1984); rather, the accounts elicited served as lens through which to visualize the discursive construction of ASPD and psychopathy.

The development of personality disorder

How does a personality become disordered? For the scientists interviewed here, this was achieved through a multifaceted matrix of interactions between somatic and societal ‘factors’—genes and environment—which acted together and upon each other in complex ways that shaped the brain and resulted in personality disorder.

This matrix was, in some ways, remarkably complex. In terms of ‘the environment’, the scientists invoked a number of actions and processes as salient in the ontogeny of personality disorder, many of which were evocative of ‘everyday’ understandings of the development of antisocial behaviour. They included parental absence and abuse, constant moving around from place to place as a child (and consequently failing to develop any strong attachments), low socio-economic status and low IQ, as well as membership in gangs and maternal drinking during pregnancy. Clearly, an individual's social ecology was deemed important in fostering the development of conditions like ASPD and psychopathy.

Nevertheless, it was the biological aspects of personality disorder that were of most interest to the respondents, and ‘genetic factors’ were emphasized as salient. The role played by genes in the development of ASPD and psychopathy was, however, viewed as unknown as yet, and difficult to ascertain. Dr A, for instance, noted that psychopathy developed because of ‘some sort of genetic predisposition and then the appropriate environmental experiences’, but ‘how these genetic predispositions interact with the environment is something we just don’t know yet’. Others agreed: while the interaction of genetics and the environment was thought important to the development of personality disorder, the scientific problem of understanding the mechanisms through which this occurred was ‘far from being solved’ (Dr E). If genes played an important aetiological role, currently it was one that was opaque to technoscientific visualization.

The ways in which genetic and environmental ‘factors’ interacted to produce personality disorder were also unclear. Underscoring the complexity of this set of conditions, the scientists suggested that different kinds of interactions could result in ASPD or psychopathy. As Dr A put it, ‘there's no single explanation for these things’. Rather, there were different aetiological routes. Such diverse ‘underlying genetic, environmental and neurological’ bases (Dr F) might, in turn, result in different ‘types’ of personality disorder. Dr E reflected explicitly on these points:

Congruent with much contemporary scientific research into psychiatric disorder (Rose, Reference Rose2007), discussions of genetics and aetiology were couched in terms of risk: genes were described as making individuals vulnerable to personality disorder, rather than determining it. In Dr E's words:

Indeed, some of the scientists took the ways in which risk was constituted and played out within the body as their main research concern. Dr H, for instance, described her research as concentrating ‘on how genetic and environmental vulnerability factors may influence brain development in a way that then biases your cognition and biases the way you feel about the world’, resulting in psychopathic-like traits in children. Risk, then, is not just an idiom for articulating aetiology: it is also a calculable object of scientific interest.

Talk of risk has a potent cultural and moral valence (Rosenberg, Reference Rosenberg2007). While conceiving of the role of genetics in terms of vulnerabilities and susceptibilities may be a ‘rational’ response to a complex, multimodal condition, framing the aetiology of personality disorder in this way also acts to buttress scientific work on these conditions against allegations of ‘reductionism’ and ‘determinism’. Certainly, a non-deterministic conception of genetics seemed important for the scientists to put across during the interview:

MP: OK. So just to sort of paraphrase your views on the underlying causes of psychopathy, there's a kind of genetic predisposition—

Dr C: —Vulnerability.

MP: Vulnerability. And that interacts with environmental factors, and that results—that could result in a form of psychopathy?

Dr C: It is […] So the idea is that you have, there might be genetic vulnerabilities that, I don’t know, might get manifested in relation to particular traits, callousness, and lack of empathy. But it might be that the environment in which […] that individual finds themselves in promotes […] forms of delinquent behaviour, and that at some point of course those behaviours will start to satisfy and stack up in relation to the diagnostic criteria [for psychopathy]. And none of this is unique to me, this is just, kind of the orthodoxy that most neurobiologists will give you.

In correcting my paraphrasing of his commentary on personality disorder, Dr C underscored the point that biology was not destiny. This motif was explicit within several of the accounts elicited. For example, when Dr H spoke about a biological basis to antisocial personalities, he asserted:

Dr E also added a cautionary statement to his discussion of the aetiology of psychopathy:

While the respondents were explicit in their assertions that biology did not cause personality disorder, they were, nevertheless, all active researchers into the somatic aspects of these conditions. This ambivalence between holism and reductionism was most evident in discussions of children and adolescents with so-called CU traits’. On the one hand, it was not considered a foregone conclusion that such children would later develop psychopathy:

On the other hand, the ‘prognosis’ was not good:

In light of this, the scientists, for the most part, advocated a degree of state interventionism in children and adolescents who, on the basis of their behaviour, were at risk of developing personality disorder. As Dr A reflected,

Clearly, ASPD and, in particular, psychopathy are considered complex conditions by those who research them—they do not simply reduce to one or more ‘faulty’ genes. Navigation of this complexity was achieved through recourse to a developmental story of genetic and environmental ‘factors’, interacting together and upon each other in ways that led to the development of personality disorder. Evocative of the ‘narrative of enlightened geneticisation’ argued by Hedgecoe (Reference Hedgecoe2001) to lie within scientists' written accounts of schizophrenia, this story subtly prioritized genetics, though genes were framed as vulnerability factors, rather than determinants, of these disorders—a discursive repertoire Rose (Reference Rose2007) has observed in wider scientific writings and commentary on the genetics of violence and aggression. In spite of their uncertainty regarding the precise details of the development of ASPD and psychopathy, the scientists were nevertheless confident that aetiology was heterogeneous on three counts. First, in terms of the entities involved: various genetic and environmental factors were thought to interact in the development of personality disorder. Second, in regard to the multimodality of aetiology: different combinations of factors could result in ASPD or psychopathy. Lastly, in respect to what might be called the pluripotentiality of aetiology: diverse developmental pathways could result in different ‘types’ of pathology that could still fit within the rubric of ASPD or psychopathy. We can therefore see that by assigning roles to both soma and society in the development of personality disorder, the ontology of these conditions is rendered less certain and more challenging to elucidate.

The expression of personality disorder

In spite of strong opinions about aetiology broadly, the scientists interviewed were, to varying degrees, not especially concerned with the specific intricacies of the development of ASPD and psychopathy. They were, in Dr D's words, ‘agnostic with respect to aetiology’. Aetiology was less important than the ways in which ASPD and psychopathy were expressed, biologically and behaviourally. It was on these correlates that the scientists’ research focused; in particular, the ways in which personality disorder manifested within the brain, which was seen as the locus—but not necessarily the cause—of ASPD and psychopathy. The neural architecture of the brain was key to the development of personality disorder, though the mechanisms of its construction were intricate and opaque.

Not surprisingly, given their professional focus, all the scientists thought that some kind of organic correlate to personality disorder was evident within the brain, irrespective of aetiology. This might be structural (linked to the anatomy of the brain), functional (associated with the cognitive processes occurring within the brain), or both. These cerebral characteristics could be measured in different ways; for instance, through functional magnetic resonance imaging (fMRI), electroencephalography (EEG), and other physiological and psychological tests, such as facial muscle response to stimuli intended to elicit fear. These methods were used to infer a particular neural structure or mechanism that would explain the differences in behaviour and cognition in groups of personality disordered individuals compared to groups of ‘normal’ individuals.

In terms of their behaviour and interpersonal relations, adults categorized with ASPD and psychopathy were not thought of as enjoyable to be in contact with. Rather, they were ‘difficult, unpleasant and troublesome’ (Dr I), and behaved antisocially. This general description extended to children—most of the scientists thought ASPD and psychopathy could be recognized in children, perhaps as young as six. In light of this, Dr I, for instance, thought that individuals characterized with psychopathy ‘are always going to be labelled as bad’. He elaborated further:

The kinds of antisocial behaviour and personality traits articulated as characteristic of personality disordered individuals were wide-ranging, including generalized rule-breaking, physical violence, rape, child molestation and murder. Like the environmental factors implicated by the respondents in the development of ASPD and psychopathy (e.g. poor parenting), the behaviours taken by the scientist to be an expression of these disorders therefore reflected everyday understandings of ‘bad’ people.

If there were a variety of ways personality disorder could develop, there were also numerous mechanisms through which it might be expressed: not every individual diagnosed with ASPD or psychopathy exhibited the same constellation of antisocial behaviours or traits. As Dr E recalled, early in his career he was struck by the diversity of behaviours and styles of interaction apparent in individuals characterized with psychopathy:

Similarly, there were differences between the disorders ASPD and psychopathy. ASPD was expressed through antisocial (often criminal) behaviour; individuals were considered to have ASPD if they exhibited a particular array of behaviours, and these persisted over time. Psychopathy, on the other hand, was more complex. While it too was expressed through antisocial behaviour, the disorder could also be recognized through a particular style of interaction, and by personality and emotional traits that lent themselves to such behaviours and interactive modes—lack of guilt and empathy, for instance. Dr D's views on psychopathy summarize well those of the other scientists:

While psychopathy may be considered a heterogeneous assemblage of personality traits, styles of interaction, and antisocial behaviour, it is the performance of antisocial acts that is key to an individual becoming classified with the disorder (or the child or youth equivalents). It is only through severe antisocial behaviour that individuals enter a social context (e.g. prison) where an opportunity for diagnosis is presented. It might, then, be asked whether an individual must perform antisocial behaviour of a degree and quality that results in entry into such a social context—in other words, to be recognized as formally antisocial—in order to meet the psychopathy, or ASPD, criteria.

This question—is the expression of criminal antisociality key to personality disorder?—was addressed to some of the respondents; in other cases, an answer emerged without the query explicitly posed. It appeared to be an issue engendering some ambivalence, as illuminated below:

Dr B began by maintaining that ‘the pathology is the behaviour’, but then moved towards arguing that it was the underlying pathology (psychopathy) rather than behaviour (antisocial acts) that was important to examine. Implicitly, this suggests that some pathology caused behaviour. Nevertheless, Dr B's own research constituted behaviour as salient: despite contesting its importance, much of Dr B's research had taken place in prisons, using individuals who had been formally categorized as antisocial through the act of sentencing as a result of criminality.

Discussion with the respondents around the importance of a history of formally antisocial behaviour when classifying an individual as personality disordered was generally framed around so-called ‘successful psychopaths’. Successful psychopaths were described as individuals who exhibited psychopathic traits, but who did not necessarily enact criminal antisocial behaviour (Babiak and Hare, Reference Babiak and Hare2006). At the very least, successful psychopaths were competent at hiding or deflecting their antisocial behaviour, preventing them from entering into a social context such as a prison where the possibility of diagnosis emerged. The extract below is representative of the respondents' views on successful psychopaths:

Dr E's reflections again reveal an ambivalence regarding whether the pathology is antisocial behaviour, or whether the pathology causes it. Furthermore, in extending the category of psychopathy to individuals who do not perform antisocial behaviour, Dr E brings the ‘disorder’ of psychopathy and ‘ordinary’ social deviancy into even closer alignment.

In discussing the ways in which alleged psychopaths might become ‘successful’, the respondents again drew on everyday notions about the development of personality. In particular, it was suggested that the means through which an individual with psychopathy might become ‘successful’ were primarily environmental: a particular set of life circumstances might shape the expression of the personality disorder such that any propensity to perform antisocial behaviours is curbed, or an individual might develop the social and intellectual capital to remain unnoticed. In Dr B's words:

Clearly, the scientists viewed ‘the environment’ as a powerful mediator through which personality disorder was expressed. Nevertheless, while ‘the manifestation of the psychopathy may depend on culture […] the underlying characteristics do not’ (Dr A).

From this discussion of the expression of personality disorder, it can be seen that, in line with the official criteria for the characterization of ASPD and psychopathy, the respondents considered the expression or clinical presentation of these conditions to be primarily through (criminally) antisocial behaviour. ASPD was almost solely expressed through behaviour, while psychopathy was a more deeply rooted pathology. The kinds of antisocial behaviour and personality traits suggested by the respondents were diverse, and reflected everyday understandings of ‘bad’ people. Accordingly, a wide variety of individuals could feasibly meet the criteria, especially for ASPD. Yet, in particular circumstances, individuals with ASPD or psychopathy might act in ways that were antisocial, but not necessarily criminal. Discussion of such individuals was characterized by ambivalence regarding whether personality disorder caused antisocial behaviour, or was antisocial behaviour. Regardless of these uncertainties, the scientists were more confident in their views on what mediates the expression of personality disorder. Similar to the scientific style of thought documented by Rose as evident in investigations of those ‘genetically at risk’ for antisocial behaviour (2007: 241), the environment was viewed as key to shaping this individualistic expression of personality disorder, resulting in the particular constellation of traits and behaviours that were recognizable to official terminological standards as either ASPD or psychopathy.

Discussion

This analysis casts light on the complex linkages made by neuroscientists between the realms of soma, psyche and society. It is clear that while genes are viewed as playing an important role in the development of ASPD and psychopathy, they are by no means construed as determining these conditions. Rather, genes are perceived as risk factors, influencing individual susceptibility to the later development of personality disorder (cf. Hedgecoe, Reference Hedgecoe2001; Rose, Reference Rose2007). The aetiological models constructed of ASPD and psychopathy also incorporated a number of ‘factors’, including so-called ‘environmental’ components. Each of these factors was viewed as interacting with the others in a complex and opaque matrix of association (cf. Shostak, Reference Shostak2003).

The complexity and opacity ascribed to ASPD and psychopathy underscores the different kinds of neuroscientific research that exist for this set of conditions, and the various ambivalences engendered in the scientists who study them. Is ‘personality disorder’ a set of behaviours and styles of interaction, or a brain dysfunction? Is there such a thing as a ‘successful psychopath’, and if so how is he or she different to one that is ‘unsuccessful’? These ambivalences draw attention to, first, the oscillation between different kinds of disease concepts (Canguilhem, Reference Canguilhem1998 [1966]) structuring theory and research into personality disorder, and thus the lack of consensus regarding its ontology, and, second, the ‘kind-making’ (Hacking, Reference Hacking2002) scientific investigation achieves even as ontological uncertainty endures. It is precisely because of the multimodality attributed to the causal processes of aetiology and expression that these uncertainties exist. If there was such a thing as ‘a gene for psychopathy’, the ontology of personality disorder could more readily be ‘fixed’; it would have less interpretative flexibility (Pinch and Bijker, Reference Pinch and Bijker1984) and, therefore, the potential for expansion of the use of the diagnostic would be lessened. Without the role for ‘the environment’ assigned by scientists in the aetiology and expression of these conditions, it is difficult to see how state intervention could be viewed as beneficial to ‘risky’ children, or how debate around the existence and pathological status of ‘successful psychopaths’ could emerge.

In reflecting on the framing of personality disorder by neuroscientists, this article has aimed to stimulate new questions about neuroscientific research into mental disorder. Long-standing critiques of biological reductionism are rendered problematic by the complex linkages scientists make between psyche, soma and society. If individuals with personality disorder are reduced to their genetics and neurology, they are also reduced to their social ecology, the multidimensional web of actors, structures and experiences within which they are situated—psychopaths are ‘ecologized’ almost as much as they are ‘neurologized’ (cf. Shostak, Reference Shostak2003). Contemporary neuroscience thus performs multiple and nuanced reductions, and in so doing demarcates and (re)configures the relationships between the domains of biology, psychology and society in the production of personhood.

However, the normative implications of such new geometries demand attention. The models of ‘the environment’ implicit in scientific research into behaviour and personality may be relatively unsophisticated compared to those employed by sociologists and anthropologists (Dingwall et al., Reference Dingwall, Nerlich and Hillyard2003), and their resonance with mundane, everyday understandings of the development of antisociality is striking. Furthermore, the degree to which biopsychosocial understandings potentially legitimate category expansion and controversial techniques for the governance of risky individuals (Rose, Reference Rose1998) is concerning. While critiques of reductionism and determinism may no longer adequately capture the nuances of contemporary neuroscientific research, the need for a critical sociology of ontology remains acute.