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This article argues that a new diagram is emerging in the criminal justicesystem as it encounters developments in the neurosciences. This doesnot take the form that concerns many ‘neuroethicists’ – it does not entaila challenge to doctrines of free will and the notion of the autonomouslegal subject – but is developing around the themes of susceptibility,risk, pre-emption and precaution. I term this diagram ‘screen and inter-vene’ and in this article I attempt to trace out this new configurationand consider some of the consequences.
criminal justice, law, neuroscience, risk, screening
In March 2008 Gary Pugh, the director of forensic science and the DNAspokesman for the UK’s Association of Chief Police Officers, attracted muchpublicity when he called for a debate on the measures required to identifyfuture offenders. He suggested that badly behaved primary school children– aged between 5 and 11 years – might have their DNA ‘fingerprints’ storedin the UK’s National DNA Database. He said: ‘If we have a primary meansof identifying people before they offend, then in the long term the benefitsof targetting younger people are extremely large. . . . We have to find whoare possibly going to be the biggest threat to society.’ Of course, the DNAprofile that would be stored on the database would be non-coding – just foridentification purposes – but the sample itself is retained, and, although Pugh
did not raise this possibility, it is entirely possible that, at some point, thiscould have been analysed for anomalies in coding regions related to brainfunctions; say, for neurotransmitters or receptors, that might be linked to thechild’s behavioural problems.1 Pugh was not a lone voice arguing for earlyidentification – many claim that those who will become prolific criminals startoffending young, and some research claims that by the time they reach 28,those who have had childhood conduct problems cost society up to 10 timesmore than those without (Romeo, Knapp and Scott, 2006; Scott, Knapp,Henderson et al
., 2001) and that adults with ‘personality disorder’ are excep-tionally costly to society (National Institute for Mental Health in England,2003). While those who think this way differ in their accounts of causation,and their suggestions as to the measures that are required, all seem agreed thatearly identification and intervention is the way to go (Harrington and Bailey,2003; Kim-Cohen, Moffitt, Taylor et al
., 2005; Margo and Stevens, 2008).
These arguments bring together two closely related senses of risk. The
first, is the desire to identify risky individuals
– that is to say, those who willpresent a future risk to others
– before the actual harm is committed. Thesecond is the hope that one might be able to identify individuals at risk
–those whose particular combination of biology and life history makes themthemselves s
usceptible to some future condition – here personality disorder,impulsivity, aggressivity or whatever, but more generally susceptibility forany psychiatric disorder. They bring these two senses of risk – risk to othersand risk to the self – together in a socio-political and cultural context with anumber of salient features. First, in domains from education to psychiatrywe have seen the rise of the belief that advances in neurobiology are centralto understanding individual conduct, both normal and pathological.2 Second,while there are many non-biological screening techniques in use, a wholerange of new technologies, notably those from behavioural genetics and brainscanning, claim that they can identify the precursors, signs or markers offuture riskiness in advance, presymptomatically or asymptomatically – thatthey can identify a ‘susceptible individual’.3 Third, we inhabit a culture of pre-caution, prevention and pre-emption, where the logic of many practices forthe conduct of conduct, and the obligation of those who must govern conduct,is to act early, to seek to prevent future undesirable events materializing, evenif one is acting only on the possibility that they might occur (Ericson andDoyle, 2003; Ewald, 2001; Sunstein, 2005). Whether it is early interventionfor children at risk of developing psychiatric disorders, early intervention forpersons convicted of minor offences who may go on to more serious crimes,or early diagnosis and intervention in cases of Mild Cognitive Impairmentthat may lead on to Alzheimer’s, many of those working in these areas sharethe view that, as the introduction to a recent collection of research papers putit, ‘earlier is almost always better’ (Lebowitz, 2004: 349). And while predic-tions are always probabilistic, decisions and actions are determinate, and tend
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
to assume the worst outcome and act to mitigate or prevent it – this is theobligation of risk management (Power, 2004).
This is the context – the conjuncture – that I want to reflect upon today.
Over the last two decades there has been a revived interest in the biology ofcriminality. But this does not search for the biological roots of crime in general,as did the earlier biological criminology (Rafter, 1997). It focuses specificallyon the biological basis of particular types of undesirable behaviour – thosethat involve impulsive or aggressive conduct and an apparent weakening ofthe conventional workings of guilt and remorse (Denno, 1990; Cauffman,Steinberg and Piquero, 2005; Fishbein and Henry, 2002). We can identify anumber of research pathways here, all of which converge on the brain. Thereare attempts to identify neurochemical anomalies that correlate with lowimpulse control or aggression (Brunner, 1996; Crusio, 1996; Miczek, deAlmeida, Kravitz et al
., 2007). There is the use of brain-scanning techniquesto see if there are characteristic patterns of brain activity in those who commitviolent or aggressive acts, or those who lack remorse or a sense of guilt(Bufkin and Luttrell, 2005; Krämer, Jansma, Tempelmann et al
., 2007; Raine,Buchsbaum and LaCasse, 1997; Raine, Buchsbaum, Stanley et al
There is research on localization of functions, seeking to identify brain regionsor neural circuits activated in aggression or impulsivity (Chen, Porjesz,Rangaswamy et al
., 2007; Hollander and Evers, 2001). There is geneticresearch, which today does not seek ‘genes for crime’ but tries to identify thespecific variations at the level of single nucleotides, or SNPs, that may belinked to low impulse control in specific biographical and environmental con-texts (Brunner, 1996; Brunner, Nelen, Breakefield et al
., 1993; Caspi, McClay,Moffitt et al
., 2002; Caspi and Moffitt, 2006; Wasserman and Wachbroit,2001). And, in a more directly forensic context, there is research that tries touse brain-scanning techniques to identify deception, for lie detection purposesin the interrogation of suspects or witnesses (Haynes and Rees, 2006; Kozel,Padgett and George, 2004; Kozel, Revell, Lorberbaum et al
., 2004; Langleben,Schroeder, Maldjian et al
These developments have generated much speculation: predictions of the
imminent convergence of behavioural genetics, neuroscience and law (Garlandand Frankel, 2006); florid claims-making on the part of some neurobiologists(‘brain overclaim syndrome’) (Kirchmeier, 2004; Mobbs, Lau, Jones et al
.,2007; Redding, 2006; Zeki and Goodenough, 2004); and much worrying onthe part of neuroethicists (Glannon, 2007; Illes, 2005; Levy, 2007; Marcus,2002; Parens, Chapman and Press, 2006; Wolpe, Foster and Langleben, 2005).4Will these developments do away with the idea of free will, upon which our
legal systems depend? Will defence lawyers claim that the responsibility oftheir client for a crime was mitigated – that it was the client’s genes, or brain,that made him or her commit the act? Should we think of crime as a disease,and with what consequences? Would the use of ‘brain-scanning’ in the legalsystem violate ‘neural privacy’? And much more in the same vein. Is thereany evidence for such speculations? Let us begin with the courtroom, withcriminal trials.
First, how about the ‘genetic defence’
– parodied as ‘my genes made me do
it’? The case that has been most widely discussed is that of Stephen Mobley,accused of murdering the manager of a Domino’s pizza store in 1991. Hislawyers sought to introduce genetic evidence – not to support a defence ofnot guilty but in mitigation of sentence. This was based on a family historywhich was claimed to show several generations of violence, aggression andbehaviour disorder in uncles, aunts and grandparents. The lawyers arguedthat this was relevant because of Han Brunner’s study which showed a linkbetween a particular syndrome – borderline mental retardation accompaniedby violence and aggression – and a point mutation in a gene regulating theproduction of an enzyme – monoamine oxidase A – linked to changes inlevels of various neurotransmitters (Brunner, Nelen, Breakefield et al
., 1993).5The Brunner study has become something of an exemplar to all futureattempts to find a genetic basis and a neurochemical mechanism for impulsiveor violent crime, seeming to show a clear causal pathway between a basesubstitution, the alteration in the structure and function of an enzyme, a deter-minate effect on a neurotransmitter linked to conduct and hence to that patho-logical conduct itself. But the court in the Mobley case refused to admit thisevidence. The grounds were similar to those used in earlier ‘biological’ defences– for example, the XYY cases in the 1970s (Saulitis, 1979), and the pre-menstrual syndrome cases in the 1980s (Allen, 1984). What the courts demandis a reasonably certain causal connection between the biological or geneticcondition in question and the specific act of criminal conduct. The Brunnerstudy was more complicated than popular reports implied. And Brunner him-self explicitly rejected this interpretation of his research, arguing that
the notion of an ‘aggression gene’ does not make sense, because it beliesthe fact that behaviour should and does arise at the highest level ofcortical organization, where individual genes are only distantly reflectedin the anatomical structure, as well as in the various neurophysiologi-cal and biochemical functions of the brain . . . although a multitude ofgenes must be involved in shaping brain function, none of these genesby itself encodes behaviour. (Brunner, 1996: 16)
Nonetheless his study has led to a host of follow-up research, some of whichI will discuss presently. But the point remains stubbornly true: there is a
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considerable distance between the probabilistic world of genetic research andthe deterministic thinking of the courts.
Although genetic arguments have been used by the defence in other cases,
in order to mitigate responsibility – such as the Kip Kinkel and Cary Staynercases which I discuss below – I know of no case where a genetic defence hassucceeded. Thus in Stayner’s, the defence called Dr Allison McInnes, assist-ant professor of psychiatry and human genetics at the Mount Sinai School ofMedicine in New York, who showed the jury a genealogical table of Stayner’sfamily history, with putative sufferers from mental disorders marked in differ-ent colors. Fresno Bee
reporter Cyndee Fontana described the testimony thus:
The story of Cary Stayner’s family tree rose in bursts of bright colorfrom a white horizontal chart. . . . Yellow for psychosis. Green forobsessive-compulsive disorder. Red for substance abuse. Purple forpedophilia. Even more colors for more mental diseases ranging throughfour generations down to Stayner himself – the fruit of a family genepool marked by psychiatric disorders. ‘So many different mental dis-orders’, said Dr McInnes as she led a jury through the branches of menand women, the flashes of color, that yielded the man convicted lastweek of murdering three tourists in February 1999.
Second, what of evidence from brain scans?
Some – for instance the US
Law and Neuroscience Project – suggest this will have a major impact in thecourts.7 Scans have been used in personal injury cases in the courtroom whereissues of brain injury are involved. Positon Emission Tomography (PET) andMagnetic Resonance Imaging (MRI) evidence of brain tumours has, on atleast one occasion, been used successfully to support a claim of insanity. Inthe famous case of John Hinckley, who was found ‘not guilty by reason ofinsanity’ for his attempt to assassinate Ronald Reagan the defence claimedthat computerized axial tomography (CAT) scans of the brain providedorganic evidence that Hinckley was schizophrenic.8 Hinckley’s acquittal onthe grounds of ‘not guilty by reason of insanity’ (NGRI) gave added impetusto the US campaign to reform the insanity and diminished capacity defences,which were severely limited in some 39 states, transformed into ‘guilty butmentally ill’ in 8 others (a verdict that allows any sentence up to and includingdeath), and abolished entirely in Illinois and Idaho (Moran, 1991).9 Nonethe-less, evidence from the new technologies for visualizing the brain found itsway into the American courts in the 1980s (Anderson, 1992).10 But, as far asI am aware, later attempts by defence lawyers in the USA to use scans todemonstrate ‘functional’ abnormalities – that is to say, where there is nolesion or injury – have not passed the test of reliability required for novelscientific evidence to be accepted by the courts in criminal cases.
Thus in the case of Kip Kinkel in Oregon, who murdered both his parents
and then returned to his school and shot a number of schoolchildren, thedefence called a pediatric neurologist who showed images from a singlephoton emission computed tomography (SPECT) scan apparently showingareas of decreased blood flow in the prefrontal cortex, the temporal occipitaland parietal lobes, and suggested that this was consistent with researchshowing a correlation between deficiencies in grey matter in these regionsand the onset of childhood schizophrenia. The judge, however, referred to a1996 change to the Oregon State constitution which shifted the focus ofcriminal punishment from ‘the principle of reformation’ to ‘the protectionof society’, and argued that the protection of society should be given mostimportance in his ruling in this case. He sentenced Kinkel to 25 years for themurders, and a further 40 months for each attempted murder, making a totalof more than 111 years in prison without parole. The subsequent appealfailed, the judge stating that the ‘protection of society’ consideration heldgreater weight than any other sentencing guidelines.11 And, in the 2002 trialof Cary Stayner for the horrific sexual assault and murder of three touristsin Yosemite, defence lawyers supported their plea of ‘not guilty by reasonof insanity’ with evidence from a host of psychiatrists.12 Experts sharply dis-agreed over the significance of Stayner’s brain scans, Dr Joseph Wu, for thedefence, seeing abnormalities in the images that could account for the defen-dant’s violent tendencies, while Dr Alan Waxman, called by the prosecution,saw nothing of the sort: on 26 August 2005, the jury took less than 5 hoursto find Stayner guilty of three counts of first-degree murder.
If such arguments from functional brain imaging were to gather strength,
however, what would be the implications? Not, I suspect, to eliminate thelegal fiction of freedom of will. When the judiciary defend the non-genetic,non-psychiatric fictions of free will, autonomy of choice and personalresponsibility, this is not because legal reasoning considers this to be a scien-tific account of the determinants of human conduct.13 Rather, the criminaljustice system deems it necessary to act on the basis of this image of the humanbeing for reasons to do with prevailing notions of moral and political order.
Indeed, the trend of contemporary legal thought, especially in the USA, isto operate on the premise of the inescapability of moral responsibility andculpability. On this basis, no appeal to biology, biography or society shouldbe allowed to weaken moral responsibility for the act, let alone to diminishthe requirement that the offender be liable to control and/or punishment. Inthis context, the argument from biology is likely to have its most significantimpact, not in diminishing the emphasis on free will necessary to a findingof guilt, but in the determination of the sentence. This is unlikely to be in thedirection of mitigation. For if antisocial conduct is indelibly inscribed in thebody of the offender, reform appears more difficult, and mitigation of punish-ment inappropriate. More likely are arguments for the long-term pacification
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
of the biologically irredeemable individual in the name of public protection.
This view seems to be gaining hold, even if it means the rejection of many‘rule of law’ considerations, such as those concerning the proportionality ofcrime and punishment.
But there is, however, another area where I think that neurobiology will
have a more significant impact. Would it be possible to identify individualswhose propensity to such conduct arises from genetic or neurochemicalanomalies or is, in some other way, inscribed in their biology? Perhaps toidentify them before any offending had taken place? For those who followthis line of reasoning, early diagnosis coupled with preventive interventionmay enable individuals so afflicted to be diverted from their path to crimi-nality (Farrington and Coid, 2003). This returns us to the question of riskwith which I began.14 Before turning to neurobiology, let us consider the wayin which the problem of risk is posed at the points where the mental healthsystem and legal systems intersect.
Over the last 20 years, mental health legislation and procedures in almost allwestern countries have become pervaded by risk-thinking (Alberg, Hatfieldand Huxley, 1996; Coid, 1996; Crichton, 1995; Moon, 2000; Rose, 1998a; Rose,1996; Steadman, 2000).15 The question of risk to others was a central concernin recent reform of the UK mental health legislation.16 The Foreword to the2002 Consultation Document on this bill recognized that only ‘a very few’people pose a risk to others ‘because of their illness’. But, nonetheless, thefocus of the proposed legislation was on risk assessment, risk management,risk communication between professionals and agencies, psychiatric treat-ment of mentally disordered offenders to reduce the risk of reoffending, and,of course, the use of the mental hospital as a site for the detention of thosethought to pose a risk to ‘the public’ irrespective of whether they are ‘treat-able’ and for as long as this risk of serious harm to others is judged to persist.
It is well known that there are many technical problems in predicting a
rare event, especially when the base rate of such events within the populationis extremely low – as it is with violent acts committed by those of us whohave received inpatient treatment for mental health problems. The historianof statistics Gerd Gigerenzer, in his Reckoning with Risk
, quotes the estimatemade by John Monahan for the US Supreme Court in 1980: the ‘best estimateis that two out of three predictions of long-term future violence made bypsychiatrists are wrong’ (Gigerenzer, 2002).17 Monahan was drawing on hisown research at the start of the 1980s which showed that in only 1 out of 3cases in which psychiatrists predicted violence did violence occur, despitethe fact that the subjects were institutionalized populations with a history of
violence and a mental illness diagnosis. Monahan estimated that the reverseerror – to wrongly predict there will be no
violent act – is much less frequent,and seems to occur in about 1 out of 10 cases. His influential 1993 paper withSteadman and others, entitled ‘From Dangerousness to Risk Assessment’,argued for a shift away from a binary and fixed distinction – dangerous/notdangerous – in favour of a continuous, day-to-day risk assessment involvinglocating the potentially risky person at the appropriate point on a continuum.
As his colleagues put it:
If an actuarially valid array of risk markers for violence could be reliablyidentified, clinicians could be trained to incorporate these factors intotheir routine practice, and the accuracy of clinical predictions of violenceamong the mentally disordered would be commensurately increased.
(Steadman, Monahan, Robbins et al
., 1993: 13)
In their early work, Monahan and Steadman were concerned to reduce thethreat to civil liberties resulting from the overdiagnosis of psychiatric patientsas dangerous. It is ironic, then, that the current political demand for riskassessment arises not from the fear of too much
detention, but from the fearof too little
The whole point of the shift from dangerousness to risk was the recog-
nition that behaviour is a product of multiple dynamic factors in a complexsituation. Robert Castel, in an insightful paper entitled ‘From Dangerousnessto Risk’ published a couple of years before Monahan and Steadman’s argu-ment, identified this trend very well – a move away from seeing dangerous-ness as an inherent part of an individual’s makeup towards a calculation ofrisk based on multiple factors (Castel, 1991). Within such a risk algorithm,the mental health status of the specific individual dissolves into this complexof factors – housing, employment, marital status, substance misuse and thelike. The point about such factors is that they are not inscribed within theperson. They are not diagnoses based on symptoms of illness. And they varyacross time and space. This conception of the situational genesis of violencemay be accurate. But to actualize it in practice would require a quite imprac-tical continuous monitoring of the everyday life of the ‘community mentalpatient’. So the reality is inescapable: the risk estimate is attached, not to thesituation, but to the individual.
How can we account for the prevalence of risk-thinking in psychiatry?
Some researchers claim to find clear evidence of a strong relation betweensevere mental illness, notably schizophrenia, and violent offending (Brennan,Mednick and Hodgins, 2000; Raine, Brennan and Farrington, 1997). But thenumber of homicides committed by those with a mental health diagnosis isstable, and the proportion of all murders is falling. Each year in the UK, thereare about 3,000 deaths from transport accidents, 2,000 from falls in the home,perhaps as many as 4,500 from suicide, around 700 from homicide, of which
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
around 70 – or 10 per cent – have been committed by people with a mentalillness diagnosis – a figure which has stayed more or less constant over thelast 20 years (Taylor and Gunn, 1999).18, 19 So what is the threat that gener-ates this fear of such violent or predatory monsters, and this demand for riskmanagement, out of all proportion to their actual contribution to violence orharm? I suspect this is something to do with that apparently harmless categoryof ‘the public’. In our ‘advanced liberal’ societies, there is a fundamental divi-sion between ‘we, the public’ who can, in our imagination, conduct ourselvesresponsibly according to the norms of civility, and those others that threatenus (Rose, 2000b). On the one hand there are fantasies of security, imaginedcommunities where normal individuals and families can live an untroubledlife of freedom. And, as its inescapable reciprocal, there is a constant fear ofpredatory monsters. A host of measures respond to this perception – gatedcommunities, closed circuit television cameras, the use of architectural devices– designed to ward off those who are thought to threaten this security. Thedemand for risk management of those who have a psychiatric diagnosis isone more way of seeking to manage the insecurities that the fantasy ofsecurity itself generates and intensifies. Risk assessment, or the demand forit, has a significance which is more symbolic than instrumental – it answersnot to the reality of dangers but to the politics of insecurity.
Mary Douglas and Aaron Wildavsky famously argued that ‘each form of
social life has its own typical risk portfolio’ (Douglas and Wildavsky, 1982:6). A risk portfolio is a way of selecting, out of all possible, real or imaginedthreats and harms, those that shall be the focus of individual or collectiveattention. This selection is, inescapably, done in relation to moral evaluationsshaped by cultural norms. Risk, in relation to mental disorder, is certainlyhigh in the risk portfolio for many – the perception that mental illness carriesthe risk of violence towards others, and alternatively that violence is, at root,a matter of mental pathology. This perception, rather than any increase inactual harms, underlies the promulgation of laws and other measures to focusrisk assessment and risk management on psychiatric patients. But what placesthe risks of those in this heterogeneous category so high in the risk portfolioof public, media and politicians?
Perhaps this can be understood, in part, by the ways in which risk-thinking,
in psychiatry, brings together two rather different senses of risk. In the first,as we have seen, there is a continuum of risk. In principle we can all be placedon this continuum, for – given certain circumstances – each of us mightcommit violent acts, and those who are young, are male and consume alcoholmight find ourselves rather high on such a scale. However, the arbitrarycategories of persons placed high on our contemporary ‘risk portfolio’emerge from another, older sense. This is not a continuum but a binary oppo-sition between the normal and the abnormal. In this opposition, some peopleare fundamentally different. They are ‘monstrous individuals’. A monstrous
individual is an anomaly, an exception. This is not merely one who divergesfrom a norm, but one who is of a radically different nature, implacably patho-logical, evil. These are the ‘predators’ of popular imagination – sex offenders,paedophiles, serial killers and, as the newspapers would put it, derangedmental patients freed to kill again. And, of course, these are the people whoare dangerous because of their ‘personality disorders’ who caused so muchconcern in the UK in the early years of this century, because it seemed thatthey escaped both mental health and criminal legislation: hence a change inthe law to enable them to be detained so long as they posed ‘a grave risk tothe public’.
I call this ‘governing through madness’. By this I mean the ways in which
contemporary politics of mental health has come to be shaped in response toa more general demand for a politics of community protection and publicdefence: anxiety about the risks posed by those with mental health problemsthus becomes one element in the justification of a more general shift in thelogics of regulation. Psychiatry itself has been reoriented within these strat-egies of control formulated in terms of risk. To satisfy the public and politi-cal demand for the identification of the potentially monstrous, psychiatricrisk-thinking has come to connect the routine management of those with ahistory of psychiatric troubles and the problem of the identification of theexception along a single dimension of risk assessment. Risk assessment in thename of the prevention of relapse has become entwined with strategies forpre-emptive intervention in the name of community safety; with the dream– or nightmare – that it is possible to identify and exclude those who areincorrigibly risky and potentially monstrous – incarceration without reform.
Historical precedents would suggest that such strategies are unlikely toreduce the overall frequency of the very rare incidents they seek to prevent.
But they are likely to result in threshold-lowering and net-widening, andthe detention of many individuals who are capable of leading lives that mightsometimes be troublingly different but would pose no dangers to others(Cohen, 1985).
The shift from dangerousness to risk has not displaced an earlier attempt –to read danger in the makeup of the individuals themselves. Consider tworecent developments in the UK. The first goes under the name of ‘Dangerousand Severe Personality Disorder’ or DSPD. The second goes under the nameof the Indeterminate Public Protection Sentence. Let me begin with DSPD.
The concern that led to the formulation of this category arose from a peculiarparadox in mental health legislation – under the Acts passed since the 1950s,an individual could only be detained against his or her will in a psychiatric
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hospital if their condition was treatable. But there were some characters, proneto commit unpleasant acts ranging from urinating in the street to violence,whose disorders were not considered to be psychiatric illnesses – althoughthey were diagnosed by psychiatrists – but disorders of personality: not statesof illness but traits of the person. Traits, for psychiatrists, were enduringfeatures of personality that might be managed but they could not be ‘treated’.
So those individuals, often termed psychopaths, could not be detained underthe mental health legislation. But nor could they be detained under the crim-inal law except by means of a specific sentence after a finding of guilt for aparticular act that they had already committed. In the classical retrospectivegaze of the criminal law, individuals could not be detained simply becauseauthorities or experts thought it likely that they would commit certain actsin the future. Hence, the problem for those who would govern risk, for theiraim is indeed to govern the future.
Of course, to some extent concern with such persons is coextensive with
psychiatry itself. In 1835 Pritchard identified a condition that he termed‘moral insanity’:
. . . a morbid perversion of the natural feelings, affections, inclinations,temper, habits, moral dispositions, and natural impulses without anyremarkable disorder or defect of the intellect or knowing or reasoningfaculties and in particular without any insane delusion or hallucination.
. . . The moral and active principles of the mind are strongly pervertedor depraved; the power of self government is lost or greatly impaired,and the individual is found to be incapable not of talking or reasoningupon any subject proposed to him, but of conducting himself withdecency and propriety in the business of life. (Pritchard, 1835: 6)
Forty years later, Maudsley wrote: ‘[It is] a form of mental alienation whichhas so much the look of vice or crime that many people regard it as an un-founded medical invention’ (Maudsley, 1874). And it was this condition thatbecame the psychopath: the Oxford English Dictionary
tells us that the PallMall Gazette
first used this term in 1885: ‘
We give M. Balinsky’s explanationof the new malady. “The psychopath . . . is a type which has only recentlycome under the notice of medical science. . . . Beside his own person and hisown interests, nothing is sacred to the psychopath.”’ In the UK’s MentalDeficiency Act 1914, these people were referred to as ‘moral defective’ (UKMDA 1914) and in the legislation of 1927, as ‘moral imbeciles’ (UK MDA1927). The UK’s Mental Health Act 1959 introduced the term ‘PsychopathicDisorder’ and over the 1970s, psychiatrists began to explore the world of‘Personality Disorder’ and ‘Anti-Social Personality Disorder’ (McNeil, 1970).
This is not the place to go into this history in any depth, just to locate themost recent expression of this problematization: termed in the UK ‘Danger-ous and Severe Personality Disorder’.
This term was introduced in 1999 in a report entitled ‘Managing Danger-
ous People with Severe Personality Disorder’ although it was neither apsychiatric diagnosis nor a legal category (Home Office and Department ofHealth, 1999). It seems to have been understood as an extension of the diag-nosis of antisocial personality disorder (ASPD) – which appears to be mostclosely associated with the notion of psychopathic disorder, the legal termused in UK mental health legislation to refer to people who have ‘a persist-ent disorder or disability of mind . . . which results in abnormally aggressiveor seriously irresponsible conduct’. The Diagnostic and Statistical Manual ofMental Disorders
) definition of this condition is
. . . a pervasive pattern of disregard for and violation of the rights ofothers occurring since age 15, as indicated by three (or more) of thefollowing: failure to conform to social norms with respect to lawfulbehaviors as indicated by repeatedly performing acts that are groundsfor arrest; deceitfulness, as indicated by repeated lying, use of aliases,or conning others for personal profit or pleasure; impulsivity or failureto plan ahead; irritability and aggressiveness, as indicated by repeatedphysical fights or assaults; reckless disregard for safety of self or others;consistent irresponsibility, as indicated by repeated failure to sustainsteady work or honor financial obligations; lack of remorse, as indicatedby being indifferent to or rationalizing having hurt, mistreated, or stolenfrom another. (American Psychiatric Association, 2000: 649–50)
The initial move in the UK was to assert that ASPD should ‘no longer be
a diagnosis of exclusion’ – that is to say, that those with this diagnosis shouldand could be treated, although not all would associate ‘inclusion’ with theextension of the powers of the Mental Health Act to compulsorily detain andtreat persons so diagnosed. But pretty soon, the strategy for ASPD mergedwith that for DSPD. Over £100 million has been spent on setting up a DSPDprogramme which declares itself dedicated to ‘Ensuring the public is pro-tected from some of the most dangerous people in society’.20 In other words,including those with DSPD by excluding them – by confining them in securefacilities in the name of public protection.
At about the same time as the DSPD programme was being established,
the UK government instituted some other ‘public protections measures’ in theCriminal Justice Act 2003 including something known as an ‘indeterminatesentence for public protection’.21 This enables judges, not only to set a min-imum tariff for a prison sentence, but to require the defendant to satisfy theauthorities that he or she is fit for release at the end of the allotted stretch,and does not pose any threat to the community. Individuals considered to bea continuing threat can be detained for indefinite periods, on the grounds ofan expert psychiatric judgement of their dangerousness, even if they have been
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convicted of a minor offence such as setting a fire. An Indeterminate PublicProtection Order is in effect a life sentence for individuals judged to be risky,or from whom the public is deemed in need of protection: as with a lifesentence, even if released, the individual is on a lifetime licence and can berecalled to prison at any time. Initially designed as a measure to detain a smallnumber of exceptionally dangerous individuals, by 2007 almost 3,000 peoplewere being detained in prison under these provisions, with the numberexpected to rise to over 12,000 by 2012.22
I think I have said enough to indicate that, in the UK at least, the hunt is
on for measures to identify those who are at risk of risk. The same is true inthe United States, as we will see presently. It is in this context that we canlocate current concerns about the neurobiology of antisocial conduct. Let meturn directly to this issue.
As in the UK, in the United States in the 1990s, there was a belief that therewas something of an epidemic of crimes of aggression, impulsivity, lack ofself-control. Whereas in the past, some had argued that criminality itself wasa disease, now the argument was slightly different: violence was a publichealth problem. In the early 1990s, the US National Institutes of MentalHealth launched the National Violence Initiative. Psychiatrists would seekto identify children likely to develop criminal behaviour and would employintervention strategies with them. The official report from this initiativeissued in 1993 and 1994 in four volumes called for more research on bio-logical and genetic factors in violent crime (Reiss and Roth, 1993; Reiss, Rothand Miczek, 1994). It also called for research into new pharmaceuticals thatmight reduce violent behaviour. By 1992, the US federal government, inpartnership with the Macarthur Foundation, was sponsoring a large-scaleinitiative entitled the ‘Program on Human Development and CriminalBehavior’ to the tune of some $12 million per year.23 The project aimed atscreening children for biological, psychological and social factors that mayplay a role in criminal behavior, and proposed to follow subjects over an8-year period, with a view to ultimately identifying biological and bio-chemical markers for predicting criminality. While this umbrella programwas withdrawn as a result of controversy surrounding the violence initiative(Wasserman, 1995), resulting in part from some injudicious remarks by thehead of the programme, Dr Frederick Goodwin, individual projects continuedto be sponsored by the federal government.
While critics saw this as a dangerous programme of social control, prop-
onents saw it somewhat differently. Diane Fishbein of the US Departmentof Justice argued that
Once prevalence rates are known for genetically influenced forms ofpsychopathology in relevant populations, we can better determine howsubstantially a prevention strategy that incorporates genetic findingsmay influence the problem of antisocial conduct . . . [At a minimum theevidence] suggests the need for early identification and intervention.
(Fishbein, 1996: 91–4)
Indeed, as Daniel Wasserman has pointed out, biological criminologists didnot believe that their work would discover ‘causes of crime’ but hoped that itmight identify markers and genes associated with that behaviour (Wasserman,1996).
I have already mentioned the Han Brunner study, linking aggressive beha-
viour and lack of impulse control to variations in the gene sequence regulatingthe monoamine oxidase A. This study, and some others by the same team,has been cited hundreds of times in the subsequent 15 years. It has becomea model for a certain style of reasoning which tries to trace a more or lessdirect line from a single nucleotide polymorphism in a coding sequence, toa variation in the structure and function of the protein – the enzyme – forwhich it coded, to an increased susceptibility to pathological conduct. Reason-ing in these terms, a cascade of papers were published in the closing years ofthe 20th century and the early years of the 21st claiming to have discoveredsusceptibility loci
in sequences coding for aspects of the neurotransmittersystems in the brain, relating to depression, anxiety disorders, and the dis-orders of children such as Attention Deficit Hyperactivity Disorder (ADHD)and conduct disorder (Manuck, Flory, Ferrell et al
Much of this work was done with animal models from fruit flies to rodents
(Hendricks, Fyodorov, Wegman et al
., 2003). Thus, for example, in 2003, EvanDeneris and his colleagues at Case Western University, working with mice,reported the discovery of the Pet-1 gene – only active in serotonin neurones– which when knocked out produced elevated aggression and anxiety in adultscompared to wild type controls. The university press release pointed out that
Serotonin is a chemical that acts as a messenger or neurotransmitterallowing neurons to communicate with one another in the brain andspinal cord. It is important for ensuring an appropriate level of anxietyand aggression. Defective serotonin neurons have been linked to exces-sive anxiety, impulsive violence, and depression in humans. . . . Anti-depressant drugs such as Prozac and Zoloft work by increasing serotoninactivity and are highly effective at treating many of these disorders.
(Press release, ‘Researchers discover Anxiety and Aggression Gene inMice; opens New Door to Study of Mood Disorders in Humans’, 2003)
And Deneris himself comments: ‘The behavior of Pet-1 knockout mice isstrikingly reminiscent of some human psychiatric disorders that are charac-terized by heightened anxiety and violence.’24
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
In similar vein, Miczek et al
., in their 2007 paper on the ‘Neurobiology
of Escalated Aggression and Violence’, move seamlessly from fruit flies torodents and humans: they write:
Psychopathological violence in criminals and intense aggression in fruitflies and rodents are studied with novel behavioral, neurobiological,and genetic approaches that characterize the escalation from adaptiveaggression to violence. . . . One goal is to delineate the type of aggres-sive behavior and its escalation with greater precision; second, the pre-frontal cortex (PFC) and brainstem structures emerge as pivotal nodesin the limbic circuitry mediating escalated aggressive behavior. . . . Bymanipulating either the fruitless
genes in the brains ofmale or female flies, patterns of aggression can be switched with malesusing female patterns and vice versa. . . . New data from feral rats pointto the regulatory influences on mesocortical serotonin circuits in highlyaggressive animals via feedback to autoreceptors and via GABAergicand glutamatergic inputs. Imaging data lead to the hypothesis that anti-social, violent, and psychopathic behavior may in part be attributableto impairments in some of the brain structures (dorsal and ventral PFC,amygdala, and angular gyrus) subserving moral cognition and emotion.
(Miczek, De Almeida, Kravitz et al
., 2007: 11803)
Considering the implications of this kind of research on behavioral genomicsfor violence prevention in 2003, Morley and Hall, of the Australian Instituteof Criminology, listed candidate gene variants that have been nominated ashaving a potential bearing on an ‘individual’s liability to develop antisocialbehavioural characteristics’ – variants in the genes for elements of the sero-tonergic system linked to impulsivity, those for elements in the dopaminergicsystem linked to ADHD, those for elements in the noradrenergic systemlinked to ADHD, impulsivity and hostility, and those linked to the activityof enzymes involved in the metabolism of neurotransmitters linked toADHD, impulsivity, aggression, conduct disorder and criminal conviction– nonetheless stressing that ‘an individual will only have a significantlyincreased risk of engaging in antisocial behavior if they carry a large numberof variant genes’ (Morley and Hall, 2003: 4).25 And they conclude that while‘Genetic research is beginning to identify genetic variants that may have somebearing on an individual’s liability to develop antisocial behavioural character-istics’ this was not a matter of single genes – instead, the issue was relocatedin the contemporary style of thought about ‘susceptibilities’. Indeed theirreport was entitled ‘Is there a Genetic Susceptibility to engage in CriminalActs’, and argued that it was likely that ‘a large number of genetic variantswill be identified that, in the presence of the necessary environmental factors,will increase the likelihood that some individuals will develop behaviouraltraits that will make them more likely to engage in criminal activities’ (Morleyand Hall, 2003: 4–5).
This then is the style of thought that is taking shape, not only in relation
to antisocial behaviour but also in relation to other problems – polygenicsusceptibilities that increase or decrease susceptibility to environmentalfactors, and hence in appropriate (or inappropriate) circumstances will lead toan undesired outcome. The reference paper for humans themselves is usuallythat by Caspi and his colleagues (2002) which has been cited hundreds oftimes in the years that have followed. This was based on research with a largecohort study, and followed Brunner in focusing on the link between the genefor monoamine oxidase A (MAOA) and violent conduct. But its novelty layin the claim to have discovered ‘gene-environment interactions’. The paperclaimed that ‘a functional polymorphism in the gene encoding the neuro-transmitter-metabolizing enzyme monoamine oxidase A (MAOA
)’ moder-ated the effect of familial environment, in this case the effect of maltreatment.
‘Maltreated children with a genotype conferring high levels of MAOA
expres-sion were less likely to develop antisocial problems. These findings may partlyexplain why not all victims of maltreatment grow up to victimize others, andthey provide epidemiological evidence that genotypes can moderate children’ssensitivity to environmental insults’ (Caspi, McClay, Moffitt et al
., 2002:851). The authors concluded that although individuals with the combinationof low activity MAOA and violence were only a small proportion of thecohort, they accounted for 44 per cent of those with convictions for violenceand hence ‘these findings might inform the development of future pharmaco-logical treatments’ (ibid.: 853). This was the first of a slew of studies by thisteam that were considered by many to change the way in which the relationbetween genes and environment was conceived in psychiatric disorders:genetic variations at the SNP level were now thought of as producing suscep-tibilities that were triggered in response to environmental insults. And becausethey were identifiable sequences that could in principle be identified in child-hood by gene-sequencing, the susceptibility to maltreatment might be identi-fied early and intervened on in the name of prevention.
What might be the implications of this line of research? Perhaps the most
likely is the development of programs of screening to detect individualscarrying these markers. Neurobiological expertise could thus provide thebasis for risk prevention strategies by a variety of agencies of social control,leading to pre-emptive intervention, perhaps by pharmaceuticals, perhaps byother measures. We are already seeing the rolling-out of programmes suchas TMAP (the Texas Medication Algorithm Project) for screening adults inrelation to major psychiatric conditions,26 whose version for screeningchildren (TCMAP) proved particularly controversial due to claims that it wasacting as a powerful marketing tool for pharmaceutical companies.27 OtherUS screening programmes for children include Teenscreen for screeningteenagers,28 together with programmes for identifying young children withADHD. As far as I am aware, none of these yet uses neurobiological or
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
genetic tests. But it is certainly possible to envisage the development ofschool-based strategies, with pre-emptive treatment a condition of continuingschooling. Indeed, now that ADHD is no longer considered a transient dis-order of childhood, but potentially a lifetime condition, and indeed a bio-marker of later psychopathy, we see yet another instance of the categoryexpansion that might result from the large-scale adoption of screen-and-intervene strategies for problematic conduct.
In another field, given the rise of measures for public protection such as
those I have described in the UK, one might imagine post-conviction screen-ing of petty criminals, with compliance with treatment made a condition ofprobation or parole. Or one can envisage scenarios in which screening andtherapy are offered to disruptive or delinquent employees as an alternativeto termination of employment. There are suggestive precedents here in theways in which psychiatric medications such as Antabuse for alcoholics andlithium for manic depression, were introduced in the USA. And biologicalexpertise might be called upon to screen for genetic markers and neuro-chemical abnormalities, in order to evaluate the levels of risk posed byoffenders, or non-offenders with a mental illness diagnosis prior to dischargefrom prison or hospital. Release would be dependent on compliance with adrug regime. But to conclude, let me give you one example from the UK toillustrate the way in which these relations between genes, brains and beha-viour are now being conceptualized.
Consider, for example, the programme of research funded by the Medical
Research Council, the Department of Health and the Home Office, andcarried out at the Institute of Psychiatry, King’s College London (Viding,Blair, Moffitt et al
., 2005; Viding, Jones, Frick et al
., 2008; Viding, Larssonand Jones, 2008). This illustrates quite clearly the line of reasoning – perhapsthe style of thought – that is taking shape here (Odgers, Moffitt, Poultonet al
., 2008). The research has argued as follows. First, that one particularsub-type of antisocial behaviour, that with ‘callous and unemotional traits’ –AS-CU – is a precursor of adult psychopathy. Second, that the characteristicsof childhood AS-CU and adult psychopathy map onto one another – in bothchildren and adults we see lack of empathy, lack of guilt and remorse, shallowaffect and manipulative conduct, and in such children we can also see pre-cursors of adult violence, such as cruelty to animals and enjoyment ofaggression. Third, if we look at studies of psychopaths, psychological testsshow them to be poor at empathizing with others and bad at recognizingtheir fear and sadness, and brain scans show them to have a disruption of oneparticular part of the brain, the amygdale, which is, so it seems, implicatedin these ‘affective’ defects. Fourth, if we take twin pairs aged around 7 years,some monozygotic and some dizygotic, who have been assessed for AS-CUand carry out functional Magnetic Resonance Imaging (fMRI) scans on them,we find the same deficits in the brains’ ‘affect circuitry’ in the AS-CU subjects
as we see in adult psychopaths. Finally, if we use classical twin study methods,taking environmental factors into account, we find a much higher correlationof these brain patterns in the genetically identical twins than in non-identicaltwins – i.e. the trait is highly heritable, and suggests a strong genetic vulner-ability. Hence, it is argued, we should search for the precise Single NucleotidePolymorphism (SNP) level variations that underlie this vulnerability. Butnote, for this line of reasoning, what we have here is a vulnerability, a suscep-tibility. It is not surprising, then, that those working on this study are closelylinked to the Caspi and Moffitt research group, who aim to identify the geneenvironment interactions which provoke vulnerability into frank psycho-pathy (Caspi, McClay, Moffitt et al
., 2002; Kim-Cohen, Moffitt, Taylor et al
.,2005; Odgers, Moffitt, Poulton et al
., 2008). The message is not fatalism butearly identification and early intervention into the home and family, usingbehaviour therapy, cognitive therapy and psychopharmaceuticals – for thiscan reshape brain mechanisms in order to nip those ‘budding psychopaths’in the bud.
I think that, in many departments of life, we are seeing the emergence of anew ‘human kind’: the susceptible individual. In the developments I havediscussed here, this takes the form of the person with an elevated neuro-biological risk of being the perpetrator of aggression or violence. This is notmerely the modern version of an older idea of the dangerous individual, forbiology here is not destiny. As in other areas of contemporary genomics, therelation between biology and criminality is being posed in terms of ‘suscep-tibility’, and the shaping, exacerbation or mitigation of that susceptibility overa life-course as a consequence of biography, experience and environment.29This way of thinking, therefore, is so powerful because it is imbued with hopeas well as anxiety. The hope, on the part of many researchers, practitionersand clinicians, is that these susceptibilities can be identified and hence opena pathway to preventive intervention which would steer the susceptible indi-vidual onto a more favourable path, one less damaging to herself or himselfand less costly to others. Yet the anxiety on the part of policy-makers, andthe priority given to the precautionary principle, have the potential to leadto a less optimistic future, in which widespread screening for biomarkers offuture psychopathology or undesirable conduct, notably those made possibleby developments in genetic profiling and brain-scanning, would lead to asignificant increase in preventive interventions in the name of public protec-tion. This is more likely in an environment in which psychiatric professionalshave already been given the obligation of governing, and being governed, inthe name of risk. And it will find a favourable ecological milieu in a political
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
and public culture suffused by insecurity and imbued with a fear of all thosewho appear unable to adopt the forms of responsible and prudent self-management that are obligatory in our current societies of freedom. In anyevent, perhaps we need to pause, and to ask ourselves what are the benefits,and what are the dangers, of this emerging logic for the conduct of conduct:not so much ‘discipline and punish’, but ‘screen and intervene’.
The material presented in this article draws extensively on the text of Chapter 8 ofmy book The Politics of Life Itself
(Princeton, NJ: Princeton University Press, 2006),although it is reframed in the current argument. Versions of the paper were givenat a workshop organized by the European Network of Neuroscience and Society,Harvard, May 2008 and a symposium at the Centre Koyré, Paris, May 2008, and theNeurocultures Workshop organized by the Brain, Self and Society project at the BIOSCentre of the LSE and the Brainhood project of the Max Planck Institute, Berlin inFebruary 2009. I thank the organizers and participants of these events for all theircomments. As my aim was to propose a general argument on the basis of an overviewof a wide range of materials, I have chosen to retain the spoken form in this article.
1 For a discussion of the loose controls on research undertaken on the UK’s
National Forensic DNA database, see Nuffield Council on Bioethics (2009).
2 See, for a UK example, the programme on ‘Understanding Individual Behaviour’
launched by the ESRC as one of their ‘grand challenges’ in their Strategic Planfor 2005–10:
Understanding Individual Behaviour and its Relationship to Biological andSocial Determinants
: Solving many of the challenges facing UK societydepends on improving the effectiveness with which individuals can takecontrol of their own lives. This involves the relationship between indi-vidual behaviour and a range of biological, technological and social influ-ences. . . . By 2010 we will have
: Collaborated with the Medical ResearchCouncil to support social neuroscience research aimed at linking ourgrowing knowledge of brain mechanisms to human and social behavior . . .
available at: http://www.esrcsocietytoday.ac.uk/ESRCInfoCentre/Images/Strategic_Plan_2005–10_tcm6–12995.pdf
On neuroscience as a key to educational policy, see the mission statement of
the University of London’s recently established Centre for Educational Neuro-science at: http://www.educationalneuroscience.org.uk/mission.html
Or, on the crucial importance of neurobiology in psychiatry, see Lee, Ng et
. (2008); Sachdev (2002); and Yudofsky and Hales (2002).
3 An ISI search shows a gradual increase in articles on susceptibility in psychiatry
over the 1990s and 2000s: some 891 articles on susceptibility in psychiatry werepublished in 2008, 829 in 2007 and 752 in 2006; 420 in 1998, 411 in 1997 and 322in 1996.
4 I will not discuss an earlier phase of speculation on crime as a disease, e.g. Mark
and Ervin (1970), or the more extreme claims of Adrian Raine (Raine, Brennan etal
., 1994); Farrington (1997); Scarpa and Raine (1997) and Raine and Liu (1998).
5 Brunner (1996) discusses the implications of his research in rather different terms.
6 See under ‘Updates’, accessed 29 August 2005: http://www.crimelibrary.com/
serial_killers/predators/stayner/ Dr McInnes describes her current research areaas neurobehavioral genetics.
7 http://www.lawandneuroscienceproject.org/8 The Hinckley case and subsequent cases using brain scans are discussed in Denno
9 In fact, the implications of the Hinckley case are complicated because, under US
federal law, the prosecution had to prove beyond reasonable doubt that thedefendant was sane at the time of the offence; in most individual states and otherjurisdictions the defence must prove by the preponderance of evidence that thedefendant is insane – a standard which would probably have led to a convictionfor Hinckley.
10 By 1992, for the first time in the USA, a court allowed an expert to draw upon
evidence from a PET scan in determining the defendant’s sanity, although in theend the matter was resolved by lowering the charge from murder to man-slaughter and avoiding a trial: see People v.
Weinstein, 591 NYS.2d 715 (Sup. Ct.
1992). The court concluded that expert evidence and consideration of the resultsof a PET scan and other physiological tests – to indicate a cyst and metabolicimbalances in the defendant’s brain – was not unreasonable in making a diag-nosis of insanity, but agreed to negotiate a reduced charge from murder tomanslaughter, rather than going to trial. In the trial of Michael Person, in NewHaven, Connecticut, in early 1998, prosecutors contested the attempts of defencelawyers to present the jury with PET scans showing brain abnormalities, and tointroduce the findings of Adrian Raine on the increased prevalence of abnormalbrain scans in convicted murderers in seeking to reduce the charge from murderto manslaughter. Another early case involving a request to introduce brain scanswas that of Jack Dempsey Ferrell, who was convicted in 1995 of the first-degreemurder of his girlfriend in 1992. At his appeal hearing before the Supreme Courtof Florida in 2005, Ferrell contended that his counsel at his first trial should havesupported arguments that he had suffered neurological impairment with a brainscan. At hearings between the original trial and the final appeal, the state hadobjected to the request for SPECT scans to be conducted, not only because therewas already a diagnosis of frontal lobe brain damage which had been taken intoaccount as a mitigating factor, but because no scan could show how the physicalbrain affected Ferrell’s capacity to function. The Supreme Court of Florida, inits ruling of 16 June 2005 (No. SC03–218), was of the view that ‘a particularizedshowing of necessity is the polestar for whether any diagnostic test should beauthorized’ and that this had not been demonstrated in Ferrell’s case.
11 More recently some have suggested that Kinkel was suffering from adverse
effects of Prozac and Ritalin that he had allegedly been taking at the time of themurders and extended this claim to the young people responsible for a numberof other school shootings in the USA. See, for example, Dan Edwards, accessed29 August 2005, at: http://www.geocities.com/StNektarios/BIOPSYCH.html
‘SCREEN AND INTERVENE’: GOVERNING RISKY BRAINS
12 The fullest account of this case that I have been able to find is that provided in
2005 by Court TV and accessed 30 August 2005 at: http://www.crimelibrary.
com/serial_killers/predators/stayner/ I have drawn on that report here.
13 Rose (2000a).
14 Raine’s work, cited above, also has come to focus on the issue of risk and predic-
tion (additionally, see Raine, 2002).
15 Of course, concern with troubling and troublesome individuals who appear to
fall between the jurisdiction of the two great apparatuses of confinement – thecriminal justice system and the psychiatric system – is long-standing. However,as I and others have argued, the shift from dangerousness to risk thinking, whichcan probably be dated to the 1980s, and is firmly in place in most countries bythe 1990s, marks a significant mutation. The work of Monahan and Steadman,which I discuss below, is exemplary here. See Duggan (1997), Rose (1996) andRose (1998a, 1998b).
16 In the UK, the Consultation Document on the Draft Mental Health Bill of June
2002 makes an interesting distinction between danger and risk. ‘Some people . . .’,the ministers say in their Foreword, ‘because of their illness, can be a danger tothemselves, whilst a very few can, at times, pose a risk to others.’ This distinc-tion of danger and risk is not sustained in the arguments around the Bill (Depart-ment of Health, 2002).
17 The original comment can be found in Monahan (1981).
18 Homicide figures vary from around 600 to 750 depending on the method of
calculation. See Office of National Statistics (2003).
19 On the basis of their examination of public inquiries into homicides by people
with mental illness, Munro and Rumgay argue that improved risk assessmenthas only a limited role in reducing homicides and that more deaths could beprevented by improved mental health care irrespective of the risk of violence(Munro and Rumgay, 2000).
20 A special supplement of the British Journal of Psychiatry
, in 2007, was devoted
to articles debating the nature and efficacy of the DSPD programme – see BritishJournal of Psychiatry
190(suppl. 49) (2007) (doi: 10.119 2 / bjp.19 0. 5. s1). Thefigure of £100 million does not include the cost of building the four DSPD unitsat Special Hospitals. The cost of confining an individual in a high-securityhospital is over £200,000 per patient per year (Maden, 2007).
21 The sentences are set out by the National Offender Management Service of the
Ministry of Justice at: http://noms.justice.gov.uk/managing-offenders/sentences/punishment/Life-sentences/
For a discussion and rather critical review of the Indeterminate Sentence for
Public Protection by Her Majesty’s Inspectors for Prison and for Probation, see:http://inspectorates.homeoffice.gov.uk/hmiprisons/thematicreports1/IPP_thematic_(2008).pdf
22 The 2007 figures are from the Ministry of Justice, Sentencing Statistics 2007,
England and Wales
(2009: 36). These figures include both the sentence of IPPand the related sentence of Extended Sentence for Public Protection. The extrap-olation, credited to a Home Office official, is given in a discussion of the sentencesby David Rose (no relation) in the New Statesman
in 2007, and can be found at:http://www.newstatesman.com/politics/2007/03/risk-prison-sex-act-life
23 http://www.ncjrs.gov/App/Publications/abstract.aspx?ID=11254724 Accessed 3 May 2008 at: http://www.sciencedaily.com/releases/2003/01/
25 They helpfully provide an analysis of candidate genes for antisocial behaviors
and a glossary at: http://www.aic.gov.au/publications/tandi2/tandi263.html
26 Accessed 24 February 2009 at: http://www.dshs.state.tx.us/mhprograms/
kids/TCMAP was suspended in September 2008.
28 Accessed 24 February 2009 at: http://www.teenscreen.org/teenscreen-schools-
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NIKOLAS ROSE is the James Martin White Professor of Sociology and thedirector of the BIOS Centre at the London School of Economics and Politi-cal Science.
: London School of Economics and Political Science – BIOS Centre,Houghton Street, London, WC2A 2AE, UK. [email: firstname.lastname@example.org]
Muzaffar ad-Din Schah auch Mozaffar ad-Din Schah (* 1853; † 1907) regierte von 1896 bis 1907 als Schah von Persien. Muzaffar ad-Din Schah war mit einer unbekannten Anzahl Frauen verheiratet, hatte 7 Söhne und 15 Töchter. Sein Nachfolger wurde sein ältester Sohn Mohammed Ali. Konzessionen und Kredite Der älteste überlebende Sohn von Naser al-Din Schah, Mass'oud Mirza Zel -e S
T A B L E T S / C H E W A B L E T A B L E T S / O R A L G R A N U L E S Composition Each tablet/sachet contains: Active Ingredient Tablets: Each 10 mg Tablet contains 10.4 mg montelukast sodium, equivalent to 10mg free acid. Chewable Tablets: Each 5 mg chewable tablet contains 5.2 mg montelukast sodium, equivalent to 5 mg free acid. Each 4 mg chewable tablet contains 4.2 mg monteluka