- Email: [email protected]
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse
Medical Hypotheses (2006) 67, 702–708
http://intl.elsevierhealth.com/journals/mehy
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse Rick Howard
*
Peaks Academic & Research Unit, Rampton Hospital, Retford, UK Division of Psychiatry, School of Community and Health Sciences, Forensic Psychiatry Section, University of Nottingham, Duncan McMillan House, Porchester Road, Nottingham NG3 6AA, UK Received 29 March 2006; accepted 30 March 2006
Summary This paper questions the assumption that personality disorder and dangerousness are causally linked, and suggests that insofar as a relationship between them exists, it is mediated by early-onset alcohol abuse. The latter, by impairing the function of prefrontal cortex during adolescence, a critical period of its development, putatively leads to deficits in goal-directed behaviour and emotional self-regulation that place the individual at high risk of becoming chronically antisocial in adulthood. Evidence is adduced in support of the hypothesis from the literature on: (i) the comorbidity of personality disorder and alcohol abuse; (ii) frontal lobe deficits in psychopaths; and (iii) life-course persistent offenders. Some testable predictions from the hypothesis are presented, together with its implications; most importantly, that measures to prevent serious antisocial behaviour in adulthood should target at-risk individuals prior to their commencing heavy drinking during adolescence. c 2006 Elsevier Ltd. All rights reserved.
Introduction The medico-legal context Personality disorders represent a medico-legal problem that refuses to go away. In the 1970s and early 1980s, British psychiatrists became increasingly reluctant to use the ‘‘Psychopathic Disorder’’ label to detain people under the 1959 Mental Health Act (MHA), with the consequence that personality disordered offenders were increas* Tel.: +44 1777880503. E-mail address: [email protected].
ingly more likely to serve prison sentences than be detained in high-security hospitals. This trend was dramatically reversed in the early 2000s following two infamous cases of personality disordered individuals who committed horrendous crimes on their release from prison – those of Michael Stone, convicted in 1998 of the murder of Lin and Megan Russell, and Roy Whiting, convicted of the murder of Sarah Payne in 2001. These cases forced the UK government to re-think mental health legislation, culminating in a reform Bill that proposed removal of both the treatability requirement enshrined in the 1983 MHA, and of the distinction contained in both the 1959 and 1983 Acts, between the
0306-9877/$ - see front matter c 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2006.03.050
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse psychopathically disordered and the mentally ill offender. Instead, both were to be subsumed under the category of ‘‘mental disorder’’, defined (in an entirely circular way) as ‘‘Any disability or disorder of mind or brain which results in an impairment or disturbance of mental function’’. Recently, the UK government announced it was abandoning attempts to introduce new mental health legislation, preferring instead to amend existing legislation. It remains to be seen how, or when, this will eventuate. Pending a review of mental health law, the UK government initiated a pilot assessment and treatment programme for individuals having what is referred to as a ‘‘Dangerous and Severe Personality Disorder’’ (DSPD). Classifying an individual as ‘‘DSPD’’ requires the conjunction of three elements: firstly, dangerousness, operationalised in terms of ‘‘high risk’’ for harm to others; secondly, severe personality disorder, where severity is operationalised in terms of: (i) the presence to a sufficient degree of psychopathic traits, or (ii) sufficient number of different personality disorders; and thirdly (and most importantly) a functional link between the personality disorder and dangerousness. A functional link between personality disorder and dangerousness is premised on the assumption that personality disorder, of sufficient severity, is in some way a causal antecedent of dangerousness. While an assumption of causality is frequently made by psychiatrists, there currently exists very little, if any, scientific evidence to support such a causal link between personality disorder and dangerousness. Two major problems bedevil the verification of such a link. Firstly, an association between personality disorder of any particular type and antisocial (e.g., criminal) behaviour may be flawed by the fact that the criteria defining the personality disorder, as in the case of antisocial personality disorder, include measures of antisocial (e.g., criminal) behaviour. This renders the association necessarily true, but only in the trivial sense that statements such as ‘‘All black swans are black’’ is true, i.e., true by definition. Secondly, an association between personality disorder and dangerousness does not necessarily imply that the one causes the other. Two critical questions, therefore, need to be addressed in relation to DSPD: firstly, which (if any) of the personality disorders is linked to dangerousness? and secondly, what is the mechanism that mediates the link? Given an association between (some types of) personality disorder (in particular, psychopathy) and dangerousness, is there a direct causal link between the two? Or is there a third variable that
703
mediates the relationship between personality disorder and dangerousness? It will be argued that it is early-onset alcohol abuse, rather than personality disorder per se, that accounts for the association between personality disorder and dangerousness. Before presenting a detailed and explicit statement of the hypothesis, the evidence for a relationship between psychopathy and dangerousness will be critically reviewed.
Psychopathy and dangerousness Evidence is accruing that PCL-defined psychopathy, a constellation of interpersonal (e.g., glibness, superficial charm, manipulativeness), affective (a callous lack of remorse, superficial affect) and behavioural (impulsive, irresponsible, emotional under-control) traits (see Fig. 1), is associated with criminality, even when indices of antisocial behaviour are excluded from the measurement of psychopathy [1]. In other words, certain ‘‘psychopathic’’ personality traits appear to be associated with antisocial behaviour. However, there are at least four reasons for questioning a causal relationship between psychopathy (and antisocial traits in general) and dangerousness, and for supposing that any association between them might be attributable to a history of alcohol abuse. Firstly, there exists a high degree of comorbidity between personality disorder (and antisocial personality disorder in particular) and drug and alcohol abuse [2,3]. This means that any association found between psychopathy and dangerousness is likely to be confounded by the possible presence of early-onset alcohol abuse, which has been found [2] to characterise individuals with a diag-
Figure 1 The three facets of psychopathy (after Cooke and Michie, 2001).
704
Howard
nosis of antisocial personality disorder. Secondly, early-onset alcohol abuse has been reported [4], in longitudinal studies such as the Dunedin Multidisciplinary Health and Development Study, to be a major risk factor for later antisocial behaviour, including violence. Almost half of males from this community sample whose subsequent criminal careers were characterised as ‘‘lifecourse persistent’’ received a diagnosis of alcohol dependence at age 18 [5]. Thirdly, studies have shown that alcohol abuse and dependence are highly prevalent among samples of mentally disordered offenders [6], with early-onset (before age 19) alcohol abuse being particularly prevalent among such offenders [7]. Fourthly, considerable overlap of antisocial traits has been reported [8] between senior business managers and mentally disordered offenders, both mentally ill and personality disordered. Results suggested that impulsive ‘‘acting out’’ was the critical feature that differentiated personality disordered offenders from business managers. This tendency to act out is identifiable with the behavioural facet of psychopathy shown in Fig. 1. This casts serious doubt on the possibility of a causal link between psychopathy and dangerousness in the absence of a tendency to act out. This is supported by findings from studies [9,10] comparing ‘‘successful’’ (unconvicted) with ‘‘unsuccessful’’ (convicted) psychopaths. The latter scored higher than the former on the behavioural (impulsivity) facet of psychopathy, but not on the affective and interpersonal facets.
Figure 2
The hypothesis The evidence reviewed above argues against an assumption of a direct causal relationship between psychopathy and dangerousness. No necessary relationship can be said to exist between any personality disorder – including psychopathy – and dangerousness. Rather, any relationship between personality disorder and dangerousness is mediated by early-onset alcohol abuse, which is the critical intervening variable. By impairing the function of prefrontal cortex during a critical period of its development (adolescence), early-onset alcohol abuse is hypothesised to lead to deficits in the neuropsychological substrates of goal-directed behaviour and emotional self-regulation, placing the individual at high risk for becoming a life-course persistent offender in adulthood. This neurodevelopmental model is shown schematically in Fig. 2. The presence in early adolescence of disinhibitory psychopathology, including conduct disorder and impulsivity arising from a variety of antecedents (e.g., child abuse, genotypic variation and the interaction between them), predisposes the individual to a vicious cycle of increasing and accelerating use of alcohol, with consequent progressive impairment of prefrontal cortex function. This results in greater impulsivity and hence greater abuse of alcohol, and so the cycle repeats itself, until the individual emerges into adulthood with compromised frontal lobe function and with the status of being at high risk for offending throughout adulthood.
A schematic representation of the hypothesis.
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse
Origins of the hypothesis This model had its origins in the finding [11] that an electrophysiological correlate of affective impulsivity, the contingent negative variation (CNV) recorded in a Go/No Go avoidance paradigm, was degraded in offenders with a history of predominantly early-onset alcohol abuse. This so-called Go/No Go CNV is degraded in patients with dorsolateral prefrontal lesions [12], implying that the degradation of the Go/No Go CNV previously reported [11] was the result of impaired frontal cortex function consequent upon early-onset alcohol abuse. Mentally disordered offenders, regardless of their legal classification or clinical diagnosis, in whom the Go/No Go CNV was degraded were found [13,14] to be at greater risk of re-offending both generally and violently. This suggested that it was early-onset alcohol abuse that accounted for both the degraded Go/No Go CNV found in earlyonset alcohol abusers, and for the greater dangerousness (in terms of risk of re-offending) found in ‘‘high risk’’ mentally disordered offenders. A logical inference from this is that a major risk factor for dangerousness in adulthood may be earlyonset alcohol abuse, and that frontal brain impairment may be the mechanism that mediates the effect of early alcohol abuse on antisocial behaviour. It is important to note that the present hypothesis is not suggesting that psychopathy is caused by early alcohol abuse. Indeed, childhood manifestations of psychopathy, in the form of conduct disorder and affective deficiency, precede, and are a known risk factor for, adolescent alcohol abuse. The present hypothesis proposes that psychopathy is a developmentally evolving process: if, and only if, its early manifestations are followed by a pattern of increasing adolescent alcohol abuse will psychopathy represent an increased risk of harm to others. Successful psychopaths are, according to the hypothesis, those who manage to avoid the accretions of neuropsychological impairment wrought by adolescent alcohol abuse. While they have many of the interpersonal and affective traits of psychopathy shown in Fig. 1, they crucially lack the impulsive and irresponsible behavioural style that would otherwise predispose them to engage in antisocial, including violent, behaviour.
Significance of the hypothesis The significance of this hypothesis lies in its implications for prediction of dangerousness and the treatment of dangerous offenders, and for the prevention of violence. First, if the hypothesis is cor-
705
rect, assessment of early alcohol abuse, and of frontal lobe pathology, should play a key role in the risk assessment of offenders prior to their release. Second, attempts to treat individuals with severe and dangerous personality disorders should take cognizance of the possibility that these individuals are (if the hypothesis is correct) neuropsychologically impaired and may not be capable of benefiting from treatments that work with neuropsychologically intact individuals. Rather than using treatments that have been found to be effective in other patient groups, special treatment approaches may need to be developed that do not rely on high cognitive capacity. Implications for the prevention of violence will be dealt with in the final section of this paper.
Evaluation of the hypothesis Is early-onset alcohol abuse an antecedent of personality disorder? The high degree of comorbidity reported [15,2] to occur between alcohol abuse and personality disorder in general, and antisocial personality disorder in particular, has already been alluded to above. According to the current hypothesis, earlyonset alcohol abuse plays a causal role in the aetiology of some aspects of personality disorder, particularly its association (when such exists) with dangerousness. The extant epidemiological literature does not provide definitive confirmatory evidence for this, since such evidence would require data from longitudinal studies, which are lacking. A notable exception is a recent study [16] showing that adolescent alcohol use mediates the relationship between abuse during childhood and borderline personality disorder (BPD) in adulthood. In other words, results of this study indicated that, consistent with the current hypothesis, adolescent alcohol abuse was a sine qua non of adult BPD. What remains to be demonstrated is firstly, that the same is true of other personality disorders; and secondly, that the degree and duration of adolescent alcohol abuse is related to the degree of dangerousness posed by BPD, and other personality disordered, patients. Do psychopaths show a frontal lobe dysfunction? The issue of possible frontal lobe/executive dysfunction in psychopaths exemplifies the confounding effect of alcohol abuse in studies that compare psychopaths with non-psychopaths. A frontal lobe abnormality has been postulated to occur in psychopaths since at least the 1970s, when a frontal syndrome, labelled ‘‘pseudopsychopathy’’,
706 was described [17] as having some, but not all, the features of psychopathy. In the 1970s it was postulated by some Swedish researchers, e.g., [18] that a frontal dysfunction in psychopaths underlay their inhibitory deficit. Since that time reports either have [19] or have not [20] confirmed the hypothesis of frontal lobe dysfunction in psychopaths, variously defined (the so-called gold-standard measure is the Psychopathy Checklist-Revised [21]). At times the deficit was reported [22] in a sub-region of prefrontal cortex (PFC), the ventromedial PFC, but a behavioural measure sensitive to orbitofrontal lesions, the Iowa Gambling Task, sometimes has (e.g., [23]) and at other times has not (e.g., [24]) been reported to show differences comparing psychopaths with non-psychopaths. An executive dysfunction [9] or a structural (on fMRI) frontal abnormality [10] has been reported as present in ‘‘unsuccessful’’ (convicted) but not ‘‘successful’’ (unconvicted) psychopaths. As mentioned above, these groups differed in their scores on the behavioural facet, but not on the interpersonal/affective facets, of psychopathy. Since the behavioural facet is known to correlate with drug/alcohol use, it is plausible that the group difference in prefrontal volume and executive function is accounted for by a group difference in a history of alcohol or drug use (notwithstanding that the groups were reported not to differ in current alcohol/drug dependence). This explanation of the difference in frontal structure and function is supported by the fact that in antisocial (belligerent) alcoholics frontal dysfunction is not only present but its extent is strongly correlated with duration of alcohol abuse [25]. A recent fMRI study [26] confirms that as far as the structural frontal differences between psychopaths and non-psychopaths are concerned, they are entirely accounted for by between-group differences in alcohol abuse (in the case of orbitofrontal and dorsolateral cortices) or education (in the case of medial frontal cortex). One is drawn inexorably to the conclusion that differences in frontal brain structure and function exist in psychopaths only insofar as they are comorbid for earlyonset alcohol use.
How does ‘‘dangerous and severe personality disorder’’ relate to life-course persistent offending? Life-course persistent offenders are those who show a chronic and recurring pattern of criminality that starts during childhood and extends throughout the lifespan. Their antisocial and criminal behaviour shows high versatility, commonly includes violence, and shows low desistance during adult life
Howard [27]. Their characteristics have been studied by Moffitt and colleagues in the context of the Dunedin Multidisciplinary Health & Development study, and results generally confirm a high degree of neuropsychological dysfunction in this small (estimated at 5–8% of the population) group of offenders who account for a disproportionate amount of violent crime. Personality characteristics of life-course persistent offenders include the psychopathic traits of alienation, callousness and impulsivity. As already mentioned, early-onset alcohol dependence is present in about one half of life-course persistent offenders. When the characteristics of DSPD offenders come to be described in detail, they will likely overlap to a high degree with those of lifecourse persistent offenders.
Predictions Certain testable predictions follow from the hypothesis. Firstly, if mentally disordered offenders, regardless of their clinical diagnosis or their legal classification as personality disordered or mentally ill, with a history of early-onset alcoholism (EOA) are compared with those without such a history, the former will show a greater incidence of antisocial behaviour, indexed by past criminal offending, current institutional behaviour, and future re-offending. Secondly, with regard to psychopathy scores, it would be predicted that patients with EOA would, in comparison with patients with late-onset or nil alcoholism, score high on the behavioural (impulsivity) facet of psychopathy measured by the PCL, but not on other facets. Thirdly, with regard to severity of personality disorder, it would be predicted that patients with EOA would fall at the high-severity end of the spectrum, and that those classified as DSPD would be over-represented among such patients. Conversely, if one compared DSPD patients with other personality disordered patients, the former would show a greater prevalence of EOA than the latter. Fourthly, mentally disordered offenders with EOA will show more evidence of frontal lobe dysfunction than those with either late-onset alcoholism or no history of alcoholism. Lastly, it would be predicted from a longitudinal study that was able to track alcohol use from late childhood through adolescence into adulthood, that the longer the duration of adolescent alcohol abuse (i.e., the earlier the onset), and the greater the amount of alcohol used during adolescence, the greater would be the likelihood that the hallmark characteristics of the life-course persistent offender would emerge in adulthood.
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse
Discussion and some implications Two important implications of the hypothesis have already been mentioned above. Perhaps the most important implication, however, is that measures to prevent serious antisocial behaviour should target individuals at risk for engaging in heavy alcohol consumption in adolescence, before they start heavy drinking, in order to prevent the cascade of events depicted in Fig. 2 from leading to chronic antisocial behaviour in adulthood. Heavy alcohol abuse in adolescents is often accompanied by use of other psychotropic drugs such as cannabis, which also impairs frontal lobe function and compounds the adverse consequences of heavy alcohol use. This is a particular problem in those who are predisposed, by virtue of pre-existing personality problems and neuropsychological impairment, to suffer such consequences. The problem is one of identifying such individuals and preventing them from becoming absorbed into a teenage drugs-and-alcohol culture. This is rapidly becoming normative among UK adolescents, as indicated by the most recent survey [28] of drug and alcohol use among UK secondary school children. This showed that 45% of 15-year-olds, males and females alike, had drunk an alcoholic drink in the previous week, the average consumption among 15-year-old drinkers being 12.9 U per week. Drinking and cannabis use were strongly correlated, and 26% of 15-year-olds had used cannabis in the previous year. Confirmation of the hypothesis put forward here would increase the urgency with which a solution to this problem of identifying at-risk individuals among teenage drug and alcohol users would need to be pursued.
References
[7]
[8] [9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19] [20]
[21] [22]
[1] Cooke DJ, Michie C, Hart SD, Clark DA. Reconstructing psychopathy: clarifying the significance of antisocial and socially deviant behaviour in the diagnosis of psychopathic personality disorder. J Pers Disord 2004;18:337–57. [2] Hesselbrock MN, Meyer RE, Keener JJ. Psychopathology in hospitalized alcoholics. Arch Gen Psychiat 1985;42:1050–5. [3] Morgenstern J, Langenbucher J, Labouvie E, Miller KJ. Comorbidity of alcoholism and personality disorders in a clinical population: prevalence rates and relation to alcohol typology variables. J Abnorm Psychol 1997;106:74–84. [4] Arsenault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin study. Arch Gen Psychiat 2000;57:979–86. [5] Moffitt TE. Personal communication; 2003. [6] Quayle M, Clark F, Renwick SJ, Hodge J, Spencer T. Alcohol and secure hospital patients: I. An examination of the
[23]
[24]
[25]
[26]
707
nature and prevalence of alcohol problems in secure hospital patients. Psychol Crime Law 1998;4:27–41. Lumsden J, Hadfield J, Littler S, Howard R. The prevalence of early onset alcohol abuse in mentally disordered offenders. J Forensic Psychiat Psychol 2005;16:651–9. Board BJ, Fritzon K. Disordered personalities at work. Psychol Crime Law 2005;11:17–32. Ishikawa SS, Raine A, Lencz T, Bihrle S, LaCasse L. Autonomic stree reactivity and executive functions in successful and unsuccessful psychopaths. J Abnorm Psychol 2001;110:423–32. Yang Y, Raine A, Lencz T, Bihrle S, LaCasse L, Colletti P. Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biol Psychiat 2005;57:1103–8. Neo LH, McCullagh P, Howard R. An electrocortical correlate of a history of alcohol abuse in criminal offenders. Psychol Crime Law 2001;7:105–17. Rosahl SK, Knight RT. Role of prefrontal cortex in generation of the contingent negative variation. Cereb Cortex 1995;2:123–34. Howard RC, Lumsden J. A neurophysiological predictor of re-offending in special hospital patients. Crim Behav Ment Health 1996;6:147–56. Howard RC, Lumsden J. CNV predicts violent outcomes in patients released from special hospital. Crim Behav Ment Health 1997;7:237–40. Morgenstern J, Langenbucher J, Labouvie E, Miller K. The comorbidity of alcoholism and personality disorders in a clinical population: prevalence rates and relation to alcohol typology variables. J Abnorm Psychol 1997;106:74–84. Thatcher DL, Cornelius JR, Clark DB. Adolescent alcohol use disorders predict borderline personality. Addict Behav 2005;30:1709–24. Elliot FA. Neurological aspects of antisocial behaviour. In: Reid WH, editor. The psychopath: a comprehensive study of antisocial disorders and behaviours. New York: Brunner/ Mazel; 1978. p. 146–89. Schalling D. Psychopathy-related personality variables and the psychophysiology of socialisation. In: Hare RD, Schalling D, editors. Psychopathic behaviour: approaches to research. New York: Wiley; 1978 [Chapter 6]. Gorenstein EE. Frontal lobe functions in psychopaths. J Abnorm Psychol 1982;91:368–79. Hare RD. Performance of psychopaths on cognitive tasks related to frontal lobe function. J Abnorm Psychol 1984;93:133–40. Hare RD. The hare psychopathy checklist. Revised: 2nd ed. Toronto: Multi-Health Systems Inc.; 2003. Lapierre D, Braun CMJ, Hodgins S. Ventral frontal deficits in psychopathy: neuropsychological test findings. Neuropsychologia 1995;33:139–51. Mitchell DGV, Colledge E, Leonard A, Blair RJR. Risky decisions and response reversal: Is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? Neuropsychologia 2002;40:2013–22. Schmitt WA, Brinckley CA, Newman JP. Testing Damasio’s somatic marker hypothesis with psychopathic individuals: Risk takers or risk averse? J Abnorm Psychol 1999;108:538–43. Howard RC. Personality, ways of coping and cognitive functions in hospitalised alcoholics. In: Joyce P, editor. Development, personality and psychopathology. Christchurch, NZ: Christchurch School of Medicine; 1994. p. 235–48. Laakso MP, Gunning-Dixon F, Vaurio O, Repo-Tiihonen E, Soininen H, Tiihonen J. Prefrontal volumes in habitually
708 violent subjects with antisocial personality disorder and type 2 alcoholism. Psychiat Res-Neuroim 2002;114:95–102. [27] Piquero AR, Moffitt TE. Life-course persistent offending. In: Adler JR, editor. Forensic psychology. Concepts, debates and practice. Cullompton, UK: Willan Publishing; 2004. p. 177–96.
Howard [28] Fuller E. Smoking, drinking and drug use among young people in England in 2004. London: The Stationery Office; 2005. Available from (http:www.dh.gov.uk/Home/fs/en). [29] Cooke DJ, Michie C. Refining the construct of psychopathy: Towards a hierarchical model. Psychol Assess 2001;13:171–88.
http://intl.elsevierhealth.com/journals/mehy
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse Rick Howard
*
Peaks Academic & Research Unit, Rampton Hospital, Retford, UK Division of Psychiatry, School of Community and Health Sciences, Forensic Psychiatry Section, University of Nottingham, Duncan McMillan House, Porchester Road, Nottingham NG3 6AA, UK Received 29 March 2006; accepted 30 March 2006
Summary This paper questions the assumption that personality disorder and dangerousness are causally linked, and suggests that insofar as a relationship between them exists, it is mediated by early-onset alcohol abuse. The latter, by impairing the function of prefrontal cortex during adolescence, a critical period of its development, putatively leads to deficits in goal-directed behaviour and emotional self-regulation that place the individual at high risk of becoming chronically antisocial in adulthood. Evidence is adduced in support of the hypothesis from the literature on: (i) the comorbidity of personality disorder and alcohol abuse; (ii) frontal lobe deficits in psychopaths; and (iii) life-course persistent offenders. Some testable predictions from the hypothesis are presented, together with its implications; most importantly, that measures to prevent serious antisocial behaviour in adulthood should target at-risk individuals prior to their commencing heavy drinking during adolescence. c 2006 Elsevier Ltd. All rights reserved.
Introduction The medico-legal context Personality disorders represent a medico-legal problem that refuses to go away. In the 1970s and early 1980s, British psychiatrists became increasingly reluctant to use the ‘‘Psychopathic Disorder’’ label to detain people under the 1959 Mental Health Act (MHA), with the consequence that personality disordered offenders were increas* Tel.: +44 1777880503. E-mail address: [email protected].
ingly more likely to serve prison sentences than be detained in high-security hospitals. This trend was dramatically reversed in the early 2000s following two infamous cases of personality disordered individuals who committed horrendous crimes on their release from prison – those of Michael Stone, convicted in 1998 of the murder of Lin and Megan Russell, and Roy Whiting, convicted of the murder of Sarah Payne in 2001. These cases forced the UK government to re-think mental health legislation, culminating in a reform Bill that proposed removal of both the treatability requirement enshrined in the 1983 MHA, and of the distinction contained in both the 1959 and 1983 Acts, between the
0306-9877/$ - see front matter c 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2006.03.050
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse psychopathically disordered and the mentally ill offender. Instead, both were to be subsumed under the category of ‘‘mental disorder’’, defined (in an entirely circular way) as ‘‘Any disability or disorder of mind or brain which results in an impairment or disturbance of mental function’’. Recently, the UK government announced it was abandoning attempts to introduce new mental health legislation, preferring instead to amend existing legislation. It remains to be seen how, or when, this will eventuate. Pending a review of mental health law, the UK government initiated a pilot assessment and treatment programme for individuals having what is referred to as a ‘‘Dangerous and Severe Personality Disorder’’ (DSPD). Classifying an individual as ‘‘DSPD’’ requires the conjunction of three elements: firstly, dangerousness, operationalised in terms of ‘‘high risk’’ for harm to others; secondly, severe personality disorder, where severity is operationalised in terms of: (i) the presence to a sufficient degree of psychopathic traits, or (ii) sufficient number of different personality disorders; and thirdly (and most importantly) a functional link between the personality disorder and dangerousness. A functional link between personality disorder and dangerousness is premised on the assumption that personality disorder, of sufficient severity, is in some way a causal antecedent of dangerousness. While an assumption of causality is frequently made by psychiatrists, there currently exists very little, if any, scientific evidence to support such a causal link between personality disorder and dangerousness. Two major problems bedevil the verification of such a link. Firstly, an association between personality disorder of any particular type and antisocial (e.g., criminal) behaviour may be flawed by the fact that the criteria defining the personality disorder, as in the case of antisocial personality disorder, include measures of antisocial (e.g., criminal) behaviour. This renders the association necessarily true, but only in the trivial sense that statements such as ‘‘All black swans are black’’ is true, i.e., true by definition. Secondly, an association between personality disorder and dangerousness does not necessarily imply that the one causes the other. Two critical questions, therefore, need to be addressed in relation to DSPD: firstly, which (if any) of the personality disorders is linked to dangerousness? and secondly, what is the mechanism that mediates the link? Given an association between (some types of) personality disorder (in particular, psychopathy) and dangerousness, is there a direct causal link between the two? Or is there a third variable that
703
mediates the relationship between personality disorder and dangerousness? It will be argued that it is early-onset alcohol abuse, rather than personality disorder per se, that accounts for the association between personality disorder and dangerousness. Before presenting a detailed and explicit statement of the hypothesis, the evidence for a relationship between psychopathy and dangerousness will be critically reviewed.
Psychopathy and dangerousness Evidence is accruing that PCL-defined psychopathy, a constellation of interpersonal (e.g., glibness, superficial charm, manipulativeness), affective (a callous lack of remorse, superficial affect) and behavioural (impulsive, irresponsible, emotional under-control) traits (see Fig. 1), is associated with criminality, even when indices of antisocial behaviour are excluded from the measurement of psychopathy [1]. In other words, certain ‘‘psychopathic’’ personality traits appear to be associated with antisocial behaviour. However, there are at least four reasons for questioning a causal relationship between psychopathy (and antisocial traits in general) and dangerousness, and for supposing that any association between them might be attributable to a history of alcohol abuse. Firstly, there exists a high degree of comorbidity between personality disorder (and antisocial personality disorder in particular) and drug and alcohol abuse [2,3]. This means that any association found between psychopathy and dangerousness is likely to be confounded by the possible presence of early-onset alcohol abuse, which has been found [2] to characterise individuals with a diag-
Figure 1 The three facets of psychopathy (after Cooke and Michie, 2001).
704
Howard
nosis of antisocial personality disorder. Secondly, early-onset alcohol abuse has been reported [4], in longitudinal studies such as the Dunedin Multidisciplinary Health and Development Study, to be a major risk factor for later antisocial behaviour, including violence. Almost half of males from this community sample whose subsequent criminal careers were characterised as ‘‘lifecourse persistent’’ received a diagnosis of alcohol dependence at age 18 [5]. Thirdly, studies have shown that alcohol abuse and dependence are highly prevalent among samples of mentally disordered offenders [6], with early-onset (before age 19) alcohol abuse being particularly prevalent among such offenders [7]. Fourthly, considerable overlap of antisocial traits has been reported [8] between senior business managers and mentally disordered offenders, both mentally ill and personality disordered. Results suggested that impulsive ‘‘acting out’’ was the critical feature that differentiated personality disordered offenders from business managers. This tendency to act out is identifiable with the behavioural facet of psychopathy shown in Fig. 1. This casts serious doubt on the possibility of a causal link between psychopathy and dangerousness in the absence of a tendency to act out. This is supported by findings from studies [9,10] comparing ‘‘successful’’ (unconvicted) with ‘‘unsuccessful’’ (convicted) psychopaths. The latter scored higher than the former on the behavioural (impulsivity) facet of psychopathy, but not on the affective and interpersonal facets.
Figure 2
The hypothesis The evidence reviewed above argues against an assumption of a direct causal relationship between psychopathy and dangerousness. No necessary relationship can be said to exist between any personality disorder – including psychopathy – and dangerousness. Rather, any relationship between personality disorder and dangerousness is mediated by early-onset alcohol abuse, which is the critical intervening variable. By impairing the function of prefrontal cortex during a critical period of its development (adolescence), early-onset alcohol abuse is hypothesised to lead to deficits in the neuropsychological substrates of goal-directed behaviour and emotional self-regulation, placing the individual at high risk for becoming a life-course persistent offender in adulthood. This neurodevelopmental model is shown schematically in Fig. 2. The presence in early adolescence of disinhibitory psychopathology, including conduct disorder and impulsivity arising from a variety of antecedents (e.g., child abuse, genotypic variation and the interaction between them), predisposes the individual to a vicious cycle of increasing and accelerating use of alcohol, with consequent progressive impairment of prefrontal cortex function. This results in greater impulsivity and hence greater abuse of alcohol, and so the cycle repeats itself, until the individual emerges into adulthood with compromised frontal lobe function and with the status of being at high risk for offending throughout adulthood.
A schematic representation of the hypothesis.
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse
Origins of the hypothesis This model had its origins in the finding [11] that an electrophysiological correlate of affective impulsivity, the contingent negative variation (CNV) recorded in a Go/No Go avoidance paradigm, was degraded in offenders with a history of predominantly early-onset alcohol abuse. This so-called Go/No Go CNV is degraded in patients with dorsolateral prefrontal lesions [12], implying that the degradation of the Go/No Go CNV previously reported [11] was the result of impaired frontal cortex function consequent upon early-onset alcohol abuse. Mentally disordered offenders, regardless of their legal classification or clinical diagnosis, in whom the Go/No Go CNV was degraded were found [13,14] to be at greater risk of re-offending both generally and violently. This suggested that it was early-onset alcohol abuse that accounted for both the degraded Go/No Go CNV found in earlyonset alcohol abusers, and for the greater dangerousness (in terms of risk of re-offending) found in ‘‘high risk’’ mentally disordered offenders. A logical inference from this is that a major risk factor for dangerousness in adulthood may be earlyonset alcohol abuse, and that frontal brain impairment may be the mechanism that mediates the effect of early alcohol abuse on antisocial behaviour. It is important to note that the present hypothesis is not suggesting that psychopathy is caused by early alcohol abuse. Indeed, childhood manifestations of psychopathy, in the form of conduct disorder and affective deficiency, precede, and are a known risk factor for, adolescent alcohol abuse. The present hypothesis proposes that psychopathy is a developmentally evolving process: if, and only if, its early manifestations are followed by a pattern of increasing adolescent alcohol abuse will psychopathy represent an increased risk of harm to others. Successful psychopaths are, according to the hypothesis, those who manage to avoid the accretions of neuropsychological impairment wrought by adolescent alcohol abuse. While they have many of the interpersonal and affective traits of psychopathy shown in Fig. 1, they crucially lack the impulsive and irresponsible behavioural style that would otherwise predispose them to engage in antisocial, including violent, behaviour.
Significance of the hypothesis The significance of this hypothesis lies in its implications for prediction of dangerousness and the treatment of dangerous offenders, and for the prevention of violence. First, if the hypothesis is cor-
705
rect, assessment of early alcohol abuse, and of frontal lobe pathology, should play a key role in the risk assessment of offenders prior to their release. Second, attempts to treat individuals with severe and dangerous personality disorders should take cognizance of the possibility that these individuals are (if the hypothesis is correct) neuropsychologically impaired and may not be capable of benefiting from treatments that work with neuropsychologically intact individuals. Rather than using treatments that have been found to be effective in other patient groups, special treatment approaches may need to be developed that do not rely on high cognitive capacity. Implications for the prevention of violence will be dealt with in the final section of this paper.
Evaluation of the hypothesis Is early-onset alcohol abuse an antecedent of personality disorder? The high degree of comorbidity reported [15,2] to occur between alcohol abuse and personality disorder in general, and antisocial personality disorder in particular, has already been alluded to above. According to the current hypothesis, earlyonset alcohol abuse plays a causal role in the aetiology of some aspects of personality disorder, particularly its association (when such exists) with dangerousness. The extant epidemiological literature does not provide definitive confirmatory evidence for this, since such evidence would require data from longitudinal studies, which are lacking. A notable exception is a recent study [16] showing that adolescent alcohol use mediates the relationship between abuse during childhood and borderline personality disorder (BPD) in adulthood. In other words, results of this study indicated that, consistent with the current hypothesis, adolescent alcohol abuse was a sine qua non of adult BPD. What remains to be demonstrated is firstly, that the same is true of other personality disorders; and secondly, that the degree and duration of adolescent alcohol abuse is related to the degree of dangerousness posed by BPD, and other personality disordered, patients. Do psychopaths show a frontal lobe dysfunction? The issue of possible frontal lobe/executive dysfunction in psychopaths exemplifies the confounding effect of alcohol abuse in studies that compare psychopaths with non-psychopaths. A frontal lobe abnormality has been postulated to occur in psychopaths since at least the 1970s, when a frontal syndrome, labelled ‘‘pseudopsychopathy’’,
706 was described [17] as having some, but not all, the features of psychopathy. In the 1970s it was postulated by some Swedish researchers, e.g., [18] that a frontal dysfunction in psychopaths underlay their inhibitory deficit. Since that time reports either have [19] or have not [20] confirmed the hypothesis of frontal lobe dysfunction in psychopaths, variously defined (the so-called gold-standard measure is the Psychopathy Checklist-Revised [21]). At times the deficit was reported [22] in a sub-region of prefrontal cortex (PFC), the ventromedial PFC, but a behavioural measure sensitive to orbitofrontal lesions, the Iowa Gambling Task, sometimes has (e.g., [23]) and at other times has not (e.g., [24]) been reported to show differences comparing psychopaths with non-psychopaths. An executive dysfunction [9] or a structural (on fMRI) frontal abnormality [10] has been reported as present in ‘‘unsuccessful’’ (convicted) but not ‘‘successful’’ (unconvicted) psychopaths. As mentioned above, these groups differed in their scores on the behavioural facet, but not on the interpersonal/affective facets, of psychopathy. Since the behavioural facet is known to correlate with drug/alcohol use, it is plausible that the group difference in prefrontal volume and executive function is accounted for by a group difference in a history of alcohol or drug use (notwithstanding that the groups were reported not to differ in current alcohol/drug dependence). This explanation of the difference in frontal structure and function is supported by the fact that in antisocial (belligerent) alcoholics frontal dysfunction is not only present but its extent is strongly correlated with duration of alcohol abuse [25]. A recent fMRI study [26] confirms that as far as the structural frontal differences between psychopaths and non-psychopaths are concerned, they are entirely accounted for by between-group differences in alcohol abuse (in the case of orbitofrontal and dorsolateral cortices) or education (in the case of medial frontal cortex). One is drawn inexorably to the conclusion that differences in frontal brain structure and function exist in psychopaths only insofar as they are comorbid for earlyonset alcohol use.
How does ‘‘dangerous and severe personality disorder’’ relate to life-course persistent offending? Life-course persistent offenders are those who show a chronic and recurring pattern of criminality that starts during childhood and extends throughout the lifespan. Their antisocial and criminal behaviour shows high versatility, commonly includes violence, and shows low desistance during adult life
Howard [27]. Their characteristics have been studied by Moffitt and colleagues in the context of the Dunedin Multidisciplinary Health & Development study, and results generally confirm a high degree of neuropsychological dysfunction in this small (estimated at 5–8% of the population) group of offenders who account for a disproportionate amount of violent crime. Personality characteristics of life-course persistent offenders include the psychopathic traits of alienation, callousness and impulsivity. As already mentioned, early-onset alcohol dependence is present in about one half of life-course persistent offenders. When the characteristics of DSPD offenders come to be described in detail, they will likely overlap to a high degree with those of lifecourse persistent offenders.
Predictions Certain testable predictions follow from the hypothesis. Firstly, if mentally disordered offenders, regardless of their clinical diagnosis or their legal classification as personality disordered or mentally ill, with a history of early-onset alcoholism (EOA) are compared with those without such a history, the former will show a greater incidence of antisocial behaviour, indexed by past criminal offending, current institutional behaviour, and future re-offending. Secondly, with regard to psychopathy scores, it would be predicted that patients with EOA would, in comparison with patients with late-onset or nil alcoholism, score high on the behavioural (impulsivity) facet of psychopathy measured by the PCL, but not on other facets. Thirdly, with regard to severity of personality disorder, it would be predicted that patients with EOA would fall at the high-severity end of the spectrum, and that those classified as DSPD would be over-represented among such patients. Conversely, if one compared DSPD patients with other personality disordered patients, the former would show a greater prevalence of EOA than the latter. Fourthly, mentally disordered offenders with EOA will show more evidence of frontal lobe dysfunction than those with either late-onset alcoholism or no history of alcoholism. Lastly, it would be predicted from a longitudinal study that was able to track alcohol use from late childhood through adolescence into adulthood, that the longer the duration of adolescent alcohol abuse (i.e., the earlier the onset), and the greater the amount of alcohol used during adolescence, the greater would be the likelihood that the hallmark characteristics of the life-course persistent offender would emerge in adulthood.
How is personality disorder linked to dangerousness? A putative role for early-onset alcohol abuse
Discussion and some implications Two important implications of the hypothesis have already been mentioned above. Perhaps the most important implication, however, is that measures to prevent serious antisocial behaviour should target individuals at risk for engaging in heavy alcohol consumption in adolescence, before they start heavy drinking, in order to prevent the cascade of events depicted in Fig. 2 from leading to chronic antisocial behaviour in adulthood. Heavy alcohol abuse in adolescents is often accompanied by use of other psychotropic drugs such as cannabis, which also impairs frontal lobe function and compounds the adverse consequences of heavy alcohol use. This is a particular problem in those who are predisposed, by virtue of pre-existing personality problems and neuropsychological impairment, to suffer such consequences. The problem is one of identifying such individuals and preventing them from becoming absorbed into a teenage drugs-and-alcohol culture. This is rapidly becoming normative among UK adolescents, as indicated by the most recent survey [28] of drug and alcohol use among UK secondary school children. This showed that 45% of 15-year-olds, males and females alike, had drunk an alcoholic drink in the previous week, the average consumption among 15-year-old drinkers being 12.9 U per week. Drinking and cannabis use were strongly correlated, and 26% of 15-year-olds had used cannabis in the previous year. Confirmation of the hypothesis put forward here would increase the urgency with which a solution to this problem of identifying at-risk individuals among teenage drug and alcohol users would need to be pursued.
References
[7]
[8] [9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19] [20]
[21] [22]
[1] Cooke DJ, Michie C, Hart SD, Clark DA. Reconstructing psychopathy: clarifying the significance of antisocial and socially deviant behaviour in the diagnosis of psychopathic personality disorder. J Pers Disord 2004;18:337–57. [2] Hesselbrock MN, Meyer RE, Keener JJ. Psychopathology in hospitalized alcoholics. Arch Gen Psychiat 1985;42:1050–5. [3] Morgenstern J, Langenbucher J, Labouvie E, Miller KJ. Comorbidity of alcoholism and personality disorders in a clinical population: prevalence rates and relation to alcohol typology variables. J Abnorm Psychol 1997;106:74–84. [4] Arsenault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin study. Arch Gen Psychiat 2000;57:979–86. [5] Moffitt TE. Personal communication; 2003. [6] Quayle M, Clark F, Renwick SJ, Hodge J, Spencer T. Alcohol and secure hospital patients: I. An examination of the
[23]
[24]
[25]
[26]
707
nature and prevalence of alcohol problems in secure hospital patients. Psychol Crime Law 1998;4:27–41. Lumsden J, Hadfield J, Littler S, Howard R. The prevalence of early onset alcohol abuse in mentally disordered offenders. J Forensic Psychiat Psychol 2005;16:651–9. Board BJ, Fritzon K. Disordered personalities at work. Psychol Crime Law 2005;11:17–32. Ishikawa SS, Raine A, Lencz T, Bihrle S, LaCasse L. Autonomic stree reactivity and executive functions in successful and unsuccessful psychopaths. J Abnorm Psychol 2001;110:423–32. Yang Y, Raine A, Lencz T, Bihrle S, LaCasse L, Colletti P. Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biol Psychiat 2005;57:1103–8. Neo LH, McCullagh P, Howard R. An electrocortical correlate of a history of alcohol abuse in criminal offenders. Psychol Crime Law 2001;7:105–17. Rosahl SK, Knight RT. Role of prefrontal cortex in generation of the contingent negative variation. Cereb Cortex 1995;2:123–34. Howard RC, Lumsden J. A neurophysiological predictor of re-offending in special hospital patients. Crim Behav Ment Health 1996;6:147–56. Howard RC, Lumsden J. CNV predicts violent outcomes in patients released from special hospital. Crim Behav Ment Health 1997;7:237–40. Morgenstern J, Langenbucher J, Labouvie E, Miller K. The comorbidity of alcoholism and personality disorders in a clinical population: prevalence rates and relation to alcohol typology variables. J Abnorm Psychol 1997;106:74–84. Thatcher DL, Cornelius JR, Clark DB. Adolescent alcohol use disorders predict borderline personality. Addict Behav 2005;30:1709–24. Elliot FA. Neurological aspects of antisocial behaviour. In: Reid WH, editor. The psychopath: a comprehensive study of antisocial disorders and behaviours. New York: Brunner/ Mazel; 1978. p. 146–89. Schalling D. Psychopathy-related personality variables and the psychophysiology of socialisation. In: Hare RD, Schalling D, editors. Psychopathic behaviour: approaches to research. New York: Wiley; 1978 [Chapter 6]. Gorenstein EE. Frontal lobe functions in psychopaths. J Abnorm Psychol 1982;91:368–79. Hare RD. Performance of psychopaths on cognitive tasks related to frontal lobe function. J Abnorm Psychol 1984;93:133–40. Hare RD. The hare psychopathy checklist. Revised: 2nd ed. Toronto: Multi-Health Systems Inc.; 2003. Lapierre D, Braun CMJ, Hodgins S. Ventral frontal deficits in psychopathy: neuropsychological test findings. Neuropsychologia 1995;33:139–51. Mitchell DGV, Colledge E, Leonard A, Blair RJR. Risky decisions and response reversal: Is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? Neuropsychologia 2002;40:2013–22. Schmitt WA, Brinckley CA, Newman JP. Testing Damasio’s somatic marker hypothesis with psychopathic individuals: Risk takers or risk averse? J Abnorm Psychol 1999;108:538–43. Howard RC. Personality, ways of coping and cognitive functions in hospitalised alcoholics. In: Joyce P, editor. Development, personality and psychopathology. Christchurch, NZ: Christchurch School of Medicine; 1994. p. 235–48. Laakso MP, Gunning-Dixon F, Vaurio O, Repo-Tiihonen E, Soininen H, Tiihonen J. Prefrontal volumes in habitually
708 violent subjects with antisocial personality disorder and type 2 alcoholism. Psychiat Res-Neuroim 2002;114:95–102. [27] Piquero AR, Moffitt TE. Life-course persistent offending. In: Adler JR, editor. Forensic psychology. Concepts, debates and practice. Cullompton, UK: Willan Publishing; 2004. p. 177–96.
Howard [28] Fuller E. Smoking, drinking and drug use among young people in England in 2004. London: The Stationery Office; 2005. Available from (http:www.dh.gov.uk/Home/fs/en). [29] Cooke DJ, Michie C. Refining the construct of psychopathy: Towards a hierarchical model. Psychol Assess 2001;13:171–88.