Introduction
Individuals with conduct disorder (CD) in youth and antisocial personality disorder (ASPD) in adulthood are responsible for a large proportion of violent crime (Falk et al., 2014; Martinez et al., 2017). Within this group, about one-third meet criteria for callous-unemotional (CU) traits in youth and psychopathy (ASPD+P) in adulthood, offending earlier, more widely, and more severely than those without psychopathy (ASPD-P) (Kosson et al., 2006). Despite the high prevalence of ASPD+/-P in forensic and penal settings (Fazel and Danesh, 2002; Coid et al., 2009b) and the large social and financial burden associated with ASPD+/-P (Heeks et al., 2018), evidence for successful treatments is lacking (Gibbon et al., 2020; Khalifa et al., 2020), and understanding of causative mechanisms remains limited.
The identification of causative mechanisms relating to neurocognitive factors that contribute to the development of ASPD and its heterogeneity may be particularly important. Studies have begun to offer insight. This includes evidence for difficulties in emotion recognition and empathic responding (Blair, 2007; Marsh and Blair, 2008; Dawel et al., 2012; Decety et al., 2013; Schönenberg and Jusyte, 2014), reinforcement-based learning (Budhani et al., 2006; Dolan, 2012; De Brito et al., 2013; Gregory et al., 2015; Hughes et al., 2016; Glimmerveen et al., 2022a), and attention (Hamilton and Newman, 2018; Baliousis et al., 2019; Baskin-Sommers and Brazil, 2022). Improved knowledge of the underpinnings of these dysfunctions could help identify important treatment targets and lead to the development of stratified, focused interventions, the potential for which has been previously demonstrated (Baskin-Sommers et al., 2015).
Despite this promise, there are several important challenges which constrain the potential of neurocognitive testing in ASPD and psychopathy. Key amongst these are (1) inconsistent phenotypic characterization of heterogeneous samples; (2) unreliable/inconsistent task design and selection; (3) poor task engagement; and (4) the lack of longitudinal studies. Below, we discuss these in turn and make suggestions for optimization of future research.
Key challenges in neurocognitive assessment in ASPD+/-P
Inconsistent phenotypic characterization
While some dimensional understanding of ASPD is important, a pragmatic approach to addressing heterogeneity of ASPD is to stratify them into more biologically homogenous subtypes (Brazil et al., 2018). Together with the divergent offending profiles of ASPD+/-P, accumulating evidence suggests that individuals with ASPD+P compared to those with ASPD-P have shared but also distinct neurobiological/neurocognitive features (Kosson et al., 2006; Gregory et al., 2012, 2015; De Brito et al., 2013; Pera-Guardiola et al., 2016; Marsden et al., 2019).
Such stratification, however, requires a consistent definition of psychopathy. The Psychopathy Checklist-Revised (PCL-R) is the most widely used assessment tool in clinical forensic and penitential populations (Hare, 1991), but considerable debate persists about the most appropriate construct of psychopathy (Cooke and Michie, 2001; Hare and Neumann, 2008). This has led to the use of other tools including self-report questionnaires, which may have lower reliability, since individuals with ASPD+/-P might not tell the truth or have enough insight (Brinkley et al., 2001; Sellbom et al., 2007; Gonsalves et al., 2013). The assessment of community-dwelling individuals with subclinical psychopathic traits also limits the ability to form a consistent understanding of psychopathy (e.g., Esser and Eisenbarth, 2021; Friedman et al., 2021). Considering the prevalence of subclinical psychopathic traits in the community (Coid et al., 2009a), this is not problematic per se. However, it is questionable whether such findings are applicable to clinical samples, where more severe neurocognitive deficits might have different underpinnings. Finally, even studies of clinical psychopathy which use the PCL-R choose different cut-off points. Evidence suggests that a cut-off point of 25 should be used for European samples (as opposed to 30 for US samples) (Cooke and Michie, 1999), likely due to cultural factors, however this is not always adhered. Furthermore, some studies might refer to their sample as “high” on psychopathy despite scores only indicating subclinical levels of psychopathy (e.g., Domes et al., 2013; Weidacker et al., 2017).
Together, these inconsistencies contribute to incongruent results in neurocognitive assessments, which complicates the development of clear neuropsychological models of ASPD+/-P. Ongoing research into the most appropriate construct of psychopathy remains of importance. However, perhaps the time has come to develop a large-scale collaborative protocol that agrees on the most appropriate tools to measure psychopathy within clinical forensic research. This would not preclude using multiple metrics of psychopathy. Indeed, sufficiently well-powered, pre-registered neurocognitive studies would allow for meaningful investigation into which constructs correlate best with potential biomarkers.
Unreliable/inconsistent task design and selection
For any given neurocognitive function, there are myriad tasks claiming to provide reliable metrics. However, these often slightly vary from one another. This leads to problems when comparing or collating findings and may partially explain inconsistent or contradictory results found in ASPD+/-P samples that are otherwise similar (Griffiths and Jalava, 2017). A key example is empathy deficits. Despite being a clinical feature of ASPD (First et al., 2015) and a critical component of the psychopathy construct (Hare, 1991), a recent systematic review found that ASPD+/-P was not associated with deficits in neurocognitive paradigms of empathy (Marsden et al., 2019). While underpowered studies in a population where recruitment is difficult may be a factor, it is also likely that inconsistency in task design and selection plays a role. Empathy is a broad concept with many facets. Neurocognitive research of empathy suggests several underpinning neurocognitive mechanisms (Bird and Viding, 2014), however there are competing theories about how it is best conceptualized (see Decety and Ickes, 2011; Zaki and Ochsner, 2012; Blair, 2018). The most common distinction is made between cognitive empathy (including mentalizing and theory of mind) and affective empathy (including experience sharing and emotional contagion). However, even when studies attempt greater specificity, for example by reference to mentalization, different researchers may in fact be referring to subtly different neurocognitive functions (Choi-Kain and Gunderson, 2008). This complicates the development and interpretation of tasks measuring empathy.
Evidence suggests some shared, but some distinct elements of empathic profiles in ASPD+/-P. Adults with ASPD+/-P show relatively normal performance on some aspects of cognitive empathy (Blair et al., 1996; Dolan and Fullam, 2004; Shamay-Tsoory et al., 2010), though those with ASPD+P fail to automatically take others' perspective (Drayton et al., 2018). In contrast, individuals with ASPD+/-P appear to diverge in key aspects of affective empathy. Studies indicate that brain regions involved in implicit responsivity to others' pain and emotional faces may be hyporesponsive in ASPD+P (Decety et al., 2013, 2014; Contreras-Rodríguez et al., 2014). Contrarily, individuals with ASPD-P are thought to be hyperresponsive to emotional stimuli, particularly fear and threat (Schönenberg and Jusyte, 2014; Hodgins et al., 2018). Hence, disentangling the relative contributions of deficits in cognitive and affective components of empathy by using consistent and reliable task designs may be crucial in developing treatments for specific deficits. The recent development of EmpaToM, a validated tool which delineates cognitive and affective empathy, is a step in the right direction (Kanske et al., 2015). This has already been used to demonstrate deficits in affective empathy, but not theory of mind, in male violent offenders (Winter et al., 2017).
Poor task engagement
Poor attention, lack of interest or motivation to participate in activities which are not self-beneficial, irresponsibility, and propensity for lying are all inherent pathological features of ASPD, and particularly, psychopathy. These features complicate assessment procedures and could lead to false positive and false negative findings. For instance, a lack of effort due to poor motivation could lead to significantly poorer performance on common outcome measures such as accuracy and reaction times than would be expected in real-life scenarios. In contrast, false negative findings could emerge due to unreliable performance. Individuals with psychopathy, where pathological lying is a feature, may be prone to report inaccurate responses, not reflecting their true emotional reaction, in tasks measuring explicit responses to emotions.
An example of the interpretation of task findings being complicated by potential poor engagement can be found in a recent fMRI experiment (Tully, 2021), which was designed to capture the neural circuitry of cooperation versus retaliation using the “Dealmaking” game (White et al., 2016). This study included male violent offenders with ASPD-P who were clinically characterized by high reactive aggression and low tolerance to frustration and threat. Based on previous findings in similar populations (White et al., 2013, 2014; ?), and assuming that their clinical profiles would be reflected in their task-based decision-making, it was predicted that they would decide to “reject and punish” unfair financial offers. Instead, they typically accepted unfair offers and punished less frequently than healthy non-offending controls (though findings were not statistically significant) (Tully, 2021). While it is possible this reflects the absence of neuropsychological differences between ASPD-P and controls, other explanations seem more feasible. It may be that the lack of actual monetary incentives meant subjects were not sufficiently motivated, or that subjects became bored or uninterested, as was reflected in some feedback comments collated separately. The experiment also found no activation of threat circuitry on fMRI, which would support the view that the task did not elicit a cooperation vs. retaliation decision in the ASPD-P group.
Future research may benefit from strategies to mitigate such risks. To disentangle true task effects from the potential impact of inherent clinical symptoms, it may be valuable to include experimental manipulations measuring attention. Furthermore, approaches to increase the motivation and engagement of individuals with ASPD and psychopathy should be considered. For example, a recent study highlighted the importance of adequate and tangible incentives or personalized rewards (Glimmerveen et al., 2022b). One time- and cost-effective solution is the incorporation of control items or performance validity tests (Greher and Wodushek, 2017; Sweet et al., 2021). This can be helpful toward identifying data that should be excluded from analysis due to poor engagement. It is also important that all participants receive the same precise instructions, to avoid different understandings of the task. For example, effort might fluctuate if participants are focusing on fast vs. accurate responses (Ging-Jehli et al., 2021). Lastly, it is important to consider task difficulty. Tasks that are too simple may promote boredom, whereas tasks that are too difficult may hinder effort (Cornacchio et al., 2017).
Lack of longitudinal studies
Since CD+/-CU traits is the psychopathological developmental precursor of ASPD+/-P, several pivotal large cohort studies have followed the trajectories of youth with CD for up to several decades (Frick and Viding, 2009; Frick et al., 2013; Assink et al., 2015; Jolliffe et al., 2017; Moffitt, 2018; Carlisi et al., 2020; Farrington, 2020; Lasko and Chester, 2021). These have provided crucial insights by identifying early cognitive risk factors for differential pathways toward life-course persistent antisocial behavior and offer improved understanding of protective and promotive factors. However, they have been limited by the relative lack of thorough neurocognitive testing. This means that the understanding of how specific neurocognitive mechanisms change over time is still limited. In contrast research of other neurodevelopmental disorders such as autism has shown that the neurobiological underpinnings may continue to develop differently throughout adulthood, highlighting the importance of longitudinal assessments across the lifespan (Magiati et al., 2014). This may be especially important in ASPD+P, which has many features consistent with neurodevelopmental disorders, including considerable heritability and a male preponderance (Viding et al., 2005; Baron-Cohen et al., 2011; Yildirim and Derksen, 2012). Longitudinal studies could also identify important distinctions in the trajectories of males and females with psychopathy (Tully et al., 2022). In keeping with this view, other authors have identified neuropsychological markers, but also their patterns of change over time, as essential in order to develop personalized medicine approaches (Blair et al., 2022). Encouragingly, large-scale collaborations in the study of antisocial youths have begun to adopt this approach (Casey et al., 2018; Freitag et al., 2018). These important developments align with a wider move toward replicability and transparency in psychological research (Munafò et al., 2017).
Conclusion
We have highlighted four key issues that continue to limit neurocognitive testing in ASPD+/-P, relating to both psychometric assessment and study methodology. Alongside specific improvements in task design and execution and longitudinal assessments, a recurring theme within potential solutions is a consistent, collaborative approach. Large-scale collaborative studies guided by scientific discourse among experts is required to move toward a personalized medicine approach that uses neurocognitive markers as treatment targets for ASPD+/-P. This is essential if we are to help alleviate the personal, social and financial burden associated with these complex disorders.
Funding
JG is in receipt of a PhD studentship funded by the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London (grant code IS-BRC-1215-20018).
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Author disclaimer
The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care.
Statements
Author contributions
JG and JT were responsible for the conceptualization of the topic and the writing and development of the manuscript. NK provided additional input and editorial support on the manuscript. All authors contributed to the article and approved the submitted version.
Acknowledgments
We would like to thank Dr. Stuart White for his helpful thoughts on an earlier draft of this article.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
References
1
AssinkM.van der PutC. E.HoeveM.de VriesS. L. A.StamsG. J. J. M.OortF. J. (2015). Risk factors for persistent delinquent behavior among juveniles: a meta-analytic review. Clin. Psychol. Rev.42, 47–61. 10.1016/j.cpr.2015.08.002
2
BaliousisM.DugganC.McCarthyL.HubandN.VöllmB. (2019). Executive function, attention, and memory deficits in antisocial personality disorder and psychopathy. Psychiatry Res.278, 151–161. 10.1016/j.psychres.2019.05.046
3
Baron-CohenS.LombardoM. V.AuyeungB.AshwinE.ChakrabartiB.KnickmeyerR. (2011). Why are autism spectrum conditions more prevalent in males?PLoS Biol.9, e1001081. 10.1371/journal.pbio.1001081
4
Baskin-SommersA. R.BrazilI. A. (2022). The importance of an exaggerated attention bottleneck for understanding psychopathy. Trends Cogn. Sci.26, 325–336. 10.1016/j.tics.2022.01.001
5
Baskin-SommersA. R.CurtinJ. J.NewmanJ. P. (2015). Altering the cognitive-affective dysfunctions of psychopathic and externalizing offender subtypes with cognitive remediation. Clin. Psychol. Sci.3, 45–57. 10.1177/2167702614560744
6
BirdG.VidingE. (2014). The self to other model of empathy: providing a new framework for understanding empathy impairments in psychopathy, autism, and alexithymia. Neurosci. Biobehav. Rev.47, 520–532. 10.1016/j.neubiorev.2014.09.021
7
BlairR. J. R. (2007). “Empathic dysfunction in psychopathic individuals,” in Empathy in Mental Illness, eds. T. F. D. Farrow and P. W. R. Woodruff (Cambridge: Cambridge University Press), 3–16.
8
BlairR. J. R. (2018). Traits of empathy and anger: implications for psychopathy and other disorders associated with aggression. Philos. Trans. R. Soc. B Biol. Sci.373, 1–8. 10.1098/rstb.2017.0155
9
BlairR. J. R.MathurA.HainesN.BajajS. (2022). Future directions for cognitive neuroscience in psychiatry: recommendations for biomarker design based on recent test re-test reliability work. Curr. Opin. Behav. Sci.44, 101102. 10.1016/j.cobeha.2022.101102
10
BlairR. J. R.SellarsC.StricklandI.ClarkF.WilliamsA.SmithM.et al. (1996). Theory of mind in the psychopath. J. Forensic Psychiatry7, 15–25. 10.1080/09585189608409914
11
BrazilI. A.van DongenJ. D. M.MaesJ. H. R.MarsR. B.Baskin-SommersA. R. (2018). Classification and treatment of antisocial individuals: from behavior to biocognition. Neurosci. Biobehav. Rev.91, 259–277. 10.1016/j.neubiorev.2016.10.010
12
BrinkleyC. A.SchmittW. A.SmithS. S.NewmanJ. P. (2001). Construct validation of a self-report psychopathy scale: does Levenson's self-report psychopathy scale measure the same constructs as Hare's psychopathy checklist-revised?Pers. Individ. Dif.31, 1021–1038. 10.1016/S0191-8869(00)00178-1
13
BudhaniS.RichellR. A.BlairR. J. R. (2006). Impaired reversal but intact acquisition: Probabilistic response reversal deficits in adult individuals with psychopathy. J. Abnorm. Psychol.115, 552–558. 10.1037/0021-843X.115.3.552
14
CarlisiC. O.MoffittT. E.KnodtA. R.HarringtonH.IrelandD.MelzerT. R.et al. (2020). Associations between life-course-persistent antisocial behaviour and brain structure in a population-representative longitudinal birth cohort. Lancet Psychiatry7, 245–253. 10.1016/S2215-0366(20)30002-X
15
CaseyB. J.CannonierT.ConleyM. I.CohenA. O.BarchD. M.HeitzegM. M.et al. (2018). The adolescent brain cognitive development (ABCD) study: imaging acquisition across 21 sites. Dev. Cogn. Neurosci.32, 43–54. 10.1016/j.dcn.2018.03.001
16
Choi-KainL. W.GundersonJ. G. (2008). Mentalization: ontogeny, assessment, and application in the treatment of borderline personality disorder. Am. J. Psychiatry165, 1127–1135. 10.1176/appi.ajp.2008.07081360
17
CoidJ.YangM.UllrichS.RobertsA.HareR. D. (2009a). Prevalence and correlates of psychopathic traits in the household population of Great Britain. Int. J. Law Psychiatry32, 65–73. 10.1016/j.ijlp.2009.01.002
18
CoidJ.YangM.UllrichS.RobertsA.MoranP.BebbingtonP.et al. (2009b). Psychopathy among prisoners in England and Wales. Int. J. Law Psychiatry32, 134–141. 10.1016/j.ijlp.2009.02.008
19
Contreras-RodríguezO.PujolJ.BatallaI.HarrisonB. J.BosqueJ.Ibern-RegàsI.et al. (2014). Disrupted neural processing of emotional faces in psychopathy. Soc. Cogn. Affect. Neurosci.9, 505–512. 10.1093/scan/nst014
20
CookeD. J.MichieC. (1999). Psychopathy across cultures: North America and Scotland compared. J. Abnorm. Psychol.108, 58–68. 10.1037/0021-843X.108.1.58
21
CookeD. J.MichieC. (2001). Refining the construct of psychopathy: towards a hierarchical model. Psychol. Assess.13, 171–188. 10.1037/1040-3590.13.2.171
22
CornacchioD.PinkhamA. E.PennD. L.HarveyP. D. (2017). Self-assessment of social cognitive ability in individuals with schizophrenia: appraising task difficulty and allocation of effort. Schizophr. Res.179, 85–90. 10.1016/j.schres.2016.09.033
23
DawelA.O'KearneyR.McKoneE.PalermoR. (2012). Not just fear and sadness: Meta-analytic evidence of pervasive emotion recognition deficits for facial and vocal expressions in psychopathy. Neurosci. Biobehav. Rev.36, 2288–2304. 10.1016/j.neubiorev.2012.08.006
24
De BritoS. A.VidingE.KumariV.BlackwoodN.HodginsS. (2013). Cool and hot executive function impairments in violent offenders with antisocial personality disorder with and without psychopathy. PLoS ONE8, e65566. 10.1371/journal.pone.0065566
25
DecetyJ.IckesW. (2011). The Social Neuroscience of Empathy, eds. J. Decety and W. Ickes (Cambridge, MA: MIT Press).
26
DecetyJ.SkellyL. R.KiehlK. A. (2013). Brain response to empathy-eliciting scenarios involving pain in incarcerated individuals with psychopathy. JAMA Psychiatry70, 638–645. 10.1001/jamapsychiatry.2013.27
27
DecetyJ.SkellyL. R.YoderK. J.KiehlK. A. (2014). Neural processing of dynamic emotional facial expressions in psychopaths. Soc. Neurosci.9, 36–49. 10.1080/17470919.2013.866905
28
DolanM. (2012). The neuropsychology of prefrontal function in antisocial personality disordered offenders with varying degrees of psychopathy. Psychol. Med.42, 1715–1725. 10.1017/S0033291711002686
29
DolanM.FullamR. (2004). Theory of mind and mentalizing ability in antisocial personality disorders with and without psychopathy. Psychol. Med.34, 1093–1102. 10.1017/S0033291704002028
30
DomesG.HollerbachP.VohsK.MokrosA.HabermeyerE. (2013). Emotional empathy and psychopathy in offenders: an experimental study. J. Pers. Disord.27, 67–84. 10.1521/pedi.2013.27.1.67
31
DraytonL. A.SantosL. R.Baskin-SommersA. R. (2018). Psychopaths fail to automatically take the perspective of others. Proc. Natl. Acad. Sci. USA.115, 3302–3307. 10.1073/pnas.1721903115
32
EsserS.EisenbarthH. (2021). Emotional learning and psychopathic personality traits: the role of attentional focus and intention to learn. Motiv. Sci.8, 191–206. 10.1037/mot0000256
33
FalkÖ.WalliniusM.LundströmS.FrisellT.AnckarsäterH.KerekesN. (2014). The 1% of the population accountable for 63 % of all violent crime convictions. Soc. Psychiatry Psychiatr. Epidemiol.49, 559–571. 10.1007/s00127-013-0783-y
34
FarringtonD. P. (2020). The integrated cognitive antisocial potential (ICAP) theory: past, present, and future. J. Dev. Life-Course Criminol.6, 172–187. 10.1007/s40865-019-00112-9
35
FazelS.DaneshJ. (2002). Serious mental disorder in 23000 prisoners: a systematic review of 62 surveys. Lancet359, 545–550. 10.1016/S0140-6736(02)07740-1
36
FirstM. B.WilliamsJ. B. W.BenjaminL. S.SpitzerR. L. (2015). User's Guide for the SCID-5-PD (Structured Clinical Interview for DSM-5 Personality Disorder). Arlington, VA: American Psychiatric Association.
37
FreitagC. M.KonradK.StadlerC.De BritoS. A.PopmaA.HerpertzS. C.et al. (2018). Conduct disorder in adolescent females: current state of research and study design of the FemNAT-CD consortium. Eur. Child Adolesc. Psychiatry27, 1077–1093. 10.1007/s00787-018-1172-6
38
FrickP. J.BlairR. J. R.CastellanosF. X. (2013). “Callous-unemotional traits and developmental pathways to the disruptive behavior disorders,” in Disruptive Behavior Disorders, Advances in Development and Psychopathology: Brain Research Foundation Symposium Series, Vol. 1, eds P.H. Tolan and B. L. Leventhal (New York, NY: Springer), 69–102. 10.1007/978-1-4614-7557-6_4
39
FrickP. J.VidingE. (2009). Antisocial behavior from a developmental psychopathology perspective. Dev. Psychopathol.21, 1111–1131. 10.1017/S0954579409990071
40
FriedmanN. P.RheeS. H.RossJ. M.CorleyR. P.HewittJ. K. (2021). Genetic and environmental relations of executive functions to antisocial personality disorder symptoms and psychopathy. Int. J. Psychophysiol.163, 67–78. 10.1016/j.ijpsycho.2018.12.007
41
GibbonS.KhalifaN. R.CheungN. H. Y.VöllmB. A.McCarthyL.GibbonS.et al. (2020). Psychological interventions for antisocial personality disorder (review). Cochrane Database Syst. Rev.9, CD007668. 10.1002/14651858.CD007668.pub3
42
Ging-JehliN. R.RatcliffR.ArnoldL. E. (2021). Improving neurocognitive testing using computational psychiatry—a systematic review for ADHD. Psychol. Bull.147, 169–231. 10.1037/bul0000319
43
GlimmerveenJ. C.MaesJ. H. R.BrazilI. A. (2022a). “Psychopathy, Maladaptive Learning and Risk Taking,” in Psychopathy, History, Philosophy an Theory of the Life Sciences 27, eds. L. Malatesti, J. McMillan, and P. Sustar (Springer, Cham), 189–211.
44
GlimmerveenJ. C.MaesJ. H. R.BultenE.ScheperI.BrazilI. A. (2022b). So what'cha want? The impact of individualised rewards on associative learning in psychopathic offenders. Cortex149, 44–58. 10.1016/j.cortex.2022.01.006
45
GonsalvesV. M.McLawsenJ. E.HussM. T.ScaloraM. J. (2013). Factor structure and construct validity of the psychopathic personality inventory in a forensic sample. Int. J. Law Psychiatry36, 176–184. 10.1016/j.ijlp.2013.01.010
46
GregoryS.BlairR. J. R.FfytcheD.SimmonsA.KumariV.HodginsS.et al. (2015). Punishment and psychopathy: a case-control functional MRI investigation of reinforcement learning in violent antisocial personality disordered men. Lancet Psychiatry2, 153–160. 10.1016/S2215-0366(14)00071-6
47
GregoryS.FfytcheD.SimmonsA.KumariV.HowardM.HodginsS.et al. (2012). The antisocial brain: psychopathy matters. A structural MRI investigation of antisocial male violent offenders. Arch. Gen. Psychiatry69, 962–972. 10.1001/archgenpsychiatry.2012.222
48
GreherM. R.WodushekT. R. (2017). Performance validity testing in neuropsychology: Scientific basis and clinical application - a brief review. J. Psychiatr. Pract.23, 134–140. 10.1097/PRA.0000000000000218
49
GriffithsS. Y.JalavaJ. V. (2017). A comprehensive neuroimaging review of PCL-R defined psychopathy. Aggress. Violent Behav.36, 60–75. 10.1016/j.avb.2017.07.002
50
HamiltonR. B.NewmanJ. P. (2018). “The response modulation hypothesis: formulation, development, and implications for psychopathy,” in Handbook of Psychopathy, ed. C. J. Patrick (New York, NY: Guilford Press), 80–93.
51
HareR. D. (1991). Manual for the Hare Psychopathy Checklist-Revised. 2nd ed. New York, NY: Guilford.
52
HareR. D.NeumannC. S. (2008). Psychopathy as a clinical and empirical construct. Annu. Rev. Clin. Psychol.4, 217–246. 10.1146/annurev.clinpsy.3.022806.091452
53
HeeksM.ReedS.TafsiriM.PrinceS. (2018). The Economic and Social Costs of Crime. Available online at: https://www.gov.uk/government/publications/the-economic-and-social-costs-of-crime (accessed April 6, 2020).
54
HodginsS.ChecknitaD.LindnerP.SchifferB.De BritoS. A. (2018). “Antisocial personality disorder,” in The Wiley Blackwell Handbook of Forensic Neuroscience, I and II, eds A. R. Beech, A. J. Carter, R. E. Mann, and P. Rotshtein (Hoboken, NJ: John Wiley and Sons). 10.1007/s00278-019-0357-x
55
HughesM. A.DolanM. C.StoutJ. C. (2016). Decision-making in psychopathy. Psychiatry Psychol. Law23, 521–537. 10.1080/13218719.2015.1081228
56
JolliffeD.FarringtonD. P.PiqueroA. R.LoeberR.HillK. G. (2017). Systematic review of early risk factors for life-course-persistent, adolescence-limited, and late-onset offenders in prospective longitudinal studies. Aggress. Violent Behav.33, 15–23. 10.1016/j.avb.2017.01.009
57
KanskeP.BöcklerA.TrautweinF. M.SingerT. (2015). Dissecting the social brain: Introducing the EmpaToM to reveal distinct neural networks and brain–behavior relations for empathy and theory of mind. Neuroimage122, 6–19. 10.1016/j.neuroimage.2015.07.082
58
KhalifaN. R.GibbonS.VöllmB. A.CheungN. H. Y.McCarthyL. (2020). Pharmacological interventions for antisocial personality disorder (review). Cochrane Database Syst. Rev.9, CD007667. 10.1002/14651858.CD007667.pub3
59
KossonD. S.LorenzA. R.NewmanJ. P. (2006). Effects of comorbid psychopathy on criminal offending and emotion processing in male offenders with antisocial personality disorder. J. Abnorm. Psychol.115, 798–806. 10.1037/0021-843X.115.4.798
60
LaskoE. N.ChesterD. S. (2021). What makes a “successful” psychopath? longitudinal trajectories of offenders' antisocial behavior and impulse control as a function of psychopathy. Personal. Disord. Theory, Res. Treat. 12, 207–215. 10.1037/per0000421
61
MagiatiI.TayX. W.HowlinP. (2014). Cognitive, language, social and behavioural outcomes in adults with autism spectrum disorders: a systematic review of longitudinal follow-up studies in adulthood. Clin. Psychol. Rev.34, 73–86. 10.1016/j.cpr.2013.11.002
62
MarsdenJ.GlazebrookC.TullyR.VöllmB. (2019). Do adult males with antisocial personality disorder (with and without co-morbid psychopathy) have deficits in emotion processing and empathy? A systematic review. Aggress. Violent Behav.48, 197–217. 10.1016/j.avb.2019.08.009
63
MarshA. A.BlairR. J. R. (2008). Deficits in facial affect recognition among antisocial populations: a meta-analysis. Neurosci. Biobehav. Rev.32, 454–465. 10.1016/j.neubiorev.2007.08.003
64
MartinezN. N.LeeY. J.EckJ. E. O. S. (2017). Ravenous wolves revisited: a systematic review of offending concentration. Crime Sci.6, 1–16. 10.1186/s40163-017-0072-2
65
MoffittT. E. (2018). Male antisocial behaviour in adolescence and beyond. Nat. Hum. Behav.2, 177–186. 10.1038/s41562-018-0309-4
66
MunafòM. R.NosekB. A.BishopD. V. M.ButtonK. S.ChambersC. D.Percie Du SertN.et al. (2017). A manifesto for reproducible science. Nat. Hum. Behav.1, 1–9. 10.1038/s41562-016-0021
67
Pera-GuardiolaV.BatallaI.BosqueJ.KossonD.Pifarr,éJ.Hernández-RibasR.et al. (2016). Modulatory effects of psychopathy on wisconsin card sorting test performance in male offenders with antisocial personality disorder. Psychiatry Res.235, 43–48. 10.1016/j.psychres.2015.12.003
68
SchönenbergM.JusyteA. (2014). Investigation of the hostile attribution bias toward ambiguous facial cues in antisocial violent offenders. Eur. Arch. Psychiatry Clin. Neurosci.264, 61–69. 10.1007/s00406-013-0440-1
69
SellbomM.Ben-PorathY. S.StaffordK. P. (2007). A Comparison of MMPI-2 Measures of Psychopathic Deviance in a Forensic Setting. Psychol. Assess.19, 430–436. 10.1037/1040-3590.19.4.430
70
Shamay-TsooryS. G.HarariH.Aharon-PeretzJ.LevkovitzY. (2010). The role of the orbitofrontal cortex in affective theory of mind deficits in criminal offenders with psychopathic tendencies. Cortex46, 668–677. 10.1016/j.cortex.2009.04.008
71
SweetJ. J.HeilbronnerR. L.MorganJ. E.LarrabeeG. J.RohlingM. L.BooneK. B.et al. (2021). American academy of clinical neuropsychology (AACN) 2021 consensus statement on validity assessment: update of the 2009 AACN consensus conference statement on neuropsychological assessment of effort, response bias, and malingering. Clin. Neuropsychol.35, 1053–1106. 10.1080/13854046.2021.1896036
72
TullyJ. (2021). “Investigating the effect of oxytocin and the neurochemistry of antisocial personality disorder and psychopathy using neuroimaging,” in Decisions to Co-Operate or Retaliate in Violent Antisocial Personality Disordered Men With and Without Psychopathy (Ann Arbour, MI: ProQuest Dissertations Publishing), 130–158.
73
TullyJ.FreyA.FotiadouM.KollaN. J.EisenbarthH. (2022). Psychopathy in women: insights from neuroscience and ways forward for research. CNS Spectr.1–13. 10.1017/S1092852921001085
74
VidingE.BlairR. J. R.MoffittT. E.PlominR. (2005). Evidence for substantial genetic risk for psychopathy in 7-years-olds. J. Child Psychol. Psychiatry46, 592–597. 10.1111/j.1469-7610.2004.00393.x
75
WeidackerK.SnowdenR. J.BoyF.JohnstonS. J. (2017). Response inhibition in the parametric Go/No-Go task in psychopathic offenders. Psychiatry Res.250, 256–263. 10.1016/j.psychres.2017.01.083
76
WhiteS. F.BrislinS. J.MeffertH.SinclairS.BlairR. J. R. (2013). Callous-unemotional traits modulate the neural response associated with punishing another individual during social exchange: a preliminary investigation. J. Pers. Disord.27, 99–112. 10.1521/pedi.2013.27.1.99
77
WhiteS. F.BrislinS. J.SinclairS.BlairR.J.R. (2014). Punishing unfairness: Rewarding or the organization of a reactively aggressive response?Hum. Brain Mapp. 35, 2137–2147. 10.1002/hbm.22316
78
WhiteS. F.Van TieghemM.BrislinS. J.SypherI.SinclairS.PineD. S.et al. (2016). Neural correlates of the propensity for retaliatory behavior in youths with disruptive behavior disorders. Am. J. Psychiatry173, 282–290. 10.1176/appi.ajp.2015.15020250
79
WinterK.SpenglerS.BermpohlF.SingerT.KanskeP. (2017). Social cognition in aggressive offenders: impaired empathy, but intact theory of mind. Sci. Rep.7, 1–11. 10.1038/s41598-017-00745-0
80
YildirimB. O.DerksenJ. J. L. (2012). A review on the relationship between testosterone and the interpersonal/affective facet of psychopathy. Psychiatry Res.197, 181–198. 10.1016/j.psychres.2011.08.016
81
ZakiJ.OchsnerK. N. (2012). The neuroscience of empathy: progress, pitfalls and promise. Nat. Neurosci.15, 675–680. 10.1038/nn.3085
Summary
Keywords
neurocognitive assessment, neuropsychological tests, antisocial personality disorder, psychopathy, challenges
Citation
Griem J, Kolla NJ and Tully J (2022) Key challenges in neurocognitive assessment of individuals with antisocial personality disorder and psychopathy. Front. Behav. Neurosci. 16:1007121. doi: 10.3389/fnbeh.2022.1007121
Received
29 July 2022
Accepted
16 August 2022
Published
02 September 2022
Volume
16 - 2022
Edited by
Matthew J. Robson, University of Cincinnati, United States
Reviewed by
Morten Hesse, Aarhus University, Denmark
Updates
Copyright
© 2022 Griem, Kolla and Tully.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Julia Griem julia.griem@kcl.ac.uk
This article was submitted to Pathological Conditions, a section of the journal Frontiers in Behavioral Neuroscience
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.