The Relation Between Impulsive-Antisocial Personality Traits and The Amygdala: A Meta-Analysis
Masterthesis Forensic Child and Youth Care Sciences Graduate School of Child Development and Education University of Amsterdam I.H. van Dijk & P.C.M van den Heuvel 10477179 & 5745179 First assessor: Prof. Dr. G.J.J.M Stams Second assessor: Dr. T. Van Leeuwen Amsterdam, January 2016
Abstract
The neurobiological perspective is a new approach that might contribute to the development of an effective intervention for clients with conduct disorder or psychopathy. It is assumed that these impulsive-antisocial personality traits are often associated with structural and/or functional deficits in the amygdala. By use of a multi-level meta-analysis this study
investigated the relation between impulsive-antisocial personality traits on the one hand and the amygdala on the other hand. A systematic literature research resulted in k = 21 studies with 40 effect sizes. The meta-analysis yielded an overall medium-to-large effect size of r = .34, which proved to be heterogeneous. Differences between studies accounted for 91.7% of the variation among effect sizes. None of the moderators (gender, sample type, age, nature of disorder) provided an explanation for the between study variance. In conclusion, there is a moderate-to-strong association between the amygdala and conduct disorder and psychopathy. However, more research is necessary, in particular involving areas of the brain that are connected with the amygdala, to explain differences in effect sizes between studies.
Introduction
Conduct disorder and psychopathy, or impulsive-antisocial personality traits, are described as persistent patterns of antisocial behavior in which the basic rights of others or major age-appropriate societal norms or rules are violated, and which may already begin in childhood or early adolescence and continue into adulthood (American Psychiatric
Association, 2013). Currently there are hardly any effective behavioral interventions for youth and adults with such severe and complex emotional and/or behavioral problems (Weisz, Ugueto, Cheron & Herren, 2013b). Therefore, a neurobiological approach should be
considered in the treatment of these disorders (Cornet, De Kogel, Nijman, Raine & Van der Laan, 2014; Weisz, Kuppens, Eckshtain, Ugueto, Hawley & Jensen-Doss, 2013a). The groundwork for such approach is provided by the work of Blair (2013), who recently reviewed the neurobiology of psychopathic traits in youths particularly focusing on the amygdala, and which is the direct motive to conduct the present meta-analysis.
Current behavioral interventions for juveniles with severe conduct problems only seem to work within ideal circumstances, which usually cannot be generated under clinically
representative conditions (Weisz et al., 2013b). This is even less so in the forensic field, where effective treatment is compromised by coercive measures and lack of treatment motivation (Lambie & Randell, 2013; Parhar, Wormith, Derkzen, & Beauregard, 2008). To date, there is a lack of research on how to improve treatments under clinically representative conditions (Weisz et al., 2013b). Even the most advanced and comprehensive treatment for conduct problems under highly controlled conditions, Multisystemic Therapy (MST), does not seem to work for forensic youth under clinically representative conditions (Van der Stouwe, Asscher, Stams, Deković & Van der Laan, 2014). This lack of effect with current interventions is possible due to the fact that the forensic field mainly has to deal with
unmotivated patients, early dropouts or that the justice system hinders the necessary conditions for effective judicial interventions.
Lack of effective treatment is highly problematic, but it also provides space for new perspectives on effective treatment. Recently, Cornet et al. (2014) reviewed the
neurobiological perspective of interventions for youth with conduct disorder, also because neurobiological factors have the power to predict the efficiency of treatments. This is important because short, early and effective interventions should be tailored to the right population and account for both age and the neurobiological make-up of clients (Salekin, 2002).
In fact there is evidence showing that neurobiological interventions can be an
alternative for those who do not benefit from the treatment as currently offered (Cornet et al., 2014; Finger, 2008; Jones, 2009; Marsh, 2008;), including medicamental treatments, with or without psychotherapy (Weisz et al., 2013a). A recent review by Blair (2013) on the
neurobiology of psychopathic traits in youth discusses how specific functional impairments in specific neural systems give rise to the development of psychopathic traits. According to Blair (2013), characteristics of psychopaths (such as lack of empathy, decision-making and
processing distress cures) are related to (functional and structural) deficits in the amygdala, both in children and in adults.
The amygdala is a complex brain structure, composed of multiple subareas, and it is involved in processing sensory information that may have an effect on behavior (LeDoux, 2007). This almond shaped structure is part of the limbic system and located in the ventral temporal lobe. In order to perform and behave normally and successfully, the amygdala should be intact. Inabilities of or damage to the amygdala can cause many behavioral deficits in emotional processing, fear conditioning and behavior, which can be linked with a variety of psychiatric disorders (LeDoux, 2007).
Several studies have reported a link between impulsive-antisocial personality traits and the amygdala at a functional level. Youth and adults with those disorders showed significant differences in activation in the amygdala, while they were exposed to dynamic visual stimuli, such as fearful or neutral faces, compared to the control group (Carré, Hyde, Neumann, Viding & Hariri, 2013; Decety, Michalska, Akitsuki & Lahey, 2009; Marsh et al., 2008; Jones, Laurens, Herba, Barker & Viding, 2009). Marsh et al. (2008) showed how adults with callous-unemotional traits had a dysfunctional amygdala and did not show greater response to fearful expressions where comparisons did (Marsh et al., 2008). Jones et al. (2009) have shown that healthy comparisons do have significant stronger amygdala activity in response to fearful expressions compared with boys with conduct problems and callous-unemotional traits.
In addition to differences at a functional level, there is evidence for differences in amygdala structure. Yang, Raine, Narr, Colleti and Toga (2009) found significant volume reductions in the amygdala in psychopaths in comparison with a control group. Those
reductions correlated significantly with psychopathy scores. Also other studies indicated that individuals with impulsive-antisocial personality traits showed volume reductions in the amygdala compared to healthy comparisons (Ermer, Cope, Nyalakanti, Calhoun & Kiehl, 2012). However, Boccardi et al. (2011) found the amygdala of psychopaths to be larger compared to the amygdala of healthy comparisons.
Thus there is accumulating evidence showing that deficits in the amygdala might be related to impulsive-antisocial personality traits. In order to examine the strength of the relation between functioning of the amygdala and impulsive- antisocial personality traits as well as factors that may moderate this relation, a multilevel meta-analysis was conducted. With this method it is possible to get a complete coverage of all relevant studies concerning this topic (Crombie & Davies, 2009). Conform requirements of a proper meta-analysis, we
explored outcomes from various categories using moderator analysis, such as study and participant characteristics (age, gender, diagnosis) to see whether they have any effects on the main outcomes (Crombie & Davies, 2009). For example, structural deficits in the amygdala may have different effects on impulsive-antisocial personality traits compared to functional deficits. Those outcomes may be relevant for further research and interventions. This might bring us one step closer to the long desired answer for significant tools in the development of an effective treatment for the problematic population as described. In the current meta-analysis, the main focus is the association between the impaired functional and structural amygdala and impulsive-antisocial personality traits.
Based upon the studies included in this meta-analysis, three hypotheses were tested. The first hypothesis is that the participants with impulsive-antisocial personality traits will have less functional reactivity in the amygdala compared to the healthy control group. The second hypothesis is that the participants with impulsive-antisocial personality traits will have more deficits in amygdala volume and morphology compared to the control groups as used in the resources in the multi-level meta-analysis. The third hypothesis is that psychopathy is stronger associated with deficits in amygdala, both structural and functional, than conduct disorder, because individuals with psychopathic traits tend to have a longer history of deviant behavior (Moffitt, Caspi, Harrington & Milne, 2002).
Methods Selection of studies
Empirical studies available between 2005 and 2015 focusing on impulsive-antisocial personality traits associated with amygdala reactivity or structure were included in the current multi-level meta-analysis. Most input for this meta-analysis has been obtained from Blair’s review (2013) about the neurobiology of psychopathic traits in youth. The relevant studies on conduct disorder, psychopathic traits and psychopathy in his review, which have examined
relations with amygdala structure or reactivity, were selected. After examining this selection of relevant studies, there was a second selection within the used references in the relevant studies. Furthermore one overall electronic database, Google Scholar, was searched using the following key words: ‘psychopathy’, ‘psychopathic traits’, ‘psychopaths’, ‘sociopathy’, ‘sociopaths’, ‘dissocial personality disorder’, ‘anti personality disorder’ and ‘conduct disorder’ in combination with ‘amygdala’.
Multiple inclusion criteria were formulated. First, the studies must include participants with diagnosed or self reported conduct disorder or psychopathy. There was a distinction between clinically diagnosed, not properly diagnosed but in detention, and not clinically diagnosed conduct disorder or psychopathy. Comorbid disorders were included as well. Second, the studies had to examine the relation between conduct disorder or psychopathy and the amygdala. This association either was functional or structural. Third, the studies should describe statistical results. And last, the studies must be published between 2005 and 2015 to preserve quality of measurements.
The initial search resulted in 21 studies (with #ES = 40 effect sizes, and N = (1,565) participants) that met the inclusion criteria. All studies contained independent data sets. Table 1 provides an overview of the included studies and their characteristics.
Moderators
Various potential moderators were identified and divided into sample and study characteristics. Study characteristics added in the moderator analysis were publication status, publication year, the continent of research (USA, Europe), research design, total sample size, proportion male, whether conduct disorder and psychopathy were self reported or officially diagnosed, the impact factor of the journal in which the study was published and the use of experimental stimuli. Sample characteristics were type of sample (clinical sample or community sample), age, gender, nature of the disorder, comorbidity, onset of disorder,
location of the amygdala (left or right) and the structure or function of the amygdala. Significant moderators were also tested for interaction-effects.
Calculation and analysis of effect sizes
Effect sizes, correlation coefficients, from the included studies in this multi-level analysis were calculated according the formulas from Lipsey and Wilson (2001). Positive effect sizes indicate that those results are consistent with our hypotheses; a high indication of conduct disorder/psychopathy is related with less activity or atypical structure of the
amygdala. Negative effect sizes indicate that conduct disorder and psychopathy are positively related to amygdala reactivity/structure. An effect size was coded as zero in case the study only reported that the relation was not significant (Lipsey & Wilson, 2001). The continuous moderators, including publication year, impact factor, mean sample age and proportion boys/men, were centered around their means. For categorical variables with more than two categories, dichotomous dummy variables were created. Outliers in effect sizes (> 3.27 SD from the mean; Tabachnik & Fidell, 2007) were winsorized to the highest effect size in the normal range.
The assumption of independent effect sizes underlying traditional meta-analytic methods was violated because we computed the overall mean effect size from more than one effect-size per study (Hox, 2002; Lipsey & Wilson, 2001). We therefore applied a multi-level approach to the current meta-analysis in order to deal with the interdependency of effect sizes (Cheung, 2014; Van den Noortgate & Onghena, 2003). A three-level model random effects model was used to account for three levels of variance, including the sampling variance for each effect size (level-one), the variance between effect sizes within studies (level-two), and the variance between studies (level-three) (Wibbelink & Assink, 2015). We used likelihood-ratio-tests to compare the deviance scores of the full model and the models without variance parameters on level two or three to determine if the level-two and -three variances were
significant, indicating heterogeneity of effect sizes within or between studies, respectively. In case the effect sizes were heterogeneous, we conducted moderator analysis, since the
differences between the effect sizes may be explained by outcome, study and sample characteristics. The current meta-analysis was conducted in R, using the metafor-package, restricted maximum likelihood estimation and the Knapp and Hartung-method (Viechtbauer, 2010; Weisz et al., 2013; Wibbelink & Assink, 2015).
File drawer bias
In this multi-level analysis, it was aimed to include all studies previously conducted that met the inclusion criteria (Lipsey & Wilson, 2001). However, some studies may not have been published due to non-significant or unanticipated results, and therefore difficult to locate. This may result in the so called “file drawer bias”, and can lead to larger estimations than the true effect size (Rosenthal, 1995). In order to check for file drawer bias, we first made a funnel plot in MIX 2.0 (Bax, 2011). If the plot is shaped like a funnel, publication bias is not likely (Duval & Tweedie, 2000). Second, we tested for funnel plot asymmetry by regressing the standard normal deviate (effect size divided by its standard error) against the effect size’s precision (inverse of the standard error) in SPSS (Egger, Smith, Schneider, & Minder, 1997). In case Egger’s test was significant, we conducted a trim-and-fill analysis (Duval & Tweedie, 2000). Finally, we calculated Rosenthal’s fail-safe number in R. This number estimates how many studies would have been included to change the possible significant association in this current study into a non-significant result. In case the fail-safe number is larger than the critical value of 5 * k + 10, in which k is the number of effect sizes, it can be concluded that file drawer bias is unlikely (Rosenthal, 1991).
Results
This multi level meta- analysis included 21 studies (k) from 2005 to 2015. The total sample of N = 1,565 children and adults consisted of n = 1,009 children (below 21 years) and
n = 556 adults (above 21 years) and total sample sizes ranged from 16 to 254 participants. The mean age of the participants was 22.14 years (SD = 9.29). The included studies were conducted in Europe (k = 8) and the USA (k = 13). In total, the coded studies produced 40 distinct effect sizes, each reflecting an effect of a structural or functional association in the amygdala with impulsive-antisocial personality traits.
The results of this multi-level-meta-analysis are presented in Table 1. A medium-to-large overall effect was found (r = .34) between impulsive-antisocial personality traits and the amygdala, which indicates that conduct disorder and psychopathy were associated with more deficits in the amygdala, difference in structure or less functional activity. The moderator analysis shows that conduct disorder did have a borderline significant stronger correlation with deficits in the amygdala than with psychopathy (p = .081). The table presents the strength of the overall effect-size and the results of the borderline significant moderator analyses.
Table 1
Significant (p = < .05) and borderline significant (p < .10) results of multilevel-meta-analysis on the relation between conduct disorder/ psychopathy and functioning/structure of the amygdala
Note. k = number of studies; #ES = number of effect sizes; t0 = difference in mean r with zero; t1 = difference in mean r with reference category; mean r = mean effect size (r); F(df1, df2) = n omnibus test. * p <.05, ** p <.01, *** p < .001 k #ES β₀ (mean r) T0 β₁ T1 F(df1, df2) Overall relation between psychopathy/ CD and amygdala 20 40 .34 3.978*** Moderator analyses Continue moderators Publication year 21 40 .33 4.030 -.061 -1.725 F(1,38) = 2.977 Mean age 21 40 .31 3.747 -.016 -1.824 F(1,43) = 3.397 N total 21 40 .47 4.236 -.002 -1.843 F(1,38) = 3.397 Categorical moderators Psychopathy 22 45 .15 1.060 .316 1.794 F(1,38) = 3.217 Conduct Disorder 22 45 .43 4.420***
In order to test if there was publication bias, Egger’s test was executed and proved not to be significant (t = -1.250, p = .219), which indicates that there was no funnel plot
asymmetry (Egger et al., 1997). Because of this, a trim-and-fill analysis was not necessary to execute. Rosenthal’s fail safe number was 3281, which indicates that to decrease the overall effect size in this multi-level-meta-analysis from significant to non-significant, more than 3281 effect sizes from zero must be retrieved in other studies. The critical value of this analysis (5 * 40 + 10 = 210) is smaller than the fail-safe number. Therefore, we can conclude that it is unlikely that we have a file drawer bias (Egger et al., 1997; Rosenthal, 1991).
The likelihood-ratio-test on the second level of variance showed a non-significant variance between effect sizes within studies (σ2level 2 = .00, χ2 (1) = .00; p = 1.0). However, the likelihood-ratio-test on the third level of variance showed a significant variance between studies (σ2
level 3 = .147, χ2 (1) = 47.256; p < .0001). About 8% of the total effect-size variance was accounted for by the sampling variance (level-one), 0% by the variance between the effect sizes within studies (level-two) and 91.7% of the total effect-size variance was accounted for by the variance between studies (level-three). We assumed that some heterogeneity between studies might be explained by outcome, study and sample
characteristics. Therefore, we conducted moderator analyses. Nonetheless, as mentioned before, these analyses only showed borderline significant moderators (Table 1).
No study characteristics were found to moderate the relation between impulsive- antisocial personality traits and the amygdala. Publication year (p = .093) and total sample size (p = .073) were nearly significant.
The impact factor of the journal in which the study was published, research design, proportion male, whether conduct disorder or psychopathy was measured through self-report or official records, brain measures (structural or functional), the continent of research and the
use of experimental stimuli did not influence the strength of the association between impulsive-antisocial personality traits and the amygdala.
No sample characteristics moderated the relation between impulsive-antisocial personality traits and the amygdala. Only the mean age of the sample (p = .076) was nearly significant. Age, gender, nature of the disorder, comorbidity, onset of disorder, location of the amygdala (left or right) and the structure or function of the amygdala did not moderate the relation between impulsive-antisocial personality traits and the amygdala. All moderators that were borderline-significant (i.e., trends) were entered in a multivariate analysis, but these trends did not remain borderline significant. Finally, we tested for interaction-effects, but no significant interaction effects were found. To conclude, 91.7% of the between study variance in effect sizes remained unexplained.
Discussion
The aim of this study was to examine the relation between the impaired functional and structural amygdala and the development of impulsive-antisocial personality traits. We found a moderate-to-strong overall effect size. This effect was heterogeneous, with 91.7% of the differences in effect sizes distributed between studies. It can be stated that this variance was hardly explained by the tested moderators. It is remarkable that we were not able to explain the 91.7% variance between studies. If the tested moderators have no significant effect whatsoever, there should be other explanations for this unexplained variance. Notably, the amygdala does not operate by itself (Blair, 2013). There are many other brain structures and neurotransmitters involved in the relation between the amygdala and impulsive-antisocial personality traits. For example, the prefrontal cortex, the striatum and dopamine system in the included studies were also associated with conduct disorder and/or psychopathy (Blair, 2013; Finger et al., 2011). This study only focused on the amygdala, and may therefore be limited in discovering significant moderating effects.
One unexpected trend, which should therefore be interpreted with care, indicated that conduct disorder was more related to the amygdala than psychopathy. A possible explanation is that during puberty and adolescence the brain is reorganizing (Blakemore & Choudhury, 2006). Both the emotional and cognitive systems are being developed. According to
Blakemore and Choudhury (2006), the brain is more sensitive for input during this period of reorganization. Therefore juveniles with conduct disorder are in a sensitive reorganization and therefore may react stronger than mostly adults with psychopathy to the experimental input, such as fearful faces.
There are a few limitations concerning our study. First of all, there was a lack of statistical power. A second limitation is that all studies based their diagnoses on the DSM IV. As result of the transition from DSM IV to DSM 5 there are changes in classification, the diagnosis of conduct disorder was extended with a specifier called ‘limited prosocial
emotions’ (Blair, 2013). It is possible that this change of classification caused differences in diagnoses, which could potentially lead to different results.
For future research we first suggest that multiple brain structures should be included. Currently there is only a small amount of research available about these functional
connections (Gabard-Durnam et al., 2014). Like previously said, the amygdala does not work all by itself. For example, the prefrontal cortex is very important as well for the development of impulsive-antisocial personality traits (Blair, 2013; Glenn, Raine, & Schug, 2009). In the prefrontal cortex interpersonal factors are developed like decision making, reactions to punishment and reward, callous unemotional traits, lying and manipulation (Blair, 2013; Glenn et al., 2009). All these characteristics are important factors in conduct disorder and psychopathy. Next to that, Gabar-Durnam et al. (2014) found evidence for functional connectivity between the amygdala and other (sub)cortical regions and limbic regions, especially the medial prefrontal cortex, insula, posterior regions and the parahippocampal
gyrus. All studies about the amygdala and functional connectivity in the (sub)cortical regions are relevant to this subject. When multiple brain structures, such as the prefrontal cortex are included in future meta-analyses, different outcomes may be found. Secondly, it might be interesting to include samples that are not yet available, and which contain diagnosed conduct disorder or psychopathy according to the DSM 5.
A total of 91.7% of the between studies variance could not be explained by the
potential moderators in this study. More knowledge about the functional connectivity between the amygdala and other (sub)cortical regions might be enlightening for this unexplained variance. At this point conclusions should be interpreted carefully. For now, the results of this multi-level meta-analysis show a medium-to-large overall-effect for the association between the amygdala and impulsive-antisocial personality traits. The magnitude of the effect
highlights the scientific relevance of the study, and so we recommend to further examine impulsive-antisocial personality traits and the amygdala and other brain structures.
Finally, it should be emphasized that the large between-study heterogeneity of the strong association between impulsive-antisocial personality traits and the amygdala sets limits to interpretation of this association, since there is hardly any explanation for the between study differences. Notably, as Miller (2010) correctly remarked, the association between a biological factor and a psychological phenomenon, does not reduce the psychological condition to a biological event. For now, it is safe to conclude that impulsive-antisocial personality traits constitute complex disturbances that depend both on brain functioning and the social environment. However, more research on amygdala functioning is necessary in order to understand how the amygdala plays a role in impulsive-antisocial behavior of humans.
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Table 1
Significant (p = < .05) and borderline significant (p < .10) results of multilevel-meta-analysis on the relation between conduct disorder/ psychopathy and functioning/structure of the amygdala
Note. k = number of studies; #ES = number of effect sizes; t0 = difference in mean r with zero;
t1 = difference in mean r with reference category; mean r = mean effect size (r); F(df1, df2) = n omnibus test. * p <.05, ** p <.01, *** p < .001 k #ES β₀ (mean r) T0 β₁ T1 F(df1, df2) Overall relation between psychopathy/ CD and amygdala 20 40 .34 3.978*** Moderator analyses Continue moderators Publication year 21 40 .33 4.030 -.061 -1.725 F(1,38) = 2.977 Mean age 21 40 .31 3.747 -.016 -1.824 F(1,43) = 3.397 N total 21 40 .47 4.236 -.002 -1.843 F(1,38) = 3.397 Categorical moderators Psychopathy 22 45 .15 1.060 .316 1.794 F(1,38) = 3.217 Conduct Disorder 22 45 .43 4.420***
Table 2
Characteristics of included studies
Study Study characteristics Sample characteristics
Author Year N # r (M) Impact
factor Desig n Diagnos e Continen t Experiment al Nature of disorder Struc/ Func
Gender Age Sample type Boccardi et al. 2011 51 2 (-.36) 2,68 Cross Official Europe No Psych Struc Male > 21 Clinical Carré et al. 2013 199 3 (.21) 2,873 Cross Self-rep America Yes Psych Func Mixed < 21 Commun Decety et al. 2008 16 3 (.90) 3,473 Cross Official America Yes CD Func Mixed < 21 Clinical Ermer et al. 2012 296 4 (.15) 4,974 Cross Official America No Psych Struc Male > 21 Clinical Ermer et al. 2013 191 2 (.09) 6,354 Cross Official America No CD Struc Male < 21 Clinical Fairchild et al. 2013 42 1 (.22) 5,669 Cross Self-rep Europe No CD Struc Female < 21 Clinical Fairchild et al. 2011 90 6 (.40) 10,226 Cross Self-rep Europe No CD Struc Male < 21 Clinical Herpetz et al. 2008 44 1 (-.50) 5,669 Cross Self-rep Europe Yes CD Func Male < 21 Clinical Huebner et al. 2008 46 2 (-.55) 6,354 Cross Self-rep Europe No CD Struc Male < 21 Clinical Hyde et al. 2014 103 2 (.06) 4,974 Cross Self-rep Europe Yes Psych Func Mixed > 21 Commun Jones et al. 2009 30 1 (.48) 13,559 Cross Official America Yes CD Func Male < 21 Commun Larson et al. 2013 49 1 (.32) 3,209 Cross Official Canada Yes Psych Func Male > 21 Clinical Marsh et al. 2011 28 1 (.39) 2,682 Cross Official America Yes CD Func Mixed < 21 Clinical Marsh et al. 2008 36 1 (.53) 13,559 Cross Official America Yes CD Func Mixed < 21 Clinical Marsh et al. 2013 35 2 (.46) 5,669 Cross Official America Yes CD Func Mixed < 21 Clinical Sebastian et al. 2012 47 1 (.48) 13,747 Cross Official America Yes CD Func Male < 21 Commun Sterzer et al. 2005 27 1 (.61) 9,472 Cross Official Europe Yes CD Func Male < 21 Clinical Sterzer et al. 2007 24 1 (.58) 6,132 Cross Official Europe No CD Struc Male < 21 Clinical Viding et al. 2012 46 2 (.41) 13,559 Cross Self-rep America Yes CD Func Male < 21 Commun Yang et al. 2009 59 2 (.40) 13,747 Cross Official America No Psych Struc Mixed > 21 Clinical Yang et al. 2010 53 2 (.26) 4,974 Cross Official America No Psych Struc Mixed > 21 Commun Note. N = number of participants; # r (M) = number of effect sizes (mean); impact factor = impact factor of journal; cross = cross-sectional
design; long = longitudinal design; self-rep = diagnose self reported; official = officially diagnosed; continent = location of study; experimental = use of experimental stimuli during brain scan; psych = psychopathy; CD = conduct disorder; struc = structural measures of amygdala; func = functional measures of amygdala;; < 21 = mean age below 21 years old; > 21 = mean age above 21 years old; commun = community sample; clinical = clinical sample.
Figure 1. Funnelplot Funnelplot Correlation S ta n d a rd E rr o r 0 .2 7 7 0 .2 0 8 0 .1 3 9 0 .0 6 9 0 .0 0 0 -0.50 0.00 0.50 1.00
Appendix A
Flow chart of search results Search results (k = 27,600)
Digital Databases
Google Scholar: 27,572 Screening Review Articles: 28
Excluded on title, abstract and duplicate citations: 27,552
Full studies retrieved for detailed evaluation (k = 48)
Excluded: 25
Literature reviews (not emperical): 8 Inappropriate sample: 17
Selection based on full article tekst (k = 22)
Included in meta-analysis (k = 21 )
Appendix B
References of included studies
1. Boccardi, M., Frisoni, G. B., Hare, R. D., Cavedo, E., Najt, P., Pievani, M., Rasser, P.E. , Laakso, M. P., Aronen, H. J., Repo-Tiihonen, E., Vaurio, O., Thompson, P.M., & Tiihonen, J. (2011). Cortex and amygdala morphology in psychopathy. Psychiatry Research: Neuroimaging, 193(2), 85-92. doi: 10.1016/j.pscychresns.2010.12.013 2. Carré, J. M., Hyde, L. W., Neumann, C. S., Viding, E., & Hariri, A. R. (2013). The neural
signatures of distinct psychopathic traits. Social neuroscience, 8(2), 122-135. doi: 10.1018/17470919.2012.703623
3. Decety, J., Michalska, K. J., Akitsuki, Y., & Lahey, B. B. (2009). Atypical empathic responses in adolescents with aggressive conduct disorder: a functional MRI investigation. Biological psychology, 80(2), 203-211.
doi:10.1016/j.biopsycho.2008.09.004
4. Ermer, E., Cope, L. M., Nyalakanti, P. K., Calhoun, V. D., & Kiehl, K. A. (2012). Aberrant paralimbic gray matter in criminal psychopathy. Journal of abnormal psychology, 121(3), 649-658. doi: 10.1037/a0026371
5. Ermer, E., Cope, L. M., Nyalakanti, P. K., Calhoun, V. D., & Kiehl, K. A. (2013). Aberrant paralimbic gray matter in incarcerated male adolescents with psychopathic traits. Journal of the American Academy of Child & Adolescent Psychiatry, 52(1), 94-103. doi:10.1016/j.jaac.2012.10.013
6. Fairchild, G., Hagan, C. C., Walsh, N. D., Passamonti, L., Calder, A. J., & Goodyer, I. M. (2013). Brain structure abnormalities in adolescent girls with conduct disorder. Journal of Child Psychology and Psychiatry, 54(1), 86-95. doi: 10.1111/j.1469-
7. Fairchild, G., Passamonti, L., Hurford, G., Hagan, C. C., von dem Hagen, E. A., van
Goozen, S. H., Goodyer, I. M., & Calder, A. J. (2011). Brain structure abnormalities in early-onset and adolescent-onset conduct disorder. Brain, 168(6).
doi:10.1176/appi.ajp.2010.10081184
8. Herpertz, S. C., Huebner, T., Marx, I., Vloet, T. D., Fink, G. R., Stoecker, T., Jon Shah, N., Konrad, K. & Herpertz-Dahlmann, B. (2008). Emotional processing in male
adolescents with childhood-onset conduct disorder. Journal of Child Psychology and Psychiatry, 49(7), 781-791. doi: 10.1111/j.1469-7610.2008.01905.x
9. Huebner, T., Vloet, T. D., Marx, I., Konrad, K., Fink, G. R., Herpertz, S. C., & Herpertz-Dahlmann, B. (2008). Morphometric brain abnormalities in boys with conduct
disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 47(5), 540-547. doi: 10.1097/CHI.0b013e3181676545
10. Hyde, L. W., Byrd, A. L., Votruba-Drzal, E., Hariri, A. R., & Manuck, S. B. (2014). Amygdala reactivity and negative emotionality: divergent correlates of antisocial personality and psychopathy traits in a community sample. Journal of Abnormal Psychology, 123 (1), 214 - 224. doi:10.1037/a0035467
11. Jones, A., Laurens, K., Herba, C., Barker, G., & Viding, E. (2009). Amygdala
hypoactivity to fearful faces in boys with conduct problems and callous-unemotional traits. American Journal of Psychiatry, 166(1), 95-102.
doi:10.1176/appi.ajp.2008.07071050
12. Larson, C. L., Baskin-Sommers, A. R., Stout, D. M., Balderston, N. L., Curtin, J. J., Schultz, D. H., Kiehl, K. A., & Newman, J. P. (2013). The interplay of attention and emotion: top-down attention modulates amygdala activation in psychopathy.
Cognitive, Affective, & Behavioral Neuroscience, 13(4), 757-770. doi:10.3578/s13415-013-0172-8
13. Marsh, A. A., Finger, E. C., Fowler, K. A., Adalio, C. J., Jurkowitz, I. T., Schechter, J. C., Pine, D. S., Decety, J., & Blair, R. J. R. (2013). Empathic responsiveness in amygdala and anterior cingulate cortex in youths with psychopathic traits. Journal of Child Psychology and Psychiatry, 54(8), 900-910. doi:10.1111/jcpp.12063
14. Marsh, A. A., Finger, E. C., Fowler, K. A., Jurkowitz, I. T., Schechter, J. C., Yu, H. H., & Blair, R. J. R. (2011). Reduced amygdala–orbitofrontal connectivity during moral judgments in youths with disruptive behavior disorders and psychopathic traits. Psychiatry Research: Neuroimaging, 194(3), 279-286.
doi:10.1016/j.pscychresns.2011.07.008
15. Marsh, A., Finger, E., Mitchell, D., Reid, M., Sims, C., Kosson, D., Towbin, K. E., Leibenluft, E., Pine, D. S. & Blair, R., 2008). Reduced amygdala response to fearful expressions in children and adolescents with callous- unemotional traits and disruptive behavior disorders. American Journal of Psychiatry, 165(6), 712-720.
doi:10.1176/appi.ajp.2007.07071145
16. Sebastian, C. L., McCrory, E. J., Cecil, C. A., Lockwood, P. L., De Brito, S. A., Fontaine, N. M., & Viding, E. (2012). Neural responses to affective and cognitive theory of mind in children with conduct problems and varying levels of callous-unemotional traits. Archives of general psychiatry, 69(8), 814-822.
doi:10.1001/archgenpsychiatry.2011.2070
17. Sterzer, P., Stadler, C., Krebs, A., Kleinschmidt, A., & Poustka, F. (2005). Abnormal neural responses to emotional visual stimuli in adolescents with conduct disorder. Biological psychiatry, 57(1), 7-15. doi:100.1016/j.biopsych.2004.10.008
18. Sterzer, P., Stadler, C., Poustka, F., & Kleinschmidt, A. (2007). A structural neural deficit in adolescents with conduct disorder and its association with lack of empathy.
19. Viding, E., Sebastian, C. L., Dadds, M. R., Lockwood, P. L., Cecil, C. A., De Brito, S. A., & McCrory, E. J. (2012). Amygdala response to preattentive masked fear in children with conduct problems: the role of callous-unemotional traits. American journal of psychiatry, 169(10), 1109-1116. doi:
20. Yang, Y., Raine, A., Narr, K. L., Colletti, P., & Toga, A. W. (2009). Localization of deformations within the amygdala in individuals with psychopathy. Archives of General Psychiatry, 66(9), 986-994. doi: 10.1001/archgenpsychiatry.2009.110
21. Yang, Y., Raine, A., Colletti, P., Toga, A. W., & Narr, K. L. (2010). Morphological alterations in the prefrontal cortex and the amygdala in unsuccessful psychopaths. Journal of abnormal psychology, 119(3), 546. doi: 10.1037/a0019611
