Amygdala Reactivity and Negative Emotionality: Divergent Correlates ofAntisocial Personality and Psychopathy Traits in a Community Sample

Luke W. HydeUniversity of Michigan

Amy L. Byrd and Elizabeth Votruba-DrzalUniversity of Pittsburgh

Ahmad R. HaririDuke University

Stephen B. ManuckUniversity of Pittsburgh

Previous studies have emphasized that antisocial personality disorder (APD) and psychopathy overlap highlybut differ critically in several features, notably negative emotionality (NEM) and possibly amygdala reactivityto social signals of threat and distress. Here we examined whether dimensions of psychopathy and APDcorrelate differentially with NEM and amygdala reactivity to emotional faces. Testing these relationshipsamong healthy individuals, dimensions of psychopathy and APD were generated by the profile matchingtechnique of Lynam and Widiger (2001), using facet scales of the NEO Personality Inventory-Revised, andamygdala reactivity was measured using a well-established emotional faces task, in a community sample of103 men and women. Higher psychopathy scores were associated with lower NEM and lower amygdalareactivity, whereas higher APD scores were related to greater NEM and greater amygdala reactivity, but onlyafter overlapping variance in APD and psychopathy was adjusted for in the statistical model. Amygdalareactivity did not mediate the relationship of APD and psychopathy scores to NEM. Supplemental analysesalso compared other measures of factors within psychopathy in predicting NEM and amygdala reactivity andfound that Factor 2 psychopathy was positively related to NEM and amygdala reactivity across measures ofpsychopathy. The overall findings replicate seminal observations on NEM in psychopathy by Hicks andPatrick (2006) and extend this work to neuroimaging in a normative population. They also suggest that onecritical way in which APD and psychopathy dimensions may differ in their etiology is through their opposinglevels of NEM and amygdala reactivity to threat.

Keywords: neural reactivity, statistical suppression, psychopathic personality inventory, fearlessness,crime

Supplemental materials: http://dx.doi.org/10.1037/a0035467.supp

Aggression and antisocial conduct comprise attributes of two re-lated psychopathologies, antisocial personality disorder (APD) andpsychopathy. APD is recognized by early involvement in antisocialacts, reckless disregard for the rights of others, and a persistent patternof impulsive and irresponsible behavior. Psychopathy subsumes manyof the same traits as APD, but in addition, includes characteristicinterpersonal and affective features, such as superficial charm, deceit-ful and manipulative behavior, callousness, and lack of empathy orremorse. Factor analytic reduction of one prominent psychopathyindex, the Psychopathy Checklist-Revised (PCL-R; Hare, 1991),

commonly yields two factors, termed Factor 1 (F1) and Factor 2 (F2;although see Cooke & Michie, 2001). F1 reflects psychopathy’sdistinctive interpersonal and unemotional qualities, whereas F2 tapsthe expressions of antisocial disposition and impulsivity common toboth psychopathy and APD (although note that the APD diagnosisdoes include some F1 symptoms including deceitfulness and lack ofremorse). Hence, most psychopaths meet criteria for APD (at least inprison settings, see Babiak, Neumann, & Hare, 2010), but mostpeople with APD are not judged psychopathic (Patrick, 2007). Al-though these factors (i.e., F1, F2) and constructs (i.e., APD, psychop-athy) are highly correlated, they often show differential associationswith outcome variables (Benning, Patrick, Hicks, Blonigen, &Krueger, 2003; Hicks, Markon, Patrick, Krueger, & Newman, 2004)and even predict outcomes such as suicide in opposite directions(Hicks & Patrick, 2006; Verona, Hicks, & Patrick, 2005).

The asymmetric relationship of psychopathy and APD hasprompted much speculation regarding etiologic factors that mightdifferentiate the two disorders (although the differences betweenAPD and psychopathy are quite understudied in comparison to thebulk of work comparing psychopathy F1 and F2). Differences inNEM are often cited as one distinguishing aspect, and it is well-established that psychopathic individuals respond minimally to

Luke W. Hyde, Department of Psychology, Center for Human Growthand Development, Survey Research Center at the Institute for SocialResearch, University of Michigan; Amy L. Byrd and Elizabeth Votruba-Drzal, Department of Psychology, University of Pittsburgh; Ahmad R.Hariri, Department of Psychology and Neuroscience, Institute for GenomeSciences and Policy, Duke University; Stephen B. Manuck, Departments ofPsychology and Psychiatry, University of Pittsburgh.

Correspondence concerning this article should be addressed to Luke W.Hyde, Department of Psychology, University of Michigan, 2251 East Hall,530 Church Street, Ann Arbor, MI 48109. E-mail: LukeHyde@umich.edu

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Journal of Abnormal Psychology © 2014 American Psychological Association2014, Vol. 123, No. 1, 214–224 0021-843X/14/$12.00 DOI: 10.1037/a0035467

214

situations thought to induce negative emotions such as experimen-tal exposure to threat and stressors (Arnett, 1997; Lorber, 2004;Patrick, Bradley, & Lang, 1993). These findings have often beeninterpreted as reflecting low levels of anxiety or fear (Fowles,1980; Lykken, 1957) specific to psychopathy (especially F1),whereas those with APD often show greater anxiety and fear(Lorber, 2004; Patrick et al., 1993).

Suppressor Effects

Although low anxiety is described as a core component ofpsychopathy (Cleckley, 1976), studies linking NEM to globallydefined psychopathy yield mixed findings (Hare, 1991; Harpur,Hare, & Hakstian, 1989; Schmitt & Newman, 1999). As Hicks andPatrick (2006) note, the psychometric characteristics of the PCL-Rmay obscure the role of anxiety, which is a core component ofNEM, in psychopathy. In particular, it has been argued that NEMmay covary negatively with the callous detachment described bythe PCL-R’s first factor, but positively with the impulsive andantisocial traits of the second factor, thereby tending to suppress astatistical association of NEM with globally defined psychopathy(Patrick et al., 1993). Providing support for this claim, Patrick(1994) found trait negative affect to covary negatively with F1 andpositively with F2 when adjusting by partial correlation for theoverlap of F1 and F2.

More recently, Hicks and Patrick (2006) described this relation-ship between PCL-R factors and NEM as an instance of “cooper-ative suppression,” which occurs when entering two correlatedpredictor variables in a regression model increases the beta-coefficient of one or both predictors above their bivariate associ-ations with the predicted variable (Paulhus, Robins, Trzesniewski,& Tracy, 2004). The two predictors may be highly correlated andthe inclusion of both variables (and thus partitioning of sharedvariance) in the same model may uncover opposing relations withthe dependent measure (Mackinnon, Krull, & Lockwood, 2000). Ina study assessing multiple facets of negative affect among incar-cerated adult males, Hicks and Patrick (2006) confirmed oppositerelations of NEM with PCL-R F1 and F2, and these divergentassociations strengthened appreciably when F1 and F2 were en-tered simultaneously as predictors. These findings, along withsupport from a similar study in children (Frick, Lilienfeld, Ellis,Loney, & Silverthorn, 1999), suggest that global measures ofpsychopathy, such as the PCL-R, may obscure an underlyingheterogeneity of antisocial pathology that encompasses both thecallous, unemotional characteristics (i.e., low NEM) of the iconicpsychopath as well as the affective lability (i.e., high NEM) andimpaired impulse control pathognomonic of APD.

Personality Dimensions

Much of the work on NEM and antisocial behavior has beendone primarily in psychopathy, focusing on the PCL-R, eventhough APD is far more common as a disorder (Patrick, 2007).Moreover, much of this research focuses only on the extreme ofthe distribution represented by criminal psychopathy ignoring thedimensionality of psychopathy and APD-related traits (e.g., Edens,Marcus, Lilienfeld, & Poythress, 2006; Widiger, 1993). Consistentwith a recent emphasis on dimensional representations of psychop-athy and personality disorders generally (e.g., Benning, Patrick,

Blonigen, Hicks, & Iacono, 2005; Trull & Durrett, 2005), it mayalso be asked whether analogous associations extend across thenormative range of personality differences. In this regard, the firstaim of this study was to determine if the findings of Hicks andPatrick (2006) extend to analogous dimensional measures of APDversus psychopathy-related traits in a nonpatient community sam-ple.

One method to address the dimensional nature of personalityfrom normal to abnormal is to describe personality disorder traitsas constellations of basic dimensions of personality, particularlyusing the Five Factor Model (FFM) of personality (Widiger &Costa, 1994), which can be measured by personality assessmentinstruments such as the NEO Personality Inventory Revised(NEO-PI-R; Costa & McCrae, 1995). To measure dimensions ofpersonality disorders using the NEO-PI-R, researchers have usedan expert consensus approach in which experts rated facets of theFFM to create prototypes of personality disorders (Lynam &Widiger, 2001; Miller, Lynam, Widiger, & Leukefeld, 2001). Thisprototype matching system effectively creates dimensional mea-sures of personality disorders ascertained through a standard mea-sure of personality that fit with FFM conceptions of each disorder,as well as assesses these traits from the normal to abnormal range.In line with this method, we used FFM derived scores from theNEO-PI-R within a community sample to test associations be-tween NEM and personality dimensions of APD and psychopathy.

Applicability to Neural Models of Psychopathyand APD

Given the well-established link between various aspects ofNEM and amygdala reactivity to social threat and distress (e.g.,Carré, Fisher, Manuck, & Hariri, 2012; Etkin et al., 2004; Fakra etal., 2009), it is possible that the divergent relationships betweenpsychopathy, APD, and NEM also exist at the neural level, par-ticularly as evidenced by amygdala reactivity to social signals ofthreat, such as angry facial expressions, and social signals ofdistress, such as fearful facial expressions. In fact, among psycho-paths, response deficiencies in experimental paradigms tappingaspects of NEM such as fear and emotional learning (especiallydeficits in fear potentiated startle), are hypothesized to be theproduct of reduced reactivity of subcortical threat systems, espe-cially the amygdala (Blair, 2006). Moreover, empirical studiesshow that psychopathy is related to reduced amygdala reactivityduring paradigms tapping threat and affective processing (for areview, see Hyde, Shaw, & Hariri, 2013). Less work has examinedamygdala reactivity in individuals with APD, but there is evidencefor greater amygdala reactivity under similar stimulus conditionswhen comparing nonpsychopathic antisocial samples with controlssuch as adults with intermittent explosive disorder (Coccaro, Mc-Closkey, Fitzgerald, & Phan, 2007), youth with conduct problemsbut not callous traits (Herpertz et al., 2008; Viding, Sebastian, etal., 2012), male community volunteers high on trait aggression andhigh on trait anxiety (Carré et al., 2012), and college students highon social deviance dimensions of the Psychopathic PersonalityInventory (PPI; Gordon, Baird, & End, 2004).

Furthermore, recent studies that examined antisocial versus psy-chopathy traits demonstrated divergent correlations between anti-social and psychopathy traits with amygdala reactivity to maskedfear faces in youth (e.g., Viding, Sebastian, et al., 2012) and in a

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215AMYGDALA REACTIVITY

college sample (Gordon et al., 2004). In this second study, Gordon,Baird, and End (2004) found that those scoring high on F1 of thePPI demonstrated attenuated amygdala reactivity to a range ofemotional faces, whereas those scoring high on F2 displayedincreased amygdala reactivity. Moreover, a recent study of ado-lescents used a theory of mind task to demonstrate divergentrelationships with amygdala reactivity within a suppression frame-work between callous-unemotional traits (i.e., psychopathy) andconduct problems (i.e., antisocial behavior; Sebastian et al., 2012).These studies suggest that, like NEM, amygdala reactivity toemotional faces, may be related in opposite directions: negativelyto the callous detachment characteristic of psychopathy and posi-tively to the antisocial and impulsive behavior of APD (for evi-dence that this association may be specific to threat and distressi.e., fear and anger faces, see: Carré et al., 2012; Coccaro et al.,2007; Marsh & Blair, 2008; Viding, Sebastian, et al., 2012).Therefore, the second major aim of this study was to extendsuppression work on NEM to neural function and test the hypoth-esis that amygdala reactivity to threat and distress (i.e., anger andfear faces) is related in divergent directions to psychopathy andAPD traits, and that this relationship with amygdala reactivityexplains (i.e., mediates) the divergent relationship between NEMand psychopathy and APD traits. That is, psychopathy is hypoth-esized to be related to lower NEM through relatively lesseramygdala reactivity, and APD is hypothesized to be related tohigher NEM through relatively greater amygdala reactivity. Addi-tionally, as previous studies have emphasized either fear or angerfaces as stimuli, we tested whether these divergent relationshipswere specific to amygdala reactivity to anger versus fear faces.

Finally, although the primary goal of this study was to extendsuppression findings to FFM conceptualizations of APD and psy-chopathy, previous work in this area (e.g., Hicks & Patrick, 2006)has examined factors within psychopathy (i.e., F1, F2). Thus, afinal aim of the study was to examine the extent to which findingsusing FFM generated measures of APD and psychopathy would beparalleled by FFM generated measures of F1 and F2 psychopathy.However, as conceptualizations of these factors vary across instru-ment and measurement (i.e., the PCL-R conceptualization of F1 isquite different then the PPI conceptualization of F1: Hare &Neumann, 2008), we included two different measures of F1 andF2—one based on the structure of the PCL-R and one based on thestructure of the PPI. As PCL-R F1 and F2 have substantial overlapwith the unique aspects to psychopathy and APD, respectively, weexpected results using PCL-R guided measures to be similar tothose found with APD and psychopathy measures, particularlywhen overlap between F1 and F2 is partialed. However, as PPI F1and F2 are generally found to be uncorrelated with each other(Marcus, Fulton, & Edens, 2013), we did not expect suppressioneffects with PPI F1 and F2. Moreover, as PPI F1 (fearless domi-nance) is thought to tap fear deficits more directly (Lilienfeld et al.,2012), we expected PPI F1 to be the more highly related to lowNEM and low amygdala reactivity to threat and distress thanPCL-R F1.

The Current Study

A central goal of the current study was to examine the differ-ential association of APD and psychopathy traits with the out-comes of threat- and distress-related amygdala reactivity and

NEM, with a secondary goal to examine how these findings mightvary by different personality based measures of factors withinpsychopathy. To attain continuous measures of personality disor-der traits, a previously validated profile matching count techniquewas used to create highly overlapping but distinct measures ofpsychopathy and APD from NEO-PI-R profiles (Lynam & Widi-ger, 2001; Miller, Bagby, Pilkonis, Reynolds, & Lynam, 2005;Miller et al., 2001), as well as FFM generated measures of F1 andF2 based on the PCL-R using the NEO-PI-R (Derefinko & Lynam,2006; Widiger & Lynam, 1998) and the PPI using the Multidi-mensional Personality Questionnaire (Benning et al., 2005).Amygdala reactivity was measured using an fMRI task designed torobustly engage the amygdala through the presentation of sociallysalient signals of threat and distress (Fakra et al., 2009; Manuck,Brown, Forbes, & Hariri, 2007). Psychopathy (and F1) was hy-pothesized to be negatively related to amygdala reactivity andNEM, whereas APD (and F2) was expected to be positively relatedto both constructs. Moreover, we expected results to be strongerwhen controlling for correlated variance in APD and psychopathy.Furthermore, we hypothesized that differences in NEM betweenAPD and psychopathy would be accounted for by differences inamygdala reactivity. Finally, we expected results to be similarwhen using F1 and F2 based on the PCL-R structure, and in asimilar direction, but without suppression, using the uncorrelatedF1 and F2 based on the PPI. The present study was conductedusing data from a study of men and women in the communitywhere a greater range of personality was possible and in whichrelationships between these traits and neural reactivity could beexamined dimensionally and in a sample much larger than relatedneuroimaging studies (e.g., Marsh et al., 2008; Veit et al., 2002).

Method

Participants

A total of 103 participants were recruited from the University ofPittsburgh Adult Health and Behavior (AHAB) Project, an archivaldatabase encompassing detailed measures of behavioral and bio-logical traits among a community sample of 1,379 nonpatient,healthy adult volunteers (Fakra et al., 2009; Manuck et al., 2007).Participants were middle-aged adults (mean age � 44.5 years;SD � 6.8; range: 31–54 years) and 45% were male (for moredetails see Supplemental Materials and Fakra et al., 2009; Hyde,Manuck, & Hariri, 2011; Manuck et al., 2007). Participants re-ported their race as follows: 88% European American, 7% AfricanAmerican, and 4% other races (e.g., Asian American, multiracial).

Procedures

Amygdala reactivity paradigm. The experimental fMRI par-adigm consisted of four blocks of a face-processing task inter-leaved with five blocks of a sensorimotor control task (Carré et al.,2012; Fakra et al., 2009; Manuck et al., 2007). During the face-processing task, subjects viewed a trio of faces (expressing eitheranger or fear) and selected one of two faces (bottom) identical toa target face (top). Each face processing block consisted of siximages, balanced for gender and target affect (angry or fearful), allderived from a standard set of pictures of facial affect (Ekman &Friesen, 1976). During the sensorimotor control blocks, subjects

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216 HYDE, BYRD, VOTRUBA-DRZAL, HARIRI, AND MANUCK

viewed a trio of simple geometric shapes (circles, vertical andhorizontal ellipses) and selected one of two shapes (bottom) iden-tical to a target shape (top). Each sensorimotor control blockconsisted of six different shape trios. A variable interstimulusinterval during face processing was used to allow for estimation ofexpression-specific neural activation.

Bold fMRI acquisition parameters. Each participant under-went scanning with a Siemens 3-T MAGNETOM Allegra (Sie-mens AG, Erlangen, Germany), which is characterized by in-creased T2� sensitivity and fast gradients (slew rate, 400 T/m/s),which minimize echospacing, thereby reducing echoplanar imag-ing geometric distortions and improving image quality. Bloodoxygen level dependent (BOLD) functional images were acquiredwith a gradient-echo echoplanar imaging sequence (TR/echotime � 2,000/25 milliseconds, FOV � 20 cm, matrix � 64_64),which covered 34 interleaved axial slices (3-mm slice thickness)aligned with the AC-PC plane and encompassing the entire cere-brum and most of the cerebellum.

Image processing and analysis. Whole-brain image analysiswas completed using the general linear model of SPM2 (WellcomeDepartment of Imaging Neuroscience, London, United Kingdom).Images for each participant were realigned to the first volume inthe time series, spatially normalized into a standard stereotacticspace (Montreal Neurological Institute template) using a 12-parameter affine model, and smoothed to minimize noise andresidual difference in gyral anatomy with a Gaussian filter set at 6mm FWHM. Voxelwise signal intensities were ratio-normalized tothe whole-brain global mean. These preprocessed data sets wereanalyzed using second level random-effects models that accountedfor both scan-to-scan and participant-to-participant variability todetermine task specific regional responses.

Following preprocessing, linear contrasts employing canonicalhemodynamic response functions were used to generate BOLDcontrast estimates for general reactivity to facial expressions (i.e.,all faces � shapes, angry face � shapes, fearful faces � shapes)for each individual. Individual contrast images (i.e., weighted sumof the beta images) from these three contrasts were then used insecond-level random effects models that account for both scan-to-scan and participant-to-participant variability to determine meancondition-specific regional responses using one-sample t tests. Allanalyses were thresholded at a voxel level of p � .05, FDRcorrected for multiple comparisons across the entire brain volume.

Regions of interest. BOLD contrast estimates (i.e., mean sig-nal) were extracted from clusters exhibiting a main effect of task

using the signal above threshold within anatomically defined re-gions of interest (ROIs). Because of the structural and functionalheterogeneity of the amygdala (Davis & Whalen, 2001; Whalen etal., 2001), we examined the ventral and dorsal amygdala indepen-dently to determine whether individual differences in personalitymap on to the amygdala’s principal input and output regions,respectively, using previously used ROI masks for the ventral,dorsal, and whole amygdala (see Supplemental Materials andHyde, Manuck, & Hariri, 2011). This approach was motivated byprevious imaging research demonstrating that individual differ-ence factors map on to specific subregions of the amygdala (Etkinet al., 2004; Manuck et al., 2010).

Measures

NEO-PI-R. The NEO-PI-R (Costa & McCrae, 1992) is aself-report questionnaire developed to assess normal personalitydimensions based on the FFM. It consists of 240 items, which arerated on a 5-point scale ranging from 0 (strongly disagree) to 4(strongly agree) and provides a score for the five domains of adultpersonality and six “facet” scales that tap associated features orattributes of the corresponding dimension. Many studies using theNEO-PI-R have consistently shown good validity, reliability andpsychometric properties (e.g., high internal consistency and long-term stability over 3 to 6 years across the five domains; Costa &McCrae, 1992), including the present study (for the five broaderdomains � � .73–.87).

APD and psychopathy traits. FFM continuous APD andpsychopathy scores were calculated using the expert consensusprototype matching approach of Lynam and Widiger (2001). Ex-perts rated prototype scores of all 10 DSM–IV personality disor-ders (and psychopathy: Miller et al., 2001) across the 30 facets ofthe FFM on the NEO-PI-R. Thus for APD and psychopathy,experts generated a profile of facet-level scores for a prototypicindividual with APD or psychopathy. These profiles can be thenused to generate “scores” for relative APD and psychopathy traitsin individuals by using a sum of scores on facets maximallydescriptive of the disorder from the prototype profiles (Decuyper,De Clercq, De Bolle, & De Fruyt, 2009; Miller et al., 2005). Thesemethods have been shown in multiple samples as valid continuousmeasures of personality disorder traits (Lynam & Widiger, 2001;Miller, 2012; Miller et al., 2005). See Table 1 for means andstandard deviations of study measures and Supplemental Table 1for a description of how these dimensions were formed.

Table 1Bivariate Correlations

Mean (SD) 1 2 3 4 5 6

1. Gender .562. Age 44.6 (6) �.093. APD 225 (28) .03 �.154. Psychopathy 285 (26) �.14 �.05 .86���

5. Right amygdala reactivity .88 (.6) �.20� �.12 .12 .076. Left amygdala reactivity .88 (.7) �.21� �.13 .12 .04 .76���

7. Negative Emotionality 24.6 (12.5) .11 �.25� .28�� �.03 .07 .17

Note. SD � standard deviation. Gender 0 � male, 1 � female. APD � antisocial personality disorder traits. Right and Left amygdala reactivity refer toextracted values based on the main effects of the All Faces � Shapes contrast.� p � .05. �� p � .01. ��� p � .001.

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217AMYGDALA REACTIVITY

Negative emotionality. NEM scores were generated using theNEM scale from the abbreviated version of the MultidimensionalPersonality Questionnaire–Brief Form (MPQ-BF; Manuck, Craig,Flory, Halder, & Ferrell, 2011; Patrick, Curtin, & Tellegen, 2002).

Measures of psychopathy factors. As noted above, we alsotested alternate ways of assessing our dependent variables bycreating F1 and F2 psychopathy scores. The first way was to createF1 and F2 scores based on the structure of the PCL-R usingWidiger and Lynam’s (1998) rational assignment of NEO-PI-Rdomains to create PCL-R guided F1 and F2 scores using Derefinkoand Lynam’s (2006) operationalization of this assignment at thefacet level. Thus, NEO-PI-R facet scores were weighted andsummed as described previously (Derefinko & Lynam, 2006, p.265) to create F1 and F2 scores. The second approach we used wasto create F1 and F2 scores based on a different conceptualizationof psychopathy (i.e., the structure derived from the PPI) andmeasured via items from a different personality questionnaire (i.e.,the MPQ-BF). Thus, we created scores of PPI F1 (fearless domi-nance) and PPI F2 (impulsive antisociality) by multiplying regres-sion weights described by Benning, Patrick, Blonigen, Hicks, andIacono (2005) with z-scores on the appropriate MPQ scales (asmeasured by the MPQ-BF, see above) to create a measure offearless dominance and a measure of impulsive antisociality fromMPQ scale scores.

Statistical Analysis

Primary dependent variables were the BOLD contrast estimatesextracted bilaterally from the mean signal in clusters of activationin the whole, ventral, and dorsal amygdala ROIs. Associations ofFFM-Psychopathy and FFM-APD scores with amygdala reactivitywere examined in regressions using IBM SPSS statistics v.20.Consistent with past studies (e.g., Hyde et al., 2011) gender wascontrolled for in all regressions given its main effect on amygdalareactivity in this sample (see Table 1).1 In all regression analyses,extracted amygdala reactivity values were regressed first on APDor psychopathy scores separately, and then onto APD and psy-chopathy scores simultaneously to assess for overlapping versusunique relationships between psychopathy and APD dimensionsand amygdala reactivity. As APD and psychopathy trait scoresdemonstrated a high correlation (see Table 1), collinearity was aconcern and thus tolerance was monitored with scores below 0.10considered problematic (Cohen, Cohen, West, & Aiken, 2003). Weused bootstrapped corrected confidence intervals to test for statis-tically significant mutual suppression where applicable using the“indirect” macro for SPSS (Preacher & Hayes, 2008). We alsoprovide “Sobel” tests to provide a measure of effect size ofsuppression effect and to be consistent with past studies in this area(Hicks & Patrick, 2006). Similar to mediation in which boot-strapped confidence intervals can be used to test the significance ofchange in a coefficient from IV to DV after the addition of a thirdvariable, these same tests can be used to determine the statisticalsignificance of the change in the coefficient due to suppressionwhen a third suppression variable is added (MacKinnon, Krull, &Lockwood, 2000). Thus, in these analyses, a confidence intervalnot containing zero was indicative of statistically significant sup-pression through a significant change in the regression coefficientwhen adding a third variable. In the results below, p values arederived from bootstrapped bias corrected confidence intervals and

z values are provided as effects sizes derived from Sobel tests(although note that Sobel tests are less powerful and only providedfor a gross effect size measure).

Results

Descriptive Statistics and Correlations

Table 1 presents descriptive statistics and correlations amongstudy variables. APD scores were positively related to NEM butpsychopathy scores were not significantly related to NEM sug-gesting that, when taken alone, only APD is related in the hypoth-esized positive direction with NEM. Psychopathy and APD scoresdemonstrated small, nonsignificant positive correlations withamygdala reactivity across all contrasts, suggesting that, whentaken alone, neither construct predicted amygdala reactivity.

Relationship With Negative Emotionality

To investigate the hypothesis that a major difference betweenAPD and psychopathy is level of negative emotionality, two hier-archical regressions predicting NEM were conducted (all regres-sions controlled for gender): In the first regression, psychopathyscores were entered first, followed by APD scores; in the secondregression, APD scores were entered first followed by psychopa-thy scores. In independent regressions, psychopathy traits were notsignificantly related to NEM (B � �.008 SE � .048, ns), whereasAPD traits were positively associated with NEM (B � .124, SE �.042, p � .01). However, when both constructs were entered in thesame regression, they each demonstrated significant relationshipswith NEM and in opposite directions, indicative of mutual sup-pression (psychopathy: B � �.524, SE � .078, p � .001; Sobelz � 5.4, 95% CI does not contain 0, and APD: B � .542, SE �.072, p � .001, Sobel z � �5.7, 95% CI does not contain 0). Thus,in extending past findings to APD and psychopathy measures(Hicks & Patrick, 2006), high APD traits were related to greaterNEM, whereas high psychopathy traits were related to lesser

1 Note that we controlled for gender in this study because there are maineffects of gender on amygdala reactivity in many past studies using thissample (e.g., Hyde et al., 2011), including the current study (see Table 1).We also reran all analyses without controlling for gender. The pattern offindings is the same throughout all of the regressions when controlling ornot controlling for gender. However, several statistically significant effectsbecame less significant in some regressions (i.e., p � .05), specificallythose not controlling for gender and predicting reactivity to Faces �Shapes in the left amygdala (psychopathy B � �.006, SE � .005,� � �.24, p � .21; APD B � .008, SE � .005, � � .33, p � .09) and leftdorsal amygdala (psychopathy B � �.009, SE � .006, � � �.28, p � .14;APD B � .011, SE � .006, � � .37, p � .06), as well as those predictingAnger � Shapes in the right amygdala (psychopathy B � �.002, SE �.001, � � �.23, p � .24; APD B � .002, SE � .001, � � .31, p � .11).In each of these cases the effect is still in the same direction and of similarmagnitude (especially when considering the size of the �) but p valueschanged when not controlling for gender. Additionally, we have alsoconducted moderated multiple regression analyses with gender as a mod-erator of all effects. When examining if any possible gender differences arestatistically significant, via moderated multiple regression, none of theinteraction terms were statistically significant (i.e., all interaction termps � .10, most interaction term ps � .30). Additionally, as interactionterms can add to collinearity concerns, we monitored measures of col-linearity and found that the addition of these interaction terms causedunacceptable levels of collinearity (e.g., tolerance � .10).

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218 HYDE, BYRD, VOTRUBA-DRZAL, HARIRI, AND MANUCK

NEM, but only when the overlap of these two constructs waspartialed out.

Mutual Suppression of Amygdala Reactivity

Table 2 presents the results of hierarchical regressions predict-ing amygdala reactivity while controlling for gender. Regressionswere run in the same manner as above, with amygdala reactivity asthe outcome instead of NEM. Across analyses, a similar trendemerged: APD traits alone were positively, although nonsignifi-cantly, related to amygdala reactivity. When accounting for psy-chopathy traits, however, this relationship increased and becamesignificant in several ROIs, suggesting that partialing out overlapwith psychopathy strengthened the positive association withamygdala reactivity. Psychopathy traits demonstrated a similareffect: Generally, psychopathy traits showed nonsignificant posi-tive associations with amygdala reactivity. However, when APDscores were accounted for, the association between psychopathytraits and amygdala reactivity was negative and, in many ROIs,significant. Moreover, when examining the significance of thesuppression effect, in almost all models in which psychopathy orAPD became significant predictors of amygdala reactivity, thesuppression effect was statistically significant (see Table 2).

Although this trend was relatively consistent across ROIs andcontrasts, psychopathy and APD traits demonstrated statisticallysignificant associations in a suppression framework within thefollowing specific amygdala regions of interest and contrasts:left amygdala (all faces), left dorsal amygdala (all faces), rightamygdala (anger faces), left amygdala (anger faces), left dorsalamygdala (anger faces), and right ventral amygdala (anger faces).Results were strongest in the left amygdala, in dorsal regions, andto the Anger � Shapes contrast. None of the amygdala ROIs forthe Fear � Shapes contrast were significantly predicted by APDand psychopathy traits (see Supplemental Table 2). Thus, thesuppression results appeared to be primarily driven by reactivity toanger and to be particularly strong in the dorsal amygdala.2

Amygdala Reactivity as Explanation for NEMSuppression Results

We examined whether suppression effects on NEM might beaccounted for by parallel effects on amygdala reactivity (i.e., todetermine whether divergent relationships with amygdala reactiv-ity account for the divergent relationships between NEM, psychop-athy, and APD). To test this question, we explored two mediationmodels in which APD and psychopathy traits predicted NEM andexamined whether this path was mediated by amygdala reactivity.To test this mediating relationship we selected the two ROIs (leftamygdala and left dorsal amygdala reactivity to All Faces �Shapes) that showed significant suppression relationships withAPD and psychopathy traits and were related to NEM (� � .20,p � .05 and � � .22, p � .02, respectively). In both models, theaddition of amygdala reactivity (left whole and left dorsalamygdala reactivity) to the regression, did not affect the signifi-cance of the relationship of psychopathy with NEM, nor therelationship of APD with NEM, nor was there any statisticalevidence of mediation effects (all z statistics � .65, all boot-strapped 95% confidence intervals contained 0). Moreover, resultswere similarly nonsignificant if NEM and amygdala reactivity

were conceptually reversed in the model (e.g., NEM as mediatingthe relationship between APD and psychopathy and amygdalareactivity). Thus, the extent to which NEM and amygdala reactiv-ity have similarly divergent relationships with psychopathy andAPD traits does not appear to be due to overlapping variance thatthe two constructs share (see Venables, Hall, & Patrick, 2013 forevidence that boldness may be a better construct for separatingAPD and psychopathy).

Exploratory Analyses With AdditionalConceptualizations of Antisocial Constructs

NEO-derived PCL-R factors. Although our primary focuswas on extending mutual suppression work to NEO-based mea-sures of APD and psychopathy, there are other compelling ways toderive similar constructs that could help clarify the extent to whichour findings are generalizable to measures of factors within psy-chopathy that are less highly correlated. The most similar approachis to use Derefinko and Lynam’s (2006) approach to use NEO-PI-R facets to create PCL-R guided F1 and F2 scores. Within thissample, these F1 and F2 dimensions were correlated at lowerlevels (r � .42, p � .001; Supplemental Table 3). Using the sameapproach as above to test for suppression relationships with NEM,F1 did not predict NEM either alone or in a suppression regression(ps � .23), whereas F2 positively predicted NEM in a regressionalone (B � .22, SE � .05, p � .001) and when controlling for F1(B � .23, SE � .07, p � .001), with no suppression effects.

When examining relationships with amygdala reactivity usingthese F1 and F2 scores, we found few instances of significantsuppression (see Supplemental Table 4; only two marginally sig-nificant suppression relationships with F2 scores predicting rightand left dorsal amygdala reactivity to anger faces). Generally F1and F2 were unrelated to amygdala reactivity alone or whencontrolling for each other. Unexpectedly, right dorsal amygdalareactivity to fear was positively and significantly related to F1. Insum, F2 predicted NEM without suppression and, in contrast toresults with APD and psychopathy dimensions, neither PCL-Rbased factor predicted amygdala reactivity, even when partialingtheir overlap.

MPQ derived PPI factors. We also used a second and moredivergent approach to examine F1 and F2 scores by using dimen-sions derived from another instrument and another conceptualiza-tion of psychopathy to determine the extent to which our findingsvary by instrument and conceptualization of psychopathy factors.In this case, we used MPQ-derived factors based on the structureof the PPI (Benning et al., 2005). As the PPI contains factors thatare generally orthogonal (Marcus et al., 2013) and in this samplethe factors were correlated only very modestly (r � .17, p � .10),we did not expect mutual suppression. However, as F1 (fearlessdominance) is thought to assess fear deficits more directly (seeLilienfeld et al., 2012) and overlaps less with PCL F1 scores, wetested these factors to determine if PPI F1 and F2 would yield a

2 Given the high correlation between APD and psychopathy scores,collinearity was monitored through tolerance values in each regression andthe lowest value of tolerance was still above “problematic” levels of 0.10(tolerance within all regressions in this study � 0.24). Moreover, in allregressions, the standard errors of the predictor variables did not changedramatically as would be expected in the case of problematic collinearity.

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219AMYGDALA REACTIVITY

similar or different pattern of results in predicting NEM andamygdala reactivity (Marcus et al., 2013; Patrick, 2007).

In relationship to NEM, we found that PPI F1 (marginally)negatively predicted NEM alone (B � �3.14, SE � 1.8, p � .10)and significantly when controlling for F2 (B � �5.3, SE � 1.3,p � .001), and surprisingly (because these two factors are nothighly correlated), demonstrated a significant suppression effect(z � 1.78, p � .05). PPI F2 did positively predict NEM alone (B �11.9, SE � 1.5, p � .001) and when controlling for F1 (B � 12.8,SE � 1.4, p � .001) demonstrating weak suppression effects (z �1.59, p � .05). When examining amygdala reactivity as the out-come, we found that PPI F2 was robustly and positively correlatedwith amygdala reactivity to most of the contrasts and across mostof the amygdala subregions, with no evidence of mutual suppres-sion (see Supplemental Table 5). Interestingly, F1 was not corre-lated with amygdala reactivity alone or when overlapping variancewas partialed out. Overall, PPI factors replicated suppression ef-fects found in regards to NEM and showed a robust positiverelationship between F2 and amygdala reactivity to both angry andfearful faces, but no evidence of F1 and amygdala associations orsuppression effects.

Discussion

In summary, we replicated and extended the findings of Hicksand Patrick (2006) by showing that dimensional variability in trait

measures of APD and psychopathy in a community sample dem-onstrated suppression effects in their relationship with NEM: APDwas positively and psychopathy was negatively correlated withNEM, but only when the shared variance of the two constructs waspartialed (which was similarly replicated using PPI psychopathyfactors). Moreover, consistent with a study in youth using a dif-ferent neuroimaging task (Sebastian et al., 2012), we found thatthis same relationship also existed with amygdala reactivity: APDdimensions were positively and psychopathy dimensions werenegatively correlated with threat-related amygdala reactivity, par-ticularly left dorsal amygdala reactivity to anger, when controllingfor the overlap of APD and psychopathy. Although NEM andamygdala reactivity had similar relationships with psychopathyand APD traits, and have been correlated in many studies includingour current work, amygdala reactivity did not mediate the rela-tionship between NEM and APD or psychopathy. Finally, inexploring different measurements of similar constructs, we foundthat NEO-derived PCL-R F2 and MPQ derived PPI F2 bothpositively predicted NEM and PPI F2 positively predictedamygdala reactivity. However, results across PCL-R F1 and F2, aswell as PPI F1, and NEO-based psychopathy scores were moreinconsistent. PPI measures of F1 and F2 did replicate divergentrelationships with NEM.

Overall, these findings support the notion that, even to the extentthat APD and psychopathy may be highly overlapping constructs,

Table 2Hierarchical Regressions of APD and Psychopathy Dimensions Predicting Amygdala Reactivity

All faces � Shapes contrast

Entire amygdala Dorsal Ventral

Right Left Right Left Right Left

PsychopathyB alone (SE) .001 (.002) .000 (.003) .003 (.003) .000 (.003) �.001 (.002) .001 (.002)Standardized � .05 .01 .09 .007 �.03 .04B with APD (SE) �.006 (.005) �.011 (005) �.004 (.006) �.014 (.006) �.006 (.005) �.001 (.004)Standardized � �.26 �.41� �.12 �.44� �.27 �.03Suppression effect (z) 1.97 2.35� 1.34 2.46� 1.41 .53

APDB alone (SE) .003 (.002) .003 (.002) .004 (.003) .004 (.003) .001 (.002) .001 (.002)Standardized � .12 .13 .14 .13 .04 .06B with psychopathy (SE) .007 (.004) .011 (.005) .007 (.006) .015 (.006) .006 (.004) .002 (.004)Standardized � .35� .48� .24 .51� .28 .09Suppression effect (z) �1.37 �2.05� �.62 �2.24� �1.4 �.19

Anger faces � Shapes contrastPsychopathy

B alone (SE) .000 (.001) .000 (.001) .000 (.001) .000 (.001) .000 (.001) .001 (.001)Standardized � .01 �.01 .04 �.04 �.003 .09B with APD (SE) �.003 (.001) �.002 (.001) �.002 (.002) �.004 (.002) �.003 (.001) .000 (.001)Standardized � �.38� �.38� �.25 �.53�� �.41� �.02Suppression effect (z) 2.80�� 2.50�� 1.80� 2.93�� 2.00� .70

APDB alone (SE) .001 (.001) .001 (.001) .001 (.001) .001 (.001) .001 (.001) .001 (.001)Standardized � .12 .10 .12 .10 .11 .10B with psychopathy (SE) .003 (.001) .003 (.001) .003 (.002) .004 (.002) .003 (.001) .001 (.001)Standardized � .45� .43� .34� .56�� .45� .12Suppression effect (z) �2.00� �2.00� �1.36 �2.69�� �1.77� �.11

Note. N � 103. Unstandardized regression coefficients reported (B) with standardized coefficients (�) reported in the line below. Gender was controlledfor in the first step of all analyses. “Sobel” tests were used to examine the effect size of mutual suppression effects and significance (p � .05) is denotedfrom bootstrap bias corrected confidence intervals.� p � .10. � p � .05. �� p � .01.

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220 HYDE, BYRD, VOTRUBA-DRZAL, HARIRI, AND MANUCK

two components that may distinguish these dimensions are NEMand amygdala reactivity. Thus, NEM and amygdala reactivity maybe key constructs of interest in research that seeks to understandetiologic differences between APD and psychopathy (see alsoVenables et al., 2013 which suggests that boldness, which is bothbroader and narrower than NEM may be a more ideal constructthat differentiates APD from psychopathy). Although some re-search has examined differential associations between factors ofpsychopathy (F1/F2) and NEM or amygdala reactivity, evaluationsof these relations with APD as an outcome are rare and thusimportant given the higher prevalence of APD. Our findings add togrowing research in this area and highlight the importance ofexamining these constructs (APD, psychopathy) separately butconcurrently in the same model. Specifically, the current findingssuggest that NEM and amygdala reactivity may not show zero-order relations with a unidimensional measure of psychopathy orAPD when considered by themselves within the normal range offunctioning (where these dimensions may be highly overlapping),but only when their overlap is considered (or, in the case ofpsychopathy, when F1 and F2 are separated).

Comparisons to Past Work on Amygdala Reactivity inAntisocial Populations

Although the NEM findings are in line with previous research andextend those findings to a community sample, the novel relationshipbetween amygdala reactivity, APD, and psychopathy dimensionsbears further consideration. Certainly the negative association be-tween psychopathy and amygdala reactivity is consistent with severalother studies in youth and adults (Hyde et al., 2013). However, thesestudies generally focused on total psychopathy scores or groups ofyouth high on callous-unemotional traits and conduct problems anddid not examine suppression relationships. Thus, it is unclear why nosignificant zero-order (nonsuppression) relationships between psy-chopathy dimensions and amygdala reactivity emerged in this study(although this similar effect was seen in Sebastian et al., 2012 and PPIF2 in this study showed robust zero-order correlations with amygdalareactivity). It could be that this relationship is much weaker dimen-sionally in a healthy sample. Without partialing out APD dimensions,the current psychopathy measure in healthy adults may be capturingmild antisociality (as it contains both F1 and F2) rather than anythingspecific to psychopathy (as evidenced by high correlations betweenthe APD and psychopathy measures). Therefore, it was not until wepartialed out the overlapping variance of APD from the psychopathydimension that we saw more of a “classic” relationship between theunique F1 components of psychopathy and amygdala reactivity. Cer-tainly there is extreme divergence across many traits between healthyadults and criminal psychopaths, which underscores the utility oftesting these relationships across the continuum of functioning, par-ticularly when exploring biological correlates which are likely to havedimensional relationships with behavior (Ofrat & Krueger, 2012;Plomin, Haworth, & Davis, 2009).

The current results also appear to be consistent with two recentneuroimaging studies emphasizing that APD and psychopathy dimen-sions have divergent relationships with amygdala reactivity. In thefirst study of a different community sample, we found that, whilecontrolling for the overlap of four psychopathy facets, amygdalareactivity to fear was negatively associated with the interpersonal facetof psychopathy (part of F1), whereas amygdala reactivity to anger was

positively associated with the lifestyle facet of psychopathy (part ofF2; Carre, Hyde, Neumann, Viding, & Hariri, 2013). In a secondrecent study of youth, similar suppressor effects in amygdala reactiv-ity emerged using dimensions of callous-unemotional traits and con-duct problems (Sebastian et al., 2012).

Locating Results Within Subregions of the Amygdala

Consistent with past studies examining neural correlates of bothanxiety and anger traits in the current sample (Carré et al., 2012;Hyde et al., 2011), the dorsal amygdala region that encompassesthe central nucleus, sublenticular extended amygdala, and nucleusbaysalis of Meynert, was most strongly related to APD and psy-chopathy in a suppression framework. These components of ourdorsal amygdala ROI collectively represent major output pathwaysthrough which the amygdala can drive behavioral and physiologicarousal (Davis, Johnstone, Mazzulla, Oler, & Whalen, 2010).Previous work on psychopathy has not examined subregions of theamygdala, although one recent review has emphasized the impor-tance of this approach (Moul, Killcross, & Dadds, 2012). Thecurrent findings highlight the ability to examine subregions of theamygdala and the need for more attention to the heterogeneity ofthe amygdala in future neuroimaging studies of psychopathy.

Specificity of Amygdala Reactivity to IndividualFace Types

In the current study we found stronger relationships between vari-ables when examining amygdala reactivity to angry rather than fearfulfacial expressions, whereas many past studies have specifically linkedpsychopathy to amygdala hyporeactivity to fearful faces (e.g., Jones,Laurens, Herba, Gareth, & Viding, 2009; Viding, Fontaine, & Mc-Crory, 2012), with one study showing this effect was specific to fearand not anger (Marsh et al., 2008). However, these studies were donein youth, focused only on callousness plus antisocial behavior, andused neutral faces as a contrast (rather than the simple somatosensorycontrol stimuli used in the present study); thus, it is hard to comparethese results directly (although see Marsh & Blair, 2008). In contrast,previous studies on adults with impulsive aggression (Coccaro et al.,2007), have highlighted the importance of the response of theamygdala to anger rather than fear (see also Carré et al., 2012). Moreresearch is needed to examine theories (e.g., Blair, 2007) that empha-size the unique importance of fearful facial expressions (vs. anger) ineliciting individual differences in amygdala reactivity that areuniquely associated with psychopathy and if the link betweenamygdala reactivity and various facial expressions will differ in rel-ative strength depending on sample characteristics (e.g., high on APDvs. psychopathy traits). Moreover, it should be noted that there wereno main effects of a contrast comparing amygdala reactivity withangry versus fearful facial expressions, thus we cannot directly test theproposition that our results were highly specific to angry facial ex-pressions.

Additionally, it is unclear why amygdala reactivity failed to medi-ate the mutual suppression relationship of psychopathy and APD toNEM. Although amygdala reactivity and NEM were correlated in thisstudy, it is likely that amygdala reactivity is also correlated with otherpersonality dimensions that may also differ between APD and psy-chopathy (e.g., components of extraversion; see Supplemental Table1). Moreover, NEM, although related to amygdala reactivity, is likely

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221AMYGDALA REACTIVITY

influenced by a complex network of neural regions, which is notwholly captured by amygdala reactivity. Similarly, it should be notedthat NEM is a complex factor containing multiple negative emotions(e.g., anger, sadness) and psychopathy itself is not associated withreductions in all negative emotions (e.g., anger; see Carré et al., 2012for findings separating some of these emotions apart in this sample).Thus, our lack of mediation results may be due to conflating multiplenegative emotions into one measure of NEM.

Comparison Among Measures of Psychopathy Factors

Supplemental analyses examining specific psychopathy subfactorsfrom different measures, yielded interesting and complex results. Themost consistent and highly correlated factor across all measures wasof general antisociality (e.g., APD, PCL-R-based F2, PPI-based F2).All three of these measures tapping antisociality demonstrated signif-icant positive relationships with NEM and both the APD and PPI F2measures yielded positive relationships with amygdala reactivity tothreat (and to some extent distress). However, findings with psychop-athy dimensions and PCL-R and PPI dimensions of F1 were moredivergent, likely based on the differing measurement and conceptu-alization of F1 and the “unique” components of psychopathy (e.g.,PCL-R F1 is conceptually different than PPI fearless dominance andthese factors were virtually uncorrelated in this study). Thus, it may besafest to conclude that our current findings are most robust in linkingamygdala reactivity and NEM positively to antisociality across mul-tiple measures whereas any links between F1/psychopathy are moredependent on the measurement instrument employed. Finally, theseresults highlight that current NEO-derived measures of psychopathyand APD share much of their variance (i.e., these two measures werevery highly correlated) and tap a similar construct (and thus may notbe an ideal measure of what they each purport to assess). Furthermore,their overlap must be partialed to allow for unique relationships withcriterion variables to emerge. These caveats should be consideredwhen using the NEO-PI-R to assess psychopathy and APD.

Limitations

Although this study had many strengths, including the use of awell-established task for eliciting amygdala reactivity, the ability toseparate differential contributions of specific threat- versus distress-related facial expressions and amygdala subregions, a relatively largesample size for a neuroimaging study, and the ability to test dimen-sional relationships in traits expressed in a community sample, thereare some limitations worth noting. First, this study examined associ-ations in a healthy community sample that is unlikely to contain anyindividuals meeting criteria for clinically diagnosed APD or psychop-athy. Thus, this investigation examines how these dimensions operatewithin healthy individuals and should not be generalized to psychiat-ric or criminal populations. Moreover, it should be noted that therewere near-zero correlations between gender and measures of APDand F2, which run counter to a large body of literature demonstratinghigher levels of these dimensions in males. These near-zero correla-tions may reflect unique aspects of this sample or the ways in whichthese measures were generated (although this relationship was con-sistent across all three measures). Second, as noted above, we did notuse neutral faces within our neuroimaging paradigm and thus cannotdirectly compare our results with studies directly contrasting angryand fearful expressions with neutral expressions. Third, we used

dimensional measures of APD and psychopathy that were derivedfrom the NEO-PI-R and we did not have any “traditional” measuresof psychopathy. Our findings did vary when based on other person-ality derived measures and our results likely would differ had we useddiagnostic criteria, self-report, or interview-based measures (e.g., theSCID-II, PPI, PCL-R). Moreover, this FFM method of generatingAPD and psychopathy traits resulted in highly correlated variables.Although we monitored closely for problems of collinearity, and havepresented results from other, less correlated, measures, it is importantto note that suppression effects are most likely to occur with highlycorrelated predictors. Moreover, as noted above, given their highoverlap and lack of zero-order correlations with NEM and amygdalareactivity, the APD and psychopathy measures appear to have diffi-culty separating the two constructs they purport to measure (i.e., APDvs. psychopathy which should not be as highly correlated). Addition-ally these measures contain some problematic features including theinclusion of anxiety into the APD score (which is not a criterion forclinically assessed APD), and the fact that psychopathy includes muchof the diagnostic criteria for APD (mostly through psychopathy’s F2with some F1 aspects). Fourth, it is important to note that this samplewas of middle-aged adults and thus differs developmentally frommany studies that have focused on adolescents or young adults/college students. Overall, these results should be interpreted withinthe larger literature on APD, psychopathy, NEM, and amygdalareactivity across development in both clinical and normative popula-tions.

Conclusions and Implications

The present findings suggest that APD and psychopathy traits in acommunity sample differ critically in their levels of NEM andamygdala reactivity, particularly when the overlap between APD andpsychopathy are taken into account. Thus, accounting for the sharedvariance between the constructs helps to separate etiologic factors thatare unique to these two overlapping constructs (e.g., levels of NEM,amygdala reactivity). The present findings help to replicate seminalwork by Hicks and Patrick (2006) and to extend the findings to APDversus psychopathy, using dimensional measures of these constructsin a healthy sample. Moreover, the present findings expand thisframework to the neural correlates of these antisocial dimensions andemphasize the differences between these two constructs at the per-sonality and neural level. Finally, by comparing various measures ofpsychopathy factors, our study highlights concurrence across mea-sures of antisociality in predicting higher NEM and higher amygdalareactivity. In the long term, in helping to better understand the differ-ences in etiology between these disorders, we hope that this basicresearch will eventually usefully inform larger efforts for early pre-vention strategies and personalized interventions based on differencesin early emerging temperaments, such as NEM (e.g., Dadds & Rho-des, 2008).

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Received March 5, 2013Revision received November 8, 2013

Accepted November 20, 2013 �

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224 HYDE, BYRD, VOTRUBA-DRZAL, HARIRI, AND MANUCK