The strongest evidence to date for a relationship between brain structure and/or function and antisociality implicates the prefrontal cortex. This is not surprising, given the region’s key multiple functions which include the inhibition of behavioral impulses and the regulation of emotions generated by underlying subcortical structures such as the amygdala. Structural imaging investigations have indicated significant gray matter reductions in the prefrontal regions of individuals characterized by aggression and antisocial behavior. For example, Raine, Lencz, Bihrle, LaCasse, and Colletti (2000), using structural MRI, found an 11 % reduction in prefrontal gray matter in individuals with ASPD compared to those without. Two prefrontal sub-regions—the orbitofrontal cortex (OFC) and dorsolateral prefrontal cortex (DLPFC)—have most consistently been found to be impaired in antisocial, violent individuals. Evidence from multiple sources suggests that the DLPFC mediates executive functions (Dinn & Harris, 2000), and is involved with the temporal integration of behavior. The OFC modulates sensitivity to reinforcement contingencies (Dinn & Harris, 2000), and is involved with the inhibition of inadequately motivated actions, and with the modulation of aggressive behavior and autonomic reactivity. In humans, this system contributes more to social and self-awareness than the DLPFC (Damasio, 1994. Laakso et al. (2002) in one of the few structural imaging studies to date examining prefrontal sub-regions found significantly reduced orbitofrontal and dorsolateral prefrontal cortex volume in individuals with ASPD, which is consistent with functional imaging studies that have indicated abnormal orbitofrontal and dorsolateral prefrontal functioning during performance of cognitive and emotional tasks in antisocial individuals (e.g., Müller et al., 2003; Raine et al., 1994; Schneider et al., 2000). Structural studies of white matter have also produced interesting, if at times inconsistent, findings. While Kruesi and Casanova (2006) found a trend toward reduced white matter/whole brain volume ratios in the corpus callosum but not in the prefrontal area in youth liars relative to antisocial controls and healthy volunteers, Yang et al. (2005) found a 22–26 % increase in prefrontal white matter along with a 36–42 % reduction in prefrontal gray/white matter ratios in adult pathological liars. Functional imaging studies have also provided evidence for prefrontal dysfunction in individuals with antisocial behaviors and disorders and have further implicated this region in anger and aggression in non-clinical populations. For example, utilizing fMRI in normal controls who were insulted, Denson, Pedersen, Ronquillo, and Nandy (2009) found general aggression to be associated with increased activity within the left anterior cingulate cortex (ACC; a region associated with anger intensity), while displaced aggression related to increased activity in the medial prefrontal cortex (an area linked to emotion regulation and self-reflections). Additionally, Goethals et al. (2005), using SPECT, found reduced regional cerebral blood flow (rCBF) in right temporal and prefrontal regions in individuals with borderline personality disorder and ASPD, compared to controls. Overall, these findings suggest that impairments in the prefrontal cortex, particularly the orbitofrontal and the dorsolateral prefrontal regions, may make key contributions to the pathogenesis of antisocial behavior in individuals with antisocial disorders.

The prefrontal cortex, however, is not alone in its demonstrated associations with antisociality, crime, and violence. Temporal lobe damage has long been known to result in blunted emotional responses (Klüver & Bucy, 1939), similar to those seen in antisocial violent individuals. Indeed, a number of PET studies indicating prefrontal dysfunction in their antisocial, violent subjects also showed reduced temporal functioning. For example, Soderstrom, Tullberg, Wikkelsoe, Ekholm, and Forsman (2000) revealed reduced rCBF in both the frontal and temporal cortices in perpetrators of violence compared to controls. Hirono, Mega, Dinov, Mishkin, and Cummings (2000) also found decreased rCBF in the left anterior temporal cortex and bilateral dorsofrontal cortex in individuals convicted of impulsive violent offenses. In another PET study focusing on temporal regions, Volkow et al. (1995) found rCBF abnormalities in prefrontal and temporal medial regions in violent psychiatric patients. Finally, Juhász, Behen, Muzik, Chugani, and Chugani (2001) found a significant correlation between a higher severity of aggression and lower metabolism in the bilateral medial prefrontal and left temporal cortex in aggressive children with epilepsy.

Structural MRI investigations have also identified fronto-temporal abnormalities in antisocial individuals. De Brito et al. (2011) found decreased white matter concentrations in the right superior frontal lobe, right dorsal anterior cingulate, right superior temporal gyrus, and left precuneus in children (ages 10–13) with psychopathic tendencies. Sato et al. (2011) reported that structural gray matter differences in the superior temporal sulcus/gyrus region distinguish psychopaths from controls (Sato et al., 2011). Additionally, using structural MRI, Barkataki, Kumari, Das, Taylor, and Sharma (2006) found whole brain volume and temporal lobe reductions in men with ASPD compared to controls. Using voxel based morphometry (VBM), Huebner et al. (2008) found a 6 % gray matter volumetric reduction in the bilateral temporal lobes, including left amygdala, left hippocampus, and the orbitofrontal and ventromedial regions in boys with CD and ADHD-along with volumetric increases in cerebellar gray matter. Temporal but not frontal/prefrontal lobe reductions have also been observed in adolescents diagnosed with early-onset CD and histories of ADHD (Kruesi, Casanova, Mannheim, & Jonson-Bilder, 2004) and impulsive-aggressive men (Dolan, 2010—20 % volumetric reductions compared to controls in this study). Overall, imaging studies have demonstrated that the temporal lobe—alone or in concert with a larger fronto-temporal circuit—may make significant contributions to aggression, violence, and disorders of antisociality.

Within the temporal region, antisocial and violent behavior has been associated with deficits in subcortical structures such as the amygdala-hippocampal complex. The amygdala plays a key role not only in the reception and production of emotion, but also in the processing of fear conditioning, while the hippocampus is involved in emotional memory. Several studies have reported functional and structural abnormalities in the amygdala-hippocampal complex in antisocial aggressive individuals. Criminal psychopaths, for example, have shown decreased amygdala-hippocampal activations during the viewing of negative affective pictures (Kiehl et al., 2001). Reduced hippocampal rCBF has also been demonstrated in violent perpetrators compared to controls (Soderstrom et al., 2000). Other functional MRI studies (e.g., Dolan, 2010) have identified amygdala activation abnormalities to various angry/neutral/sad facial comparisons in adolescent and young adult males with early or late-onset CD (Passamonti et al., 2010). Using fMRI, Sterzer, Stadler, Krebs, Kleinschmidt, and Poustka (2005) found adolescents with CD showed reduced activation in the right dorsal anterior cingulate cortex (ACC) when viewing neutral and negative images compared to controls, and reduced amygdala activation when viewing negative images in those with high aggression. Additionally, recent structural MRI data has shown reduced whole brain and hippocampal volumes in individuals with schizophrenia with a history of violence (Barkataki et al., 2006), and reductions in hippocampal and parahippocampal volumes in murderers with schizophrenia (Yang et al., 2010) VBM data have also indicated bilateral amygdala volumetric reductions in adolescent males with early or late-onset CD (Fairchild et al., 2011). Together, these findings suggest that temporal lobe deficits, particularly in the amygdala and hippocampus, may predispose an individual to a lack of fear for punishment and result in the disruption of normal moral development.

Gender differences in brain structure have been noted by numerous authors, with men (after correcting for body size and age) generally having larger brains than women (Burgaleta et al., 2012; Fan et al., 2010; Rushton & Ankney, 2009), attributed to the nearly four billion more neurons in the adult male brain (Pakkenberg & Gundersen, 1997, in Rushton & Ankney, 2009). While numerous imaging studies of antisocial disorders have utilized all-male participants (e.g., Bagcioglu et al., 2014; Barkataki et al., 2006; Fairchild et al., 2011; Huebner et al., 2008; Passamonti et al., 2010), those involving mixed-gender samples are much less common. In one rare imaging study of individuals with ASPD involving actual gender comparisons, Raine, Yang, Narr, and Toga (2011) used structural MRI to examine gender differences in regional brain volume between adult male and female temporary employment agency workers with and without diagnoses of ASPD, along with independently recruited female controls. Males with ASPD showed an 8.7 % reduction in orbitofrontal gray matter volume, a 17.3 % reduction in middle frontal gray matter volume, and a 16.1 % reduction in right rectal gray matter volume compared to male controls. In both males and females, orbitofrontal and middle frontal volumetric reductions were significantly associated with increased ASPD symptomatology and criminal offending. Compared to females, males overall had reduced orbitofrontal and middle frontal gray matter volume; and controlling for these volumetric differences reduced the gender difference in ASPD/antisocial behavior by 77.3 %. Based on these findings, the authors hypothesized that gender differences in antisocial behavior may be partly attributable to structural gender differences in the prefrontal cortex. In all, while this may be first imaging evidence for a brain structural profile of antisocial behavior unique to men, future investigations in this area are clearly needed.

While deficits in measures of general intelligence (e.g., IQ or Full Scale IQ) are the best-replicated neuropsychological correlate of antisociality, violence, and crime among non-mentally ill individuals (Wilson & Herrnstein, 1985), the identification of component verbal versus spatial/performance intelligence deficits has proven useful in understanding the etiological underpinnings of antisocial behavior. Widely reported among adult antisocial populations is reduced verbal as opposed to spatial/performance IQ—perhaps indexing deficits in left hemispheric functioning (Raine, 1993). Verbal IQ reductions appear largely characteristic of antisocial children and adolescents (Barker et al., 2007; Brennan, Hall, Bor, Najman, & Williams, 2003; Raine, 1993; Teichner & Golden, 2000; Vermeiren, De Clippele, Schwab-Stone, Ruchkin, & Deboutte, 2002)—including those with CD (Déry, Toupin, Pauzé, Mercier, & Fortin, 1999)—and have been shown to predict later delinquency at age 18 for persistent, high-level offending beginning in preadolescence (Moffitt, Lynam, & Silva, 1994). Verbal deficits may undermine the development of language-based self-control mechanisms (Luria, 1980), leading ultimately to failure of socialization (Eriksson, Hodgins, & Tengström, 2005), although the juvenile offender with verbal intelligence deficits may have a more positive prognosis, with environmental modifications and therapy (Teichner & Golden, 2000). Interestingly, general intellectual performance or verbal intelligence deficits have not been reported in individuals with antisocial personality disorder and psychopathy (Barkataki et al., 2006; Kosson, Miller, Byrnes, & Leveroni, 2007), although verbal dysfunction may be related to some specific psychopathic traits (i.e., criminal versatility and violence; Rasmussen, Almvik, & Levander, 2001). Thus, while global and/or verbal IQ deficits may be associated with adult antisociality in general, they may not be associated with specific subsets of antisocial trait constellations.

Additionally, the literature related to global verbal intelligence in juvenile psychopathy (itself a largely unexplored and controversial topic; Salekin, 2006) is scant. Verbal deficits were not observed by Loney, Frick, Ellis, and McCoy (1998) in children with conduct problems characterized by Callous-Unemotional traits (CU traits—related to adult psychopathy; Frick et al., 2003), and verbal intelligence was shown to be related positively with the superficial and deceitful interpersonal style traits and inversely with the affective processing-disturbance traits of psychopathy in juvenile prisoners (Salekin, Neumann, Leistico, & Zalot, 2004). Overall, verbal deficits in populations of antisocial youth appear relatively consistent, although future investigations of psychopathic youth may help clarify heterogeneous verbal IQ findings among antisocial juveniles.

Gender differences. While a significant number of neuropsychological studies have examined general, verbal, and performance IQ deficits in antisocial males and females across the lifespan, both combined and separately, few studies have attempted to identify a pattern of verbal and/or intelligence deficits unique to male antisocial populations. Examined separately, females with antisocial disorders have shown neuropsychological deficits comparable to those reported in antisocial males. For example, Pajer et al. (2008) found reduced performance across several neuropsychological domains, including intelligence (i.e., IQ), language, visuospatial skills, verbal memory, executive functioning, and achievement, in adolescent females with CD compared to normal controls. However, Goodman (1995) compared boys and girls (ages 5–16), grouped by behavioral problems (CD, mixed disorders of conduct and emotion, emotional disorders, and other disorders) to healthy controls; and results indicated increased IQ scores in males compared to females in each behavioral group, although group differences only approached significance. Arcia and Conners (1998), on balance, found no gender differences over the lifespan of individuals with ADHD with respect to IQ, neuropsychological performance, or teacher or parent ratings of disruptive behavioral problems. David Wechsler originally argued that the aforementioned performance IQ > verbal IQ discrepancy would be less-characteristic of delinquency in females, but this was based on results from only one study (Isen, 2010). In a recent meta-analysis of 131 studies of antisocial individuals from different age groups, Isen (2010) found the aforementioned PIQ > VIQ discrepancy to be characteristic of females as well as males. Furthermore, results across 14 studies of females with antisocial behavior indicated that this discrepancy is slightly larger for females. As such, it may be that specific patterns of verbal and performance deficits may characterize antisocial males and females separately, though more work is needed in this area.

Executive functioning (EF) is an umbrella term for the cognitive processes allowing for goal-oriented, contextually appropriate behavior, and effective self-serving conduct (Lezak, Howieson, Loring, Hannay, & Fischer, 2004; Luria, 1980). Deficits in EF, as indicated by performance errors on neuropsychological measures of strategy formation, cognitive flexibility, or inhibition (i.e., categorization, maze-tracing, Stroop interference, card sorting, verbal fluency, and tower tests; and go/no-go and gambling tasks), are thought to represent frontal lobe impairment. Morgan and Lilienfeld’s now-classic (2000) meta-analysis of 39 studies found overall EF deficits in antisocial individuals compared to controls, and strongest effects for the Porteus Mazes test Q score (i.e., crossed lines, pencil lifts, and changed directions—errors purportedly reflecting impulsivity).

Evidence for EF deficits in delinquent children and adolescents with CD has varied historically depending upon sample characteristics, control groups, assessment measures, operationalizations of EF, and methodology (Moffitt & Henry, 1989; Teichner & Golden, 2000). Findings have recently been mixed, with executive dysfunction characterizing some antisocial youths (Cauffman, Steinberg, & Piquero, 2005; Dolan & Lennox, 2013; Kronenberger et al., 2005; Nigg et al., 2004; White et al., 1994) and not others (Moffitt et al., 1994; Nigg et al., 2004). This may reflect, however, the development of EF along with the ongoing mylenation of the frontal cortex into adolescence and beyond (Nigg et al., 2004; Raine, 2002), which may explain differences in executive functioning deficits among children and adults. Nestor (1992), for example, found impairments in EF in older (i.e., middle-aged) but not younger (i.e., early adulthood) maximum security hospital patients. Blair (2006) found orbitofrontal task deficits to be more pronounced in psychopathic adults than psychopathic children. Additionally, comorbid hyperactivity and aggression may influence neuropsychological performance (Raine, 2002; Séguin, Nagin, Assad, & Tremblay, 2004). Furthermore, antisocial behavior and executive dysfunction may be related developmentally, and certain EF deficits may have serious developmental consequences such as inattention, impulsivity, and problematic understanding of the negative implications/impact of behavior. This may lead to an impaired ability to mentally maintain abstract ideas of ethical values and future contingencies while focusing upon immediate rewards, and inhibit modification of behavior in response to social feedback (Moffitt & Henry, 1989).

Executive dysfunction has also more recently been associated with aggressive (e.g., male batterers) and ASPD populations (Dolan & Park, 2002; Stanford, Conklin, Helfritz, & Kockler, 2007, property offending (Barker et al., 2007), and reactive versus instrumental violent offenders (Broomhall, 2005). Adult psychopathy has not demonstrated consistent associations with general EF deficits (Blair & Frith, 2000; Dinn & Harris, 2000; Hiatt & Newman, 2006; Kosson et al., 2007), although recent neuropsychological evidence suggests that psychopathy may be characterized more by deficits in orbitofrontal functioning (Blair et al., 2006). Additionally, uncaught (successful) psychopaths have demonstrated better dorsolateral prefrontal task performance compared to unsuccessful psychopaths and controls (Ishikawa, Raine, Lencz, Bihrle, & Lacasse, 2001).

Gender differences. Empirical support for a neuropsychological profile of executive dysfunction unique to males who are defiant, aggressive, or violent is mixed. Many neuropsychological studies utilizing all-male participants (e.g., Giancola & Zeichner, 1994; Séguin, Pihl, Harden, Tremblay, & Boulerice, 1995; Spellacy, 1977; see also Morgan & Lilienfeld, 2000, for a review) have identified similar deficits in executive functioning in individuals characterized by antisocial behavior and disorders. In fact, Speltz, DeKlyen, Calderon, Greenberg, and Fisher (1999) found that preschool boys with early onset conduct problems with both ODD and ADHD demonstrated reduced verbal and executive functioning abilities compared to those with ODD alone.

On balance, studies involving gender comparisons have produced findings which are somewhat discordant. For example, in a sample of children with aggressive behavior, Raaijmakers et al. (2008) found reduced executive functioning abilities in 4-year-old boys compared to girls, and increased impulse control and verbal skills in girls—thought to represent faster maturation in girls. Giancola, Roth, and Parrott (2006) found executive functioning mediated the relationship between difficult temperament and aggression (i.e., increased performance on executive functioning measures was associated with decreased negative temperament and aggression) for men but not women. Brennan et al. (2003), in a study of 370 Australian adolescents, identified an interaction of biological risk factors (i.e., low age 5 vocabulary ability, poor age 15 VIQ and executive functioning, prenatal/birth complications, maternal illness during pregnancy, and infant temperament) and social risk factors that predicted life-course persistent aggression in boys and girls, and predicted life-course persistent versus adolescent-onset aggression in boys. Social risk factors were stronger predictors of later aggression, although these authors suggest an interaction of early social risks with later biological risks to predict persistent aggression; and that lifetime, cumulative interactions of these risks are stronger predictors of persistent aggression in boys than are risks specific to childhood or adolescence. However, Herba, Tranah, Rubia, and Yule (2006) found no gender differences in performance on neuropsychological measures of motor response inhibition, verbal inhibition, and cognitive interference inhibition in adolescents marked by conduct problems. Overall, such heterogeneity in findings may reflect the aforementioned methodological limitations of EF studies in antisocial populations in general. Nonetheless, they are at least consistent with results produced by imaging and neurological studies of violent, aggressive, and antisocial persons.