Adolescents with lack of empath are at higher risk of developing psychopathic traits


A pioneering study with the Portuguese population shows that adolescents with high levels of callous-unemotional traits demonstrate lower levels of anticipated guilt towards the possibility of committing an immoral act and struggle to judge an immoral act as a wrong one.

Researchers have evaluated the callous traits, that is, the lack of empathy and disregard for the wellbeing and feelings of others, of 47 adolescents between 15 and 18 years old.

The teenagers watched video animations portraying examples of moral transgressions, such as incriminating someone or keeping money that fell from someone else’s pocket.

“This approach allowed us to create more realistic scenarios that happen in daily life,” explains Oscar Gonçalves, a neuroscientist at Proaction Lab and co-author of the study.

The adolescents were asked how guilty they would feel if they were the ones to commit the moral transgressions and how wrong they think the actions were.

Although the callous-unemotional traits in adolescents are known to be precursors of psychopathy in adulthood, the results of the study differ from what is known about psychopaths.

“Adults with psychopathic traits show low levels of anticipated guilt but consider immoral actions as wrong. However, in our study, adolescents with high CU levels show levels of guilt and judge immoral actions as less wrong,” explains Margarida Vasconcelos, first author.

However, researchers have found evidence of a dissociation between moral emotions and moral judgment, that is, between the feelings of guilt and the judgment of immoral actions.

“Even in adolescents with sub-clinical levels of callous-unemotional traits, this dissociation typical in psychopathy in adulthood is already happening during development,” explains the study coordinator Ana Seara Cardoso.

The results of the study will “contribute to the development of a severe anti-social behavior model” and allow the “development of intervention targets, rehabilitation and early prevention of anti-social behavior,” says Ana Seara Cardoso.

Aggressive and antisocial behaviours are the leading cause of child and adolescent referrals to mental health clinicians and can lead to a diagnosis of conduct disorder1. However, not all patients receiving this diagnosis show the same pathophysiology. One form of conduct disorder is marked by the presence of psychopathic traits and will be the main focus of this Review. Psychopathic traits have a core callous– unemotional component (for example, lack of guilt and empathy) and an impulsive–antisocial component2. They are detectable early in childhood and persist into adulthood3,4. Clinically, understanding psychopathic traits is important, as their presence can interfere with socialization5 and currently available conduct-disorder treatments6,7.

There has been rapid progress in our understanding of the neurobiology of psychopathic traits, particularly the callous–unemotional component, over the past 5 years. Indeed, partly as a result of neurobiological studies8–10 a form of callous–unemotional specifier (termed ‘limited prosocial emotions’) has been introduced to the conduct disorder diagnosis in the fifth edition of the Diagnostic and Statistical Manual (DSM-5)11. To qualify for this specifier, an individual must have displayed two of four characteristics in the previous 12 months in multiple settings. These characteristics are lack of remorse or guilt; callousness (that is, lack of empathy); lack of concern about performance (for example, at school); and shallow or deficient affect (a lack of expression of feelings to others). A different form of conduct disorder is associated with increased risk of mood and anxiety disorders and emotional lability (BOX 1).

Box 1
Different forms of conduct disorder
Patients receiving a diagnosis of conduct disorder do not all have the same pathophysiology. One set of neurodevelopmental impairments — decreased amygdala responsiveness to distress cues and decreased striatal and ventromedial prefrontal cortex (vmPFC) sensitivity to reinforcement signals that are critical for successful decision making (FIG. 1) — can lead to a diagnosis of conduct disorder associated with psychopathic traits. Another set of dysfunctions can also lead to a diagnosis of conduct disorder, as explained below.

Mammals demonstrate a graded and instinctual response to threat: distant threats induce freezing; as the threats draw closer, they induce flight; and, finally, reactive aggression is induced when they are very close and escape is impossible184. Reactive aggression involves unplanned, enraged attacks on the object perceived to be the source of the threat or frustration. Animal studies have shown that reactive aggression is mediated by a circuit that runs from the medial amygdala, largely via the stria terminalis to the medial hypothalamus, and from there to the dorsal half of the periaqueductal grey (PAG)185–188.

This circuitry is assumed to mediate reactive aggression in humans as well189 (see the figure). Certainly, several recent functional MRI studies have identified these regions to be involved in defensive reactions to threat in humans190–192. This circuitry is assumed to be regulated by frontal cortical regions, particularly the vmPFC and, potentially, regions of the anterior cingulate cortex (ACC).

If the basic threat circuit (amygdala–hypothalamus–PAG) is overly responsive, either because of prior priming or inadequate regulation, the individual is more likely to respond to a threat with reactive aggression than with freezing or flight53. In youths with conduct problems and low callous–unemotional traits, this circuit is overly responsive, as evidenced by, for example, increased amygdala responses to fearful expressions49. Moreover, they are more likely to display higher levels of threat-based and frustration-based reactive aggression193. Such individuals probably represent many of the 40% with conduct disorder who also meet criteria for a mood or anxiety disorder194. Notably, a high rating for psychopathic traits (which characterizes the other form of conduct disorder) is typically associated with a decreased risk for anxiety and mood disorder symptoms, particularly when the relationship between anxiety on the one hand, and antisocial and impulsive behaviour on the other hand is accounted for195–197. This inverse relationship between psychopathic traits and mood and anxiety disorders is unsurprising, as increased amygdala responsiveness is also commonly associated with mood and anxiety disorders198. By contrast, psychopathic traits are associated with decreased amygdala responsiveness8,10,30,48–50,83.

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This Review discusses why psychopathic traits in youths are associated with an increased risk of antisocial behaviour and aggression. I use a cognitive neuroscience approach; that is, I consider how specific functional impairments in specific neural systems give rise to the development of psychopathic traits. I then use cognitive neuroscience findings to interpret both data on genetic and environmental risk factors for aggression and data on potential treatment possibilities. Finally, I present an integrative model of psychopathic traits, conduct disorder and aggression more generally.

A cognitive neuroscience approach

Youths with psychopathic traits show two main cognitive impairments. The first is a specific form of empathic dysfunction. Indeed, the clinical literature has long associated psychopathy with empathy impairment12,13. However, the term empathy subsumes two critical processes that are distinct at both the cognitive and the neural level14: cognitive empathy involves the representation of the intentions and thoughts of other individuals (also known as theory of mind)15, whereas emotional empathy involves affective responses to emotional displays of other individuals and to verbal descriptions of the emotional states of other individuals. Psychopathic traits are not associated with reductions in cognitive empathy but they — and particularly the callous–unemotional component — are associated with reductions in specific forms of emotional empathy (in particular, responding to the fear, sadness, pain and happiness of others). This functional impairment is associated with reduced amygdala and ventromedial prefrontal cortex (vmPFC) responsiveness to distress cues (FIG. 1).

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Figure 1
Core regions implicated in, and functions disrupted by, psychopathic traitsa | Core regions implicated in psychopathic traits: the amygdala, the caudate (which is part of the striatum) and the ventromedial prefrontal cortex (vmPFC). In addition to these core regions, the anterior insular cortex (AIC) and the dorsomedial PFC (dmPFC) may also be implicated. b | Functional impairments associated with psychopathic traits. In individuals with psychopathic traits, impaired processing of distress cues results in impaired learning about actions that harm others (stimulus-reinforcement learning), which involves the amygdala. In addition, impaired prediction error signalling in these individuals, which involves the striatum, causes impairments in both stimulus-reinforcement and response–outcome learning. As a result, the expected value of objects, cues and responses are poorly learnt and represented (in the vmPFC), and decision making is impaired. Response conflict resolution (which involves the dmPFC), initiation of response change (which involves the AIC) and response implementation (caudate) — functions implicated in guiding an individual away from suboptimal behavioural choices — are thought to be generally intact in individuals with psychopathic traits. These regions are also recruited to guide an individual away from suboptimal behavioural choices based on expected value information, that is, because the response about to be made is associated with punishment. Individuals with psychopathic traits show reduced recruitment of these areas on the basis of expected value information.

The second cognitive impairment in youths with psychopathic traits is impairment in aspects of decision making, specifically in reinforcement learning and the representation of reinforcement expectancies. This impairment may relate more to the impulsive–antisocial component of psychopathic traits and is also seen, at least partially, in patients with other externalizing disorders, such as attention-deficit hyperactivity disorder (ADHD), and in those at risk of developing drug addiction. This functional impairment is associated with dysfunction in the vmPFC and striatum (FIG. 1).

Cognitive empathy
It has been known for some time that adults with psychopathic traits show no impairment in cognitive empathy16–18. This finding has been replicated recently in adolescents with psychopathic traits19,20. A recent functional MRI (fMRI) study examined participants who were using information about the intentions and beliefs of other individuals to predict their behaviour21. This study demonstrated that youths with psychopathic traits show normal recruitment of the medial frontal cortex (including the vmPFC), temporal parietal junction, posterior cingulate cortex and temporal pole when engaged in this cognitive empathy task. These are all regions that have been implicated in cognitive empathy in healthy individuals22–24.

Emotional empathy
Empathic reactions can be evoked by facial cues, auditory cues, body postures and even text. Emotional empathy has a communicatory function: the emotional cues of others impart specific information to the observer25,26, and emotional empathy is the observer’s ‘translation’ of this communication. It has been argued that different facial expressions provide different communicatory signals, initiate different forms of reinforcement-based learning and are processed by neural systems that are at least partially distinct25.

The emotional empathy impairment in youths (and adults) with psychopathic traits is selective. For example, they have normal recognition of expressions of anger and disgust (for meta-analytic reviews of the literature, see REFS 27,28), and blood oxygen level-dependent (BOLD) responses to angry expressions are similar to those in typically developing adolescents (the response to disgust expressions has not been tested)8,29,30.

By contrast, they display impaired processing of both distress cues (that is, expressions of fear, sadness or pain) and happy expressions; studies quite consistently show impaired recognition of fearful and, to a lesser extent, sad and happy expressions in youths (and adults) with psychopathic traits31–36. These findings have been confirmed in recent meta-analytic reviews of the literature27,28. The impaired recognition of fearfulness and sadness also applies to vocal tones35,37 and body postures38.

In addition, youths with psychopathic traits show reduced autonomic responses to fearful and sad expressions and pain in other individuals, as well as atypical electroencephalography responses to pain in others39–43. In line with findings of reduced responsiveness to the distress of others, children with high callous–unemotional traits state that they are less concerned (relative to children with low callous–unemotional traits) that aggressive behaviour will result in suffering in the victim44. Importantly, although youths with psychopathic traits show a reduced response to emotional stimuli (whether indexed by autonomic or amygdala activity), the response is not absent, and increasing the intensity of an emotional stimulus — through morphing31 or by orientating the participant’s attention towards the eyes — reduces or removes group differences in fearful expression recognition34,45.

In healthy individuals, amygdala activation by distress cues leads to both increased arousal (via projections to the brainstem) and increased attention to these cues. This increased attention reflects the reciprocal connections between the amygdala and temporal cortex, such that amygdala activity will stimulate the neurons that represent the emotionally salient features of the eliciting cue, further strengthening the representation of these features and increasing the probability that they will ‘win’ the competition for representation46.

In the case of fearful expressions, the eye region is a particularly emotionally salient feature47 and representation of the eyes will thus be particularly strengthened when a healthy individual sees a fearful face. As a result of stimulus-reinforcement learning, an association is formed between the ‘social punishment’ of the fearful or sad facial expression and any representations of objects or actions associated with this expression. Which object is associated will be specified by the expresser’s eye gaze 29.

The deficits in emotional empathy shown by adolescents with psychopathic traits involve amygdala dysfunction31. Indeed, fMRI studies in adolescents with psychopathic traits have consistently shown reduced amygdala responses to images of faces with fearful expressions8,10,30,48,49. Furthermore, youths with conduct disorder who have psychopathic traits show reduced amygdala and rostral medial frontal cortical responses to images of other individuals in pain47,50. The impaired recognition of happy expressions may also relate to amygdala dysfunction, but this has not yet been empirically confirmed. It is the callous–unemotional component of psychopathic traits that seems to be particularly associated with the reduced amygdala response to distress cues10,48.

Appropriate processing of distress cues is critical for socialization. Many studies in humans and animals have shown the role of emotional expressions in the transmission of the value of actions and objects. For example, humans value positively those actions and objects that make care-givers smile and avoid actions and objects for which care-givers show fear51,52. Similarly, individuals approach objects associated with happiness in another individual and avoid objects associated with fear or disgust in another individual.

The amygdala allows the association of the stimulus (the object or action towards which the expression was displayed) with the reinforcement (the expression itself), so that the object or action becomes associated with a value53. Indeed, recent animal studies have confirmed a critical role for the amygdala in observational fear54. In individuals with psychopathic traits, reduced processing of distress cues by the amygdala would lead to reduced aversion for actions that harm others, so that the individual is more likely to commit actions that harm others to achieve their goals (BOX 2).

Box 2
Care-based moral judgements
The deficits in emotional empathy and reinforcement-based decision making in adolescents with psychopathic traits affect social cognition in these individuals, particularly the formation of appropriate care-based moral judgements (that is, judgements about transgressions that result in harm to another individual (for example, one person hitting another), known as care-based transgressions). It has been argued that emotion has an important role in care-based moral judgments199–202. Specifically, care-based judgments rely on the amygdala associating the aversive emotional response to the victim’s distress with the representation of the action that caused this distress and on the ventromedial prefrontal cortex (vmPFC) representing the value of the transgression53.

Adults with psychopathic traits show reduced amygdala and vmPFC activity in response to care-based transgressions and a weaker correlation between their amygdala response and their rating of the severity of care-based transgressions compared with control participants203,204. Similarly, youths with psychopathic traits show reduced amygdala activity and reduced amygdala–vmPFC functional connectivity when making moral judgements83. There is also behavioural evidence that youths (and adults) with psychopathic traits show impaired care-based moral reasoning69,199. In addition, a recent study showed that adolescents with psychopathic traits give less to charities when such giving comes at a personal cost205.

Perhaps the most interesting finding regarding the altered moral reasoning in individuals with psychopathic traits is that it is selective for care-based transgressions. Indeed, their moral judgement of conventional transgressions (which concern social normative behaviour and are heavily reinforced by the anger of hierarchy figures (for example, not talking during class)) and disgust-based transgressions (transgressions that may elicit disgust reactions from observers — often against forms of sexual activity)69,199,206–208 is normal69,199,209,210. In addition, adults with psychopathic traits (adolescents have not yet been tested) judge care-based transgressions less seriously than control individuals, whereas there are no differences in how they judge the severity of conventional and disgust-based transgressions209–211.

It has been argued that the ability to respond to emotional reactions of others is critically important in socialization (including in judging social transgressions). As partially independent emotional learning systems are thought to allow the learning of valence information provided by different emotional expressions25,53, a selective impairment in processing care-based transgressions may be due to impairment in a particular emotional learning system.

Specifically, distress cues (for example, from people subjected to care-based transgressions) are processed by the amygdala; the inferior frontal cortex is involved in processing angry expressions (which occur during conventional transgressions; for a meta-analytic review of the expression literature, see REF. 212); and the insula is important for processing disgust expressions (which occur during disgust-based transgressions)200.

Thus, the selective impairment in recognizing distress cues but not disgusted or angry expressions in individuals with psychopathic traits (for meta-analytic reviews of the literature, see REFS 27,28) is in agreement with the finding that such individuals show impaired processing of care-based transgressions but normal processing of conventional and disgust-based transgressions69,199,209,210.

Emotional empathy also has a communicatory function: it is critical for learning the social value of actions and objects and important for appropriate decision making. In healthy individuals, the strength of the representation of the distress of the victim is inversely related to the probability of an aggressive response55. Brain regions that are important for representing the valence of objects and actions and for using this information to guide choices towards or away from these objects and actions include the vmPFC and anterior insular cortex (see below)56–59.

Furthermore, there is considerable evidence, including from lesion studies, that the vmPFC and insular cortex are critical for empathic responding60–63. Youths with conduct disorder show reduced rostral vmPFC activation in response to observing pain in other individuals50, as well as reduced insula responses when using emotional reactions from other individuals to predict the subsequent behaviour of these individuals21. In both cases, the activity reduction in these areas was correlated with the severity of psychopathic50 or callous–unemotional21 traits.

In summary, these findings suggest that adolescents with psychopathic traits not only form weaker associations between representations of actions that harm others and the aversive consequences of these actions to other individuals but also apply this information less during decision making. Such individuals are more likely to commit actions that will harm other individuals, because they are less likely to be deterred from committing such actions by any expectations regarding the distress the action would cause in the victims.

Emotional learning and decision making
Youths with psychopathic traits show pronounced impairments in emotional learning and decision making. This reflects not only reduced responsiveness to the social reinforcers (emotional expressions) considered above but also deficits in the processes underlying aversive conditioning, passive avoidance learning64, operant extinction2,65,66 and reversal learning67,68. These impairments manifest when making moral judgements69 and in other decision-making paradigms70.

It should be noted that reduced aversive conditioning has so far been assessed and found only in adult individuals with psychopathic traits71,72. However, youths with conduct disorder have also been reported to show reduced aversive conditioning73, and a propensity for aversive conditioning at the age of 3 years predicts future antisocial behaviour74.

Youths with psychopathic traits show deficits in the capacity to link outcomes (rewards or punishments) with stimuli or responses, and this is due to dysfunction within the amygdala, striatum (caudate and nucleus accumbens) and vmPFC75. In addition, there is evidence that the use of outcome information by the anterior insula, inferior frontal cortex and dorsomedial PFC (dmPFC) to guide the individual away from suboptimal behavioural choices58,59 is disrupted in adolescents with psychopathic traits76.

Clinically, this impairment may manifest in many destructive behaviours: for example, deciding to mug people on the street corner on which the individual was almost arrested the night before or to fight someone in response to mild provocation (in other words, to ‘be a man’), despite repeated negative consequences of such behaviours. The effective use of reinforcement outcome information during decision making requires two components.

The first is the appropriate representation of the reward or punishment received when an action has been performed. Prediction error signalling is critical for this56,77. Prediction error signals are thought to spur reinforcement learning (mediated by both the amygdala and striatum): the greater the prediction error, the greater the change in the reinforcement associated with the stimulus78. The second component is the appropriate representation of the expected value when considering whether to perform an action.

The vmPFC is involved in encoding received rewards56,57. Youths with psychopathic tendencies64 and conduct disorder79, or with increased levels of antisocial behaviour80, show reduced vmPFC response to the receipt of a reward (although there is one report that youths with externalizing disorders show heightened responsiveness to rewards81).

This is thought to reflect disrupted prediction error signalling9,64,76. Many studies in healthy adults have shown that the size of the positive prediction error (when a reward is larger than expected) is correlated with activity within the striatum56,57. This positive association between positive prediction errors and activity within the striatum also exists in healthy youths, but it is less strong in adolescents with psychopathic traits76. Given the importance of prediction error signalling for initiating reinforcement learning78, reduced prediction error signalling should result in poorer, and slower, learning of the reinforcements associated with objects and actions.

One particularly interesting feature of prediction error signalling in youths with psychopathic traits concerns their response to punishment. Punishments that are worse than expected are typically associated with a reduction in striatal activity in healthy adults and youths56,57. By contrast, adolescents with psychopathic traits showed a positive relationship between prediction errors to punishment and activity within the striatum76.

This is in agreement with earlier studies that showed increased responses to unexpected punishment within the vmPFC and striatum in youths with psychopathic traits and in antisocial youths more generally64,80. The reason for these increased, as opposed to decreased, striatal and vmPFC responses to unexpected punishment remains unclear, but it probably contributes to their decision-making impairment.

The representation of expected value is also disrupted in youths with psychopathic traits. Studies have shown a positive correlation between the expected value associated with a response or a stimulus and activity within the vmPFC in healthy adults and adolescents56,57. Thus, as the expected value associated with a stimulus increases (that is, the stimulus is an increasingly good predictor of reward), the individual is more likely to respond to that stimulus.

By contrast, in a recent model-based fMRI study, youths with psychopathic traits showed a weaker association between expected value and both choice behaviour and vmPFC activity during choice than healthy youths76. Thus, youths with psychopathic traits are poorer at using and representing expected value information, and this may impair their decision making.

Interestingly, healthy adolescents also show a stronger correlation between expected value and activity within the anterior insula, inferior frontal cortex and dmPFC than adolescents with psychopathic tendencies when avoiding stimuli that it would have been better to approach (because appropriate representation of expected values would predict that responding would engender reward)76.

The anterior insula, inferior frontal cortex and dmPFC have been implicated in guiding the individual away from suboptimal choices58,59. Although one study suggested that the functioning of the anterior insula and dmPFC is disrupted in individuals with psychopathic traits82, this disruption is only partial. The recruitment of both regions is comparable to that seen in healthy youths in tests in which they are altering their behaviour in immediate response to punishment cues or during response conflict9,83. As such, the reduced activity may reflect problems in the use of expected value information rather than disruption in these regions perse.

Notably, although youths with conduct disorder and psychopathic traits show the above deficits in decision making and its computational underpinnings, there are no clear indications that these deficits are related to the severity of psychopathic traits specifically.

This is in contrast to the empathy dysfunction discussed above: repeated findings have shown that weaker responses in the amygdala, vmPFC and anterior insula to empathy cues are associated with higher severity of psychopathic traits8,21,48,50. Decision-making deficits may not be specific to psychopathic traits but may also occur in individuals showing high levels of externalizing behaviour.

For example, both individuals with ADHD84–86 and children of alcoholics, who are at risk of developing various externalizing problems, including drug addiction and conduct disorder87,88, show reduced striatal activity in anticipation of rewards89,90. This shared dysfunction may underpin the high comorbidity of conduct disorder with ADHD91 and substance dependence92.

In summary, adolescents with psychopathic traits show reduced representation of reward outcomes and expected value in the vmPFC, as well as reduced reward prediction error signalling and potentially highly atypical punishment prediction error signalling in the striatum. These computational impairments probably underlie the severe decision-making impairments seen in this population. However, these deficits (at least the reduced striatal response to reward) are partially shared by other populations that show increased externalizing behaviour.

Conclusions and future directions
Psychopathic traits are characterized by core impairments in empathy, particularly in the processing of distress cues, and core impairments in decision making, specifically in prediction error signalling and the representation of reward outcomes and expected value. These impairments are associated with dysfunction in the amygdala, vmPFC and striatum, although other brain areas may also be involved (FIG. 2). These impairments, with some exceptions, are also seen in adults with psychopathic traits (BOX 4). Studies in animals are increasing our understanding of these computational impairments.

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Figure 2
A framework for understanding conduct disorder
This model shows the aetiological (genetic and environmental), neural, cognitive and behavioural aspects of conduct disorder. Genetic factors reduce amygdala activation, specifically in response to distress cues, and consequently reduce emotional empathy. Genetic factors may also influence striatal and ventromedial prefrontal cortex (vmPFC) responsiveness to prediction error and expected value information and thereby lead to impaired decision making, but this has yet to be empirically demonstrated. Owing to the extensive interconnections between the amygdala, striatum and vmPFC, early dysfunction in one area is likely to be associated with dysfunction in the others. Perinatal factors, such as maternal substance abuse during pregnancy, can affect the functional integrity of these regions. All of these factors may lead to similar dysfunction at the cognitive level and may result in callous–unemotional traits and in increased antisocial behaviour and instrumental aggression. Impairments in decision making increase the risk that these individuals fail to achieve their goals, become frustrated and demonstrate frustration-based reactive aggression. Specific genetic polymorphisms as well as exposure to trauma, violence and neglect can result in increased amygdala responsiveness, specifically to threat cues. Such increased responsiveness increases threat sensitivity and the likelihood that a threat triggers reactive aggression (as opposed to freezing or escape behaviour). Increased amygdala responsiveness is also associated with an increased risk for anxiety disorders. Thus, patients meeting criteria for conduct disorder can have callous–unemotional traits or high levels of anxiety: callous–unemotional traits are associated with reduced amygdala responses to threat, whereas anxiety is associated with increased amygdala responses to threat. This suggests that there are at least two forms of conduct disorder. The first is referred to here as ‘conduct disorder with psychopathic traits’ and includes behaviours marked in red. The second is known as ‘conduct disorder associated with anxiety and emotional lability’ and includes the behaviours marked in blue (also see BOX 1). Both forms are likely to show under-regulated responses to social provocation (marked in green).

Box 4
Comparing youths and adults with psychopathic traits
Cognitive neuroscience studies have shown similarities and differences between youths and adults with psychopathic traits (see the table; following recent methodological criticisms about some work on adults with psychopathic traits232, this comparison includes only clinical populations that are matched for IQ or for whom IQ differences are statistically considered).

Youths with psychopathic traits and adults with psychopathic traits are notably similar in terms of their functional impairments. Both show reduced psychophysiological responsiveness to the distress of others and impaired recognition of emotional (particularly fearful and sad) expressions, extinction, reversal learning and care-based moral judgement. Adults with psychopathic traits also show impairment on aversive conditioning tasks, but such studies have not yet been conducted in younger individuals.

A comparison of structural MRI (sMRI) studies shows that amygdala volume is reduced in both youths and adults with psychopathic traits. Findings regarding the integrity of the uncinate fasciculus in these groups are inconsistent. In addition, adults with psychopathic traits seem to have reduced structural integrity of the ventromedial prefrontal cortex (vmPFC), but there are no consistent findings in younger patients.

Functional MRI (fMRI) studies have shown reduced functional connectivity between the amygdala and vmPFC in both youths and adults with psychopathic traits. Findings of reduced amygdala responses to emotional provocation in adults with psychopathic traits are similar to reduced amygdala responses to fearful expressions found in youths with psychopathic traits. But studies that specifically examined the response to fearful expressions in adults with psychopathic traits have typically not shown reduced amygdala responses233–235 (but see REF. 236). However, it is difficult to draw conclusions from these studies, as only the study that reported group differences actually observed an amygdala response to fearful expressions in the comparison individuals236.

fMRI studies have shown that youths with psychopathic traits have reduced responsiveness to reward within the vmPFC64,76. However, reward responsiveness has not been investigated in adults with psychopathic traits. Of the two fMRI studies in adults with psychopathic traits that have reported vmPFC dysfunction, one study reported reduced vmPFC differential responsiveness to moral versus non-moral images204, whereas the second study reported increased vmPFC activity in individuals identifying another person’s emotional responsiveness237. Given the differences in task between these two studies and the lack of specific investigations of reward responsiveness, it is not currently possible to conclude whether there is consistency between youths and adults with respect to vmPFC functioning.

Functional impairments (neurocognitive testing)
Psychophysiological responsiveness to the distress
of others
Reduced (as measured by skin
conductance responses)39
Reduced (as measured by skin conductance
Expression recognitionImpaired27,28Impaired27,28
Aversive conditioningUnclearImpaired71
Reversal learningImpaired68Impaired241
Care-based moral judgementImpaired69Impaired199,242,243
sMRI findings
vmPFCInconsistent findingsReduced121,245,246
Uncinate fasciculusInconsistent findingsReduced connectivity103–105
fMRI findings
Amygdala-vmPFC functional connectivityReduced8,83,106Reduced104
Amygdala responsiveness to emotional cuesReduced8,10,30,48,49Reduced203,204,247
vmPFC responsivenessReduced to reward64,76Inconsistent findings

In short, cognitive neuroscience findings in youths and adult with psychopathic traits are relatively similar — this is perhaps not surprising and indicates that the underlying pathophysiology is similar. It is likely that future studies will identify differences. For example, long-term drug abuse, which is increased in individuals with psychopathic traits228, may have progressively deleterious effects on brain structure and function, and may exacerbate pre-existing pathophysiology and cause additional dysfunctions.

A molecular neuroscience-level understanding of this disorder is crucial for the development and refinement of treatments, but this is currently only at an early stage. Importantly, it is now possible to model aspects of the empathy and decision-making impairments in animals. For example, mice show observational learning from the emotional displays of other mice54, and rats can perform a task that is very similar to the passive avoidance task used to study individuals with psychopathic traits179,180. Such animal models allow us to target brain areas for molecular investigation that cognitive neuroscience studies of psychopathic traits have shown to be relevant to the disorder.

Perhaps the most important promise of neurobiological studies into psychopathic traits is that they may identify biomarkers that can provide differential diagnoses and predict long-term prognosis and treatment efficacy. Although differential diagnoses can be provided on the basis of an individual’s overt behaviour and their self-report of impairment, they are prone to environmental influences on behaviour, inaccuracies in self-report and clinician biases. It can be argued that, at least in the future, diagnosis by identifying pathophysiology is more likely to be relevant for treatment decisions181.

Currently, we only have putative fMRI and neurocognitive biomarkers of psychopathic traits8,76. Studies will need to be conducted to determine whether they predict long-term prognosis and treatment efficacy. With respect to prognosis, some preliminary findings show that reduced amygdala volume, reduced aversive conditioning and lower error-related brain activity predict future offending74,182,183.

These will need to be confirmed. Currently, we have no data on whether the putative fMRI and neurocognitive biomarkers of psychopathic traits predict treatment response. Moreover, we have no data on whether current treatments alter the pathophysiology of psychopathic traits. But fMRI studies will allow us the possibility of determining whether current (and novel) treatments address the underlying pathophysiology rather than the immediate behavioural manifestation of this pathophysiology.

There has been rapid development in our understanding of the cognitive neuroscience of psychopathic traits over the past 5 years — the first fMRI studies into the neural correlates of psychopathic traits in youths only appeared in 2008 (REFS 8,9). The collection of data is accelerating and new avenues of research, such as modelling the functional impairments in animals and molecular neuroscience approaches, are becoming available. It is perhaps time to believe that we will soon be able to more effectively help adolescents with psychopathic traits.

reference link:

Original Research: Open access.
Callous-Unemotional Traits Moderate Anticipated Guilt and Wrongness Judgments to Everyday Moral Transgressions in Adolescents” by Margarida Vasconcelos et al.. Frontiers in Psychiatry


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