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Psychophysiological Investigation of Psychopathy: From Robert Hare to Contemporary Research

  • Open Access
  • 01-03-2026
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Abstract

Psychophysiological reactivity has been a critical emphasis in the quest to understand the underlying mechanisms of psychopathy. The combination of reduced affective responding and antisocial behavior in psychopathy sparked questions that called for a structured assessment of the features of this condition – a need that Robert D. Hare addressed through his development of the Psychopathy Checklist, which became the focus of extensive research into autonomic and central nervous system activity and reactivity. This paper reviews the impact of Hare’s initial work on subsequent research which aims at understanding the role of physiological processes in psychopathy and related psychopathic traits as a neurodevelopmental disorder, as somatic aphasia, and as a condition of low fear reactivity and resistance to external stressors, in successful as well as unsuccessful psychopathy. Avenues for future research highlighted by this review include the consideration of developmental trajectories across measures and in relation to the different facets of psychopathy.

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Introduction

Hervey Cleckley described in a subgroup of his inpatients (Cleckley, 1941), which he termed psychopathic, a diminishment of reactivity in situations that normally evoke anxiety or fear, and difficulty learning from experiences involving punishment. These descriptions initiated research on reinforcement learning mechanisms, including punishment based learning (Hare 1965b, 1972), in order to understand the underlying mechanisms. Why was it that psychopathic individuals exhibited deficient emotional reactivity? Would their ostensible cold-blooded mask of sanity be reflected in physiological correlates?
Intrigued by these questions, Robert D. Hare conducted pioneering studies on the psychophysiological underpinnings of fear-based learning using classical conditioning, and due to this work undertook to develop an innovative criterion based assessment tool for psychopathy, the Psychopathy Checklist (PCL; Hare, 1980). Characteristics of low anxiety or fear and failure to learn from punishment were reflected in the PCL’s callous/lack of empathy and shallow affect items, and also in its need for stimulation item (Hare, 1980, 2003). Hare’s seminal early work on classical conditioning and physiological reactivity to threat cues contributed to the development of fear-based theories of psychopathy including Fowles’ (1980) impaired behavioral inhibition system (BIS) conceptualization and Blair’s (2008) amygdala deficit model. Since, the nature and bases of affective response deficits in psychopathy remains a topic of intense interest among researchers, with such deficits being suggested as a driving factor in aggressive and antisocial behavior (Blair, 2007, 2022; Lykken, 1993).
As a tribute to the seminal work of Robert Hare, this article reviews the literature that speaks to some key psychophysiological mechanisms underlying psychopathic behavior, in particular as assessed by the PCL family of assessments (Forth et al., 2003; Hare et al., 2019). We pay particular attention to the ways in which the seminal research contributions from Dr. Hare’s laboratory have flourished and significantly shaped contemporary contributions to the etiology of psychopathy. In doing so we highlight a variety of different psychophysiological perspectives that reflect the diverse and distinctive contributions that Dr. Hare has made to the field, and which promise to have traction in the future. We begin by considering psychopathy as a neurodevelopmental disorder and somatic aphasia as potential core underlying mechanisms and follow this with a discussion of the role of low fear, reduced error-processing, and stress-resistance as psychophysiological characteristics of psychopathy. After a section discussing successful psychopathy as an aspect that was highlighted by Robert Hare, we finish with an outlook on unresolved questions that remain regarding the underlying mechanisms of psychopathy as reflected in its psychophysiological correlates.

Psychopathy as a Neurodevelopmental Disorder

The PCL, first published in 1980 (Hare, 1980), was not the only critical contribution that Robert Hare made. Ten years earlier in 1970 Hare published “Psychopathy: Theory and Research” (Hare, 1970). As the first empirically-oriented book on psychopathy, this slim volume quickly became the go-to publication for psychopathy researchers in the 1970’s. The beauty of the book was that in just 118 pages of text, it succinctly summarized everything that was known at the time on not just psychophysiological correlates and the assessment of psychopathy, but also its social processes and treatment. While it went on to influence a great deal of psychophysiological research in the ensuing decades, it contained a rough diamond that was overlooked in the gold-rush pursuit for the etiology of psychopathy: the idea that psychopathy may have a neurodevelopmental basis.

Differences in Resting State Slow-wave EEG Activity

In his short 9-page chapter on electroencephalogram (EEG), Hare highlighted findings from EEG studies of psychopaths dating back to the 1940’s and early 1950’s (Hare, 1970). Going back to research during World War II for example, Hill and Watterson (1942) found that 48% of those with a psychopathic personality had slow-wave EEG activity compared to 15% of controls. A later review summarizing extensive research from 14 studies based on approximately 1,500 psychopaths further confirmed that 31–58% had some form of EEG abnormality. Hare went on to review many more studies, leading him to the conclusion that:
“…EEG studies of psychopathy have produced rather consistent results. One finding, that the widespread slow-wave activity found in psychopaths bears a certain resemblance to the EEG patterns usually found in children, has led to a cortical immaturity hypothesis of psychopathy” (p.35).
As ever, Hare was judicious in evaluating this hypothesis. How could it explain why some individuals with EEG abnormalities do not become psychopaths? How exactly does slow-wave EEG result in psychopathic behavior? And how can it explain links between the social environment and psychopathy? Nevertheless, Hare believed that there was some substance to this hypothesis that was worthy of pursing. The only problem was that this provocative idea was never really pursued.
Despite raising this challenging hypothesis on the etiology of psychopathy, the idea effectively fell by the wayside, and was only seriously taken up in one review paper which focused exclusively on the idea that psychopathy was a neurodevelopmental disorder (Gao et al., 2009). The very early and indeed large body of psychophysiological research on psychopathy which had started with resting EEG eventually progressed into event-related potentials (ERPs), autonomic measures of electrodermal and cardiovascular activity, and cognitive and affective paradigms capturing more phasic rather than tonic activity (Eisenbarth et al., 2013; Gao & Raine, 2009; Patrick, 1994; Raine, 1989). As we will see, this has led to a rich and informative body of research, but it was never to touch on the concept of neurodevelopment for one simple reason: with rare exceptions (Gao et al., 2010), there is a dearth of longitudinal psychophysiological research on measures such as P300 and the startle blink reflex. In contrast, resting EEG research with its strong grounding in medicine had at an early stage established a very large cross-sectional data-base that charted changes in EEG spectra across age, allowing the excess slow-wave EEG on psychopathy to be mapped onto the presence of excessive slow-wave EEGs in typically developed children. This in turn established the concept that the brains of highly psychopathic individuals are characterized by differences in brain development.

The Neurodevelopmental Hypothesis

What constitutes a neurodevelopmental disorder is rarely if ever defined in the field and can be easily misinterpreted. Establishing a neuropsychological or genetic basis to a condition does not in and of itself qualify that condition as a neurodevelopmental disorder which instead encompasses multiple features. In brief, a neurodevelopmental disorder has its origins in childhood (frequently before grade school), is characterized by abnormalities in brain structure and function throughout development, is accompanied by neurocognitive impairments, has a significant genetic basis, runs a relatively stable course throughout development, without remission or relapse; and continues into adult life, resulting in impaired social, academic, or occupational functioning (Raine, 2018).
We would argue that psychopathy quite clearly is a neurodevelopmental disorder. Psychopathy has its origins in early temperament. For example, in one longitudinal study Glenn et al. (2007) found that 28-year-old adults with a psychopathic personality as measured by Hare’s self-report psychopathy scale were characterized at age 3 years by a lack of fear and a more disinhibited temperament. An extensive body of brain imaging research on psychopathy has clearly documented structural and functional abnormalities in not just highly psychopathic adults (Blair, 2008; Yang & Raine, 2009), but also throughout development in children with callous-unemotional behavior. For example, longitudinal functional imaging research on 283 children documented that abnormal functional connectivity between the medial prefrontal cortex and cingulo-opercular network at birth predicted both higher callous-unemotional traits and lower empathy at age 3 (Brady et al., 2023). Cross-sectional structural imaging research has similarly documented an association between increased callous traits and decreased frontal and temporal cortical surface area in 2,146 10-year-old children (Bolhuis et al., 2019). Extensive research had not just documented a significant genetic basis to psychopathy (Tuvblad et al., 2014; Viding et al., 2005), but also significant neurocognitive impairments (Blair, 2019; Viding & McCrory, 2012). Psychopathy runs a stable course, with reviews arguing that psychopathic-like behavior in childhood and adolescence looks very much like psychopathy in adulthood (Lynam & Gudonis, 2005) and has been linked to callous-unemotional traits and the limited prosocial emotions specifier of conduct problems. Long-term outcomes in psychopathy have been argued to be poor (Stone, 1993), and impaired social, academic, and occupational functioning is near-prototypical in adult life of a highly psychopathic individual (Hare, 2003).
Not only does psychopathy meet core criteria for defining a neurodevelopmental disorder, but this condition is also consistent with other associated features of neurodevelopmental disorders. For example, neurodevelopmental disorders tend to be more common in males, and there is a strong, consistent gender difference in psychopathy that favors males (Cale & Lilienfeld, 2002), a difference which has been argued to be mediated by low resting heart rate (Ling et al., 2023). Furthermore, neurodevelopmental disorders are often comorbid with other neurodevelopmental disorders, and the neurodevelopmental disorder of ADHD has been argued in developmental research to be a core feature of the “fledgling psychopath” (Lynam, 1998). Base rates of neurodevelopmental disorders are often low at about 1–2% (e.g., autism, schizophrenia), and the base rate of psychopathy has similarly been estimated to be low in the general population at approximately 1%, although a higher base-rate of 3.6% has been estimated for the general UK population based on the PCL: SV (Coid & Yang, 2008). In addition, as with other neurodevelopmental disorders, psychopaths are usually a source of significant concern to family members.
Thus, Hare’s seminal highlighting of the cortical immaturity hypothesis more than half a century ago that was predicated exclusively on increased resting slow-wave EEG in psychopaths had profound implications for the consideration of psychopathy as a neurodevelopmental disorder. We will discuss wider implications later in this article.

Psychopathy and Reduced Reactivity to External Stressors and Errors

Robert Hare was a pioneer in the psychophysiological study of emotional processing in psychopathy. His earliest studies on this topic were inspired by two precedent-setting works. One was the portrayal of psychopathy in Cleckley’s (1941, 1976) book, “The Mask of Sanity”, which emphasized affective deficits including lack of remorse and inability to learn from punishment. The other was David Lykken’s (1957) experimental study of anxiousness and fear reactivity in youthful offenders exhibiting psychopathy as described by Cleckley. Drawing on Lykken’s findings and concepts from learning theory (e.g., Miller (1978); Mowrer (1960); Hare (1965a) postulated that psychopathy involves an unusually steep gradient of fear arousal, such that threat-predictive cues fail to evoke the normal anticipatory fear that inhibits actions resulting in punishment. He tested this hypothesis in a series of classic laboratory studies with incarcerated offenders (e.g., Hare 1965b, c) in which he operationalized fear in terms of increases in electrodermal activity (“galvanic skin response”). One of these studies (Hare 1965c) introduced the “countdown” paradigm, entailing measurement of physiological reactivity during anticipation of a signaled noxious event such as shock, which became a cornerstone of theorizing in the psychopathy area (Fowles, 1980; Hare et al., 1978; Lykken, 1995; Patrick, 1994).
Research over the years since Hare’s seminal studies demonstrating reduced anticipatory fear response in psychopathic offenders has examined reactivity to external stressors of other types such as threat cues, physical pain, and social pressure. In addition, another way in which affective reactivity in psychopathy has been studied is in the context of making mistakes, where the recognition of errors can lead to a stress response. Of note, reduced learning from mistakes, along with lack of stress reactivity, were notable features described by Cleckley in his clinical account of psychopathy. We review research along each of these lines in the subsections that follow.

Reduced Reactivity to External Stressors

An aspect of psychopathic personality that Cleckley described as an “absence of nervousness” (1941) is represented in Hare’s PCL-R’s “Shallow affect” item. Stress can arise from different sources, including aversive perceptual stimuli (e.g., threatening visual images, unpleasant sounds), physical challenges such as endurance of pain stimulation, and social challenges such as the need to make a speech. Stressors of these types typically elicit physiological responding, including autonomic nervous system reactivity, muscle tension, hormonal reactions, and related neurophysiological reactions (Kudielka et al., 2009; Kyle & McNeil, 2014; Vanhollebeke et al., 2022; Zis et al., 2022).
Consistent with the idea that psychopathic individuals are generally resistant to stress (Cleckley, 1941), psychopathy has been associated with reduced autonomic nervous system reactivity despite self-reported stress (Gao et al., 2012; Verona et al., 2004). Another consistent finding has been that offenders defined as psychopathic using Hare’s (1991, 2003) PCL-R – in particular, those scoring very high on the PCL-R’s interpersonal-affective (Factor 1) symptoms – fail to show startle-blink potentiation during viewing of aversive picture stimuli, indicating a lack of defensive reflex priming in the face of threat (Patrick et al., 1993; Patrick, 1994). In addition, acute pain seems to be perceived less intensely by individuals from the community scoring high on psychopathy, as evidenced both by increased behavioral tolerance (Brislin et al., 2016; Miller et al., 2014) and reduced neurophysiological response (Brislin et al., 2022). These results for high-psychopathic community participants dovetail with Hare’s (1972) finding of reduced electrodermal reactivity to the experience of a needle injection in male prisoners rated high in psychopathic features.
By contrast, findings regarding physiological responsivity of psychopathic individuals in social stress situations have been mixed. One study found that only the testosterone-cortisol ratio at baseline was related to psychopathy (both affective and lifestyle factors), but not the cortisol response to controllable and uncontrollable stressors (Glenn et al., 2011). Another study employing community participants found that higher psychopathy was related to increased behavioral approach to angry facial expressions, but not to cortisol or testosterone reactivity in this task (Dapprich et al., 2021). However, other work has shown that community participants high on the disinhibition and meanness facets of psychopathy exhibit lower cortisol reactivity to a stronger social stress task using the Trier Social Stress Test (Konzok et al., 2021).
Given the scarcity of investigations in incarcerated populations, further psychophysiological research on resistance to social stress in psychopathy is warranted, especially given the need for larger samples and methodological consistency across outcome measures. Such studies should also focus on behavior and reactivity in dyadic interactions to achieve a better understanding of the underlying mechanisms of aberrant social behavior in high-psychopathic individuals.

Deficient Error Processing

Hare’s early work on threat processing highlighted the role of feedback or error processing. A key human function required to regulate behavior is to monitor one’s own behavior and its effects on oneself and on the environment. It allows one to adjust behavior as a function of the motivation to avoid errors. Individuals high on psychopathy have been found to show less passive avoidance learning (Blair et al., 2004) and stimulus reinforcement learning (Von Borries et al., 2010). In reaction to committing an error, two components in the EEG have been identified, the Error Related Negativity (ERN), which appears following errors regardless of awareness of their occurrence, and the error positivity (Pe), which appears specifically in relation to awareness of error commission (Falkenstein et al., 1991; Hewig et al., 2011). Importantly, ERN and Pe appear with and without feedback about the error’s occurrence.
A recent systematic review and meta-analysis focusing on these error monitoring components and psychopathy addressed the need for aggregating research focusing on neurophysiological components reflecting error processing (Vallet et al., 2020). The 16 studies included in this meta-analysis were based on a variety of task types (Eriksen flanker, Go/NoGo, Simon’s, learning- and empathy-related tasks), forensic and non-forensic samples, as well as a variety of psychopathy measures. In accordance with two earlier systematic reviews (Clark et al., 2019; Schulreich, 2016), meta-analytic evidence showed a reduced ERN related to the PCL-R total score with a small effect size (Cohen’s d = 0.10), and with the impulsive-antisocial component of psychopathy, but no significant reduction of the ERN in relation to the affective component of psychopathy (Vallet et al., 2020). This effect pattern reflects the functional distinction between the components of psychopathy that was also evident, as described above, for fear processing (Patrick, 1994). Importantly, the reduced ERN effect for the impulsive-antisocial component of psychopathy was mainly present for non-forensic samples, not for incarcerated samples, which seems to point to small and non-specific correlate of psychopathic personality traits. In addition, stronger effects (Cohen’s d = 0.25) have been reported across studies based on the Disinhibition dimension of Patrick’s TriPM (2010).
For the Pe, which reflects awareness of errors, Vallet and colleagues’ meta-analysis found evidence for a significant reduction related to the overall psychopathy score (Cohen’s d = −0.21), not to its factors, based on a smaller subset of studies (Vallet et al., 2020). Therefore, the overall conclusion for error processing and psychopathy seems to be that antisocial, externalizing components of psychopathy might be related to reduced neurophysiological error processing, but not affective components and more so in non-forensic samples. This might indicate that error processing correlates could be more specific and only reflect the disinhibition component of psychopathy (see also in younger samples, e.g. Paiva et al., 2020; Ribes-Guardiola et al., 2020).
Taken together, Robert D. Hare’s work on reduced anticipatory fear response in psychopathic offenders had substantial impact on the development of subsequent investigations into processing of external stressors yielding important implications for the psychophysiological underpinnings of thrill-seeking and stress tolerance. However, not all external impacts seem to be processed differently in psychopathy, therefore, future work will need to differentiate the context of those external stimuli to build foundations for potential treatment targets.

Psychopathy as Somatic Aphasia

Reduced physiological responsiveness to stressors/threat seen in those with high psychopathic traits may be associated with their low sensitivity to internal physiological changes and thus lack of fear experiences. In another seminal work of Hare, he pointed to the potential relevance of resting state neural activity (1970). He suggested that resting state neural activity might be related to a classical clinical description of psychopathic traits, which involves the disconnect between physiological and self-report indicators of emotional reactivity. According to Cleckley’s (1976) original conceptualization of psychopathy, one definitive diagnostic marker for this condition is a disconnect between linguistic and experiential components of emotion, a condition he called “semantic aphasia”. Cleckley’s idea was that psychopaths have difficulty understanding the emotional content of words, an impairment that could underly many of their symptoms, in particular their inability to understand the significance of their antisocial actions.
Taking this idea further, interoception, which includes awareness (one’s conscious feeling of physiological processes in the body) and accuracy (one’s ability to accurately perceive the physiological process), has been argued to be crucial to the subjective experience of emotion (e.g., Damasio, 1994). The inability to recognize and understand one’s own bodily signals may contribute to emotion processing deficits and lack of empathy (e.g. Ainley et al., 2016), important features of psychopathy (Northam & Dadds, 2020; Waller et al., 2020). Neuroimaging evidence has also implicated a primary interoception network, including the insular-frontotemporal region, in emotion processing and regulation (Adolfi et al., 2017), and its disruption has been found in individuals with psychopathic traits (Yang & Raine, 2009). However, the notion that psychopaths have fundamental issues with recognizing and understanding their internal bodily signals and emotional experiences has not been examined widely until relatively recently.
Interoceptive awareness and accuracy can be assessed through self-report or objective measures such as skin conductance levels and heart rate (Murphy et al., 2019). In one of the earliest studies to directly examine interoception in psychopathy, 138 adult men recruited from local temporary employment agencies completed a stressor in which they were asked to give a 2-min speech about their worst faults while their skin conductance responses and heart rate were recorded (Gao et al., 2012). Psychopathic traits were assessed using the PCL-R. A disconnect which the authors termed “somatic aphasia” was documented between perceived bodily reactions and objective measures of physiological reactivity in those high in psychopathic traits. In particular, this deficit was found to be associated with the affective-interpersonal factor of psychopathy. In a later study attempting to replicate these findings, male and female participants from college and community settings (n = 114) completed a social stressor task in which they were socially excluded by peers while their skin conductance and heart rate responses were recorded (Gao et al., 2026). They were then asked to rate their bodily sensations during the task, and self-reported psychopathic traits on the Psychopathic Personality Inventory – Revised (PPI-R; Lilienfeld & Widows, 2005). It was found that lower interoceptive accuracy, reflected by a disconnect between psychophysiological reactivity and self-reports of bodily reaction, was associated with the self-centered impulsivity dimension of psychopathy.
A few studies have also found the interoception deficits to be associated with the impulsivity-antisocial factor or secondary psychopathy. Nentjes et al. (2013) found that reduced heartbeat detection accuracy was associated with the PCL-R Facet 4 (antisocial) but no other facet scores in 75 male personality disordered offenders. In a study using the Triarchic Psychopathy Measure (TriPM; Patrick, 2010) to assess psychopathic traits, Ellis, Schroeder, Patrick, and Moser (2017) found that individuals who scored high on boldness demonstrated reduced emotional reactivity, as indexed by smaller late positive potential response to negative versus neutral picture stimuli, although their self-reported emotional reactivity was similar to those with low boldness. Instead, those high on boldness tend to over-report experiencing greater emotional reactivity when asked to increase or decrease their emotions. This over-reporting may reflect their efforts to conceal blunted emotional responses, or their enhanced attention to the emotional content of the pictures when cued to (Ellis et al., 2017).
In one recent study of 64 male and female inmates (Lamoureux & Glenn, 2021), psychopathic traits assessed by the PCL-Screening Version (Hart et al., 1995), and interoceptive ability was assessed using a heartbeat tracking task and a self-report measure. No significant relationships were found between levels of psychopathic traits and interoceptive awareness or accuracy.
Taken together, the empirical evidence to date has generally supported the notion of Hare that psychopaths show a disconnect between physiological activity and experiences of emotion, in terms of interoception deficits. Individuals high on psychopathic traits seem to have difficulty accurately perceiving their own bodily signals, although findings are not entirely consistent. Using self-report combined with objective psychophysiological measurements, studies have generally found that reduced interoception is associated with the Factor 2 of PCL-R or secondary psychopathy. Future studies with larger samples and multi-modality methods (i.e., self-report, behavioral performance, and physiological recording) are needed to further determine the interoception deficits in psychopathy. Pressing questions include what brain mechanisms may underlie this condition, and whether longitudinal research can establish whether interoception deficits are part of the characteristics of a neurodevelopmental disorder of psychopathy.

Psychopathy - Its Successful and Unsuccessful Variants

One line of Hare’s work has focused on a specific psychopathic population that is successful beyond not being in prison or a forensic institution, such as in the workplace or in specific social contexts (Babiak & Hare, 2007; Hare, 1994; Mullins-Sweatt et al., 2010). Hare (2002) stated that “Not all psychopaths are in prison. Some are in the board room”, and in fact, studies have demonstrated that the base rate of psychopathy in the upper ranks of corporations may be as high as 3% compared with 1% in the general population (Babiak et al., 2010). Further, his work has suggested that the latent dimensions and general nature of psychopathy are same across a wide diversity of samples, including offenders, psychiatric, community, and corporate samples (Babiak et al., 2010; Babiak & Hare, 2006; Hare & Neumann, 2008). Inspired by this work, increasing number of studies have been conducted to explain the differences and similarities between successful and unsuccessful psychopathy.
One of the major challenges faced in this research area of successful psychopaths concerns the inconsistency or ambiguity in the literature on conceptualizing, operationalizing, and measuring “successful” psychopathy (Glenn & Raine, 2014; Steinert et al., 2017; Wallace et al., 2022). In one of the earlier definitions, successful psychopaths were defined as individuals scoring high in psychopathy who have never been convicted of a crime. Using this definition, Ishikawa, Raine, Lencz, Bihrle, and LaCasse (2001) recruited successful (higher PCL-R score and no prior convictions) and unsuccessful psychopaths (higher PCL-R score with at least one criminal conviction) together with non-psychopathic controls from local employment agencies in the Los Angeles area. It was found that although unsuccessful psychopaths showed reduced heart rate stress reactivity and impaired executive functioning (Wisconsin Card Sorting task) as typically seen in incarcerated psychopaths, successful psychopaths from the community showed heightened stress reactivity and significantly outperformed non-psychopathic controls on the executive functioning task. In a different sample using the same recruitment technique and operationalization of “successful psychopathy”, Gao et al. (2011) found that unsuccessful psychopaths reported experiencing more childhood physical abuse, and more importantly, they showed reduced P3 amplitudes to target stimuli, demonstrating their difficulties in allocating attention to task-relevant stimuli. In contrast, successful psychopaths had larger P3 amplitudes and shorter P3 latency to irrelevant non-target stimuli, suggesting enhanced cognitive abilities in this subgroup. It is therefore hypothesized that enhanced autonomic and CNS functioning, along with better executive functioning, may protect a subgroup of psychopaths from being detected and arrested, while allowing them to still perpetrate significant harm to others in the community (Gao et al., 2020; Gao & Raine, 2010).
In this regard, Patrick et al. (2009)’s triarchic model of psychopathy emphasizes three core phenotypic constructs (Disinhibition, Boldness, Meanness) and provides a framework that is particularly relevant to the workplace. According to the moderated-expression model, successful psychopathy is explained by protective factors that play a buffering role against psychopathic manifestations of maladjustment and deviance (Hall & Benning, 2006; Lilienfeld et al., 2015). Specifically, it proposes that external factors or certain psychopathic traits such as boldness or fearless dominance, moderate the effect of core psychopathic traits such as affective deficits on severe antisocial behaviors. Therefore, enhanced autonomic responding and executive functioning (Ishikawa et al., 2001), superior brain functioning (Gao et al., 2011), and positive childhood experiences (Waller et al., 2013), characteristics likely associated with the boldness and fearless dominance features of psychopathy, may help these individuals adopt more socially adaptive strategies and protect them from manifesting serious antisocial behavior. This is turn decreases the likelihood of being incarcerated or premature death (Gao & Raine, 2010). High intelligence has also been theorized to play such a protective role, although empirical studies are needed to test if higher levels of intelligence may reduce the risk of deviant behaviors exhibited by those with psychopathic traits (Persson & Lilienfeld, 2019; Wall et al., 2013).Alternatively, some have proposed that successful psychopaths show a pattern that is different from the pattern of other psychopaths. According to this differential-configuration model, some adaptive features, such as fearless dominance or boldness, may be the key to distinguish those who are successful from others (Lilienfeld et al., 2015). Finally, a few studies have failed to support the notion that some psychopathic traits contribute to a successful life and questioned the existence of successful psychopaths (Kiehl & Lushing, 2014). It is important to note that psychophysiological evidence for the latter two theories is lacking.
In conclusion, despite the burgeoning interest in successful psychopathy, there is not a unified approach to define and conceptualize this construct, likely due to lack of clear conceptualization of “success” for psychopaths (Wallace et al., 2022). Overall, some adaptative features, such as boldness and other features from Factor 1 of the PCL-R, may contribute to their success in workplace and other social contexts. Nonetheless, more search is needed to allow a better understanding of the theoretical mechanisms together with a working definition of successful psychopathy. Most of the research to date has relied on a diverse mixture of self-report measures and rating inventories. Given that psychopathic individuals may be manipulative and dishonest, future work should integrate self-report and other-observant methods to provide more reliable and valid measures of psychopathic traits. Furthermore, significant amount of the research to date has utilized undergraduate students who by definition have achieved significant success; as such establishing the correlates of further success may be susceptible to ceiling effects. Finally, almost all research is cross-sectional, precluding inferences regarding temporal precedence. Prospective longitudinal research is needed to understand the directionality of the relationships.

Open Questions and Future Directions

Though some questions that Robert Hare initiated with his aim to understand reinforcement learning in psychopathy have been answered, differences in learning as reflected in psychophysiological measures are still under investigation. In fact, throughout this paper, we have argued that there are a lot of open questions that need further investigation to clarify the developmental pathways of psychopathy reflected in psychophysiological correlates and to derive indications for treatment (Kyranides et al., 2017).
There are wider implications from the perspective of psychopathy as a neurodevelopmental disorder. First, if the field was to reconceptualize psychopathy as a neurodevelopmental disorder, that classification could potentially be used as a mitigating factor in criminal cases. In much the same way that an autism-spectrum diagnosis may influence jurors’ perceptions (Berryessa et al., 2015), viewing psychopathy as a condition that emanates from very early factors beyond the individual’s control could influence decisions in death penalty cases. Whether this would be construed as a welcome or unwelcome development is a matter of some debate.
Second, there could be implications for risk assessment. On the one hand, if psychopathy is viewed as neurodevelopmental in nature, sentencing could be longer for psychopaths if it were felt that their neurodevelopmental nature meant that the individual could not be treated. Similarly, parole prospects may be diminished if it were believed that the neurodevelopmental underpinnings of the condition precluded future change in behavior. On the other hand, treatment opportunities need to be further investigated as the current knowledge about successful treatment in adults (as opposed to young people) is very limited.
Third, considering adult psychopathy as neurodevelopmental in origin could result in most children with significant callous-unemotional traits also being considered to suffer from a neurodevelopmental condition. This in turn may attract greater clinical attention to this condition and result in a redoubling of efforts to develop interventions for this childhood condition based on empirical findings for effective treatments (Fleming et al., 2023; Perlstein et al., 2023), and potentially prevent its development into adult psychopathy. Indeed, if psychopathy is a neurodevelopmental disorder, then interventional efforts would likely be most effective when they start in early childhood or infancy, or indeed as some have called for, as early as the newborn period (Brady et al., 2023). Whether it would be ethically advisable to screen and intervene at an early age is again a matter of debate.
If we were to derive a list of priorities for future research based on the open questions, these should include the following considerations.
  • Considering psychopathy as a neurodevelopmental disorder given the physiological intricacies that Hare’s research started asks for longitudinal studies that include neurophysiological resting state and reactivity measures.
  • While Hare’s research started with a male offending populations, his research already suggested the need for consistently investigating gender differences across the research.
  • The differential role of psychopathy subtypes, e.g. dominance of presentation based on Factor 1 or 2 of the PCL-R and overlap with self-reported psychopathic traits need to be standard in psychopathy research.
  • Tracing back to the slow-wave EEG activity differences, combining functional and structural brain imaging methods with autonomic nervous system methods and behavioral outcomes to allow the systematic investigation of psychophysiological mechanisms in the behavioral context.
  • Systematically review and meta-analyze the relationship between correlates of PCL-R and self-report assessed psychopathy, especially to increase the understanding of successful versus non-successful psychopathy.

Conclusions

There are several conclusions that can be drawn from the psychophysiological research on psychopathy to date. First, there is strong evidence for psychopathy demonstrating characteristics of a neurodevelopmental disorder, which needs to be considered in future investigations into psychophysiological correlates of PCL-assessed psychopathy. Second, low resting heart rate seems to be an important indicator for psychopathy and as a precursor of callous-unemotional traits. Third, the evidence for a reduced interoceptive awareness in psychopathy might relate to low resting heart rate and the related low physiological reactivity to fear-eliciting cues. Fourth, subjective and physiological responding to emotional stimuli cannot be equated, but this dissociation between responses within the same person to a single cue is actually providing us not only with insights into the nature of psychopathy but also into the nature of human emotional reactivity more broadly (Marsh, 2013). Last but not least, increasing our understanding of the psychophysiological correlates in successful (compared to non-successful) psychopathy needs to advance to be able to differentiate psychopathy from its related but yet different construct, antisocial personality disorder (Leistico et al., 2008). As Robert Hare has described the move towards integration of models, theories using neuro- and psychophysiological measures: “A notable trend is the interest shown by neuroscientists in using psychopathy as a vehicle for evaluating their own models of behavior, personality, and brain function. The result may ultimately be an integration of psychopathy theory and research with more general psychobiological, behavioral genetic, developmental, and personality models.” (Hare & Neumann, 2008 p. 240).

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Titel
Psychophysiological Investigation of Psychopathy: From Robert Hare to Contemporary Research
Auteurs
Hedwig Eisenbarth
Christopher J. Patrick
Yu Gao
Adrian Raine
Publicatiedatum
01-03-2026
Uitgeverij
Springer US
Gepubliceerd in
Journal of Psychopathology and Behavioral Assessment / Uitgave 1/2026
Print ISSN: 0882-2689
Elektronisch ISSN: 1573-3505
DOI
https://doi.org/10.1007/s10862-026-10274-8
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