Why one of the most stigmatized neurological conditions may also be one of the most misunderstood
The word “psychopath” conjures images of serial killers and corporate predators, Hannibal Lecter behind glass or Patrick Bateman with an axe. But the neurological profile we call primary psychopathy, characterized by constitutional differences in emotional processing rather than antisocial behaviour, may be better understood not as proto-criminality, but as a form of neurodivergence: a different way of being human, one that exists on a spectrum and carries both challenges and advantages depending on context.
This reframing is not about excusing harm or romanticizing predation. It is about recognizing that our current framework, developed in prisons, designed to predict recidivism, and saturated with moral condemnation, fails the many people with these neurological differences who never commit crimes, who contribute to society, and who deserve a path to self-understanding that doesn’t require them to see themselves as monsters in waiting.
The Forensic Framework and Its Limitations
To understand why a reframing is needed, we must first understand how psychopathy came to be defined. The dominant framework in both research and clinical practice is Robert Hare’s Psychopathy Checklist-Revised (PCL-R), developed in the 1970s and 1980s. The PCL-R assesses twenty items grouped into two factors. Factor 1 captures affective and interpersonal traits: shallow affect, callousness, lack of remorse, manipulativeness. Factor 2 captures antisocial and lifestyle traits: impulsivity, irresponsibility, criminal versatility, early behavioral problems.
Hare developed this instrument in prisons, studying incarcerated populations to identify individuals at highest risk of reoffending. As a predictive tool for criminal justice contexts, the PCL-R has proven useful. But somewhere between its narrow forensic origins and its current cultural dominance, it became the definition of psychopathy itself, and that is where the problems begin.
The first problem is selection bias. When your entire research sample comes from prisons, you will inevitably conclude that your construct predicts criminality. This is circular: develop a tool in prison, identify “psychopaths” in prison, conclude that psychopathy equals criminal. But this tells us nothing about the prevalence or expression of these traits in people who never enter the criminal justice system; surgeons, crisis negotiators, bomb disposal technicians, or the estimated one to three percent of the general population who would score high on Factor 1 traits while leading ordinary, law-abiding lives.
The second problem is etiological conflation. Factor 1 and Factor 2 traits have fundamentally different origins. Factor 1 traits, the affective and interpersonal characteristics, show strong heritability, appear early in development, and correspond to measurable neurological differences. They are constitutional. Factor 2 traits, by contrast, are often trauma-induced, environmentally shaped, and associated with adverse childhood experiences. Lumping them together in a single construct obscures these crucial distinctions.
Jennifer Skeem and David Cooke’s landmark 2010 analysis, published in Psychological Assessment, argued that criminal behavior is not a central component of psychopathy but rather a downstream consequence that depends on other factors. When you separate Factor 1 from Factor 2, the relationship between core psychopathic traits and violence becomes much weaker than commonly assumed. The monster narrative dissolves under scrutiny.
The third problem is perhaps the most insidious: the moralization of neurology. Under the current framework, reduced affective empathy is not treated as a processing difference but as a moral failing. People with these traits are not described as wired differently; they are described as lacking conscience, as manipulative, as evil. The very language used “cold,” “callous,” “remorseless” transforms neurological variation into character indictment.
We would not say that a person with color blindness lacks moral fiber because they cannot distinguish red from green. We would not suggest that someone with prosopagnosia is deliberately refusing to recognize faces. Yet the same courtesy is not extended to those whose brains process emotional information differently. The assumption that feeling what others feel is prerequisite to treating them well, that morality requires emotional mirroring, is so deeply embedded in our culture that we forget it is an assumption at all.
Inside the Brain: The Neurological Basis of Primary Psychopathy
If we are to argue that primary psychopathy belongs under the neurodivergence umbrella, we must first establish that it has a clear neurological basis. The evidence here is remarkably robust, in some ways, more so than for conditions already accepted as neurodivergent.
Kent Kiehl has spent decades scanning the brains of thousands of individuals, documenting consistent differences in those with high psychopathy scores. His work, synthesized in his 2006 paper in Psychiatry Research and his book The Psychopath Whisperer, points to dysfunction in the paralimbic system, the brain regions involved in processing emotion, especially the amygdala and surrounding structures.
The amygdala differences are perhaps the most replicated finding. Individuals with high Factor 1 traits show reduced amygdala volume and reduced reactivity to stimuli that would normally trigger fear or distress responses. This is not about being immune to all emotion, anger, frustration, and pleasure may be experienced normally or even intensely. But the specific circuits that respond to others’ fear, that generate the visceral discomfort of witnessing suffering, that produce the physiological markers of guilt and shame, these are attenuated.
Adrian Raine’s work, chronicled in The Anatomy of Violence, documents differences in prefrontal-limbic connectivity. The communication pathways between the brain’s emotional centers and its rational decision-making regions operate differently in individuals with high psychopathy scores. This does not mean impaired reasoning, indeed, reasoning may be enhanced by reduced emotional interference, but it does mean that emotional inputs are weighted differently in the decision-making process.
The fear response itself is measurable. In studies using the startle reflex paradigm, individuals with primary psychopathic traits show attenuated startle responses to threatening stimuli. Their physiological fear response, increased heart rate, sweating, cortisol release, is dampened. Again, this is not a choice or a moral failing. It is hardware.
Perhaps most compellingly, Essi Viding’s 2005 twin study, published in the Journal of Child Psychology and Psychiatry, found substantial genetic risk for callous-unemotional traits in seven-year-olds. The heritability estimates are comparable to or higher than those for other conditions we readily accept as neurodevelopmental. These traits are present from early development, not acquired through bad choices or moral corruption.
James Fallon’s case adds an unexpected dimension. A neuroscientist who had spent years studying the brains of psychopaths, Fallon discovered through his own research that he possessed the neurological markers and genetic risk factors for psychopathy. His book The Psychopath Inside chronicles his attempt to reconcile this discovery with his life as a husband, father, and researcher who had never committed a violent crime. Fallon attributes his trajectory partly to a stable, loving upbringing, suggesting that environment can profoundly shape how these neurological differences manifest.
R. J. R. Blair’s 2013 review in Nature Reviews Neuroscience synthesizes the developmental neurobiology, emphasizing that the neural differences observed in adults with psychopathic traits are present in children with callous-unemotional traits, and that these differences affect specific emotional learning processes rather than representing global cognitive impairment.
Two Kinds of Empathy: A Crucial Distinction
To understand primary psychopathy accurately, we must distinguish between two empathy systems that are often conflated in popular discourse.
Affective empathy is the capacity to feel what others feel, to experience emotional resonance with their states. When you wince watching someone stub their toe, when your chest tightens seeing a child cry, when you cannot help but smile at someone else’s joy, that is affective empathy. It is automatic, visceral, and involuntary.
Cognitive empathy is the capacity to understand what others feel, to model their mental states, take their perspective, predict their reactions. This is what psychologists call “theory of mind.” It is more deliberate, more intellectual, and does not require feeling the emotions in question.
Simone Shamay-Tsoory’s 2009 research in Brain demonstrated that these are dissociable systems, supported by different neural circuits. Damage to one can leave the other intact. And in primary psychopathy, we see a characteristic pattern: affective empathy is reduced or absent, while cognitive empathy is often intact or even enhanced.
This distinction matters enormously. The common assumption is that someone who does not feel your pain cannot understand or respond appropriately to it. But this is simply false. A person with reduced affective empathy can still recognize that you are suffering, can still understand that suffering is bad for you, can still choose to help alleviate it, they just will not feel the automatic emotional pull that typically motivates such behavior. They must rely instead on cognitive understanding and deliberate choice.
Paul Bloom’s book Against Empathy argues provocatively that cognitive empathy plus rational ethical frameworks may actually produce better moral outcomes than affective empathy alone. Affective empathy is biased: we feel it more strongly for those who look like us, for individuals rather than groups, for nearby rather than distant suffering. A surgeon who felt the pain of every incision would be unable to operate. A triage nurse who became emotionally overwhelmed by each patient would fail to make the hard decisions necessary to save the most lives.
This is not to say that reduced affective empathy has no costs, clearly it does. But the assumption that morality requires emotional mirroring is philosophically contestable. Immanuel Kant built his entire ethical framework on reason, not sentiment. John Rawls asked us to reason from behind a veil of ignorance, deliberately setting aside our emotional attachments. The idea that one can behave ethically through rational commitment rather than emotional resonance is well-established in moral philosophy, it simply has not penetrated our cultural understanding of psychopathy.
The Case for Neurodivergence: Why Primary Psychopathy Qualifies
Neurodivergence, as a concept, emerged from the autism rights movement in the late 1990s. Judy Singer coined the term to describe neurological differences as natural human variation rather than pathology, a shift from “disorder” to “difference” framing. The neurodiversity paradigm now encompasses autism, ADHD, dyslexia, dyspraxia, Tourette syndrome, and other conditions characterized by constitutional differences in brain development and function.
The criteria for inclusion are not perfectly codified, but certain characteristics emerge across accepted neurodivergent conditions: clear neurological basis, presence from early development, high heritability, representation of variation rather than degeneration, existence on a spectrum, and context-dependent functionality (advantages in some environments, disadvantages in others).
Primary psychopathy meets every one of these criteria. The neurological basis is well-documented, arguably better documented than for some conditions already under the umbrella. The traits are present from childhood, as demonstrated by research on callous-unemotional traits in young children. The heritability is substantial. The condition represents variation in emotional processing, not cognitive degeneration. It exists on a spectrum, from mild trait elevation to more pronounced presentations. And it shows clear context-dependence: the same traits that might predispose someone to antisocial behavior in a chaotic, violent environment might produce an exceptional emergency room physician, military strategist, or crisis negotiator in the right context.
The parallel with autism is instructive. Within living memory, autism was understood as a devastating pathology, often blamed on “refrigerator mothers” whose coldness supposedly caused their children’s withdrawal. Autistic people were institutionalized, subjected to harmful “treatments,” and denied agency. The reframing of autism as neurodivergence, pioneered by autistic self-advocates and eventually embraced by much of the research community, transformed outcomes. It enabled autistic people to understand themselves without shame, to access accommodations rather than cures, to have their strengths recognized alongside their challenges, and to build communities of mutual support.
Both autism and primary psychopathy involve atypical social-emotional processing, though in different directions. Both are stigmatized based on worst-case presentations. Both involve genuine challenges alongside genuine advantages. And both would benefit from a framework that treats difference as difference rather than as deficiency or evil.
Kevin Dutton’s research on “successful psychopaths” individuals with high Factor 1 traits who have achieved success in fields like surgery, law, and business demonstrates that these traits are not inevitably paths to harm. Scott Lilienfeld’s 2015 review on “successful psychopathy” in Current Directions in Psychological Science identifies individuals who score high on fearless dominance and stress immunity while showing low antisocial behavior. Gao and Raine’s 2010 neurobiological model in Behavioral Sciences & the Law distinguishes successful from unsuccessful psychopaths based on intact prefrontal functioning. These are not exceptions that prove the rule; they may represent the rule that forensic-focused research has obscured.
The Hard Questions: Addressing Objections
A proposal this significant cannot proceed without engaging serious objections. There are at least four that demand honest attention.
“Psychopathy is associated with harm. You cannot include something dangerous in a framework about acceptance.”
This objection carries real weight. The statistical association between psychopathic traits and harmful behavior is not zero, even when we focus on Factor 1 alone. Some people with these traits do cause genuine suffering, and victims’ experiences cannot be dismissed.
But several points complicate this picture. First, the harm association is significantly confounded by Factor 2 traits and by forensic sampling bias. When Skeem and colleagues examined Factor 1 alone in non-forensic populations, the relationship to violence weakened substantially. Second, most people with primary psychopathic traits never commit crimes we simply do not study them because they are not in our prisons or clinics. Third, environment powerfully mediates outcomes: Fallon’s case illustrates how the same neurological profile can produce very different life trajectories depending on context.
Fourth, and crucially, autism and ADHD can also be associated with harmful behaviors. Autistic meltdowns can involve aggression. ADHD impulsivity can lead to actions that hurt others. We do not exclude these conditions from the neurodivergence framework for that reason. We recognize that explanation is not excuse, that neurological understanding does not eliminate accountability, and that most people with these conditions navigate the world without harming others.
The same framework should apply to primary psychopathy. Reframing it as neurodivergence does not mean excusing bad behavior. It means separating “wired differently” from “destined to harm.” People remain accountable for their choices regardless of their neurology. What changes is the default assumption from “dangerous until proven otherwise” to “different, with behavior depending on choices and circumstances.”
I acknowledge, however, that any reframing must not become a shield for bad behavior. “I have reduced affective empathy” cannot become a get-out-of-jail-free card. The language matters. The framework must maintain behavioral standards while offering a less stigmatizing path for those who meet them.
“This dilutes neurodivergence and harms existing communities.”
Neurodivergent communities have fought hard for recognition and acceptance. It is reasonable to ask whether adding a condition associated with manipulation and harm might contaminate that hard-won progress.
The response here must be humble rather than assertive. The criteria for neurodivergence are met on principled grounds, the neurological basis is real, the developmental origin is clear, the heritability is established. The category is already expansive, including conditions as different as dyslexia (a reading difference) and Tourette syndrome (a movement difference). There is no principled reason to exclude emotional processing differences.
But I acknowledge that existing neurodivergent communities may not want this association. The framing should be developed in dialogue, not imposed. Perhaps the right model is “separate but allied,” under the conceptual umbrella of neurodivergence without demanding inclusion in specific communities or support groups. Different conditions have different needs and should not be homogenized.
“People will use this as an excuse for bad behavior.”
This is perhaps the most common objection, and it is not unfounded. The history of “my brain made me do it” defenses is troubling, and extending this framework to a condition already associated with manipulation invites abuse.
But this problem is not unique to psychopathy. Every neurological explanation faces the same challenge. People have claimed their ADHD made them cheat, their autism made them inappropriate, their depression made them abusive. We manage these claims not by refusing to acknowledge the conditions, but by maintaining that explanation is not excuse. Understanding why someone did something does not mean they are not responsible for doing it.
The alternative; continued stigmatization, does not prevent bad behaviour either. It simply forces people with these traits into hiding, denies them access to support, and makes it harder to develop adaptive strategies. A person who cannot acknowledge their reduced affective empathy cannot develop compensatory mechanisms for it.
The risk is real and must be actively managed through language and framing. “I have reduced affective empathy, so I must work harder to consider others’ perspectives” is very different from “I have reduced affective empathy, so I cannot help hurting people.” The framework must emphasize the former while vigilantly rejecting the latter.
“The science is not settled enough for this reframing.”
Science is never perfectly settled, and epistemic humility is warranted. There are genuine debates about whether psychopathy is best understood as categorical or dimensional, about how separable Factor 1 and Factor 2 really are, about the precise neural mechanisms involved. Edens and colleagues’ 2006 taxometric analysis in the Journal of Consulting and Clinical Psychology found evidence for dimensional rather than categorical structure, suggesting psychopathic traits exist on a continuum rather than as a discrete category.
But the bar cannot be perfection. The neuroscience of Factor 1 traits is actually quite robust, more robust than the evidence was for autism or ADHD when their reframings began. Waiting for perfect certainty means people continue to suffer under a framework that treats them as monsters. At some point, the evidence becomes sufficient to act while remaining open to revision.
I accept that the reframing should be held provisionally and updated with new evidence. Overclaiming would undermine credibility. This is not a definitive pronouncement but an invitation to shift the conversation, to begin exploring what would follow if we took the neurodivergence framing seriously while remaining alert to evidence that might challenge it.
What We Would Gain: The Benefits of Reframing
If the objections can be addressed, what would be gained by adopting a neurodivergence framework for primary psychopathy?
For individuals with these traits, the benefits would be profound. Consider the difference between “my brain processes emotions differently” and “I am fundamentally broken and potentially evil.” The first framing allows for self-understanding without self-hatred, for acknowledging challenges while also recognizing strengths. It opens the door to seeking support, something nearly impossible under the current framework, where disclosing psychopathic traits risks being treated as a danger rather than a person seeking help.
For families and children, the benefits are equally significant. Parents of children with callous-unemotional traits currently face a devastating prognosis: your child may be a future psychopath. The neurodivergence framework would offer something different: your child’s brain develops emotional processing differently; here is how to support them, channel their traits positively, and help them build a good life. Viding and McCrory’s 2018 review in Psychological Medicine emphasizes that developmental trajectories are not fixed and that early intervention can shape outcomes. The fear would be replaced by guidance. The stigma would be replaced by strategy.
For society, the benefits include better talent utilization. People with primary psychopathic traits are overrepresented in certain high-functioning roles: surgery, emergency response, military special operations, crisis negotiation. These are not accidents; these are environments where reduced fear response, emotional detachment under pressure, and clear-eyed decision-making are genuine assets. A neurodivergence framework would enable earlier identification of these traits and proactive matching to contexts where they are adaptive rather than waiting to see if they manifest as crime.
For science, the benefits include access to populations that current research neglects. Nearly everything we know about psychopathy comes from prisons and forensic clinics. A destigmatized framework would enable recruitment of non-forensic samples, community studies, developmental research that follows children from early trait identification through adulthood. We would finally learn the full range of outcomes associated with these traits, not just the worst ones.
Implementation: From Theory to Practice
What would this reframing look like in concrete terms?
Screening would shift from risk assessment to developmental identification. Instead of asking “is this child likely to become a criminal?” we would ask “does this child show affective processing differences that might benefit from early support?” The goal would be accommodation rather than surveillance, understanding how to help the child develop prosocial strategies, not flagging them for future monitoring. Salekin’s 2017 review in the Journal of Child Psychology and Psychiatry emphasizes that psychopathic traits in children are malleable and that intervention approaches show promise.
Education would adapt to different learning styles. For children with reduced affective empathy, teaching ethics through emotional appeals (“how would you feel if someone did that to you?”) is ineffective because they genuinely do not feel it the same way. Alternative approaches—game theory, rational ethics, contractual frameworks, explicit social scripts, can be equally effective at producing prosocial behavior while working with rather than against the child’s neurology.
Career guidance would identify high-fit roles early. Instead of discovering in adulthood that one’s traits are well-suited to certain professions, individuals could be guided toward paths where their neurology is an asset. Mentorship from successful adults with similar traits could provide models of how to channel the profile positively.
Therapy and coaching would adapt to different emotional architectures. Current therapeutic approaches often assume neurotypical emotional processing, building emotional awareness, increasing empathic resonance, processing feelings. For someone whose brain does not generate those responses, such approaches are frustrating at best and alienating at worst. Adapted approaches would focus on cognitive strategies, behavioral commitments, and rational frameworks for prosocial behavior.
Language itself might evolve. “Primary psychopathy” carries so much forensic baggage that some researchers have suggested alternative terminology. “Low-affective-empathy neurodivergence” is clunky but descriptive. Whatever the eventual terminology, it should describe the neurological difference without the moral condemnation embedded in current language.
Conclusion: Toward a Different Conversation
The argument presented here is not that primary psychopathy is unproblematic, that people with these traits face no genuine challenges, or that society has no legitimate interests in preventing harm. The argument is that our current framework, forensic in origin, moralized in application, stigmatizing in effect, fails both individuals with these traits and the society that might benefit from their contributions if properly channeled.
Reframing primary psychopathy as neurodivergence would not solve all problems. Some people with these traits will still make harmful choices, just as some neurotypical people do. But it would offer a path forward that does not require seeing oneself as a monster, that enables help-seeking rather than hiding, that focuses on channeling traits productively rather than merely suppressing them, and that might ultimately produce better outcomes for everyone.
Fifty years ago, autism was understood as a tragedy to be prevented, a disorder to be cured, a deviation to be corrected. Parents were blamed, children were institutionalized, autistic voices were silenced. Today, while challenges remain, the landscape has transformed. Autism is understood as a neurological difference, autistic people are recognized as full participants in society, and the “cure” framework has given way to one of accommodation and acceptance.
The same shift is possible for primary psychopathy. It will be harder, the association with harm is stronger, the stigma is deeper, the cultural resistance is fiercer. But the scientific basis is there, the conceptual framework is there, and most importantly, the people who would benefit are already there: living with these traits, struggling against the monster narrative, seeking understanding in a world that offers only condemnation.
The answers are not certain, the path is not clear, and the resistance will be substantial. But for the people who need this framework; who exist right now, who are struggling right now, who deserve better than what we currently offer, the conversation cannot wait for perfect consensus. It needs to start now.
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