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Criminal Minds

On November 7, 1974, an attractive dark-haired man in his late twenties approached a young woman in a Utah mall. He flashed a police badge and calmly informed her that someone had broken into her car. Following the interaction, both the man and woman left the mall to inspect the car. Although she determined nothing was taken, he asked her to file a report at the police station; she agreed, and they drove away in his Volkswagen Bug [1].

The woman, Carol DaRonch, was 18 years old at the time. The man was notorious serial killer Ted Bundy, a man responsible for over 30 murders, convicted of three, and executed in January of 1989 [1]. Once DaRonch was in his car, Bundy attempted to handcuff her, but she escaped. Her escape eventually led to his capture; police arrested him nine months later, found handcuffs in his car, and connected him to a sinister web of murders and missing women [1].

Public fascination with Bundy persisted, not because of this string of gruesome crimes, but due to his charm and charisma. Underneath these appealing qualities, there was a severe lack of remorse and empathy, boundless egocentrism, and an aptitude for manipulation. Ted Bundy, alum of the University of Washington, is remembered today as a textbook psychopath.

In reality, there is no clinical psychopathy diagnosis. The Diagnostic Statistical Manual 5th Edition (DSM-5), which outlines criteria for various psychological disorders, provides antisocial personality disorder (APD) as the closest disorder to psychopathy [2]. APD is characterized first by impairments in personality functioning, including egocentrism, self-esteem gained from power, lack of empathy, and difficulty forming and maintaining intimate relationships. Robert Hare’s Psychopathy Checklist – Revised (PCL-R), measures psychopathic tendencies with a series of interview questions that scores individuals on 20 traits [3]. These traits are divided into two categories: the first evaluates emotional detachment and the second assesses antisocial behavior. Many violent criminals score high in the latter, which includes impulsiveness and violent behavior [4]. The first category measures a variety of affective-interpersonal traits, including deceitfulness, callousness, and hostility, explaining psychopaths’ infamous manipulative side and lack of empathy [2]. To receive the label of “psychopath,” an individual must score high in both categories of the PCL-R [4].

Approximately one percent of the human population—and up to 75 percent of incarcerated males within the United States—meets the diagnostic criteria for APD. Among this incarcerated population, about one quarter meet PCL-R requirements for psychopathy [4]. Although it lacks a clinical DSM-5 diagnosis, psychopathy is incredibly common statistically. The presence of psychopaths is not new to society: stories of people lacking a “moral center” span both cultures and time [5]. Despite this long documented existence in society, little is known about the causes of psychopathy. Our understanding of neurobiological abnormalities related to psychopathic behavior began with case studies of acquired psychopathy, or pseudo-psychopathy. Thus far, research in correlational studies has implicated the limbic and frontal lobe areas, including the prefrontal cortex and the orbitofrontal cortex resting just below it [5].

In 1848, Phineas Gage paved the way for our understanding of prefrontal cortex function in perhaps the most famous case in neuropathology [6]. While working on a railroad, a premature explosion sent an iron rod through Gage’s left cheek, which emerged through the top of his skull. Miraculously, he lived—but not without adverse consequences. Prior to the injury, Gage had been a model foreman and was considered dependable and even-tempered. Afterwards, Gage’s doctor, John Harlow, described him as “fitful, irreverent, and profane.” Dr. Harlow determined that the iron had removed part of the frontal lobe, including the prefrontal cortex. This discovery corroborated animal studies, conducted by David Ferrier, in which primates displayed profound changes in personality after having their prefrontal cortex removed. These findings led current researchers to suggest that damage to the prefrontal cortex may result in dramatic personality changes [6].

Over a century later, there are two theoretical models of psychopathy that rely on different brain abnormalities to explain the disorder. One of these models is the violence inhibition control mechanism, or VIM [7]. The VIM draws a parallel between mechanisms of aggression control observed in animals with a similar mechanism in humans. This theory heavily implicates the amygdala, a brain structure assumed to be linked to aggression and fear. The VIM relies on the demonstration of submission to an adversary to cease that adversary’s aggressive behavior. Consider a fight between two dogs: if one dog submits and exposes his underbelly, the aggressor will likely cease the attack. From this observed behavior in animals, and a presumably analogous counterpart in humans, Blair developed a primitive, operational definition of morality. If this VIM system malfunctions, and submission cues no longer activate a withdrawal response in the aggressor, this may constitute a cognitive “lack of empathy.” Additionally, Blair suggests that abnormal amygdala activation may underlie abnormal aggression and violent behavior [7]. Implication of the amygdala in violent behavior is not unique to psychopaths: a study comparing the positron emission tomography (PET) scans of violent murderers, including both psychopathic and non-psychopathic individuals, found abnormal amygdala activation in murderers’ brains when compared to non-murderer controls.

The murderers’ brains had decreased amygdala activation in the left hemisphere and increased activation in the right hemisphere [8]. The key takeaway from this study is that there are both psychopathic and non-psychopathic murderers, and each group tends to exhibit violent behavior as well as abnormal amygdala activation.

A study conducted by Antonio Damasio and colleagues further elaborated on the role of the prefrontal cortex in developmental psychopathy [9]. A man known as EVR, a successful businessman, husband, and father, was diagnosed with a brain tumor in 1975. He underwent surgery, resulting in a partial removal of the orbitofrontal cortex, a division of the frontal lobe. Following the surgery, EVR declared bankruptcy, divorced his wife, and relocated to a mental asylum. EVR’s case prompted Damasio to conduct a study comparing prefrontal lesion patients like EVR, patients with lesions outside of prefrontal areas, and undamaged brain controls in how they responded to social situations. His team proceeded to develop one of the most prominent theories of developmental psychopathy, which is the second model [9].

The second model is the somatic marker hypothesis, or SMH, first proposed by Antonio Damasio and colleagues [9]. It suggests that the ventromedial prefrontal cortex functions by connecting an emotional or somatic state to a potential decision outcome based on previous experiences of positive and negative consequences. When this system malfunctions, an individual can become incapable of attaching emotional meaning to certain consequences, creating a brain that fails to respond normally to social situations and does not learn from its mistakes [9]. Another study provided additional support for the SMH upon finding that psychopathic participants and orbitofrontal lesion patients exhibited similar gambling behavior. These patients did not display “punishment learning”—the acquired sensitivity to stimuli with negative consequences—compared to controls [10]. Furthermore, the aforementioned PET scan study conducted on murderers’ brains revealed lower activation in many areas of the frontal lobe, including the prefrontal cortex [8].

An essential part of the SMH is the ventromedial cortex [9]. This area is critical to our ability to re-experience emotional responses and perhaps our ability to empathetically experience those of others [11]. When an environmental stimulus activates our emotional response, a neural pathway involving the ventromedial cortex, insular cortex, and amygdala is activated, which then activates the body’s physiological response. Re-experiencing the stimulus at a later time results in activation of the ventromedial cortex, which in turn activates the amygdala and brainstem nuclei to produce a virtual somatic state that excludes the body and operates entirely cerebrally [11]. Damasio conjectured that this cerebral response is implicated both in remembering somatic states and the ability to virtually experience another’s somatic state based on one’s own past experiences.

Achieving this virtual somatic state allows us to maintain an automatic response to socially meaningful stimuli that guides us towards socially acceptable behavior. Disruption in the neural circuit that produces somatic states results in under-arousal to socially meaningful images and consequently abnormal social conduct. While direct connections between conscious perception and brain function elude neuroscientists today, the somatic marker hypothesis provides a foundation for what may constitute a psychopathic inability to display punishment learning from past experiences or achieve a virtual somatic state. This renders the psychopath incapable of responding in a socially appropriate way to meaningful images—what can be construed as a lack of empathy.

The psychopathic individuals mentioned thus far have been presented as a homogenous group. However, some studies suggest divisions among psychopaths themselves. One study compared “unsuccessful” psychopaths, who have been convicted of a crime, with “successful” psychopaths, who have not [12]. Structural MRI, or magnetic resonance imaging, revealed decreased gray matter volume in the prefrontal cortex within the unsuccessful psychopath group scans. Gray matter is composed of neuron cell bodies and synapses; in this case, a reduction in gray matter volume signifies a loss of neurons and may constitute under-activity in specific brain regions. This under-activity resembles the prefrontal cortex damage seen in other pseudo-psychopathic patients [12].

Clearly, not all psychopaths are criminals. An array of interacting factors contribute to psychopathy, including genetics, environmental influence, and individual experience. A spectrum exists even within psychopathy. James H. Fallon, professor of psychiatry and human behavior at the University of California, Irvine, discusses his own research of psychopathy in his book, The Psychopath Inside [13]. Fallon had been acting as an expert witness for murder cases in which the defendant pled not guilty by reason of insanity. According to Fallon, he noticed patterns of brain inactivity in the murderers’ PET scans that indicated an underactive orbitofrontal cortex, ventromedial cortex, and amygdala. Following a random chain of events, he also noticed that his own PET scan closely resembled the scans of murderers pleading insanity [13]. While Fallon utilized only his own expertise while reviewing his PET scan, and speculates on epigenetic causes for his “successful” psychopathy, no conclusive research has been conducted in predicting psychopathy. More research is needed to determine causal relationships from what is currently mostly correlational research.

The search continues for the specific neural mechanisms underlying a psychopathic brain. Research is being conducted into how psychopaths emerge by quantifying the influence of genetics versus environmental stimuli. Still, there are many unanswered questions. Can brain scans or genetic testing early in child development indicate predisposition to psychopathy? What must occur, environmentally, for psychopathic tendencies to transform into criminal activity? If a direct brain mechanism is verified, is corrective treatment possible? The current answers are conjecture at best. Researchers will likely spend years studying these questions. At the moment, there is only speculation on the neurobiological distinction between violent, psychopathic criminals and the successful psychopaths who walk among us. No one knows definitively what separates the prominent professor and researcher of neuroscience, James H. Fallon, from the cold and manipulative serial killer, Ted Bundy.

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  1. “Theodore Robert Bundy.”, Accessed 9 April 2017.
  2. American Psychiatric Association. (2012). Criteria for the Personality Disorders. Diagnostic Statistical Manual, n/a, 5.
  3. Hare, R. D. (1998). The Hare PCL-R: Some issues concerning its use and misuse. Legal and Criminological Psychology, 3, 101-122.
  4. Weber, S., Habel, U., Amunts, K., Schneider, F. (2008). Structural brain abnormalities in psychopaths—a review. Behavioral Sciences and the Law, 26, n/a, 7-28.
  5. Kiehl, K. A., Hoffman, M. B. The criminal psychopath: history, neuroscience, treatment, and economics. Journal title,
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  9. Damasio, A. R., Tranel, D., Damasio, H. (1990). Individuals with sociopathic behavior caused by frontal damage fail to respond autonomically to social stimuli. Behavioural Brain Research, 41, 2, 81-94.
  10. Van Honk, J., Hermans, E. J., Putman, P., Montagne, B., Schutter, D. J. (2002). Defective somatic markers in sub-clinical psychopathy. Neuroreport, 13, 8, 1025-1027.
  11. Philippot, P. and Feldman, R. S. (2004). The Regulation of Emotion. New Jersey: Lawrence Erlbaum Associates, Inc.
  12. Yang, Y., Raine, A., Lencz, T., Bihrle, S., LaCasse, L., Colletti, P. (2005) Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biological Psychiatry, 57, 10, 1103-1108.
  13. Fallon, J. (2013). The Psychopath Inside, A Neuroscientist’s Personal Journey into the Dark Side of the Brain. New York: Penguin Group.

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