On August 1, 1966, twenty-five-year-old Charles Whitman went to the top of the University of Texas Tower carrying guns and ammunition. Having earned a sharpshooter's badge in the Marines, he was an excellent marksman. For over 90 minutes, he shot at anyone he saw. He killed 13 people that day before he was killed by Austin police. This was the worst school shooting in American history until the shooting at Virginia Tech in 2007. The night before he went to the Tower, he killed his mother and his wife.
Those who knew Whitman were shocked, because he had always appeared to be a talented young man with good character. He earned his Eagle Scout Badge when he was only 12 years old, which made him one of the youngest boys to earn that honor in the history of the Boy Scouts. But then as he neared his 25th birthday, he changed.
Whitman had been going to doctors and psychiatrists with complaints that something was wrong with him mentally--that he felt overly aggressive and had thoughts of killing people. He also felt tremendous pain in his head. In the suicide note that he left, he asked that there should be an autopsy of his brain to see what was wrong, which might improve the scientific understanding of the biological causes of mental illness leading to violence.
Texas Governor John Connolly appointed a commission of experts to study the causes of Whitman's behavior. They found evidence of a tumor the size of a pecan pressing on his amygdala. They said that while it was possible that this had contributed to his violent emotions, there was not enough scientific understanding of how brain lesions like this influence thought and behavior to reach any firm conclusion that this was a contributing cause for his murderous actions.
Scientists have continued to debate this. Some have seen evidence that his brain tumor was probably a partial cause of his crime. Others have pointed to many other possible causes from his life experience. Whitman's father had physically and emotionally abused him and his mother. His mother was forced to run away from his father and move to Austin to be close to her son. These and other psychological stressors could have led to Whitman's mental break driving him to his violent self-destructive behavior. Far from being the cause of his criminal violence, his brain tumor might have been only a coincidental occurrence.
And yet there are some cases of people with no history of criminal propensities who become criminal shortly after suffering brain lesions, which suggests some causal connection between the crime and the brain disorder.
If we understood how certain kinds of brain damage might increase the probability of criminal behavior, could that help us in predicting and punishing such behavior? Does criminality become less blameworthy when it is at least partially caused by neurological disorders? Or should we say that as long as someone like Whitman fully understands what he is doing and chooses to do it, even as he knows that it is wrong, his blameworthiness is not reduced?
And if we understood what went wrong in Whitman's brain to create his criminal mind, could this also help us understand what must go right in a normal brain to create a moral mind?
It should be easier today than it was in 1966 to answer these questions, because since the 1990s, the technology of brain scanning--particularly, MRI--has allowed us for the first time to see images of the structure and functioning of both criminal minds and moral minds in the brain. We now have many case studies of people who have had damage in particular parts of the brain, who then show criminal behavior sometime after that damage, and the brain scans can identify the areas of the brain that have been damaged.
There are, however, at least four problems in these studies. The first is the problem of individual differences. Most people who have damage to the same part of the brain do not become criminals. So there must be factors other than brain damage that vary for different individuals with different genetic propensities, different neural circuitry, and different life histories that explain why some become criminals, and others do not. For example, Phineas Gage suffered massive damage to his ventromedial prefrontal cortex, and while people with that kind of brain lesion often become criminals, Gage did not.
The second problem is that the lesions that seem to cause criminality occur in several different parts of the brain. While lesions in the prefrontal cortex are most commonly associated with criminal behavior, lesions in other parts of the brain are sometimes associated with criminality. Similarly, while the normal functioning of the prefrontal cortex seems to be required for good moral judgment, the neuroscientific study of morality has identified many other areas of the brain that contribute to moral experience.
The third problem is that the plasticity of the brain allows the brain to reorganize its neural circuitry after damage has occurred, so that healthy parts of the brain can take on some of the functionality that was lost in the damaged part.
The fourth problem is that it is not clear how the correlation between brain damage and criminality should influence our legal standards of criminal responsibility and punishment. Does neuroscience promote a deterministic explanation of human behavior that denies the free will presupposed in the law? Or can our concepts of moral responsibility and free will be seen as compatible with neuroscientific explanations of criminal behavior?
Before thinking through those problems, let's review a few case histories illustrating how brain lesions can be connected to criminality.
TWO CASES OF EARLY-ONSET PFC DAMAGE
Antonio Damasio and his colleagues have reported two cases of young adults with impaired social and moral behavior apparently caused by early prefrontal cortex lesions occurring before they were 16 months old (Anderson et al. 1999). When the researchers first saw them, subject A was a 20-year-old woman, and subject B was a 23-year-old man. Both had been raised in stable, middle-class homes with college-educated parents who were attentive to their children. Both patients had socially well-adapted siblings who were normal in their behavior.
Patient A had been run over by a vehicle when she was 15 months old. She recovered quickly. When she was three years old, her parents noticed that she did not respond to verbal or physical punishment. She became ever more disruptive over her childhood, until she reached age 14, and she was placed in a special treatment center. She stole from her family and was arrested repeatedly for shoplifting. She gave birth to a baby at age 18, but she showed no interest in caring for the child. She never sought employment. When jobs were arranged for her, she was soon fired for being undependable and disruptive in the workplace. She became completely dependent on her family and social agencies for financial support and management of her life. She never expressed guilt for her misconduct. She blamed other people for her problems.
Patient B had had a right frontal tumor surgically removed at age three months. He recovered, and he showed normal development during his early childhood. But at age nine, he showed remarkably flat emotions combined with occasional explosive outbursts of anger. After graduating from high school, his behavioral problems intensified. He could not hold a job. He frequently engaged in violent assaults. He became a petty thief. He fathered a child, but provided no paternal care. He expressed no guilt for his misbehavior.
Neuropsychological evaluations of both patients showed that they had normal intellectual ability. In this, they were like patients with adult-onset lesions of the frontal cortices in that their immoral conduct could not be explained by their lacking mental ability. This is what Damasio identifies as the refutation of Immanuel Kant's claim that moral judgment is a purely rational activity.
The neuroimaging studies of these two patients showed that both had damage to prefrontal regions of the brain, with no evidence of damage in other areas. The lesion in subject A was bilateral--with damage in both the left and right polar and ventromedial prefrontal cortices. The lesion in subject B was unilateral--in the right prefrontal region.
When they were presented with verbal scenarios of social dilemmas and interpersonal conflicts, both patients failed to identify the primary issues in these dilemmas and failed to propose ways to resolve conflicts. In this, they differed greatly from patients with adult-onset prefrontal lesions, who have a factual knowledge of social rules applied to verbal scenarios, although they have no emotional commitment to these rules in their own real life situations. So it seemed that while the adult-onset patients had at least learned the social norms of good conduct before their brains were damaged, although they were unable to obey those social norms in their own lives, the early-onset patients had never learned those social norms at all.
Patients A and B were also tested for their ability to make decisions that are personally advantageous to them. They participated in the Iowa Gambling Experiment, which was designed by Damasio's student Antoine Bechara to be a lifelike simulation of how human beings must make decisions in the face of uncertainty, in which we weigh likely gains and losses as we seek a personally advantageous future in which our net gains exceed our net losses. The Player sits in front of four decks of cards labeled A, B, C, and D. The Player is given a loan of $2,000 and told that the goal of the game is to lose as little as possible of the loan and to make as much extra money as possible.
The Player turns cards, one at a time, from any of the four decks, until the experimenter says to stop. The Player is told that turning each card will result in earning a sum of money, and that occasionally turning a card will result in both earning some money and having to pay some money to the experimenter. The amount to be earned or paid is not known until the card is turned. The Player is not allowed to keep written notes to tally how much has been earned or paid at any point.
The turning of any card in decks A and B pays $100, while the turning of any card in decks C and D only pays $50. For every 10 cards turned over in decks A and B, at least one card will require a high payment, with a total loss of $1,250. For every 10 cards turned over in decks C and D, at least one card will require a much lower payment, with a total loss of $250. Consequently, over the long term, decks A and B are disadvantageous because they cost more (a loss of $250 in every 10 cards); and decks C and D are advantageous because bring an overall gain (a gain of $250 in every 10 cards).
Players cannot predict exactly the gains and losses in their play of the cards, but normally players can guess that the high gain/high risk decks--A and B--are the "bad" decks, and the low gain/low risk decks--C and D--are the "good" decks that will yield the highest payoffs in the long run. But patients who have suffered damage to the ventromedial prefrontal cortex prefer to pick cards from decks A and B, and because of the the high penalties they incur, they are bankrupt halfway into the game. This is what patients A and B did when they played the game: they chose the high gain/high risk decks, although they must have known that this would be bad for them in the long run.
We see here the normal human tendency to be more concerned with the present than with the future--to choose what gives us high gains in the present even though this will bring high losses in the future. But normally morally mature human beings learn to exercise prudent self-control in overcoming this tendency by choosing the low gain/low risk returns in the present if that is likely to lead to higher gains in the future. Those with frontal lobe damage, however, seem to have an exaggerated tendency to go for the present high reward rather than bank on the future. So what's wrong with them?
Damasio's answer is based on his "somatic marker hypothesis"--the idea that good decision-making about what is personally advantageous and socially appropriate is guided by moral emotions in the mind that are rooted in the visceral feelings of the body, and that these somatic markers are processed in the ventromedial prefrontal cortex (vmPFC) and the amygdala. Frontal lobe patients have all of the intellectual capacities--such as working memory, attention, and language--required for decision-making, but they do not feel the somatically marked emotions necessary for motivating good decisions. These patients suffer from "acquired psychopathy," because they are like psychopaths in that they know the difference between right and wrong, but they don't care--they don't feel those moral emotions like guilt, shame, and regret that normally motivate human beings to do what is right and avoid what is wrong.
Antonio and Hanna Damasio decided to test this by using a polygraph to monitor skin conductance response--also called electrodermal activity--while people are playing the Iowa Gambling Game, because skin conductance response measures unconscious neurophysiological arousal (Bechara et al. 1996; Damasio 1994). When we feel a strong emotion, our autonomic nervous system slightly increases the secretion from our skin's sweat glands. Usually, this increase is too small for us to notice it. But it can be detected by using a pair of electrodes connected to the skin and a polygraph. The slight increase in sweat reduces the resistance to the passage of an electrical current. And so if a low-voltage electrical current is passed between the two electrodes, the polygraph can detect the change in the amount of current conducted.
As measured by this skin conductance response, both normal people and frontal lobe patients showed emotional arousal a few seconds after turning over a card and seeing the reward or punishment. It was also found that as the game continued, in the time immediately before they selected a card from a bad deck, normal people showed a skin conductance response, indicating that their bodies were generating an unconscious signal about the badness of the deck, and the magnitude of this signal increased over the course of the game. Normal people did not show this at the start of the game. This was a response they had to learn while playing the game: their brains were signaling a warning about the likely bad future consequences of selecting cards from the bad decks.
But the frontally damaged patients did not show any anticipatory skin conductance responses! Their brains were not sending any visceral predictive warning about a likely bad future outcome from selecting from the bad decks. Even if they knew they were making a bad choice, they did not feel how bad it would be for them. Even if they were as capable as normal people of making a cognitive estimate of the badness of their choice, the frontally damaged patients did not feel the somatic alarm signal that motivated normal people to avoid a bad choice. Here, again, we see how good moral judgment requires not just pure reason or pure emotion but the interaction of both moral reason and moral emotion. Knowing what is good for us is not good enough if we do not feel it.
Notice also here that Damasio assumes a broad conception of moral judgment as concerned not just with what is socially appropriate but also with what is personally advantageous. A lot of the neuroscientific studies of moral psychology identify morality with what is good for society, and thus seem to assume that what is good for the individual is a matter of selfish interest beyond morality. But Damasio's use of the Iowa Gambling Experiment is a test of how prudent individuals are in choosing what is good or advantageous for themselves as individuals. Thus, Damasio agrees with the traditional conception of Aristotle and others that prudence--the correct choice of what is good for oneself--is a moral virtue, even the supreme virtue, and that morality generally is self-perfective or self-regarding. But since we are social animals, what is good for us individually includes the social good. (I have written previously about the morality of prudence here.)
THREE CASES OF ADULT-ONSET PFC DAMAGE
Elliot was 35 years old when Damasio first met him. In Descartes' Error, Damasio called him "A Modern Phineas Gage," because he had suffered damage to his frontal lobes as a young adult just like Gage; and like Gage this caused a radical change in his personality.
Elliot had been a good husband and father. He had had a successful professional career working with a business firm. He was admired by his younger siblings and his colleagues. But then something happened to him that changed him. He began to have severe headaches. He could not concentrate. He could not complete his work projects. He seemed to have lost his sense of responsibility.
Elliot's doctors discovered that he had a brain tumor the size of a small orange that was pressing against both frontal lobes. Although the tumor was not malignant, its growth was destroying brain tissue. The tumor and the damaged frontal lobe tissue had to be surgically removed.
His physical and cognitive recovery from the surgery seemed good. He was walking and speaking like normal. He was just as smart as he had always been. But his family and friends noticed that his personality had changed. As Damasio said, "Elliot was no longer Elliot."
He was so poor at organizing his work schedule that he was fired from his job. He lost other jobs as well. He invested all of his savings in foolish business ventures that ended in bankruptcy.
His wife divorced him. He married again and then was divorced a second time. He drifted around with no source of income. When Damasio first saw him, he was living under the care of a sibling.
Elliot was intelligent. He had a good memory. He had a great fund of knowledge about the world and about what was happening in his life. But his life was chaotic because he could not make good decisions about his life, and he could not plan for the future. One could conclude, Damasio observed, that as was the case for Gage, "his free will had been compromised" (Damasio 1994, 38).
MRI studies of Elliot's brain revealed that he had the same brain damage as Gage--in the ventromedial areas of the prefrontal cortices. These are the part of the brain identified by Damasio as necessary for practical reasoning and decision making.
Standardized tests revealed that Elliot had a superior intellect. His mental capacities for perception, memory, learning, language, attention, and mathematics were all good. But even with all of these intellectual abilities, he still could not make good decisions about his personal and social life.
The problem with Elliot, Damasio finally realized, was not in the character of his intelligence but in his emotions--or rather in the absence of emotions. Elliot could recount all of the tragic events in his life with an attitude of calmness, as if he were a dispassionate spectator of his own life. He knew that his life had been ruined, but he felt nothing about it.
To test this emotional flatness, Damasio put Elliot through a series of psychophysiological experiments. He was shown images of emotionally charged visual stimuli--such as houses burning or collapsing in earthquakes, or people injured in gory accidents or drowning in floods--and he felt no emotion. Normally, when people see such emotional images, they show a strong skin conductance response. But Elliot showed no skin conductance response at all--just like others with frontal damage. In fact, he said that he knew that before his brain damage, he would have felt some deep emotions in response to such images, but now he could not feel those emotions, although he understood that he should feel them.
Elliot was presented with a long series of hypothetical scenarios of ethical dilemmas, financial decisions, and social problems; and then he was asked to generate solutions. He was very good at this. But then at the end of one session, after he had come up with lots of possible choices for action, he remarked: "And after all this, I still wouldn't know what to do!"
He could think of many hypothetical solutions to hypothetical problems, but he still could not decide what to do in real life situations. His impairment was not a lack of social knowledge or understanding but a lack of emotional reactivity that would give motivational weight to his choices in real life. As Damasio said, "the cold-bloodedness of Elliot's reasoning prevented him from assigning different values to different options, and made his decision-making landscape hopelessly flat" (Damasio 1994, 51).
When Elliot played the Iowa Gambling Game, he was fully engaged, and he clearly wanted to win. But like other frontal damage patients, he could not resist taking cards from the "bad" decks; and he showed no anticipatory skin conductance response prior to choosing the "bad" decks. Even after playing the game repeatedly, he could not correct his mistakes.
Although Elliot's case is rare, there are a few other well-studied cases of adult-onset PFC damage followed by criminal or otherwise deviant behavior. For example, Christina Meyers and her colleagues have reported the case of a man they name J.Z., who had a brain tumor removed in 1962 at the age of 33, which damaged his left orbital frontal lobe. He suffered a change of personality like that of Elliot: he seemed to show something similar to psychopathic personality or antisocial personality disorder (Meyers et al. 1992).
Before his surgery in 1962, J.Z. was a stable and reliable husband, father, and worker. He had worked at the same clothing store for many years. After the surgery, his behavior at work and at home became disordered and disruptive. He lost his job, and he never again had steady employment. He lost most of his family's savings in wild business deals. His wife divorced him. When he reported for a neuropsychological evaluation at Baylor College of Medicine in 1987, he was 58 years old, unemployed, and living with his mother.
Speaking during his evaluation, J.Z. "freely reported being involved in criminal activities and said he had three billion dollars hidden away in West Germany" (Meyers et al. 1992, 123). But to me this sounds so ridiculously boastful that his talk about "criminal activities" sounds dubious.
Meyers and her colleagues decided that his personality showed the traits of "antisocial personality disorder." According to the American Psychiatric Association's Diagnostic and Statistical Manual-III-R of 1987, an adult can be identified with this disorder if he has at least four of the following 10 traits: (1) lack of consistent work behavior; (2) non-conformance to usual social norms; (3) tendency to be irritable and aggressive, (4) repeated problems honoring financial obligations, (5) failure to plan ahead or impulsive behavior, (6) untruthfulness, (7) recklessness with regard to personal safety; (8) inability to function as a responsible parent; (9) inability to sustain a monogamous relationship for more than one year; and (10) lack of remorse. Meyers and her team saw at least 5 of these traits in J.Z.--1, 4, 5, 6, and 10.
J.Z. did not, however, satisfy one crucial criterion for this antisocial personality disorder: this disorder had not started in his childhood. So like Damasio, Meyers calls this acquired antisocial personality disorder, as distinguished from developmental antisocial personality disorder.
Robert Blair and Lisa Cipolotti (2000) have reported a similar case of acquired antisocial personality disorder after frontal lobe damage. J.S. was a 56-year-old man in 1996 when he suffered trauma to the right frontal region of his brain. A CT brain scan showed damage to the right orbitofrontal cortex and to the left amygdala. Prior to this, he had worked successfully as an electrical engineer. He was known as a quiet man who was never aggressive. But after the brain injury, he became aggressively violent. When he was in a rehabilitation hospital, he assaulted the nurses. He frequently damaged property. Like J.Z., J.S. satisfied some of the criteria in the DSM for antisocial personality disorder.
THE MATRICIDAL DAUGHTER
Charles Whitman murdered his mother. The killing of a mother by her child is rare. But when it does happen, the killer is almost always a son rather than a daughter. So the story of the woman in Chile with adult-onset PFC damage who murdered her mother is surprising.
When Gricel Orellana and her colleagues first saw this woman at a hospital in Chile in 2009, she was 64 years old, and she had recently tried to kill a relative by poisoning her and then attempting to drown her in a bathtub. This woman had had auditory hallucinations that God was commanding her to murder her relative. As recommended by a forensic psychiatrist, a court declared her "not guilty by reason of insanity," and remanded her to psychiatric care (Orellana et al. 2013).
Amazingly, the court had made the same ruling--not guilty by reason of insanity--only two years earlier when she had murdered her mother. She had tried unsuccessfully to strangle her mother with a scarf, and then the next day she drowned her in a bathtub. She had followed her religious hallucinations telling her to kill her mother as a sacrifice to God.
This woman's shocking behavior had begun in 1985, when she was 40 years old, after she had had surgery to remove nasal polyps, and the surgery damaged her right ventromedial prefrontal cortex. Before 1985, her life was normal, and she showed no unusual behavior, although she fought with her mother constantly. After the surgery, her personality changed radically. Her behavior became so disruptive that she could not maintain any stable social relationships. She could not keep any regular jobs.
In 1993, she developed visual and auditory hallucinations with religious messages, which included God's command to kill her mother. A psychiatrist diagnosed her as suffering from paranoid schizophrenia.
In 2009, a MRI of her brain confirmed that she had damage to the right ventromedial prefrontal cortex, which apparently had come from her 1985 surgery. Like some of the other PFC lesion patients, this could have caused her "acquired psychopathy."
Orellana and her colleagues administered the same tests that Damasio had used with Elliot, including the Iowa Gambling Task, and they found the same evidence of poor decision-making and emotional flatness that is characteristic of psychopaths.
LESION NETWORK LOCALIZATION OF CRIMINAL BEHAVIOR
These 6 cases of frontal lobe damage followed by personality changes that resemble antisocial personality disorder are included in the 17 brain lesion cases associated with criminal behavior studied by Ryan Darby and his colleagues (Darby et al. 2018). Although the most common lesion location was the vmPFC/orbitofrontal cortex, in at least seven of these 17 cases, the brain damage did not extend into these areas. Three of the lesions were in the medial temporal lobe and amygdala, three in the anterior lateral temporal lobe, one in the dorsomedial prefrontal cortex, and one in the ventral striatum.
Darby and his colleagues suspected that the behavioral impairments caused by these lesions resulted not so much from damage to any one particular region itself but from the disruption of the connections between brain regions. We can explain criminality as caused by some impairment of the brain's normal capacity for moral judgment. The neuroscientific study of morality has shown that the neural basis for moral judgment cannot be located in any one area of the brain, because the "moral brain" is actually a large functional network connecting many different areas of the brain (Fumagalli and Priori 2006; Greene and Young 2020; Mendez 2009; Young and Dungan 2012). As expected, Darby's group was able to show that all of the lesions were functionally connected to the same network of brain regions for moral judgment--including regions involved in morality, value-based decision making, and theory of mind.
UNNATURAL FREE WILL, NATURAL DETERMINISM, AND NATURAL FREEDOM
So what does this teach us about whether we can hold people morally and legal responsible for their criminal behavior? As I have indicated in a previous post, there are at least three possibilities. First, we might argue that no matter what the biological science of natural causality claims, we have a "free will" to exercise a supernatural or immaterial freedom of will that is an uncaused cause of our thinking and acting, and without this, we have no grounds for holding people responsible for their behavior.
Second, we might argue that neuroscience and the other biological sciences show that all human thinking and acting is determined by natural biological causes; and so "free will" is illusory, and we cannot hold people responsible for what they do, because they had no choice.
The third possibility is somewhere in between these two extremes. How we think and act is not compelled by natural causes. But neither can we exercise "free will" understood as some spiritual or immaterial power that is an uncaused cause acting outside and beyond natural causality. We have the power to act as we choose regardless of the cause of the choice. The fact that all of our behavior is caused does not mean that it is compelled. When we freely choose to think or act, what we do has been caused by our beliefs and desires, but this causation is not compulsion, and so we can be held legally or morally responsible for this.
Sometimes people are compelled by biological causes to behave in ways that they have not freely chosen. So we might agree that the woman in Chile who killed her mother suffered from some form of paranoid psychosis: she heard the voice of God commanding her to kill her mother. We might agree that she was innocent by reason of insanity, because she could not distinguish right from wrong.
But most of us most of the time have enough freedom of choice that we can be held responsible for our behavior. Even most of those people with psychopathic brains do not become criminals. Gage and Elliot might have had "acquired psychopathy" because of their frontal lobe damage, but they did not become violent criminals.
REFERENCES
Anderson, Steven W., Antoine Bechara, Hanna Damasio, Daniel Tranel, and Antonio Damasio. 1999. "Impairment of Social and Moral Behavior Related to Early Damage in Human Prefrontal Cortex." Nature Neuroscience 2: 1032-1037.
Blair, Robert J. R., and Lisa Cipolotti. 2000. "Impaired Social Response Reversal: A Case of 'Acquired Sociopathy.'" Brain 123: 1122-1141.
Damasio, Antonio. 1994. Descartes' Error: Emotion, Reason, and the Human Brain. New York: G. P. Putnam's Sons.
Darby, R. Ryan, Andreas Horn, Fiery Cushman, and Michael D. Fox. 2018. "Lesion Network Localization of Criminal Behavior." Proceedings of the National Academy of Sciences 115: 601-606.
Fumagalli, Manuela, and Alberto Priori. 2012. "Functional and Clinical Neuroanatomy of Morality." Brain 135: 2006-2021.
Greene, Joshua, and Lianne Young. 2020. "The Cognitive Neuroscience of Moral Judgment and Decision-Making." In David Poeppel, George Mangun, and Michael Gazzaniga, eds., The Cognitive Neurosciences, 1003-1013. Cambridge: MIT Press.
Mendez, Mario F. 2009. "The Neurobiology of Moral Behavior." CNS Spectr. 14: 608-620.
Meyers, Christiana, Stephen Berman, Randall Scheibel, and Anne Hayman. 1992. "Case Report: Acquired Antisocial Personality Disorder Associated with Unilateral Left Orbital Frontal Lobe Damage." Journal of Psychiatric Neuroscience 17: 121-25.
Orellana, Gricel, Luis Alvarado, Carlos Munoz-Neira, Rodrigo Avila, Mario Mendez, and Andrea Slachevsky. 2013. "Psychosis-Related Matricide Associated with a Lesion of the Ventromedial Prefrontal Cortex." Journal of the American Academy of Psychiatry and Law 41: 401-406,
Young, Liane, and James Dungan. 2012. "Where in the Brain Is Morality? Everywhere and Maybe Nowhere." Social Neuroscience 7: 1-10.
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