The Anatomy of Violence (47 page)

Figure 8.6
   
Functional
neuroanatomical model of violence highlighting cognitive,
affective, and
motor processes

Turning to the affective processing deficits we see outlined in the top center of
Figure 8.6
, the neural structures I have highlighted are the
amygdala/
hippocampal complex, the
insula, the
anterior cingulate, and
the
superior temporal gyrus.
Impairments to these regions can result in an inability to understand the mental states of others,
¹¹⁴
learning and
memory impairments,
¹¹⁵
lack of disgust,
impaired
moral decision-making,
¹¹⁶
lack of guilt and embarrassment,
¹¹⁷
lack of empathy,
¹¹⁸
poor
fear conditioning,
¹¹⁹
poor emotion regulation,
¹²⁰
and reduction in uncomfortable emotions associated with moral transgressions.
¹²¹
These affective impairments can then result in being undeterred from perpetrating gruesome acts on others,
¹²²
callous disregard for others’ feelings,
¹²³
poor conscience development,
¹²⁴
and being unmotivated to avoid social transgressions.
¹²⁵
It’s easy to see how such a set of traits may in turn raise the likelihood of violence.

At the
motor level on the right-hand side of the figure,
brain areas include the
dorsolateral pre
frontal cortex,
orbitofrontal cortex, and the
inferior frontal cortex. Brain impairments here result in response
perseveration,
¹²⁶
motor impairments involving a failure to inhibit inappropriate responses,
¹²⁷
impulsivity,
¹²⁸
the failure to shift response sets and passively avoid punishment,
¹²⁹
and motor excess.
¹³⁰
In the social context of everyday life this results in the failure to invoke alternative response strategies for conflict resolution,
¹³¹
the repetition of maladaptive social behavior,
¹³²
poor impulse control,
¹³³
the failure to avoid punishment, and disruptive behavior.
¹³⁴

We see here a flow from basic brain processes to more complex cognitive, emotional, and motor constructs that then translate to real-world practical behaviors that we know characterize violent offenders. It’s certainly not a simple model, because violence is not a simple behavior. Yet it conveys the complexity of the problem we are dealing with when we try to put just the brain pieces of the puzzle together. You can imagine the even greater complexity involved when we come to including the macro-social and psychosocial processes that interact with these brain pieces. Furthermore, while I have included multiple frontal, temporal, and parietal regions, imaging research on violence is still a fledgling field. I’ve certainly simplified it here. There are many more brain regions involved, including the
septum,
¹³⁵
the
hypothalamus,
¹³⁶
and the
striatum,
¹³⁷
among many others.

You may also wonder how violence in particular arises from these cognitive, affective, and motor forces. I view violence at a dimensional, probabilistic level. The greater the number of impaired cognitive, affective, and motor neural systems, the greater the likelihood of violence
as an outcome. If, for example, you make poor
decisions
and
you don’t feel guilt
and
you act impulsively, then that will exponentially increase the likelihood of violence—all other things being equal.

As I hope I have clarified so far, there is not one unique cause of violence. That is why violence is so hard to fathom—and one of the reasons it’s fascinating for scientists and the public alike. That is true for the brain too. For some social scientists it’s easy to think of the brain as a big blob—and yet in reality it’s a mesmerizing mélange of diverse regions, each with intriguing basic
functions that contour criminal outcomes. We can see from the brain to basic cognitive-affective-motor processes to social behaviors that raise the risk of riotous behavior that the anatomy of violence is very complex.

Biology by itself is just not sufficient. Instead, we need social risk factors to pull the trigger on an outcome of violence. Although I have here emphasized early
social deprivation in the violence jigsaw puzzle, I want to leave the brain uppermost in your mind. That’s because the brain goes to the heart of this book’s argument—the seeds of sin are brain-based. Despite decades in which scientists emphasized environmental and social processes, the brain is the cardinal transgressor.

This should not be a bitter pill for either social scientists or neuroscientists to swallow. We can get to bad brains through bad genes or bad environments—or, as I have argued in this chapter, through the combination of both. As you read this, greater appreciation for the complexity of violence combined with recent advances in neuroscience are paving the way for a much more sophisticated and integrated journey toward discovering crime causation, a journey that builds on the decades of painstaking sociological and psychological research on crime that social scientists can take credit for. What were two competing
perspectives should now be more sensibly viewed as complementary in explaining the causes of crime. For traditional criminologists, what was once an old foe can become a new friend in the fight against violence.

Finally, we should return to our point of departure.
Henry Lee Lucas was concocted from a horrendous home brew of head injury, malnutrition, humiliation, abuse, alcoholism, abject poverty, neglect,
maternal rejection, overcrowding, a bad
neighborhood, a criminal household, and a total lack of love. Violent offenders in general have a history of abuse and early deprivation,
¹³⁸
and with some exceptions
noted earlier, this history particularly characterizes the backgrounds of
serial killers.
¹³⁹
Lucas also had structural and functional brain
impairments, as revealed by
MRI and
EEG examinations, with the frontal poles particularly affected, along with the temporal
cortex.
¹⁴⁰
Toxicology tests also revealed particularly high
cadmium and
lead levels,
heavy metals that we have seen impair brain structure and function.
¹⁴¹
He can be pieced together and understood from distal structural and functional brain impairments that result in the more proximal
cognitive, emotional, and behavioral risk factors for violence—bad
decision-making at the cognitive level,
callousness at the emotional level, and disinhibition at the behavioral level. These constitute key components of the puzzle making up this multiple
murderer.

One unresolved piece remains. Why were all of his
victims female? Henry Lucas’s first official murder victim was his own mother, whom he killed with a knife when he was drunk. While he believed he was only slapping her with his hand, he later realized that he held a knife when he hit her neck. He was twenty-three years old, and was sentenced to twenty years in prison for second-degree murder, as she ultimately died of a heart attack.
¹⁴²

Almost his last victim was
Becky Powell, a twelve-year-old juvenile
delinquent he had met when he was forty and developed an ambiguous relationship with. At one level he was a loving surrogate father for three years, making sure she was fed, clothed, and cared for—a better parent than he had had. At another level he educated her in stealing and
burglary and became her lover. During a tiff when drunk, he stabbed the teenager through the heart, again with a knife. After having
sex with her dead body he cut her up into pieces, stuffed her into two pillowcases, and buried her in a shallow grave. He would visit that grave several times, talking to Becky’s remains and weeping in
remorse.
¹⁴³
It was the only truly loving relationship he had experienced in his whole life, bringing about a radical change in Lucas, who, surprisingly, confessed to his
killings soon after being arrested on a mere weapons charge.

So at opposite ends in Lucas’s life we find two
love-hate female relationships, with maternal abuse as the core cause of his many killings. Consider the dreadful deprivation of his childhood and the abuse heaped upon him by his alcoholic prostitute mother. The deprivation that she likely experienced herself as a child was passed down to Henry Lee Lucas not just environmentally, not just genetically, but likely
epigenetically. We’ve noted how maternal care is one important ingredient
in epigenetics—in gene expression. The complete lack of maternal care likely turned off important genes in Lucas that normally inhibit
violence—and turned on genes that promote it. Genetic inheritance passed from one generation to the next. Yet the
social environment was truly the factor that turned Lucas into a murderous psychopath.
¹⁴⁴
His
mother had all the hallmarks of a hateful psychopath, and in killing her, Henry was virtually reliving his intergenerational genetic destiny of psychopathy. As Lucas said himself, “I hated all my life. I hated everybody.”
¹⁴⁵
He especially hated his mother, and that hatred was in all likelihood turned against other women, even those like Becky Powell whom he came closest to loving.

Recall also the puzzling picture of Carlton
Gary, who similarly lacked secure parental bonds and suffered significant early deprivation and malnutrition. Among other perplexing issues in this case is why a handsome
African-American man with glamorous girlfriends would resort to raping women over the age of fifty-five. Unusually, all were interracial homicides. All seven of his
victims were white women—and yet only 1 in 10 homicides in the United States are interracial. Could this unusual pattern of violence stem from the fact that his mother and his aunt, who also raised him, worked as housekeepers for elderly, prosperous white women? Could complaining, cantankerous white women living at a time when overt racism was more common than it is today have led to hostilities from Gary’s caregivers that were passed down to him? Or, alternatively, could Gary’s hatred for elderly white women derive from his despising a mother who scarcely existed for him—a subtle redirection of aggression, as we saw for Henry Lee Lucas? And did epigenetics play a supporting role, with deprivation altering gene expression in Lucas for a rebound back to his mother?

What could have been done to save Henry Lee Lucas from a life of serial homicide, and, ultimately, death from heart failure in prison—to say nothing of saving his innocent victims?
¹⁴⁶
Are Lucas, Gary, and others like them a lost cause right at the beginning, in early
childhood? Genes and brain predispositions to violence are not immutable. As we continue to piece together the different factors, social and biological, that play a role in predisposing individuals to violence, we become better placed to develop appropriate prevention and intervention programs. And that will be the focus of our next chapter—how we might prevent people like Henry Lee Lucas and Carlton Gary from becoming killers.

Danny seemed to be a hopeless case. In spite of a well-to-do home environment in Los Angeles, complete with the support and care of loving, attentive parents, by the age of three he was stealing constantly. Further into childhood he became a compulsive and adept liar. At the tender age of ten, Danny was not just staying out all night, he was buying and selling
drugs. He was known by other neighborhood kids as a nasty piece of work, and because it was a middle-class neighborhood they steered well clear of him. And it wasn’t for lack of trying on his parents’ part. As his mother recalled, “No matter what the discipline was, or the consequences of his
misbehavior, it was never enough. There was no stopping him. We were really at a complete loss for answers.”
¹

Danny grew older and stronger, and essentially commandeered his parent’s house. He stole cars and appropriated his mother’s jewelry for drug dealing. He was getting F’s in school. He was a precocious abuser of drugs, graduating from
cannabis to speed to cocaine to crystal meth. When he was fifteen he was sentenced to eighteen months in a juvenile detention center. It’s a familiar story, with all the early telltale signs of a life of crime, and likely
violence too—perhaps another
Jeffrey Landrigan in the making.

Out of sheer desperation his parents entered him in a
biofeedback treatment clinic after his release from the detention center. These alternative-medicine clinics assess the physiological profiles of individuals
with clinical problems to ascertain whether any physiological imbalance can be corrected. How? By helping them become more aware of their biology and teaching them to change their
brain. At that point, neither Danny nor his parents actually had any hope that the treatment would do any good. They felt they were just going through the motions—but they turned out to be wrong.

The first clinical evaluation confirmed excessive slow-wave activity in Danny’s pre
frontal cortex—a classic sign of chronic under-arousal. Then came thirty sessions of biofeedback. Danny sat in front of a computer screen with an electrode cap on his head, which measured his brain activity as he played Pac-Man on the computer. Danny controlled Pac-Man, trapped in a maze, and his task was to move around, gobbling up as many pellets as he could. He could only move Pac-Man by maintaining sustained
attention—by transforming his frontal slow-wave
theta activity into faster-wave
alpha and
beta activity. If his attention lapsed, Pac-Man stopped. By maintaining his concentration, Danny was able to retrain his under-aroused, immature cortex, which had constantly craved immediate stimulation, into a more mature and aroused brain capable of focusing on a task.

It was hardly a quick fix. For Danny, the biofeedback training lasted for nearly a year. But a metamorphosis took place over the course of his thirty treatment sessions. He was radically transformed, from an inattentive, F-grade teenager on a downward spiral toward prison into a mature, straight-A, career-oriented student who ended up passing his exams with distinction. It was a complete reversal of fortune.