The Anatomy of Violence

by Adrian Raine

  But before moving on, let’s underscore an important fact: no proposed cause of offending—whether it be social or neurobiological—inevitably results in crime and violence. While the dramatic case of Phineas Gage from Vermont in 1848 originally set up the prefrontal dysfunction theory of psychopathic and antisocial behavior, three more clinical cases strike a chord of caution lest we take this theory too far.

  THE SPANISH PHINEAS GAGE

  The first is the remarkable case of an individual known as the Spanish Phineas Gage—referred to here as SPG—a twenty-one-year-old university student living in Barcelona. It was 1937, the Spanish Civil War was raging, and nobody was safe. One fateful day he found himself upstairs in a house being pursued by the opposition in this civil struggle. Almost cornered, he threw open the window, climbed out onto the windowsill, and made a bold attempt to escape by shinnying down the drainpipe on the outside wall.

  Unfortunately for SPG, the pipe was old, and it broke away from the wall. SPG clung on to it for dear life, falling down onto a spiked metal gate. His head was impaled on the gate, with a spiked point entering the left side of his forehead, injuring his left eyeball, and coming out through the right side of his forehead. It selectively damaged his prefrontal cortex, just as the metal tamping rod had blasted a discrete hole through Phineas Gage’s brain.

  People came to the rescue. They were able to cut through the bar, with SPG conscious all the time throughout the ordeal. He even helped his rescuers to get him off the gate. As with Gage they quickly got him to medical care, delivering him to the Hospital de la Santa Creu i Sant Pau in Barcelona.62 The damage to his prefrontal cortex was quite extensive, and, just like Gage, he lost vision in his left eye. Again like Gage he survived the horrific accident, and it was not long before he was back on his feet, creating a new life for himself. And yet again it truly was a new life. Just like Gage, he was impatient, restless, impulsive, and would move from one thing to another, unable to properly finish any single task.

  Yet here the striking parallel ends between the American and the Spanish Phineas Gages. Despite having the usual executive dysfunction that one expects from such a head injury, and despite his impulsivity, SPG did not develop the antisocial, psychopathic personality that characterized Gage. Why not?

  The answer once again lies at least in part in the environment. At the time of the accident, he was engaged to his childhood sweetheart. As they once said in Rome, amore vincit omnia—love conquers all. And over in Barcelona love helped conquer the antisocial sequelae that we might normally have expected from this dreadful prefrontal damage. SPG’s sweetheart stood by him, and three years after the horrific accident, they were married. Unlike Gage, SPG had spousal support, and his support system did not end there. For the rest of his life he was able to hold down a steady job in one location, unlike Gage, who drifted around for a significant period of his life.

  How could this be possible, you may say. You are by now becoming an adroit neuropsychologist, and you know that prefrontal damage invariably leads to the inability to sustain attention, to complete a task, to shift strategies in tackling problems, and to plan ahead. This was indeed true of SPG, who showed significant impairments on frontal-lobe executive tasks. But the environment is again the answer. His parents were wealthy and owned a family firm where SPG was employed for the rest of his life. His poor executive functioning meant that he was never a particularly good worker. He could do only basic manual tasks and always had to be closely supervised and checked. Yet a job it was, and with it came security and occupational functioning.

  Lady Luck was not finished with SPG. He not only had a devoted wife and caring, affluent parents to support him, but he also went on to have two loving children who were destined to play a role in his psychosocial rehabilitation. In the words of his daughter:

  As a child, I realized that my father was a “protected” person. When I was young I soon saw what the “problem” was, although I had always suspected it. At 17, I became part of this protection, and I still am.63

  SPG could hold his broken head high throughout his life. He was always able to bring home the bacon after his hard day’s work. He had occupational functioning. He had family functioning. He had love in his life from all quarters. As many of you likely know if you reflect on episodes in your own lives, love truly can overcome enormous adversity. For me this case highlights the critical importance of psychosocial protective factors that can guard against a life of crime in the face of horrendous prefrontal damage.

  As with Gage, we see in SPG a man who was not antisocial before the accident that caused the prefrontal damage. Let’s now turn to our second chord of caution, but here our case was antisocial before the head injury.

  THE RUSSIAN-ROULETTE URCHIN FROM UTAH

  This second case study dates from approximately 2000 and concerns a thirteen-year-old-boy from Utah who by all accounts was a bit of a Johnny-gone-rotten.64 For most of his short life, he had been rotten to the core, with a well-documented history of conduct disorder, risk-taking, hyperactivity, and attention-deficit disorder. Sadly, his parents had long since lost their parental rights, and he lived in a foster home. He was a bad kid, but bear in mind that genes and an early negative home environment likely worked against him to make him what he was.

  One day the lonely lad was playing Russian roulette by himself with a .22-caliber pistol. After all, despite the natural beauty of the state, what else is there for a hyperactive, stimulation-seeking, conduct-disordered boy to do in Utah? With the pistol perched underneath his chin and the barrel pointing straight up, he pulled the trigger. The loaded chamber turned, the wheel of fortune spun, and the pistol went off. He succeeded in punching a hole right through his prefrontal cortex.

  Again our case was rushed to the hospital. Yet again he miraculously survived his deadly game. The CT scan taken soon after he arrived at the hospital showed that the bullet had punched a neat hole through his brain, selectively damaging the very middle part of his prefrontal cortex in much the same way that Phineas Gage’s medial prefrontal cortex was damaged by the tamping rod. If he had wanted to selectively take out this very midline part of the medial prefrontal cortex, frankly, the poor youngster could not have done a better job.

  The really unusual aspect of this case is, well, nothing. I mean, nothing really unusual happened afterward. Despite losing at Russian roulette, the boy did not have such a bad ending. His social workers, foster parents, psychologist, and all legal authorities who had been managing his case agreed that he was completely unchanged by the brain damage. He was the same unruly, conduct-disordered urchin that he always had been. But he was not worse. He did not even show any additional cognitive deficits.

  As the Americans say, “What gives?” The neuropsychologist Erin Bigler, who reported this case, reasoned that the young teenager had succeeded in knocking out only the piece of his medial prefrontal cortex that was already dysfunctional, the part that had been causing the conduct disorder in the first place. This second case study highlights a truism—that prefrontal damage does not by any means always result in behavioral change in the antisocial direction, particularly if, unlike the American and Spanish Phineas Gage cases, the individual was not normal to begin with.

  THE PHILADELPHIA CROSSBOW MAN

  Our third case takes this principle to another level. It underscores the point that there can be marked differences in outcome when prefrontal damage strikes. It is yet another Gage-like accident, and, as with the Utah Russian-roulette case, we are dealing with an individual with a deeply entrenched preexisting antisocial condition. But on this occasion there is an astonishing change in behavior after the accident.

  This chord of caution deals with a thirty-three-year-old man from Philadelphia who had a history replete with antisocial and aggressive behavior throughout his life—a life-course persistent offender who was pathologically aggressive. He was also depressed. In fact, he was very depressed. He decided to end his life—but in an unusual way. He took a cr
ossbow and—in a manner remarkably reminiscent of the Russian-roulette case—he placed the bow underneath his chin, with the arrow bolt pointing straight up, and he released the trigger.

  Like a tamping rod, the bolt shot right up into his prefrontal cortex, and as was the case with the Spanish Phineas Gage, the deadly projectile lodged firmly in his brain. Like the other victims we have witnessed, he was rapidly rushed to medical care. Yet again it’s a strange survival story. This unhappy and deeply troubled man was taken to my university hospital—the Hospital of the University of Pennsylvania—to have the bolt extracted from his brain. It selectively damaged the medial prefrontal cortex, just as it had been with Gage and our Russian-roulette case. The missiles in all three cases had essentially the same trajectory, entering from the lower part of the head and exiting from the top of the front part of the skull.

  There was a new twist in this case. As with Gage, the Philadelphian Crossbow Man was radically changed by the prefrontal damage—but in the opposite direction. Gage had been transformed from a normal man into a psychopathic-like individual. The Philadelphia Crossbow Man was instead transformed from an aggressive, irritable, emotionally labile antisocial into a quiet, docile, and content man.

  The pathological aggression was eradicated overnight. The depression disappeared in a jiffy. It was a miracle cure. Indeed, the only neuropsychiatric symptom that resulted from the damage to a man who had been seriously depressed was that, in the words of his clinician, he became “inappropriately cheerful.”65 He simply cheered up.

  This third case study again reveals the complexity of the relationship between brain and behavior, and highlights the striking differences in outcome that can occur as a function of damage to the prefrontal cortex. In the crossbow case, the fact that this disturbed and depressed individual became jolly after the accident is not entirely surprising. Puerile jocularity is one neurological symptom of damage to the prefrontal cortex, and this is what we see here. Indeed, puerile jocularity also characterized the Spanish Phineas Gage. Apparently, he spent a lot of time telling the same old lame jokes and being overly cheerful.66 So when at your next work party you meet that disinhibited, loquacious extravert who tells bad jokes and laughs at them like there is no tomorrow, make a neurological note to yourself and suspect either a spiked bar, a crossbow bolt—or perhaps just plain old frontal-lobe dysfunction.

  Clearly we must be cautious with our prefrontal cortical explanation of crime. Prefrontal damage doesn’t always produce antisocial behavior. But let us not forget that overall there is a link between prefrontal structure and violence based on MRI and neurological studies, so we have to be equally cautious not to discount the hypothesis that prefrontal brain damage causes violence.

  Let’s take this idea a step further from a developmental standpoint. Neurological studies have shown us that brain damage in childhood and adulthood can raise the odds of violence. Now we’ll use structural MRI to delineate more precisely that moment in time when something goes badly amiss in brain development—and here we must go back even beyond birth.

  BORN TO BOX?

  We saw in the Introduction that Cesare Lombroso was fascinated with the idea of a physical brain difference that marked out the born criminal. While no criminal is really “born bad,” I believe there is a “neurodevelopmental” brain abnormality in some offenders—a brain that does not grow in quite the way it should.

  One indication of brain maldevelopment very early on is a neurological condition called cavum septum pellucidum. Normally everyone has two leaflets of gray and white matter fused together called the “septum pellucidum” that separate the lateral ventricles—fluid-filled spaces in the middle of the brain. You can see that black space in the normal brain in the left image of Figure 5.5, together with the white septum pellucidum line that divides the black ventricles. During fetal development there is in addition a smaller fluid-filled, cave-like gap—or “cavum”—right in between these two leaflets. You can see this black gap separating the two white leaflets of the septum pellucidum in the brain depicted in the right image of Figure 5.5. As the brain rapidly grows during the second trimester of pregnancy, the growth of your limbic and midline structures—the hippocampus, amygdala, septum, and corpus callosum—effectively press the two leaflets together until they fuse. This fusion is completed between three and six months after you are born.67 But when limbic structures do not develop normally, the cavum between the two leaflets remains—hence the term cavum septum pellucidum.

  When we scanned the brains of our subjects from the temp agencies, we found that nineteen of them had cavum septum pellucidum—just like the one shown in the right image of Figure 5.5. We called these the cavum group—those with a visible marker of very early brain maldevelopment. We compared them to individuals with normal brains. Those with cavum septum pellucidum had significantly higher scores on measures of both psychopathy and antisocial personality disorder compared with controls. They also had more charges and convictions for criminal offenses.68

  Figure 5.5

  This research design is the “biological high risk” design. You don’t see it too often. We are taking those with the neurobiological abnormality and comparing them with those without the abnormality. But we can also slice this particular pie another way. Let’s instead start off by taking those with psychopathy, and compare them to non-antisocial controls on the degree to which they have cavum septum pellucidum. Fusion of the septi pellucidi from back to front during fetal development is partly on a continuum. It’s a bit like when you zip up your jeans—the zip might not close all the way and there is a gap left. So we can measure the extent to which the septum pellucidum is “zipped up,” so to speak.

  What we find is that psychopaths have a greater degree of incomplete closure of the septum pellucidum, reflecting some amount of disruption to brain development. But it’s not just psychopathy. This is also true of those with antisocial personality disorder as well as those with criminal charges and convictions. It cuts across the whole spectrum of antisocial behaviors.

  We see here in the classic clinical design—where we compare those with and without a clinical disorder—a convergence of findings that match those from the biological high-risk design. Different research designs converge on the same conclusion—there is an early neurodevelopmental basis to crime occurring even before the child is born. The evidence for a neurodevelopmental basis to criminal and psychopathic behavior is mounting.69 As much as traditional criminologists and sociologists would hate to admit it, Lombroso was partly right.

  We don’t know what specific factors can account for the limbic maldevelopment that gives rise to cavum septum pellucidum. We do know, however, that maternal alcohol abuse during pregnancy plays a role.70 So while talk of a neurodevelopment abnormality sounds like genetic destiny, environmental influences like maternal alcohol abuse may be just as important.

  There is an interesting twist to the link between cavum septum pellucidum and crime. In our study we found that brain maldevelopment was especially linked to features of antisocial personality related to lifelong antisocial behavior—things like a reckless disregarded for self and others, lack of remorse, and aggression. Interestingly, boxers are more likely to have cavum septum pellucidum than controls. Is that because the brain damage is caused by being biffed about in the boxing ring rather than the other way around?

  Researchers think not, and instead have touted the provocative idea that those with cavum septum pellucidum are “born to box.”71 Their idea is that cavum septum pellucidum nudges the individual into developing an aggressive personality. Those with aggressive tendencies are more likely to take up boxing, making good use of their natural aggression. But could trauma and head injury in our temp workers result in cavum septum pellucidum? We controlled for these factors, as well as many psychiatric confounds, and results remained unchanged. Cavum septum pellucidum by itself predisposes people to antisocial, psychopathic, and aggressive behavior.

  For some, therefore, i
t’s an early neurodevelopment disorder that puts their limbic system out of kilter and places them on a path to crime. Add in a degree of frontal-lobe dysfunction, and they lose full control of their basic instincts—whether it’s sex or aggression or both.

  FEARLESS ALMONDS

  It’s worth repeating that the complexity of the brain matches the complexity of the causes of crime. When we learn more about our neurobiology in forthcoming decades, we’ll see that multiple brain systems are complicit. We have dug down from the surface of the prefrontal cortex into the very deepest chasms of the brain—the cavum septum pellucidum. To mine more knowledge on violence, let’s now move away from the very center of the brain into that dysfunctional limbic system that seems not to be developing properly in psychopaths. The key culprit dwelling in this neural neighborhood? We think it’s the amygdala.

  The amygdala is an almond-shaped structure lying in a deep cortical fold inside the brain—an area called the medial surface of the temporal lobe. There is one in each hemisphere of the brain, about three-quarters of the way down from the top of the brain depicted in Figure 5.6. This part of the brain is critically involved in the generation of emotion. No brain area is more important in the minds of neuroscientists for emotion than the amygdala. Recall that one of the striking features of the psychopath is a lack of affect and emotional depth. Juxtapose this obvious clinical observation with the equally obvious role of the amygdala in the generation of fear, and you come up with a surprisingly simple hypothesis—that the amygdala is structurally abnormal in psychopaths.

  Figure 5.6 Coronal slice of the brain showing the left and right amygdala toward the base of the brain