The Anatomy of Violence

by Adrian Raine

  Third, we’ll shift gears a bit in terms of causation. Weinstein’s case illustrates how a medical illness late in life can cause brain impairment—but what about younger offenders? We saw in chapters 3 and 4—where we touched on brain imaging and psychophysiology—that violent offenders have functional brain impairments. Rather like your car when it misfires or your computer when it runs slowly, there is something just not working right with offenders’ brains. So far, we have viewed this as a software problem. Maybe a bad birth messed up the program for normal development, or maybe poor nutrition was the culprit. But now what I’m suggesting is the possibility of hardware failure. The idea is that criminals have broken brains—brains anatomically different from those of the rest of us.

  Taking a leaf out of Lombroso’s nineteenth-century book Criminal Man, I’ll argue that the world’s first criminologist was absolutely correct in espousing structural brain abnormalities as a predisposition to violence. He may have been wrong on the precise location in the vermis of the cerebellum, or the ethnic hereditability of these traits, but he was right on the mark in arguing for a structural mark of Cain. This may sound like we’re back to the “born criminal” and the destiny of genetics. While I have insisted so far that there is indeed in good part a genetic basis to violence, I’ll also highlight here the critical importance of the environment in helping to cause the structural brain deformations that we find in offenders.

  Fourth, and finally, Weinstein’s case deals with severe violence, but are structural brain deformations restricted only to aggressive behavior? I’ll argue that they are not, and that their influence runs the gamut of antisocial behaviors and extends into nonviolent crimes—including even deception and white-collar crime. We’ll start this part of our journey with a trip back to those temporary-employment agencies in Los Angeles.

  BACON-SLICING THE BRAIN

  As you’ll recall from our earlier discussion of Randy Kraft and Antonio Bustamante, back in 1994 Monte Buchsbaum and I, along with my colleague Lori LaCasse, had shown from our PET functional imaging work that murderers have poor functioning in the prefrontal cortex as well as the amygdala and hippocampus. We had clearly demonstrated for the first time a functional brain abnormality in these homicidal offenders.5 At that time we were quite ecstatic.

  Yet that exhilaration was tempered by a dose of skepticism. For one thing, this was a forensic sample—they were all referred by their defense teams, who suspected that something might be wrong. Would our findings apply to the general population? For another thing, they were all murderers—would our results apply to those who showed a broad range of antisocial behavior? Furthermore, we had shown the presence of functional abnormalities, but we had not really tested Lombroso’s hypothesis of physical brain anomalies. How could we overcome these methodological challenges?

  The answers all came from temporary-employment agencies. You’ll recall from chapter 4 that while prospecting in California I struck gold at temp agencies. There we were able to recruit psychopaths and individuals with antisocial personality disorder. These individuals are free-range violent offenders who are running around right now in the community committing rape, robbery, and murder while you read this book. Robert Schug, one of my gifted PhD students with unusual forensic skills, conducted painstaking in-depth clinical interviews with our participants to assess which ones were psychopaths. We then set to work scanning our sample using anatomical magnetic resonance imaging—aMRI. Unlike functional imaging, aMRI gives a high-resolution image of the anatomy of the brain—just what we need for prying into the structure of the criminal brain.

  After just four minutes with a subject we are able to acquire many images of the brain’s structure. Then the hard work begins. After brain scanning, we use sophisticated computer software combined with our detailed knowledge of brain anatomy. We identify landmarks in the brain scans that pinpoint exactly where the orbitofrontal cortex and amygdala are. As with a bacon-slicer, we dissect the brain into slices as thin as one millimeter. There are over a hundred of these slices as we move in a coronal direction—from the forehead to the very back of the head. Having a thin slice of a brain results in good spatial resolution—we can visualize tissue as tiny as one cubic millimeter. Just as for your digital camera or TV, the higher the number of pixels within a given area, the better the resolution, and the clearer and sharper the picture.

  Then, on each slice, using our neuroanatomical landmarks—the sulci, or grooves, in the brain—we painstakingly trace the area of the brain structure in question. You can see one slice from the prefrontal cortex on the left side of Figure 5.1, in the color-plate section. On the right side you can also see a three-dimensional rendering of a quadrant cut out of the skull to reveal below it the underlying brain tissue in one of our subjects. Just like a slice of bacon that has both red meat and white fat, our brain slices have two tissue types. We first have to trace around the “gray” matter in each slice—the meat, colored green here. This separates the neural tissue from the fat—the white matter—so that we can compute the area of neurons. Add up all these gray neuronal areas across all slices, and we have the number we want—the cortical volume of the brain region of interest.

  So what do we find in the prefrontal cortex? Those with a diagnosis of antisocial personality disorder—lifelong persistent antisocial behavior—had an 11 percent reduction in the volume of gray matter in the prefrontal cortex.6 White matter volume was normal. Antisocial bacon has plenty of fat—just not enough meat, not enough neurons. As we saw in chapter 3, the prefrontal cortex is centrally involved in many cognitive, emotional, and behavioral functions, and when it is impaired, the risk of antisocial and violent behavior increases.

  Our antisocial individuals did not differ from controls in whole-brain volume, so the deficit was relatively specific to that critical prefrontal cortical region. But perhaps the brain deficit is not causing antisocial behavior. After all, antisocial individuals often abuse alcohol and drugs, and this could account for the prefrontal gray matter reduction. We therefore created a control group who did not have antisocial personality disorder, but who did abuse drugs and alcohol. We then compared the two groups. The result? The antisocial group had a 14 percent reduction in prefrontal gray volume compared with the drug-abuse control group, a slightly bigger group difference than that between normal controls and antisocials.

  So drugs are not the cause of the structural brain deficit, but questions still remain. Prefrontal structural deficits have been found in other psychiatric disorders. We also know that those with antisocial personality disorder have higher rates of other mental illnesses, including schizotypal personality, narcissism, and depression.7 Could the brain impairment have nothing to do with antisocial personality disorder but instead be linked to a different clinical disorder that our antisocials also happened to have?

  To deal with this, we created a psychiatric control group that was not antisocial but that was matched with the antisocial group on all the clinical disorders that the antisocial group had. Yet again, we found that the antisocial group had a 14 percent prefrontal volume reduction compared with this psychiatric control group. Our findings cannot be explained away by a psychiatric third factor.

  Could the answer instead be family factors? In this case, we think not. We controlled for a whole host of social risk factors for crime, including social class, divorce, and child abuse, but found that the prefrontal cortex–antisocial relationship held firm. And unlike the case of Herbert Weinstein, there were no visible lesions in our antisocial subjects that could account for the volume reduction.

  We are left with the possibility that this structural impairment has a subtle early origin. For whatever reason—be it environmental or genetic—the brain is not developing normally throughout infancy, childhood, and adolescence. We’ll come back to this “neurodevelopmental” idea later.

  The MRI brain scan of Herbert Weinstein showed enormous structural impairment that was very visible. But if you were to compare the M
RI scan of an antisocial individual with that of a normal person, you would not see the 11 percent reduction in gray-matter volume. That reduction corresponds to just half a millimeter in thickness of the thin outer cortical ribbon that is colored green in Figure 5.1.8 The difference is visually imperceptible not just to your eye but also to the eye of the world’s best-trained neuroradiologist. Indeed, an expert neuroradiologist would actually judge the brain scan of the antisocial individual to be quite normal. And yet it’s not.

  We know it’s not normal only because we are not making a clinical judgment such as medical practitioners make who are looking for visible tumors. We are not taking a brief, global look at this slice to discern outright signs of pathology, as is common neuroradiological practice. We are not looking for a big hole in our slice of bacon. Instead, we are spending hours painstakingly computing the precise volume of gray matter in the prefrontal cortex using brain-imaging software. Doing that, we can identify small differences that have important clinical significance. Herbert Weinstein is just the tallest tree in a forest of brain-impaired offenders. Below such visibly striking cases are a host of violent offenders with more subtle but equally significant prefrontal impairments. Yet in clinical practice such sharks will slip away entirely unnoticed.

  Let’s face it, findings come and go. Our study was the first to demonstrate a structural brain abnormality in any antisocial group. But perhaps it was just a fluke. We therefore conducted a meta-analysis that pooled together the findings of all anatomical brain-imaging studies conducted on offender populations—twelve in all—and found that this specific area of the brain is indeed structurally impaired in offenders.9 Since this meta-analysis, yet more studies have observed prefrontal structural abnormalities in offenders.10 The findings are not a fluke.

  To make better sense of what we found, and to understand more fully the implications of this specific structural brain abnormality, we need to take a quick trip to a neurologist’s clinic in Iowa. As it happens, it is the clinic of the neurologist who consulted in the pretrial hearing of Herbert Weinstein—Antonio Damasio.

  I have briefly mentioned earlier how Damasio, then at the University of Iowa and now at the University of Southern California, made truly groundbreaking contributions to our knowledge of how the brain works. A lot of this knowledge has come from the study of unfortunate individuals who, for one reason or another, have suffered a head injury resulting in brain damage. The silver lining to these clouds, from a scientific standpoint, is that by taking together all the clinical patients with damage to one specific brain region, and by comparing them to patients with lesions in different areas, we can draw conclusions on the critical functions of that brain region. Together with his equally brilliant wife, Hanna Damasio, and other colleagues, Antonio has made fascinating deductions from these patients about the functions of some areas of the prefrontal cortex and related regions, including the amygdala.

  One group of patients had lesions localized to the ventral prefrontal cortex, the lower region of frontal cortex. It includes the orbitofrontal cortex, which sits right above your eyes, and the ventromedial prefrontal cortex, which is in line with your nose. The patients showed a striking pattern of cognitive, emotional, and behavioral features that set them apart not just from normal controls, but also from patients with lesions outside of this brain area.11

  First, at an emotional level, while their electrodermal response system is otherwise intact and responsive, patients with ventral prefrontal damage do not give skin-conductance responses to socially meaningful pictures such as disasters and mutilations. The ventral prefrontal cortex is involved in coding social-emotional events. It connects to the limbic system and other brain areas to generate appropriate emotional responses within a social context, measured here by a sweat response. Without that neural system in place, the individual is emotionally blunted—and we saw earlier that psychopaths and those with antisocial personality disorder are similarly emotionally blunted and lacking in empathy.

  Second, at a cognitive level, such neurological patients make bad decisions. In a psychological test called the Iowa gambling task, which was developed by the neurologist Antoine Bechara, subjects have to sort cards into one of four piles. Depending on which pile they place their card in they get monetary rewards or punishments. Unbeknownst to the subject, the decks are loaded. If they pick decks A or B, they might initially get large rewards, but eventually they are hit by even larger losses. Decks C and D give smaller rewards but they also yield much smaller punishments. Over the course of one hundred card plays, normal subjects learn about halfway through to avoid the high-reward/high-loss decks A and B. They instead persist in picking decks C and D, which ultimately give them the best payoff. They show good decision-making in the face of competing rewards and punishments. Patients with ventral prefrontal lesions don’t. They instead keep making bad decisions by picking the bad decks.12

  Even more interesting is what normal individuals show in terms of their sweat responses during the task. About halfway through the task they become cognitively aware of which decks are bad, and which are good. Just prior to that, when they are consciously unaware of the good and bad decks, they contemplate picking from a bad deck. What Antoine Bechara saw on the polygraph was a skin-conductance response (a somatic marker), a bodily alarm bell warning them that they were about to embark on a risky move. Subconsciously, their body knows that bad news is just around the corner, and that they should hold back on their response—but consciously their brain does not. Very soon after this somatic alarm bell rings, normal individuals change their strategy and switch to the good decks—and they become cognitively aware of what’s going on. The ventromedial lesion patients? No alarm bell. So they continue to pick cards from the bad decks.

  It’s not surprising, then, that psychopaths make bad decisions and mess up their own lives as well as those unfortunate enough to be within their social circle. As we saw in chapter 4, the lack of autonomic, emotional responsivity results in an inability to reason and decide advantageously in risky situations. This in turn is very likely to contribute to the impulsivity, rule-breaking, and reckless, irresponsible behavior that make up four of the seven traits of antisocial personality disorder. So we can understand how structural abnormalities to the prefrontal cortex could later result in antisocial personality—they could be the cause of the functional autonomic abnormalities we documented in the last chapter.

  The third striking characteristic of these patients, at a behavioral level, is that they exhibit psychopathic-like behavior. A classic example of this, which took place more than 150 years ago and highlights the intricate link between brain and personality, is the case of Phineas Gage. It’s an unusual story that has been told before in neuroscience circles, but it is well worth retelling here.

  THE CURIOUS CASE OF PHINEAS GAGE

  Gage was a well-respected, well-liked, industrious, and responsible foreman working for the Great Western Railway. The fateful day was September 13, 1848. He was organizing the destruction of a large boulder lying in the path of the projected railway track. The work team had chiseled a hole into the boulder for the gunpowder and sand. The gunpowder was then poured into the hole. It was four-thirty in the afternoon.13

  The next step should have been an apprentice pouring sand on top of the gunpowder. Gage was standing by with a metal tamping rod that was three feet seven inches long and one and a quarter inches in diameter. He was on the verge of using the rod to tamp down and compress the sand on top of the gunpowder to potentiate the explosion. At that critical moment, Gage was distracted by a conversation with his co-workers. After a few seconds he turned back to the boulder, believing that sand had been placed on top of the gunpowder. It had not. He tamped down with the rod right on top of the exposed gunpowder. The metal rod rubbed against the rock and created a spark that ignited the gunpowder. It transformed the tamping rod into a lethal spear that blasted its way right through the head of Phineas Gage.

  Gage had been stooped
over the hole as he tamped down with his hand. The rod entered his lower left cheek and exited from the top-middle part of his head, creating an open flap of bone on the top of his skull. You can see this flap in Figure 5.2 and the bone-shattering damage the rod created. The deadly missile flew through the air, landing eighty feet away, while Gage was hurled to the ground.

  Understandably, all the railway workers thought Gage was as dead as a doornail. But after a couple of minutes he began to twitch and groan, and they realized that he was still alive. They put him into an oxcart and took him to the nearest town. He was carried upstairs into a hotel room and a doctor was summoned. What was the treatment in the nineteenth century when you had a tamping rod blown through your brain? Rhubarb and castor oil.

  Figure 5.2 Skull of Phineas Gage

  You would not think Gage stood a snowball’s chance in hell of surviving. But what a miraculous remedy rhubarb and castor oil turned out to be! Gage lost his left eye, but in no less than three weeks, he was out of bed and back on his feet. Within a month Gage was walking around town creating a new life for himself. And it truly was a new life. For in the words of his friends, acquaintances, and employers, he was “no longer Gage”:

  He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operations, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man. Previous to his injury, although untrained in the schools, he possessed a well-balanced mind, and was looked upon by those who knew him as a shrewd, smart businessman, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and acquaintances said he was “no longer Gage.”14