The Anatomy of Violence (24 page)

Something snapped inside Herbert. He grabbed his wife by the
throat and throttled the life out of her. There she was, dead on the floor. That did not look too good, so Herbert opened the window, picked his wife’s dead body up, and threw her out. She did a free fall twelve floors down onto East Seventy-second Street, landing on the sidewalk below. Herbert thought it would look like an accident, but on reflection he realized it still didn’t look very good. So he crept out of the building, only to be nabbed by the police. They charged him with second-degree
murder.

Things were looking bad for Weinstein, but he was a wealthy man and had a good defense team. And his lawyers suspected something unusual in the case. He did not have any prior history of crime or violence. They referred Herbert for a
structural
brain scan using
MRI.
¹
They followed this up with a
PET scan, which maps brain functioning. If you could see the images you wouldn’t have to be the world’s leading neurologist to notice that his brain is broken. It was incredibly striking—there was a big chunk missing from the pre
frontal cortex. What exactly was happening here? Unknown to anyone—including Weinstein himself—a
subarachnoid cyst was growing in his left frontal lobe. This cyst displaced brain tissue in both frontal and
temporal cortices.

The neurologist
Antonio Damasio was consulted during a pretrial hearing to render his opinion on Weinstein’s ability to think rationally and control his emotions.
Skin-conductance data were admitted alongside the brain-imaging data to argue that Weinstein had an
impaired ability to regulate his emotions and make rational decisions. The defense team went with an
insanity defense, and Judge
Richard Carruthers was favorably impressed by Damasio’s arguments and the testimony of the imaging experts. In a novel pretrial bargain, the prosecution and defense agreed to a plea of
manslaughter.
²
This carried a seven-year sentence in contrast to the twenty-five-year sentence Weinstein would have served if he had been convicted of second-degree murder.

It was a monumental decision. No court had ever used PET in this way in a criminal trial.
³
For the first time, brain-imaging data had been used in a capital case prior to the trial itself to bargain down both the crime and the ensuing punishment.
⁴

The case of Herbert Weinstein highlights yet again the importance of the brain in predisposing someone to violence. More specifically, the case suggests that a
structural
brain deficit in the left prefrontal cortex results in a
functional
brain abnormality that in turn results in violence.
Cysts such as Weinstein’s have an unknown cause and can grow for a long time. They can also be benign, but experts in the case testified that the cyst resulted in brain dysfunction that substantially impaired Weinstein’s ability for rational thinking. That bolstered the credibility of his insanity defense.

Recall from
chapter 3
that impairment to the frontal cortex is particularly associated with
reactive aggression. Revisiting the events from that night we can see that Weinstein’s violence was reactive in nature. Arguments had preceded the attack, and his wife had attempted to scratch his face. These are the aggressive verbal and physical stimuli that provoked Weinstein’s violent response. Recall our earlier argument that
spousal abuse can be caused by a lack of prefrontal regulatory control over the
limbic regions of the brain, resulting in reactive aggression in the face of emotionally provocative stimuli. Factor in to the equation that Weinstein had no prior history
in any shape or form
of aggressive or antisocial behavior. In terms of timing, it seems reasonable to suppose that the onset of this medical condition was a direct cause of Weinstein’s extreme reactionary violence.

In this chapter we’ll build on Weinstein’s case in four different ways. We will burrow further into the anatomy of violence by arguing that the brains of some offenders are
physically different
from those of the rest of us.

First, for Herbert Weinstein the structural brain abnormality is so striking that we can all see it. But I’ll argue that many violent offenders have structural abnormalities. They may be so subtle that even highly experienced neuroradiologists cannot detect the abnormality, yet they can in practice be detected using brain imaging and state-of-the-art analytic tools.

Second, while Weinstein’s brain abnormality likely had its onset in adulthood, I’ll suggest that for most other offenders, something has gone wrong with their brain development very early in
life. I’ll advance a “
neurodevelopmental” theory of crime and violence—the idea that the seeds of sin are sown very early on in life.

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.

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 MRI 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.