Mind Reader

How looks can kill

People obsessed with their appearance suffer from a biological disorder, researchers now say. But not so fast: It's still our culture that warps our brains.

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How looks can kill

Anybody so inclined can see the psychological demons behind Michael Jackson’s facial work-in-progress. In contemporary psychiatric jargon, such morbid obsession with one’s looks is called body dysmorphic disorder (BDD), from “dysmorph,” the Greek word for misshapen. Though few are as alarming as Jackson, we all know folks who are preoccupied with the shape of their nose, the cleft of their chin or the size of their breasts, and are constantly seeking the latest cosmetic fix, be it surgery, Botox, collagen, fat injections or various implants. Estimates of the incidence of BDD vary widely; there is no yardstick for when body image concerns should be considered excessive and presumably pathological. A good guess is that BDD occurs in about 1 to 2 percent of the general population, but in as much as 7 to 30 percent among those seeking repeated cosmetic surgery.

Such patients are easy to mock; some less than sympathetic journalists have dubbed BDD the “imagined ugliness syndrome.” However, to the sufferers, every bodily deviation from perceived perfection is both real and profoundly disturbing. Many become socially isolated, have difficulty holding jobs and suffer from serious depression. In a prospective study, over 50 percent of patients with BDD admitted to thoughts of suicide, with an attempted suicide rate of 2 to 3 percent per year, and an overall suicide rate of greater than 20 percent.

Because BDD is a serious disorder with potentially tragic consequences, a better understanding of its root causes would be a welcome medical advance. But how are we to think about a condition that is associated with widely disparate personality types and seems so driven by cultural pressures? Unlike mental illnesses such as schizophrenia and bipolar disorder, where biology clearly plays a major role, it’s hard to see how excessive concern with the shape of one’s nose or lips arises from brain mechanisms gone askew.

Now medical researchers believe they have found a biological cause. In December, a team of UCLA psychiatrists conducted an fMRI study of BDD patients. Their results suggest that BDD patients may suffer from faulty visual processing, causing them to have skewed images of themselves and others. While it’s an intriguing study and could provide some insights into BDD, it is ultimately inconclusive and underscores the fallacy of basing behavior on fMRI brain scans.

At UCLA’s obsessive-compulsive-disorder treatment program, James Feusner and colleagues asked 12 patients with BDD and 13 normal control patients to examine a series of photographs of unfamiliar faces, while undergoing fMRI (functional magnetic resonance imaging) scans. Each face was shown in three versions: an unaltered photo, a blurry image that eliminated detail and a photo that exaggerated facial outlines. Previous fMRI research has suggested that each category — – normal, blurry or exaggerated — is processed by separate neural pathways. When the image was normal or blurry, control subjects used neural pathways involved in analyzing the face as a whole; only when presented with exaggerated facial features did the control patients activate neural pathways known to focus on details. However, the BDD group viewed all three categories via the neural pathways that zero in on details, while not engaging those pathways that evaluate the face as a single unit.

Feusner’s interpretation is that BDD patients’ “brain hardware is fine, but there’s a glitch in the operating software that prevents patients from seeing themselves as others do … There is an abnormality in how BDD patients’ brains interpret what they see.” Though not offering an explanation of why “their brains are programmed to extract details — or fill them in where they don’t exist,” Feusner says that “BDD has a biological link and can no longer be attributed solely to our society’s focus on appearance.” He adds that in the future, patients’ brains might be retrained to perceive faces more accurately.

The study has been widely reported as being the first demonstration of “a biological reason for BDD patients’ distorted body image.” Newsweek opined, “Doctors and patients can only hope that such tangible evidence of pathology will help remove the stigma attached to most mental illnesses.”

But can an fMRI determine a “glitch in the brain software” or that a mental condition is the reflection of an underlying brain abnormality? Can it make the arbitrary determination of whether a behavioral disorder has a primary psychological or biological basis? To approach these questions, let me briefly present a classic study of brain development that offers a basic insight into the “biology” of “hard-wiring.” Though I’ve chosen a simple rat study, the underlying principle of neural organization applies equally to humans.

The rat’s auditory cortex — the part of the brain that processes incoming sounds — continues to develop for about two weeks after birth. After that, the circuitry becomes relatively fixed. This two-week postnatal window of brain plasticity allows researchers to study how changes in experience during that time might affect what will be seen as “hard-wired” neural circuitry.

The auditory cortex of rats (and humans) is subdivided so that neurons in different regions preferentially respond to a relatively narrow bandwidth of sound. For example, some cells respond to high-pitched sounds but not low-pitched ones, while others respond to low-pitched sounds but not high-pitched ones. By exposing adult rats to different-frequency sounds while recording electrical activity from individual cortical neurons, researchers have been able to create topographic maps of which regions of the normal rat auditory cortex respond to which frequencies.

But the circuitry of the adult auditory cortex depends upon what the rat hears during the critical two-week postnatal period. If rats are exposed to a full range of ambient sound, the adult cortex will have a normal sound frequency distribution. If during the first two weeks of life, rats are exposed to only a single sound frequency, the adult rats will have many more neurons and a greater cortical area devoted to this frequency, and far fewer neurons and a diminished cortical representation for other frequencies. In short, the developing brain uses environmental cues to determine its final structure.

Now, to get a sense of the problem in attributing causation to fMRI findings, pretend that you are a neuroscientist who has just received your latest shipment of lab rats. They arrive without any accompanying papers documenting involvement in any prior experiments. One, Helen, seems different from the others; she never responds to her dinner bell. Being curious, you slip poor Helen into the fMRI scanner. To your surprise, you discover that high-pitched sounds produce very little cortical activation in her, when compared with her cage mates.

It would be logical to conclude that Helen’s decreased auditory cortex activation correlates with her inability to hear high frequencies. You would be justified in issuing the not-very-meaningful observation that there is a biological link between Helen’s defective hearing and the structural anatomy of her auditory cortex. But here’s where modern neuroscience needs to have a healthy dose of self-restraint: You can describe correlations; you cannot ascribe causation.

Without Helen’s pediatric history — knowing what sound frequencies she was exposed to as a baby rat — you could not know that her adult fMRI findings represented a normal response to an abnormal auditory environment during a crucial phase of brain development. You wouldn’t be justified in using the fMRI findings to postulate a possible underlying brain disorder, disease or software glitch. FMRI measures brain activity at any given instant. It does not tell us why this activity is occurring; it cannot tell us about the root causes of behavior.

I suspect that the UCLA study is documenting the human equivalent of Helen. Rather than offering an insight into a possible biological cause of BDD, the UCLA study may be a more sophisticated way of showing what we already know — that childhood events can physically shape the developing brain into a different way of seeing the world.

Though some degree of brain plasticity persists throughout life, the earliest years, when the brain is under development, are the most crucial. It is easy to see how a young child — criticized by parents or schoolmates for ears that stick out too far, or a nose that is too big or too long — might begin comparing herself with the gold standards offered up by TV, movies and magazines. Each new image is yet another opportunity for self-evaluation. This process invites a feature-by-feature comparison, and what originated as a purely psychological state — dissatisfaction with one’s appearance — gradually is converted into a biological tendency to see facial details rather than the entire face.

The UCLA study also underscores the difficulty of distinguishing between “emotional” and “biological” causes of a mental disorder. With BDD, it is easy to argue that a child may have a genetic predisposition to obsessions — seen in families with obsessive-compulsive disorder — and so might be more inclined to ruminate over each perceived facial feature flaw. But against this genetic backdrop, keep in mind that Helen was a completely normal rat whose abnormal brain function was exclusively the result of environmental deprivation.

Even conventional language contributes to the confusion of emotional vs. biological. If a person believes that a perfectly normal-shaped nose is too wide and ugly, and his fMRI is different from those of a control group, is his problem now “real” as opposed to “all in his mind”? All beliefs, no matter how bizarre or ill-founded, will be manifest as physical brain changes. Demonstrating these changes says nothing about the realness of the belief, nor does it document the presence of a tangible pathology.

Even with these caveats, the UCLA fMRI study may be giving us a very different insight into the evolution of BDD. Ride a subway and watch a 10-year-old girl reading a teen fashion magazine, her index finger intently tracing the outline of a waif-thin model’s collagen-fattened lips, and then, with a sullen sense of defeat, examine her own reflection in the subway window. I can’t know with certainty, but I suspect that the UCLA study is documenting the power of our culture of appearance to shape our ability to see ourselves and others, even to the extent of creating or at least facilitating a psychiatric disorder of monumental consequences.

Since the beginning of time, parents have worried about kids’ role models. Can bad ones be destructive? Neuroscience is saying yes. So perhaps it’s time to see our obsession with “perfect” features as being as toxic as secondhand smoke or exposure to pesticides, as likely to cause mental problems as war is to cause post-traumatic stress disorder in soldiers. Kids deserve better. They need to learn from parents and authority figures that self-esteem isn’t dependent upon a cookie-cutter imitation of the celebrity du jour. The best medicine is preventive medicine. And the best single preventive for BDD is the simple lesson that beauty comes in all sizes, shapes and personalities.

Robert Burton, M.D., is the former chief of neurology at Mount Zion-UCSF Hospital and the author of "On Being Certain: Believing You Are Right Even When You're Not." His column, "Mind Reader," appears regularly in Salon.

The man who lost his past

The documentary film "Unknown White Male," about a New York stockbroker who loses his memory, is medically implausible. But it offers an important lesson about an overlooked illness.

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The man who lost his past

Hollywood loves amnesia. From “Spellbound” to “The Manchurian Candidate,” “Memento” to “Eternal Sunshine of the Spotless Mind,” “Mulholland Drive” to wonderful old sci-fi epics like “The Alligator People,” somebody is always losing his memory in movies. No matter how good or bad, these films share one powerfully seductive quality; being fictitious, they allow us to suspend our disbelief in the biological plausibility of amnesia in exchange for the romantic notion of erasing our pasts. They allow us to feel what it would be like to recover lost and cherished memories, or to establish an entirely fresh identity from new or even implanted memories.

But how are we to look at fictitious amnesia presented as factual truth? That question has been haunting me for weeks, ever since I rented the 2006 documentary “Unknown White Male.” On the film’s official Web site, director Rupert Murray introduces his film as the “startling story of Doug Bruce, a man who, for no apparent reason, lost 37 years of life history, who lost every memory of his friends, his family and every experience he had ever known. This true story follows Doug in the hours and months following his amnesia, as he tries to piece his life back together and has to discover the world anew.” When the film was first released, it received mostly positive reviews. Roger Ebert called it “an intriguing and disturbing film.” Some critics, on the other hand, sensed that it was a hoax.

After having viewed the movie twice, and interviewing Murray, I have little doubt that the movie was made in good faith. Yet Bruce’s condition is medically implausible. To me, the real attraction of the movie is that it transforms a viewer into an armchair neurologist, forced to diagnose a bizarre memory loss that has stumped the experts. I cannot imagine a better medical training film for sorting out a neurological from a psychiatric disease, for determining whether a patient’s condition is real or imagined.

When we meet him, Bruce is a retired British stockbroker and photography student living in New York City. One day in 2003, he suddenly awakens on the subway to Coney Island, completely stripped of his past; he doesn’t even know his own name. He does complain of bumps on his head and a headache, but he isn’t aware of having been mugged. Bruce begins his adventure by walking into a police station to seek help. After a series of tests, including MRI and CT scans, reveal no related physical problem, Bruce is hospitalized on the Coney Island Hospital psych ward. The name that a nurse enters in his chart is Unknown White Male. He has no identification but does have a slip of paper with a telephone number, which conveniently leads to a former girlfriend.

Bruce’s reimmersion into daily life and into his past is filmed by Murray, an old friend of Bruce’s from London and a budding filmmaker. To aid viewers in his journey of self-rediscovery, Bruce provides Murray with his own video footage that he began shooting within a week of losing his memory. Included are conversations with the camera, shots of him returning to his Greenwich Village loft and even his airport reunion with his father and sisters, neither of whom he recognizes or remembers. Describing his first encounter with his father, Bruce said, “My father is not at all what I expected.” The viewer is left to ponder how someone without a memory of his father would have expectations of what he would be like.

To understand Bruce’s amnesia, imagine how you’d think and act if you had completely lost your personal identity. You’d be sunk in profound terror and confusion. Without a personal background and sense of self, what could you do? What would you want to do? Without a significant fund of prior knowledge about the nature of the world, you would neither understand your confusion nor know what future steps to take to sort things out.

This raises the first serious problem with Bruce’s story: Imagining future actions requires past knowledge. In an April 2007 article in the journal Neuropsychologia, a Harvard research team headed by psychologist and memory expert Daniel Schacter suggests that the primary role of memory might not be for reminiscence but rather to facilitate thinking about the future.

In a series of fMRI studies, healthy young volunteers have shown similar areas of brain activation when thinking about past personal memories and when imagining themselves in future events. The Harvard researchers state that “there is no adaptive advantage conferred by simply remembering, if such recollection does not provide one with information to evaluate future outcomes.” Supporting evidence for their conclusion is a vast body of neurological literature documenting that patients with damage to areas of the brain vital for laying down past memories have impaired ability to elaborate future scenarios. So, to the extent that one is stripped of one’s past, one is cut off from one’s future. Conversely, to the extent that one’s behavior suggests some understanding of a future, one must not be entirely cut off from one’s past.

For Bruce to turn himself in to the police implies some knowledge that the police might be helpful — a scenario that requires access to prior knowledge of how police behave in general. To carry around a video camera and film his meetings with “old” friends and family, Bruce would have to have some understanding that there was some future value to shooting the film. Without a recollection of his past, he wouldn’t be able to project when and where such a movie might be shown, or even who might want to see it. Similarly, in an article that questioned the veracity of the film, the Washington Post asked why Bruce, only days after the incident, registered the e-mail address Unknownwhitemale@yahoo.com? How would Bruce understand that this address might be of future value?

During a phone interview, Murray explained to me that Bruce lost his personal (episodic) memories, but retained his semantic (impersonal factual knowledge of the world, such as that a Chevrolet is a type of automobile) memories. In large part, Murray bases this distinction on his interpretation of the writings of Schacter, as well as on Schacter’s discussion of episodic and semantic memory in the movie. But there’s more to situational memory than this arbitrary distinction. Knowing the dictionary definition of police isn’t sufficient to predict how the police might or might not respond under a wide variety of circumstances, or even if they can be trusted. Think of the complicated and even contradictory impulses you have when someone in a bar suddenly hollers out, “Call the police.” Everything from your past experience to geographic location colors your understanding of the word police.

In the movie, Murray refers to Bruce’s amnesia as representing a fugue state, a psychological condition of no known cause in which one temporarily (for days or weeks) loses all sense of self. But Bruce’s amnesia has persisted to the present. Murray is now unwilling to pin any specific label on Bruce, telling me that none of the experts was able to provide a final diagnosis. In his interview on camera, Schacter suggests that Bruce’s memory loss falls into the category of functional or psychogenic amnesia — two interchangeable terms used to describe a condition of profound loss of past memories, unassociated with any impairment of new memory formation and not explainable by any known medical illness. Schacter affirms that, in the case of Bruce, there isn’t any available scientific evidence to explain how such a profound amnesia might have occurred.

In their daily practice, neurologists most commonly confront acute memory loss in a syndrome known as transient global amnesia (TGA). Occurring primarily in healthy people over 50, the specific cause isn’t known. The most popular explanations are that there is temporary interruption of the blood supply or an electrical “short circuit” in the regions of the temporal lobe that process and store new and retrieve old memories. Typically, such patients are acutely confused and disoriented; they have great difficulty creating new memories (anterograde amnesia). Their inability to recall old memories (retrograde amnesia) can extend back 10 to 20 years prior to the episode. But it is never complete. In the most thorough study of patients in the throes of an acute TGA attack, UC-San Diego neuroscientists demonstrated that a significant amount of apparently lost personal memories could be retrieved when the examiner asked more probing questions about the patients’ pasts. Another hallmark of memory impairment in TGA patients is that they — unlike Bruce — do not forget who they are. Personal identity is uniformly retained.

Even in patients with chronic amnesia resulting from severe brain injury, alcoholism or encephalitis, retrograde amnesia isn’t total. More recent memories are affected more than remote memories. A patient might lose months or even years of his memory immediately preceding his brain insult, but memories from long ago — greater than 10 to 20 years — tend to be preserved. By the time retrograde memory loss is total and all personal identity is lost (as with the profoundly demented), patients have become completely helpless and unable to take care of their most basic needs. I’m not aware of a single well-documented case of a patient who suffered a complete loss of personal memory while able to accurately lay down new memories.

If a neurological explanation for Bruce’s memory impairment is out of the question, is there any justification for a psychological cause? Although the movie offers no specific instance of psychic trauma, it repeatedly mentions that Bruce’s mother’s death from cancer a few years earlier may have been the triggering emotional event.

Even so, we are faced with the same problem: Emotional trauma must ultimately work by changing brain chemistry. If you get depressed and forgetful after the death of a close family member, the triggering event is purely psychological, but the depression and forgetfulness result from neurotransmitters such as serotonin going haywire. With memory impairment from post-traumatic stress disorder, elevated levels of stress hormones such as cortisol can be found, as can MRI evidence of reduced hippocampal volume, the part of the brain responsible for processing and storing new memories. In other words, psychic trauma plies its undesirable effects through physical brain changes. But there is no evidence linking physical changes with psychologically induced amnesia, either in Bruce or in the neurological literature.

In the absence of hard scientific evidence for psychogenic amnesia, neurologists might expect to find some epidemiological evidence for it. They might expect to see it among survivors of concentration camps, 9/11, the Columbine massacre or airplane crashes. Yet this isn’t the case. There isn’t a recognizable clinical syndrome in which high-stress survivors forget who they are. Instead, many suffer from not being able to forget. As Holocaust survivor Jorge Semprun wrote in his extraordinary memoir, “Literature or Life,” getting on with life required a constant effort to forget; he called it “a studied amnesia.” A 1998 review of psychogenic amnesia in the British Journal of Psychiatry failed to find any convincing data that could demonstrate psychogenic amnesia following major emotional trauma.

That brings us face to face with a fundamental question raised by “Unknown White Male”: Is psychogenic amnesia a real medical condition? Part of the problem is that there is no definitive test to prove whether a patient is actively faking or truly experiencing memory loss. If we knew the exact fMRI patterns for “true” and “feigned” amnesia, and a patient unequivocally demonstrated the “feigned” pattern, the patient could always argue that such findings only represented unconscious brain activity of which he was blissfully unaware.

In 1986, Schacter argued that “there are few well established facts regarding the nature of simulated amnesia, and no evidence that experts can distinguish accurately between genuine and simulated amnesia.” By 1999, only a third of 300 board-certified psychiatrists polled felt that psychogenic amnesia should be included without reservations in DSM-IV (the psychiatric diagnostic manual); only 25 percent felt that the diagnosis was supported by strong scientific evidence. By 2006, psychiatrists from Johns Hopkins and Columbia-Presbyterian medical centers concluded that psychogenic amnesia “remains best conceptualized as a relatively rare form of illness-simulating behavior rather than a disease.”

So is Bruce’s simulated amnesia a pure scam for financial gain or, as some have suggested, a bid for celebrity? Is it the reflection of a serious mental illness (factitious disorder), in which patients feel an inner need to be seen as ill or injured? Perhaps. But even this dubious psychiatric distinction can only be based on guesswork about what Bruce is experiencing.

Like most movie reviewers, I am satisfied that Murray’s intentions for making the movie were straightforward and legitimate. Indeed, Murray’s thoughtful conversation echoed much of the psychiatric literature on the origin of simulated disease. Referring to the possibility that Bruce’s amnesia was a hoax, Murray said, “There is no empirical data one way or the other.” He told me that none of Bruce’s many diagnostic tests, including standard MRI and fMRI, showed any convincing reason for the amnesia. Neither did Bruce’s visits to multiple psychiatrists. “At the end of the day, all you can go on is your own personal experience, your own personal intuition,” Murray said. “Who knows what happened. Maybe at some point in his mind he did want to become someone else. I really don’t know.”

Knowing that Bruce’s amnesia was likely feigned, either consciously or unconsciously, I watched the film a second time. Again I was swept up in the story. It was as though I wanted to believe, even when I knew better. This is exactly the draw of the movie. Bruce’s story taps into a universal desire for a fresh start — the tabula rasa upon which we can rewrite our life history. Here’s Bruce, magically and without explanation, accomplishing what most of us only dream of: neutralizing the bad memories that make our pasts into emotional minefields. He validates our deepest desire to believe that the mind is sufficiently powerful to overcome its own obstacles and begin anew. He shows us that despite what science may say at a given time, it may never be the full explanation, giving each of us full license to believe in the veracity of wildly implausible human behavior. “One of the unique aspects of brain disorders is that there are endless unique cases in science, and seemingly the unexplainable become explainable later on,” Murray told me.

In his review of “Unknown White Male,” Ebert asked, “Is that person any more or less real to us if the film is truthful or fraudulent?” The overriding issue raised by the movie, though, isn’t scam or fraud; it’s about how certain psychiatric conditions exist solely as reflections of how we interpret human behavior. In a question-and-answer session among Murray, the film’s producer, Beadie Finzi, and a movie audience, included on the DVD, Finzi summarized her conviction that Bruce’s amnesia is “true” by saying, “The facts are that everyone who does know him, who has ever known him, is completely convinced that this has happened.” Although Schacter and others have already shown that there is no decent method for distinguishing simulated from genuine amnesia, the filmmakers, most of Bruce’s former friends, and most viewers and movie critics believe that Bruce’s amnesia is “real.”

For me, the most startling consequence of the movie is that so many are willing to put aside the present-day neuroscience of memory in favor of relying upon gut feelings and personal experience. This is hardly a sound approach to categorizing psychiatric disease, and yet this is precisely the logic that has perpetuated the myth of psychogenic amnesia as a bona fide medical condition.

The movie is a powerful reminder of how other simulated medical conditions — such as Munchausen syndrome, in which patients injure themselves to gain attention and emotional support — are often overlooked or denied by friends and family, and even some doctors, precisely because they trust their gut feelings rather than prevailing medical evidence. These patients often embark on extended medical pilgrimages, going from doctor to doctor, hospital to hospital, convinced that they are misunderstood patients who only want to get better. This may apply to Bruce, although, sadly, he may not be aware of it. The failure to recognize simulated illness is a commonplace medical error with often tragic results, ranging from broken families to serious self-generated diseases and utter disruption of a patient’s life.

In the end, “Unknown White Male” is a true story of a simulated illness. But when it comes to Bruce’s amnesia, it is only a movie.

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Robert Burton, M.D., is the former chief of neurology at Mount Zion-UCSF Hospital and the author of "On Being Certain: Believing You Are Right Even When You're Not." His column, "Mind Reader," appears regularly in Salon.

We’re prejudiced, now what?

Scientists now tell us bias toward others may be innate. But that doesn't mean we have to behave like Bill O'Reilly.

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We're prejudiced, now what?

All good people agree,
And all good people say,
All nice people, like Us, are We
And every one else is They

— Rudyard Kipling

I am stuck in rush-hour traffic. Maybe I can find a decent radio program to distract myself from the blasting horns, angry looks and cussing behind rolled-up windows. But the radio is worse than the traffic. On NPR, a Washington think tank guru is arguing that “my 30-plus years of studying the Middle East has convinced me that democracy is more appropriate for some cultures than others.” A second NPR station is airing a debate on the medical rights of “illegal aliens.” On Fox, Bill O’Reilly is talking about a recent dinner in Harlem, N.Y., with Al Sharpton: “I couldn’t get over the fact that there was no difference between Sylvia’s restaurant and any other restaurant in New York City. I mean, it was exactly the same, even though it’s run by blacks.”

Everywhere I turn, someone is honking at the other guy. Once upon a time, when psychology was king of the behavioral hill, I thought that prejudice could be explained by upbringing, cultural influences, socioeconomic disparities and plain old wrong thinking. Despite any hard evidence from soft sciences, I nursed the vaguely optimistic belief that education and the teaching of tolerance might make a dent in the bigotry and racism of “others.” And yet sitting in stalled traffic, I cannot shake the irrational feeling that “those in the other cars” are different from “us in our car.” If my mind seems intent upon making such ludicrous and meaningless distinctions, is there more here than meets the purely psychological I?

Psychologists have long talked about our tendency to form “in groups” based upon skin color, accents (the Parisian vs. the “country French”) and hairstyle (try to look at green spiked hair and a crew cut without drawing inferences of fundamental differences in personality). In his 1954 book, “The Nature of Prejudice,” psychologist Gordon Allport observed that many white Americans live in a “state of conflict.” On one hand, they may be ideologically opposed to prejudice, but on the other, they possess underlying tendencies to think and act in racially biased ways.

Neuroscience is now providing tantalizing hints as to how these tendencies might occur. In 2000, two fMRI (functional magnetic resonance imaging) studies allowed the first visualizations of the underlying neuroanatomy of prejudice. In one study, Allan Hart, an Amherst social psychologist, found that when white and black subjects were given brief subliminal glimpses of faces of the other race, both showed increased activity in the amygdala, a small set of nuclei within the medial temporal lobes, believed to be responsible for processing the emotional significance of a stimulus.

In a separate study, New York University neuroscientist Elizabeth Phelps found that the degree of increased amygdala activity directly correlated with both physiological and psychological testing evidence for prejudiced responses. Most important, these biased subjects were unaware of having seen the faces or of having any emotional response. Based upon these and subsequent confirming studies, the amygdala is now thought to be integral to the biology of unconscious discrimination.

Given that the amygdala has long been recognized to be instrumental in emotional processing, particularly in relationship to learning, perception and expression of fear, it has seemed reasonable to interpret such studies as showing that viewing different-colored skin might trigger fear or apprehension. However, Phelps and others have cautioned that the amygdala also responds more generally to the emotional intensity of a stimulus — not only fear but also ambiguity, vigilance and even some states of uncertainty that can have a positive outcome. So, given our present state of knowledge, fMRI activation of the amygdala should not be taken as unequivocal evidence that the fear and anxiety are the primary unconscious responses to racial or ethnic differences; the activation could represent a nonspecific state of heightened emotional arousal.

Naturally, evolutionary biologists are quick to point out the obvious adaptive benefits of immediate unconscious recognition of any difference that might indicate a potential enemy or predator. UCLA anthropologist Rob Boyd has written extensively that being attuned to ethnic differences allows individuals to identify others who share the same cultural norms; sharing similar expectations makes social interaction a lot easier than mixing it up with those with different expectations.

At an equally basic neural level, reflexive detection of differences is an essential aspect of how we learn through pattern recognition. For example, the brain contains primary modules for distinguishing colors. These neural systems operate outside of awareness. One cannot choose not to see a color difference. Even at a young age, such differences contribute to our worldview. According to studies by University of Michigan psychologist Lawrence Hirschfeld, 3-year-old children already attribute significance to skin color and appear to believe that race is the most important physical characteristic in determining what sort of person one is.

The evidence is pouring in; at bottom, we seem programmed to seek out and create meaning out of perceived differences. The question that continues to hound me: Is it possible to break this cycle of prejudgment?

A relatively new and utterly intriguing approach to seeing how prejudice may have evolved and taken root in our brains is “agent-based computational modeling.” This imposing mouthful is nothing more than a clever description of using computers to study how complex systems arise out of basic elements. The technique is relatively straightforward. You create tiny computer programs (agents) with only a few sets of instructions. You then place them on a computer grid and watch their interactions over thousands of trial periods.

Such computer models are now commonly used to predict such disparate activities as consumer behavior, seasonal migration of birds, sexual reproduction, the transmission of diseases and even how culture spreads and becomes established. In evolutionary models, individual characteristics and behavioral strategies can be followed over multiple generations to see how successful behaviors gradually gain dominance. It is presumed that, over time, the optimal strategy for survival will emerge from initially random encounters.

Using this technique, University of Michigan political scientist Robert Axelrod and his colleague Ross Hammond of the Brookings Institution in Washington, D.C., have studied how ethnocentric behavior may have evolved even in the absence of any initial bias or prejudice. To make the model as simple as possible, they made each agent one of four possible colors. None of the colors was given any positive or negative ranking with respect to the other colors; in the beginning, all colors were created equal. The agents were then provided with instructions (simple algorithms) as to possible ways to respond when encountering another agent. One algorithm specified whether or not the agent cooperated when meeting someone of its own color. The other algorithm specified whether or not the agent cooperated with agents of a different color.

The scientists defined an ethnocentric strategy as one in which an agent cooperated only with other agents of its own color, and not with agents of other colors. The other strategies were to cooperate with everyone, cooperate with no one and cooperate only with agents of a different color. Since only one of the four possible strategies is ethnocentric and all were equally likely, random interactions would result in a 25 percent rate of ethnocentric behavior. Yet their studies consistently demonstrated that greater than three-fourths of the agents eventually adopted an ethnocentric strategy. In short, although the agents weren’t programmed to have any initial bias for or against any color, they gradually evolved an ethnocentric preference for one’s own color at the expense of those of another color.

Axelrod and Hammond don’t claim that their studies duplicate the real-world complexities of prejudice and discrimination. But it is hard to ignore that an initially meaningless trait morphed into a trigger for group bias. Contrary to how most of us see bigotry and prejudice as arising out of faulty education and early-childhood indoctrination, Axelrod’s model doesn’t begin with preconceived notions about the relative values of different colors, nor is it associated with any underlying negative emotional state such as envy, frustration or animosity. Detection of a difference, no matter how innocent, is enough to result in ethnocentric strategies.

Even more striking, there isn’t any conventional “thought” associated with this prejudice; it emerges in the same way as ants build ant colonies, and cities and societies form without prior planning or specific intention. Nowhere in the agent’s minuscule “mind” is there any line of code on how best to proceed; there is no built-in suggestion that discrimination might provide better rates of reproduction or survival.

In “The Selfish Gene,” Richard Dawkins said in his characteristic blunt manner, “We are survival machines — robot vehicles blindly programmed to preserve the selfish molecules known as genes.” No matter how inflammatory Dawkins’ rhetoric might sound, his observation is consistent with the conclusions of Axelrod’s agent-modeling studies.

So is this powerful self-interest strategy truly in the genes, and even if it is, can it be modified by experience and education? It’s clear that ethnocentricity is the optimal strategy when mutual distrust is the default position between different groups. But a variety of game theory simulations, like the prisoner’s dilemma, designed to study cooperation vs. noncooperation between two people or groups, suggest that under certain circumstances, mutual cooperation is the preferable strategy.

In a worldwide competition held by Axelrod, academics were asked to create a variety of programs for how agents might best interact for long-term survival. The winner was a simple program, tit for tat, which specified that an agent would always cooperate with another agent at their first encounter; after that, one agent would adopt whatever strategy the opponent demonstrated. If the other guy (agent) responds favorably to your initial offer, cooperation ensues. If the opponent rejects cooperation, you abandon niceness and revert to mutual mistrust. Tit for tat showed that a single attempt at cooperation, prior to knowing how the other agent would respond, resulted in a better long-term outcome for both agents. Trust, in other words, is good.

If such computer simulations are applicable to human behavior, the moral is transparently frustrating. In meeting someone perceived as being different, we must offer initial trust and cooperation without any guarantee that the other person will reciprocate. But anyone who has resolved to adopt the doctrine of unilateral compassion and “turn the other cheek” knows how difficult such self-sacrificing behavior is to initiate unilaterally.

The encouraging news: Axelrod has used such studies to show how cooperative behavior can evolve from mechanisms that, by natural selection, are inherently selfish. The not-so-good news: It isn’t at all clear how humans can overcome basic emotions such as fear, anger, the urge for retribution or just a heightened emotional arousal that make initial cooperation so antithetical to how we normally react to perceived differences.

Nevertheless, Elizabeth Phelps has repeatedly emphasized that the behavioral studies demonstrating unconscious bias “do not indicate that this behavior is ‘hard-wired,’ or unchangeable.” In her 2000 study, she demonstrated that our unconscious biased responses (amygdala activation) can be significantly reduced by experience and familiarity. In other words, emergent prejudiced behavior isn’t an inescapable aspect of our biology.

Admittedly, one of the greatest obstacles to a frank discussion of bias is the repugnance of prejudice. As ugly traits go, racist and bigot are right up there with pedophile and cannibal. But somehow we need to get over our puritanical revulsion with aspects of our biology that we find morally unacceptable. Being politically correct and denying the presence of unconscious bias has been shown to have its own downside. In a clever fMRI study, psychologist Jennifer Richeson has demonstrated that trying not to have inappropriate racial thoughts can actually tax brain activity and result in lesser performance on psychological tests that require maximal attention and concentration.

There’s no doubt that ethnocentric philosophies can be deliberate attempts to justify everything from eugenics to xenophobia. But cognitive science is also showing how many of our thoughts begin outside of awareness. It isn’t much of a leap to believe that conscious thoughts, including racist or ethnocentric beliefs, are after-the-fact rationalizations for unconscious behaviors that have survival benefits. (In fMRI studies, activation of the amygdala corresponded with the subjects making racially biased decisions, despite being unaware of feeling any bias.) If so, we shouldn’t be surprised that the most cogent arguments against discrimination rarely shake biased beliefs.

For me, real bigotry begins with the hubris and arrogance of those like Bill O’Reilly who insist that their assessment of others is purely based upon reason and conscious deliberation, as opposed to being colored by involuntary and unrecognized elements of prejudice. For us to treat others with real trust, we must begin by acknowledging our biases and consciously doing the hard mental work to overcome them. We may not be able to prevent biased opinions from arising, but we do retain the veto power over whether to believe in and act on them.

We are left with two options. We can pretend we are free of bias, and avoid thinking about how to deal with our own deeply ingrained tendency to discriminate. Or we can take a lesson from neuroscience, and even from dumb computer agents, which can switch from noncooperation to cooperation if they learn that it is in their best interests.

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Robert Burton, M.D., is the former chief of neurology at Mount Zion-UCSF Hospital and the author of "On Being Certain: Believing You Are Right Even When You're Not." His column, "Mind Reader," appears regularly in Salon.

The light’s on, but is anybody home?

An extraordinary brain study concludes that a woman in a vegetative state is aware of herself. It's a dangerous claim that could throw families and physicians into turmoil.

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The light's on, but is anybody home?

In a recent article in the Archives of Neurology, a team of British and Belgian neuroscientists describe a clinically unconscious accident victim who can, on command, imagine herself playing tennis and walking around her house. By showing that her functional brain imaging studies (fMRI) are indistinguishable from those of healthy volunteers performing the same mental tasks, the researchers claim that the young woman’s fMRI “confirmed beyond any doubt that she was consciously aware of herself and her surroundings, and was willfully following instructions given to her, despite her diagnosis of a vegetative state.”

Their extraordinary conclusions are beyond provocative; they raise profound questions about the very notion of consciousness. What’s more, they could throw thousands of families and doctors into utter turmoil. As with the Terri Schiavo controversy, patient advocacy groups, self-serving lawyers and politicians with personal agendas could use the study’s stamp of certainty as a given.

Yet the study’s conclusions are not beyond a doubt. There are plenty of questions about whether this young woman is conscious and capable of choice.

Let’s briefly look at the study. In mid-2005, a 23-year-old woman sustained massive head injuries in an auto accident. Following multiple brain surgeries and five months of rehabilitation attempts, she remained unresponsive. According to her treating physicians, she could open her eyes but could not respond to any commands; she could not voluntarily look in the direction of a voice; there was no evidence of orientation or emotional response. They determined that she was in a permanent vegetative state — a neurological categorization of patients who emerge from coma, appear to be awake, but show no signs of awareness of self or environment.

Before the recent advances in functional brain imaging, most neurologists, based upon their bedside observations and brain wave studies, would have agreed that the woman, though “awake,” was extremely unlikely to have a significant private mental life — either in terms of personal awareness or willful mental activity. (This failure to differentiate between awake and aware was a major feature of the Schiavo affair.) But new tools bring new opportunities; her doctors wondered if the fMRI could provide additional understanding of the clinically unresponsive brain. What if the fMRI could demonstrate residual consciousness and self-awareness, perhaps even the ability to respond to commands?

Their proposed study was quite simple. While inside an fMRI scanner, the unresponsive woman was asked by the researchers to perform three mental tests: relax, imagine playing tennis, and imagine walking around the various rooms in her home. The tasks were chosen because of their ability to activate different areas of the brain. Imagining playing tennis would light up the supplementary motor area, a region involved in imagining as well as performing coordinated movements. In contrast, imagining moving from room to room in a house activated those regions, such as the posterior parietal lobe, that contribute to imaginary or real spatial navigation.

At first glance, the results are startling. The patient was able to activate the same general brain regions as conscious volunteers serving as controls in the test; according to the authors, the images were statistically indistinguishable.

But are the authors’ conclusions justified? Should we accept that the patient really was consciously aware and able “to understand instructions, carry out different mental tasks, and exhibit willed voluntary behavior in the absence of any overt action.”

Traditionally, consciousness has been considered a subjective and private experience. Unless we subscribe to Las Vegas versions of telepathy, we are dependent upon what a person’s mind tells us about what that mind is doing. We ask someone what they are thinking or how they are feeling; if they don’t answer, we are left guessing at the meaning of sighs, grunts and bits of body language and gesture.

Are we to now believe that an fMRI can tell us the level and nature of a patient’s consciousness even when the patient can’t respond? Putting aside for a moment the very considerable questions of fMRI methodology, and interpretation, are we ready to accept technology as the final word in assessing mental states?

This is not simply an academic question applicable to a single patient. Tens of thousands of patients in a persistent vegetative state linger in long-term care facilities. Others remain under the radar, being cared for at home by their families. The estimated annual cost of medical treatment for them is between $1 billion and $7 billion a year. Once larger numbers of patients are evaluated via fMRI, it is quite likely that we will find others with similar degrees of activation on a variety of mental tasks. Family members will be asked to understand, interpret and act on the scan reports. I cannot imagine a worse medical nightmare than being told that a clinically unconscious spouse or child has been shown on fMRI to have an active imagination and substantial self-awareness, especially when the findings don’t alter the grim prognosis or substantiate the value of greater rehabilitative efforts. Before putting a family through such agonizing dilemmas, we neurologists should be reasonably certain that what the fMRI shows does correspond to actual mental states in the seemingly unconscious.

But how could we make such a determination? How can you objectively confirm what is, at bottom, a subjective experience?

Stymied, I decided to take a step back and review what the fMRI has shown in other states of diminished consciousness. But to understand what we see on such scans, we need to first look at how the brain processes information. For a quick example, consider how a visual image is formed and projected into consciousness.

Your retina detects a yellow-and-black fluttering. The information is sent to the primary visual cortex. Specialized collections of neurons (modules) process different aspects of vision, such as the detection of vertical or horizontal motion, lines and edges, determination of color. The output of these modules then flows into higher order networks — first within the visual association areas, and then into more widely distributed circuitry for non-visual elements, such as the remembrance of seeing a similar pattern hovering over a mountain lake, a trip to a natural science museum with your grandfather, the cover of a book on chaos theory, a scary scene from “Silence of the Lambs.” Finally, through mechanisms both utterly mysterious and widely distributed throughout the brain, this unconsciously constructed perception is delivered into awareness; you suddenly “see” a monarch butterfly floating in front of you.

If we were to watch this process on fMRI, we would see activation of the primary visual cortex, secondary visual association areas, as well as more widely distributed non-visual areas that contribute to your understanding of and feelings toward a butterfly. But we would not see the image’s transition from unconscious to conscious perception. Consciousness isn’t generated by a specific brain area that can be directly visualized. The fMRI can show us the precursors of a perception: It cannot tell us if the person is actually aware of that perception.

To put this into everyday terms, imagine your morning commute. You settle into your car, turn on the news and you’re immediately immersed in the latest presidential scandal. In what seems only seconds later, you find yourself at work. You have no specific awareness of having made the 10-mile drive. Nevertheless, if you had been wearing a portable fMRI helmet, your scan would have shown various areas of brain lighting up as your brain successively processed a wide variety of inputs that you may or may not remember having heard or seen. You may consider making turns or applying the brakes as intentional actions, but in fact your unconscious mind was making intentional and deliberate choices while the conscious “you” was on autopilot.

When judging a patient’s degree of personal awareness and ability to make willful decisions, it’s important to distinguish between choices that can only be made consciously (such as consistently choosing to blink once for yes or twice for no) and choices that might be more reflexive and occur outside of consciousness. In short, we need to know if a choice is truly deliberate or merely the unconscious activation of neural circuitry.

So is it possible that this young woman’s fMRI scans are not reflective of conscious intention and choice? Maybe her injury destroyed her ability to make unconscious thoughts conscious, but left her auditory pathways and subconscious processing mechanisms sufficiently intact to “hear” and respond to the researchers’ questions.

Although it’s too early to draw definitive conclusions, several recent fMRI studies point in this direction. In the March 2007 Journal of Neurology, Chinese researchers have studied the ability of unconscious patients to recognize their own names. Of seven persistent vegetative patients presented with a familiar voice saying their name (the same technique used when asking unconscious young women to relax), three showed activation of the primary auditory cortex and two also activated higher order association areas in the temporal lobe. So, are we to conclude that such patients are secretly conscious, or are they merely unconsciously registering recognition of their own names? And how would we know?

Imagine being at a cocktail party. You are intently talking to one person; all other conversations are mercifully tuned out. Suddenly you are aware that someone across the room has mentioned your name. Neural circuitry previously trained to recognize your name did what it was trained to do; the conscious “you” neither willed this activation nor asked to be notified when your name came up. Seen in this light, the Chinese researchers elegantly demonstrate how extensive areas of brain specific for language processing can be activated in unconscious patients. The study does not tell us whether these patients were actually aware of hearing their names, nor does it tell us that this processing was consciously willed.

These studies may be the earliest fMRI demonstrations of how much cognition actually occurs at a purely unconscious level. Indeed, Nicholas Schiff of Cornell Medical School, who specializes in disorders of impaired consciousness, has repeatedly cautioned that preservation of isolated neural networks (like name recognition) shouldn’t be construed as representing conscious awareness; rather, such activity might be seen as evidence for parts of the brain operating outside of awareness.

Back to the young woman imagining playing tennis. Since the appearance of the preliminary version of the study in Science in 2006, there has been a flurry of criticisms, ranging from how to construct a study that can separate out conscious choice from more automatic unconscious processing, to the larger question of whether the fMRI is capable of confirming the presence of consciousness. The authors haven’t budged.

On his Web site, the lead author, Cambridge neuroscientist Adrian Owen, has expanded his conclusion by suggesting that the performance of these mental tasks might be a way that non-communicative patients “may be able to use their residual cognitive capabilities to communicate their thoughts to those around them by modulating their own neural activity.” Imagine being the young woman’s parent and reading that just maybe your unconscious daughter could communicate with you, if only science could perfect the proper techniques.

The dream of technology clarifying personal experience carries a huge moral burden. I’ve lived through the era when the electro-encephalogram (EEG) was correlated with everything from borderline personality to impulsive, even homicidal behavior. In criminal trials, EEGs were commonly flaunted as evidence for diminished capacity. Patients without clinical seizures were treated with major league anticonvulsants simply because they had minor brain-wave irregularities. With time and experience, enthusiasm for the specificity of EEGs subsided; the neurological community learned that a wide variety of “irregular” findings might be nothing more than the far ends of the distribution of normal findings.

Now the new fair-haired kid on the neurological block is the fMRI. The underlying principle of fMRIs is fairly straightforward. Areas of brain that are active need more oxygen; this increased oxygen use is reflected as hot spots on the scan. But fMRI accuracy, reliability and interpretations remain debatable, especially when it comes to studying complex mental activities with relatively primitive and indirect measurements of blood flow. At best, the fMRI is the physiological equivalent of an aerial photograph of a house. It can tell you which rooms are lighted, even the amount of electricity being used in any room, but it cannot tell you what is going on in a lighted room, or even if anyone is home and is aware of the light.

Despite numerous discussions of technical limitations — the April 2005 Scientific American article “Fact or Phrenology” is an excellent overview — the fMRI has captured the popular imagination big time. In 2006, there were 1,500 fMRI articles in professional journals. Some studies have been meticulous and provide superb insights into brain function. Others have been trivial, if not downright silly, such as why consumers might prefer Coke to Pepsi, or how fMRI can conclusively determine if you are lying. There are those that border on science fiction, such as German neuroscientist John-Dylan Haynes’ suggestion that one day the computer should be able to read minds. “Every thought is associated with a characteristic pattern of activation in the brain. By training a computer to recognize these patterns, it becomes possible to read a person’s thoughts from patterns of their cerebral activity.”

My primary concern isn’t with the variable quality of fMRI studies; we are all aware that science proceeds via fits and starts, the good and the bad sorted out over time. For me, the problem is one of ethical responsibility to patients and their families. And there is the issue of social responsibility. Science doesn’t exist in a vacuum; I would hate to see such preliminary and controversial studies cited as evidence for otherwise untenable or extreme social policies.

Perhaps Owen and his colleagues are correct and this unfortunate woman has fleeting moments of consciousness and is trying to communicate her thoughts. But perhaps the study shows nothing more than preserved bits of neural machinery capable of making unconscious choices. There cannot be a definitive conclusion until we understand every aspect of brain function and have demonstrated precisely what neural states correspond to specific conscious experiences. Until this mythical time arrives, pronouncements of fMRI confirmation of consciousness aren’t science; they are bald speculations and should be so labeled.

Scientists dealing with human lives have the obligation to heed the Hippocratic Oath: primum non nocerum. Above all, do no harm. The study by Owen and co. provides provocative insights into the degree of residual cognitive processes that can be preserved in a clinically unconscious patient. That is enough. Whether this unfortunate young woman has elements of consciousness lurking beneath her unresponsive behavior is not a question that can be answered through technology.

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Robert Burton, M.D., is the former chief of neurology at Mount Zion-UCSF Hospital and the author of "On Being Certain: Believing You Are Right Even When You're Not." His column, "Mind Reader," appears regularly in Salon.

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