Playing Scared (11 page)

The stain had traveled to four regions of the brain. He resumed his cutting into the rats’ brains, sounding the tone, cutting, and sounding the tone once again, until, by the process of elimination, he hit pay dirt: the amygdala. “We do not tremble because we are afraid or cry because we feel sad,” LeDoux wrote, echoing William James. “We are afraid because we tremble and sad because we cry.”

Without an amygdala, a rat loses all fear. In some experiments, amygdala-less rats (ones whose amygdalae have been surgically removed) happily clamber on top of sleeping cats and nip at their ears. A person whose amygdala is damaged can’t recognize the expression of fear on another person’s face.

The amygdala leaps into overdrive whenever we feel threatened. It is our internal guard dog, always on the lookout
for a moving shadow, a slammed gate, a knock at the door. When an engine backfires on the street, the amygdala receives the information and makes us jump, ready to fight or flee, before the prefrontal cortex (the conscious brain) weighs in. The whole process takes twelve milliseconds, during which the amygdala waits around—like a brilliant math student marking time while her more ordinary classmates catch up—for the higher brain to run its processing and figure out if there’s a problem.

Fear conditioning is not only lightning fast; it is the most effective learning. There is little forgetting when it comes to fear. That has been understood and even exploited for hundreds of years, as psychologist James McGaugh details in his 2003 book,
Memory and Emotion
:

“In medieval times, before writing was used to keep historical records, other means had to be found to maintain records of important events, such as the granting of land to a township, an important wedding or negotiations between powerful families. To accomplish this, a young child about seven years old was selected, instructed to observe the proceedings carefully, and then thrown into a river. In this way, it was said, the memory of the event would be impressed on the child and the record of the event maintained for the child’s lifetime.”
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One of the breakthroughs in understanding the link between fear and memory came in 1911, when Swiss neurologist and psychologist Édouard Claparède came across an amnesiac patient in a Geneva clinic. The woman retained all her old memories but was unable to create new ones. Though Claparède greeted her each day, she never remembered him; each time he entered her room, it was like a first meeting in which he had to
introduce himself all over again. One day, he hid a pin in his hand and reached out to shake her hand, pricking her. The next day, as usual, she did not remember him. But when he went to shake her hand, she withheld it, recognizing a threat.
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That’s because fear learning is laid down in the amygdala, separately from the learning of people’s names, the Pythagorean theorem, or how to drive a stick shift. Most long-term memories reside in the hippocampus, where they have a tendency to weaken and dissolve over time. That little seahorse in the brain is one of the first regions affected by Alzheimer’s disease. But fear memories can’t afford to weaken, turn fallible, or go up in smoke. Our survival as a species depends on our ability to remember that the touch of a flame destroys, the bite of a rattlesnake is shot through with poison, and a charging hyena has murder on the brain. Sometimes there are no second chances. Evolution has done all it can to ensure that fear memories remain unshakable—“implicit” in neuroscience lingo, “unconscious” in Freudian. The amygdala is what keeps them that way. The stronger the emotional response signaled by the amygdala, the better the chance we’ll remember it. With a single bad experience, we can become conditioned to fear things that are totally harmless. And it doesn’t matter whether the threat is external or internal, real or imagined: The brain responds the same.

That fact begs a critical question: If fear learning is so powerful, how realistic is it to hope to overcome a lifetime of stage fright? Can the hapless musician or nerve-ridden actor retrain his or her amygdala and so reclaim some degree of poise? Or is it a fool’s errand, destined to fail because of the
very nature of fear acquisition? Scientists are addressing the broader question of whether fear can be reversed. Much of the research is funded by the U.S. Department of Defense, which has an obvious interest in the extinction of traumatic memories. Nearly three hundred thousand veterans from the wars in Iraq and Afghanistan have been diagnosed with post-traumatic stress disorder. Health care for a veteran with PTSD costs three and a half times as much as it does for one without the disorder. The human and financial toll is overwhelming, with medical care costs exceeding $2 billion. But the government’s research holds potential far beyond the military. Anxiety disorders represent the most common mental illness in the country. They affect 18 percent of the adult population, or forty million people, according to the National Institute of Mental Health. In addition to PTSD, they include obsessive-compulsive disorder, panic disorder, generalized anxiety disorder, and social phobia (of which performance anxiety is a subset).

The most common form of treatment is known as “extinction training.” In the laboratory, the idea is simple enough: Stop shocking the poor rat whenever it hears the tone and then repeat that pattern again and again and again—as many times as it takes for the animal to learn that the tone doesn’t necessarily signal pain. Had LeDoux repeated his routine enough times, his rats might have behaved differently. Psychologists use the same approach with their clients, only they call it “exposure therapy.” What they have learned, along with lab scientists, is that human anxieties and phobias are more resistant to extinction than animal fears. It’s easier to get
a rat to stop jumping at a buzzer than it is to get a phobic driver across the George Washington Bridge.

But exposure therapy remains the best treatment for anxiety disorders such as mine, according to Michael Fanselow, a neuroscientist at the University of California at Los Angeles. “When we’re afraid, part of the fear response is an increase in blood pressure and heart rate. What often happens—and this is especially the case in public-performing fears—you get these changes, which in turn make the fear worse, which makes your blood pressure and heart rate go up even more. So you get into this positive feedback loop.” He recommended a combination of beta-blockers and exposure training, which—coming as it did from one of the top neuroscientists in the country—hardly sounded like state-of-the-art advice.

Beta-blockers are the dirty little secret of the classical music world. “They shut down the feedback loop,” Fanselow said. As for exposure training, it’s what every mother tells her kid at one time or another. Get back on the horse, toast your brother at his wedding, play yet another recital. Has nothing changed? Psychologists have for years applied the principle of exposure therapy to treat claustrophobics, locking them in car trunks and coffins—an escape hatch at the ready. They have helped people with arachnophobia face down their fear of spiders and cajoled others with a fear of heights into glass elevators. Current technique relies on a gradual desensitization, beginning with mild triggers before building up little by little. So, for example, a person who is terrified of spiders will at first be exposed to pictures of spiders, before being brought face-to-face with a spider in a cage. Eventually, the spider will
be let out, allowed to crawl about, and, if all goes well, be touched and petted by the arachnophobe.

This graduated exposure is used to treat yet another common and embarrassing performance anxiety. Paruresis is the inability to urinate in the presence of others, and it happens more often to men than women. Like most social phobias, shy bladder syndrome, as it is also called, derives from a fear of negative evaluation by others. But here the results can be unusually extreme. People who suffer from this syndrome will often go to great lengths to avoid urinating, even traveling across the world without visiting a bathroom. “The record appears to be three to five days, which seems way out there on the spectrum,” said Steven Soifer, an expert on paruresis. He is the founder of three nonprofits (the Shy Bladder Institute, the International Paruresis Association, and the American Restroom Association), author of two self-help books, and a tireless advocate for cleaner, more private public restrooms.

Soifer works each year with hundreds of men and women. He asks them to drink copious amounts of water and then to travel from toilet to toilet. Their first field trip is usually to a hotel room, where they are assigned the job of urinating with the door closed while a buddy waits outside. Next, they work their way to a bathroom with the door open just a crack. The goal or “feared item” of choice is a large public bathroom, preferably in a casino or shopping mall. A professor of social work at the University of Memphis, Soifer traces his own lifelong problem with paruresis to junior high school, when some kids tried to break down the door of the bathroom stall in which he was sitting. “Based on all the workshops I’ve done, I
can confidently say that the most common reason is bullying of some sort—either at school or at home, by parents or siblings,” he said. “Most people who were publicly embarrassed or had some kind of trauma could develop these symptoms.”

Scientists used to think of memories as photographs, their details fixed the instant they are recorded. Today, the accepted view is that memories are stored like individual files on a shelf; each time one is pulled down for viewing, it is altered or “reconsolidated,” even if only minimally, before being put back in storage. Each new version sits beside the old one, like the history of a computer document that’s gone through multiple revisions. They all remain in your hard drive.

Extinction training doesn’t work by outright destroying a memory. Rather, it gradually defuses a memory through repeated reconsolidations. The sooner this process begins after a trauma, the greater the chance that the traumatic memory can be disrupted and pushed aside. How soon after a trauma must the process begin in order to be effective? What is the window for optimum results? In a 2007 experiment at New York University, three groups were subjected to a series of electric shocks—all administered whenever an orange square appeared on their computer screens. The fear conditioning worked; all three groups developed an aversion to the orange square. Over the next few days, researchers experimented with varying methods of extinction training to rid the subjects of their newfound fear. The first group was brought back and shown the square—shock-free—to reactivate their fearful memory. Ten minutes later, they were shown it again. Voilà! Their fear was gone. The second group was similarly reacquainted with
the orange square, but didn’t receive their extinction training until six hours later. The subjects in this group didn’t fare as well as the first; they never did lose their fear of the orange square. Neither did the members of the third group, who were never shown the square again, never reminded of the fearful memory—and never given the chance to alter it. The experiment showed that scientists could selectively block a conditioned fear memory in humans with a behavioral manipulation. The implication was clear: Find that window—somewhere between ten minutes and six hours—and it might be possible to treat even the most intractable fears. Possibly without drugs.

The search for a chemical fix to curtail fear dates back to ancient tribes on the Siberian steppes. The shamans of the Koyak and Wiros tribes created a drug made from
Amanita muscaria
, the distinctive red-and-white mushroom commonly known as fly agaric. They discovered that when a warrior urinated after eating this mushroom, the potency of the drug in his urine was many times greater than in the mushroom alone. Warriors stored the urine and drank it on the eve of battle to give themselves courage. In time, they began feeding the mushroom to reindeer and then gathering the animal’s urine, which made for an even more effective brew. It seems the compound passed unmetabolized through the reindeer’s kidneys, increasing the potency still further.
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In North Africa in the thirteenth century, the Crusaders fought a band of Muslim warriors known as “hashshashin,” so called because—as legend has it—they ingested hashish before battle to reduce fear and control pain. The English
word
assassin
is reputedly derived from these hashish eaters, who made a practice of ambushing their Christian enemies. In the sixteenth century, the Incas of Peru prepared for battle against the Spaniards by chewing on coca leaves, the source of cocaine. British soldiers traditionally have been offered a double jigger of rum to steel their nerves, while Russian soldiers get vodka. During World War II, the Russians got a mild tranquilizer prepared from valerian, an herb that’s long been associated with valor,
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while the Americans and British were fed amphetamines to increase confidence and aggression and elevate morale.
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During the war in Iraq, American troops were provided with stimulant medications including Ritalin and Adderall to boost wakefulness and learning.

Published reports have described Pentagon-funded research into smart drugs to create a fearless “supersoldier.” If only such a drug had been available on London’s West End when Sir Laurence Olivier confided his stage terror to the actress Dame Sybil Thorndike and her husband. “Take drugs, darling,” she said. “We do.”

Today’s most widely prescribed drugs for anxiety—Anafranil, Ativan, BuSpar, Celexa, Effexor, Lexapro, Lyrica, Klonopin, Paxil, Prozac, Tofranil, Xanax, Zoloft—are overkill for a midlevel manager who just happens to be scared stiff about his upcoming presentation before the board of directors. That’s why performers and public speakers are far more likely to dose up with a beta-blocker: “For Public Speaking” is the off-label use routinely stamped on prescription bottles. Though never approved for stage fright, the beta-blocker—usually propranolol—is the standby drug for performance anxiety.
According to one study, propranolol slightly improved the test results of medical students. Another study found that high school seniors who took it outperformed their classmates on a repeat of the SATs. But it is in music performance that the drug occupies a special niche; it’s joked that an IV drip of propranolol hangs over every orchestra pit. Beta-blockers—so called because they block the heart’s adrenaline-responsive beta-receptors—work by slowing nerve impulses through the heart. They make the heart pump less forcefully, lowering blood pressure and reducing demand for oxygen. They also act as a balance to the body’s autonomic system, which regulates breath, heart rate, digestion, perspiration, urination, and sexual arousal.