How We Decide (6 page)

The target was moving fast. The time for deliberation was over. Riley issued the order to fire; two Sea Dart surface-to-air missiles were launched into the sky. Seconds passed. Riley nervously stared at the radar screen, watching his missiles race toward the object at speeds approaching Mach I. The blinking green blips appeared to be drawn to the target, like iron filings to a magnet. Riley waited for the interception.

The explosion echoed over the ocean. All of the blips immediately disappeared from the radar screen. Whatever had been flying toward the USS
Missouri
helplessly fell into the sea, just seven hundred yards in front of the American battleship. A few moments later, the captain of the HMS
Gloucester
entered the radar room. "Whose bird is it?" he asked Riley, wanting to know who was responsible for destroying the still unidentified target. "It was ours, sir," Riley responded. The captain asked Riley how he could be sure he'd fired at an Iraqi missile and not at an American fighter jet. Riley said he just knew.

THE NEXT FOUR HOURS
were the longest ones of Riley's life. If he had shot down an A-6, then he had killed two innocent pilots. His career was over. He might even be court-martialed. Riley immediately went back to review the radar tapes, looking for any scrap of evidence suggesting that the blip really was an Iraqi missile. But even when he had the luxury of time and analysis, Riley still couldn't definitively identify the target; the tapes were completely ambiguous. The mood on the HMS
Gloucester
quickly grew somber. Investigative teams were sent out to view the wreckage still floating on the ocean surface. An immediate inventory of all Coalition planes in the area was conducted.

The captain of the HMS
Gloucester
heard the news first. He walked over to Riley's bunk, where Riley was trying, in vain, to get some sleep. The results of the investigation were in: the radar blip was a Silkworm missile, not an American fighter jet. Riley had single-handedly saved a battleship.

Of course, it's possible that Riley had just gotten lucky. After the war was over, British naval officers carefully analyzed the sequence of events preceding Riley's decision to fire the Sea Dart missiles. They concluded that based on the radar tapes, it was impossible to distinguish between the Silkworm and a friendly A-6. Although Riley had made the correct decision, he could have just as easily been shooting down an American fighter jet. His risky gamble had paid off, but it had still been a gamble.

That, at least, was the official version of events until the summer of 1993, when Gary Klein started to investigate the Silkworm affair. A cognitive psychologist who consults for the Marine Corps, Klein was informed that nobody could explain how the radar blip had been identified as a hostile missile. Even Riley didn't know why he'd considered that early-morning blip so dangerous. He assumed, like everybody else, that he'd just gotten lucky.

Klein was intrigued. He had spent the last few decades studying decision-making in high-pressure situations, and he knew that intuition could often be astonishingly insightful, even if the origin of those insights was obscure. He was determined to find the source of Riley's fear, to figure out why this particular blip had felt so scary. So he went back to the radar tapes.

He soon realized that Riley had gotten used to seeing a very consistent blip pattern when the A-6s returned from their bombing sorties. Because Riley's naval radar could pick up signals only over water—after a signal went "wet feet"—he was accustomed to seeing the fighter jets right as they flew off the Kuwaiti coast. The planes typically became visible after a single radar sweep.

Klein analyzed the radar tapes from the predawn missile attack. He replayed those fateful forty seconds over and over again, searching for any differences between Riley's experience of the A-6s returning from their sorties and his experience of the Silkworm blip.

That's when Klein suddenly saw the discrepancy. It was subtle, but crystal clear. He could finally explain Riley's intuitive insight.

The secret was the timing. Unlike the A-6, the Silkworm didn't appear off the coast right away. Because it traveled at such a low altitude, nearly two thousand feet below an A-6's, the signal of the missile was initially masked by ground interference. As a result, it wasn't visible until the
third
radar sweep, which was eight seconds after an A-6 would have appeared. Riley was unconsciously evaluating the altitude of the blip, even if he didn't know he was doing it.

This is why Riley got the chills when he stared at the Iraqi missile on his radar screen. There was something strange about this radar blip. It didn't feel like an A-6. Although Riley couldn't explain why he felt so scared, he knew that something scary was happening. This blip needed to be shot down.

The question still remains: how did Riley's emotions manage to distinguish between these two seemingly identical radar blips? What was happening inside his brain when he first saw the Silkworm missile, three sweeps off the Kuwaiti coast? Where did his fear come from? The answer lies in a single molecule, called dopamine, that brain cells use to communicate with one another. When Riley stared at the radar screen, it was most likely his dopamine neurons that told him he was looking at a missile and not an A-6 fighter jet.

The importance of dopamine was discovered by accident. In 1954, James Olds and Peter Milner, two neuroscientists at McGill University, decided to implant an electrode deep into the center of a rat's brain. The precise placement of the electrode was largely happenstance; at the time, the geography of the mind remained a mystery. But Olds and Milner got lucky. They inserted the needle right next to the nucleus accumbens (NAcc), a part of the brain that generates pleasurable feelings. Whenever you eat a piece of chocolate cake, or listen to a favorite pop song, or watch your favorite team win the World Series, it is your NAcc that helps you feel so happy.

But Olds and Milner quickly discovered that too much pleasure can be fatal. They placed the electrodes in several rodents' brains and then ran a small current into each wire, making the NAccs continually excited. The scientists noticed that the rodents lost interest in everything. They stopped eating and drinking. All courtship behavior ceased. The rats would just huddle in the corners of their cages, transfixed by their bliss. Within days, all of the animals had perished. They died of thirst.

It took several decades of painstaking research, but neuroscientists eventually discovered that the rats had been suffering from an excess of dopamine. The stimulation of the NAcc triggered a massive release of the neurotransmitter, which overwhelmed the rodents with ecstasy. In humans, addictive drugs work the same way: a crack addict who has just gotten a fix is no different than a rat in an electrical rapture. The brains of both creatures have been blinded by pleasure. This, then, became the dopaminergic cliché; it was the chemical explanation for sex, drugs, and rock and roll.

But happiness isn't the only feeling that dopamine produces. Scientists now know that this neurotransmitter helps to regulate
all
of our emotions, from the first stirrings of love to the most visceral forms of disgust. It is the common neural currency of the mind, the molecule that helps us decide among alternatives. By looking at how dopamine works inside the brain, we can see why feelings are capable of providing deep insights. While Plato disparaged emotions as irrational and untrustworthy—the wild horses of the soul—they actually reflect an enormous amount of invisible analysis.

Much of our understanding of the dopamine system comes from the pioneering research of Wolfram Schultz, a neuroscientist at Cambridge University. He likes to compare dopamine neurons (those neurons that use dopamine to communicate) to the photoreceptors on the retina, which detect the rays of light entering the eye. Just as the process of sight starts with the retina, so the process of decision-making begins with the fluctuations of dopamine.

As a medical student in the early 1970s, Schultz grew interested in the neurotransmitter because of its role in triggering the paralyzing symptoms of Parkinson's disease. He recorded from cells in the monkey brain, hoping to find which cells were involved in controlling the body's movements. But he couldn't find anything. "It was a classic case of experimental failure," he says. "I was a very frustrated scientist." But after years of searching, Schultz noticed something odd about these dopamine neurons: they began to fire just before the monkey was given a reward, such as a pellet of food or a bit of banana. (The rewards were used to get the monkeys to move.) "At first I thought it was unlikely that an individual cell could represent anything so complicated as food," Schultz says. "It just seemed like too much information for one neuron."

After hundreds of experimental trials, Schultz began to believe his own data; he realized he had accidentally found the reward mechanism at work in the primate brain. In the mid-1980s, after publishing a series of landmark papers, Schultz set out to decipher this reward circuitry. How exactly did a single cell manage to represent a reward? And why did it fire
before
a reward was given?

The Schultz experiments followed a simple protocol: he sounded a loud tone, waited for a few seconds, and then squirted some drops of apple juice into the mouth of a monkey. While the experiment was unfolding, Schultz was probing the monkey brain with a needle that monitored the electrical activity inside individual cells. At first, the dopamine neurons fired only when the juice was delivered. The cells were responding to the actual reward. However, once the animal learned that the tone preceded the arrival of juice—this required only a few trials—the same neurons began firing at the sound of the tone instead of at the sweet reward. Schultz called these cells "prediction neurons," since they were more concerned with
predicting
rewards than actually receiving them. (This process can be indefinitely extended: the dopamine neurons can be made to respond to a light that precedes the tone that precedes the juice, and so on.) Once this simple pattern was learned, the monkey's dopamine neurons became exquisitely sensitive to variations on it. If the cellular predictions proved correct, and the reward arrived right on time, then the primate experienced a brief surge of dopamine, the pleasure of being right. However, if the pattern was violated—if the tone was played but the juice never arrived—then the monkey's dopamine neurons decreased their firing rate. This is known as the prediction-error signal. The monkey felt upset because its predictions of juice were wrong.

What's interesting about this system is that it's all about
expectation.
Dopamine neurons constantly generate patterns based on experience: if this, then that. They learn that the tone predicts the juice, or that the light predicts the tone that predicts the juice. The cacophony of reality is distilled into models of correlation that allow the brain to anticipate what will happen next. As a result, the monkeys quickly learn when to expect their sweet reward.

After refining this set of cellular forecasts, the brain compares these predictions to what actually happens. Once the monkey is taught to expect juice after a certain sequence of events, its dopamine cells carefully monitor the situation. If everything goes according to plan, its dopamine neurons secrete a little burst of enjoyment. The monkey is happy. But if these expectations aren't met—if the monkey doesn't get the promised juice—the dopamine cells go on strike. They instantly send out a signal announcing their mistake and stop releasing dopamine.

The brain is designed to amplify the shock of these mistaken predictions. Whenever it experiences something unexpected—like a radar blip that doesn't fit the usual pattern, or a drop of juice that doesn't arrive—the cortex immediately takes notice. Within milliseconds, the activity of the brain cells has been inflated into a powerful emotion. Nothing focuses the mind like surprise.

This fast cellular process begins in a tiny area in the center of the brain that is dense with dopamine neurons. Neuroscientists have known for several years that this region, the anterior cingulate cortex (ACC), is involved in the detection of errors. Whenever the dopamine neurons make a mistaken prediction—when they expect juice but don't get it—the brain generates a unique electrical signal, known as error-related negativity. The signal emanates from the ACC, so many neuroscientists refer to this area as the "oh, shit!" circuit.

The importance of the ACC is revealed by the layout of the brain. Like the orbitofrontal cortex, the ACC helps control the conversation between what we know and what we feel. It sits at the crucial intersection between these two different ways of thinking. On the one hand, the ACC is closely connected to the thalamus, a brain area that helps direct conscious attention. This means that if the ACC is startled by some stimulus—like the bang of a gunshot it didn't expect—it can immediately focus on the relevant sensation. It forces the individual to notice the unexpected event.

While the ACC is alerting the consciousness, it's also sending signals to the hypothalamus, which regulates crucial aspects of bodily function. When the ACC is worried about some anomaly—for instance, an errant blip on a radar screen—that worry is immediately translated into a somatic signal as the muscles prepare for action. Within seconds, heart rate increases, and adrenaline pours into the bloodstream. These fleshly feelings compel us to respond to the situation
right away.
A racing pulse and sweaty palms are the brain's way of saying that there's no time to waste. This prediction error is urgent.

But the ACC doesn't just monitor erroneous predictions. It also helps remember what the dopamine cells have just learned, so that expectations can be quickly adjusted in light of new events. It internalizes the lessons of real life, making sure that neural patterns are completely up to date. If it was predicted that juice would arrive after the tone, but the juice never arrived, then the ACC makes sure that future predictions are revised. The short-term feeling is translated into a long-term lesson. Even if the monkey is unaware of what, exactly, the ACC has memorized, the next time it's waiting for a squirt of juice, its brain cells are prepared. They know exactly when the reward will arrive.