Complications (17 page)

According to the new theory, pain and other sensations are conceived as “neuromodules” in the brain—something akin to individual computer programs on a hard drive, or to tracks on a compact disc. When you feel pain, it’s your brain running a neuromodule that produces the pain experience, as if someone pressed the
PLAY
button on a CD player. And a great many things can press the button (besides a neurosurgeon zapping the right neuron with low DC voltage). The way Melzack explains it, a pain neuromodule is not a discrete anatomical entity but a network, linking components from virtually every region of the brain. Input is gathered from sensory nerves, memory, mood, and other centers, like members of some committee in charge of whether the music will play. If the signals
reach a certain threshold, they trigger the neuromodule. And then what plays is no one-note melody. Pain is a symphony—a complex response that includes not just a distinct sensation but also motor activity, a change in emotion, a focusing of attention, a brand-new memory.

Suddenly, a simple toe-stubbing no longer seems so simple. In this view, the signal from the toe still has to make it through the spinal-cord gate, but thereafter it joins a lot of other signals in the brain—from memories, anticipation, mood, distractions. Altogether, they may combine to activate a toe-pain neuromodule. In some people, however, the physical stimulus may be canceled out and the stubbed toe hardly noticed. There’s nothing surprising here so far. But now we can imagine—and this is the most radical implication of Melzack’s ideas—that the same neuromodule can go off, generating genuine toe pain, without a toe’s having been stubbed at all. The neuromodule could—like Site 23 in Mark Taylor’s brain—become primed like a hair trigger. Then virtually anything could set it off: a touch, a stab of fear, a sudden frustration, a mere memory.

The new theory about the psychology of pain has, almost perversely, helped give direction to the pharmacology of pain. For pharmacologists, the Holy Grail of chronic-pain treatment is a pill that would be more effective than morphine but lack its side effects, such as dependence, sedation, and motor impairment. If an overactive neuronal system is the problem, then what one needs is a drug that will damp it down. That’s why, in what a decade ago might have seemed a strange development, pain specialists increasingly prescribe anti-epileptic drugs, like carbamazepine and gabapentin, for their most difficult-to-treat patients. After all, that’s what these drugs do: they tune brain cells to modulate their excitability. So far, these kinds of drugs work only for some people—Quinlan has been on gabapentin for more than six months without much effect—but drug companies are hard at work on a new generation of similar “neuro-stabilizing” compounds.

Neurex, for example, a small Silicon Valley biotechnology company (now called Elan Pharmaceuticals), not long ago designed a pain drug from the venom of the Conus sea snail following such thinking. Venoms are, needless to say, biologically potent, and, unlike most of the proteins from nature that scientists have tried to use as drugs, they evade the body’s mechanisms for breaking proteins down. The trick is to tame the venom, to modify it so it is medically useful. The Conus venom was known to kill by blocking specific pathways in the brain that are necessary in order for neurons to fire. With a few alterations, however, Neurex scientists created Ziconotide, a drug that only slightly inhibits those pathways. Instead of shutting brain cells down, it seems to merely mute their excitability. In initial clinical trials, Ziconotide effectively controlled chronic pain from cancer and from AIDS. Another new generation analgesic in development is Abbott Laboratories’ ABT-594, a compound related to a poison secreted by an Ecuadorian frog,
Epibpedobates tricolor
. In animal experiments that were published in the journal
Science
, ABT-594 proved to be as much as fifty times as potent as morphine in relieving pain. Companies have other pain drugs in the pipeline, too, including a class of drugs known as NMDA antagonists, which also work by reducing neuronal excitability. One of these could turn out to be the painkiller that Quinlan and patients like him are looking for.

At best, however, these drugs represent only a halfway solution. The fundamental problem for research is how to stop the pain system in such patients from going haywire in the first place. The stories that people tell of their chronic pain typically start with an initial injury. So, historically, we have tried to prevent chronic pain by preventing acute strains. A whole ergonomics industry has developed around this idea. Yet the lesson from Ross’s pain clinic and Lenz’s operating table is that the antecedents of pain lie elsewhere than in the muscle and bone of patients. In fact, some forms of chronic pain behave astonishingly like social epidemics.

In Australia during the early 1980s, workers—particularly keyboard operators—experienced a sudden outbreak of disabling arm pain, which doctors labeled “repetition strain injury,” or RSI. This was not a mild case of writer’s cramp but a matter of severe pain, which started with minor discomfort during typing or other repetitive work and progressed to invalidism. The average time that a sufferer lost from work was seventy-four days. As with chronic back pain, no consistent physical abnormalities or effective treatment could be found, yet the arm pain spread like a contagion. It had hardly existed before 1981, but by its peak, in 1985, enormous numbers of workers were affected. In two Australian states, RSI disabled as much as 30 percent of the workforce in some industries; at the same time there were pockets of workers who were almost entirely unaffected. Clusters appeared even within a single organization. At Telecom Australia, for example, the incidence of RSI among telephone operators in a single city varied widely between departments. Nor could investigators find any connection between RSI and the physical circumstances of the workers—the actual repetitiveness of their jobs or the ergonomics of their equipment. Then, as suddenly as it had begun, the epidemic crashed. By 1987, it was essentially over. In the late 1990s, Australian researchers were complaining that they couldn’t find enough RSI patients to study.

Chronic back pain has been with us for so long that it is hard conceptually—and even politically—to step back and recognize its social etiology, let alone figure out how cultural factors make an individual’s pain system go awry. The Australian pain epidemic demonstrates the power of those factors to cause genuine, disabling pain on a national scale, and yet our knowledge of these causes and how to control them is meager. We know from a variety of studies that social-support networks—a happy marriage and satisfying employment, say—protect against disabling back pain. We know, statistically speaking, that being given certain diagnostic labels and being provided disability pay (and thus a kind of official recognition and validation) can perpetuate chronic pain. In Australia, for example, many
researchers believe that two major factors that sparked the epidemic were the coining of RSI as a diagnostic label and early action by the government to insure compensation for the syndrome as a work-related disability. When the diagnosis fell out of favor with physicians, and disability coverage became harder to get, the incidence of the symptoms associated with the disorder plummeted. It also appeared that initial publicity about the possible portents of arm pain and concerted campaigns in some places to increase the reporting of arm pains or to institute ergonomic changes only contributed to the epidemic. More recently, in the United States, a debate has erupted over the origins of a similar workplace epidemic, called, variously, repetitive-stress injury, repetitive-motion disorder, and—in the currently favored nomenclature—cumulative-trauma disorder. Once again, the salient risk factors seem to be social rather than physical.

Back and arm pain are not unique in having nonphysical causes. Studies have shown that social conditions play a dominant role in many chronic-pain syndromes, including chronic pelvic pain, temporomandibular-joint disorder, and chronic tension headache, to name just a few. Again, none of this should be taken to mean that people are faking it. As Melzack’s account suggests, pain that doesn’t arise from physical injury is no less real than pain that does—in the brain it is precisely the same. And so a compassionate approach toward chronic pain means investigating its social coordinates, not just its physical ones. For the solution to chronic pain may lie more in what goes on around us than in what is going on inside us. Of all the implications of the new theory of pain, this one seems to be the oddest and the most far-reaching: it has made pain political.

I
n the beginning, the nausea didn’t seem anything to worry about. Amy Fitzpatrick was eight weeks pregnant—with twins, as an ultrasound had revealed—and, having watched her sister and her friends go through their pregnancies, she understood that nausea was simply part of the deal. Her first episode was certainly inconvenient, though. She was on New York City’s F.D.R. Drive, piloting her Honda Civic to work through the frantic rush of morning traffic. Speeding along at fifty miles per hour, she realized that she was about to throw up.

Fitzpatrick was twenty-nine years old, tall, with long, thick black hair set against pale Irish skin and a dimpled, almost teenage face that sometimes made it hard for people to take her seriously, despite her Wharton M.B.A. She lived in Manhattan, where her husband was an investment banker, and she commuted to Manhasset, on Long Island, where she worked as a management consultant for the North Shore Health System. It was a brisk March morning, and she needed to find somewhere to pull over fast.

As she got off the F.D.R. onto the ramp to the Triborough Bridge, her head was swimming and her stomach was roiling. She was in what scientists call the “prodromal phase of emesis.” Salivation increases, sometimes torrentially. The pupils dilate. The
heart begins to race. The blood vessels in the skin constrict, increasing pallor—NASA scientists have even used skin sensors to detect space sickness in astronauts, who are sometimes reluctant to admit experiencing nausea. People break out in a cold sweat. Fatigue and often drowsiness occur in minutes. Attention, reflexes, and concentration wane.

While all this is going on, the stomach develops abnormal electrical activity, which prevents it from emptying and causes it to relax. The esophagus contracts, pulling the upper portion of the stomach from the abdomen, through the diaphragm, and into the chest, forming a kind of funnel from stomach to esophagus. Then, in a single movement, known as the “retrograde giant contraction,” the upper small intestine evacuates its contents backward into the stomach in preparation for vomiting. In the lower small intestine, smaller rhythmic contractions push the contents into the colon.

As Fitzpatrick came off the exit ramp, the lanes opened out like a fan, and all the drivers around her jockeyed for position. She looked for a place to pull over on the right side of the road, but there wasn’t any. She started to cut across the lanes to the left, aiming for a no-man’s-land between the traffic going into the toll booths and the traffic coming out from the other direction. She began to retch, and she fished out an empty plastic grocery bag. Then she vomited. Some of the vomit hit the dress and jacket she wore. Some got into the bag she held with one hand. She kept her eyes open and kept the car steady, though, and made it out of the traffic. Then she braked to a halt, bent forward against her shoulder belt, and brought up whatever she had left.

The vomiting act itself has two phases. The retching phase involves a few rounds of coordinated contractions of the abdominal muscles, the diaphragm, and the muscles of respiratory inspiration. So far, nothing has come out. In the expulsive phase, the diaphragm and the abdomen undergo a massive, prolonged contraction, generating intense pressure in the stomach; when the esophagus relaxes,
it’s
as if someone had taken the plug off a fire hydrant.

Vomiting usually makes people feel better, at least for a little while, but Fitzpatrick didn’t feel any better. She sat there with the cars rushing by, waiting for the sick feeling to pass, but it didn’t. Eventually, still queasy, she drove over the bridge, turned the car around, went home, and climbed into bed. Over the next few days, she began to lose her appetite, and strong odors became intolerable. Easter came that weekend, and she and her husband, Bob, drove down to Alexandria, Virginia, to see her family. She was barely able to tolerate the ride, and had to spend it lying flat on the backseat. It would be months before she could make it back to New York.

At her parents’ home, her symptoms rapidly escalated. That weekend, she was unable to hold down any food or liquid at all. She became thoroughly dehydrated. The Monday after Easter, she spent a few hours at the hospital and got replenished with intravenous fluid. She saw her mother’s obstetrician, who reassured her that nausea and vomiting were normal during pregnancy, and gave her some common, practical advice: stay away from strong odors and cold liquids, and try to get down small amounts of food whenever possible—perhaps dry crackers and other carbohydrates. Since Fitzpatrick’s symptoms were normal, the doctor didn’t want to consider prescribing drugs. Pregnancy sickness, she pointed out, usually goes away by the fourteenth, at most the sixteenth, week of pregnancy.

Fitzpatrick was determined, but she found that she couldn’t tolerate anything except a bite of cracker or toast. By the end of the week, she needed more hydration, and the doctor arranged for a visiting nurse to come to her parents’ house and administer IV fluids. Fitzpatrick continually felt that she was on the verge of throwing up. She had been someone who could eat almost anything; now the smell of the blandest foods made her gag. She had always loved stomach-churning amusement park rides; now riding in a car or just standing up
or
tilting her head brought on severe motion sickness. She couldn’t make it down the stairs. Even in bed, watching TV or focusing on a magazine made her head reel. Over the next couple of
weeks, she would vomit five or six times a day. She lost twelve pounds instead of gaining weight, as a woman bearing twins should have. The worst of it was the sense that she was losing control of her life. The management executive in her couldn’t stand it. Here she was, back in the house she had grown up in. Her mother had to take a leave from teaching high school to care for her. She felt as if she were a helpless child.