The Pain Chronicles

by Melanie Thernstrom

  “It was easier to be alone with the pain,” she said. Like the wounded animal that instinctively separates itself from the herd, many patients with chronic pain are alone. “I couldn’t hold anyone,” another woman who was suffering from a frozen shoulder explained to me. “My hands were full with pain.”

  Because the head is the exclusive home of four of the five senses by which the brain is informed of the outside world, it is commensurately well protected by sensory nerves. Indeed, with the exception of the hands, the brain devotes more space to processing sensory information from the head than it does to the entire rest of the body. Damage to facial nerves thus has the capacity to cause great suffering.

  Dr. Carr asked Lee to describe the headaches. Like most of the hundred-odd patients I observed in various pain clinics trying to describe their suffering, Lee seemed stumped by the question. Elaine Scarry characterizes pain as not only not a linguistic experience, but as a language-destroying experience. “Whatever pain achieves, it achieves in part through its unsharability, and it ensures this unsharability through its resistance to language,” she writes, citing Virginia Woolf’s famous observation that “English, which can express the thoughts of Hamlet and the tragedy of Lear, has no words for the shiver and the headache . . . [L]et a sufferer try to describe a pain in his head to a doctor and language at once runs dry.”

  Part of the curse of pain is that it sounds untrue to people who don’t have pain. Patients grope at metaphors that seem melodramatic, both far-fetched and clichéd. “A hot, banging pain, like an ice pick,” a homeless man described the diabetic neuropathy that scalds his thighs and feet as the small nerves die, deprived of oxygen by the disease. “It heats up and then sticks it in, again and again,” he told Dr. Carr. “It holds my feet in the fire.” He broke off, his face twisting into the particular stricken bewilderment that I observed on the faces of patients whom I watched in different pain clinics describe their afflictions: What is tormenting me and why?

  “It’s like being slammed into a wall and totally destroyed,” Lee said. “It makes you want to pull every hair out of your head. There’s nothing I can do to defend myself. It’s like knives are going through my eyes.” She started to weep again.

  I felt the need to interrupt—to contradict or console. But Dr. Carr sat calmly as she blotted her face, his concentration fixed, his hands folded reassuringly across his lap, with the equable, impersonal kindness of a priest or a cop. Almost all of the patients during the long day broke down during their appointments. Perhaps because their lives echo the chaos in his own blue-collar Irish-Catholic upbringing as the son of an alcoholic bartender, he said, he isn’t alarmed when patients scream at him. He is neither indifferent to emotion nor distracted by it; at all times, his focus is on the culprit—the shape-shifter, the pain.

  Dr. Carr asked Lee to close her eyes, and he tapped her head with the stiff corner of an unopened alcohol wipe. Within a few minutes he had found a clear pattern of numbness that suggests that one of the main nerves in her face—the occipital nerve—was severed during her surgery. It was clear from their differing expressions that Dr. Carr regarded this as revelation—the demystification of her pain—and that Lee had no idea why.

  I felt her bewilderment: What was the connection between tapping with an alcohol wipe and the bottomless sorrow of her experience?

  Lee’s voice became small as she asked, “If the nerve was cut, how could it cause pain?”

  THE UNDEADNESS OF DEAD NERVES

  How, indeed?

  It is only recently that such phenomena have been understood. Doctors used to be entirely confident that severed nerves could not transmit pain—they’re severed! Nerve cutting was even seen as the solution for many pain syndromes in the nineteenth and the first half of the twentieth centuries, a treatment no more effective than the old European practice of cauterizing wounds with boiling oil (standard until Ambroise Paré ran out of oil on the battlefield one day and noticed the next morning that the patients he had neglected to cauterize had fared better than those whose limbs had been helpfully scalded with boiling oil).

  Americans are routinely schooled about many things, yet the inner workings of our bodies remain more remote than the turning of the planets. Certainly I had no model in my mind of the nervous system. I knew that severed nerves in the spinal cord cause paralysis. But I did not know that there are different types of nerves and that movement is enabled by motor neurons, whereas pain is transmitted by sensory neurons. Damaged or severed sensory nerves can cause only numbness, but they can also grow back irregularly and begin firing spontaneously, producing stabbing, electrical, or shooting sensations. Destroying sensory nerves as a treatment for pain usually makes sense only in the case of terminally ill patients who will die before the nerves begin to regenerate.

  “Sensory nerves can come back,” Dr. Scott Fishman quipped, “and when they do, they come back angry.”

  Indeed, nerve damage is now understood to be the cause of many chronic pain syndromes. The undeadness of dead nerves is at the center of the mystery of chronic pain—the ghost ringing the church bell in the empty steeple, signaling destruction on the land. Much chronic pain is now understood to be neuropathic—a pathology of the nervous system originating either in damage to the central nervous system of the brain and spinal cord or in damage to peripheral sensory nerves.

  I took notes on science, medical terms, and studies in a pink spiral-bound notebook, which (unlike my green “Patient Interviews” or my yellow “Representation of Pain in Art, Lit, and Religion” notebooks) I presumed would be the boring notebook. In fact, I had allotted science my favorite color in order to offset its expected tedium. But the more I researched the science of chronic pain, the less dry and the more menacing it seemed.

  Physical pain changes the body in the same way that emotional loss watermarks the soul. The body’s pain system is not hardwired, but soft-wired (what neuroscientists call “plastic”), and it can be maladaptively molded by pain to increase its pain sensitivity. Ordinarily we think of neuroplasticity as being a positive trait: as the brain adapts to its circumstances and learns new things, new nervous pathways are laid down and old neural pathways disappear, the way the forest reclaims an untrodden path. But in the case of persistent pain, neuroplasticity is negative. The nerves in the spinal cord become hyperexcitable and begin spontaneously firing and recruiting other nerves in their service, and the whole system revs up to be increasingly responsive to pain, in a phenomenon discovered by the pain researcher Clifford Woolf and termed peripheral sensitization (when hypersensitivity occurs in the periphery of the body) or central sensitization (when hypersensitivity occurs within the central nervous system).

  While the threshold to trigger the damage-detecting sensory neurons (nociceptors) is normally set by evolution at a relatively fixed point for all members of a species, peripheral sensitization and central sensitization lower that threshold, so that ordinary stimuli become painful. Central and peripheral sensitization routinely happen in a mild way after any injury, to protect the area. If you burn yourself, for example, an hour later a circle of redness will develop around the wound as the injured nerves transmit messages to the neighboring nerves, and the whole area develops an abnormal sensitivity. This heightened sensitivity serves the adaptive function of discouraging contact with the damaged tissue. If you take a bath, warm water that feels pleasant on most of your body will suddenly sting the burned area. To someone whose nervous system has been sensitized by a migraine, loud noise or bright light will hurt.

  Normally, the wound begins to heal and the sensitization disappears. But in some chronic pain syndromes the sensitivity endures. Harmless stimuli—pressure or light touch—become painful, in a phenomenon known as allodynia. Ordinarily, light touch is transmitted by different nerves from those that register pain. In allodynia, however, the light-touch nerves change so that they function as pain nerves. To someone suffering from allodynia (which can afflict sufferers of the pain syndromes tr
igeminal neuralgia, postherpetic neuralgia, fibromyalgia, and peripheral neuropathy caused by injury or by a disease such as diabetes), tears can scald, a caress can feel like a blow, and the light pressure of a sock can feel like the hot iron shoes in which the wicked queen in “Snow White” was forced to dance until she died. Patients become, literally, afraid to move.

  While allodynia involves harmless stimuli being misperceived as pain, chronic pain sufferers can also suffer from heightened sensitivity to painful stimuli, in a process known as hyperalgesia that involves an amplification of pain signals (in the periphery, or in the spinal cord, or in the brain itself). Hyperalgesia can endure long after its initial protective function has been served.

  Pain begets pain. The longer that pain pathways relay pain messages, the more efficient those pathways become, causing greater pain to be transmitted, the way a stream carves a path through land, so that over time, it flows more quickly and turns into a river. Research by Allan Basbaum at the University of California, San Francisco, has shown that progressively deeper levels of pain cells in the spinal cord are activated with prolonged injury.

  Hyperalgesia is a feature of many pain syndromes. Diabetic neuropathy, for example, can damage the nerves in one foot, causing local pain and numbness in it. Yet as the sufferer’s entire nervous system is changed by pain over time, the other foot can become hyperalgesic as well, even though the nerves in that foot appear to be normal. Like the multiplying swarms of demons who slipped through the unguarded openings of the ancients’ bodies to gorge on their blood and feast on their organs, the pain that pain spawns is ever more malign.

  In short, I scrawled on the cover of the pink notebook, “Bad, bad news.”

  NEUROPATHIC PAIN SYNDROMES

  Understanding chronic pain as a disease of the central nervous system sheds light on the riddle of chronic pain, solving the question of why, for many pain syndromes, there is no clear cause and why, even in pain syndromes where there is a clear-cut cause of pain, the cause bears no clear relation to the severity of the pain. Terrible osteoarthritis can be accompanied by mild (or no) pain, while mild degenerative osteoarthritic changes can cause crippling agony.

  Ordinary conditions cause extraordinary pain—in some people. MRIs show only bones and tissue; doctors look at the patient’s scan and say, “Your back looks fine, the swelling is gone” or “The bone’s all healed,” and they conclude that there is no reason for the patient still to be suffering. One study indicated that a full one-third of damaged disks looked normal on an MRI; another study indicated that nearly half of patients under sixty who had visibly degenerated disks on an MRI felt normal. The problem does not always lie in the tissue and bones; it can lie in the invisible hydra of nerves that MRIs often cannot detect.

  Not all chronic pain is neuropathic. There is also muscular pain, nociceptive pain (pain that stems from tissue damage or inflammation), and psychogenic pain (physical pain that is caused, augmented, or prolonged by emotional factors). Pain-causing conditions usually involve multiple types of pain. However, many chronic pain complaints, like backache, that were once assumed to be wholly musculoskeletal, are now thought to have a hidden neuropathic component. Over time, neuropathic pain leads to musculoskeletal pain. Nerve pain makes muscles spasm, which in turn interferes with normal use of the area, which causes weakness and eventually atrophy. Changes in the person’s mood and sleep and finally personality set in, and the original problem—the nerve injury—becomes harder to detect.

  “There’s tremendous ignorance about neuropathic pain,” commented Dr. Clifford Woolf, a Harvard professor who is one of the world’s foremost researchers of neuropathic pain. “Most doctors don’t know to look for it.”

  Many unexplained chronic pain syndromes that appear not to be coupled with any nerve injury may be a result of a neurobiological amplification of pain signals that leads to central sensitization and hyperalgesia. With IBS (irritable bowel syndrome), which causes unexplained intestinal distress, for example, the abnormality may not originate in the intestines themselves, but rather in the person’s central nervous system.

  Another good example is fibromyalgia, a baffling syndrome that disproportionately affects women, the symptoms of which include chronic muscular pain, fatigue, depression, and heightened sensitivity to touch. Patients feel as if they have been “beaten up,” as one patient put it, or are achy from a flu that never goes away. The disturbance appears to reside not in their muscles, but in their nervous systems. Fibromyalgia patients have been shown to have lower pain thresholds and altered chemistry in their spinal cords and in the parts of their brains involved in regulating pain. They also suffer from a dysregulation of the neurotransmitter dopamine (which is intimately involved in feelings of well-being) and a dysregulation of the neurotransmitters serotonin and norepinephrine (which are involved in both depression and pain modulation). The predilection to develop fibromyalgia is likely to be genetic.

  Although fibromyalgia has been studied since the seventeenth century, it was not formally recognized as a disease until 1987, and many physicians continue to believe it is a psychological disorder. Of the dozens of women I saw in pain clinics during my research who were suffering from fibromyalgia, every one had had the experience of being disbelieved and being asked questions such as “Are you having marital problems?” in an insinuating tone, as if that were the cause of their pain. (And many were; chronic disease usually causes marital problems.)

  Dr. Richard Gracely and Dr. Daniel Clauw have examined fibromyalgia patients and patients suffering from lower-back pain that has no identified cause. In one study, they attached a small device to the base of subjects’ thumbnails that applied pulsing pressure at varying levels ranging from innocuous to painful. The investigators discovered that the subjects with fibromyalgia and back pain said they experienced mild pressure as painful, while the healthy control subjects experienced the squeeze as only slightly unpleasant.

  Were those patients just—as British doctors like to say—moaners? Before the invention of functional brain imaging (a technique that allows researchers to take a video of sorts, or a 3-D movie, of the brain as it responds to pain), the question would have been unanswerable. Doctors’ impressions of patients’ credibility would have been mainly a reflection of their own personalities and whether they were inclined to believe or disbelieve patients. But in the Gracely and Clauw study, functional imaging was able to see that the patients were truthfully describing their experiences as the imaging documented activation in the pain-processing areas of the brain—activation that was not seen in the control subjects’ brains until the pressure on their thumbs was dramatically increased.

  What was the pain-processing circuitry in my brain like? I wondered when I read about the study. Was there a brain imaging study I could volunteer for?

  SURGICAL PAIN SYNDROMES

  Surgeons warn patients of many remote risks, from blood clots to the possibility of anesthesia producing a fatal reaction, but they often don’t mention (and perhaps remain largely unaware of) the much more likely possibility of developing chronic neuropathic pain. One of Dr. Carr’s patients was a wealthy man whose life was ruined by having a nerve nicked during plastic surgery to correct protruding ears. Another patient acquired chronic chest pain after being treated in a hospital for a collapsed lung, when a tube was inserted in her chest—one of the body’s most nerve-rich areas. One poignant category of patients in pain clinics is that of those who have had surgery specifically to treat chronic pain, but instead, whose surgery worsened their pain, an outcome for which they say they had no warning. Pain following the common back surgery of laminectomy (which removes part of the vertebral bone and sometimes surrounding ligaments and muscles as well) is so common that it has a name (post-laminectomy syndrome).

  The classic method of performing a thoracotomy (a chest incision that cuts through ribs to gain access to the heart, lungs, or other organs) carries a high risk of lasting pain. In one study, 30 percent of patients repor
ted pain four years after their surgery. “If you ask thoracic surgeons,” Dr. Woolf said, “they would say, these are big life-threatening situations—heart surgery or cancer. The fact that the patient has pain for the rest of his life is not important—they feel, ‘I saved your life, what do you expect?’ Pain is not seen as life threatening. And until patients have pain, they can’t imagine what it’s like—the way it’s there all the time and makes you miserable.”

  A significant percentage of cancer survivors suffer from chronic pain, stemming either directly from their tumors or from their treatment (radiation and chemotherapy can damage nerves just as surgery can). Moreover, survivors often have difficulty finding doctors willing to prescribe opioids once their pain no longer enjoys the social sanctification accorded by malignancy.

  A landmark 1997 University of Toronto study by Dr. Anna Taddio and others has troubling implications about the impact of pain on infants and children. The study compared the pain responses of groups of infant boys who were uncircumcised, circumcised with an anesthetic cream, and circumcised without anesthesia. Four to six months later, the group who had been circumcised without anesthesia had the lowest pain threshold, crying longer and showing more visible signs of pain at their first inoculations, providing evidence that there is enduring cellular pain memory when damage is inflicted upon the immature nervous system.

  A CLASSIC MISINTERPRETATION

  At some level, every doctor is familiar with central sensitization because they know that a patient who comes in with twenty years of back pain is more than twenty times less likely to get well than one who comes in after just six weeks (a fact I wish I had appreciated before my pain settled in).