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Pain Center
updated Friday, March 27, 2009

Perspectives in Intractable Pain Management An analysis of current diverging viewpoints

Healthcare Professionals' Perspective Fear of Addiction

Ultimately, clinicians want to relieve 100% of their patients pain; however, false notions of addiction blind them to the fact that opioids are safe, effective analgesics that relieve pain almost completely.1 To understand how opioids are effective for intractable pain without threat of addiction, it is necessary to understand what addiction is.

Addiction Defined

Addiction is defined by the American Society of Addiction Medicine as the abuse of any psychoactive substance with compulsion and loss of control despite adverse consequences.11 The American Medical Association Task Force defines addiction as a chronic disorder characterized by the compulsive use of a substance resulting in physical, psychological, or social harm to the user and continued use despite the harm.11 In other words, addiction involves a dependence upon a drug to experience euphoria despite harm to oneself or others.

Opioid use for intractable pain is not associated with dependency upon a drug despite harm to oneself.3 In fact, opioids increase intractable pain patients quality of life.

Patients do become physically dependent upon opioids3 because, without appropriate opioid therapy, they would continue to feel pain. Also, according to Aaron Gilson, Researcher at the Pain and Policy Studies Group at the University of Wisconsin, initial tolerance to opioids may result and, if abruptly taken off opioid treatment, withdrawal symptoms may arise. However, as Gilson goes on to explain, tolerance and withdrawal symptoms resulting from opioid treatment for intractable pain do not indicate addiction. These are simply physiological reactions to opioids. Studies have shown that less than 1% of those taking appropriate levels of opioids for pain management become addicted.1,4

Difference between pain patients and addicts

The difference between pain patients and addicts seeking euphoria is that patients can take increasing doses of opioids, as pain persists, without severe side effects while addicts cannot.4 As intractable pain continues to persist, usually a sign of disease progression, pain patients may require higher increments of opioids to relieve pain. Fortunately, opioids taken for intractable pain do not have a ceiling dosagea dosage where the drug can no longer treat a higher level of pain.12 In fact, according to Dr. William Hurwitz, pain patients who would otherwise be incapacitated by pain can increase their quality of life by taking dosage levels of opioids that would kill the average person.4

Although not proven, researchers believe that pain patients and addicts respond to opioids differently because the nervous pathway that transports intractable pain develops little to no tolerance to opioids. The nervous pathways that transport acute pain and pleasure do develop significant tolerance to opioids.7

Coalition of Pain Experts Offers Guidance on Measures to Prevent Misuse and Abuse of Pain Medications; Calls for Treating Chronic Pain as a Chronic Disease

PALM BEACH, Fla.An ad hoc coalition of leading pain specialists and representatives from key clinical and patient advocacy organizations convened in November 2008 to address the growing problem of misuse and abuse of pain medications, and to strengthen support for recognizing chronic pain as a distinct disease statean important step toward improving the diagnosis and treatment of patients with pain.

The roundtable included representatives from primary care and specialty medicine, nursing, nurse practitioners, and physician assistants, as well as representatives from the American Academy of Pain Medicine, the American Pain Society, the  American Chronic Pain Association, National Pain Foundation, the American Pain Foundation, and other leaders in the pain community.

The goals were to review the barriers to diagnosis and treatment of acute and chronic pain in clinical and community settings; increase public awareness of the disparities in pain treatment based on gender, race, ethnicity, and age, and provide recommendations to enable clinicians to overcome these barriers; implement management strategies to provide adequate pain relief for a spectrum of patients, including those who may be at highest risk for medication misuse, abuse, and diversion; and discuss emerging technologies to deter misuse, abuse, and diversion of opioids.

Roundtable participants began by delineating some of the current obstacles to meeting their goals, and then collaborated on possible solutions. One of the major obstacles, they argued, is the inconsistency of guidelines for the diagnosis and treatment of pain, which represent a number of individual organizations and pain societies. Therefore, reorganizing the organizations and societies in the pain community into a single united group could enhance cooperation and eliminate fragmented guidelines and treatment standards. Similarly, the lack of standardized procedures for patient assessments (which should include physical examination and functional evaluation before and during treatment) has led to a lack of outcomes data in pain medicine. Development of protocols for outcomes studiesparticularly studies that look at the effects of pain and treatment of pain on function and quality of lifeas well as the generation of best practices can help overcome these obstacles..

The medical communitys focus on global outcomes of treatment, rather than on patient-specific outcomes, is yet another obstacle to optimal treatment for pain. But by having patients actively involved in their management plan, healthcare providers can become more knowledgeable patient advocates with legislators, insurers, and other medical professionals. Because it is not possible to provide complete relief to all patients with pain, education about realistic treatment outcomes is key for both patients and healthcare providers. For example, by becoming active members of their treatment teams, patients may realize improved quality of life despite persistence of a certain level of pain.

Opioids are not appropriate for all patients with painfor example, those whose pain is mediated through inflammatory pathways, who are more effectively treated with anti-inflammatory drugs. Nor are opioids appropriate for patients who may misuse/abuse/divert these medications. However, this obstacle may be resolved by drugs in development that utilize novel tamper-resistant and abuse-deterrent technologies.  Furthermore, physicians prescribing of opioids has become limited not only by their abuse potential but also by the increased possibility of litigation and changes in medical insurance and governmental policies.

In the past 10 years, adolescents and young adults have escalated their abuse and non-medical use of opioids. In 2006, 10% of youths aged 12 to 17 were current illicit drug users, with 3% using prescription drugs nonmedically, and nearly 20% of young adults aged 18 to 25 used illicit drugs, with more than 6% using psychotherapeutics nonmedically.  At the same time, many (or even most) parents remain largely unaware that their children may be abusing drugs.

Roundtable participants agreed that many of these obstacles to effective diagnosis and management of pain could be resolved by making pain medicine a primary medical specialty. As a positive first step, they said, a 2-year fellowship or 4-year residency program in pain medicine should be established in the medical curriculum. Training for pain medicine specialists would include all facets of pain management (for example, anesthesiology, physiatry, psychiatry, rehabilitation). The benefits of this expertise in pain medicine could then be extended by incorporating pain management principles into other programs, promoting learning for nurse practitioners, physician assistants, and other allied health professionals.

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Study suggests physician concerns over widely publicized prosecutions are disproportionate to actual numbers of legal and regulatory actions

Contacts:  

Lorell R. LaBoube, Center for Practical Bioethics
(816)221-1100,  

Drew Carlson, Federation of State Medical Boards
(817) 868-4043

Angelita Plemmer, National Association of Attorneys General
(202)326-6047

September 9, 2008

Some doctors under treat pain partially out of an unrealistic fear of legal repercussions, causing many chronic-pain patients to continue to suffer even though effective pain medications may be available to help them.

A new study in the September 9 issue of Pain Medicine shows that between 1998 and 2006, only a tiny number of U.S. doctors actually appear to have been prosecuted or administratively sanctioned for improperly prescribing powerful pain medications. Over this eight year span, best-available data and records indicate that only about one in 1,000 practicing physicians was tried or sanctioned for offenses of this type. 

Study findings include the following:

725 physicians were identified as having been prosecuted or sanctioned for such violations during the nine-year time frame, or only about 0.1% of nearly 700,000 practicing patient care physicians in the US.

Most of the patient care doctors identified in such cases were primary care physicians rather than specialists in other fields, including pain medicine. Among the 725 physicians involved in these cases, only 25 were pain medicine specialists or self-identified as such. In contrast, General Practice/Family Medicine physicians accounted for 285.

In 2005 and 2006, the Drug Enforcement Administration reports having investigated an average of only 4-5 doctors per state each year for possible criminal offenses connected with improper prescription or handling of pain medications. 

Compared with physicians in the national workforce, significantly more of the study physicians were male, aged 55 or over, and lacked board certifications

The authors of the study say a balanced approach is required, one that will allow doctors to responsibly prescribe powerful pain medications without fear, while allowing enforcement agencies to continue preventing the diversion and misuse of regulated pain-controlling drugs.

"This study is the most comprehensive and systematic attempt to gather information on the numbers and types of physicians who actually have been tried and convicted for offenses involving improper prescribing or handling of controlled-substance pain medications," said Myra Christopher, president and CEO of the Center for Practical Bioethics.

The study analyzes the numbers and types of cases and physicians involved, criminal and administrative charges brought, and case outcomes and sanctions. It also examines the characteristics of the small number of physicians who have been involved in such cases, including medical specialty, age and medical school.
 
The study was authored by nine individuals associated with the Balanced Pain Policy Initiative, an undertaking of the Center for Practical Bioethics, the National Association of Attorneys General, and the Federation of State Medical Boards.

Christopher said results of this research suggest that physician fear of regulatory scrutiny cannot be explained by the actual rates of prosecution or administrative review. Reasons for this fear are more complex than an objective assessment of risk would suggest, she said.

"However, it is essential to address the problem, because this fear on the part of physicians can change prescribing behaviors and undermine the treatment of pain," said Christopher.

"Physicians and law enforcement must resolve competing perceptions surrounding the need to treat patients for pain and the need to prevent the diversion of drugs for illicit purposes," said Christopher. "All sides must work to achieve a balance between aggressive pain treatment and legal/regulatory policies that support the greater needs of society."

An estimated 70 million Americans suffer from chronic pain, resulting in more than 50 million lost workdays each year.

Links:

Authors and Affiliations
Key Findings
key Implications
Balanced Pain Policy Initiative Objectives and Working Group

Founded in 1984, the Center for Practical Bioethics is an independent organization nationally recognized for its work in practical bioethics. More than a think tank, the Center puts theory into action to help people and organizations find real-world solutions to complex issues in health and healthcare.

The Federation of State Medical Boards is a national not-for-profit organization representing the 70 medical boards of the United States and its territories, including 14 state boards of osteopathic medicine. Its mission is continual improvement in the quality, safety and integrity of health care through the development and promotion of high standards for physician licensure and practice.

The National Association of Attorneys General (NAAG) was founded in 1907 to help Attorneys General fulfill the responsibilities of their office and to assist in the delivery of high quality legal services to the states and territorial jurisdictions. NAAG fosters an environment of "cooperative leadership," helping Attorneys General respond effectively individually and collectively - to emerging state and federal issues.

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Who hasn't wished she could watch her brain at work and make changes to it, the way a painter steps back from a painting, studies it and decides to make the sky a different hue? If only we could spell-check our brain like a text, or reprogram it like a computer to eliminate glitches like pain, depression and learning disabilities. Would we one day become completely transparent to ourselves, and fully conscious of consciousness consciously create ourselves as we like?

The glitch I'd like to program out of my brain is chronic pain. For the past 10 years, I have been suffering from an arthritic condition that causes chronic pain in my neck that radiates into the right side of my face and right shoulder and arm. Sometimes I picture the pain soggy, moldy, dark or perhaps ashy, like those alarming pictures of smokers' lungs. Wherever the pain is located, it must look awful by now, after a decade of dominating my brain. I'd like to replace my forehead with a Plexiglas window, set up a camera and film my brain and (since this is my brain, I'm the director) redirect it. Cut. Those areas that are generating pain cool it. Those areas that are supposed to be alleviating pain hello? I need you! Down-regulate pain-perception circuitry, as scientists say. Up-regulate pain-modulation circuitry. Now.

Recently, I had a glimpse of what that reprogramming would look like. I was lying on my back in a large white plastic f.M.R.I. machine that uses ingenious new software, peering up through 3-D goggles at a small screen. I was experiencing a clinical demonstration of a new technology real-time functional neuroimaging used in a Stanford University study, now in its second phase, that allows subjects to see their own brain activity while feeling pain and to try to change that brain activity to control their pain.

Over six sessions, volunteers are being asked to try to increase and decrease their pain while watching the activation of a part of their brain involved in pain perception and modulation. This real-time imaging lets them assess how well they are succeeding. Dr. Sean Mackey, the study's senior investigator and the director of the Neuroimaging and Pain Lab at Stanford, explained that the results of the study's first phase, which were recently published in the prestigious Proceedings of the National Academy of Sciences, showed that while looking at the brain, subjects can learn to control its activation in a way that regulates their pain. While this may be likened to biofeedback, traditional biofeedback provides indirect measures of brain activity through information about heart rate, skin temperature and other autonomic functions, or even EEG waves. Mackey's approach allows subjects to interact with the brain itself.

"It is the mind-body problem right there on the screen," one of Mackey's collaborators, Christopher deCharms, a neurophysiologist and a principal investigator of the study, told me later. "We are doing something that people have wanted to do for thousands of years. Descartes said, 'I think, therefore I am.' Now we're watching that process as it unfolds."

Suddenly, the machine made a deep rattling sound, and an image flickered before me: my brain. I am looking at my own brain, as it thinks my own thoughts, including these thoughts.

How does it work? I want to ask. Just as people were once puzzled by Freud's talking cure (how does describing problems solve them?), the Stanford study makes us wonder: How can one part of our brain control another by looking at it? Who is the "me" controlling my brain, then? It seems to deepen the mind-body problem, widening the old Cartesian divide by splitting the self into subject and agent.

But most of all I want to know: Will I be able to learn it?

For most of history, the idea of watching the mind at work was as fantastical as documenting a ghost. You could break into the haunted house slice the brain open but all you would find would be the house itself, the brain's architecture, not its invisible occupant. Photographing it with X-rays resulted only in pictures of the shell of the house, the skull. The invention of the CT scan and magnetic resonance imaging (M.R.I.) were great advances because they reveal tissue as well as bones the wallpaper as well as the walls but the ghost still didn't show up. Consciousness remained elusive.

A newer form of M.R.I., functional magnetic resonance imaging (f.M.R.I.), used with increasingly sophisticated software, is accomplishing this, taking "movies" of brain activity. Researchers are able to watch the brain work, as the films show parts of the brain becoming active under various stimuli by detecting areas of increased blood flow connected with the faster firing of nerve cells. These films are difficult to read; researchers puzzle over the new images like Columbus staring at the gray shoreline, thinking, India? Most of the brain is uncharted, the nature of the terrain unclear. But the voyage has been made; the technology exists. Pain a complex perception occupying the elusive space spanning sensation, emotion and cognition is a particularly promising area of imaging research because, researchers say, it has the potential to make great progress in a short time.

Perhaps more than any other aspect of human existence, persistent pain is experienced as something we cannot control but desperately wish we could. Acute pain serves the evolutionary function of warning us of tissue damage, but chronic pain does nothing except undo us. Pain is the primary complaint that sends people to the doctor. Of the 50-odd million sufferers in the United States, half cannot get adequate relief from their chronic pain. Many do not even have a diagnosis.

Unlike acute pain, chronic pain is now thought to be a disease of the central nervous system that may or may not correlate with any tissue damage but involves an errant reprogramming in the brain and spinal cord. The brain can generate terrible pain in a wound that is long healed, in a body that is numb and paralyzed or in the case of phantom-limb pain in a limb that no longer even exists.

Although there have been many theories about how pain works in the brain, it is only through neuroimaging that the process has actually been observed. It is now clear that there is no single pain center in the brain. Rather, pain is a complex, adaptive network involving 5 to 10 areas of the brain transmitting information back and forth.

This network has two pain systems: pain perception and pain modulation, which involve both overlapping and distinct brain structures. The pain-modulatory system constantly interacts with the pain-perception system, inhibiting its activity. Much chronic pain is thought to involve either an overactive pain-perception circuit or an underactive pain-modulation circuit.

Like everyone who suffers from chronic pain, I find it hard to believe that I have a pain-modulation circuit. The aspect of my pain I feel most certain about is that it is not voluntary: I cannot modulate it. And this belief is reinforced every single day that I suffer from pain, which is every day. Yet I know that pain is not a fact, like a broken bone; it's a perception, like hunger, about a physical state ("an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage," as the International Association for the Study of Pain defines it). And it's a mercurial perception; under certain circumstances the pain-modulatory system works like a spell and the brain completely blocks out pain.

Soldiers, athletes, martyrs and pilgrims engage in battles, athletic feats or acts of devotion without being distracted by the pain of injuries. When the teenage surfer Bethany Hamilton's arm was bitten off by a shark, she felt pressure, but "I didn't feel any pain I'm really lucky, because if I felt pain, things might not have gone as well," she said (articulating one reason the modulatory system evolved: if she had thrashed about in pain, she would have bled until she drowned).

In addition to being activated by stress, the pain-modulatory system is triggered by belief. The brain will shut down pain if it believes it has been given pain relief, even when it hasn't (the placebo effect), and it will augment pain if it believes you are being hurt, even if you aren't (the nocebo effect). The brain's modulatory system relies on endogenous endorphins, its own opiatelike substances. The nature of a placebo has long been a source of speculation and debate, but neuroimaging studies have shown the way a placebo actually helps to activate the pain-modulatory system.

In a recently published study led by Dr. Jon-Kar Zubieta at the University of Michigan Medical School, the brains of 14 men were imaged after a stinging saltwater solution was injected into their jaws. They were then each given a placebo and told that it would positively relieve their pain. The men immediately felt better and the screen showed how. Parts of the brain that release endogenous opiates lighted up. In other words, fake opiates caused the brain to dispense real ones. Like some New Age dictum, philosophy becomes chemistry; believing becomes reality; the mind unites with the body.

Other studies have shown that opiates and other medications rely on a placebo to achieve part of their effect. When subjects are covertly given strong opiates like morphine, they don't work nearly as well as they do if the subjects are told they are being given a powerful pain reliever. Even real medications require some of the brain's own bounty.

Conversely, thinking about pain creates pain. In studies at Oxford University, Irene Tracey has shown that asking subjects to think about their chronic pain, for example, increases activation in their pain-perception circuits. Distraction, on the other hand, is a great analgesic; when Tracey's volunteers were asked to engage in a complicated counting task while being subjected to a painful heat stimulus, she could watch the pain-perception matrix decrease while cognitive parts of the brain involved in counting lighted up. At McGill University, Catherine Bushnell has shown that simply listening to tones while being subjected to a heat stimulus decreased activity in the pain-perception circuit.

"There is an interesting irony to pain," comments Christopher deCharms, who worked with Mackey designing and carrying out the Stanford study. We were talking in his office at Omneuron, a Menlo Park medical-technology company he founded three years ago to develop clinical applications of neuroimaging. "Everyone is born with a system designed to turn off pain. There isn't an obvious mechanism to turn off other diseases like Parkinson's. With pain, the system is there, but we don't have control over the dial."

The goal of the Stanford technique is to teach people to control their dials to activate their modulatory systems without requiring the extreme stress of fleeing from a shark or the deception of a placebo. The hope of neuroimaging therapy (as deCharms calls the Stanford technique) is that repeated practice will strengthen and eventually change the ineffective modulatory system to eliminate chronic pain, the way long-term physical therapy can change muscular weakness. The scan would thus be more than a research tool: the scan itself would be the treatment, and the subject his or her own researcher.

Only once do I recall having a glimmer of my own pain-modulatory system at work: a hidden power that emerged, dispensed with pain and then returned to some forgotten fold in my brain, where I have never been able to locate it again. The event did not take place on a battlefield or a marathon course or in a temple; it was in a basement of the Stanford University medical center three years ago. At the time, Mackey had designed an earlier study that did not use imaging technology but focused on how suggestion alters pain perception. Although I was not formally enrolled in the study, I asked if I could undergo a clinical demonstration. My experience illustrated the power of suggestion in an unexpected fashion.

A metal probe attached to the underbelly of my arm heated up and cooled down at set intervals. I was told that although the heat probe would feel uncomfortable, my skin would not be burned. During one exposure, I was instructed to think of the pain as positively as possible, during another to think of it as negatively. After each sequence, I was asked to rate my pain on a 0-to-10 scale, with 10 being the worst pain I could imagine.

Although I discovered that I could make the pain fluctuate depending on whether I was imagining that I was sunbathing or was the victim of an inquisition, I still rated all the pain as low ranging from a 1 to a 3. If 10 was being slowly burned alive, I felt I should at least be begging for mercy to justify a rating of 5. So I insisted that Mackey turn up the dial so I could get a real response. But even during the moments when I was actively trying to imagine the pain as negatively as possible, it remained in a mental box of "not even burned," which kept it from really hurting: hurting, that is, the way a burn would.

As it turned out, I got a second-degree burn that later darkened into a square mark. Mackey was more than a little dismayed as we watched the reddening skin pucker, but I was thrilled. Naturally the protocol had been carefully designed not to injure anyone, yet in my case that protection had failed because of the very phenomenon it was designed to study: expectation the effect of the mind on pain or placebo.

I had recently spent several weeks observing Mackey in the university's pain clinic, where he is associate director. I was so convinced that Mackey then a tall sandy-haired 39-year-old with a deep interest in technology (he got a Ph.D. in electrical engineering before he went to medical school) and an air of radiant integrity would not burn me that my brain had not perceived the stimulus as a threat and generated pain. I admired him, I trusted him, I was positive that he wouldn't hurt me. And, ipso facto, he hadn't.

Mackey's genius as a practitioner, I thought, lay partly in his ability to similarly inspire patients. "When I started working with pain patients, I realized how much of the treatment involved trying to reverse learned helplessness," he said to rally them out of the despair ingrained from years of unremitting pain and cajole their minds to chip in its own analgesic to their therapies. "The purpose of this study is to show patients their mind matters," Mackey said.

The mark of the burn is barely visible now, but for a couple of years afterward, at times when my chronic pain was making me miserable, the sight of it would both encourage and reproach me. Here is the ultimate proof that my mind can control pain, I would think, yet I didn't know how to make it wake up and do so. I could take the edge off the pain by conjuring positive images, but the effects didn't last, and I never again had the remarkable placebo response that masked a second-degree burn. In fact, a mild burn from spilling tea on my hand one day brought tears to my eyes.

When the real-time neuroimaging study began, I couldn't wait to try it.

The area of the brain that the scanner focuses on is the rostral anterior cingulate cortex (rACC). The rACC (a quarter-size patch in the middle-front of the brain, the cingular cortex) plays a critical role in the awareness of the nastiness of pain: the feeling of dislike for it, a loathing so intense that you are immediately compelled to try to make it stop. Indeed, the pain of pain, you might say, its defining element, is the way in which the sensation is suffused with a particular unpleasantness researchers refer to as dysphoria. Since pain is a perception, it's not pain if you don't experience it as hurting. You can feel hot or cold or pressure, and note them simply as stimuli, but when they exceed a certain intensity, the rACC kicks in, and suddenly they become painful, riveting your attention and causing you to recoil.

Many pain-reducing techniques aim to manipulate the conscious awareness of pain. Distraction, placebo, meditation, imagining pleasant scenes and hypnosis all result in a reduction of rACC activation when they work. Patients who have undergone a radical surgical treatment occasionally used for pain (as well as for mental illness) called a cingulotomy, in which the rACC is partly destroyed, report that they are still aware of pain but that they don't "mind" it anymore. Their emotional response has receded.

The image I saw while lying in the f.M.R.I. machine at the time of the recent Stanford study was not literally my rACC but a visual analogue of it that is easier to see: a 3-D image of a fire. The flames represent the degree of activation in your rACC: when it is low, the flames are low; when rACC activation is high, the flames flare. The study involves five 13-minute scanning runs, each consisting of five cycles of a 30-second rest followed by a 1-minute interval in which you try to increase rACC activation and then a 1-minute interval in which you try to decrease rACC activation.

Before my scan began, I was prepped in different mental strategies for increasing and modulating my pain. Everyone's brain works a bit differently, though, so subjects have to experiment in the scanner to see what is most effective for them. For some, trying to distract themselves from their pain works best; for others, focusing on their pain like embracing a Zen koan seems to be what triggers their pain-modulatory system. When deCharms used neuroimaging therapy on himself to try to alleviate his chronic neck pain, he concentrated on the pain itself and felt it "suddenly melt away." He said that a patient described the feeling as being "like a runner's high" (a state that has been shown to involve the release of endogenous endorphins).

Increase Your Pain, the screen commanded, as the first run began. I tried to recall the mental strategies in which I had been prepped for increasing pain: Dwell on how hopeless, depressed or lonely you felt when your pain was most severe. Sense that the pain is causing long-term damage.

Dwelling on the hopeless loneliness of my pain certainly made the flames of my rACC spark. The mental image that I found increased my pain the most, however, was the one that matched the visual analogue of the rACC: Picture a hot flame on your painful area. Try to make the flame grow in the painful area, and imagine it actually burning your flesh.

Having recently read Ariel Glucklich's extraordinary "Sacred Pain," I had plenty of details of the burning of heretics and witches available to me. I had only to imagine the smell of sizzling hair to make the flames of my rACC explode.

Decrease Pain, the screen commanded.

The suggested pain-reduction strategies, however, did little to quell the flames on the screen. I pictured suffocating the pain with banal positive imagery: flowing water or honey, something soft and gentle, but my mind kept slipping back to the progress of the auto-da-fé, and the rACC fire flared.

Feel that sensation, but tell yourself that it is just a completely harmless, short-term tactile sensation.

Pilgrims and devotees all around the world choose to inflict pain upon themselves during sacred rites from being nailed to crosses to dangling from hooks. For them, pain is an occasion for euphoria, not dysphoria. There are many historical records of the equanimity saints and martyrs often possessed during torture. The second-century Jewish martyr Rabbi Akiva, for example, continued to recite a prayer with a smile on his lips while the flesh was being combed from his bones. "All my life," he explained to the puzzled Roman general orchestrating his execution, "when I said the words 'You shall love the Lord your God with all your heart, with all your soul, and with all your might,' I was saddened, for I thought, When shall I be able to fulfill this command? Now that I am giving my life and my resolution remains firm, should I not smile?"

As Glucklich writes, the conviction that pain is a spiritual opportunity seems paradoxically anesthetizing or, as a scientist would say, religious states of conviction can robustly activate the pain-modulatory system.

During my next Decrease Pain interval, instead of trying to picture a vacation, I imagined myself as a martyr, lucidly reciting Though I walk through the valley of the shadow of death while being burned at the stake. My rACC activation I noted respectfully quieted. Then I remembered that the 23rd Psalm seems to have Christian associations, and since I was presumably being tortured for being half-Jewish, a Jewish prayer might be more appropriate. Unless, that is, I was being accused of witchcraft, in which case, I might be generally disillusioned with Judeo-Christian prayer. As I tried to settle on a fantasy, I noticed that my rACC stayed low: Irene Tracey's theory of the modulating effects of distraction. By the last run, I had the strategies down heretic-martyr: rACC down; heretic-victim: rACC up.

The results of the scan, Mackey showed me, revealed significant brain control. A week later, I was scanned again, this time in the offices of Omneuron. I could feel that it was easier to control my rACC with less reliance on elaborate fantasy; I was interacting more directly with my brain.

This learning effect was clearly seen in the recent Stanford study (which was financed in part by the National Institutes of Health). The first phase of the study looked at 12 subjects with chronic pain and 36 healthy subjects. (The healthy participants were subjected to a painful heat stimulus in the scanner and tried to modulate their responses. The chronic-pain patients, however, simply worked to reduce their own pain.) The chronic-pain patients who underwent neuroimaging training reported an average decrease of 64 percent in pain rating by the end of the study. (Healthy subjects also reported a significant increase in their ability to control the pain.)

"One big concern we had," Mackey says, "is, Were we creating the world's most expensive placebo?" To ensure against that, Mackey trained a control group in pain-reduction techniques without using the scanner (as in his previous study) to see if that was as effective as employing a $2 million machine. Mackey also tried scanning subjects without showing them their brain images or tricking subjects by feeding them images of irrelevant parts of the brain or feeding them someone else's brain images. "None of these worked," Mackey says, "or worked nearly as well." Traditional biofeedback also compared unfavorably; changes in pain ratings of subjects in the experimental group were three times as large as in the biofeedback control group.

The second phase of the study, which is now under way, is designed to assess whether neuroimaging therapy offers long-term practical benefits to a larger group of chronic-pain patients. After the six sessions designed to teach them to regulate their pain, they will be observed for at least six months. The idea is to see whether they can fundamentally change their modulation system so that it can reduce pain all the time without constantly and consciously thinking about it. If so, the technique would not simply provide shelter from the storm of pain; it would bring about climate change.

"I believe the technique may make lasting changes because the brain is a machine designed to learn," deCharms says. The brain is soft-wired (plastic) rather than hard-wired: whenever you learn something new, new neural connections are believed to form and old, unused ones to wither away. (Researchers refer to this as activity-dependent neuroplasticity.) In other words, if you actively engage a certain brain region, you can alter it.

Many diseases of the central nervous system involve inappropriate levels of activation in particular brain regions that change the way they operate (negative neuroplasticity). Some regions experience atrophy, while other regions become hyperactive. (For example, epilepsy involves hyperactivity of cells; stroke, Parkinson's and other diseases involve the atrophy of nerve cells.) With chronic pain, it is believed that additional nerve cells, recruited for transmitting pain, create more pain pathways in the nervous system, while nerve cells that normally inhibit or slow the signaling, decrease or change function.

In addition, chronic pain results in a significant loss of other kinds of brain cells. A. Vania Apkarian at Northwestern University found that while the brain of a healthy person shrinks 2.5 percent a year, in a person with chronic back pain, it shrinks an additional 1.3 percent annually in the areas that involve rational thinking. I know chronic pain interferes with my concentration at times, but I never imagined that it could be truly impairing it! The Stanford technique may mitigate this harm by teaching people how to increase the efficacy of the healthy cells.

Moreover, the technique may offer a particular advantage over drug therapy. It is very difficult to design drugs to fix a problem in a specific region of the brain because the receptors that drugs target, like the opiate receptors, generally appear in multiple systems throughout the brain (which is partly why drugs almost always have side-effects). Neuroimaging therapy, on the other hand, is designed to teach control of a localized brain region.

"The technique gives people a tool they didn't know they had," Mackey says, "cognitive control over neuroplasticity. We don't fully understand how this feedback mechanism is working, but it provides tangible evidence that people can change something in their own brains, which can be very empowering. It takes Buddhist monks 30 years of sitting on a mountain learning to control their brains through meditation we're trying to jump-start that process." As to how exactly it works how the decision-making parts of the brain (the prefrontal regions of the cortex) cause the change in the rACC "Heck if I know!" he says. "How do we get the brain to do anything? We can map out the anatomical circuits involved and the general functions of those circuits, but we can't tell you the mechanism by which any cognitive decision is translated into action."

If neuroimaging therapy could treat pain, could it rewire the brain to fix other diseases, like depression, stroke and learning disabilities, or exercise the brain in ways that would make it cleverer and more adept at certain skills? Neuroimaging has shown, for example, that the part of the brains of London cabdrivers that regulates spatial relations is larger than usual and that learning to juggle creates visible changes in parts of the brain involved with motor coordination during three months of training. I'm constantly getting lost and dropping things. Could I exercise and strengthen those areas more quickly by, say, thinking about maps in the scanner than by driving around London?

"What is the limit to neuroimaging therapy?" deCharms muses. "Could you learn to target the reward or serotonin system and up-regulate happiness? Could you augment psychotherapy by allowing the patient and the therapist to watch the brain?" an idea Omneuron is already exploring, by bringing therapists and patients to the scanner and imaging patients' brains as they undergo the sessions. "After all, talk therapy is about learning to understand thought processes to understand neural substrates and change them," he says.

How deep can the insights that functional imaging might offer really go?

What I'd like to do most is not fix problems or improve skills but use imaging as a vehicle for self-transparency. Instead of puzzling about my motivations, I'd like to be able to read my mind completely, like a book: for imaging to be the Plexiglas window through which I could finally see the ghost.

"Hmm," Dr. Scott Fishman, chief of the pain-medicine division at the University of California, Davis, said dubiously when I brought up this notion. "I'm not sure that functional imaging is actually looking at the mind. The mind is like a virtual organ it doesn't have a physical address that we know about. Functional imaging provides a two-dimensional snapshot of a three-dimensional or a four-dimensional event of this entity of the mind. Right now, imaging is just looking at the brain; we have to be honest about that." Imaging shows the level of activation of different parts of the brain, from which we can extrapolate something about the mind, he points out, "but what we really need to see is how the parts talk to each other and the complex nuances of their language."

The brain has more than a hundred billion neurons. All functional imaging can tell us now is that a few hundred million of them in various areas become more active at certain times. It's as if you were trying to conduct a symphony by watching a silent film of the concert. You would see the players in the bass section active at one moment, vigorously gesturing, and then the rest of the orchestra would join in, but you couldn't hear the notes or how they form strands of melody and harmony and meld together to create the ethereal experience.

"Consciousness is not neurons firing consciousness is a transcendent emergent phenomenon that depends on the firing of neurons," says Dr. Daniel Carr, an eminent pain researcher who is now the C.E.O. of Javelin Pharmaceuticals. "The gears of a watch rotate and keep time, but the turning of the gears is not time. The question is, Is neuroimaging a picture of the experience of consciousness or is it a picture of a mechanism associated with that experience? Can there actually be a picture of an experience? Does a picture of a funeral or a wedding show you experiences? Or is there an unbridgeable gap there because you need to already understand the experience in order to interpret the photos? If a higher being told us how consciousness works, could we understand the explanation?"

Melanie Thernstrom is a contributing writer for the magazine. She is working on a book about pain.

This article was reported by Ivanhoe.com, who offers Medical Alerts by e-mail every day of the week. To subscribe, go to: http://www.ivanhoe.com/newsalert/.

SOURCE: Arthritis & Rheumatism, 2005;52:1577-1584

Focus on Pain (Travell) Seminar Orlando, 2003 (notes by Devin J. Starlanyl)

One of the best seminars with new research in the fields of fibromyalgia syndrome (FMS) and chronic myofascial pain (CMP) for care providers is the Focus on Pain (Travell) Seminar.  The following is an account of some of the highlights of the March 6-9, 2003, Focus on Pain Seminar in Orlando, Florida. This seminar series has been organized by Robert Gerwin, MD.  Dr .Gerwin, a neurologist with vast experience in myofascial pain, was one of the first doctors to recognize the importance of the work of Travell and Simons.  Click here to read entire piece.

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Attitudes toward opioid use for chronic pain:

Pain Res Manag. 2003 Winter;8(4):189-94. Morley-Forster PK, Clark AJ, Speechley M, Moulin DE.
St. Joseph's Health Care, London, Canada.

OBJECTIVES: To measure chronic pain patient volumes seen in primary care practice; to determine what medications physicians choose for the treatment of moderate to severe chronic pain; to identify barriers to the use of opioids in the treatment of chronic pain; and to assess physicians' attitudes toward the current management of chronic pain in
Canada.

DESIGN: A computer-assisted telephone survey of 100 regionally representative Canadian physicians with a defined interest in palliative care (PC, n=30) or noncancer pain (GP, n=70).

SETTING: A survey was conducted by Ipsos-Reid in June 2001. Only physicians who met the eligibility criteria of having written 20 or more prescriptions for moderate to severe pain in the preceding four weeks or
having devoted 20% of time to palliative care were eligible to participate.

RESULTS: In one month, the average number of patients with moderate to severe chronic pain seen by PCs was 94.2; the average seen by GPs was 44.7. The pain experienced by 83.3% of GP patients was noncancer
related. For chronic cancer pain, an opioid analgesic was the treatment of choice of 79% of physicians (48% preferred morphine, 21% codeine, 10% other). For moderate to severe chronic noncancer pain, opioids were the
first-line treatment of only 32% of physicians (16% preferred codeine, 16% major opioids) because a significant number preferred either nonsteriodal anti-inflammatory drugs (29%) or acetaminophen (16%).
Thirty-five per cent of GPs and 23% of PCs would never use opioids for noncancer pain, even when described as severe. Chronic pain was deemed by 68% of physicians to be inadequately managed. Almost 60% thought that
pain management could be enhanced by improved physician education. Identified barriers to opioid use included addiction potential (37%) and side effects (25%). Seventeen per cent of GPs and 10% of PCs thought
that regulatory sanctions limited opioid prescribing.

CONCLUSIONS: Even among physicians experienced in chronic pain treatment, there is a reluctance to use opioids for severe nonmalignant pain. One-half of the survey participants believed that there was a need for improved physician education in pain management, including the use
of opioids.

PMID: 14679412

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New Textbook Teaches Pain Management  September 8, 2003 05:07 PM EDT

WASHINGTON - An estimated 50 million Americans suffer from persistent pain, yet most medical students have no courses focused on treating pain, according to the American Academy of Pain Medicine. "Untreated pain, tragically, is an epidemic in the United States," Dr. Louis Sullivan, former Health and Human Services secretary, said Monday as he announced an initiative to promote education on pain management at the country's medical schools.

The American Academy of Pain Medicine has developed a Web-based textbook that will be available to medical students without charge beginning September 2004. It covers the neurobiology of pain, patient evaluation and common types of pain, such as cancer and pediatric pain, and includes self-tests.

The project is financed by a grant from the Purdue Pharma Fund, a branch of the drug company that makes the painkiller OxyContin.

Dr. Daniel Carr, director of the project and a professor of pain research at Boston's New England Medical Center, said the textbook focuses on medical and behavioral treatments for pain, because they are backed by more research than alternative therapies such as acupuncture.

Only 3 percent of medical schools require students to take a course on pain management, according to a survey of 125 schools by the Association of American Medical Colleges in 2000 and 2001.

Developed with the participation of the Association of American Medical Colleges, the new textbook will be tested in he coming months at the Morehouse School of Medicine, in Atlanta; the University of Connecticut School of Medicine, in Farmington, Conn.; and the Texas College of Osteopathic Medicine, in Fort Worth, Texas.

While millions of Americans suffer from pain in silence, the abuse of prescription drugs is well documented. Nearly 3 million young people, age 12 to 17, said they had used prescription drugs for nonmedical reasons at least once, according to a January 2003 government report. OxyContin, a brand name for the drug oxycodone, is among the most-abused prescription medications.

Nevertheless, project director Carr said, "The burden of undertreated pain dwarfs overtreated pain" in the overall society. American Academy of Pain Medicine: http://www.painmed.org

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Does chronic pain predict future psychological distress?
McBeth J, Macfarlane GJ, Silman AJ.Pain. 2002 Apr;96(3):239-45.

Arthritis Research Campaign (ARC) Epidemiology Unit, School of Epidemiology and Health Sciences, Stopford Building, University of Manchester, Oxford Road, M13 9PT, Manchester, UK.


Cross-sectional studies have consistently shown a relationship between chronic widespread pain, the clinical hallmark of fibromyalgia, and psychological distress. These studies cannot distinguish the direction
of any causal relationship. Recent population based studies have reported that such pain is predictive of future distress. However,chronic pain is often associated with physical and psychological
co-morbid features which may confound this relationship. The aim of thisstudy was to examine the hypothesis that chronic widespread pain increases the risk of future distress after adjusting for the effects of
possible confounding factors.

A population based survey of 1953 individuals identified subjects' psychological status and whether they
satisfied criteria for chronic widespread pain. At baseline co-morbid features of chronic widespread pain, including reporting other somatic symptoms, abnormal illness behaviour, health anxiety, fatigue and low
levels of self-care, were measured. All subjects were followed up after 12 months to determine levels of psychological distress. Subjects with chronic widespread pain at baseline were much more likely to be
distressed at follow up (OR=4.0, 95% CI (2.5,6.3)). As levels of distress at follow up may simply reflect those at baseline the association was adjusted for baseline levels of distress. Chronic widespread pain was, however, still associated with future distress although the relationship was slightly attenuated (odds ratio, OR=3.0,
95% CI (1.8,5.1)).

To examine our main hypothesis a final analysis was undertaken adjusting this association for those co-morbid features assessed at baseline. Following these adjustments chronic widespread pain was no longer significantly associated with future distress (OR=1.5, 95% CI (0.8,2.9)). Chronic widespread pain was associated with
increased levels of psychological distress at follow up. However, a more rigorous analysis indicated that the association between baseline pain status with future distress was explained by concomitant features of
chronic pain rather than pain per se. These findings indicate that it is those persons with chronic widespread pain in the presence of other physical and psychosocial factors who will become distressed.

PMID: 11972995

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Modern nerve stimulators to kill pain
International Science & Technology Center 13.11.2003


Managing pain may one day be as easy as sticking on a Band-AidTM.

336666666666666666666666666666
Russian researchers at the company BIOFIL Ltd. in Sarov are
developing a line of miniature transcutaneous electrical nerve
stimulation (TENS) devices that work as a non-drug alternative to
pain relief and are small enough for patients to use without
hindering daily life.

TENS technology is an accepted (FDA approved) and effective way to
handle acute or chronic pain associated with diseases affecting
muscles and joints. There are no known side effects and it is not
addictive, but does require a physician's prescription. A standard
device consists of an electric pulse generator and connecting
electrodes that are placed directly on the skin in the painful area.
Electric pulses are applied and travel through the skin to the target
area. The device, however, never penetrates the skin and provides
non-invasive therapy.

Currently, TENS devices are expensive, bulky, and heavy, which has
limited their use to hospitals and outpatient centers. The BIOFIL
product line of miniature devices allows the patients to use the unit
during their daily routines. The patient can vary the intensity of
the electric pulses by manipulating a control unit that features an
LCD display and push-button controls.

The product line includes devices that may be applied as a small
Band-AidTM-like adhesive containing expendable stimulating
electrodes. In a similar concept, the BIOFIL group is also designing
orthopedic splints, brackets, and bandages with built-in stimulators.
A third type of model gives the patient "remote control" of a pain
region.

The group at BIOFIL Ltd., a 1991 spin-off of the Russian Federal
Nuclear Center VNIIEF, began developing the miniature TENS devices in
1998 in cooperation with Lawrence Livermore Laboratories (Washington,
DC) and Cyclotec Medical Industries, Inc. (Lauderhill, FL). Following
this work, Livermore Lab and BIOFIL received funding from the
Department of Energy IPP program for a 2-year ISTC project beginning
in 2002. Research at BIOFIL will further develop the TENS technology
for their portable biomedical devices, perform pilot runs for
clinical testing, and prepare for production and commercialization,
in cooperation with the U.S. industry partner, Cyclotec Medical
Industries.

The target markets for the miniature TENS devices includes
rehabilitation following surgery or trauma, home health care, sports
medicine, industrial medicine, and emergency care.

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The epidemiology of chronic generalized musculoskeletal pain.

Best Pract Res Clin Rheumatol. 2003 Aug;17(4):547-61.Tore Gran J.
Department of Rheumatology, National Hospital Rikshospitalet,
Sognsvannsveien, Oslo, Norway

Chronic widespread musculoskeletal pain has been subjected to
several epidemiological studies during the last decade. According
to these, approximately 10% of the general population report such
complaints, clearly indicating chronic widespread musculoskeletal
pain as a major health problem in the Western world. Almost
unanimously, all studies found higher rates of such complaints
among women compared with men, but the mechanisms responsible for
the skewed gender ratio remain unknown.  Chronic widespread
musculoskeletal pain is the clinical hallmark of fibromyalgia and
has been the subject of numerous epidemiological studies. The
prevalence of fibromyalgia is reportedly 3-5%, again with a
significant female predominance. Although the aetiopathogenesis
of both fibromyalgia and chronic widespread musculoskeletal pain
without other features of fibromyalgia remains an enigma, there
is a body of evidence suggesting psychological and sociocultural
factors as important for contracting such pain syndromes.
PMID: 12849711

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Researchers find gene involved in pain relief

University of Toronto Researchers at the University of Toronto, The Hospital
for Sick Children and the Amgen Institute have discovered a genetic mechanism
involved in pain modulation that could lead to an entirely new approach to
pain control.
    The results of their research are published in the Jan. 11
issue of the journal Cell. In the study, genetically engineered mice lacking
a gene called DREAM (downstream regulatory element antagonistic modulator)
showed a dramatic loss of pain sensitivity compared to mice who had the DREAM
gene. "This is an exciting development," says study co-author Professor
Michael Salter, director of the University of Toronto Centre for the Study of
Pain and a senior scientist at The Hospital for Sick Children. "There's a
great interest in this finding because it's so different from the traditional
approaches researchers have been taking to pain management."
    The work was done in the laboratory of principal investigator Professor Josef Penninger at
Amgen by graduate students Mary Cheng and Graham Pitcher, lead authors of the
study. The DREAM gene's role in reducing production of the chemical dynorphin
had been previously identified. DREAM produces a protein that suppresses the
genetic machinery that reads the DNA code for dynorphin, which decreases
dynorphin production. Dynorphin is a peptide normally produced in the body.
Known as an endorphin, it is produced in response to pain or stress. "We knew
about DREAM and its role in dynorphin expression, but the purpose of this
study was to determine DREAM's actual physiological function," says Salter.
     When the DREAM gene was absent in mice, the researchers discovered increased
production of dynorphin in the region of the spinal cord involved in
transmitting and controlling pain messages. The mice, they discovered, had
decreased sensitivity to acute, inflammatory and neuropathic pain. "The
attenuated pain response was evident for all types of pain in all types of
tissue tested," says Salter. "The fact that even mice with neuropathic
pain-the kind of sharp, chronic pain resulting from nerve injury-experienced
this effect is exciting because the medical community currently doesn't have
any widely effective treatments for this debilitating type of pain."
     Current approaches to pain management focus on drugs such as morphine that stimulate
cell receptors for the endorphin family of proteins, also called the
endogenous opioid system, or drugs such as aspirin that block the enzyme
cyclo-oxygenase.
    The DREAM gene, however, works in an entirely different way
by binding directly to DNA and regulating the expression of a protein in the
endogenous opioid system. "These findings point to a novel pharmacological
approach to pain management where researchers will be looking for drugs that
could block the ability of DREAM to bind to DNA or simply prevent the
production of DREAM," says Salter. The mice in the study who lacked the DREAM
gene were otherwise completely normal and showed no reduction in their motor
function, learning or memory. They also did not become addicted to the pain
control chemicals their bodies produced, which may prove to be an advantage
over the potentially addictive drugs such as morphine that act on opioid
receptors. "Pain is a huge, silent public health crisis that is only
beginning to be addressed by researchers," Salter says. "Evidence of the
severity of this crisis can be found in the fact that the U.S. government has
declared 2001-2010 the Decade of Pain Research and Management. This
declaration highlights a growing awareness of the vast problem of untreated
or under-treated pain, and we hope this research will contribute in a
significant way to current efforts by scientists to confront this challenge."

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Evidence of involvement of central neural mechanisms in generating
fibromyalgia pain.
Curr Rheumatol Rep  2002 Aug;4(4):299-305 Staud R.
University of Florida, Division of Rheumatology and Clinical Immunology,
PO Box 100221, Gainesville, FL 32610-0221, USA.

Fibromyalgia syndrome (FMS) is characterized by widespread pain,
fatigue, sleep abnormalities, and distress. Because FMS lacks consistent
evidence of tissue abnormalities, recent investigations have focused on
central nervous system mechanisms of pain. Abnormal temporal summation
of second pain (wind-up) and central sensitization have been described
recently in patients with FMS. Wind-up and central sensitization, which
rely on central pain mechanisms, occur after prolonged C-nociceptor
input and depend on activation of nociceptor-specific
neurons and wide dynamic range neurons in the dorsal horn of the spinal
cord.  Other abnormal central pain mechanisms recently detected in
patients with FMS include diffuse noxious inhibitory controls. These
pain inhibitory mechanisms rely on spinal cord and supraspinal systems
involving pain facilitatory and pain inhibitory pathways. Brain-imaging
techniques that can detect neuronal activation after nociceptive stimuli
have provided additional evidence for abnormal central pain mechanisms
in FMS. Brain images have corroborated the augmented reported pain
experience of patients with fibromyalgia during experimental pain
stimuli. In addition, thalamic activity, which contributes significantly
to pain processing, was decreased in fibromyalgia. However, central pain
mechanisms of fibromyalgia may not depend exclusively on neuronal
activation. Neuroglial activation has been found to play an important
role in the induction and maintenance of chronic pain. These findings
may have important implications for future research and the treatment of
fibromyalgia pain.

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Weather and the pain in fibromyalgia: are they related?

E A Fors1 and H Sexton2 1 Department of Psychiatry and Behavioural Medicine and Multidisciplinary
Pain Centre, University Hospital of Trondheim, Norway 2 Psychiatric Research Centre for Finnmark and Troms, Tromsö, NorwayObjectives: To examine the association between fibromyalgic pain and weather to determine the nature of their interrelationship.

Methods: The daily pain ratings of 55 female patients previously diagnosed
with fibromyalgia were recorded on visual analogue scales (VAS) over 28
days. These ratings were then related to the official weather parameters and
a composite weather variable using time series methodology. Effect sizes r
were calculated from the t values and df.

Results: A composite weather variable did not significantly predict changes
in pain, either the same day (t=-1.15, df=1483, p=0.25) or on the next day
(t=-1.55, df=1483, p=0.12)-that is, the weather was not a factor for changes
in the subjective pain of FM. Patients' pain did not predict weather change
in this sample, and neither same day (t=-0. 69, df=1483, p<0.49) nor
previous day pain (t=-1.31, df=1483, p<0.19) predicted weather changes. A
post hoc exploratory analysis showed that those with <10 years of
fibromyalgia experienced significantly greater weather sensitivity to pain
(t=- 2.73, df=389, p<0.006) than those with longer illness.

Conclusion: A statistically significant relationship between fibromyalgic
pain and the weather was not found in this sample, although it is possible
that a group of patients with less chronic fibromyalgia might be weather
sensitive. Correspondence to: Dr E A Fors, Department of Psychiatry and Behavioural Medicine, NTNU, PO Box 3008 Lade, NO-7441 Trondheim, Norway;

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Sleep and chronic pain. Challenges to the alpha-EEG sleep pattern as a pain specific sleep anomaly
Journal: J Psychosom Res 2003 Jan;54(1):77-83 Authors: Rains JC, Penzien DB. Affiliation: Center for Sleep Evaluation, Elliot Hospital, One Elliot Way, Manchester, NH, USA NLM Citation: PMID: 12505558

OBJECTIVE: The alpha-EEG sleep anomaly has been associated with chronic benign pain syndromes. Although controversial, the anomaly is believed by some to be an important biologic correlate of certain otherwise poorly explained painful conditions (e.g., fibromyalgia and chronic fatigue syndrome). To shed further light on this phenomenon, this study compared the sleep and psychological characteristics of chronic pain patients who exhibited the alpha-EEG sleep anomaly with pain-free psychiatric and medical patients who also were found to exhibit the alpha-EEG anomaly.

METHODS: The alpha-EEG sleep was identified in the polysomnographic records of 5% of over 1000 consecutive sleep patients. Objective sleep parameters, daytime sleepiness and psychological characteristics (Minnesota Multiphasic Personality Inventory [MMPI] scores) of patients exhibiting this anomaly were examined.

RESULTS: The alpha-EEG anomaly was identified in only 5% of the total patient sample. Patients with the alpha-EEG anomaly could be further classified into three diagnostic subgroups: chronic pain, psychiatric and other medical/sleep disorders, The subgroups were compared on sleep parameters and psychological characteristics. Less than 40% of the patients exhibiting the alpha-EEG anomaly experienced chronic pain. Chronic pain patients evidenced disturbed sleep patterns and psychological characteristics that were for the most part similar to those observed1000 in some pain-free medical and psychiatric patients. Only the medical subgroup exhibited objective daytime sleepiness. The alpha-EEG sleep disturbance was not accounted for by psychological characteristics.

CONCLUSIONS: These findings challenge the notion that alpha-EEG sleep is of direct etiological significance in producing the pain complaint among patients with chronic pain since the alpha-EEG sleep was not a sufficient condition for pain.

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Chronic pain and difficulty in relaxing postural muscles in patients with fibromyalgia and chronic whiplash associated disorders.1: J Rheumatol 2001 Jun;28(6):1361-8 
Elert J, Kendall SA, Larsson B, Mansson B, Gerdle B. Department of Rehabilitation Medicine, INR, Faculty of Health Sciences, Pain and Rehabilitation Centre, University Hospital, Linkoping, Sweden.

OBJECTIVE: To investigate if muscle tension according to the surface electromyogram (EMG) of the shoulder flexors is increased in consecutive patients with fibromyalgia (FM) or chronic whiplash associated disorders (WAD).

METHODS: A total of 59 consecutive patients with FM (n = 36) or chronic WAD (n =23) performed 100 maximal isokinetic contractions combined with surface electromyography of the trapezius and infraspinatus. A randomized group of pain-free female (n = 27) subjects served as control group. Peak torque initially (Pti) and absolute and relative peak torque at endurance level (PTe, PTer) were registered as output variables, together with the EMG level of unnecessary muscle tension, i.e., the signal amplitude ratio (SAR).

RESULTS: The patient groups had a higher level of unnecessary tension initially and at the endurance level. The patients had lower absolute output (PTi and PTe), but the relative levels (PTer) did not differ comparing all 3 groups. Subjects with FM had significantly higher body mass index (BMI) than the other groups. BMI did not influence the SAR but correlated positively with PTi.

CONCLUSION: The results confirmed earlier findings that groups of patients with chronic pain have increased muscle tension and decreased output during dynamic activity compared to pain-free controls. However, the results indicated there is heterogeneity within groups of patients with the same chronic pain disorder and that not all patients with chronic pain have increased muscle tension.

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Pain Research Comes into Its Own Molecular biology may provide answers to relief

"Previously, scientists generally believed that glia played no role in pain because they lack axons and therefore were incapable of cell-to-cell signaling. But now, some researchers believe that glial activation can create, maintain, or expand pain in response to peripheral injury and
inflammation, according to Linda R. Watkins, professor in the department of psychology and the Center for Neurosciences at University of Colorado, and the article's lead author.

The recent findings suggest a new approach to pain control, because all current clinical therapies are focused on altering neuronal, rather than glial, function, Watkins says. The finding opens a promising new target for pharmacological treatments and may have significant implications for
drug development aimed at controlling clinical pain, she says. Pain "is a dynamic process where activated glia interact both with pain messages arriving at the spinal cord and with spinal cord neurons whose job it is to relay that message up to the brain," Watkins says. "This is a whole
new level of pain processing [that] promises to expand our understanding not only of pain, but also of glial-neuronal interactions, since there is certainly no reason to believe that pain is the only phenomenon where glial-neuronal interactions will prove to be important."

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How to find relief from the pain that wont go away  By Winnie Yu

Twenty years ago, Julie Lydon of Norwood, Massachusetts, started to experience lower back pain. Soon she couldnt stand up straight, and her muscles stiffened when she sat for too long. Her body throbbed, and she was tired all the time. Doctors ran a battery of tests, looking for cancer, leukemia, anything. Finally, after 15 long years, Julie had a diagnosis: fibromyalgia.

This chronic disorder, marked by unending pain and fatigue, affects up to 10 million Americans, the majority of whom are women. But many patients have a hard time getting diagnosed since the exact causes of fibromyalgia are unclear, there is no blood test available and symptoms can vary widely. As scientists continue to study this mysterious ailment, promising discoveries are being made to help patients with fibromyalgia better understand and manage their condition.

New studies, new Discoveries
According to researchers, fibromyalgia does have a biological basis. A study done at the National Institutes of Health and Georgetown University found pain signals in the brain scans of fibromyalgia sufferers that did not appear in scans of people without the disease. Researchers also found that fibromyalgia patients brains respond differently to pain.

Other findings could explain the intense pain that patients feel. Fibromyalgia patients have higher than normal levels of the neural hormone substance P. This hormone, found in spinal fluid, sends pain signals after an injury. At the same time, people with fibromyalgia have lower levels of serotonin, a neurotransmitter that reduces pain.
Other hormones may also be culprits. Those with fibromyalgia have lower levels of certain growth hormones, which help the body attain the deep, restorative sleep it needs. Fibromyalgia patients also secrete lower amounts of certain stress hormones, causing them to respond less effectively to stress.

Studies suggest that genes may also play a role. Now that weve started to map the human genome, research suggests that there may be twenty genes or more that could be responsible for fibromyalgia, says Kim Jones, Ph.D., R.N., assistant professor at the Oregon Health & Science University in Portland and a fibromyalgia researcher. People with a greater number of potentially affected genes may require little or no environmental stimulation to turn on their fibromyalgia genes. Others may need more stimuli. Among the environmental factors under investigation by the Arthritis Foundation are physical trauma, viral or bacterial infections and emotional distress.

Drug Companies Look Ahead
The growing body of physical evidence has inspired pharmaceutical companies to explore new drugs to treat fibromyalgia, says Daniel Clauw, M.D., a professor of medicine at the University of Michigan and a fibromyalgia researcher who coauthored the NIH-Georgetown study. There are at least three companies doing clinical trials to get drugs approved for fibro, says Dr. Clauw. Like existing therapies (see The Rx Factor, right), the new drugs can relieve symptoms but wont cure the disease. Because we dont know the cause, we are stuck treating the symptoms, says Daniel Rooks, Ph.D., director of the Be Well! Tanger Center for Health Management at Beth Israel Deaconess Medical Center in Boston.

Diet Makes a Difference
Some researchers believe that people with fibromyalgia should reduce their intake of certain foods. For instance, too much monosodium glutamate (MSG) and aspartame may aggravate pain. Excess calories could cause weight gain that, in turn, may worsen pain.

Eating a balanced diet will help support the immune system, says Leslie Bonci, R.D., a spokeswoman for the American Dietetic Association and director of sports nutrition at the University of Pittsburgh Medical Center.

That means getting enough protein, essential fatty acids, antioxidants and vitamins A, C and E. Foods such as tuna, chicken, yogurt and peanut butter are good sources of protein. Fresh fruits and vegetables, dried fruits and frozen veggies are all good sources of antioxidants and vitamins A, C and E. And essential fatty acids, such as omega-3s, are found in fatty fish, such as tuna and salmon, as well as in ground flaxseed.

The Age-Old Remedy: Exercise
Even though medication offers relief, experts say exercise is an essential treatment for fibromy-algia. Exercise is a must, says Dr. Rooks. Theres nothing better for improving function and outlook.

Andrea Whitaker, 46, of Cambridge, Massachusetts, agrees. The worst thing I can do is not move, says Andrea, who was diagnosed with fibromyalgia six years ago. Staying immobile is a definite trigger. My muscles just freeze up.

According to Don L. Goldenberg, M.D., medical advisor for the Arthritis Foundation, a patient should focus most on cardiovascular workouts such as walking or water aerobics. Besides improving general fitness, cardiovascular exercise improves immunity and elevates mood, he says.

Stretching is also important. The intense pain of the disease tightens muscles, causing them to shorten and lose range of motion. Stretching is critical for preventing muscle injury, says Robert Bennett, M.D., professor of medicine at the Oregon Health & Science University and a longtime researcher in the field. Ideally, you should gently stretch each muscle group twice a day for about four to five minutes.

Strength training also plays a role. A study by Drs. Bennett and Jones found that specially tailored twice-weekly strength-training classes paid off even more than flexibility training did. Jane Walpole has known this for years. In 1989, the 50-year-old from Tigard, Oregon, developed fibromyalgia so severe she abandoned her career as a dentist and gave up kayaking and skiing. Several years later, while caring for her premature niece, Jane found herself constantly lifting the 4 1/2-pound infant. It was painful at first, but she persevered. As the baby gained weight, Jane grew stronger. Now she lifts free weights two or three times a week. Exercise and weight lifting relieve pain. You just have to take it slow and listen to your body, she says.

Slow Down and Breathe
Before he got sick at age 39, Steve Lindsay, of Tenants Harbor, Maine, worked long hours as a sculptor and teacher. In his free time, he liked to garden, row and hike. All of a sudden my lifestyle fell apart, says Steve, who would wake up feeling as though hed climbed a mountain without preparing the day before. Now 50, Steve says he has learned to accept the limitations imposed by fibromyalgia. I cant do everything I used to do, he says. I have to pace myself and take it easy.
Stress can also exacerbate symptoms. Cognitive behavioral therapy helps teach relaxation techniques, such as deep breathing, meditation, and techniques for coping with stress. Patients are encouraged to simplify their lives by paring down social obligations and accepting their own limitations.

The Rx Factor
Even with exercise and lifestyle changes, many fibromyalgia patients need medication to help relieve pain, fatigue and other symptoms associated with the disease.

To prevent inflammation, nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil) and naproxen (Aleve), and cox-2 inhibitors such as celecoxib (Celebrex) and rofecoxib (Vioxx)

For relief of minor pain, analgesics such as acetaminophen (Tylenol) or a more powerful prescription drug

For muscle pain, muscle relaxants such as cyclobenzaprine (Flexeril)

For severe pain, strong prescription painkillers such as tramadol (Ultram); opiate agonists; or narcotics, which include oxycodone (OxyContin), propoxyphene (Darvocet) and meperidine (Demerol)

For persistent pain in specific locations, injections of anesthetics such as lidocaine

To alleviate sleep deprivation, low doses of tricyclic antidepressants such as amitriptyline (Elavil) and nortriptyline (Aventyl); sedatives such as zolpidem (Ambien); or selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac), paroxetine (Paxil) and sertraline (Zoloft)

Medications to treat other ailments that sometimes accompany fibromyalgia, such as irritable bowel syndrome, migraine headaches, restless leg syndrome and cold intolerance

Is There Any Alternative?
Although no alternative remedies have been scientifically proven to treat fibromyalgia, many doctors recommend nutritional supplements, vitamins and minerals along with prescription drugs. When I first started out, I prescribed only traditional treatments, says Stuart Erner, M.D., an internist in Albany, New York, who has treated fibromyalgia since the late 1980s. But I was not getting much response, so I started using nutritional supplements and herbal remedies. The combined approach is generally more effective than traditional remedies alone, he says. Below, a few of his recommended supplements.*

Coenzyme Q10 may boost energy, fight off infection and improve cognitive functioning.

Melatonin and valerian are believed to help promote deep sleep.

Magnesium and malic acid are thought to relieve pain and fatigue.

5-hydroxytryptophan (5-HTP) helps improve sleep and mood and reduces carbohydrate cravings.

St. Johns wort may ease depression.

* Always check with your doctor before using supplements, as they can interfere with other medications.

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Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale.
Journal: Pain 2001 Nov;94(2):149-158
Authors: Farrar JT, Young JP, LaMoreaux L, Werth JL, Poole RM.
Affiliation: Department of Biostatistics and Epidemiology, University of
Pennsylvania School of Medicine, Blockley Hall, Room 816, 423 Guardian
Drive, 19104, Philadelphia, PA, USANLM Citation: PMID: 11690728

Pain intensity is frequently measured on an 11-point pain intensity numerical rating scale (PI-NRS), where 0=no pain and 10=worst possible pain. However, it is difficult to interpret the clinical importance of changes from baseline on this scale (such as a 1- or 2-point change). To
date, there are no data driven estimates for clinically important differences in pain intensity scales used for chronic pain studies.

We have estimated a clinically important difference on this scale by relating it to global assessments of change in multiple studies of chronic pain. Data on 2724 subjects from 10 recently completed
placebo-controlled clinical trials of pregabalin in diabetic neuropathy, postherpetic neuralgia, chronic low back pain, fibromyalgia, and osteoarthritis were used. The studies had similar designs and
measurement instruments, including the PI-NRS, collected in a daily diary, and the standard seven-point patient global impression of change (PGIC), collected at the endpoint.

The changes in the PI-NRS from baseline to the endpoint were compared to the PGIC for each subject. Categories of 'much improved' and 'very much improved' were used as determinants of a clinically important difference and the relationship to the PI-NRS was explored using graphs, box plots, and sensitivity/specificity analyses. A consistent relationship between the change in PI-NRS and the PGIC was demonstrated regardless of study, disease type, age, sex, study result, or treatment group.

On average, a reduction of approximately two points or a reduction of approximately 30% in the PI-NRS represented a clinically important difference. The relationship between percent change and the PGIC was also consistent regardless of baseline pain, while higher baseline scores required larger raw changes to represent a clinically important difference.

The application of these results to future studies may provide a standard definition of clinically important improvement in clinical trials of chronic pain therapies. Use of a standard outcome across
chronic pain studies would greatly enhance the comparability, validity, and clinical applicability of these studies.

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Intrathecal Bupivacaine for Chronic Pain: A Review of Current Knowledge
Timothy R. Deer MD, Mario Serafini DO, Eric Buchser MD, F. Michael Ferrante MD, Samuel J. Hassenbusch MD, PhD

Objective.This article presents an overview of the use of intrathecal bupivacaine (with and without opioid), focusing on laboratory data and clinical use for chronic pain. Some background on epidural use is included to support the intrathecal literature.

Materials and Methods.Currently available literature (MEDLINE) regarding the use of intrathecal bupivacaine is reviewed. Prior to presenting the intrathecal bupivacaine data, an overview of data related to bupivacaine stability, microbiology, preclinical toxicology, and pharmacokinetics is presented, along with a brief review of the epidural bupivacaine literature.

Results.Based on the current available literature, intrathecal bupivacaine appears to be a safe and acceptable method of treatment for chronic pain in both cancer and noncancer patients. The stability and bacteriologic studies support the use of bupivacaine in external or implantable drug administration devices. Toxicity studies in laboratory animals suggest complications only at plasma levels that would not be seen at clinically relevant doses of intrathecal administration. Bupivacaine is a clinically effective addition to intrathecal opioids. Bupivacaine administration is more effective intrathecally, providing better pain relief than epidural administration. Reports of complications are infrequent. Further studies are needed to define the use of intrathecal bupivacaine and should include long-term safety. Compatibility studies will also be needed when bupivacaine is used in combination with other agents. In addition, outcome studies are needed specifically to differentiate use of intrathecal bupivacaine based on the source and mechanism of pain.

Conclusions.While there are few long-term randomized prospective studies at this point, we conclude that intrathecal bupivacaine appears to be a safe and efficacious treatment in both cancer and noncancer pain.

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Unexplainable nondermatomal somatosensory deficits in patients with chronic nonmalignant pain in the context of litigation/compensation: a role for involvement of central factors?J Rheumatol 2001 Jun;28(6):1385-93 Mailis A, Papagapiou M, Umana M, Cohodarevic T, Nowak J, Nicholson K. Comprehensive Pain Program, Toronto Western Hospital, and Department of Medicine, University of Toronto, Toronto, Ontario, Canada. MID: 11409135

OBJECTIVE: To address the prevalence and characteristics of nondermatomal   somatosensory deficits (NDSD) in subjects with chronic pain in the context of compensation/litigation.

METHODS: Data were collected via standardized history, examination, and patient- as well as physician-drawn body maps in a consecutive series of 194 subjects seen for the purpose of an independent medical examination.

RESULTS: Forty-nine subjects (25.3%) with primarily widespread pain (often diagnosed as fibromyalgia) presented with hemisensory or quadrotomal deficits to pinprick and other cutaneous stimuli on the side of lateralized pain or worse pain. The NDSD limbs often had impairment of vibration sense (not infrequently associated with "forehead vibration split"), reduced strength, dexterity or movement, and extreme sensitivity to superficial skin palpation or profound insensitivity to deep pain. Spatial, temporal, qualitative, and evolutionary patterns of NDSD emerged associated with cognitive/affective symptoms. NDSD subjects were more often born outside Canada, more likely to be injured at work, present with abnormal pain behavior, and have negative investigations.

CONCLUSION: NDSD are a prevalent problem associated with chronic pain. Future research should explore the prevalence of NDSD in other pain populations, the role of personality and related factors, and the underlying biological substrate of these deficits.

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Efficacy and Safety of Intrathecal Opioid/Bupivacaine Mixture in Chronic Nonmalignant Pain: A Double Blind, Randomized, Crossover, Multicenter Study
by the National Forum of Independent Pain Clinicians (NFIPC) Y. Eugene Mironer MD*, John C. Haasis MD, Iva Chapple MD, Christopher Brown RN-FNPC*, John R. Satterthwaite MD

Objective.Intrathecal opioid/local anesthetic mixtures are a popular alternative in contemporary treatment of chronic nonmalignant pain. Unfortunately, its use is based solely on retrospective studies or anecdotal reports.

Materials and Methods.A double blind, randomized, crossover, multicenter study was performed in 24 patients with intrathecal pumps. For four consecutive months, their pumps were refilled with either the original opioid or its mixture with different concentrations of bupivacaine(4, 6, or 8 mg/day).

Results.Only one patient experienced mild side effects from intrathecal bupivacaine. A strong placebo response was observed in all patients when they entered the study. Addition of bupivacaine to the intrathecal opioid failed to produce significant improvement in pain control.

Conclusion.At currently used doses, intrathecal opioid bupivacaine mixtures are not more efficacious in the treatment of chronic nonmalignant pain than opioid alone.

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Abstract - Opioids in non-cancer pain: a life-time sentence?

Dellemijn, P. L. (2001).
European Journal of Pain:Ejp 5(3): 333-9.

There is continuing reluctance to prescribe strong opioids for the
management of chronic non-cancer pain due to concerns about side-effects,
physical tolerance, withdrawal and addiction. Randomized controlled trials
have now provided evidence for the efficacy of opioids against both
nociceptive and neuropathic pain. However, there is considerable variability
in response rates, possibly depending on the type of pain, the type of
opioid and its route of administration, the time to follow-up, compliance
and the development of tolerance.

Five patients were selected with nociceptive or neuropathic pain in whom other pharmacological or physical therapies had failed to provide satisfactory pain relief. They received transdermal fentanyl (starting dose 25 microg/h) for at least 6 weeks. Transdermal fentanyl dosage was titrated upwards as required. Transdermal fentanyl provided adequate pain relief in patients with nociceptive pain
(diabetic ulcer, osteoporotic vertebral fracture, ankylosing spondylitis) or neuropathic pain with a nociceptive component (radicular pain due to disc protrusion, herpetic neuralgia). The duration of treatment ranged from 6 weeks to 6 months for four cases.

In the case of ankylosing spondylitis, treatment was carried out for 2 years, stopped and then restarted successfully. There were no withdrawal effects or addictive behaviour on
treatment cessation, regardless of duration of the treatment. In conclusion,
strong opioids may provide prolonged effective pain relief in selected patients with nociceptive and neuropathic non-cancer pain. Transdermal fentanyl treatment can often be temporary and can easily be stopped following adequate pain relief without withdrawal effects or any evidence of
addictive behaviour.

Copyright 2001 European Federation of Chapters of the
International Association for the Study of Pain

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Unexplainable nondermatomal somatosensory deficits in patients with chronic nonmalignant pain in the context of litigation/compensation: a role for involvement of central factors?J Rheumatol 2001 Jun;28(6):1385-93 Mailis A, Papagapiou M, Umana M, Cohodarevic T, Nowak J, Nicholson K. Comprehensive Pain Program, Toronto Western Hospital, and Department of Medicine, University of Toronto, Toronto, Ontario, Canada. MID: 11409135

OBJECTIVE: To address the prevalence and characteristics of nondermatomal   somatosensory deficits (NDSD) in subjects with chronic pain in the context of compensation/litigation.

METHODS: Data were collected via standardized history, examination, and patient- as well as physician-drawn body maps in a consecutive series of 194 subjects seen for the purpose of an independent medical examination.

RESULTS: Forty-nine subjects (25.3%) with primarily widespread pain (often diagnosed as fibromyalgia) presented with hemisensory or quadrotomal deficits to pinprick and other cutaneous stimuli on the side of lateralized pain or worse pain. The NDSD limbs often had impairment of vibration sense (not infrequently associated with "forehead vibration split"), reduced strength, dexterity or movement, and extreme sensitivity to superficial skin palpation or profound insensitivity to deep pain. Spatial, temporal, qualitative, and evolutionary patterns of NDSD emerged associated with cognitive/affective symptoms. NDSD subjects were more often born outside Canada, more likely to be injured at work, present with abnormal pain behavior, and have negative investigations.

CONCLUSION: NDSD are a prevalent problem associated with chronic pain. Future research should explore the prevalence of NDSD in other pain populations, the role of personality and related factors, and the underlying biological substrate of these deficits.

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ACR: Lower-Back and Fibromyalgia Pain Linked, Possible Source Identified
By Bruce Sylvester NEW ORLEANS, LA -- October 28, 2002 --

Lower back pain appears to be caused by a malfunctioning pain pathways in the brain, in a manner similar to fibromyalgia pain, University of Michigan researchers report. "These patients get bad reputation for claiming to feel pain in places where no physiological cause can be identified. It looks like the pain has a physiological source indeed, but in problems in the brain," said investigator Richard Gracely, Ph.D, professor of rheumatology at the University of Michigan School of Medicine in Ann Arbor told United Press International. The research was presented yesterday at the annual meeting of the American College of Rheumatology in New Orleans. The investigators enrolled 15 subjects experiencing chronic lower-back pain with no apparent physical cause, such as muscle, joint or bone injury. They also recruited 15 fibromyalgia patients and 15 normal control subjects. All subjects underwent functional magnetic resonance image (fMRI) scanning simultaneous with having a device apply pulsing pressure to the base of their left thumbnail. The variable pressure included painful and non-painful levels. The researchers noted that mild pressure caused subjects with lower-back pain and fibromyalgia to report significant pain, while control subjects tolerated the same pressure with little pain. Among the back pain and the fibromyalgia patients, the same mild pressure caused brain responses in areas that process the sensation of pain. The same brain responses did not happen in control subjects until pressure was raised substantially. All subjects showed increased activity in eight areas of the brain, but lower-back pain subjects showed no increased activity in two areas that were active in both fibromyalgia subjects and normal control subjects. The fibromyalgia subjects showed increased activation in two other areas not active in back pain patients and healthy subjects. The study indicated that lower-back pain patients have enhanced pain response in some brain regions, and diminished response in others, the investigators reported. The study offers the first objective method for correlating lower-back pain to unique brain activities at the precise moment of adverse feeling. The research might eventually lead to better treatments for lower back pain and fibromyalgia, by pointing toward certain brain regions where pain-inducing disorders might be located, Dr. Gracely noted. "So the bottom line is that fibromyalgia pain and lower-back pain are really 'real,'" said Nancy Derby, spokesperson and director of public policy and education for the National Fibromyalgia Association in Orange, CA. "This pain is a moving target, it seems, and perhaps now we see a bit better where it comes starts." Lower back pain is common, especially among overweight and sedentary people and those whose work is physically demanding. Lower back pain and problems stemming from it rank as the second most frequent cause of lost work days in adults under the age of 45, second only to the common cold. The study was supported in part by the National Fibromyalgia Research Association, the U.S. Army and the National Institutes of Health. Copyright © 2003 P\S\L Consulting Group Inc.

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