Researchers are making discoveries about why the body turns against itself--and that could result in new treatments in the years ahead. Find out what's in the pipeline now for rheumatoid arthritis, multiple sclerosis and lupus.
Twenty-three and a half million. That’s how many Americans may be affected by one of the more than 80 diseases characterized as autoimmune. These disorders range from Hashimoto’s disease, the most common thyroid condition in America and a fairly controllable illness, to more complex progressive diseases, such as lupus, multiple sclerosis (MS) and rheumatoid arthritis (RA). Though each autoimmune disease appears to be distinct, scientists are finding out just how much they have in common.
Genes, for example. “Many of the same genes constitute risk factors for multiple autoimmune diseases,” says Betty Diamond, M.D., chief of the Center for Autoimmune Diseases at North Shore Long Island Jewish Health Systems in Manhassett, NY. Type 1 diabetes, for example, is associated with Hashimoto’s, Addison’s disease (in which the adrenal glands don’t produce enough cortisol) and celiac disease (in which the body loses its ability to digest gluten, a protein in wheat, rye and barley). “The same pathways might be involved in autoimmune activation, and targeting them may be therapeutic for several diseases,” says Dr. Diamond.
Most autoimmune diseases damage organs by promoting an inflammatory process. Scientists have been working to develop treatments to fight that inflammation; a number of treatments developed in the past decade that do so have been shown to slow or even stop progression of these diseases. Many of them are “biologics”—disease-modifying medications that mimic the function of complex natural compounds.
The coming years should bring additional improvements in treatment, as many more therapies are undergoing clinical testing. “Years ago, the only approach we had was to suppress the whole immune system, and now we have drugs that target just a part of the inflammatory response,” says Noel Rose, M.D., director of the Johns Hopkins Autoimmune Disease Research Center in Baltimore. “We’d like to go further, to treat the specific immune response—to turn off the autoimmune process, or arrest it. That’s where the field is going.”
Some researchers believe we are on the verge of a profound burst of knowledge that will unlock new ways to identify—and intervene in—very early changes in immune function, years before disease actually develops. The next step, says Stephen Balch, M.D., medical director of the Lupus Treatment Center in Atlanta, “is to develop a treatment that is not just specific for lupus or MS or RA but one that can attack the earliest phases in someone’s susceptibility to this autoimmune process.”
Saturday, February 16, 2008
Thursday, February 14, 2008
One Click sends along:
4. I Was Right About Bird Flu Hoax.
Number of human cases of avian flu dropped rather than rose for the first time -- from a paltry 115 in 2006 to an even more insignificant 86 in 2007. New York Times article shows scientists and governments are congratulating themselves for averting a threat that never was by stockpiling worthless vaccines, pointlessly culling hundreds of millions of birds, and pouring money into preparation efforts. I can only imagine that the flu vaccine manufacturers are laughing all the way to the bank.
Dr Mercola, Mercola.com
I'll repeat the sarcastic comment I made when the subject first came up: CDC had a vaccine for Bird Flu in 8 days, but after 18 years, still had nothing for CFS. They try to tell us how hard it is to find a virus, or a treatment, but for this hoax pandemic, they devoted all available resources and found what was needed in record time.
The difference may well boil down to the same thing as the difference between AIDS and CFS: death. We don't die -- we live a long, lingering might-as-well-be-dead, but we don't die. We commit suicide because we can't stand to live with such severe impairments, but we don't die "of" CFS. Even after Casey Fero and Sophia Mirza's autopsies showed problems caused by CFS, CDC still doesn't acknowledge that people can die from CFS. And as long as we're not dying, it's not considered urgent.
It's time for CFS patients to demand that our disease, which has been disabling people for decades, gets the concerted research effort that bird flu did. Instead of muddying the research pool with people who have depression (and therefore no virus) CDC needs to get a research pool from CFS experts who are sure their patients are correctly diagnosed. Follow up on the virus Elaine DeFreitas found nearly 20 years ago. Follow up on the other researchers' findings. Devote all of CDC's resources, the way they did for bird flu because WE DEMAND A CURE!
Wednesday, February 13, 2008
Dr. Richard Bruno theorizes that CFS/ME/fibromyalgia and post-polio are the same condition. It has been known for decades that polio and myalgic encephalomyelitis traveled in side-by-side epidemics, and that those affected with ME were later found to be immune to polio. He observes, "If you had paralysis or muscle weakness, you certainly did have myelitis, an inflammation of the motor neurons in the spinal cord."
While Dr. Bruno admitted to me that it’s unlikely that those of us born after the polio vaccine became available in the mid-1950s had "polio", the fact is that the vaccine only protects against a few of the worst strains; it is possible that the virus that we had was one of the milder variants not covered by the vaccine. Of course, since polio had been eradicated in the US three decades earlier, no one ever thought to test me for polio, so we don’t know what virus I had ... only what viruses I tested negative for. (He theorizes that when polio was conquered, it left a vacuum which was filled by another enterovirus; CFS researchers have found an enterovirus.)
While, obviously, I would recommend that the first book a new CFS patient reads is a CFS-specific book (and I put David Bell’s "Doctor’s Guide" at the top of that list; I recommend Devin Starlanyl’s books for a fibromyalgia primer), if you’ve read all the other literature and are looking for another viewpoint, Dr. Bruno’s "The Polio Paradox: What you need to know" is intriguing reading.
I come at this book from two perspectives: at about the time that I developed CFS, a friend was diagnosed with post-polio in arm muscles overused in propelling her wheelchair. The muscle weakness she describes in post-polio sounds a lot like what I describe in CFS; her medical experts nodded sagely and explained, mine told me what I was describing was "impossible". How can the same symptom be both "expected" and "impossible"?! Dr. Bruno recommends discarding the old "use it or lose it" philosophy and learn to "conserve to preserve." This has worked for me; I spent much of my career doing production typing – 100 pages a day – and then came home to do a couple hours of needlework, so, like my friend, it was my arm muscles that were overused. When I followed her doctors’ advice about setting limits on how much I used my hands/arms, it stopped the problems of ever-increasing weakness and late-day muscle failure.
Dr. Bruno describes PPS patients as "having new symptoms: overwhelming fatigue, muscle weakness, muscle and joint pain, sleep disorders, heightened sensitivity to anesthesia, cold and pain, and difficulty swallowing and breathing" and "brain fatigue", including word-finding difficulty. Sound familiar?
Molly, a patient, asks "Have you ever been so exhausted that eating a meal, let alone cooking it, simply wasn’t possible?" I see every CFS patient out there nodding in recognition, and every non-patient in total disbelief. That may be the best explanation of why calling what we have "fatigue" is the understatement of the millennium. But Dr. Bruno warns against taking pep pills; instead, for your own good, heed your body’s demand to rest.
Dr. Bruno was training in Columbia University’s Department of Rehabilitation Medicine, studying disorders of the autonomic nervous system when he dealt with a polio patient whose bad arm was always colder than his good arm. Intrigued, Dr. Bruno started researching further.
In his investigations, Dr. Bruno came on some startling information – the plan to award Disability benefits for post-polio was "shelved in favor of benefits for those with AIDS. Disability should not be an either-or proposition" and that the patients "reported 50% more Type A behavior on average than did nondisabled individuals." Three British researchers concluded that "highly motivated patients who pushed themselves beyond the competence of their damaged bodies were most likely to develop late-onset problems."
He observes that for most patients "it’s more important to appear normal ... to protect themselves from criticism and failure than it is to ... care for themselves." Just what some people have suggested about CFS: that it occurs in Type A people who cannot and will not stay home until they are completely recovered from the virus; I went back to work the day after I first sat up for an hour propped up with pillows. I pushed myself (I still do) to my limits (and sometimes beyond) because that’s the type of person I am, and I paid the price in the long run, and now take criticism for not pushing even further past my limits in order to continue to appear normal.
Pathologist David Bodian observes that the non-paralytic forms "may be associated with severe neuron damage in the spinalcord. [And] some with non-paralytic poliomyelitis do not have any damage in the spinal cord but have characteristic damage in the brain. ... [The virus] is capable of producing an encephalitis, with or without symptoms." Again, similarities with CFS. The Type II virus (documented in the 1948 Iceland outbreak of what is thought to be CFS, as well as by Dr. Sabin in Cleveland the year before) is least likely to cause paralysis but seems to damage the brain stem just above the spinal cord, while preventing infection by the high-virulence Type I virus. Coxsackie virus, which has been found in CFS patients, "can cause damage to the brain and spinal cord that is identical to polio." Dr. Bruno comments on viral proliferation in the throat; I often have throat problems just before I relapse. The evidence for the CFS/polio connection keeps mounting.
In 1934, a disease resembling the later "Iceland Disease" felled 150 doctors and nurses in the polio ward of Los Angeles General Hospital; identical symptoms were documented among 300 doctors and nurses at London’s Royal Free Hospital in 1955. At that time, infectious disease specialist Melvin Ramsey stopped calling it "atypical poliomyelitis" and started calling it "Myalgic Encephalomyelitis". Like polio, the symptoms included headache, pain, fever, and weakness. "Some ME patients reported fatigue, that they were ‘not as quick or incisive in thought’ as before their illness, ‘a decreased ability to learn, and a decline in their short-term memory’ that lasted for decades." Some patients never recovered. "Of more than a dozen ME outbreaks before the introduction of the polio vaccine in 1954, nine occurred during or immediately after outbreaks of polio, and several involved hospital staff who cared for polio patients." After the polio vaccine, "the number of ME cases went through the roof." Dr. Bruno’s theory is that nature abhors a vacuum, and when poliovirus was eliminated, another enterovirus filled the void; other doctors point out that the Sabin vaccine prevents only the 3 worst variants.
There is the fiction that if a test shows normal strength, there’s nothing wrong. However, "no manual muscle test measures your endurance, effort, or the time it takes for you to recover strength after activity." In both CFS and PPS, stamina is an issue, you "can do almost anything once." Dr. Bruno warns that every time patients "exhaust their motor neurons, they are doing damage that will eventually result in permanent weakness"; this push/crash roller coaster is another thing patients have in common. "The only cause of progressive muscle weakness is [patients] not taking care of themselves." Let me repeat that: you can avoid deterioration by honoring your limits. His advice is "if anything causes fatigue, weakness or pain, DON’T DO IT! (Or do much less of it.)" For both conditions, the recommendation is to do half the amount of work or exercise that triggers symptoms; I’m proof that you can maintain full strength with CFS, because I can still lift (though only once) the same amount I used to. "Deconditioning is one of the red herrings that doctors who know nothing ... try to feed you." (Another red herring is that your symptoms will disappear if you lose weight; research found no correlation between weight and any PPS symptom.)
Dr. Bruno observes that patients "were confronted by doctors’ ignorance about PPS, their disinterest and disdain. Many physicians dismissed new symptoms as psychosomatic. ... Even after the publication of scores of medical journal articles, international conferences, and acceptance of PPS by the American Medical Association ... [patients] are still being told by doctors that they’re lazy, crazy, fat, old or just plain lying," a situation which will sound familiar to CFS patients as well.Rather than admit that they don’t know what they’re talking about, doctors will throw out those red herrings like deconditioning, weight, depression, and prescribe exercise ... which is guaranteed to make you feel worse. Then you risk developing real depression, which he notes is triggered when patients "can no longer meet other people’s expectations and do what they think they ‘should’." It’s a result, not a cause, and the medical profession must take responsibility that sometimes the cause for the patient becoming depressed is their bullying the patient to do more than the patient is physically capable of.
He found 2/3 of patients reported muscle weakness was triggered by cold temperatures, and "specific triggers for their pain" including cold exposure, which explains why patients feel worse in winter. It is not, as some have suggested, Seasonal Affective Disorder: I used to live somewhere with very little difference in the length of the days, but certain months were cooler and damper, and those were the months I felt worse. He also tells the story of apatient who, like me, worked in an over-air-conditioned office, cold to the point that the staff complained, "She became weaker and more fatigued as her overtaxed, refrigerated motor neurons worked harder day after day to make her cold-stiffened muscles and joints move. Ultimately, enough of those overtaxed neurons failed and probably died under the cold-induced stress to cause permanent weakness." A nurse tells me the body works optimally at 76 degrees; although it may be tempting to save money by using less heating oil, be aware that you may cost yourself much more in the long run.
On my first reading, I thought it was ridiculous that Dr. Bruno felt it necessary to spell out that research has shown that pain can disturb sleep, yet, how many of my doctors missed that incredibly obvious nexus and refused me the pain pills that would have let me sleep?
Why do we have digestive problems? The vagus nerve contracts the muscles in your stomach, causing vomiting. This nerve also affects other autonomic functions. No less than Supreme Court Justice William O. Douglas said that exercise "made me feel faint; and sometimes I’d be sick at my stomach or get a severe headache." Dr. Bruno explains that a "spasm pushes on the vagus nerve, slows the heart, drops the blood pressure, and turns on the gut, causing nausea and maybe a feeling of faintness – all because the functioning of the vagus nerve is discombobulated." He warns that stretching toward the pain will make the spasm worse, so stretch only away from the side that hurts.
Now turn to p. 207, "subjects who had fainted even once reported significantly higher fatigue than those who had never fainted. And those who had fainted more than three times had the highest fatigue of all. This suggested to us that there is a relationship between fainting and fatigue – that damage to brain stem neurons controlling blood pressure, damage to those controlling heart rate, and damage to the brain activation neurons is related in anyone who has chronic fatigue, whether they've had polio or not." I’ve fainted dozens of times in my life.
In 1995, Peter Rowe found CFS patients have fatigue + blood pressure drop when they stand up, leading to the conclusion that "some CFS patients have lost the ability to regulate the size of their veins, just like polio survivors, allowing blood to pool and blood pressure to drop," probably due to brain stem neuron damage from a virus. I’d also refer you to Dr. Cheney’s comments on cardiac issues related to standing up. On that subject, Dr. Bruno poses the Cardiac Conundrum, what to do when "one indispensable muscle needs exercise while all the other muscles need rest?" and observes "arm exercise is more taxing on the heart and a more efficient form of heart exercise." However, in general "an exercise program is not required to prevent your muscles from turning to jelly." Physiatrist Jim Agre warns "For some persons, the performance of normal activities of daily living may require maximal effort, and additional exercise may lead to overuse problems." If you feel stronger on days you don’t exercise, your body is trying to tell you something. Listen to it. "Don’t stand when you can sit, and don’t sit when you can lie down."
Agre’s research found that polio patients who used pacing (resting for at least an equal length of time after working a short time) "could do 240 percent more work with fewer symptoms." Dr. Goudsmit’s research with CFS patients didn’t show quite as much success at increasing output, though it was successful at reducing symptoms.
Another intriguing finding is that patients tend to hypoglycemia. "The more challenging the mental task – like those difficult attention tests – the more sugar neurons need to function." Steroids make it even worse.
Numerous parallels between PPS/CFS/ME are listed on pages 285-287. There is no question in Dr. Bruno’s mind that they are physical, not emotional illnesses with "remarkable similarities". Both groups have white spots in brain neurons and less of the hormone ACTH, more prolactin and less dopamine, less growth hormone (which researchers believe to be the result, not the cause). "The symptoms of fatigue – in both polio survivors and CFS/ME patients – result from a virus damaging brain-activating neurons." Ten pages later, he also analyzes the parallels between PPS/CFS/fibromyalgia.
"Even more disturbing is that doctors choose to ignore more than eighty years of research indicating that ME, and its American cousin CFS, are very likely caused by one or more of the enteroviruses. More than polio survivors with PPS, those with ME and CFS have been dismissed as lazy, crazy, or outright liars by the medical community. Maybe it’s our Puritan heritage, but there are two symptoms by which people are not ‘allowed’ to be disabled: fatigue and pain."
"Just like polio survivors, those with CFS, ME and fibromyalgia have no more time to waste with doctors who don’t believe their conditions are real. ...It’s time doctors start looking at the cause ... from the brain up, instead of from the mind down, so that [patients] start getting help for their symptoms, instead of being blamed for them."
"How many PPS/CFS/fibromyalgia patients have been discarded by doctors who thought them to be lazy or faking when an anti-depressant didn’t cure their fatigue, or when physical therapy ... made weakness worse, not better? ...In this new millennium medicine must not be about doctors’ egos and their ability to ‘cure’ disease."
The message that has been sent is that "there is no disability that cannot be conquered" if patients try hard enough. "It is this ethic that allows doctors to reject patients whose conditions cannot be diagnosed with a blood test or an X-ray, to dismiss [them] as lazy or crazy." Unfortunately, there are some diseases for which we still have no cure, or even an effective treatment; the medical profession tries hard to sweep those under the rug, as well as to ignore the evidence that pushing some patients to rehab ever-harder will result in permanent disability.
Dr. Bruno notes that after reading his book "you now know more than any doctor you’re likely to meet"; this is too often the situation for CFS and fibromyalgia patients as well. "There is one thing we still don’t understand: why doctors and governments throughout the world refuse to acknowledge, let alone learn about and provide treatment."
Source: Journal of Chronic Fatigue Syndrome Vol. 14, #2, pp 7-23 Date: Summer 2007
Legal and Scientific Considerations of the Exercise Stress Test
Margaret Ciccolella, EdD, JD; Staci R. Stevens, MA; Christopher R. Snell, PhD; J. Mark VanNess, PhD - Margaret Ciccolella, Staci R. Stevens, Christopher R. Snell, and J. Mark VanNess are affiliated with the University of the Pacific, Pacific Fatigue Laboratory, Stockton, CA. - Address correspondence to: J. Mark VanNess, University of the Pacific, Stockton, CA 95211 (E-mail: email@example.com ).
This article examines the legal and scientific bases on which an exercise stress test can provide medically acceptable evidence of disability for the Chronic Fatigue Syndrome (CFS) patient. To qualify for disability benefits, a claimant must establish the existence of a serious medically determinable impairment (MDI) that causes the inability to work. The single stress test has been used to objectively establish whether a claimant can engage in "substantial gainful employment" and is an important determinant of the award or denial of benefits. A review of case law indicates problems associated with a single test protocol that may be remedied by a "test-retest" protocol. The results of a preliminary study employing this approach indicate that the test-retest protocol addresses problems inherent in a single test and therefore provides an assessment of CFS related disability consistent with both medical and legal considerations.
Denial of Benefits: Typical Scenario
Denial of related disability benefits is a common problem for the patient with a medical diagnosis of Chronic Fatigue Syndrome (CFS). The typical scenario can be described as follows: Debilitating fatigue prevents continued work and the CFS patient reports the diagnosis to his or her employer. The patient becomes a "claimant" upon application for related disability benefits from the Social Security Administration (SSA) and/or a private insurance carrier. The initial burden is on the claimant who must objectively establish the existence of a medically determinable impairment (MDI) that is serious enough to cause the inability to engage in any "substantial gainful employment." Claimant fails to provide sufficient objective evidence and disability for the inability to work is successfully challenged resulting in the denial of benefits. Appeals are available but the burden rests with the claimant to pursue a reversal of the denial.
At the appeal and regardless of the agency involved, a review of the medical record fails to provide sufficient objective evidence of a serious impairment that causes disability. While the diagnosis is accepted, the central legal issue is whether the claimant can work on a regular and ongoing basis.The medical record documents that the diagnosis is largely based on self-reports by the patient to the treating physician and that the symptoms upon which a diagnosis or MDI is made overlap with other illnesses. This makes it difficult to distinguish CFS from other illnesses. It is undisputed that there is no widely accepted definitive laboratory test for CFS. However, the record used to objectively document a FRC that precludes the ability to work on a regular and ongoing basis includes a single exercise stress test. The test shows diminished metabolic capability consistent with the ability to do at least sedentary work and the benefits are denied.
Problem: The Single Stress Test
The single stress test has been utilized to assess Function Residual Capacity (FRC) and therefore determine whether a claimant can work. The problem is that a review of case law documents that both good and poor results of a single stress test have been used to deny benefits. A good result contradicts the diagnosis of disability because it appears to show the ability to work. A poor result is subject to the criticism that the claimant malingered by deliberately failing to exert maximal effort on the test.
It is our position that utilization of a single test fails to objectively establish disability from both a legal and clinical perspective. We premise this paper on the assertion that "post-exertional malaise" is the cornerstone symptom of CFS related disability. The objective assessment of the fatigue suffered following a test is critical to the determination of ability to work on a regularand ongoing basis. Such an assessment requires integration of law and science if meaningful consequences are to result for the CFS patient.
SSA explicitly states that continued research will produce new evidence to "clarify the nature of CFS and provide greater specificity regarding the clinical and laboratory diagnostic techniques that should be used to document this disorder" (1). The purpose of this paper is to explore the utilization of a "test-retest" protocol consistent with such a mandate. The legal considerations relevant to the use of a single stress test protocol will be discussed followed by a report of preliminary "test-retest" research conducted at the Pacific Fatigue Laboratory.
Social Security Administration (SSA) Policy
Social Security Ruling (SSR) 99-2p (1999) Mettlen v. Commissioner of the SSA (2003)
Social Security rulings constitute general policy statements but they do not have the full force and effect of law. While SSA rulings are not binding upon a court, courts in fact frequently rely upon them. This reliance is evident in a review of appeals denying benefits involving both SSA and private insurance companies. For this reason, SSA policy for evaluating CFS disability claims is briefly reviewed here.
SSA accepts the definition of CFS established by an international group convened by the Centers for Disease Control and Prevention (CDC). Under the CDC definition, the hallmark of CFS is the presence of clinically evaluated and debilitating chronic fatigue that cannot be explained by another physical or mental disorder. SSA requires a dual process in the establishment of CFS disability in that a claimant must prove (1) the existence of a "medically determinable impairment" (MDI) and (2) the inability to engage in any substantial employment.
1. Establishing the MDI. Physicians sometimes cannot make a conclusive diagnosis of CFS and there is no "dipstick" laboratory test for diagnosing the condition. SSA accepts the symptom-based criteria for the diagnosis of CFS established by the CDC,1 but requires a strict timeline for the concurrence of at least four symptoms that include post-exertional malaise lasting more than 24 hours. Of the listed symptoms, post-exertional malaise is considered to represent the cornerstone symptom of CFS and is therefore is especially relevant to this paper.
While diagnosis may be based primarily on self-reported symptoms, disability requires objective evidence. For example, SSA policy explicitly disallows a finding of disability based solely on subjectively allegations of symptoms or impairments. A serious impairment (MDI) must be objectively proven. Since the medical community has not reached agreement on a definitive test, SSA allows reliance on "certain" listed laboratory findings to establish the existence of the MDI.2 The list of enumerated laboratory findings includes "an abnormal stress test" using a "medically accepted" protocol.
2. Establishing the ability to engage in any substantial employment. SSA policy considers whether a claimant has the ability to engage in "substantial gainful employment," i.e., whether the claimant can sustain work-related activities in a work setting on a regular and continuing basis. Residual functional capacity (FRC) laboratory test assesses whether the claimant, in spite of a serious impairment, has the physical and mental ability to perform activities required by competitive, remunerative work. If an applicant's FRC fails to meet the requirements of regular, previous employment, then the burden is on the Commissioner to show that the claimant can do work as it is generally performed in the "national economy" (Mettlen v. Commissioner of the SSA, 2003).
Examples of Appeals Using the Exercise Stress Test
The most common use of the stress test in appeals is to objectively establish FRC and work capacity by assessing the metabolic onset of fatigue. A single stress test is ineffective in establishing a MDI because it cannot document post-exertional malaise, a cornerstone symptom used to diagnose CFS, and does not distinguish between CFS and other illnesses. It further fails to effectively assess disability in that both good and poor performances have been used to dispute an inability to work and deny benefits. The following cases illustrate the problems when a single stress test protocol is used.
Problems Associated with a Good Result on a Single Stress Test
O'Sullivan v. The Prudential Insurance Co. of America (2002) Marshall v. Sullivan (1990)
In O'Sullivan v. Prudential (2002), the former director of human resources in a New York City hotel (claimant) appealed a private insurance company's denial of long-term benefits. Prudential discontinued the long-term disability benefits after claimant, a CFS patient with overlapping symptoms of fibromyalgia, alleged total disability. Prudential had the medical records of the claimant reviewed by a consulting physician asking her to answer two specific questions: (1) what objective medical evidence existed that rendered claimant unable to perform the sedentary duties of her job and (2) based on the medical evidence in the record, did the claimant have any restrictions or limitations of her functional ability?
The response to both questions focused in part upon the results of a single exercise stress test in which the claimant's relatively good performance appeared to demonstrate the ability to work. With regard to claimant's ability to work, Prudential's consulting physician concluded that no objective evidence existed to support claimant's inability to perform a sedentary desk job. "She was able to reach 9 METs of exercise on a stress test... more than what is generally considered minimally necessary for a sedentary job." With regard to functional ability, the physician stated that "very little documentation of [claimant's ] actual physical abilities is available in the medical records... The treadmill test documented that she is able to walk uphill for nearly 8 minutes at a time..."
During the proceedings, Prudential did not contest claimant's complaints of pain and fatigue or the fibromyalgia diagnosis. Instead, Prudential simply maintained that there was no objective medical evidence which established how the claimant's condition rendered her totally disabled.
The court addressed the question of disability by considering two issues: (1) whether claimant was unable to perform the duties of her job due to sickness and (2) whether the claimant was unable to perform the duties of any job consistent with her education, training, or experience. The court found the record devoid of any evidence that the claimant's treating physicians were aware of the duties of the claimant's job [**]and further concluded that they were apparently ignorant of her level of education, training, and experience. The court found that the claimant's treating physicians offered "little more than conclusionary assertions that do not establish that [claimant] is totally disabled." Here, while claimant was granted SSA benefits, Prudential's denial of long-term benefits was upheld.
In Marshall v. Sullivan (1990),3 claimant appealed SSA denial of benefits for chronic fatigue. Claimant was a 68-year-old accountant for the state of Virginia who was initially diagnosed with chronic infectious mononucleosis related to Epstein-Barr virus (EBV). Her treating physician concluded that she was totally disabled based upon her reports of debilitating fatigue following routine exertion and lab results showing persistent elevation of EBV antibody titers. It should be noted that by the end of her appeal EBV and mononucleosis were ruled out as causing disability and the proper diagnosis of Chronic Fatigue Immune Dysfunction Syndrome (CFIDS) was made.
In addition to her treating physicians, three additional physicians examined claimant (one each from SSA, a private insurance carrier, and the state retirement board) and all agreed that claimant was disabled. The only report to contradict claimant's disability came from the medical advisor for SSA who neither treated nor examined claimant. According to the medical advisor, the results of the treadmill test revealed a lack of disability and he found that claimant had the capacity "for at least light work." The claimant's high level of performance on the treadmill proved that she had the "residual functional capacity" to work comfortably at lower levels of activity. The Administrative Law Judge (ALJ) relied primarily on the medical advisor's opinions and the results of the treadmill test in finding claimant not disabled.
At the appeal, the ALJ was found to have improperly analyzed claimant's fatigue.
In his decision, the ALJ refers to that test [treadmill test] as `an objective tool by which the Administrative Law Judge can measure the claimant's fatigue.' This is clearly not the case; Marshall's [claimant's] performance on the treadmill revealed nothing about the increased fatigue she suffered following the test.
It was determined that the treadmill test failed to provide persuasive evidence to contradict the treating and examining physicians. Therefore, the SSA decision to deny benefits was reversed and claimant was awarded benefits. While the outcome was good for the claimant in this particular case, the risk and burden on the claimant was clear. The objective results of a single test resulted in an initial denial of benefits and the claimant was forced to pursue two appeals in order to ultimately prevail. This might have been avoided altogether had the claimant participated in a second test to objectively document the fatigue that she suffered following the first test. See discussion below.
Problems Associated with a Poor Result on a Stress Test
Coffman v. Metropolitan (2002)
In Coffman v. Metropolitan (2002), claimant appealed the denial of long-term benefits from a private insurance company. Claimant worked as a drug representative for a major company and was subsequently diagnosed with CFS, hypothroidism, vertigo, and other conditions. Metropolitan denied disability benefits claiming the medical record had "insufficient objective clinical findings" to support claimant's subjective complaints and did not support that [claimant] was "unable to perform the duties of his job." Further, Metropolitan offered expert testimony that the fatigue of a chronic nature experienced by claimant was more likely due to other conditions.
At trial, claimant offered the results of a cardiopulmonary stress test to prove a significant impairment of functional aerobic work. Claimant's treating physician stated that maximal oxygen consumption was only 61% of predicted for sedentary individuals and that this poor performance showed the inability of claimant to "sustain work."
Metropolitan responded that these conclusions were wrong because they were based on "a test which clearly revealed less than maximal effort" noting that claimant reached only 73% of his predicted maximal heart rate. Claimant's treating physician responded to the criticism asserting that claimant was on cardiac drugs (calcium channel blockers) that may have blunted heart rate and that excellent effort on the test was observed in blood pressure readings that increased from 120/80 to 200/94 and increases in oxygen pulse and respiratory rate. He further stated that hyperventilation due to anxiety accounted for a respiratory quotient (RQ) greater than one at the beginning of the test.
Metropolitan used video-surveillance showing claimant running errands with his wife, driving a car, attending church, carrying two tote bags, etc. This direct observation of claimant's activities was effectively used to contradict the claim that physical limitations precluded work and provided additional support for Metropolitan's challenge to the results of the stress test. A Metropolitan expert testified that claimant's functional capacities were "compatible with the Department of Labor Work Category definition of light to medium work." The shadow cast upon the results of the stress test and the lack of objective medical evidence to support disability resulted in a ruling that upheld Prudential's denial of benefits.
[** Similarly, one of my doctors stated unequivocally that I could work without having any clue about my job duties; on questioning, he seemed to think my function was purely decorative with no production necessary. He had received a one-page typed letter from me and without knowing who wrote it or who typed it, relied on that to say that I could work successfully. Doctors who saw me sit up for 5 minutes stated unequivocally that I could sit for 8 hours, without any proof that their extrapolation was accurate. I've never had a Residual Functional Capacity Evaluation that proved I could work for 8 hours in one day; they don't want to develop the proof that I'm telling the truth, and rely on the fact that I cannot afford to pay for such testing myself ... only to have it rejected by the judge on the assumption that a poor result could only mean malingering, as described above]
Relevance to the Need for a Test-Retest Protocol
In good result/performance cases, a claim for benefits is compromised when a single exercise stress test provides apparent and objective evidence of the ability to work that conflict with the medical record. In such cases, the record is typically replete with subjective evidence of claimant's debilitating fatigue following routine exertion that includes walks, running errands, doing household chores, etc. The failure to objectively document post-exertional malaise is a failure to distinguish fatigue from disability. As a cornerstone symptom of CFS, it is imperative to document post-exertional malaise in order to objectively demonstrate the inability to work on a regular and continuing basis. If post-exertional malaise effectively means that the patient who works on Monday will then suffer uncompromising fatigue for several days thereafter, then it is reasonable to assert that there can be no reasonable expectation of regular participation in the national economy.
Poor result/performance cases provide objective evidence for disability but have been successfully challenged on the basis that the claimant malingered on the test. This raises the important issue of the endpoint used to determine both effort and fatigue. End point respiratory quotients (RQs) are widely accepted as objective markers of effort and fatigue. RQs exceeding 1.09 at the end of an 8-12 minute test indicate that peak aerobic capacity has been met and that anaerobic metabolism explains continued participation in the test. An RQ exceeding one coupled with evidence that either (1) Peak VO_2 or (2) heart rates meeting or exceeding 85% of predicted maximal rates is compelling evidence of maximal effort on a stress test.
The ability to do errands and chores is often used as evidence of the ability to work a job every day. Video-surveillance and third-party testimony is permitted to document a claimant's daily activities, e.g., doing household chores, shopping, running errands, attending church, driving a car, etc. (Coffman v. Metropolitan, 2002). However, at least one appeal ruled that the ability to do limited daily activities is not inconsistent evidence of disability. In Smith v. Barnhart (2003), the ALJ found claimant not markedly impaired because she was able to care for her personal needs, perform some household tasks, and regularly attend church and a Bible study. At appeal, this decision was found not to reflect whether the ALJ considered evidence showing that the claimant had difficulty performing her limited daily tasks. The court cited authority that the ALJ must assess such activities by their independence, appropriateness, effectiveness, and sustainability. Additionally, the ALJ did not analyze why claimant's daily activities were inconsistent with her ability to work. "The fact that a claimant is able to engage in limited daily activities, such as washing dishes, doing laundry, and cooking meals does not necessarily demonstrate that she is not disabled."
Nonetheless, specific reference in the medical record of the caloric or metabolic requirements to perform specific jobs or tasks is important. O'Sullivan v. Prudential (2002) explicitly commented on the need for the medical record to specifically document the physician's knowledge of the metabolic requirements for certain jobs. A poor performance on a stress test may not defeat an argument that sedentary work is within the metabolic capability of a claimant. This argument may be supported by reference to Department of Labor Work Category or specific lists of routine and unskilled jobs within the capabilities of persons with aerobic impairments, e.g., stationary security guard, toll booth operator, ticket taker, car lot attendant (Swenson v. Sullivan, 1989). Evidence of the caloric requirements associated with various tasks/jobs and claimant's metabolic capability to perform would greatly support a rebuttal to the argument. This requires a test-retest protocol that measures oxygen consumption values that are readily translated into caloric equivalents.
The following preliminary study conducted at the Pacific Fatigue Laboratory is directly relevant to the issues raised above. The study examines the test-retest protocol and discussion of the results directly connects the legal and scientific considerations relevant to stress testing.
PACIFIC FATIGUE LABORATORY STUDY
In this study, the exercise test-retest protocol was examined. The objective of the study was to determine whether objective findings of post-exertional malaise could be documented and to determine whether a serial stress test could objectively distinguish fatigue caused by CFS as opposed to fatigue caused by other illnesses. A brief summary is shown in Table 1.
A standardized bicycle protocol was used in six CFS patients and six normal controls. Expired gases were collected throughout the test so that the following values could be determined: Peak oxygen consumption (VO_2peak ml/kg/min), oxygen consumption at anaerobic threshold (VO_2 @AT ml/kg/min), peak respiratory quotient (RQ), and percentage of predicted heart rate (beats/min). The premise of the study was that test-retest variability in these values should not exceed 8% (2). The rationale for examining these values in a serial protocol is as follows:
Peak VO_2 documents maximal aerobic capacity that can be used to measure fatigue, post-exertional fatigue and determine functional work capacity. Oxygen consumption values can be translated into estimates of kilocalories that in turn can be used to compare the energy requirements of various tasks. This allows for an objective determination of the ability to do work and therefore support or deny the existence of disability. Further, evidence of the attainment of Peak VO_2 is one factor that documents maximal exertion in a test.
VO_2 @AT is the intensity of physical work when anaerobic metabolism takes on a significant and increasing role in providing the energy necessary to continue work. Subjectively, this is the point in work that feels as if exhaustion will occur within a relatively short time in the absence of rest or a reduced workload. Objectively, VO_2 @AT documents one parameter on which to explain level of work that cannot be tolerated for long periods because it represents a point when fatigue begins to lead to exhaustion. This too may be translated into one's ability to produce and expend energy (kilocalories) at the onset of fatigue allowing for comparison with the energy requirements of various tasks.
Peak RQ values objectively document the relative contribution of aerobic and anaerobic metabolism at the end of a stress test. Values exceeding one indicate Peak VO_2 has been met and that anaerobic metabolism preferentially contributes to the energy necessary to continue work. Values over 1.0 are widely accepted as an important factor that shows maximal effort was exerted on a test.
85% of Predicted Maximal Heart Rate is a commonly accepted end-point representing fatigue and true effort in a stress test. There should not be exclusive or even preferential reliance on heart rate. While heart rate objectively reflects workload, it is also influenced by other factors, e.g., emotional status, influence of drugs, state of hydration. Further, it has been argued that blunted heart rates are characteristic of the CFS patient (3). Heart rate is important but should not be exclusively relied upon, especially under circumstances where objective documentation of effort is important.
DISCUSSION OF CLINICAL AND LEGAL ISSUES RELEVANT TO THE RESULTS AND A CFS DIAGNOSIS
1. Establishment of an MDI
Can the Test-Retest Protocol Support a Diagnosis by Showing Post-Exertional Malaise?
On Test 1, a side-by-side comparison of Controls and CFS patients shows the relatively "good performance" similar to the discussion above examining legal appeals. In O'Sullivan v. Prudential (2002), claimant had a maximal MET level of 9. Here, Test 1 Peak VO_2 values represent maximal MET levels of 8.11 and 7.48, respectively for Controls and CFS patients. Test 1 values alone are not compelling evidence that the CFS patients are significantly more impaired that Controls. Additionally, Peak VO_2, VO_2 @AT, and RQ values show no significant differences between the two groups. This further suggests that metabolic abnormalities are absent.
It is the comparison between tests that shows a disturbing difference between the two groups. Variability from Test 1 to Test 2 in Peak VO_2 and VO_2 @AT values documents impairment in CFS patient but not the controls. Controls show only 2-3% variability while CFS patients declined by an average of 22-27%. Based upon the premise that test-retest variability should not exceed 8%, this study indicates significant impaired metabolic capability as well as an atypical recovery response in the CFS patient but not the Controls. This is directly relevant to a finding of post-exertional malaise.
This type of analysis is precluded when only the results of a single test are available. A serial protocol is required to document debilitating fatigue. The test-retest protocol does what the single test cannot do, namely objectively document post-exertional malaise, a cornerstone symptom upon which a CFS diagnosis can be founded.
Can the Test-Retest Protocol Distinguish CFS from Other Illnesses?
There remains the problem of distinguishing CFS from other illnesses. This raises the question of what results might occur when CFS patients are compared to patients with other illnesses. Wasserman argues that test-retest variability should not exceed 8% in Peak VO_2 and VO_2 @AT values in clinical and normal groups. Weisman reports a summary of five prior studies that examined test-retest variability in patients with different illnesses. The averaged variability in Peak VO_1 and VO_2/AT among patients suffering from chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), and chronic heart failure (CHF) was 7.2% (2).
It is our contention that the dramatic decline in Peak VO_2 and VO_2 @AT values in CFS patients documented in the Pacific study is unique to CFS and, therefore, represents a basis on which to distinguish fatigue caused by CFS as opposed to fatigue caused by other illnesses. Further research is necessary but based on the results of Pacific's study, the potential to better understand and therefore articulate the nature of CFS to both medical and legal arenas is clearly possible.
2. Establishment of the Ability to Work
Can the Test-Retest Protocol More Effectively Document Functional Impairment/Ability to Work?
Metabolic charts state the caloric requirements for certain tasks and VO_2 and VO_2 @AT values can be translated into calorically based documentation of an individual's metabolic ability or state of fatigue in any number of tasks and jobs. Laboratory stress tests that produce such information may provide explicit documentation of specific tasks that may be reasonably and regularly done by the claimant. This goes to the heart of the ability to work every day at a given job and therefore "engage in substantial employment."
This is illustrated using data from the Pacific study from CFS Patients on Test 2 values of Peak VO_2 an VO_2 @AT and a hypothetical CFS patient weighing 150 pounds (68 kg). Oxygen consumption data is translated into Calories on the premise that one liter of oxygen consumed is the equivalent of approximately 5 calories produced and expended.
For example, Peak VO_2 averaged 20.5 ml/kg/min which translates to a maximal ability to aerobically produce and expend 7kcals/min. VO_2 @AT work capacity averaged 11 ml/kg/min which translates into 3.74 kcals/min3.
It is imperative to distinguish the ability to work a regular job from engaging in daily activities that permit frequent and extended rest periods.Providing specific metabolic information from a test-retest format allows discussion of job requirements in terms of Caloric requirements. This is terminology familiar even to the lay person and providesdocumentation required by policy, law, and precedent.
Can the Test-Retest Protocol Distinguish Maximal Exertion from Malingered Effort?
Peak RQ values with minimal variability and with values ranging from 1.09-1.21 give strong objective support that both groups in both tests exerted maximal effort. Unlike the Controls, the CFS Patients experienced a dramatic decline in VO_2 @AT values between tests suggesting impaired metabolism sufficiently serious to result in the onset of fatigue at a significantly lower workload. This data is the type of objective documentation that can support self-reports by CFS Patients of debilitating fatigue following routine exertion.
Proving CFS disability is a mandate for a claimant seeking associated benefits. Examination of legal considerations relevant to the proof of disability and the process of securing benefits is important to CFS research. The alliance of science and law allows for consideration of the development of laboratory findings that have the potential to better understand the nature of CFS and to provide objective and acceptable evidence for CFS disability.
It is our contention that the Pacific study on serial testing reflects this alliance. It is clear that the Pacific study is preliminary and begs further review. But the initial data suggests that the test-retest format offers a superior basis on which to establish disability consistent with SSA policy and other relevant case law. If the preliminary data holds, the contribution to the CFS patient may be immeasurable.
1. Diagnosis requires concurrence of at least four self-reported symptoms that include: (1) short-term memory loss or impaired concentration that causes substantial reduction in previous levels of performance in work, social or personal activities; (2) sore throat; (3) tender lymph nodes in the neck or auxiliary area; (4) muscle pain; (5) joint pain without redness or swelling; (6) non-refreshing sleep; and (7) post-exertional malaise lasting more than 24 hours. Social Security Ruling (SSR) 99-2p (1999).
2. The following lab findings establish the existence of a MDI in CFS patients: An elevated antibody titer to Epstein-Barr virus capsid antigen equal to or greater than 1:5120, or early antigen equal to or greater that 1:640; An abnormal MRI brain scan; Neurally mediated hypotension as shown by tilt table testing or another clinically accepted form of testing; or, Any other lab findings that are consistent with medically accepted clinical practice and are consistent with the other evidence in the case record; for example, an abnormal exercise stress test or abnormal sleep studies. Social Security Ruling (SSR) 99-2p (1999).
3. Unpublished dispositions when used in this paper are not included as legal precedent. Rather, they are included because they offer insight into the legal use and interpretation of stress tests for the CFS patient.
CASE LAW REFERENCES
Kansky v. Coca-Cola Bottling Company of New England, (2006 WL 1167781 at D. Mass). Marshall v. Sullivan, 914 F.2d. 248, Unpublished Disposition, 1990 WL 135840 (4th Cir. Va 1990). Mettlen v. Commissioner of the Social Security Administration, 2003 WL 1889011, 86 Soc.Sec.Rep.Serv. 600 (E.D. Tex. 2003). O'Sullivan v. The Prudential Insurance Co. of America, 2002 WL 484847 (S.D.N.Y.). Smith v. Barnhart, 59 Fed.Appx. 901 (7th Cir. In 2003) Unpublished Disposition. Swenson v. Sullivan, 876. F.2d 683 (9th Cir. Wa 1989).
There is no electronic version of the table.
TABLE 1. A summary of the results of the preliminary study with 6 CFS patients and 6 control subjects. The values for peak oxygen consumption (VO_2 Peak) oxygen consumption at the anaerobic threshold (VO_2 @AT), peak respiratory quotient (Peak RQ) and the percent of age-predicted maximal heart rate attained at peak exercise (Predicted HR%) are shown for the first exercise test (Test 1) and the second exercise test (Test 2) administered 24 hours later. The percent variability (Var) between Test 1 and Test 2 is shown to illustrate the magnitude of the difference in between the metabolic responses.
1. SSR 99-2p (1999 WL 271569 (S.S.A.)) April 30, 1999.
2. Weisman, I.M., & Zeballos, J. (Eds.) (2002) Clinical exercise testing. New York: Karger. In Progress in Respiratory Research (Volume 32; C.T. Bolliger, Editor).
3. VanNess, J.M., Snell C.R., Dempsey W.L., Strayer D.R., Stevens S.R. Sub- classifying Chronic Fatigue Syndrome Through Exercise Testing. Med Sci Sports Exerc 2003; 35(6), 908-913.
-------- (c) 2007 The Haworth Press
The "full text" of
Legal and Scientific Considerations of the Exercise Stress Test
Journal: J of Chronic Fatigue Syndrome, Vol 14, No. 2, 2007, pp. 61-75
Authors: Margaret Ciccolella EdD, JD, Staci R. Stevens MA,
ChristopherR. Snell PhD, Mark Van Ness PhD
that was posted to Co-Cure did not include an important table, Table 1 in
this important paper:
Test 1 Test 2 (Var)
VO2 Peak 28.4 28.9 (2%)
V02@AT 17.5 18.0 (3%)
Peak RQ 1.19 1.21 (2%)
Predicted HR% 94.8 97.6 (3%)
Test 1 Test 2 (Var)
VO2 Peak 26.2 20.5 (-22%)
V02@AT 15.0 11.0 (-27%)
Peak RQ 1.15 1.09 (5%) (TK: this should be
Predicted HR% 87.0 87.8 (1%)
Also note that this does not match the abstract for:
Diminished Cardiopulmonary Capacity During Post-Exertional Malaise
Journal, J of Chronic Fatigue Syndrome, Vol. 14, No. 2, 2007, pp. 77-85
Authors: J. Mark VanNess PhD, Christopher R. Snell PhD, Staci R. Stevens
Results: "differences between control and CFS, respectively, for test 1: ..
HR% (87.0 ± 25.4%; 94.8 ± 8.8%)."
as the heart rate is inverted.
As the authors calculated the percentage difference between test 1 and test
2 in Ciccolella et al and they are similar within groups across the two
tests, I presume it is correct. Also they explicitly say it might be a
little lower in people with CFS (1) (appended), I would imagine that the
percentages are the wrong way around in Van Ness et al i.e. it should be HR%
(94.8 ± 8.8%; 87.0 ± 25.4%)
(1) "85% of Predicted Maximal Heart Rate is a commonly accepted endpoint
representing fatigue and true effort in a stress test. There should
not be exclusive or even preferential reliance on heart rate. While heart
rate objectively reflects workload, it is also influenced by other factors,
e.g., emotional status, influence of drugs, state of hydration. Further, it
has been argued that blunted heart rates are characteristic of the CFS
(3). Heart rate is important but should not be exclusively relied
upon, especially under circumstances where objective documentation
of effort is important."
[Dr. Teicheira told me that chronic pain also damages the central nervous system, and that untreated pain may be the root cause of fibromyalgia. He had nothing good to say about any doctor who refuses to prescribe pain medication or tells the patient to "tough it out". I suffered for years without effective pain relief, and he suspects I'll suffer the rest of my life from the results of being refused appropriate treatment.]
by Northwestern University
People with unrelenting pain don't only suffer from the non-stop sensation of throbbing pain. They also have trouble sleeping, are often depressed, anxious and even have difficulty making simple decisions.
“Stuck on Full Throttle”
In a new study, investigators at Northwestern University's Feinberg School of Medicine have identified a clue that may explain how suffering long-term pain could trigger these other pain-related symptoms.
- Researchers found that in a healthy brain all the regions exist in a state of equilibrium. When one region is active, the others quiet down.
- But in people with chronic pain, a front region of the cortex mostly associated with emotion "never shuts up," said Dante Chialvo http://www.chialvo.net/index.html, lead author and associate research professor of physiology at the Feinberg School. "The areas that are affected fail to deactivate when they should." They are stuck on full throttle, wearing out neurons and altering their connections to each other.
This is the first demonstration of brain disturbances in chronic pain patients not directly related to the sensation of pain. The study was published Feb. 6 in The Journal of Neuroscience. [See abstract - “Beyond Feeling: Chronic Pain Hurts the Brain, Disrupting the Default-Mode Network Dynamics.” ]
Chronic Low Back Pain vs. Pain Free Volunteers
Chialvo and colleagues used functional magnetic resonance imaging (fMRI) to scan the brains of people with chronic low back pain and a group of pain-free volunteers while both groups were tracking a moving bar on a computer screen.
The study showed the pain sufferers performed the task well but "at the expense of using their brain differently than the pain-free group," Chialvo said.
When certain parts of the cortex were activated in the pain-free group, some others were deactivated, maintaining a cooperative equilibrium between the regions. This equilibrium also is known as the resting state network of the brain. In the chronic pain group, however, one of the nodes of this network did not quiet down as it did in the pain-free subjects.
This constant firing of neurons in these regions of the brain could cause permanent damage, Chialvo said. "We know when neurons fire too much they may change their connections with other neurons and or even die because they can't sustain high activity for so long," he explained.
"If you are a chronic pain patient, you have pain 24 hours a day, seven days a week, every minute of your life," Chialvo said. "That permanent perception of pain in your brain makes these areas in your brain continuously active. This continuous dysfunction in the equilibrium of the brain can change the wiring forever and could hurt the brain."
Chialvo hypothesized the subsequent changes in wiring "may make it harder for you to make a decision or be in a good mood to get up in the morning. It could be that pain produces depression and the other reported abnormalities because it disturbs the balance of the brain as a whole."
Study of New Pain Control Approaches "Essential"
He said his findings show it is essential to study new approaches to treat patients - not just to control their pain but also to evaluate and prevent the dysfunction that may be generated in the brain by the chronic pain.
* * *
Unfortunately, too many doctors don't understand these basic facts about pain. According to Dr. Teicheira, the structural changes begin to occur in under 48 hours, so there is never a point when a patient should be told to tough it out and come back only if the pain doesn't get better after a week or two -- that's too late.
Ironically, the stance of the director of the pain management clinic at the medical group where I was repeatedly denied pain medication is that "pain is what the patient says it is". If the patient says the pain is severe, then it's severe and should be treated as such. Unfortunately, the doctors I dealt with refused to believe me that the pain was severe enough to prevent me from sleeping, and also refused to refer me to the pain management clinic where I would have been believed.
Unfortunately, by the time I ran into Dr. Teicheira, who would have gladly testified that they'd committed malpractice, the statute of limitations had run out.
Don't let it happen to you -- do whatever it takes to get a referral to a pain management clinic. While a rheumatologist may be loathe to prescribe anything stronger than Advil for fear of government investigation leading to losing his license (which Dr. Teicheira calls an unreasonable fear if they're prescribing reasonable amounts -- only those prescribing excessive quantities to one patient have anything to fear), a pain management specialist is expected to be prescribing pain pills, and won't give you that hokey excuse for not giving you what you need.
Another excuse they'll use is that they don't want to turn you into an addict. Statistically, less than 1% of patients become addicted to their pain pills, and almost all of those can be predicted because they have an addictive personality. If you don't have a history of alcoholism, drug addiction, gambling addiction, internet addiction, etc., they have nothing to worry about.