PATIENT CONFERENCE SUMMARY
SEPTEMBER 13, 2008
by Linda Milne
“What Fibromyalgia Taught Me.”
Central to this year’s conference was the free screening of a new DVD entitled “Living with Fibromyalgia”. The 70-minute film, created by husband-wife team, Daneen Akers & Stephen Eyers. played to a packed house at the Broadway theatre. Following the film, Akers, a daughter of an FM patient, launched the afternoon conference with “What Fibromyalgia Taught Me.” Her wit and warmth, not to mention the quality of her own struggle to understand FM and assist her mother, set a tone for the conference that could be understood by one and all – patient and family.
To an audience of nods and smiles, she described FM and the guest who came to dinner and never left. Her personal frustration at her mother’s unexplained pain and fatigue was a challenge to overcome, especially as she watched her mom deal with skepticism and dismissive attitudes from the doctors she sought out for help.
The family joined together in their desire to understand this illness and the havoc it was introducing into the life of their formerly active, athletic mother – and of course their own. They searched for something the family could learn from together. They culled the Internet, talked with others and in the end realized they would make a film intended for patient and family. According to Akers “little did we know what that would entail!”
Akers noted our culture does not understand chronic, cyclical pain; but, our culture does understand and believe what we see in film. Because their creative effort chose this media they have been successful in giving us something the entire family can view together to build understanding and support. Ask anyone coping with FM and they will tell you that family validation is perhaps even more precious than self-validation.
Akers shared with the audience the lessons she has learned from FM: 1) Ignorance is NOT bliss; 2) knowledge is power, especially for family members; 3) patience is indeed a virtue, as witnessed by her own family that had bad or worse news re FM for more than 12 years, 4) we need each other, we must do more to help each other understand that our value is not based on our bodies or our productivity; 5) things are changing and it is for the better; 6) we all do better when we find ways of getting outside of ourselves and our pain; and, 7) FM patients are courageous, strong and heroic individuals. She reminded us, “Hope is the thing with feathers that perches in the soul and sings the tune without the words, and never stops at all.”
As an inspiration for us all, Akers shared pictures of her mom’s first 10k marathon since FM joined the family. This was the realization of her long-held goal of running in the Kona, HI marathon.
As a footnote to the film screening and the keynote address, OFFER sold out of the DVD “Living with Fibromyalgia.” You can purchase this item directly from Akers/Eyers by using the link here in e-news. Go to: http://www.livingwithfm.com/
"New Research and Biomarkers for FMS/CFS"
Kathleen Light, PhD, University of Utah
"New Hopeful Biomarkers in Chronic Fatigue/Fibromyalgia Syndromes'' is a report on the investigative work at the University of Utah of the husband/wife PhD team of Alan & Kathy Light along with colleagues Ron Hughen, B.S., Adrea White, PhD and Lucinda Bateman M.D.
Genes are likely to be involved in FMS and CFS in two ways: inherited genes may give you a constitutional vulnerability; then you may be exposed to a life event (such as an infection, trauma/accident, or major life stressor) that influences gene expression and the triggering onset or worsening of symptoms.
Sensory pathways involved in muscle pain and fatigue (even amount the healthy) are still not understood. Pain from working muscles that are not obviously damaged is something we all have experienced, but the pathways involved are only beginning to be documented. The same is true of muscle fatigue; and, like pain, this is a vital protective sensory experience, but even less is known about these pathways.
There is a paradox in FMS & CFS regarding exercise. Gradual increase in whole body exercise is one of the most effective treatments to slowly reduce symptoms and normalize function. Yet exercise, even at a moderate level causes worsening of pain and fatigue symptoms in these patients at 24 and 48 hours later (and sometimes much longer).
A standardized bicycle exercise protocol to at least 85% of predicted maximum heart rate was repeated twice 24 hours apart 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 age-predicted maximum heart rate (beats/min).
The controls in the study showed only 2-3% change in oxygen consumption from Test 1 to Test 2 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 24 hours after initial exercise test in CFS patients. This occurred at the same time period when CFS and FMS patients report increases in muscles pain and fatigue even at rest or during simple movements.
This raises the question: can changes seen after exercise be one way to get at biomarkers of CFS? Can Blood-based biomarkers be found that are associated with this exaggerated delayed onset muscle pain and fatigue in CFS & FMS patients? Why blood-based markers? Because these tests are traditional in medical practices and are considered objective, hard evidence. Such an approach avoids legal concerns about subjectively, malingering or biases from secondary gain (insurance or disability).
The same mild exercise task to achieve the same level of heart rate and blood pressure may have very different effects in patients with CFS & FMS vs. healthy, pain-free individuals.
RESULTS: Beginning at 30 minutes after exercise and continuing at 8, 24 and 48 hours after exercise, CFS patients with and w/o FMS increased one ion channel receptor (type P) to 4 times its pre-exercise level. Healthy subjects showed no increases at all. Based on Alan Light’s animal research, this type of receptor seems especially sensitive to fatigue.
RESULTS: Beginning at 30 minutes after exercise and continuing at 8, 24 and 48 hours after exercise, patients with FMS as well as CFS increased one ion channel receptor (type A) to 2 times its pre-exercise level. Again, healthy subjects showed no increases at all. This type of receptor seems sensitive to both muscle pain and fatigue.
RESULTS: Both CFS & FMS patients also showed increases in receptors that detect sympathetic nervous system activity (adrenergic receptors) that were 2-6 times their pre-exercise levels. Kathleen Light and Wm Maixner also found that very low dose propranolol led to reductions in clinical pain in FMS and TMD patients.
RESULTS: Those patients who were involved in exercising on a regular basis showed some reduction in their post exercise increases in these ion channel receptors and in their beta adrenergic receptors, although they were still higher than normal. This may be one way that exercise training helps reduce pain and fatigue symptoms.
RESULTS: Among CFS patients, those who were higher in fitness (which overlaps with being lower in fatigue and pain symptoms) had lower anti-inflammatory and pro-inflammatory cytokines, especially at the 8-hour post-exercise time point. There was an association between having more normal ion channel receptors and more normal cytokines
Light at the end of the tunnel. Alan and Kathy Light have hope that these post exercise blood-based measures can help us develop biomarkers for CFS and for FMS. They also offer clues as to possible targets for future interventions to reduce muscle pain and fatigue.
Caveat: We still need to know if these patterns of responses are specific to CFS/FMS but may occur in other disorders e.g. MS, post cancer fatigue.
Updates in Diagnosis and Treatment of FM"
N. Lee Smith, MD, Lifetree Pain Clinic
Dr. N. Lee Smith, MD, Director of Stress Medicine at Lifetree Pain Clinic presented Understanding FM and Related Disorders: New Possibilities.
FM is caused by a combination of primary injury and secondary effects. Neuropathic pain as a factor in FM is manifest as a dysfunction of the nervous system.
FM is diagnosed by chronic widespread pain affecting at least 11 of 18 specific tender points and overlapping hypersensitivity disorders. Studies that make a comparison of pain thresholds reveal that FM patients are hypersensitive to pain and are a prototype of central nervous system hypersensitization. When inhibition is lacking, the nervous system hypersensitizes. Factors that can contribute to having FMS are: genetics (8.5 times more likely); predisposition; neurotransmission/sleep abnormalities, triggering events such as painful trauma, infections, stress & disordered sensory processing.
Sleep abnormality is often a factor in FMS. Most patients should be screened for sleep apnea, as about 20% have it. Some meds are effective in improving deep sleep in some patients.
Pain levels can be graded from a nuisance at levels 1-3, distraction at 4-7, disabling at 8 to 9, with the worst pain being 10.
Drugs of choice are a variety of neural modulators: neural stabilizers, antidepressants, topical or injected anesthetics and other neural modulators, separately, or in combination.
Which medications to start with depends upon dominant patterns of problems. Using meds with complementary mechanisms in lower dose may be better than high doses of one mechanism. Some drugs have been studied and are negative for FMS relief. At present only two medications have received FDA approval for FMS treatment, Lyrica (Pregabalin) and Cymbalta (Duloxetine). Both raised patient functioning and lowered the perception of pain. Other meds are prescribed as off-label applications.
There is strong evidence that non-pharmacological treatments such as education, carefully paced exercise, and cognitive-behavioral therapy are helpful in treating FMS. There is some evidence that biofeedback, hypnosis, massage and hot baths may help some patients. Minimal evidence exists for ultrasound, electrotherapy, chiropractic, acupuncture and nutritional for FMS.
Ask yourself: Who Am I – the little I or THE BIG I? 1) Do I see myself as pain or illness? Do I need fixing? 2) Pain is a part of me, but it is not me; I am more. 3) I’m part of something much larger. I am free and I am connected. Pain is but a small part of the BIG I.
Early treatment is of key importance regardless of approach.
"Updates in Diagnosis and Treatment of CFS"
Lucinda Bateman, MD, Fatigue Consultation Clinic
Salt Lake City internist Lucinda Bateman, CFS & FMS specialist, offered an update in the diagnosis and treatment of CFS, opening with a brief review of three case definitions: the 1994 CDC definition, the CFS pediatric and the Canadian definition. She went on to summarize the difference between CFS and FMS saying it is largely based upon whether the major symptom is widespread pain and/or debilitating fatigue. Both syndromes are heterogeneous, with symptoms that are not mutually exclusive.
Some quick facts about CFS: PubMed lists more than 4,300 peer reviewed scientific publications about CFS, with 467 of them published since January 2007. For comparison she found 4,800 FM articles, with 667 of them coming since 1/07. It was thought CFS afflicts less than 1 million Americans. However, up-to-date CDC research, based upon the patient studies conducted in Wichita and random digit dial calls in the state of Georgia, tells us it is closer to 4 million. Direct costs (treatment) are estimated to be $2,000-$8,000 -- that’s $2-7 billion per year in US. When indirect costs (lost wages, productivity decline, etc,) are added, the cost is a staggering $18-24 billion per year.
Science has clarified what specialist providers have long suspected -- the illness is not a form of depression. CFS is typified by low-grade immune activation. MRI, PET and SPECT scans of the brain reveal abnormal white matter, abnormal brain metabolism, and something CFS patients know all too well, abnormal cognitive function (processing efficiency, memory and attention). Dr. Bateman explained the HPA (hypothalamics, pituitary, adrenal) axis and how the neuroendocrine system being blunted or dysregulated effects reaction to physical and psychological stress.
An international conference held in June 2008 presented research linking some CFS to viruses such as herpes, enteroviruses and other pathogens such as EBV, HHV-6, CMV, Lume, Ross Rives, Q fever and others. The search continues for objective markers that will lead to better diagnosis and effective treatments. There was also discussion of a ‘superantigen’ as a trigger to CFS. Data from treadmill testing, cytokine analysis, gene expression and other viral markers is still pending and will be announced at a later date. At present, treatment remains supportive, directed toward symptom management.
RNA from blood samples studied by one international researcher, London doctor Jonathan Kerr, found 88 genes differentiated ME/CFS study participants from normal controls. These expressions included both hematological and immunological disease and function, cancer, cell death, immune response and infections. His studies found seven genomic subtypes of CFS/ME: 1) cognitive, musculoskeletal, sleep, anxiety/depression; 2) musculoskeletal, pain, anxiety/depression; mild symptoms; 4) cognitive; 5) musculoskeletal, gastrointestinal; 6) post-exertional; and, 7) pain, infectious, musculoskeletal, sleep, neurological, gastrointestinal, neurocognitive, anxiety/depression.
There is a symptom treatment hierarchy, according to Dr. Bateman. It begins with activity management (pacing); followed by sleep; mood/cognition; pain; fatigue; physical conditioning; orthostatic intolerance and the micromanagement of all medical problems.
Acknowledgement was given to Peggy Allen, CNM, for her recently published work entitled “Chronic Fatigue Syndrome: Implications for Women and their Health Care Providers During Childbearing Years.” Her teenage daughter, Lauren, who has CFS, inspired her mother, a medical professional, to fill in this important gap in scientific literature.
The ultimate solution? More money for research. Examples demonstrate the challenge we face. Muscular Dystrophy, affecting about 200,000, collected $65 million in its 43rd telethon this year. Breast cancer research, afflicting about 2,400,000 in US, collects nearly $1 trillion each year from public and private funding. In contrast, CFS lags sadly behind. Funding mandated by congress through the NIH and CDC is considerably down from the 2005 high of approximately $12 million. A private fund drive launched by the CFIDS Association has raised $1 million dollars in 2008 for a variety of research. Pharmaceutical research has brought 2 FM- indicated drugs to the market this year, with more in the pipeline. By contrast, pharmaceutical efforts have produced experimental intravenous drug, Ampligen, which has yet to be approved by the FDA and Valcyte, an oral experimental drug under clinical trial at Stanford.
In closing, these helpful resources were offered: www.iacfsme.org; www.cdc.gov/cfs/, http://www.hhs.gov/advcomcfs/index.html to access the CFS Advisory Committee that reports directly to the Secretary of Health and Human Services in Wash DC, www.cfids.org, the premiere advocacy and information organization in the US and http://orwh.od.nih.gov/cfs.html to access the Trans-NIH (Nat’l Institute of Health) Working group on CFS, under the Office of Women’s Health.