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Portland Conference Highlights Fibromyalgia and CFIDS Research Advances

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By Author: Kyle Roderick • www.ProHealth.com • December 1, 1998


Sponsored by the non-profit National Fibromyalgia Research Association, (NFRA), the "New Dimensions in Fibromyalgia Syndrome" research symposium convened in Portland, Oregon, September 14 and 15.

Fibromyalgia is a medical condition characterized by chronic pain in muscles and surrounding structures, which are also unusually tender to pressure. Physicians refer to fibromyalgia syndrome (FMS) as a chronic, painful musculoskeletal disorder of unknown etiology. FMS affects about five million people in the United States and about 1.5 percent of the general population in almost every country where it has been documented. Because fibromyalgia symptoms often overlap with those of chronic fatigue immune dysfunction syndrome, also known as CFIDS or CFS, some of the presenters also discussed research findings on CFIDS patients.

According to Jacob Teitelbaum, M.D., one of the speakers at the conference, "CFIDS is a group of symptoms associated with severe chronic fatigue. The most predominant symptom or condition is that the person's fatigue has caused a persistent and substantial reduction in their activity level. Poor sleep, recurrent infections, achiness, "brain fog," increased thirst, bowel disorders, and exhaustion after minimal exertion are some of the more common symptoms."

Judging by the diverse scientific and clinical evidence presented, this conference's central fact is that significant advancements are occurring in the search for underlying causes of fibromyalgia and in understanding the disorder; its diagnosis, and approaches to treatment. Comprising a forum of twenty-two rheumatologists, fibromyalgia researchers and other physicians and scientists, the meeting was co-chaired by rheumatologists I. Jon Russell, M.D., Ph.D., and Robert Bennett, M.D., Ph.D.

The meeting also drew a representative from the National Institutes of Health (NIH). Stanley Pillemer, M.D., a rheumatologist and medical officer at the Office of the Director, National Institute of Arthritis and Musculoskeletal and Skin Diseases at the NIH, gave two presentations. One of these outlined suggestions for FMS researchers on how to design controlled FMS research studies. (Two researchers who have received FMS research grants from the National Institutes of Health, Laurence Bradley, Ph.D., and Gail Adler, M.D.; Ph.D., also addressed the conference.) Adler, an endocrinologist, discussed how many FMS symptoms resemble those of patients suffering from hormone deficiencies. While it is unknown why multiple hormone abnormalities are observed in FMS patients, she believes that understanding these may help define FMS.

"As we better understand the hormone abnormalities present in fibromyalgia, we should be able to develop tests that can detect the abnormalities that occur frequently, early in the course of the disorder," Adler said. Thus, further study of neuroendocrine dysfunction in FMS may aid in defining the etiology of the illness and help clarify the mechanisms perpetuating it. What's more, research may eventually lead to a neuroendocrine test for FMS.

In his research into FMS patients, Dr. Bradley has also studied non-patients, in order to learn more about the pain perception and psychological factors associated with health care-seeking for FMS. Thus far, he has identified 4 variables related to pain perception that distinguish both patients and non-patients with FMS from healthy controls. These are (a) low pain threshold levels at tender points and control points; (b) high scores on an index of sensory discrimination ability; (c) high cerebrospinal fluid (CSF) levels of substance P; and (d) low regional cerebral blood flow in the caudate nucleus.

While Bradley says his research into non-patients has led to advances in understanding abnormal pain perception in FMS, "it must be noted that these non-patients may not be representative of the entire population of community residents who do not seek care for FMS. In addition, we know little about persons with FMS who cope well with FMS with only primary medical care for their symptoms. Thus, there is a need for additional epidemiologic studies of patients and non-patients with FMS. And these studies should distinguish between FMS and chronic or recurrent pain associated with other disorders or comorbidities."

Dr. Russell's talk, "Investigative Pathways of Diagnosis," discussed how two neurochemical models may be related to central nervous system-mediated pain in FMS. These models are serotonin [5HT] deficiency and excesses of substance P [SP]. (Regarding serotonin, it is one of the brain's main "feel-good" neurotransmitters. Serotonin is vitally important to the overall function of the brain, as it helps promote sleep and control pain. Excessive serotonin causes somnolence and depression. The neurotransmitter SP is emitted into the spinal cord area when nerve fibers in skin, muscle and bone are injured. SP travels in all directions and facilitates the transmission of pain messages to the brain by a sequence of chemical reactions known as nociception.)

According to Russell, "New findings in these interdependent models support their validity in FMS." In his research trial involving FMS patients and controls, cerebrospinal fluid (CSF) and peripheral platelets [PLT] were collected. He found that "FMS subgroups exhibited abnormalities in both central and peripheral 5HT which correlate with FMS symptoms and suggest a clinically relevant, widespread defect in 5HT production and/or availability in FMS. FMS subgroups exhibit central abnormalities in SP levels which could be due to low 5HT and appear to change in concert with painful FMS symptoms. Therefore, subgroups of clinically similar FMS may be distinguished biologically by physiologically relevant laboratory abnormalities."

Russell's findings help the medical and patient community in that there are now two substances to test for which may lead to FMS diagnosis. Perhaps science may be nearing identification of a marker for fibromyalgia.

Lars Tanum, M.D., the symposium's sole European presenter, is a trained psychiatrist with experience in clinical medicine; he works as a clinician and researcher in the department of Psychosomatic and Behavioral Medicine at the National University Hospital in Oslo, Norway. While he doubts that FMS is caused by a psychiatric illness, Tanum has conducted two trials which show that "a portion of adult females with primary fibromyalgia and no psychiatric history do share some common features and suffer from a psychobiological dysfunction similar to what is reported among patients with panic disorder."

Tanum reported that the anti-depressant SSRI drug Paroxetine is effective in helping control distress and anxiety in FMS patients. He notes, however, that compared to other patient groups, FMS patients need more time to respond to drug treatment, and should give Paroxetine a few months to start taking effect. This slow response of FMS patients to drug treatment may partly explain the various negative drug trials involving them in the medical literature.

While Tanum's talk concerned some of the psychological aspects of FMS, Jacob Teitelbaum, M.D. an internist based in Annapolis, MD. discussed various research findings and his own clinical experiences with over 1000 fibromyalgia and CFIDS patients which show that fibromyalgia is a disease for which effective treatment exists.

Teitelbaum proposes that hypothalamic, immune and neurotransmitter dysfunction, and in addition, possibly mitochondrial dysfunction, combined with inadequate nutrition, cause the chronic illness of FMS.

While he concedes that understanding of FMS is still in the nascent stage, Teitelbaum is the senior author of the study, "Effective Treatment of Severe Chronic Fatigue States," which showed that over 85% of fibromyalgia patients improve, often remarkably, with an integrated treatment protocol. Teitelbaum is presently the senior researcher in a larger, randomized, placebo-controlled trial of this protocol, which will be completed in the spring of 1988.

Michael J. Rosner, M.D., a neurologist and professor of Neurological Surgery at the University of Alabama at Birmingham, discussed some intriguing findings relating to patients previously diagnosed with CFIDS or FMS. After observing two patients with cervical stenosis [an abnormally narrow spinal canal] whose "chronic fatigue syndrome" improved after surgery, Dr. Rosner evaluated 48 patients with CFIDS and fibromyalgia syndrome.

"We tested the hypotheses that the spinal canal would be stenotic in patients with chronic fatigue and fibromyalgia syndromes, and that decompression of craniovertebral stenosis would lead to improvement in symptomatology and objective neurologic findings."

Dr. Rosner found that there is a subset of patients with the diagnosis of CFIDS or FMS who suffer from some element of craniovertebral compression. This is primarily congenital and appears relatively normal unless more highly quantified analysis of the spinal canal is performed. Detailed neurological history and physical findings in this group of patients are consistent with a chronic myelopathy. The majority of the signs and symptoms can be reversed in these patients with the surgical procedure, craniocervical decompression.

While some of Dr. Rosner's patients had congenital cervical stenosis, others exhibited overly narrow cerebellar tonsils, and some had abnormalities of cerebro-spinal fluid outflow from the posterior fossa. For patients with simple anterior spinal cord compression, they underwent anterior cervical decompression and fusion. These conditions were corrected with the appropriate surgical procedures.

By 24+2.7 weeks after surgery, 80% of Dr. Rosner's patients felt improved in most of a list of 18 symptoms. Fifteen to 20% felt that they were unchanged with fewer than 10% feeling that they had worsened in some symptoms. By 78 + 26 weeks after surgery, patients answered a more detailed questionnaire. 10 to 15% reported they were worse in some types of symptomatology; 10 to 20% felt they were unchanged in some of their symptoms, with the remainder reporting some degree of improvement. More than half felt 50% or more improved after surgery. Nearly all patients felt some symptoms improved.

Dr. Rosner's study does not answer the question of how many patients diagnosed with CFIDS or FMS may actually sufer from craniovertebral radiological compression. The study raises the important point, however, that cervical stenosis may, in some cases, be one of the underlying causes of CFIDS or FMS.

According to NFRA activist and conference organizer Rae Marie Gleason, "Dr. Rosner's findings were very intriguing and worthy of more research because very few physician/researchers are exploring these kind of neurological connections to FMS and CFIDS. Findings presented by Dr. Rosner and his colleagues at this conference help enhance the discovery process and will encourage more funding into FMS."



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