Research is the key to finding both the etiology and potential cure to Fibromyalgia Syndrome. This page outlines some of the promising research being conducted.

• Neurohormones and brain chemicals
• Altered pain amplification
• Neuroendocrine (HPA- axis ~ hypothalamus/pituitary/adrenal)
• Low levels of growth factor (IGF-1) a marker for low levels of growth hormone (GH) secretion
• EMG (electromyogram)-guided trigger point injections
• EEG (electroencephalogram) tracing that is characteristic for fibromyalgia
• Spinal cord compression (cervical stenosis and chiari malformations)

Neurohormones and brain chemicals
We know that fibromyalgia syndrome involves a loss of pain regulation in the central nervous system (CNS) which in turn causes pain amplification. Excessive pain stimulation then appears to lead to abnormal levels of CNS neurotransmitters like serotonin, norepinephrine and Substance P that enable nerves to transmit signals in the brain. These neurotransmitter imbalances in turn create problems with the body's hormonal response to stress (i.e., inappropriate levels of cortisol, catecholamines, growth hormone and possibly thyroid hormones) which cause abnormalities in the autonomic nervous system, the system which regulates involuntary functions such as blood pressure and bowel function. Such abnormalities seem to contribute to irritable bowel syndrome, neurally mediated hypotension (low blood pressure), irritable bladder syndrome, vascular headaches, chronic fatigue, and non-restorative sleep disorders

Some of the leading FMS researchers in this country, such as I. Jon Russell, M.D., are working on identifying the biochemical abnormalities and determining how they effect fibromyalgia syndrome.

Altered pain amplification
Dr. Karl Henriksson's model for understanding fibromyalgia is based on pain and its effects. "Fibromyalgia is a combination of a chronic pain condition and a chronic stress syndrome and the two syndromes together may be considered a pain disease."

There is a wide variety of evidence that pain sensing mechanisms are altered in FMS patients.

• "There is a general agreement that the main cause of allodynia [pain sensitization ~ when stimuli which would not normally cause pain are painful] is a disturbance in the pain modulation in the central nervous system, especially at the spinal cord level"
• "activation of NMDA receptors [activated when there is a persistent or repetitive pain] leading to central sensitization and allodynia is an important factor "
• "aberrations in seratonin metabolism could contribute to deficient pain inhibition"
• "increased levels of Substance P in the cerebro-spinal fluid [common in FMS patients] could be a consequence of persistent stimulation of nociceptors [pain receptors located in the connective tissue in muscles]"

Dr. Karl Henriksson explained the connection between pain and stress syndrome which he believes creates many of the other symptoms and laboratory abnormalities in FMS, "An amplified and more or less continuous pain signal constitutes a continuous stress factor. Adaptation to this stress can lead either to an increased stress response or deficient adaptive response from the stress regulating systems [such as neuroendocrine system and autonomic nervous systems]."

Neuroendocrine (HPA- axis ~ hypothalamus/pituitary/adrenal)
Leslie Crofford, M.D., has described pituitary-adrenal hormonal abnormalities in response to stress. In her research, she will correlate cognitive function of FM patients with measures of neuroendocrine function. A basic thesis advanced is that FM patients may have both cognitive and neuroendocrine function similar to that of control subjects who are 20 to 30 years older. Indeed, cognitive testing in patients with CFS reveals changes similar to those seen in subjects of advanced chronological age. In two experiments, FM patients will be compared to age and education matched controls, as well as to education matched older adults. Neuroendocrine function will be measured as well, as will depression, pain, fatigue, and beliefs about memory function.

This approach allows a determination as to whether there are differences in cognitive function of fibromyalgia patients from others, and whether cognitive aging is a good model for understanding the cognitive effects of FM. In addition, and perhaps more importantly, the integration of a cognitive approach with a neuroendocrine approach will allow us to determine what mechanisms account for the cognitive differences - neurochemical, psychiatric, or experienced pain and fatigue. Knowing the mechanisms underlying observed cognitive deficits has important implications for treatment of the disorder as well as for understanding its etiology.

Low levels of growth factor(IGF-1) and growth hormone (GH) secretion
Low levels of insulin-like growth factor 1 (IGF-1), a surrogate marker for low growth hormone (GH) secretion, occur in about one third of [Fibromyalgia] patients who have many clinical features of growth hormone deficiency, such as diminished energy, dysphoria, impaired cognition, poor general health, reduced exercise capacity, muscle weakness, and cold intolerance. To determine whether suboptimal growth hormone production could be relevant to the symptomatology of fibromyalgia, the clinical effects of treatment with growth hormone were assessed.

EMG (electromyogram)-guided trigger point injections
David Hubbard, M.D., has described the use of EMG (electromyogram)-guided trigger point injections as a technique to improve the effectiveness of standard trigger point injections. He has also documented the experimental use of the medication phenoxybenzamine in injections which has successfully eradicated trigger points for up to two years, a tremendous improvement over current medicines that only work for about a week. Infrared laser therapy may also prove effective and safe in treating tender points.

EEG (electroencephalogram) tracing that is characteristic for fibromyalgia
Stuart Donaldson, Ph.D., has described a brain wave pattern on EEG (electroencephalogram) tracing that is characteristic for fibromyalgia. His recent study in the Canadian Journal of Clinical Medicine (June 1998) shows that the patients with cognitive dysfunction (i.e., problems remembering things involving more than one step) or "fibro-fog" improved with his photostimulation neurotherapy; in addition, their brain wave EEG tracings returned to normal. If other researchers are able to duplicate Donaldson's findings, this will represent a real breakthrough in FMS. We will then have another objective test specifically for fibromyalgia syndrome.

Spinal cord compression (cervical stenosis and chiari malformations)
Dr. Michael Rosner, a neurosurgeon, has been studying the effects of spinal cord compression and fibromyalgia. Dr. Rosner's findings prompted the NFRA to fund a pilot spinal cord compression surveillance study. Fibromyalgia researchers, Dr. Robert Bennett of Oregon Health Sciences University, Dr. I. Jon Russell of the University of Texas Health Sciences at San Antonio, and Dr. Dan Clauw of Georgetown University, will be conducting the research. The study, consulted and coordinated by Dr. Rosner, consists of newly diagnosed FM patients undergoing a neurological examination and MRI to ascertain whether spinal cord compression is present. The purpose of this investigation is to determine the percentage of patients diagnosed with fibromyalgia who have this medical condition.

FMS Research Abstracts

	What is Fibromyalgia Syndrome and what are the symptoms?		What research is being conducted on Fibromyalgia Syndrome?
	How will my doctor diagnose Fibromyalgia Syndrome?		Vitamins & supplements for Fibromyalgia Syndrome?
	How common is Fibromyalgia Syndrome?		Fibromyalgia Syndrome disability issues.
	Is Fibromyalgia contagious?		Tips on living with Fibromyalgia Syndrome.
	What treatments are available for Fibromyalgia Syndrome?		Return to FMS Information Resource Guide Index.