FM Conference Highlights

Medical Highlights from the Fibromyalgia Conference 2002
By Kathy Longley BSc (HONS)

Dr Robert Bennett - Altered Pain Pathways in Fibromyalgia

Dr Robert Bennett is a highly acclaimed professor of medicine at the Oregon Health Sciences University in Portland, Oregon USA. He has been involved in fibromyalgia research since 1979 and has published countless original studies. In his first talk he proceeded to explain the concept of "central sensitisation". In fibromyalgia the pain pathways have become highly sensitised to pain, with pain messages being amplified at the level of the spinal cord. When a pain message reaches the spinal cord it has to be transmitted to an ascending nerve, which conducts the signal up to the brain. This is achieved by using special chemicals called neurotransmitters stored at the nerve terminal. The neurotransmitters are released into the gap between the two nerves and transmit the signal by opening channels in the membrane of the ascending nerve. The main neurotransmitters involved are called glutamate and substance P. Levels of substance P have been shown to be three times higher in the spinal cord fluid of fibromyalgia patients. Also, constant incoming pain signals cause large amounts of glutamate to be released activating specialised receptors called NMDA receptors, which normally remain silent during general pain transmission. Activation of these receptors together with the abnormal levels of substance P greatly enhances the intensity of the pain signal transmitted.

Another nerve descending from the brain down to the spinal cord acts to interrupt the transmission of the pain signal, either dampening it down or filtering it out completely before it reaches the brain. This descending nerve pathway uses the neurotransmitters serotonin, GABA, and the body's natural painkillers called endorphins. Due to a deficiency in these neurotransmitters the dampening down process is ineffective allowing more intense and increased numbers of pain signals to reach the brain. These alterations in the nerve pathways involved in the transmission of pain lead to a state of hypersensitisation where pain is felt at a much lower threshold referred to as "central sensitisation". Understanding these altered mechanisms in fibromyalgia has led to the use of specific drugs targeted at the pain transmission sites in the spinal cord.

(To read about the alterations of the pain pathways in fibromyalgia and the drugs used in more detail please refer to the articles entitled "Ouch don't touch me!" parts 1 and 2 to be found in the FaMily magazine, issues December 2001 and February 2002 respectively)

Dr Kim Lawson- A link between Fibromyalgia and Potassium Channels?

Dr Kim Lawson, a Senior Lecturer in Pharmacology at Sheffield Hallam University, presented the hypothesis of dysfunctional potassium (K+) channels being the root cause for the symptoms of fibromyalgia. K+ channels are involved in fundamental cell processes and maintain electrical stability across the cellular membrane. When a cell is activated, for example a nerve cell, specific ions enter into the cell and alter the electric charge across the cellular membrane, causing the cell to become excited and therefore active. K+ ions, stored within the cell, are responsible for calming the cell down again and restoring it to its resting state. They achieve this by moving out of the cell through the K+ channels in the cell membrane to readjust the electric charge to its resting potential. Malfunctions in K+ channels have been implicated in a range of diseases. The malfunctions are generally believed to be due to mutations in the genes encoding for the proteins that make up the channels in the cell membrane. If these proteins are not formed properly the K+ ions may not be able to move across the cellular membrane effectively, leaving the cell in an activated and excited state for a longer period of time. These mutations could be either inherited or acquired, possibly as a result of trauma.

There are many different types of K+ channels distributed throughout the tissues of the body. One type called Kv 1.1 is believed to be involved in neuropathic pain. Kv 1.1 has been shown to play an important role in pain pathways and the dampening down of pain signals and when this channel is dysfunctional symptoms of hyperalgesia and a lowered pain threshold are observed, both classic symptoms of fibromyalgia. Also, the common drugs used to treat fibromyalgia like Tricyclics, SSRI's and painkillers like Tramadol are all believed to work by altering the activity of K+ channels. It is possible that these drugs are successful in combating some of the symptoms of fibromyalgia due to K+ channels been at the root cause of the problem. If this proves to be the case then new drugs targeted to the specific K+ channels involved could prove to be highly effective in treating all aspects of fibromyalgia.

Dr Jon Russell - The Neurochemical Basis of Fibromyalgia

Dr Russell is an Associate Professor of medicine at the University of Texas Health Science Centre in San Antonio, USA. He is the author of over 85 original publications into the research of fibromyalgia and holds the position of Editor-in-Chief for the Journal of Musculoskeletal pain. Dr Russell spoke about the objective abnormalities that have been found in the pain pathways of fibromyalgia patients explaining that fibromyalgia is "no longer considered merely a psychological disorder, a diagnosis to be made by exclusion, or a condition devoid of objective laboratories findings."

He brought attention to three studies carried out to measure the levels of substance P in the cerebral spinal fluid (CSF) of fibromyalgia patients. Two of these studies found three times as much substance P in the CSF of 84% of fibromyalgia patients compared to controls, while the other found a twofold increase. This significant increase in substance P was found to be specific to the central nervous system rather than the peripheral nervous system indicating that the drugs used to treat fibromyalgia need to target the central nervous system. It was also found that substance P remains high and can even increase over time. Another chemical involved in pain pathways is called nerve growth factor (NGF) and has been found to be four-times higher in the CSF of fibromyalgia patients compared to controls. This significant rise in NGF appears to be a distinguishing feature of fibromyalgia and could be responsible for the increased levels of substance P. Decreased levels of serotonin and tryptophan have also been reported in fibromyalgia research. Dr Russell explained that tryptophan can enter into one of two different biochemical pathways, one leading to the production of serotonin and the other to a chemical called kynurenine. Kynurenine levels have been found to be higher than normal in fibromyalgia indicating that tryptophan is channelled into the kynurenine pathway rather than the serotonin pathway leading to the low levels of serotonin observed.

The combined forces of the abnormal levels of these chemicals in fibromyalgia can lead to widespread allodynia (a lowered pain threshold), with the result of touch being perceived as pain.

(Dr Russell's talk will be expanded on in an upcoming article in FaMily magazine.)

Dr Jacob Teitelbaum - Fatigued to Fantastic workshop

Dr Teitelbaum runs a specialised clinic for fibromyalgia and chronic fatigue syndrome patients in Annapolis, Maryland USA. He has devised his own treatment protocol, which he has used to successfully treat over 2000 patients. This protocol has been tested in a placebo-controlled study and shown to be effective.

Dr Teitelbaum believes that fibromyalgia is caused by mitochondrial dysfunction that can lead to the dysfunction of the hypothalamus, the main hormone-producing gland in the brain. He spoke passionately about his treatment protocol explaining the importance of tackling all the major issues of fibromyalgia at the same time in order to achieve significant results. These important areas are disordered sleep, hormonal deficiencies, nutritional deficiencies and opportunistic infections. Disordered sleep can be tackled using a variety of drugs, for example, Ambien, klonopin, melatonin, amitriptyline and a range of herbal remedies like valerian, passionflower and lemon balm. He pointed out that it is better to take low levels of several sleep medications rather than a high level of just one to insure that the medications are cleared from the bloodstream by morning to prevent a sleep hangover. He stressed that it is of vital importance for people with fibromyalgia to achieve eight-and-a-half hours of solid sleep. There are numerous scientific studies reporting abnormal levels of hormones in fibromyalgia, for example, low levels of thyroid hormone, growth hormone and cortisol. In his protocol Dr Teitelbaum treats all these hormonal abnormalities and is adamant that blood tests cannot be relied upon to determine if hormone levels are low. Blood tests can apparently be very inaccurate and he advises doctors to go by the clinical symptoms presented by the patient. Nutritional deficiencies in fibromyalgia are also numerous and Dr Teitelbaum has created his own Formula to include all the nutrients required at the correct dosage levels. This Foundation Formula can be purchased over the Internet and it is worth pointing out that all of Dr Teitelbaum's profits go either to charity or are channelled back into fibromyalgia research. Opportunistic infections can include yeast like Candida, bacteria or parasites that reside in the gut interfering with the absorption of nutrients and zapping energy. Candida can be treated by a sugar-free diet combined with anti-fungal drugs and good bacteria like acidophilus. Clearing these infections from the gut and the blood stream can apparently have dramatic effects. Dr Teitelbaum continually stressed that treating one of these areas could produce some good results, however, it is essential to treat all these areas at the same time to achieve highly significant effects.

A full account of Dr Teitelbaum's protocol can be found in his book "Fatigued to Fantastic", which is available from the Fibromyalgia Association UK. It is certainly worth a read.

(The significance of the relationship between Fibromyalgia and low thyroid hormone will be examined in an upcoming article in FaMily magazine)

Dr Robert Bennett-Growth Hormone Deficiency and Fibromyalgia

In his second talk Dr Bennett explained the important link between growth hormone deficiency and the fibromyalgia and reviewed various studies he has conducted in this area. Adults deficient in growth hormone have symptoms similar to fibromyalgia, for example, low energy, muscle weakness, impaired cognition, cold intolerance and a reduced exercise capacity. Growth hormone is released in a pulsatile fashion during deep sleep and stimulates the body to undergo biochemical and mechanical repair, for example, repairing all the microtraumas in the muscles that have built up during the day. Due to deep sleep being disrupted in fibromyalgia the pulsatile release of growth hormone is greatly reduced and the body's repair systems become less effective leading to increased muscular pain. Growth hormone release is also dependent on the levels of another hormone called somatostatin. Somatostatin is an inhibitory hormone released by the hypothalamus to depress growth hormone secretion. The levels of somatostatin are believed to be elevated in fibromyalgia due to the over activity of the stress hormone CRH.

Dr Bennett has carried out studies to investigate the effects of increasing growth hormone in fibromyalgia patients. In one double blind, placebo-controlled study 25 fibromyalgia patients received growth hormone injections while another 25 patients were injected with a placebo. The 25 patients injecting growth hormone showed a prompt increase in IGF-1 levels within the first month and these levels were sustained throughout the nine-month trial. No increase in IGF-1 levels was observed in the placebo group. (IGF-1 levels in the blood reflect the amount of growth hormone secreted.) Those receiving growth hormone showed significant improvement in their symptoms compared to the placebo group. Unfortunately growth hormone is very expensive to administer and those patients who were unable to afford to continue the treatment after the study had ended suffered a relapse in their symptoms. In another study Dr Bennett investigated an alternative way of increasing growth hormone by administering a drug called pyridostigmine that works to inhibit somatostatin and these results were also very promising. Dr Bennett's work provides new ways forward to produce other successful drugs for treating fibromyalgia.

(Dr Bennett's talk will be expanded on in an upcoming article in FaMily magazine.)

These highlights are simply a sample of the inspiring and informative talks given at the conference. There were many others I don't have room to write about. I am sure you would all like to join with me in thanking all the speakers who gave up their valuable time to come and talk to us and of course to Pam and Bob Stewart for all their hard work in organising the conference.

Copyright © K.E Longley 2002
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