Clinics in London, Oxford and Bristol
At our Clinics in London, Oxford and Bristol, we treat patients who have Fibromyalgia (FM) and ME (also know as Chronic Fatigue Syndrome or CFS). These syndromes can be characterised by a set of symptoms that overlap by around 70% and Dr Muhammad Yunus believes that Myofascial Pain Syndrome is present in roughly 50% of FM and CFS diagnosed patients. Many of the therapies or approaches that are used to treat FM are also used to treat ME /CFS, and vice versa. Many doctors would consider that the link between all of these conditions is that they all show Central Sensitization (CS) - a hypersensitive Central Nervous System that produces enhanced sensitivity throughout the body.
Both FM and CFS/ME present the following characteristics, all-over body pain, post-exertional fatigue/malaise, problems with temperature control or cold intolerance, disrupted sleep, sensitivity to many stimuli including bright lights and noise, irritable bowel and bladder symptoms, headaches, brainfog, alcohol and medicine intolerance, dizziness, Neurally Mediated Hypotension, reduced cerebral blood flow in cortex and midbrain, reduced serum and/or CSF serotonin, often there is a family hereditary, low blood levels of magnesium, low brain levels of B12, and abnormal neuroimaging (i.e. MRI and Spect Scans).
Dr. Debra Buchwald (who conducted a large USA research project to evaluate the symptoms commonly reported by each condition and determine the degree to which they may or may not be related) writes that “what she found was that CFS and FM are characterised by greater similarities than differences. The distinction between CFS/FM to be sub-classified according to severity of various symptoms. For patients and their physicians, there is substantial value in the findings in both the CFS and FM literature opening up research channels of communication between both camps will benefit patients with either diagnosis”.1
Researchers in Germany found that subtle alterations of a hormonal stress response system called the HPA (hypothalamic pituitary adrenal) axis, may play a role in CFS.2 Dr. R. Bennett writes in his website “the effects of HPA axis dysregulation secretion are postulated to be relevant to Growth Hormone Deficiency in FM (low levels are a known cause of many FM problems). Neeck has hypothesized that stress is the common denominator linking the HPA axis and reduced Growth Hormone secretion in Fibromyalgia. Understanding links with chronic stress may provide some insights into mechanisms whereby environmental stressors and developmental factors interact with inherited susceptibility to modify gene expression and ultimately generate symptoms”.
Other studies show that “stress and anxiety have been shown to have adverse effects on FM in the long run. Initially, under stressful or anxiety-driven conditions, the body automatically pours out its own opiods. CFS (and possibly FM) patients have a limited supply of opiod-like substance, implying that stress and anxiety might leave the body depleted of these pain-fighting chemicals. In addition, the pain itself could cause enough stress and anxiety to make this a viscous cycle, keeping your system depleted of its self-made opiods”.3 An Italian study has shown that levels of Endorphins are substantially lower in CFS patients than controls, indicating that this could also be true for FM.
Dr. Andrew Wright, Medical Advisor to AFME, writes in 1998 that “In a recent PhD thesis, Lucinda Scott from the Department of Psychological Medicine at St. Bartholomew’s Hospital, has looked at the hypothalamic pituitary adrenal axis in CFS (ME) and comes to some conclusions supporting the fact that in people with this illness there is a failure of the normal response to biological stress and that people are unable to cope at a biological level with the said stresses”. “Stress and anxiety is an important modulator of dopaminergic neurotransmission”4 and low dopamine and the neurotransmitter GABA levels have been found in FM and hypothetically in CFS. These low or disrupted levels of dopamine and GABA appear to be part of what is causing the disfunctioning of the Sympathetic Nervous System and NMDA receptors. This is important because “The NMDA receptors in the spinal cord are know to be out of control in FM, magnifying noxious inputs at this level of the Central Nervous System”. However, “Studies have shown that stress does not cause FM and don’t let any person insinuate that your fatigue (or pain) are just symptoms of stress”. Additionally, “The Autonomic Nervous System in FM, and likely in CFS patients, can be characterised by a dominant sympathetically controlled system that is so maxed-out and overworked, that it is sluggish in its response to environmental stimuli and Central Nervous System demands.” Dr Manuel Martinez-Lavin, a key researcher in this field hypothesizes “that many people are prone to develop FM (i.e. genetic predisposition). They have a baseline hyperactive Sympathetic Nervous System, and after a triggering event (e.g., trauma, infection, etc), a central pain sensitization state develops.” Natelson goes on to add that he believes that for some people “their FM may be a form of CFS and vice versa.” 5 It would seem likely that both the disfunctioning of the HPA axis, the Autonomic Nervous System (i.e. the Sympathetic Nervous System) and the Central Nervous System are the cause of these conditions.
The first main difference between FM and ME/CFS are the levels of substance P, which intensify the pain signals sent to the brain. Substance P has been shown in two studies to be three times higher than normal in patients with FM. Dr. John Russell has also found that NGF or nerve growth factor is four times higher in patients with FM, and in adults NGF appears to play a role in the transmission of pain. This would explain why some patients experience fatigue and not pain.6 RNaseL, a cellular antiviral enzyme is frequently elevated in CFS (but not FM). Patients with Parvovirus B19 Associated Chronic Fatigue Syndrome have been shown to respond to Immunoglobulin Therapy.7 Most ME/CFS patients report a flu-like illness or infection as the cause of their illness, while most FMS patients will normally recall a trauma that triggered their illness.
Various diagnostic methods including Brain Imaging by Dr’s Wood, Russell, Olafsson, etc have shown changes in brain chemicals, resulting in central sensitization, or fibromyalgia. Only recently have doctors started to investigate the chemical Dopamine and it’s impact on chronic pain. Dr Wood has shown using Brain Imaging that dopamine has been suppressed by long term chronic stress and this results from corticotrophin releasing hormone being released and changes in the sympathetic nervous system. This is important because dopamine suppress pain and many of the other symptoms of fibromyalgia. This research is supported by Dr Andrew Holman’s clinical practice and research on FMS patients demonstrating that dopamine agonists can reduce, often significantly, many of the symptoms of FMS including pain and sleep problems. Dr Holman and other doctors have shown that dopamine agonists can reduce the symptoms of FMS better than any other medicine that has been trialled on FMS.
Prof. Davies clinical experience has been that dopamine agonists, added to other treatments that have been shown to reduce FMS and/ or Myofascial Pain Syndrome, such as trigger point injections or myers cocktails (discussed later in this article) can further reduce the symptoms of FMS and these treatments form the basis of our treatment at both our Private and Guys NHS practices. The excellent DVD “Fibromyalgia show me where it hurts” from www.LifeBeyondPain.com discusses the above in much greater detail.
Professor Davies has developed a variety of treatments to help patients with these disabling conditions, based upon the latest medical research from around the Medical world and years of clinical experience.
There have been many articles and reports on the value of graded exercise programs in ME/CFS and Fibromyalgia. However, Professor Davies is firmly of the opinion that Pacing oneself, including prolonged periods of REST for both the body and mind are essential. This opinion has recently been confirmed by a scientific study8 and in a review of previous studies that question the generally-held view that aerobic exercise programmes are a major useful treatment for ME/CFS and FM. It is Professor Davies experience that patients generally do best if they rest completely in the early stages of these conditions, then as their health and muscles improve with treatment they can first increase their activities and later on if appropriate introduce exercise. The key is to establish a good sleep routine and to avoid a ‘boom and bust’ cycle.
Pain relief is an area of much development recently and Professor Davies is using new medicines that have been shown to significantly reduce pain and also improve the sleep of these conditions (it is important to use medicines that will not disrupt deep or stage four sleep further). Upper Airway Resistance Syndrome (or UARS) is something that has recently become a major area of research for FM/CFS/ME and is a condition that affects the majority of patients with these illnesses. UARS has been shown to disrupt sleep and can also impact the hypothalamic-pituitary-adrenal axis, neural and immune system, and can initiate a variety of symptoms along with severe fatigue, pain and immune dysfunction as seen in patients with CFS/ME/FM.9 Fortunately , there are several treatments that can significantly improve UARS.10
Trigger point injections have been used since the late 1940’s in France and the 1950’s in America for a variety of soft tissue musculo-skeletal problems. Anecdotal literature abounds with success stories of patients who have suffered for considerable lengths of time with musculo-skeletal pains which have not responded to conservative therapies but did respond to trigger point injections. In a study published in the Journal of Orthopaedic Medicine 2001, treatment by intradermal sodium salicylate (aspirin) or trigger point injections were given to patients with Fibromyalgia. 9 of the 11 patients reported worthwhile symptomatic improvement after treatment. These injections help release the tension in the tightened and shortened muscles of FM/ME and should reduce the pain in these muscle areas.
Botox has been used for pain relief for several years for chronic muscle pain conditions such as Myofascial Pain Syndrome, which can often be the cause of much of the pain in FM/ME/CFS. The pain reducing effect of Botox can be more potent on a trigger point than the trigger point injections. Our medicine-sensitive patients will be pleased to hear that there are few, if any, side-effects from either injections. Many people can now get effective pain relief from either trigger point or Botox injections. Professor Davies has over 20 years experience injecting these painful areas and comments that most patients find these injections useful for their pain.
This treatment, often referred to as a Myers or IVMT, is used to provide significant relief of pain and fatigue for many patients. It is a simple Outpatient intravenous infusion of lignocaine and magnesium to reduce the NMDA receptor11 and the Sympathetic Nervous System disfunctioning (and these problems are what many doctors believe are one of the main causes of Fibromyalgia) plus B vitamins. There are several studiescited in Dr Teitelbaum’s book Pain Free 1-2-3! which show that the majority of patients Fibromyalgia improved significantly with various doses of intravenous infusions of lignocaine or magnesium. In the USA Dr David Katz is conducting a clinical trial sponsored by the National Institutes of Heath on Myers and their effect on FM, in the May 2005 issue of ImmuneSupport Dr Katz states that “he has treated more than 60 patients so far, about 80% of them have had good results”. Low magnesium12and B vitamins levels are also considered by many doctors to be a cause of fatigue and Myers Infusions can also increase these levels thereby improving fatigue for many patients. One study found preliminary evidence of reduced functional B vitamin levels, particularly pyridoxine (B-6), in CFIDS patients.13
Even people who aren’t B-12 deficient have more energy after vitamin B-12 shots, so many physicians urge fatigued patients to try B-12. In one preliminary trial, 2,500–5,000 mcg. of vitamin B-12 given by injection every two to three days led to improvement in 50–80 percent of a group of PWCs; most improvement appeared after several weeks.14 Oral magnesium or B-12 supplements are unlikely to provide the same results as they do when injected because the body cannot absorb large amounts orally.
By: Daniel Austen, Clinic Manager. Medically reviewed by Professor John E. Davies.
1) Dr Charles Lapp, et al. Fibromyalgia Network. April 2003 CFS Conference, the merging of two syndromes pp4-10.
2) Psychosomatic Medicine. 2002.
3) Fibromyalgia Network. Jan. 2003. Neuro-Hormonal differences pp2-3.
4) Malt EA, Olafsaon S, Aakvaag A, Lund A, Ursin H. Altered dopamine D (2) receptor function in fibromyalgia patients: a neuroendorcine study with buspirone in women with fibromyalgia compared to female population based controls. J Affect Discord. 2003 Jun; 75 (1): pp77-82.
5) Fibromyalgia Network, July 2004 pp1-5.
6) K Longley. Family Magazine. 2002. Pain signals out of control pp7-8.
7) Dr J R Kerr. Clinical Infectious Diseases. May 2003 Successful Intravenous Immunoglobin Therapy in 3 Cases of Parvovirus B10-Associated Chronic Fatigue Syndrome. pp100-106.
8) C Ramsey, J Moreland et al, ‘An observer-blinded comparision of supervised and unsupervised aerobic exercise regimes in Fibromyalgia’ J of Rheumatology Vol 39 No 5 (2000).
9) Timothy J Craig, D.O., S. Kakumanu. American Family Physician. Volume 65, Number 6/ March 15, 2002. pp1088. Further references pp 1090, Number’s 31, 32, 33, 34 & 35.
10) Fibromyalgia Network. Edition 67 pp12-14 and edition 68 pp9-15.
11) M R Tramer, C J Glynn, Magnesium bier’s block for treatment of chronic limb pain: a randomised, double-blind, cross-over study. PAIN, Vol. 99 (1-2) (2002) pp 235-241.
12) Jessop C. Clinical features and possible etiology of CFIDS. CFIDS Chronicle 1991;Spring:70-73.
13) Heap LC, Peters TJ, Wessely S. Vitamin B status in patients with chronic fatigue syndrome. J R Soc Med 1999;92(4):183-5.
14) Lapp CW, Cheney PR. The rationale for using high-dose cobalamin (vitamin B-12). CFIDS Chronicle Physicians’ Forum 1993; Fall:19-20.