Fibromyalgia Syndrome (Small Fibre Neuropathy- SFN)
Fibromyalgia syndrome (FMS) is a common yet generally poorly understood syndrome characterized by diffuse chronic pain accompanied by other symptoms such as fatigue, poor sleep and stiffness, often in the absence of any obvious disease or pathology. The essential features of FMS include widespread pain, fatigue, muscle stiffness, sleep disturbance and emotional distress. These symptoms are unpredictable in their severity and timing. The pain of FMS often has a burning, aching quality, and varies in severity and position. Muscles often ache after mild exercise. Multiple tender areas are essential for the diagnosis. The pain is not fixed, and it varies with a wide range of factors such as activity, age, drugs, hormonal action, diet, illness, season, stress and even weather change.
Recent research has made some significant progress. Dr Pete Smith, an immunologist on the Gold Coast has established FMS to be part of the complexity of threat receptor hypersensitivity (see later on TLRs), and he is working in an area called ion channellopathy. Other US researchers have found a very high incidence of non-myelinated small nerve fibre neuropathy (where there is significant damage to the small nerve endings especially in the skin) which explains the characteristic sensitivity to touch, and probably also explains the hypersensitivity in the vagus nerve which innervates the gut and heart producing symptoms of autonomic dysfunction (dysautonomia). Genetic researchers have firmly established a much higher than normal association with the MTHFR gene mutations, which appears to be clinically the case as well. This association is restricted by the inability at present to map all the MTHFR mutations (only 2 currently being tested in normal laboratories).
The skin biopsy results with the neuropathy are very similar to that found in many other conditions, notably diabetic (and pre-diabetic) neuropathy, Sjogrens Syndrome, Lupus connective tissue disease, Sarcoidosis, Vitamin B12 deficiency, Coeliac disease, HIV, Amyloidosis, Paraproteinaemia, Alcohol abuse and Chemotherapy. This has led researchers to look at FMS in a different light. In the past, and unfortunately even now in many areas, FMS has been considered a psychiatric problem. In FMS/SFN there is a heightened sensitivity in the threat receptors, producing anxiety-like symptoms, and stress aggravates these. It has been traditional to use TCAs (tricyclic antidepressants) but these drugs produce side effects, but may assist many people as they simply are sedating and also turn off 2 of the TLRs.
There is now increasing evidence that nerve compression can promote local as well as remote immune –mediated inflammation, resulting in activation of pain pathways nowhere near the area of compression. Patients with neuropathic pain from entrapment syndromes often present with symptoms outside the innervation area. (2) Slowly progressive mild nerve compression can produce preferential degeneration of small nerve fibres, whereas myelinated axons remain largely intact. As a consequence, changes are not seen on standard Nerve Conduction Studies. (3)
Many patients with FMS start with one or more trigger points described as myofascial points then progressively more are affected often at a time some distance from the original activating factor. While it may be increasing inflammatory responses associated with these compression syndromes, the release of a research in 2017 identifying the presence of previously undiscovered networks of interconnected fluid-filled compartments below the skin’s surface, lining the digestive tract, lungs and urinary systems, and surrounding arteries, veins and fascia between muscles may provide the missing part of this puzzle.
“Mast cells play a key role in homeostatic mechanisms and surveillance, recognizing and responding to different pathogens, and tissue injury. An abundance of mast cells reside in connective tissue that borders with the external world (the skin as well as gastrointestinal, respiratory, and urogenital tracts.) Situated near nerve fibres, lymphatics, and blood vessels, as well as coupled with their ability to secrete potent mediators, mast cells can modulate the function of local and distant structures (eg other immune cell populations, fibroblasts, angiogenesis), and mast cell dysregulation has been implicated in immediate and delayed hypersensitivity syndromes, neuropathies, and connective tissue disorders.” (1)
Many people with FMS can describe a cascade of inflammatory processes, and when these are “time-lined” it appears that Mast Cell Activation has occurred, which not only appears to explain the cascade, but also provides an insight into the neuropathy and improving outcomes for the patients.
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