Small fiber neuropathy

Hi all,

I've been diagnosed with Fibromyalgia for some time now but was in a lot of pain (and still am) with my back, I've been through every X-ray, MRI, etc etc to try to sort it out to no avail and I was getting quite upset as I was not getting any answers. Finally after more tests yesterday I got an answer. I have now been diagnosed with Small Fibre neuropathy which is a condition of the nerves just under the skin. This has now opened up more questions as to how to treat it etc etc.

I was wondering if anyone on here with Fibromyalgia also suffers with Small Fibre neuropathy?

There was a study not long ago I'm sure saying something about the pain in Fibromyalgia may come from blood vessels near the skin but if nerves near the skin are damaged as in my case, could this also be linked to the issues we suffer with Fibromyalgia??

15 Replies

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  • Hi there Andy184 It's a very good question. It as been said for some years now that the blood vessels in the hands was fibro related. I have not read any further updates since that was published. But it would be good to see just how many people suffering with fibro also suffer from small nerve neuropathy. I do suffer with it mildly in my feet. Maybe we should run a poll on how many members suffer with it in our group here. Ummm thought provoking thank you

    Mo xx

  • That's a very interesting diagnosis. In the past I had Ankylosing Spondiltis which is chronic inflammation of tissue within joints incl ribs. I had to take myself to a big city hospital to get a diagnosis of the unbearable pain in my rib cages. I saw an Orthopaedic guy who also asked the Nephrologist to be involved, they too found something damaged in my renal area BUT as an infant I had nephritis! It was decided that this early illness in life had left its mark, It was at this time I was introduced to Acupuncture and later hydrotherapy..Its quite amazing really that every ache and pain are passed off as fibro- Don't take No for an answer kick up a fuss and insist on being referered to another hospital with more qualified specialists.. Good luck, please let us know what happens.

  • Thanks Caz,

    I saw one Dr who said there was nothing wrong with me at all and I insisted on a second opinion which is when they found this. It's frightening how Drs will just dismiss you with out taking the time to investigate your illness properly

  • Hello and welcome to our friendly fibro forum where you can get support, understanding, advice and help along with a chuckle or two.

    Our mother site fmauk.org has a wealth of information, including guides and links.

    Nothing surprises me with fibro linked to many other conditions.

    Many fibromites have posted with the same diagnosis as you in addition to their fibro and it has been mooted that blood vessels are involved.

    It is also true that spinal pain through misaligned discs or arthritis can be linked to fibro so it looks like you are getting it from all sides.

    Hope you manage to find effective relief very soon and looking forward to seeing you around the forum.

    X

  • Thanks Bluebell99

  • So how do we go about running a poll Bluebell99?

  • If you would like a Poll to be done, run it by Ken, TheAuthor by PM and he will check that it is suitable and original.

    xx

  • Hi Andy184

    I sincerely hope that you are feeling as well as you possibly can be today? Welcome to the forum and it is wonderful to make your acquaintance. I have pasted below an excerpt from the *US National Library of Medicine as to what can cause it:

    *There are a variety of diseases that may result in a small fiber neuropathy, including diabetes and other glucose dysregulation syndromes (eg, impaired glucose tolerance and metabolic syndrome), thyroid dysfunction, sarcoidosis, vitamin B12 deficiency, HIV, neurotoxic medications (including many chemotherapeutic agents ...

    As for treatment they say:

    *Many cases of small fiber neuropathy will remain idiopathic, or will still require treatment of pain. There is very limited evidence for specific medications in the treatment of pain from small fiber neuropathies. Most clinical studies have examined drugs in the treatment of many neuropathic pain syndromes (such as postherpetic neuralgia and painful diabetic neuropathy).

    I am so truly sorry that I could not help you more with treatments. I have diabetic Neuropathy so I truly sympathise with you. I want to sincerely wish you all the best of luck and please take care of yourself my friend.

    All my hopes and dreams for you

    Ken

  • Hi Andy184, sorry for the long post, but the original page had adverts. Hope this is of interest.

    This new understanding of fibromyalgia will hopefully lead to better treatments, doctors and researchers say.

    Fibromyalgia affects 1% to 5% of Americans, mainly women, but until recently, scientists had no idea what might be causing its severe and mysterious pains. For decades, doctors told patients their agony was imaginary, the result of emotional hysteria, not a physical ailment.

    But this year, researchers finally began to get a handle on the condition.

    “What’s happened is in 2013 there’s been this absolute explosion of papers,” says neurologist Anne Louise Oaklander at Massachusetts General Hospital in Boston. “The whole view on this has shifted.”

    Oaklander published two studies this year showing that half or more of the cases of fibromyalgia are really a little-known condition affecting the nerves. People with this small-fiber neuropathy get faulty signals from tiny nerves all over the body, including internal organs, causing an odd constellation of symptoms from pain to sleep and digestive problems that overlap with symptoms of fibromyalgia.

    Neuroscientist Frank Rice and a team based at Albany Medical College also discovered that there are excessive nerve fibers lining the blood vessels of the skin of fibromyalgia patients — removing any doubt that the condition is physically real.

    These fibers in the skin can sense blood flow and control the dilation and constriction of vessels to regulate body temperature, Rice says, as well as direct nutrients to muscles during exercise. Women have more of these fibers than men, he says, perhaps explaining why they are much more likely to get fibromyalgia.

    “Blood vessel nerve fibers are an important target that haven’t been in our line of thinking to date in chronic pain conditions,” says Rice, now president and chief scientist at Integrated Tissue Dynamics LLC, a biotechnology research company in Rensselaer, N.Y.

    In recent years, scans of patients with fibromyalgia have revealed brain changes associated with pain, but the new research suggests these are a symptom rather than the cause of the condition.

    This new understanding of fibromyalgia will hopefully lead to better treatments, Rice and Oaklander say.

    Right now, most people are treated with the antidepressants Cymbalta made by Eli Lilly, or Savella by Forest Pharmaceuticals, or with Lyrica, a seizure medication from Pfizer — which have all been federally approved for use in fibromyalgia.

    But these drugs have side effects and don’t help everyone.

    “We’re looking now to understand more about other features of the pathology that might lead to a more targeted approach and less of a shotgun that causes side effects,” says Rice, also an adjunct professor at the University at Albany, State University of New York.

    The trigger for fibromyalgia is still a mystery, although stressful events in patients’ past have been thought to play a role.

    Rheumatologist Richard Chou says there is some preliminary evidence that the nerve damage is caused by the immune system.

    “We’re hoping some day we’ll be able to say exactly how your immune system is causing damage to the sensory nerves that results in fibromyalgia pain,” says Chou, an assistant professor at the Geisel School of Medicine at Dartmouth in New Hampshire. Researchers don’t yet know whether the pain causes the other problems of fibromyalgia — disrupting sleep, for instance — or whether both pain and sleep disturbances share the same cause.

    Fibromyalgia’s constellation of symptoms is very similar to those of chronic fatigue syndrome and Gulf War syndrome, which Oaklander’s group also studies. “If someone has more of one symptom than another they might call it one thing, like chronic fatigue, but it’s not clear that these are different,” Oaklander says

    She says researchers still have a lot to learn about these conditions, but scientists are taking them more seriously and making real progress for the first time.

    Carolyn DiSilva of Maynard, Mass., one of Oaklander’s patients, says she was stunned to learn that she had small-fiber neuropathy caused by an overactive immune system, instead of fibromyalgia.

    “I think a lot of people, they get a blanket diagnosis as fibromyalgia because doctors don’t know what’s wrong with them,” says DiSilva, 47, who has suffered from unexplained pains for about 14 years. The non-stop agony and the pins and needles that plagued her for hours at a time forced her to give up her work as a hair stylist, she says.

    Understanding what’s causing her pain has helped her, she says, because doctors and others take her problems seriously, instead of dismissing her as they used to do.

    And now that it’s clear DiSilva has an immune problem, Oaklander has put her on intravenous immunoglobulin treatments — instead of conventional fibromyalgia therapy — which seem to be making a profound difference in her health.

    DiSilva says her pain has dropped from a 10 on a 10-point scale to about a 4.

    “I always hope that someday I’ll wake up with no pain, but I’m so grateful that I’ve come this far.”

    Source of the study: usatoday.com

  • Hi Andy184 This is another article. Apologies to everyone else!

    Fibromyalgia - Ultimately a Disease of Amplified Pain

    By Mark J. Pellegrino, MD* • ProHealth.com • May 26, 2008

    Many conditions can lead to permanent changes in the pain transmission mechanism and result in chronic pain that overwhelms the body’s pain defense mechanisms. One such condition is Fibromyalgia.

    Fibromyalgia may not cause destruction along the pain pathways as other conditions I have mentioned can [rheumatoid arthritis, carpal tunnel syndrome, shingles, multiple sclerosis, for example]. However, Fibromyalgia does cause chronic abnormal changes along all the pathway components and this results in chronic pain via both peripheral (from skin, muscles and nerves) and central (from spinal cord and brain) neurological mechanisms.

    The end result of Fibromyalgia’s abnormal changes appears to be a state of pain amplification that causes severe generalized pain. Fibromyalgia is ultimately a disease of amplified pain.

    Dr. Robert Bennett has written and presented excellent information that explains why we hurt with Fibromyalgia (e.g., “Emerging Concepts in the Neurobiology of Chronic Pain: Evidence of Abnormal Sensory Processing in Fibromyalgia,” Mayo Clinic Proceedings). If we trace the pain signals through the various parts of the pain pathway (from the nociceptors - or specialized pain nerve endings – to the nerves to the spinal cord to the brain) in people with Fibromyalgia, we find various abnormalities along the way. Many studies have shed light on different points along the complete pain pathway.

    I want to briefly summarize some of these different abnormalities and possible problems encountered by Fibromyalgia pain signals on the path to the brain.

    NOCICEPTORS - Pain originates from the nociceptors

    Trauma is a common trigger of Fibromyalgia. Tissue injury - damage to the muscles and soft tissues – activates the nociceptors. Some studies have suggested that microscopic injury occurs in specific parts of the muscles (for those who want the medical names: muscle spindles, intrafusal fibers, and calcium pumps).

    Localized tissue injury probably activates arachidonic acid (a biological protein), which turns into “bad” prostaglandans (called Cox-II prostaglandins), and cause inflammation and pain.

    In addition to trauma, autoimmune factors may be another pain nerve activator. Perhaps autoimmune processes create compounds which act as irritants and activate the nociceptors chronically to the point where they become “permanently” sensitized and irritated. As a result, biochemical, hormonal, and red blood cell changes occur that interfere with the cells’ ability to receive adequate supplies of oxygen, glucose, and other nutrients. Blood flow, energy formation, and the cells’ electrical and neurological harmonies are all disrupted.

    Since the nociceptors remain “faulty,” the electrical and neurological balance remains abnormal, and nociceptors continue to be activated. Pain-producing neurotransmitters are released and accumulate as long as the nociceptors stay activated at the peripheral level (skin and muscles, especially).

    These persistent pain signals we experience may be interpreted as an itching, burning, swelling, or tingling at one end of the spectrum, or – at the other end – knife-stabbing, burning, or throbbing. One nociceptor can signal different pain signals and sensations depending on its level of irritation – the more irritated it is, the more severe the pain.

    These changes can become permanent and cause the nerves to become sensitized to the point where they are easily activated to send pain, even in the absence of any noxious stimulus.

    In other words, persistent pain signals can spontaneously arise from peripheral nerve endings and bombard the rest of the pain pathway. So, instead of waiting for outside stimulation such as trauma, pressure, temperature, or touch to signal the nociceptors, these nociceptors send pain signals on their own, without any outside help. This “spontaneous” pain is what we complain about the most!

    NERVES

    The nerves, especially the sensory nerves and the autonomic nerves, “wonder what is happening” because they are getting bombarded by all of these signals from the nociceptors. At first, they try to diminish these painful signals by using accommodation and gate mechanisms.

    However, the signals persist and they, too, undergo a sensitization process. They become hypersensitized and react with an exaggerated response instead of a normal or diminishing response (accommodation). Now we get even more pain, numbness, swelling, burning, and other sensations.

    Some of the hypersensitization may be mediated by nerve growth factor, which has been found in higher levels in Fibromyalgia. A high nerve growth factor may indicate the nerves are trying to regenerate or repair themselves. But instead of repairing the nerves so they act normal again, the opposite seems to happen. Nerve growth factor is probably enhancing the nerves’ abilities to transmit pain to the spinal cord. More pain results, not less.

    SPINAL CORD – Amplification, wind-up, allodynia, Substance P, generalization

    At the spinal cord level, the Fibromyalgia begins to take control.

    It is here that additional changes occur to perpetuate the pain and spread it to different levels. When pain generators first start firing, the spinal cord pain processing centers may act at first like a dry sponge and easily soak up all the signals. Our bodies may have many pain generators at any given time, but if they are slowly and intermittently firing, drug sponges can soak up the signals and not cause any bothersome symptoms.

    From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated, and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain.

    In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more. The additional oncoming continuous signals will spill over the wet sponge, and this leads to persistent pain.

    The two main changes that occur at the spinal cord include:

    Pain amplification (by specialized nerves called NMDA receptors)

    And loss of pain filtering (by the diffuse noxious inhibitory control system).

    Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain. This phenomenon is called “wind-up,” and is the neurological mechanism for the amplification of pain.

    Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified, and be sent to the brain as pain. The spinal cord becomes more sensitized to sending pain, lots of it. Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals.

    As a result, different sensory signals such as touch, pressure, temperature, and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature, or joint motion signals.

    This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia. Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain! We can still appreciate touch, pressure, temperature, joint movement, and other non-pain signals, but pain contaminates these signals, and we feel the pain.

    Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters.

    Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain. When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal. As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “generalization” of the Fibromyalgia.

    This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain. A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured. Over time, the pain begins to involve the mid-back, low back, and ultimately the whole body, even though these areas were never injured. The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body.

    BRAIN

    Our poor brains have no chance, do they? Any pain memory stored in the past will be re-awakened by this process. Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops. This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive. Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated.

    The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord. Changes occur:

    Serotonin levels decrease,

    Brain waves change,

    Sleep stages are affected,

    Blood flow and glucose [blood sugar] metabolism are affected.

    The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain. Fibrofog occurs. Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness, and helplessness, which can further amplify the pain.

    In patients with Fibromyalgia, functional reorganization (brain plasticity) in both sensory and motor portions of the brain has been observed, and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003). These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses. The brain makes these changes to enhance its ability to perceive pain – brain amplified pain.

    This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw, et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs. This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain.

    FIBROMYALGIA PAIN SUMMARY

    To summarize, Fibromyalgia changes our pain pathways. It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain. The main problem, in a nutshell, is amplified pain.

    The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain. What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia. Our pain signal of a “1” gets amplified and magnified, and by the time it reaches our brain, it is a “10”!

    Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals. Even tiny subconscious pain signals can get amplified, or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain.

    These are not your everyday aches and pains, these are severe pains that cannot be ignored. This severe, chronic pain can completely disrupt one’s life. And by the way, while all of this is happening, we continue to look completely normal on the outside.

    ___

    * Dr. Pellegrino, a fibromyalgia patient himself, has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center. This article is reproduced with his permission from Chapter 9 of Fibromyalgia: Up Close & Personal by Mark J. Pellegrino, MD. © Anadem Publishing, Inc. and Mark Pellegrino, MD, 2005, all rights reserved. To purchase a copy, call Dr. Pellegrino's staff at the Ohio Rehab Center (800-529-7500).

    Note: This information has not been evaluated by the FDA. It is not meant to prevent, diagnose, treat, or cure any illness, condition, or disease. It is very important that you make no change in your personal healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

  • This is one is very recent and unfortunately, very technically. I do like the first sentence, I think most would word it rather stronger!

    Pain. 2017 Jan;158(1):34-47.

    Towards a neurophysiological signature for fibromyalgia.

    López-Solà M1, Woo CW, Pujol J, Deus J, Harrison BJ, Monfort J, Wager TD.

    Author information

    Abstract

    Patients with fibromyalgia (FM) show characteristically enhanced unpleasantness to painful and nonpainful sensations accompanied by altered neural responses. The diagnostic potential of such neural alterations, including their sensitivity and specificity to FM (vs healthy controls) is unknown. We identify a brain signature that characterizes FM central pathophysiology at the neural systems level. We included 37 patients with FM and 35 matched healthy controls, and analyzed functional magnetic resonance imaging responses to (1) painful pressure and (2) nonpainful multisensory (visual-auditory-tactile) stimulation. We used machine-learning techniques to identify a brain-based FM signature. When exposed to the same painful stimuli, patients with FM showed greater neurologic pain signature (NPS; Wager et al., 2013. An fMRI-based neurologic signature of physical pain. N Engl J Med 2013;368:1388-97) responses. In addition, a new pain-related classifier ("FM-pain") revealed augmented responses in sensory integration (insula/operculum) and self-referential (eg, medial prefrontal) regions in FM and reduced responses in the lateral frontal cortex. A "multisensory" classifier trained on nonpainful sensory stimulation revealed augmented responses in the insula/operculum, posterior cingulate, and medial prefrontal regions and reduced responses in the primary/secondary sensory cortices, basal ganglia, and cerebellum. Combined activity in the NPS, FM pain, and multisensory patterns classified patients vs controls with 92% sensitivity and 94% specificity in out-of-sample individuals. Enhanced NPS responses partly mediated mechanical hypersensitivity and correlated with depression and disability (Puncorrected < 0.05); FM-pain and multisensory responses correlated with clinical pain (Puncorrected < 0.05). The study provides initial characterization of individual patients with FM based on pathophysiological, symptom-related brain features. If replicated, these brain features may constitute objective neural targets for therapeutic interventions. The results establish a framework for assessing therapeutic mechanisms and predicting treatment response at the individual level.

  • This is a link to the research on nerve endings surrounding blood vessels, it has some clear and very easy to understand diagrams and there are also photos.

    galim.org/files/pdf/Rice.pdf

    This is more research from 2013.

    Multiple Studies, One Conclusion: Some Fibromyalgia Patients Show Peripheral Nerve Pathologies

    Role of small fiber abnormalities in condition unclear

    by Stephani Sutherland on 6 Nov 2013

    Fibromyalgia syndrome (FMS) ranks among the most enigmatic and prevalent chronic pain conditions. Researchers and clinicians have searched in vain for an underlying cause for the unexplained widespread muscle pain, fatigue, and tenderness. In recent years, FMS has come to be seen as a "central" pain disorder, arising from changes in pain processing in the central nervous system. Now several new reports show evidence for peripheral nerve abnormalities in FMS patients that could contribute to their chronic pain.

    Jordi Serra of the University of Barcelona, Spain, and University College London, UK, said that together the studies—including his own work—suggest that at least some people with FMS have peripheral neuropathy and support the idea that FMS is a neuropathic pain condition. “Even though FMS is currently not considered a neuropathic disorder, it really looks the same” in some respects, Serra said.

    Peripheral nerves damaged

    One study, from Nurcan Üçeyler, Claudia Sommer, and colleagues at the University of Würzburg, Germany, compared 25 people diagnosed with FMS to 10 with depression but not pain, and similar numbers of matched healthy controls. The FMS group showed impaired peripheral sensory nerve function as measured by quantitative sensory testing—a subjective test—and by electrophysiological recording of pain-related evoked potentials. Skin biopsies revealed reduced innervation with the small fiber nerves that carry painful sensations in the legs. The group with FMS also reported higher levels of neuropathic pain symptoms. The study was published online March 9 in Brain.

    In a separate study that appeared June 5 in Pain, Anne Louise Oaklander and her team at Massachusetts General Hospital, Boston, US, reported similar findings in a group of 27 people rigorously diagnosed with FMS: Skin biopsies from the legs revealed that 41 percent of the FMS patients had loss of small fiber innervation to levels considered clinically diagnostic for small fiber peripheral neuropathy (SFPN), a condition that can cause widespread pain. FMS patients also reported more symptoms than controls did on a questionnaire designed to detect neuropathic pain, and neurologic examination indicated more evidence of SFPN. The results led the investigators to suggest that some of the group diagnosed with FMS actually had unrecognized SFPN.

    A third study presented at the November 2012 meeting of the International Association for the Study of Pain by Serra showed functional abnormalities in the small nerve fibers of FMS patients to match the anatomical differences seen by Oaklander and Sommer. Using a challenging technique called microneurography to record from individual nerve fibers in the skin, Serra had previously demonstrated hyperactivity in sensory neurons from patients with painful peripheral neuropathy (Serra et al., 2011). Serra found similarly altered conduction and firing properties in FMS patients compared to controls. That work is currently in press in the Annals of Neurology.

    A condition by any other name?

    The results raise the question of whether some patients diagnosed with FMS actually have SFPN. Sommer and colleagues stop short of calling their findings SFPN, instead describing “small fibre pathology” in the FMS patients. But Oaklander says making the diagnosis is important, because unlike FMS, which has no known cause and thus no disease-based treatment, small fiber polyneuropathies have some known causes that suggest treatment options.

    In a letter to Pain commenting on Oaklander’s study, Üçeyler and Sommer argued that such a simple explanation is unlikely, because FMS includes some symptoms that are distinct from the usual presentation of SFPN (Üçeyler and Sommer, 2013). For example, many patients with FMS experience the burning pain or nerve tingling characteristic of SFPN, but most with SFPN do not experience the hallmark FMS symptom of widespread deep tissue pain. That discrepancy led Sommer and colleagues to conclude that the nerve damage seen in the epidermis probably doesn’t underlie the deep, widespread pain of FMS, which instead might result from similar problems in the small fibers that extend to muscles, fascia, and tendons.

    In a published response, Oaklander pointed out that people with SFPN vary in their clinical presentation, which may include widespread pain (Oaklander et al., 2013). Her group previously reported finding juvenile-onset small fiber polyneuropathy in people with unexplained widespread pain, many of whom had previously received a diagnosis of FMS (see PRF related news story).

    Oaklander and colleagues stress that making the diagnosis of SFPN in some FMS patients could lead physicians to look harder for an underlying cause—such as hepatitis, diabetes, or an immune response directed at sodium channels—and perhaps suggest alternative treatments. In the current study, the investigators looked for possible causes in 13 FMS patients with identified small fiber pathology and found two had hepatitis C, three had a potential genetic cause, and eight had markers of dysimmunity.

    If an underlying cause for the peripheral nerve pathology could be identified, would it lead to improvement for FMS patients? “I like the optimistic stance,” said Roland Staud, a rheumatologist at the University of Florida, US. “I’d say yes; if you identify the main driving cause for their response, there’s a good chance they’ll [improve].”

    Daniel Clauw, who studies fibromyalgia at the University of Michigan, US, disagrees. Clauw said that while the science in the new studies is sound, he doesn’t see how the findings should change treatment for people with FMS. Until that happens, he said, “I hang my hat on CNS treatments” that modulate pain-processing circuits. Clauw went a step further and suggested that the observed nerve damage probably follows FMS rather than the other way around. “It may be a marker of a chronically overactive nervous system,” Clauw said. The central nervous system undergoes remodeling with chronic pain, he said, so why not the peripheral system as well?

    One hypothesis to explain FMS is that people with the disorder become, for unidentified reasons, extremely sensitive to nociceptive input, possibly because peripheral sensory signals not normally felt as painful become amplified in the brain and spinal cord. Whereas many people with identified peripheral nerve damage do not experience any neuropathic pain, people with FMS could have an enhanced response to such damage.

    How that amplification is set into motion remains a mystery, but FMS often develops following a traumatic event or injury, and patients might have several other concomitant pain conditions. “Fibromyalgia can be triggered or exacerbated by multiple conditions, and now it appears that small fiber neuropathy may be one of them,” said Staud.

    Another peripheral trigger?

    In other related work published May 20 in Pain Medicine, Frank Rice and colleagues at the Albany Medical College, New York, US, found different peripheral nerve abnormalities in the palms of FMS patients. Tiny blood vessels called arteriole-venule shunts (AVSs) in the hands are important for regulating body temperature and controlling blood flow to muscles during exercise. The shunts constrict in response to norepinephrine released by autonomic fibers and dilate in response to peptides released by sensory fibers, giving these afferents a dual role as receptors and effectors. Rice found that the fibers were significantly altered in the FMS patients but not in control subjects. Innervation by both fiber types was increased with FMS, and the balance was tipped so that sensory neuron endings outnumbered autonomic fibers.

    Rice postulates that the imbalance might affect thermal regulation or produce deep tissue ischemia, perhaps contributing to widespread muscle pain or fatigue. Staud appreciates the findings but said, at this stage, “the relationship to fibromyalgia is not at all clear.” Next, said Staud, experiments will be needed to correlate the anatomical findings with pain or other aspects of FMS. “I’m totally on board if he shows evidence of that,” said Staud, but “otherwise, it is an oddity that we cannot currently explain.”

    Despite their different interpretations of the recent findings, the researchers all agreed that changes in the central nervous system certainly contribute to FMS to some degree. “We are not saying the CNS is not important,” said Serra. “We are only saying that, because [pain] seems to be coming from the periphery, it makes sense to look there.”

    Staud agreed and said that in treating FMS patients, “I look for potential biological causes that could drive it from the periphery,” and these findings present another potential cause. What the findings will mean for FMS treatment remains to be seen.

    Stephani Sutherland, PhD, is a neuroscientist, yogi, and freelance writer in Southern California.

    Image: A 60-micron optical section of human skin, showing epidermal nerve fibers (thin green) penetrating into the epidermis (blue). Credit: William Kennedy and Gwen Wendelschafer-Crabb, University of Minnesota, Minneapolis, US.

    REFERENCES:

    Small fibre pathology in patients with fibromyalgia syndrome.

    Uçeyler N, Zeller D, Kahn A-K, Kewenig S, Kittel-Schneider S, Schmid A, Casanova-Molla J, Reiners K, Sommer C

    Brain. 2013 Jun; 136(Pt 6):1857-67. Epub 2013 Mar 09.

    Excessive Peptidergic Sensory Innervation of Cutaneous Arteriole-Venule Shunts (AVS) in the Palmar Glabrous Skin of Fibromyalgia Patients: Implications for Widespread Deep Tissue Pain and Fatigue.

    Albrecht PJ, Hou Q, Argoff CE, Storey JR, Wymer JP, Rice FL

    Pain Med. 2013 Jun; 14(6):895-915. Epub 2013 May 20.

  • Thanks very much Tedsmum. Very interesting

  • I also have peripheral neuropathy affecting my feet, legs and lately my hands, i am diabetic but it is extremely well controlled and has been ruled out as a cause.

    I think it's an excellent idea to run a poll on this, the subject comes up quite often.

    C.c xx

  • Wow thanks for the info Ccupcakes. It would be interesting to see how many have both.

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