Fibromyalgia Support Group
You're not alone in your pain. Fibromyalgia is a condition that can be difficult to diagnose and manage. If you're trying to cope with pain throughout your body, sleep problems, general fatigue, or other common fibromyalgia symptoms, you're in the right place. The community is here for you to talk about therapies and share your challenges.
The evidence is piling up on this. Interesting is that fibro does have to do with the immune system, and there may be effective treatments that modulate the immune system.
PAIN MEDICINE NEWS
MAY 27, 2016
Up to Half of Fibromyalgia Patients Have Hard Evidence of Small-Fiber Polyneuropathy
Palm Springs, Calif.Several recent papers show that up to half of patients with fibromyalgia have objective evidence of small-fiber polyneuropathy (SFPN), a known peripheral nerve disease that can be tested for objectively and in some cases is curable. This is the first firm evidence of a biological mechanism for fibromyalgia, a disease that was often thought to be psychosomatic.
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Anne Louise Oaklander, MD, PhD
If so many fibromyalgia patients might have SFPN, well need ways to screen and diagnose that are less expensive and labor-intensive, and more widely available, said Anne Louise Oaklander, MD, PhD, of the Departments of Neurology and Pathology at Massachusetts General Hospital and Harvard Medical School, both in Boston, at the 2016 annual meeting of the American Academy of Pain Medicine (AAPM).
As Dr. Oaklander reported, small fiber is the most common type of peripheral nerve fiber, but there is little awareness about SFPN among many medical specialists. These axons run throughout our entire body, innervating most of our organs and tissues, she said. So when people develop SFPN, they get symptoms and signs in multiple organ systems, and the underlying diagnosis can get lost in the shuffle.
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Objective Evidence of SFPN in Fibromyalgia
To test the hypothesis that some patients labeled with fibromyalgia have unrecognized SFPN causing their symptoms, Dr. Oaklanders research team prospectively measured SFPN-associated findings in 27 patients with fibromyalgia and 30 matched normal controls (Pain 2013;154:2310-2316). We made this [study] as rigorous as we could, said Dr. Oaklander. Subjects were required to meet American College of Rheumatology criteria and have a doctors note showing real-world fibromyalgia. We looked for symptoms, signs, pathology and pathophysiology consistent with SFPN, and we used the best-available validated tests.
Using diagnostic skin biopsies from the lower leg, her team found that 41% of fibromyalgia patients had axon loss severe enough to meet the standard diagnostic criteria for SFPN, versus only 3% of matched normal controls. Likewise, the teams other study of 41 patients with childhood-onset, unexplained, chronic, widespread pain, most of whom were diagnosed with juvenile fibromyalgia, showed that 59% met the criteria for definite SFPN (Pediatrics 2013;131:e1091-e1100). Moreover, some of the patients SFPN appeared to be immune mediated and improved with immunomodulatory therapies.
Dr. Oaklander mentioned that since the publication of her studies, abundant independent research affirms the discovery that between one-third and one-half of fibromyalgia patients appear to have SFPN. She noted that every manuscript, now almost a dozen, has reported similar findings. Fibromyalgia patients (Pain Med 2013;14:895-915) were shown to have the same loss of myovascular innervation as SFPN patients (Muscle Nerve 2015;51:514-521), which Dr. Oaklander believes offers a plausible explanation for their lack of stamina during exercise. A microneurographic study established that C fibers fire spontaneously and abnormally in fibromyalgia patients, just as in SFPN patients (Ann Neurol 2014;75:196-208).
Whats in a Name?
Does it make a difference whether an illness is called fibromyalgia or SFPN? According to Dr. Oaklander, there is a crucial distinction. For SFPN, objective diagnostic tests offer clarity and direction for patients and physicians. Skin biopsies and autonomic function testing, she said, permit objective diagnosis and outcomes that can be used to evaluate therapies. Plus, the medical causes of SFPN, which range from diabetes to vitamin deficiencies, often can be identified and improved, or even cured. In contrast, she said, fibromyalgia treatments address symptoms without identifying the underlying causes, since they have remained unknown.
Diagnostic Yield of Blood Tests In SFPN Patients
Dr. Oaklander presented retrospective data from 195 patients with idiopathic SFPN showing that a panel of widely available blood tests identified potential medical causes in 57% of patients, while 42% had at least one marker of dysimmunity. This also suggests that some may have potentially treatable autoimmune causes for their symptoms, Dr. Oaklander observed. She said there is additional, preliminary evidence that some patients benefit from treatment with intravenous immunoglobulin, a standard treatment for autoimmune polyneuropathy.
Blood tests can help track the underlying causes and mechanisms of SFPN, she concluded. Theres evidence, at least in the youngest patients, that there is a contribution of autoimmunity, and very preliminary evidence that, for very specific patients, there may be a role for immunomodulatory therapy.
Sean Mackey, MD, PhD, chief of pain medicine at Stanford University Medical Center, in California, and a past president of the AAPM, whose team is researching the role of glial cells in fibromyalgia, advocated the merits of studying both the central and peripheral nervous systems for widespread pain disorders.
Ultimately, said Dr. Mackey, we need a grand unified theory to show that were talking about the same thing, just from different perspectives. Were eventually going to converge, and its going to take really methodologically sound, elegant work, like Dr. Oaklanders, to help us better understand the mechanisms of these diseases.
Chase Doyle
PAIN MEDICINE NEWS
MAY 27, 2016
Up to Half of Fibromyalgia Patients Have Hard Evidence of Small-Fiber Polyneuropathy
Palm Springs, Calif.Several recent papers show that up to half of patients with fibromyalgia have objective evidence of small-fiber polyneuropathy (SFPN), a known peripheral nerve disease that can be tested for objectively and in some cases is curable. This is the first firm evidence of a biological mechanism for fibromyalgia, a disease that was often thought to be psychosomatic.
image
Anne Louise Oaklander, MD, PhD
If so many fibromyalgia patients might have SFPN, well need ways to screen and diagnose that are less expensive and labor-intensive, and more widely available, said Anne Louise Oaklander, MD, PhD, of the Departments of Neurology and Pathology at Massachusetts General Hospital and Harvard Medical School, both in Boston, at the 2016 annual meeting of the American Academy of Pain Medicine (AAPM).
As Dr. Oaklander reported, small fiber is the most common type of peripheral nerve fiber, but there is little awareness about SFPN among many medical specialists. These axons run throughout our entire body, innervating most of our organs and tissues, she said. So when people develop SFPN, they get symptoms and signs in multiple organ systems, and the underlying diagnosis can get lost in the shuffle.
ADVERTISEMENT
Objective Evidence of SFPN in Fibromyalgia
To test the hypothesis that some patients labeled with fibromyalgia have unrecognized SFPN causing their symptoms, Dr. Oaklanders research team prospectively measured SFPN-associated findings in 27 patients with fibromyalgia and 30 matched normal controls (Pain 2013;154:2310-2316). We made this [study] as rigorous as we could, said Dr. Oaklander. Subjects were required to meet American College of Rheumatology criteria and have a doctors note showing real-world fibromyalgia. We looked for symptoms, signs, pathology and pathophysiology consistent with SFPN, and we used the best-available validated tests.
Using diagnostic skin biopsies from the lower leg, her team found that 41% of fibromyalgia patients had axon loss severe enough to meet the standard diagnostic criteria for SFPN, versus only 3% of matched normal controls. Likewise, the teams other study of 41 patients with childhood-onset, unexplained, chronic, widespread pain, most of whom were diagnosed with juvenile fibromyalgia, showed that 59% met the criteria for definite SFPN (Pediatrics 2013;131:e1091-e1100). Moreover, some of the patients SFPN appeared to be immune mediated and improved with immunomodulatory therapies.
Dr. Oaklander mentioned that since the publication of her studies, abundant independent research affirms the discovery that between one-third and one-half of fibromyalgia patients appear to have SFPN. She noted that every manuscript, now almost a dozen, has reported similar findings. Fibromyalgia patients (Pain Med 2013;14:895-915) were shown to have the same loss of myovascular innervation as SFPN patients (Muscle Nerve 2015;51:514-521), which Dr. Oaklander believes offers a plausible explanation for their lack of stamina during exercise. A microneurographic study established that C fibers fire spontaneously and abnormally in fibromyalgia patients, just as in SFPN patients (Ann Neurol 2014;75:196-208).
Whats in a Name?
Does it make a difference whether an illness is called fibromyalgia or SFPN? According to Dr. Oaklander, there is a crucial distinction. For SFPN, objective diagnostic tests offer clarity and direction for patients and physicians. Skin biopsies and autonomic function testing, she said, permit objective diagnosis and outcomes that can be used to evaluate therapies. Plus, the medical causes of SFPN, which range from diabetes to vitamin deficiencies, often can be identified and improved, or even cured. In contrast, she said, fibromyalgia treatments address symptoms without identifying the underlying causes, since they have remained unknown.
Diagnostic Yield of Blood Tests In SFPN Patients
Dr. Oaklander presented retrospective data from 195 patients with idiopathic SFPN showing that a panel of widely available blood tests identified potential medical causes in 57% of patients, while 42% had at least one marker of dysimmunity. This also suggests that some may have potentially treatable autoimmune causes for their symptoms, Dr. Oaklander observed. She said there is additional, preliminary evidence that some patients benefit from treatment with intravenous immunoglobulin, a standard treatment for autoimmune polyneuropathy.
Blood tests can help track the underlying causes and mechanisms of SFPN, she concluded. Theres evidence, at least in the youngest patients, that there is a contribution of autoimmunity, and very preliminary evidence that, for very specific patients, there may be a role for immunomodulatory therapy.
Sean Mackey, MD, PhD, chief of pain medicine at Stanford University Medical Center, in California, and a past president of the AAPM, whose team is researching the role of glial cells in fibromyalgia, advocated the merits of studying both the central and peripheral nervous systems for widespread pain disorders.
Ultimately, said Dr. Mackey, we need a grand unified theory to show that were talking about the same thing, just from different perspectives. Were eventually going to converge, and its going to take really methodologically sound, elegant work, like Dr. Oaklanders, to help us better understand the mechanisms of these diseases.
Chase Doyle
Dr. Oaklander has done a number of studies, as have others. It looks like her numbers are 40 to 69%.
In this study, the patients found to have SFNP, were textbook for fibromyalgia.
Physics got Einstein. We need an Einstein for fibro...
I don't think small fiber neuropathy in fifity percent of fibro patients is going to turn out to be the cause of onset of fibro.
I'm excited by a neuro-scientist out of Univ of Alabama, Jarred Younger who postulates that the blood-brain barrier has been breached and that neuro inflammation causes the symptoms of fibro.
Here's a video https://www.youtube.com/watch?v=TH_upgDgLQ8
I wonder which criteria they're using for fibromyalgia - I don't think the ACR ever formally adopted the new criteria that were proposed in 2010.
The introduction to the article. Not just one small study.
I really am interested in that Jarred Younger video and how leptin resistance can affect pain and fatigue. WOW....I've always believed there is an inflammatory process going on and what is causing it is partially responsible for some of the symptoms of FM.
Always good debates girls.