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The 'Body' is Back in Fibromyalgia: Small Nerve Fiber Damage Suggests the Pain Begins There

  [ 185 votes ]   [ 5 Comments ]
By Cort Johnson • www.ProHealth.com • May 7, 2014


The 'Body' is Back in Fibromyalgia: Small Nerve Fiber Damage Suggests the Pain Begins There
Reprinted with the kind permission of Cort Johnson and Health Rising.

The Missing Body

“It’s commonly claimed that, despite its severity and widespread nature, FM has not been associated with an identifiable peripheral-tissue lesion.” Authors

The ‘word’ on Fibromyalgia, which was originally proposed to be a disorder of the muscles, has been that it’s a disorder of the central nervous system. Studies have found that both the pain-producing and the pain-inhibiting sides of the central nervous system in Fibromyalgia are clearly dysregulated. These are important findings, but they’re not the whole story. You wouldn’t know that from overviews of the disorder on the web where the central nervous system paradigm dominates.

Some have speculated that lower levels of a brain neurotransmitter called serotonin leads to lowered pain thresholds or an increased sensitivity to pain. Serotonin is associated with a calming, anxiety-reducing reaction. The lowered pain thresholds in fibromyalgia patients may be caused by the reduced effectiveness of the body’s natural endorphin painkillers and the increased presence of a chemical called “substance P”. Web MD

Even the National Fibromyalgia Association makes no mention of the peripheral nervous system (although it does mention cytokines) in its overview of causes.

The FM patient experiences pain amplification due to abnormal sensory processing in the central nervous system. An increasing number of scientific studies now show multiple physiological abnormalities … including: increased levels of substance P in the spinal cord, low levels of blood flow to the thalamus region of the brain, HPA axis hypofunction, low levels of serotonin and tryptophan and abnormalities in cytokine function.

The Body is Back

The evidence has been mounting over time, but over the past year it’s become clear that Fibromyalgia is not a brain or a body disorder: it’s both. Recent studies have found immune, autonomic nervous system, and muscle issues in FM. With this fourth study in the past year showing substantial damage occurring in the peripheral nervous systems, the body is back in the FM spotlight big time.

The next big question is going to be what is the chicken and what is the egg in FM. The authors of this paper are clear that they believe nerve problems in the body are the egg.

The lead author in this study, Dr. Xavier J. Caro, reported finding large-fiber neuropathy in FM patients in 2008 and was the first to report small nerve fiber problems in FM. His work with large fiber neuropathy was curtailed by the invasive, painful and costly nature of the testing, but then he turned to looking at small fiber neuropathy (SFN).

In the study, Dr. Caro and Dr. Earl Winter state their interest in the peripheral (body’s) nervous system (as opposed to the nervous system in the brain) is really quite simple. When people with FM describe their symptoms they’re describing neuropathic or nerve problems. They note that the ‘language’ of FM can seem fantastic to the uninitiated (which has undoubtably contributed to the problems the disorder has had being taken seriously by the medical profession). Terms like ‘burning’, ‘stabbing’, ‘pins and needles’, ‘hot’, even just ‘miserable’ all describe nerve problems.

For myself the hot, burning sensations I get after too much exercise are rarely found on symptom checklists. I don’t think they’ve been used as diagnostic by any physicians I’ve seen, yet for me they are a major symptom and a major part of post-exertional malaise. They are also nerve symptoms.

Nerve symptoms are very common in FM. Caro and Winter note that over 75% of their FM patients use nerve symptoms to describe their disorder, but only about 20% of rheumatoid arthritis patients do, and other studies have found even higher rates of neuropathic language in FM. In fact, people with FM use much the same language to describe their symptoms, as do diabetics who have peripheral neuropathy.

The Study

Between 2007 and 2011 Caro collected skin biopsies from about 40 FM patients and 40 healthy controls and examine their blood for immune factors. The results make up this present study.

A screen for an array of autoimmune and sensory disorders ultimately eliminated over 20% of the initial pool of FM patients due to the presence of diabetes, autoimmune disorders, hepatitis, etc.

Results

“We … report a surprisingly high prevalence of diminished ENFD (epidermal nerve fiber density) in FM.” Authors

This was an older group of FM patients (mean age 60), every single one of which had some diminished sensory perception in their lower extremities. They also had significantly decreased nerve fiber density in their feet and thighs (p = 0.0002) – a sign that their peripheral nerves had been damaged – compared to the controls. In what’s called a ‘stocking distribution’, the further down the legs they tested the more damage they found – a pattern that is often found in small fiber neuropathy.

Fourteen of 40 FM subjects had evidence of hypercholesterolemia, and 11 had hypertriglyceridemia.

The fact that pain levels were not significantly associated with nerve fiber loss suggested that the pain in FM was not solely due to that loss.

Given their past findings of large fiber neuropathy in FM, they assume the FM patients with SFN also have large fiber involvement as well.

Immune System

“We consider it likely that an immunopathogenic mechanism is at work.” Authors

The lead author in this study, Xavier J. Caro MD, is a rheumatologist and has quite a history in studying and treating FM. Thirty years ago he reported finding IgG at the dermal/epidermal junction in FM patients, and in 1989 he proposed that FM was in part an immune disorder. In this study he and his co-investigator, Earl F. Winter PhD, noted a variety of abnormal nervous system and immune findings associated with the skin in FM patients, with most of those abnormalities dating back to the late 1980s.

More recent studies have found evidence of increased mast cell activation, changes in collagen structure, and increased cytokine levels in the skin. In 2013 Caro published a chapter in a rheumatology textbook where he called Fibromyalgia a ‘neuroimmune’ disorder (“Fibromyalgia: Evaluation and therapy of a neuroimmune disorder”). One has the feeling he’s been looking forward to having this discussion for a long time.

In this study, low nerve densities were significantly correlated with increased IL-2R levels. Il-2R activates T-cells and macrophages, and high levels have been associated with autoimmune disorders including multiple sclerosis.

They noted, as have others, that intravenous immunoglobulin (IVIG) does help some people with Fibromyalgia. (In Dr. Sivieri’s experience, small fiber neuropathy in FM is associated with IgG subclass deficiencies, particularly in the IgG subclass. IgG’s or immunoglobulins refer to antibodies produced by B-cells.)

Pointing a finger straight at the immune system, the authors suggested that a ‘cytokine-related’ lesion (i.e., small fiber loss) would not be unexpected and noted that IL-2R administration in cancer patients can produce an FM-like state. (Discovery of cytokine-induced small fiber neuropathy might be a good thing because it presents the possibility of producing a drug to block IL2-R.)

Pain

Why the pain if the nerve fibers – the source of the pain – have been destroyed? Because they haven’t been completely destroyed and those that are still left are understandably upset (hyperexcitable) and they’re also communicating that upset to the secondary nerve fibers that are intact around them.

‘Central’ Sensitivity Not So Central?

The authors clearly have not been taken with the central sensitivity paradigm that’s held sway for past decade or so in FM. They bluntly stated that the two CNS factors primarily blamed for FM, wind-up and central sensitization (CS), are likely to be secondary rather than primary. They went so far as to state that there is “no credible scientific or clinical evidence that reducing, or even eliminating, CS down-regulates pathological peripheral pain input at all.”

They’re not saying that medications that reduce factors associated with central sensitization don’t work; they may reduce pain, but they play no role in reducing pain inputs from the periphery.

In the past it’s been thought that small pain inputs from the periphery or body in FM get jacked up by a process of central sensitization. These authors believe the pain inputs from the body – from the damaged nerves they and others are finding – are pathological.

If central sensitization was responsible for the pain coming in from the periphery, then diminishing it should result in reduced pain coming in from the body. But they see no evidence of that.

Instead, they provide hope that the going after the problems in the peripheral nerves can eliminate the ‘dysfunctional’ nature of the body pain in FM, and that treating the nerve problems lends itself ‘very well’ to ‘everyday clinical management’ of FM. In response to an email Dr. Caro stated that the treatment of FM is complex and that no two cases are alike but that in the main most Fibromyalgia patients require ‘immune modulators’ – an amazing statement given the current focus on the brain in FM.

But with small nerve fiber damage showing up, and studies proposing that an immune signature has been found, and with Dr. Pridgen reporting ’impressive results’ from his antiviral trial, perhaps an approach using immune modulators in Fibromyalgia isn’t so amazing after all.

Dr. Caro has written a chapter on evaluating Fibromyalgia patients and is planning to write a chapter on FM treatment. A study on immune deficiency in FM has been completed as well and will be released at a National Arthritis Conference in the fall.

If you’re thinking all this applies to FM and not to Chronic Fatigue Syndrome think again. Dr. Caro stated that he doesn’t really differentiate between the two.

Two more things: The authors don’t talk about the autonomic issues arising from small fiber neuropathy, but they do note that autonomic nerve fibers are involved. Nor do they talk about the effect of SFN on exercise. We don’t know how far the neuropathy in FM and presumably ME/CFS extends, but a loss of nerve density in the muscles would reduce muscle activation as well.

When one person with SFN noted how her muscles kept locking up the day after exercise, her neurologist explained that most muscles have several sets of nerves feeding them. When one set of nerves is ‘used up’ during exercise, the others kick in (and activate more parts of the muscles). If’s you’ve only got one set of nerve fibers left, if you keep sending messages down that nerve the muscles will just lock up. Symptomatically that sounds a lot like the muscle stiffness that I experience after exercise.

_______________


About the Author:  Cort Johnson has had ME/CFS for over 30 years. The founder of Phoenix Rising and Health Rising, Cort has contributed hundreds of blogs on chronic fatigue syndrome, fibromyalgia and their allied disorders over the past 10 years. Find more of Cort's and other bloggers' work at Health Rising.




Please Discuss This Article:   Post a Comment 

What's Up with This?
Posted by: djburloak
May 7, 2014
What possible connection or redeeming value does the (clearly sexist!) photo looking up a women's skirt have to this article?!?! Come on ProHealth!
Reply Reply

Visual Linkage Perhaps?
Posted by: hypatiajames
May 7, 2014
The picture you mention of the woman's legs is next to a sentence which mentions the "stocking distribution." The aforementioned woman is wearing stockings.... Don't presume the worst; it will just make you angrier.
Reply Reply

 
It's still Inappropriate
Posted by: djburloak
May 7, 2014
It still amounts to a contrived and inappropriate connection. Out of all the great info in this article, someone had to choose that portion to make a visual connection... especially when the camera angle is focused up, when the reference is toward the lower led. A hosiery display or rack of socks would be much less inflammatory and still enable the connection.

I do expect better of this website and all of its content.

AS for making me angry, it is more disappointing...so much for respect of the total membership of the site.

 


Biased
Posted by: IanH
May 8, 2014
Unfortunately studies using older people with FMS will see extensive peripheral fibre damage. To assert that this is a primary cause of FMS the study must do the study on a cross section of ages ie include people under the age of thirty AND those who have had FM for less than 2 years.

A mean age of 60 is not a sample supporting peripheral fibre damage.

The peripheral neuropathy is most likely the accumulating result of the immune system attack, worse in longer term cases. That is our experience. In addition, longer term cases of FM show more spinal "damage" as well as tendon shortening.
Reply Reply

 
Biased
Posted by: Niaks1211
May 16, 2014
I agree with using a 60 age group. My 19 year old daughter has suffered for years and just recently been diagnosed with FM. I myself being in my 40's have had problems in the past but with my self employed occupation of house cleaning have caused FM to rear it's ugly head.

 



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