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Small Nerve Fiber Involvement in FIbromyalgia Patients

  [ 9 votes ]   [ 1 Comment ]
www.ProHealth.com • February 17, 2014


Small nerve fiber involvement in patients referred for fibromyalgia.

By Maria Pia Giannoccaro MD, et al.

Abstract:

Introduction: Fibromyalgia (FM) is a chronic syndrome characterized by widespread pain often accompanied by other symptoms suggestive of neuropathic pain. We evaluated patients for small fiber neuropathy (SFN) who were referred for fibromyalgia (FM).

Methods: We studied 20 consecutive subjects with primary FM. Patients underwent neurological examination, nerve conduction studies, and skin biopsies from distal leg and thigh.

Results: Electrodiagnostic studies were normal in all patients. SFN was diagnosed in 6 patients by reduced epidermal nerve fiber density. These patients also showed abnormalities of both adrenergic and cholinergic fibers.

Conclusion: A subset of FM subjects have SFN, which may contribute to their sensory and autonomic symptoms. Skin biopsy should be considered in the diagnostic work-up of FM. Muscle Nerve, 2014.

Source: Muscle & Nerve, December 28, 2013. By Maria Pia Giannoccaro MD, Vincenzo Donadio PhD, Alex Incensi BSc, Patrizia Avoni PhD and Rocco Liguori MD. Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.




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Article Comments Post a Comment

We need more info
Posted by: IanH
Feb 19, 2014
We need to know the genetics of the people now to ascertain whether the SFN (small fibre neuropathy) is causing the fibromyalgia syndrome or whether it is a result of a separate pathology in which "fibromyalgia" is a symptom set eg ME/CFS.

There are several explanations as to why about 30% of people with diagnosed FM might have SFN but not all cases.

Genetics:

The genes SCN9A or SCN10A are mutated in about 35% of cases of small fiber neuropathy.

These genes code for the alpha subunits of two different sodium channels, Nav1.7 and Nav1.8.

Sodium channels transport positively charged sodium ions into cells and play a key role in a cell's ability to generate and transmit electrical signals. The NaV1.7 and NaV1.8 sodium channels are found in nociceptors that transmit pain signals to the spinal cord and brain.

The mutations cause "leakages":
The SCN9A gene mutations result in NaV1.7 sodium channels that do not close completely when the channel is turned off.

Some of the SCN10A gene mutations result in NaV1.8 sodium channels that open more easily than usual.

The altered channels allow sodium ions to flow abnormally into nociceptors. This increase in sodium ions enhances transmission of pain signals, causing individuals to be more sensitive to stimulation that might otherwise not cause pain.

In this condition, the small fibers that extend from the nociceptors degenerate over time. The cause of this degeneration is unknown, (but see my notes below). The gradual degeneration likely accounts for signs and symptoms such as the loss of temperature differentiation and pinprick sensation. So we get increased pain signaling and a degeneration of pain-transmitting fibers. This leads to a variable condition with signs and symptoms that can change over time. (This suggests an immunological cause)

Also, other health conditions can cause this disorder:
Diabetes mellitus and impaired glucose tolerance
Fabry disease
immune disorders such as celiac disease or Sjogren syndrome
sarcoidosis
human immunodeficiency virus (HIV) infection.

Immunological destabilization of the protein subunits:
The alpha subunits of the Nav1.7 channel are affected by low energy output of the Na_K_ATPase

NAv1.7 and NAv1.8 are both modulated by the Protein Kinase A and Protein Kinase C. A down regulation of PKa and/or PKc will interfere with NAv1.8 and NAv1.8 causing the above leakages. Other research has shown dysfunction in PKc and PKa pathways in ME/CFS.

So in summary we have:
genetic differences to account for some SFN
Energetics deficits and elevated ROS and NOS which can account for the SFN
Immune/mRNA pathways which can account for the SFN.

All in all these factors can account for the 30% of FM patients who have SFN. So I am suggesting that the SFN is caused by some "known" mainly immunological disruptions in FM.

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