Fibromyalgia: research update

A summary of where main-stream medicine is upto in understanding and treating Fibromyalgia

The causes of fibromyalgia are still largely unknown, but it isn’t as controversial as it used to be.

A decade ago, the condition was most often attributed to muscle and ligament problems. Many main-stream physicians declared it a psychogenic disorder (and some still do). More recently, studies have linked fibromyalgia with malfunctioning neurotransmitters, neurochemical imbalances and other neuropathic conditions.

Dr Philippe Berenger, a pain management specialist at the Cleveland Clinic say: “Today, it’s more widely accepted that fibromyalgia is primarily a neurogenic disease,” though he cautions that this “… still doesn’t explain the disease, but it’s a step forward.”

The definitions we can agree on

In 1994, the International Association for the Study of Pain (IASP) defined neuropathic pain as “initiated or caused by a primary lesion or dysfunction of the nervous system.” In 2008, the IASP’s Neuropathic Pain Special Interest Group tweaked the definition to include “disease of the somatosensory nervous system.”

Fibromyalgia fits these definitions,” says Dr. Berenger. “Although the condition has no anatomically definable lesions, it is marked by altered neurological function in the spinal cord and brain. It can, therefore, be considered a dysfunction of the central inhibitory process of pain control.”

Fibromyalgia’s link to central sensitisation

It’s clear that fibromyalgia has mechanisms and pathways associated with central sensitisation, he notes. The condition follows similar pathways as other neuropathic pain syndromes, such as complex regional pain syndrome, interstitial cystitis and irritable bowel syndrome.

All nerves in fibromyalgia patients are more sensitive than they should be — including the brain and spinal cord,” says Dr. Berenger. “Many patients have difficulty with concentration or have hypersensitivity to light, odors or sounds. Some have additional neuropathic pain syndromes or struggle with autonomic dysfunction, such as vasovagal symptoms.”

So what is “Central Sensitisation”?pho-fibro

Central sensitization has been demonstrated in animals and humans by using various triggers (e.g., mustard oil, heat, hypertonic saline injection) to activate sensory nerve cells in the skin, internal organs and muscles, that normally only respond to damage or potentially damage – and send signals to the spinal cord and brain. Sensitisation presents in various ways, here are some of the most common:

  • Tactile allodynia (that’s pain caused by touch, to you and me)

  • Hyperalgesia (increased sensitivity to pain)

  • Enhanced pressure and thermal sensitivity

  • Sensitivity spreading to neighbouring areas that are not being stimulated and even to remote regions

The increased excitability of spinal cord nerves results in sensitivity and pain lasting much longer than would normallybe the case and the areas affected by pain expanding, possibly far beyond the site of stimulation.

Newer evidence supports neurogenic claim

In 2014, researchers discovered through skin biopsy that patients with fibromyalgia had lower skin nerve fiber density than patients without fibromyalgia (1). Small fiber neuropathy, therefore, is likely another contributing factor in fibromyalgia pain — and proivdies still more evidence that the condition has neurogenic roots, notes Dr. Berenger.

What this means for treatment

Most of the drugs used today to treat fibromyalgia — like antidepressants and antiepileptics — are already focused on neurological targets,” says Dr. Berenger.

However, considering fibromyalgia as a central sensitisation disorder opens up a larger array of treatment options, he says. Agents active on the central nervous system include:

  • Sodium channel blockers

  • Calcium channel blockers

  • Serotonin-norepinephrine reuptake inhibitors (SNRI)

  • NMDA receptor antagonists

  • Nerve growth factor (NGF) inhibitors

Low-dose naltrexone is another treatment option on the horizon. One 2013 study (2) found that the drug significantly reduced pain and improved mood and general satisfaction in people with fibromyalgia. Other studies have reported similar positive responses to the drug.

Is any of it “in the mind”?

Saying that fibromyalgia is “all in the mind” isn’t entirely wrong, concludes Dr. Berenger.

Pain pathways and centres are in the brain. And we can employ techniques like mindfulness and biofeedback to control pain,” he says. “However, it’s more helpful — and accurate — to consider it a neurogenic disorder.”

Acknowledgement, links and links

To view Peak Health online’s range of Alpha-Stim products for help with fibromyalgia symptom managment, please click on the following link, which will open a new page in your web-browser: http://www.peakhealthonline.com/alpha-stim-40-c.asp

This blog post based on material provided by Consult QD, the physicians and healthcare professionals blog of Cleveland Clinic’s Department of Pain Management, to which we give grateful acknowledgement. Original source material has been edited for form and content by staff of Peak Health Online’s Well-being Library – visit us at: www.PeakHealthOnline.com

References:

(1) Caro, X. J. and Winter, E. F. (2014), Evidence of Abnormal Epidermal Nerve Fiber Density in Fibromyalgia: Clinical and Immunologic Implications. Arthritis & Rheumatology, 66: 1945–1954. doi:10.1002/art.38662

(2) Younger, J. Noor, N. McCue, R. Mackey, S. (2013) Low-dose naltrexone for the treatment of fibromyalgia; findings of a small, ramdomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels. Arthritis & Rheumatology, 65(2); 529-38. doi: 10.1002/art.37734

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