Sympathetic Nervous System Derangement Theory of Fibromyalgia

From Fibro Wiki
Jump to: navigation, search

This is the hypothesis that an “autonomic dysfunction may explain the multi-system features of fibromyalgia and that and that fibromyalgia is a sympathetically maintained neuropathic pain syndrome.” (Dorsal root ganglia, sodium channels, and fibromyalgia sympathetic pain. Martinez-Lavin M1, Solano C. Med Hypotheses. 2009 Jan;72(1):64-6.)

Martinez-Lavin et al. note: “Dorsal root ganglia (DRG) are potential sympathetic-nociceptive short-circuit sites. Sodium channels located in DRG (particularly Nav1.7) act as molecular gatekeepers of pain detection at peripheral nociceptors. Different infecting agents may lie dormant in DGR. Trauma or infection can induce neuroplasticity with an over-expression of sympathetic fibers and sodium channels in DRG. Nerve growth factor (NGF) mediates these phenotypic changes, which enable catecholamines and/or sympathetic impulses to activate nociceptors.”

These authors further remind us that primary erythromelalgia and paroxysmal extreme pain disorder (formerly familial rectal pain syndrome) are both rare DRG sodium "channelopathies" which are painful-dysautonomic syndromes.

Martinez-Lavin proposed “that enhanced DRG excitability may play a key role in fibromyalgia pain. Individuals at risk would be those with genetically determined sympathetic hyperactivity, or those with inherent sodium channelopathies.” They speculated that a “stressful environment may contribute to permanent sympathetic hyperactivity.”

They further speculated that trauma or infection might induce the “up-regulation” of sodium channels and “sympathetic sprouting in DRG through NGF over-expression.” In support of their theory they note that: “High levels of NGF have been reported in the cerebro-spinal fluid of FM patients. These post-traumatic (or post-infective) phenotypic changes would induce a sympathetically maintained neuropathic pain syndrome resulting in widespread pain, allodynia and paresthesias - precisely, the key clinical features of FM.” (Dorsal root ganglia, sodium channels, and fibromyalgia sympathetic pain. Martinez-Lavin M1, Solano C. Med Hypotheses. 2009 Jan;72(1):64-6.)

[Author’s comments: It is plausible that sympathetic nervous system or abnormalities contribute to fibromyalgia pain, but the sympathetic nervous system abnormalities do not at this time explain many aspects of fibromyalgia such as the associated sleep abnormalities, the onset, the many known risk factors and comorbidities.]

There is autonomic nervous system dysfunction that is consistent with sympathetic overactivity in fibromyalgia (Cited in Zamunér, 2015).

A continuous study of patients with fibromyalgia was done by Zamunér et al. As a result of their investigations they concluded that in patients “the higher the sympathetic drive to the heart and vessels, the higher the magnitude of chronic pain.”

They also found that both “cardiac and muscle sympathetic nerve activity baroreceptor control (post-ganglionic sympathetic discharge activity) were inversely related to the pain intensity.” (Relationship between sympathetic activity and pain intensity in fibromyalgia. Zamunér AR1, Barbic F2, Dipaola F2, Bulgheroni M2, Diana A3, Atzeni F4, Marchi A5, Sarzi-Puttini P6, Porta A7, Furlan R8. Clin Exp Rheumatol. 2015 Jan-Feb;33(1 Suppl 88):S53-7.)

Pain intensity was linearly correlated with a ratio of a measure of cardiac sympathetic activity (LFRR) to a measure of vagal modulation (HFRR). “Pain intensity was inversely correlated with the αLF index” which is a measure of cardiac baroreflex function. Pain was also inversely correlated with the baroreceptor modulation of the sympathetic vasomotor control (sBRS).

They concluded that: “the higher the sympathetic drive to the heart and vessels, the higher the magnitude of chronic pain.” (Zamunér et. Al. 2015)

Their final conclusion was that their findings support the “theoretical possibility” that “anti-adrenergic agents might lessen chronic pain intensity by reducing the under-lying excessive sympathetic activity”.

[Author’s comment: While they have demonstrated that this is a theoretical possibility, it seems unlikely given that we now know that there are a great many addition factors involved in fibromyalgia pain. It seems likely to the author that underlying the sympathetic nervous system changes in fibromyalgia there is a deeper layer of even more fundamental issues.]