Central Sensitization Theory of Fibromyalgia

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Central sensitization/Central sensitivity as the dominant current theory of fibromyalgia as of 2020[edit]

The dominant current theory as of 2017 is that fibromyalgia is a disorder that is due to central sensitization involving brain changes that cause it to be overreactive to sensory stimuli, especially mechanical pain and this result in tenderness.

Supporters of this theory note that patients are clinically oversensitive to mechanical pain and other pain stimuli. [Author’s comment: Perhaps there is a weakness in their stimulus barrier and they lack the normal abilities to block out and not overreact to sensory stimuli.]

Staud et al. state: “Many recent fibromyalgia studies have demonstrated central nervous system (CNS) pain processing abnormalities, including abnormal temporal summation of pain. In the CNS, persistent nociceptive input from peripheral tissues can lead to neuroplastic changes resulting in central sensitization and pain. This mechanism appears to represent a hallmark of fibromyalgia and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established, only minimal peripheral input is required for the maintenance of the chronic pain state.” (Psycho-physical and neurochemical abnormalities of pain processing in fibromyalgia. Staud R1, Spaeth M. CNS Spectr. 2008 Mar;13(3 Suppl 5):12-7.)

A review paper by Cagnie et al. in 2014 found that there was “moderate evidence for region-specific changes in gray matter volume, a decreased functional connectivity in the descending pain-modulating system, and an increased activity in the pain matrix related to central sensitization.” (Central sensitization in fibromyalgia? A systematic review on structural and functional brain MRI. Cagnie B1, Coppieters I2, Denecker S2, Six J2, Danneels L2, Meeus M3. Semin Arthritis Rheum. 2014 Aug;44(1):68-75.)

Fleming’s description of central sensitization[edit]

Here is Fleming et al.’s description of central sensitization from their article on its role in fibromyalgia: “Central sensitization can be defined as a state in which the central nervous system amplifies sensory input across many organ systems. This enhanced response to sensation includes plasticity at a neuronal level that increases sensitivity for future stimulation. Heightened sensitivity results in the perception of pain from non-painful stimuli (allodynia) and greater pain than would be expected from painful stimuli (hyperalgesia). Prominent visceral hypersensitivity can affect every organ system and produce intolerable discomfort. Ultimately, all of these amplified sensations, which range from the arthralgias and myalgias of FM, to headaches, abdominal complaints, and pelvic concerns, may constitute an initial presentation of CS as MUS.8,14” (Central Sensitization Syndrome and the Initial Evaluation of a Patient with Fibromyalgia: A Review. Kevin C. Fleming, M.D.1,* and Mary M. Volcheck, R.N.2Rambam Maimonides Med J. 2015 Apr; 6(2): e0020. This is an open-access article. All its content, except where otherwise noted, is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.)

[Author’s comment: The claim that every organ can be affected may be an exaggeration. Many organs, such as the spleen probably have not been studied. Nonetheless, a number of organs have been implicated in central sensitization, including the bowels and the urinary system. It is noteworthy the irritable bowel syndrome and interstitial cystitis are commonplace in fibromyalgia patients]

Fleming et al. state: “On a cellular level, CS results from multiple processes altering the functional status of nociceptive neurons. These processes include increases in membrane excitability, facilitation of synaptic strength, and decreases in inhibitory transmission (disinhibition). Affected neurons display spontaneous activity, reduced activation threshold, and enlarged receptive fields. Hypersensitivity amplifies the sensory response elicited by normal inputs such as innocuous stimuli and normal body sensations. Perceptions may no longer be coupled to the intensity, duration, or even the presence of noxious peripheral stimuli. And yet, CS results in changes in brain activity that can be detected by functional magnetic resonance or positron emission tomographic imaging and electro-physiologic studies. In this paper, we will focus on FM, which is an archetypal presentation of CS.” (Fleming et al. 2015)

Pain reflex abnormalities in fibromyalgia[edit]

Based on extensive unpublished experience by the author during the examination of normal controls and fibromyalgia patients, it was found that fibromyalgia patients, especially those that are seriously ill, have numerous exaggerated withdrawal reflexes. These examinations gave the strong clinical impression that the body has a separate withdrawal reflex for every tender point. Withdrawal reflexes are a clinical sign of over-relativity. They seem to be an indicator of central sensitization.

In one study, nociceptive flexion reflex was induced by applying cutaneous electrodes so as to stimulate the sural nerve in its retromaleolar track with an electrical stimulus. The stimulus was a set of “single rectangular impulses (0.5 msec) delivered with 6–10 second interstimulus interval, by a constant current stimulator at variable intensities (1–100 mA)”. It was delivered using a Nicolet Viking IV. (As of 2014, newer models may have superseded this, so parties interested in performing the RIII reflex should contact the manufacturer.) (Neurophysiologic evidence for a central sensitization in patients with fibromyalgia. Desmeules JA1, Cedraschi C, Rapiti E, Baumgartner E, Finckh A, Cohen P, Dayer P, Vischer TL. Arthritis Rheum. 2003 May;48(5):1420-9, available online at: https://docslide.net/documents/neurophysiologic-evidence-for-a-central-sensitization-in-patients-with-fibromyalgia.html )

Limitations and Benefits of the Central Sensitization Theory of Fibromyalgia[edit]

The theory has been very useful to help understand reactivity. It has pointed the way to clinicians as to the need to assess their fibromyalgia patients for multiple types. For example, migraine is extremely common in fibromyalgia and photophobia and sonophobia are cardinal symptoms of migraine and the are forms of over-reactivity.

The main limitation is that the theory does not explain why patients are oversensitive, nor does it offer a clear path as to what to do about it.

For further information on central sensitization and fibromyalgia[edit]

Psychosocial factors and central sensitivity syndromes. Adams LM, Turk DC1. Curr Rheumatol Rev. 2015;11(2):96-108, available in full online at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728142/. For a diagram that shows their biopsychosocial approach see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728142/figure/F1/.

Fibromyalgia: the prototypical central sensitivity syndrome. Boomershine CS1. Curr Rheumatol Rev. 2015;11(2):131-45.

How to explain central sensitization to patients with 'unexplained' chronic musculoskeletal pain: practice guidelines. Nijs J1, Paul van Wilgen C, Van Oosterwijck J, van Ittersum M, Meeus M. Man Ther. 2011 Oct;16(5):413-8.

The Central Sensitization Inventory (CSI): establishing clinically significant values for identifying central sensitivity syndromes in an outpatient chronic pain sample.

Neblett R1, Cohen H, Choi Y, Hartzell MM, Williams M, Mayer TG, Gatchel RJ. J Pain. 2013 May;14(5):438-45. (Here is a link to the inventory: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248986/#APP1.)