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Chronic Pain As A Cause Of Ans Dysfunction


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http://www.prohealth.com/library/showarticle.cfm?libid=16778

Article:

Induction of chronic non-inflammatory widespread pain increases cardiac sympathetic modulation in rats

- Source: Autonomic Neuroscience, Jan 21, 2012

By LR Oliveira, VJ Santana-Filho, et al.

[Note: The autonomic nervous system works below the level of consciousness to maintain the body’s balance – regulating blood pressure, pulse, breathing rates, etc. as needed in response to changing physical demands. Two parts of the system are sympathetic function, which involves ‘pushing’, balanced by parasympathic function, which involves relaxing. One type of autonomic dysregulation is when heart rate increases and blood pressure/volume decreases abnormally on standing, causing faint feeling (postural orthostatic tachycardia syndrome - POTS).]

Abstract:

Fibromyalgia (FM) is characterized by chronic non-inflammatory widespread pain (CWP) and changes in sympathetic function. In attempt to elucidate the pathophysiological mechanisms of FM we used a well-established CWP animal model.

We aimed to evaluate changes in cardiac autonomic balance and baroreflex function in response to CWP induction in rats. [baroreflex function refers to the body’s mechanism for maintaining blood pressure.] CWP was induced by two injections of acidic saline (pH 4.0, n=8) five days apart into the left gastrocnemius muscle. Control animals were injected twice with normal saline (pH 7.2, n=6).

One day after the second injection of acidic saline or normal saline, the animals had pulse interval (PI) and systolic arterial pressure (SAP) variability, and spontaneous baroreflex sensitivity (BRS) evaluated.

After induction of CWP, there was an increase of power in the low frequency (LF) band of PI spectrum (12.75±1.04nu), a decrease in the high frequency (HF) band (87.25±1.04nu) and an increase of LF/HF ratio (0.16±0.01), when compared to control animals (7.83±1.13nu LF; 92.16±1.13nu HF; 0.08±0.01 LF/HF).

In addition, there was an increase of power in the LF band of SAP spectrum (7.93±1.39mmHg(2)) when compared to control animals (2.97±0.61mmHg(2)). BRS was lower in acidic saline injected rats (0.59±0.06ms/mmHg) when compared to control animals (0.71±0.03ms/mmHg).

Our results showed that induction of chronic widespread pain in rats shifts cardiac sympathovagal balance towards sympathetic [pushing] predominance and decreases BRS [blood pressure/flow]. These data corroborate findings in humans with FM.

Source: Autonomic Neuroscience, Jan 21, 2012. Department of Physiology, Federal University of Sergipe, Sao Cristovao, Brazil; Graduate Program in Physical Therapy and Rehabilitation Science, University of Iowa, Iowa City, USA. [Email: visf@infonet.com.br]

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http://www.ncbi.nlm....pubmed/20428906

Abnormal overexpression of mastocytes in skin biopsies of fibromyalgia patients

Clin Rheumatol. 2010 Dec;29(12):1403-12. Epub 2010 Apr 30.

Blanco I, Béritze N, Argüelles M, Cárcaba V, Fernández F, Janciauskiene S, Oikonomopoulou K, de Serres FJ, Fernández-Bustillo E, Hollenberg MD.

Source

Department of Internal Medicine, Valle del Nalón Hospital, 33920 Langreo, Principado de Asturias, Spain. ignablanco@yahoo.com

Abstract

Formalin-fixed, paraffin-embedded skin tissue sections were collected from a matched cohort of 63 fibromyalgia syndrome (FMS) patients and 49 volunteers from the general population with both alpha1-antitrypsin (AAT) normal and deficiency variants. These tissues were examined for the expression of the broad-spectrum inhibitor AAT, the serine proteinases elastase and tryptase, the proinflammatory cytokines MCP-1 and TNFα, the endothelium biomarker VEGF, and the inflammation/nociception-related receptor PAR(2). The most relevant finding of the study was a significantly increased number of mast cells (MCs) in the papillary dermis of all FMS patients (greater than or equal to five to 14 per microscopic high power field) compared to zero to one in controls (p < 0.001). MCs strongly stained with tryptase, AAT and PAR(2) antibodies, exhibited a spindle-like shape and were uniformly distributed around blood vessels and appendages. MCP-1 and VEGF expressed weak/moderate positivity in most samples, with a higher expression in controls than in FMS patients (p < 0.001 and 0.051, respectively). No differences in elastase and TNFα were found between both groups. Moreover, no histological differences were found between samples from AAT deficiency and normal AAT phenotypes. Our results indicate that FMS is a MC-associated condition. MCs are present in skin and mucosal surfaces throughout the human body, and are easily stimulated by a number of physical, psychological, and chemical triggers to degranulate, releasing several proinflammatory products which are able to generate nervous peripheral stimuli causing CNS hypersensitivity, local, and systemic symptoms. Our findings open new avenues of research on FMS mechanisms and will benefit the diagnosis of patients and the development of therapeutics.

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http://www.prohealth...cfm?libid=16778

Article:

Induction of chronic non-inflammatory widespread pain increases cardiac sympathetic modulation in rats

- Source: Autonomic Neuroscience, Jan 21, 2012

By LR Oliveira, VJ Santana-Filho, et al.

[Note: The autonomic nervous system works below the level of consciousness to maintain the body’s balance – regulating blood pressure, pulse, breathing rates, etc. as needed in response to changing physical demands. Two parts of the system are sympathetic function, which involves ‘pushing’, balanced by parasympathic function, which involves relaxing. One type of autonomic dysregulation is when heart rate increases and blood pressure/volume decreases abnormally on standing, causing faint feeling (postural orthostatic tachycardia syndrome - POTS).]

Abstract:

Fibromyalgia (FM) is characterized by chronic non-inflammatory widespread pain (CWP) and changes in sympathetic function. In attempt to elucidate the pathophysiological mechanisms of FM we used a well-established CWP animal model.

We aimed to evaluate changes in cardiac autonomic balance and baroreflex function in response to CWP induction in rats. [baroreflex function refers to the body’s mechanism for maintaining blood pressure.] CWP was induced by two injections of acidic saline (pH 4.0, n=8) five days apart into the left gastrocnemius muscle. Control animals were injected twice with normal saline (pH 7.2, n=6).

One day after the second injection of acidic saline or normal saline, the animals had pulse interval (PI) and systolic arterial pressure (SAP) variability, and spontaneous baroreflex sensitivity (BRS) evaluated.

After induction of CWP, there was an increase of power in the low frequency (LF) band of PI spectrum (12.75±1.04nu), a decrease in the high frequency (HF) band (87.25±1.04nu) and an increase of LF/HF ratio (0.16±0.01), when compared to control animals (7.83±1.13nu LF; 92.16±1.13nu HF; 0.08±0.01 LF/HF).

In addition, there was an increase of power in the LF band of SAP spectrum (7.93±1.39mmHg(2)) when compared to control animals (2.97±0.61mmHg(2)). BRS was lower in acidic saline injected rats (0.59±0.06ms/mmHg) when compared to control animals (0.71±0.03ms/mmHg).

Our results showed that induction of chronic widespread pain in rats shifts cardiac sympathovagal balance towards sympathetic [pushing] predominance and decreases BRS [blood pressure/flow]. These data corroborate findings in humans with FM.

Source: Autonomic Neuroscience, Jan 21, 2012. Department of Physiology, Federal University of Sergipe, Sao Cristovao, Brazil; Graduate Program in Physical Therapy and Rehabilitation Science, University of Iowa, Iowa City, USA. [Email: visf@infonet.com.br]

It's funny, about 4 years ago when I began having the symptoms of near syncope/neurocardiogenic syncope--before pursuing cardiologist--I'd asked my rheume (I have fibro--osteoarthritis and pain 24/7 where glutteal muscles + tendon were avulsed off my hip bone in 2004 that was still not yet found at that time, plus EDS) if the constant pain in such a big joint could be stressing something since it is 24/7 except for when I get what little sleep I get? She said it had no bearing. Nothing has ever touched the pain (including RFA) so it's something I just tolerate as best I can using Lidoderm patches sparingly (due to high copays/authorization mandates--and I don't see the interventional radiologist who Rx'd them anymore and my ortho is readying to retire), Therma Care wraps or heating pad. I've always known there must be a link as things seemed to turn south since that happened.

Thanks for posting.

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