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Reflex Sympathetic Dystrophy (RSD and CRPS) Reflex Sympathetic Dystrophy (Complex Regional Pain Syndromes Type I) and Causalgia (Complex Regional Pain Syndromes Type II)(RSD and CRPS)

chronic stress and RSD (for Betsy)

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Unread 03-04-2010, 09:15 PM   #21
loretta
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Quote:
Originally Posted by fmichael View Post
Dear Betsy -

In the Lyrica thread you indicated that there was no known link between chronic stress and RSD/CRPS. I do not believe this to be the case. While in 2001, the research indicated that this was an open question, the reaearch that has been coming in since then suggests otherwise. As to the sate of the scirence in 2001, see, "Neuroimmune alterations in the complex regional pain syndrome," Frank J.P.M. Huygen, et al, European Journal of Pharmacology 429 (2001) 101-113 at 105:
Bruehl et al. reviewed the literature for evidence that psychological factors predispose certain individuals to development of complex regional pain syndrome type 1. The data reviewed are consistent with a theoretical model in which depression, anxiety, or life stressors may influence the development of complex regional pain syndrome type 1 through their effects on a-adrenergic activity. Conclusions regarding the etiological significance of these factors are not possible due to the dearth of high-quality studies
ŽBruehl and Carlson, 1992.. Psychological differences observed between complex regional pain syndrome type 1 and non-complex regional pain syndrome type 1 chronic pain patients provide partial support for the clinical assumptions that complex regional pain syndrome type 1 patients are more psychologically dysfunctional than other chronic pain patients (Bruehl et al., 1996). Stressful life events are more common in the complex regional pain syndrome type 1 patients (Geertzen et al., 1998).
Since then, however, it has been well documented that a particularlar pro-iflamatory cytokine, Interleukin 6 (IL6) is linked to RSD/CRPS. See, e.g., "Changes in Cerebrospinal Fluid Levels of Pro-inflammatory Cytokines in CRPS," Alexander GM, van Rijn MA, van Hilten JJ, Perreault MJ, Schwartzmann RJ, Pain, 2005; 116: 213-219, a copy of which can be accessed for free from the RSDSA Medical Articles Archive page at http://www.rsds.org/2/library/articl...ive/index.html, then scroll down where it's listed alphabetically by author under "Research."

Then, take a look at the following online article which is made available by the Proceedings of the National Acadamy of Sciences of the United States: "Chronic stress and age-related increases in the proinflammatory cytokine IL-6," Janice K. Kiecolt-Glaser, et al, PNAS | July 22, 2003 | vol. 100 | no. 15 | 9090-9095 and which you can freely link to here: http://www.pnas.org/cgi/content/full/100/15/9090

Here's the abstract:
Overproduction of IL-6, a proinflammatory cytokine, is associated with a spectrum of age-related conditions including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline. To describe the pattern of change in IL-6 over 6 years among older adults undergoing a chronic stressor, this longitudinal community study assessed the relationship between chronic stress and IL-6 production in 119 men and women who were caregiving for a spouse with dementia and 106 noncaregivers, with a mean age at study entry of 70.58 (SD = 8.03) for the full sample. On entry into this portion of the longitudinal study, 28 of the caregivers' spouses had already died, and an additional 50 of the 119 spouses died during the 6 years of this study. Levels of IL-6 and health behaviors associated with IL-6 were measured across 6 years. Caregivers' average rate of increase in IL-6 was about four times as large as that of noncaregivers. Moreover, the mean annual changes in IL-6 among former caregivers did not differ from that of current caregivers even several years after the death of the impaired spouse. There were no systematic group differences in chronic health problems, medications, or health-relevant behaviors that might have accounted for caregivers' steeper IL-6 slope. These data provide evidence of a key mechanism through which chronic stressors may accelerate risk of a host of age-related diseases by prematurely aging the immune response.

A growing body of evidence has implicated caregiving as a risk factor for health. Compared with noncaregivers, men and women who provide care to a spouse with a stroke or dementia report more infectious illness episodes (1), they have poorer immune responses to influenza virus and pneumococcal pneumonia vaccines (2–4), their wounds heal more slowly (5), they are at greater risk for developing mild hypertension (6, 7), and they may be at greater risk for coronary heart disease (8). Moreover, a prospective longitudinal study found that the relative risk for all-cause mortality among strained caregivers was 63% higher than noncaregiving controls (9). In this study, we provide evidence of one core pathway behind the diverse health risks associated with caregiving and other chronic stressors: overproduction of IL-6, a key proinflammatory cytokine that appears to enhance morbidity and mortality among older adults (10).

Recent medical literature has highlighted a spectrum of age-associated diseases whose onset and course may be influenced by proinflammatory cytokines, including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, Alzheimer's disease, periodontal disease, and frailty and functional decline. The link to cardiovascular disease, the leading cause of death, has attracted the greatest attention; the association with IL-6 is related in part to the central role that this cytokine plays in promoting the production of C-reactive protein (CRP), an important risk factor for myocardial infarction (10–12). For example, high concentrations of CRP predicted the risk of future cardiovascular disease in apparently healthy men (12).

CRP and IL-6 have other important health consequences in addition to their role in cardiovascular disease. Elevated levels of CRP and IL-6 predicted the development of type 2 diabetes in a 4-year follow-up period in healthy women after adjustments for key risk factors; among women in the highest vs. lowest quartiles, the relative risk for developing diabetes was 7.5 for IL-6 and 15.7 for CRP (13). In another study, elevated serum IL-6 levels predicted future disability in older adults, a finding that may reflect the effects of the cytokine on muscle atrophy, and/or the pathophysiologic role played by the cytokine in particular diseases (14). Proinflammatory cytokines, including IL-6, may slow muscle repair after injury and accelerate muscle wasting (15); indeed, IL-6 and CRP also play a pathogenic role in a range of diseases associated with disability among the elderly (osteoporosis, arthritis, and congestive heart failure, among others) (14).

Production of IL-6 and other proinflammatory cytokines can be directly stimulated by depression and other negative emotions and stressful experiences (16–20). Indeed, both physical and psychological stressors can provoke transient increases in proinflammatory cytokines (21, 22). Additionally, negative emotions contribute to greater risk for infection, prolonged infection, and delayed wound healing (1–5), all processes that can fuel sustained proinflammatory cytokine production. Thus, stressors can directly affect the cells of the immune system and modulate the secretion of proinflammatory cytokines. Accordingly, we argue that distress-related immune dysregulation may be one central mechanism behind a large and diverse set of health risks associated with caregiving and other chronic stressors. In this study, we tested the hypothesis that caregivers would show a steeper increase in IL-6 levels over time than noncaregiving controls. Additionally, we assessed the question of whether the cessation of caregiving would have beneficial consequences for IL-6 levels.
Here's another freely available article, tending in the same direction, "Cytokine Dysregulation, Inflammation and Well-Being," Ilia J. Elenkov, et al, Neuroimmunomodulation 2005;12:255-269 (DOI: 10.1159/000087104) and freely available at http://content.karger.com/ProdukteDB...tentOnly=false. In any event, here's the abstract from that one:
Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor- and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
I hope you will agree that this is an exciting area of research.

That said, there is, I believe, also further lierature that ties chronic stress levels to the incidence if RSD at the time the underling physical injury was sustained. I will post it as soon as I can locate it. Nevertheless, the foregoing is a start.

Mike
Hi Mike, I totally agree with connection of high stress and it's timing with the incidence of us getting RSD thru injury, surgery, etc. We had a survey pole on NT a year or so ago asking this question. There was a definite higher percentage of those getting RSD at the time of the surgery or incidence and being under high stress.
I'll be 62 in May and lost my health insurance. I'm going to apply for SSDI. I've had it 15 years and have my Drs. support. I've been hospitalized with it and on several meds. I have it full body, generalized now and internal pelvic area. Also have trigeminal nerve disorder, fibromyalgia, and PTSD. Now checking out sleep apnea or grasping for air day and night. Any suggestions would be appreciated. I've never applied for anything before and kinda clueless. My RSD followed surgery, but wasn't diagnosed for 4 years, No legal litigation in my background with RSD. Thanks Mike, Hope all goes well with you in this. Your friend, loretta with big hugs
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Unread 03-05-2010, 12:12 AM   #22
bobber
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Ive been told by several Dr's that people who are more high stressed or high anxiety are prone to Contract RSd with or without an injury,,with that staement I concur,,,,plus as Ive been told,,," The Fewer The Words, The More Powerfull The Statement" .
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