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

Yeah, that's not exactly what I meant. I clearly stated that stress may *contribute* to disease. My point was that it is not the ONLY factor.

Joan, probably not meaning to imply this, said that stress "converts to RSD." That's just not true. Stress may (in some or maybe even most cases) contribute to the incitement of RSD, but I don't think anybody will argue that a person under stress will just suddenly one day get RSD.

When I write these posts, I write exactly what I mean, and I attempt to qualify each statement I make. I was unaware of this study, and perhaps this will teach me to be a bit more cautious in the future. However, the gist of what I said still stands: stress is sometimes (not necessarily always) one of many factors that must be taken into account when determining the causes of RSD.

And, as I said, I'd like to meet a person who has no chronic stress in his or her life. In 25 years, I've never met any. Stress is too general a term to be used in such complex discussions of pathophysiology.

This is a facinating topic. Especially for the chicken-or-the-egg implications. For another full test article I just found online, check out NEUROBIOLOGY OF THE STRESS RESPONSE: CONTRIBUTION OF THE SYMPATHETIC NERVOUS SYSTEM TO THE NEUROIMMUNE AXIS IN TRAUMATIC INJURY [Review Article], Molina, Patricia E, Shock:Volume 24(1)July 2005 pp 3-10, which you can link to here: http://www.shockjournal.com/pt/re/sh...195628!8091!-1. Here"s the abstact:

Acute injury produces an immediate activation of neuroendocrine mechanisms aimed at restoring hemodynamic and metabolic counter-regulatory responses. These counter-regulatory responses are mediated by the systemic and tissue-localized release of neuroendocrine-signaling molecules known to affect immune function. This has led to the recognition of the importance of neuroendocrine-immune modulation during acute injury as well as throughout the recovery period. The period immediately after acute injury is characterized by upregulation of proinflammatory cytokine expression leading to a later period of generalized immunosuppression. The course and progression of the host recovery from traumatic injury and the integrity of its response to a secondary challenge is directly related to the effective control of the immediate proinflammatory responses to the initial insult. Among the neuroendocrine mechanisms involved in restoring homeostasis, the sympathetic nervous system plays a central role in mediating acute counter-regulatory stress responses to injury. In addition to its recognized cardiovascular, hemodynamic, and metabolic effects, the neurotransmitters released by the sympathetic nervous system have been shown to affect immune function through specific adrenergic receptor-mediated pathways. In turn, cells of the immune system and their products have been shown to influence peripheral and central neurotransmission, leading to the conceptualization of a bidirectional neuroimmune communication system. The reflex activation of this bidirectonal neuroimmune pathway in response to injury, integrated with the parasympathetic nervous system, and opioid and glucocorticoid pathways responsible for orchestrating the counterregulatory stress response, results in dynamic regulation of host defense mechanisms vital for immune competence and tissue repair. This review provides the biological framework for the integration of our understanding of the neuroendocrine mechanisms involved in mediating the stress response and their role in modulating immune function during and after traumatic injury.

It's a good article. I would urge anyone to check it out.

Mike

Yeah, it really is a question of what comes first. They only test for things like proinflammatory cytokines after someone gets RSD (or something else), and then speculation can begin about what is causing what (is the stress causing the inflammatory response or vice-versa?)

If they could predict who would get RSD, I think this would all be explained...except the same question applies, because in order to predict that phenomenon, I believe we must know the true cause of RSD. I think we all know that nobody's proven that yet, although there are a lot of theories. With Mike and Vicc on the case, who knows...

I'm glad you're having fun with this, Mike...I suppose it's a good discussion to have, but it's kind of stressing me out (ha-ha).

-Betsy

i said in the lyrica thread:

"Type A personalities, i believe, from what i have read,that because a person is already stressing themselves, even if it is in a good and positive way, it is still stress, the chance of the overstress and conversion to rsd is more possible."

i did not say stress CONVERTS to rsd.

i was simply being part of a conversation and stating what i had read many times in many different sites.
this is what i get so frustrated about, when people make a big deal about words, and they are misquoted words at that.
so if you are making a point use your own words and please either quote me or don't refer to my posting. joan

"A 2 1/2-year-old girl with reflex sympathetic dystrophy syndrome (CRPS type I): case report," F Güler-Uysal et al, Clinical Rehabilitation 2003; 1 7: 224–227 (attached) (report of a 2 1/2-year-old girl was presented for treatment by her relatives, declaring that she could not use her left hand and resisted even the touch of anyone who attempted to examine it for the last three months; patient had experienced the Marmara earthquake in Turkey in August 1999 and had been rescued after 12 hours of being trapped under the ruins; her parents had died during the same disaster and she was being followed by the Paediatric Psychiatry Clinic with diagnoses of non-organic failure to thrive and acute stress disorder).

The article also sites another piece for which I could only get an abstract:

"Stressful life events and psychological dysfunction in Complex Regional Pain Syndrome type I.," Geertzen JH, de Bruijn-Kofman AT, de Bruijn HP, van de Wiel HB, Dijkstra PU, Clin J. Pain, 1998 Jun;14(2):143-7:

OBJECTIVE: To determine to what extent stressful life events and psychological dysfunction play a role in the pathogenesis of Complex Regional Pain Syndrome type I (CRPS). DESIGN: A comparative study between a CRPS group and a control group. Stressful life events and psychological dysfunction evaluation was performed with a life event rating list and the Symptom Checklist-90 (SCL-90). SETTING: A university hospital. SUBJECTS: The CRPS group consisted of 24 patients with a history of upper extremity CRPS of less than 3 months. The control group consisted of 42 hand pathology patients waiting for elective hand surgery within the next 24 hours. MAIN OUTCOME MEASURES: Stressful life event rating was measured using the Social Readjustment Rating Scale. Psychological dysfunction was measured using the SCL-90. RESULTS: Stressful life events were experienced by 19 patients (79.2%) in the CRPS group and by 9 patients (21.4%) in the control group. This difference was significant. Testing of psychological dysfunction (SCL-90) in CRPS patients and the control group demonstrated some significant differences: male patients were more anxious than male controls; female patients were statistically more depressed, had feelings of inadequacy, and were emotionally less stable than female controls. In multivariate analysis, no significant differences were found across gender, age, or gender x group interactions. Of the SCL-90 dimensions, only insomnia correlated with the experienced stressful life events. CONCLUSION: Stressful life events are more common in the CRPS group, which indicates that there may be a multiconditional model of CRPS. The experience of stressful life events besides trauma or surgery are risk factors, not causes, in such a model.

Mike

Attached Files

A two and one half year old girl with reflex sympathetic dystrophy . . . case report.pdf (98.5 KB, 154 views)

"Hostile Marital Interactions, Proinflammatory Cytokine Production, and Wound Healing," Janice K. Kiecolt-Glaser, PhD; Timothy J. Loving, PhD; Jeffrey R. Stowell, PhD; William B. Malarkey, MD; Stanley Lemeshow, PhD; Stephanie L. Dickinson, MAS; Ronald Glaser, PhD, Arch Gen Psychiatry. 2005;62:1377-1384 [free full text at: http://archpsyc.ama-assn.org/cgi/con...ull/62/12/1377]:

ABSTRACT

Context A growing epidemiological literature has suggested that marital discord is a risk factor for morbidity and mortality. In addition, depression and stress are associated with enhanced production of proinflammatory cytokines that influence a spectrum of conditions associated with aging.

Objective To assess how hostile marital behaviors modulate wound healing, as well as local and systemic proinflammatory cytokine production.

Design and Setting Couples were admitted twice to a hospital research unit for 24 hours in a crossover trial. Wound healing was assessed daily following research unit discharge.

Participants Volunteer sample of 42 healthy married couples, aged 22 to 77 years (mean [SD], 37.04 [13.05]), married a mean (SD) of 12.55 (11.01) years.

Interventions During the first research unit admission, couples had a structured social support interaction, and during the second admission, they discussed a marital disagreement.

Main Outcome Measures Couples’ interpersonal behavior, wound healing, and local and systemic changes in proinflammatory cytokine production were assessed during each research unit admission.

Results Couples’ blister wounds healed more slowly and local cytokine production (IL-6, tumor necrosis factor , and IL-1) was lower at wound sites following marital conflicts than after social support interactions. Couples who demonstrated consistently higher levels of hostile behaviors across both their interactions healed at 60% of the rate of low-hostile couples. High-hostile couples also produced relatively larger increases in plasma IL-6 and tumor necrosis factor values the morning after a conflict than after a social support interaction compared with low-hostile couples.

Conclusions These data provide further mechanistic evidence of the sensitivity of wound healing to everyday stressors. Moreover, more frequent and amplified increases in proinflammatory cytokine levels could accelerate a range of age-related diseases. Thus, these data also provide a window on the pathways through which hostile or abrasive relationships affect physiological functioning and health.

Mike

Mike,

This entire thread is unfair to Betsy. She presented her views (which have strong scientific support), on why she doesn't think stress plays a significant role in the onset of RSD, and you come back with thousands of words in med-speak that she can't even understand, what can she say? She certainly doesn't have the education or experience to debate an attorney.

How do I know this? Because I have spent ten years researching RSD, and prior to that earned degrees is both psychology and social work, and I can't even figure out what some of those articles are saying. But I can say they have nothing to do with pathopsychology and RSD..

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

Ok I can figure that one out, and it is on-topic, but what does it say? I don't believe I'm far off in assuming that if Betsy had had the benefit(?) of my particular education she might well have said:

There are such significant differences between RSD pain and other types of chronic pain (like ours isn't controlled by opiates), and such profound differences in interactions with pshycians who know something about normal chronic pain as opposed to than number which can't even spell RSD, that its easier to think we're crazy; especially if that's what you set out to prove.

Here is a comparison between us and so many other severely disabled people in the world:

Their disability is usually visible -- and often disturbing, and natural human reactions to them could run the gamut from revulsion to sympathy to empathy to concern to total pity.

Ours is often invisible or is barely visable and natural human reactions are almost unversal: Why is that ***** using a handicapped parking space?

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).

What does this mean and how does it apply to RSD? What does an abstract about.... stress while watching someone you have loved for almost half a century disintegrate in front of you; while you drive yourself beyond exhaustion in order to keep your beloved out of a nursing home; and all the while knowing you won't win....have to do with the day to day stress we experienced before RSD?

And if you're going to argue that we were more stressed than "normal" people, give us some research proving typical RSD patients were.

I could have equally dismissed the other abstracts you used as equally irrelevant to a discussion of some sort of psychological predisposition toward RSD, but I didn't bother reading them. The literature is overwhelming on this: There are no known or suspected psychological factors in the etiology of RSD.

Any research relevant to this topic must include both RSD AND a psychological instrument (test, study, etc). If it isn't talking specifically about RSD and psychology, then it isn't talking about what we're talking about here.

If you disagree with Betsy, give reasons why you believe stress plays a role in the onset of this disease. Please don't overwhelm those you disagree with, with a bunch of words that none of us understand. That is not -- in my view -- informational or supportive...Vic

Dear Vicc and Betsy -

I certainly didn't mean to overwhelm Betsy, and my most sincere apologies if I did. One of the things that writing as a lawyer taught me to do was to string quotations together, where the reader would then rely on the quotation itself in order to understand what was being communicated. If I failed in that regard, my apologies again. But I don't believe - and take some umbrage with the suggestion - that the entire thread is unfair to her. I will attemp to explain why.

In simple terms, let's start with the article on "Hostile Marital Interactions, Proinflammatory Cytokine Production, and Wound Healing," stressful events in peoples lives can interfere with immunological responses, to the point of effecting the closure of wounds. And as a side-note, let me also add the following study:

"Marital conflict in older adults: endocrinological and immunological correlates," Kiecolt-Glaser JK, Glaser R, Cacioppo JT, MacCallum RC, Snydersmith M, Kim C, Malarkey WB, Psychosom Med., 1997 Jul-Aug; 59(4): 339-49:

OBJECTIVE: To assess endocrinological and immunological correlates of marital conflict and marital satisfaction, 31 older couples (mean age 67 years) who had been married an average of 42 years were studied. METHOD: Couples were admitted to the Clinical Research Center and a catheter was placed in each subject's arm. Blood was drawn on entry for immunological assays; for hormone analyses, five blood samples were drawn during a 30-minute conflict discussion and a 15-minute recovery session. The conflict session was recorded on videotapes that were later coded for problem-solving behaviors using the Marital Interaction Coding System (MICS). RESULTS: Among wives, escalation of negative behavior during conflict and marital satisfaction showed strong relationships to endocrine changes, accounting for 16% to 21% of the variance in the rates of change of cortisol, adrenocorticotropic hormone (ACTH), and norepinephrine (but not epinephrine). In contrast, husbands' endocrine data did not show significant relationships with negative behavior or marital quality. Both men and women who showed relatively poorer immunological responses across three functional assays (the blastogenic response to two T-cell mitogens and antibody titers to latent Epstein-Barr virus) displayed more negative behavior during conflict; they also characterized their usual marital disagreements as more negative than individuals who showed better immune responses across assays.

CONCLUSION: Abrasive marital interactions may have physiological consequences even among older adults in long-term marriages.

(I will be happy to email the full text of this one to anyone who wants it, just send me a PM with your email address.)

Now consider my insertion of the full text of "A 2 1/2-year-old girl with reflex sympathetic dystrophy syndrome (CRPS type I): case report," an anecdotal report of RSD following extreme stress, and a "plain language" discussion of the literature tying stress to RSD. Perfectly appropriate? I think so.

Then we get to the thrust of my argument, and here's where the science cuts in. I'll try to be as clear as possible. In "Chronic stress and age-related increases in the proinflammatory cytokine IL-6," Janice K. Kiecolt-Glaser, et al, PNAS, etc., the authors established that depression/stress by themselves could increase the levels of C-reactive proteins and IL6 (remember the article about wound healing and marital stress). And then we have the Schwartzman piece showing high levels of IL6 in the spinal fluids of CRPS patients. Which is if course a direct tie-in to not only the Turkish study on the 2 and 1/2 year old girl, but also the abstract of the one small study that's looked at the issue directly "Stressful life events and psychological dysfunction in Complex Regional Pain Syndrome type I.," Geertzen JH, de Bruijn-Kofman AT, de Bruijn HP, van de Wiel HB, Dijkstra PU, Clin J. Pain, 1998 Jun;14(2):143-7:

OBJECTIVE: To determine to what extent stressful life events and psychological dysfunction play a role in the pathogenesis of Complex Regional Pain Syndrome type I (CRPS). DESIGN: A comparative study between a CRPS group and a control group. Stressful life events and psychological dysfunction evaluation was performed with a life event rating list and the Symptom Checklist-90 (SCL-90). SETTING: A university hospital. SUBJECTS: The CRPS group consisted of 24 patients with a history of upper extremity CRPS of less than 3 months. The control group consisted of 42 hand pathology patients waiting for elective hand surgery within the next 24 hours. MAIN OUTCOME MEASURES: Stressful life event rating was measured using the Social Readjustment Rating Scale. Psychological dysfunction was measured using the SCL-90. RESULTS: Stressful life events were experienced by 19 patients (79.2%) in the CRPS group and by 9 patients (21.4%) in the control group. This difference was significant. Testing of psychological dysfunction (SCL-90) in CRPS patients and the control group demonstrated some significant differences: male patients were more anxious than male controls; female patients were statistically more depressed, had feelings of inadequacy, and were emotionally less stable than female controls. In multivariate analysis, no significant differences were found across gender, age, or gender x group interactions. Of the SCL-90 dimensions, only insomnia correlated with the experienced stressful life events. CONCLUSION: Stressful life events are more common in the CRPS group, which indicates that there may be a multiconditional model of CRPS. The experience of stressful life events besides trauma or surgery are risk factors, not causes, in such a model.

The evidence shows that (1) stress and depression can, without any other intervening variable, trigger the development of pro-inflamatory cytokines, (2) the same stress/depression significantly interferes with the normal functioning of the immune system, (3) pro-inflammatory cytokines are "associated" with CRPS and (4) there are at least two reports - the Turkish study and the Geertzen article - that begin to go to the direction of the causal link between "stress" and RDS/CRPS. But all that said, if anyone won't even read the materials I've included because they don't agree with the conclusions, then there's not much I can say.

Finally, I will grant that there may be a piece of the chain that could be filled in here or there, but overall, I see the evidence as powerful. And that and that alone was the point I was trying to make.

Mike

A somewhat "off-topic" post-script: This is one reason why I am a booster of utilizing "Mindfulness Based Stress Reduction", e.g. meditation and body awareness, for people with RSD: on the theory that if stress plays a role in the onset of the disease, perhaps reducing the stress will keep the disease in check. Of course, even if it doesn't work directly on the disease - and I won't warrant that it does - there are always the mindfulness and equinimity components, which do in fact "work" from my personal experience.

Hi Mike,


Thanks for your post,
I had long rejected the fact that I may have any type of predisposition that made me more likely to succumb to RSD following my accident.
It seemed to me that it in some way implied that there may have been something in my power that could have prevented it but I have tried to absolve myself of that responsibility as it is just to great a burden to carry.
It does seem however that there is something in this type A personality hypothesis as I do recognise many whom I would imagine fit that description amongst us (myself included)
My life before RSD was wonderful, I thought it could never be better but in hindsight I lived a life of permanent stress trying to balance being a wife, mother of 6, a full time highly stressful job and various community services.
My conclusion is that stress may not have been the cause of my RSD (jury still out on that one) but I do believe it has definitely impacted the outcome .
Cheers to all
Tayla