Hi everyone, I have been interested in doing pain medicine for a long time, and am strongly considering applying into it. However, I fear that with all of the changes that are going on in terms of private practices shutting down and more CRNA's being hired over MDs, I'm worried about job prospects if I choose to go the Anes-Pain route. I would like to believe that anesthesiologists have a skill set that is unique, but will the market reflect that? Thanks!
Market Desirability of Skills: Projections
- Thread starter Lolito
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Go with your passion, live below your means, and enjoy your life. All of medicine is turning to stool so you might as well enjoy what you are doing.
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Medicine will always need people who are able to treat pain and can do procedures; whether and what you get paid for them is a whole 'nother question.
The medical field has already accepted that CRNAs can do a lot of the same things anesthesiologists can do, but not everything... draw your own conclusions.
The medical field has already accepted that CRNAs can do a lot of the same things anesthesiologists can do, but not everything... draw your own conclusions.
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I'd go with crossbow skills...
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It is a skill set that is unique. It's just that, when it comes to chronic pain management, procedures are (and will continue to be) increasingly less emphasized.
Procedures, narcotics, and fee for service down. Psyche, patient education and self care up.
Plus, it doesn't help that most of the procedures work "kind of", and work "some of the time".
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I followed a dermatologist once. For some reason this derm's practice was almost 100% hemorrhoid management. It was like 40 dirty asses I looked at that day and I couldn't figure out why derm was so popular. Somehow that is related to this thread...
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They can "de-epmphasize" procedures all they want.
Have we been withholding the magic non-procedural therapy from our patients that will cure them once and for all? No?
The problems our patients present with will persist because they aren't easy to treat, and certainly not with non-procedural medicine.
We will still be faced with frustrated patients who tell us "look, I gotta do somethin' 'cause...."
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Get your x-waiver and be prepared to use it in a combined pain/addiction setting.
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1) Ignore 101N
2) The population is aging
3) Neck and back pain are not getting any less prevalent
4) If the right doctor performs the right procedure on the right patient, our stuff works almost all the time.
Physicians have been complaining about decreasing revenue since the implementation of Medicare. Yet remarkably, many of the folks on this board have beautiful homes, multiple high end vehicles, and live really nice lifestyles.
My dad's a doc. All his buddies used to gripe all time and tell me not to go into medicine (40 yrs ago). Doctors love to kvetch. The reimbursement shell game has been going on forever - feds decrease reimbursement for procedure X, field shifts to do more of procedure Y.
If your goal is to get filthy rich, become a hedge fund manager, or found the next Apple/Google/Cisco. We make plenty of money. We will continue to for a long time to come. We are recession-proof. When the market next crashes, all your wall street & /or real estate buddies will wish they were you.
2) The population is aging
3) Neck and back pain are not getting any less prevalent
4) If the right doctor performs the right procedure on the right patient, our stuff works almost all the time.
Physicians have been complaining about decreasing revenue since the implementation of Medicare. Yet remarkably, many of the folks on this board have beautiful homes, multiple high end vehicles, and live really nice lifestyles.
My dad's a doc. All his buddies used to gripe all time and tell me not to go into medicine (40 yrs ago). Doctors love to kvetch. The reimbursement shell game has been going on forever - feds decrease reimbursement for procedure X, field shifts to do more of procedure Y.
If your goal is to get filthy rich, become a hedge fund manager, or found the next Apple/Google/Cisco. We make plenty of money. We will continue to for a long time to come. We are recession-proof. When the market next crashes, all your wall street & /or real estate buddies will wish they were you.
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Some truth to that.
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No. Do not do this.
Conflict of interest when you prescribe opioids and then treat addiction at the same time.
Also you do not want to deal with the addiction population.
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Tell me the conflict. Is it the same conflict as treating renal insufficiency and heart failure?
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Free pizza in waiting room
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Or you can pretend it's all nociceptive pain
Rates of opioid misuse, abuse, and addiction in chronic pain: a systematic review and data synthesis.
Review article
Vowles KE, et al. Pain. 2015.
Show full citation
Abstract
Opioid use in chronic pain treatment is complex, as patients may derive both benefit and harm. Identification of individuals currently using opioids in a problematic way is important given the substantial recent increases in prescription rates and consequent increases in morbidity and mortality. The present review provides updated and expanded information regarding rates of problematic opioid use in chronic pain. Because previous reviews have indicated substantial variability in this literature, several steps were taken to enhance precision and utility. First, problematic use was coded using explicitly defined terms, referring to different patterns of use (ie, misuse, abuse, and addiction). Second, average prevalence rates were calculated and weighted by sample size and study quality. Third, the influence of differences in study methodology was examined. In total, data from 38 studies were included. Rates of problematic use were quite broad, ranging from <1% to 81% across studies. Across most calculations, rates of misuse averaged between 21% and 29% (range, 95% confidence interval [CI]: 13%-38%). Rates of addiction averaged between 8% and 12% (range, 95% CI: 3%-17%). Abuse was reported in only a single study. Only 1 difference emerged when study methods were examined, where rates of addiction were lower in studies that identified prevalence assessment as a primary, rather than secondary, objective. Although significant variability remains in this literature, this review provides guidance regarding possible average rates of opioid misuse and addiction and also highlights areas in need of further clarification.
Rates of opioid misuse, abuse, and addiction in chronic pain: a systematic review and data synthesis.
Review article
Vowles KE, et al. Pain. 2015.
Show full citation
Abstract
Opioid use in chronic pain treatment is complex, as patients may derive both benefit and harm. Identification of individuals currently using opioids in a problematic way is important given the substantial recent increases in prescription rates and consequent increases in morbidity and mortality. The present review provides updated and expanded information regarding rates of problematic opioid use in chronic pain. Because previous reviews have indicated substantial variability in this literature, several steps were taken to enhance precision and utility. First, problematic use was coded using explicitly defined terms, referring to different patterns of use (ie, misuse, abuse, and addiction). Second, average prevalence rates were calculated and weighted by sample size and study quality. Third, the influence of differences in study methodology was examined. In total, data from 38 studies were included. Rates of problematic use were quite broad, ranging from <1% to 81% across studies. Across most calculations, rates of misuse averaged between 21% and 29% (range, 95% confidence interval [CI]: 13%-38%). Rates of addiction averaged between 8% and 12% (range, 95% CI: 3%-17%). Abuse was reported in only a single study. Only 1 difference emerged when study methods were examined, where rates of addiction were lower in studies that identified prevalence assessment as a primary, rather than secondary, objective. Although significant variability remains in this literature, this review provides guidance regarding possible average rates of opioid misuse and addiction and also highlights areas in need of further clarification.
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Or you can pretend it's all nociceptive pain
Rates of opioid misuse, abuse, and addiction in chronic pain: a systematic review and data synthesis.
Review article
Vowles KE, et al. Pain. 2015.
Show full citation
Abstract
Opioid use in chronic pain treatment is complex, as patients may derive both benefit and harm. Identification of individuals currently using opioids in a problematic way is important given the substantial recent increases in prescription rates and consequent increases in morbidity and mortality. The present review provides updated and expanded information regarding rates of problematic opioid use in chronic pain. Because previous reviews have indicated substantial variability in this literature, several steps were taken to enhance precision and utility. First, problematic use was coded using explicitly defined terms, referring to different patterns of use (ie, misuse, abuse, and addiction). Second, average prevalence rates were calculated and weighted by sample size and study quality. Third, the influence of differences in study methodology was examined. In total, data from 38 studies were included. Rates of problematic use were quite broad, ranging from <1% to 81% across studies. Across most calculations, rates of misuse averaged between 21% and 29% (range, 95% confidence interval [CI]: 13%-38%). Rates of addiction averaged between 8% and 12% (range, 95% CI: 3%-17%). Abuse was reported in only a single study. Only 1 difference emerged when study methods were examined, where rates of addiction were lower in studies that identified prevalence assessment as a primary, rather than secondary, objective. Although significant variability remains in this literature, this review provides guidance regarding possible average rates of opioid misuse and addiction and also highlights areas in need of further clarification.
So i guess we all agree that only 8-12% of pain patients are addicts. Same as general population. Now im not saying only 10% who show up to our clinics will have addiction problems, but our job is to to determine which patient has pain, which has addiction, and which have both.
Defining addiction by dsmV or 4c's and assessing with due diligence (outside records, uds, pdmp, criminal records database) is our job. Pass go and get close monitoring and meds if functional goals are met.
Or you can demonize all patients who complain of pain and all docs whose job it is to try and help them.
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To the original OP. As you can see your question has exposed a fault line between many of us
who trained before the recognition of the current opioid epidemic and those of you who will graduate
in years to come. As a group - although not necessarily those here - IPM had a big role in the genesis
of the opioid crisis we are now facing. I think it's important to own up to it and help fix it by becoming
familiar with diagnosing OUD and offering evidence-based treatment for it.
"Some have framed efforts to reign in runaway prescribing as a threat to quality of care for those with chronic pain. As a practicing physician, I can assure you, nothing could be further from the truth. An overwhelming amount of evidence supports the compatibility of effective pain treatment with reducing opioid prescribing. High quality care for patients in pain isn’t jeopardized by such efforts, it demands it."
Caleb Alexander, MD
In a similar vein, many of us who trained prior to the recognition of the 'central pain' phenotype tend
to view most all MSK pain as nociceptive or neuropathic. This training flaw is difficult to escape,
particularly when interventions - whether they work or not - reimburse better than low-tech, evidence-based,
interventions like behavioral therapy, exercises, and life-style modifications. There are several IPM
societies that, even now, continue to ignore centralized pain, particularly those that make money off of cadaver
courses and technology. It's easy to pretend that a procedure will help, they are easy to do, and they avoid the difficult conversations about how pain can exist in the absence of nociception.
And now I await the trolls
who trained before the recognition of the current opioid epidemic and those of you who will graduate
in years to come. As a group - although not necessarily those here - IPM had a big role in the genesis
of the opioid crisis we are now facing. I think it's important to own up to it and help fix it by becoming
familiar with diagnosing OUD and offering evidence-based treatment for it.
"Some have framed efforts to reign in runaway prescribing as a threat to quality of care for those with chronic pain. As a practicing physician, I can assure you, nothing could be further from the truth. An overwhelming amount of evidence supports the compatibility of effective pain treatment with reducing opioid prescribing. High quality care for patients in pain isn’t jeopardized by such efforts, it demands it."
Caleb Alexander, MD
In a similar vein, many of us who trained prior to the recognition of the 'central pain' phenotype tend
to view most all MSK pain as nociceptive or neuropathic. This training flaw is difficult to escape,
particularly when interventions - whether they work or not - reimburse better than low-tech, evidence-based,
interventions like behavioral therapy, exercises, and life-style modifications. There are several IPM
societies that, even now, continue to ignore centralized pain, particularly those that make money off of cadaver
courses and technology. It's easy to pretend that a procedure will help, they are easy to do, and they avoid the difficult conversations about how pain can exist in the absence of nociception.
And now I await the trolls
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Speaking for the trolls, please note that 101N is incapable of civil discourse. Many practitioners of interventional pain management do not write for narcotics. Despite that, he generalizes, and casts aspersions generally on anyone who performs interventions. This despite the fact that the vast majority of such scripts are written by PCPs, not pain docs (just look at the citation he uses to back up his claim).
To be clear, central pain is not a phenotype. It is a result of an initial peripheral pain generator. Mind you, not all pain emanating from the neck or the back goes on to central pain. In fact, the very reason one performs interventions is to forestall or prevent the development of central sensitization.
Allowing these unsupported, irresponsible, overly broad generalizations to go unchallenged might allow for those still forming opinions to be influenced by 101N. Don't let his flood of citations fool you. Read the citations, and look to see if they stand for the proposition he claims (they often don't). Ask him for literature that actually backs up his claims (he can't give it to you). And question not only what he says, but what he leaves out (which is quite a lot). Ask him if he writes for opioids (he does). Ask him if he abides by the dose restrictions he would impose on the rest of us (he doesn't). Then ask yourself whether he is someone whose opinion you should respect (I'll let you reach your own conclusion on that one)
To be clear, central pain is not a phenotype. It is a result of an initial peripheral pain generator. Mind you, not all pain emanating from the neck or the back goes on to central pain. In fact, the very reason one performs interventions is to forestall or prevent the development of central sensitization.
- There is good evidence that RF works in the low back (http://www.ncbi.nlm.nih.gov/pubmed/10806505, http://www.ncbi.nlm.nih.gov/pubmed/23279154) and in the neck (http://www.ncbi.nlm.nih.gov/pubmed/22458772).
- There is good evidence that in patients with lumbar radicular pain caused by contained disc herniations, lumbar transforaminal injection of corticosteroids is effective in reducing pain, restoring function, reducing the need for other health care, and avoiding surgery (http://www.ncbi.nlm.nih.gov/pubmed/23110347).
- We can discriminate and stratify which patients are likely to respond to lumbar transforaminal epidurals (http://www.ncbi.nlm.nih.gov/pubmed/23566298).
- We can confirm that not all lumbar epidurals are equally effective (http://www.ncbi.nlm.nih.gov/pubmed/27630917)
- Diagnostic blocks have construct validity (http://www.ncbi.nlm.nih.gov/pubmed/24716821).
- Discogenic pain is a real diagnosis (http://www.ncbi.nlm.nih.gov/pubmed/23566298)
Allowing these unsupported, irresponsible, overly broad generalizations to go unchallenged might allow for those still forming opinions to be influenced by 101N. Don't let his flood of citations fool you. Read the citations, and look to see if they stand for the proposition he claims (they often don't). Ask him for literature that actually backs up his claims (he can't give it to you). And question not only what he says, but what he leaves out (which is quite a lot). Ask him if he writes for opioids (he does). Ask him if he abides by the dose restrictions he would impose on the rest of us (he doesn't). Then ask yourself whether he is someone whose opinion you should respect (I'll let you reach your own conclusion on that one)
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I'm still waiting for the explanation of how treating addiction is a conflict with pain management.
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Let me rephrase, ethically I can not justify prescribing opioids and treating addiction at the same time. Also I do not have the necessary training, skill or interest in addiction medicine.
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That's fair. You could employ people to do it for you if the need exists in your community.
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This reference identifies family medicine and primary care as the RX drivers not IPM.
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Central pain is a useful clinical concept [1,2], and a common "clinical" pain phenotype [3], but it is not the result of an initial injury. It was initially proposed - Clifford Wolff - to be caused by 'windup' at the cord level and there is some evidence that windup does occur with certain, rare types, of neural injuries. However, there is virtually no evidence to support an initial pain generator in the most common of the 'central pain' spectrum disorders: FMS, HA, TMJ, IC, IBS, HA, LBP, etc. Moreover, the most recent meta-analysis of fMRI studies doesn't seem to suggest that there is a common brain mechanism between all of the various CS species.[4]
Initially, Fredrick Wolfe thought that there was a tissue level explanation for FMS. However, by 2008 he had abandoned that belief [5] and he remains a vocal skeptic that there is simple biological explanation. Dan Clauw - who I respect- still holds hope - after 25yrs - that a tissue level explanation will be found, but he is now beginning to be more circumspect and in his most recent paper he too is calling it a spectrum disorder.[6]
"We conclude that fibromyalgia and related disorders are heterogenous conditions with a complicated pathobiology with patients falling along a continuum with one end a purely peripherally driven painful condition and the other end of the continuum is when pain is purely centrally driven."
Meanwhile, 50yrs of pain psychology research has identified that the single most powerful predictor of pain
outcome, is catastrophizing/fear-avoidance. Catastrophizing is a coping trait that is established early in life and persists. It is not the result of an injury although it is associated with adverse childhood events. And - wait for it -there is emerging evidence that catastrophizing also predicts a negative response to spine injections.
1. http://www.ncbi.nlm.nih.gov/pubmed/26266995
2. http://www.jpain.org/article/S1526-5900(16)00566-6/pdf
3. http://www.ncbi.nlm.nih.gov/pubmed/27166559
4. http://www.ncbi.nlm.nih.gov/pubmed/26717948
5. http://www.nytimes.com/2008/01/14/health/14pain.html?_r=0
6. https://www.ncbi.nlm.nih.gov/pubmed/27291641
Initially, Fredrick Wolfe thought that there was a tissue level explanation for FMS. However, by 2008 he had abandoned that belief [5] and he remains a vocal skeptic that there is simple biological explanation. Dan Clauw - who I respect- still holds hope - after 25yrs - that a tissue level explanation will be found, but he is now beginning to be more circumspect and in his most recent paper he too is calling it a spectrum disorder.[6]
"We conclude that fibromyalgia and related disorders are heterogenous conditions with a complicated pathobiology with patients falling along a continuum with one end a purely peripherally driven painful condition and the other end of the continuum is when pain is purely centrally driven."
Meanwhile, 50yrs of pain psychology research has identified that the single most powerful predictor of pain
outcome, is catastrophizing/fear-avoidance. Catastrophizing is a coping trait that is established early in life and persists. It is not the result of an injury although it is associated with adverse childhood events. And - wait for it -there is emerging evidence that catastrophizing also predicts a negative response to spine injections.
1. http://www.ncbi.nlm.nih.gov/pubmed/26266995
2. http://www.jpain.org/article/S1526-5900(16)00566-6/pdf
3. http://www.ncbi.nlm.nih.gov/pubmed/27166559
4. http://www.ncbi.nlm.nih.gov/pubmed/26717948
5. http://www.nytimes.com/2008/01/14/health/14pain.html?_r=0
6. https://www.ncbi.nlm.nih.gov/pubmed/27291641
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Here's the problem with your 50 years of psychology research: Across the board, the quality of the psychology research literature is notoriously poor. Theories of personality, coping, development, etc have shifted dramatically over the last several decades as have methods of measurement, etc. Moreover, any psychological construct that actually PREDICTS (in an experimental design use of the term) anything is useful as far as it goes, but limited by the very concept of the mind itself.
That is, it is virtually impossible to distinguish a "psychological effect" from the epiphenomenon of brain function itself. Behavior is different as you can measure assays of behavior in animal models. I don't think anyone would argue that castastrophizing/fear avoidance are negatively associated with health outcomes across a range of conditions, but its specificity to chronic pain per se has not been proven. It is equally likely that chronic pain CAUSES catastrophizing/fear avoidance. Moreover, there is no rule in life that says you can't have more than one thing wrong with you: CS, facet pain, and crazy. If you're making an argument for relative apportionment of such in treatment planning, then that seems reasonable. If you're making an argument for screening out patients for any IPM intervention on the basis of psychological factors, then I can't support that.
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In the fog of war you post with no references, because you have none.
To the OP, chronic non-cancer pain treatment is going to change soon. IPM
is not - the best or only - way to treat it.
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Interesting that, when you lump low back pain in with acknowledged somatiform disorders, you have no citation. It's a nice little bait and switch. Give quotes about FMS, and then attribute those same characteristics to something else altogether. It's deceptive. It's dishonest. It's deceitful. But it's an impressive debate tactic.
Some of us use a DRAM to risk stratify for depressed somatics (http://www.healio.com/orthopedics/s...ram-assessment-recommended-for-spine-patients, https://www.ncbi.nlm.nih.gov/pubmed/27153146, https://www.ncbi.nlm.nih.gov/pubmed/25995493). THOSE folks do poorly. THOSE folks need to receive psychological support. Not ALL patients. Not ALL non cancer pain patients not currently working. Not patients Dr. 101N, through his great and mystical power, has discerned are appropriate.
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"Interesting that, when you lump low back pain in with acknowledged somatiform disorders, you have no citation."
1. http://www.ptmovements.com/wp-conte...A-Narrative-Review-article-NJIRM-9-4-2016.pdf
2. http://www.ncbi.nlm.nih.gov/pubmed/26000680
3. https://www.researchgate.net/profil...letal_Pain/links/5595839808ae793d137b1cc9.pdf
4. http://www.ncbi.nlm.nih.gov/pubmed/16618470
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835496/
6. http://www.ncbi.nlm.nih.gov/pubmed/27445616
7. http://www.ncbi.nlm.nih.gov/pubmed/25811262
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823723/
9. http://www.ncbi.nlm.nih.gov/pubmed/7701392
10. http://www.ncbi.nlm.nih.gov/pubmed/26814298
11. http://www.ncbi.nlm.nih.gov/pubmed/14872506
12. http://www.ncbi.nlm.nih.gov/pubmed/16586062
13. http://www.ncbi.nlm.nih.gov/pubmed/20219398
12. http://www.ncbi.nlm.nih.gov/pubmed/20823782
13.http://www.ncbi.nlm.nih.gov/pubmed/24607845
14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404223/
1. http://www.ptmovements.com/wp-conte...A-Narrative-Review-article-NJIRM-9-4-2016.pdf
2. http://www.ncbi.nlm.nih.gov/pubmed/26000680
3. https://www.researchgate.net/profil...letal_Pain/links/5595839808ae793d137b1cc9.pdf
4. http://www.ncbi.nlm.nih.gov/pubmed/16618470
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835496/
6. http://www.ncbi.nlm.nih.gov/pubmed/27445616
7. http://www.ncbi.nlm.nih.gov/pubmed/25811262
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823723/
9. http://www.ncbi.nlm.nih.gov/pubmed/7701392
10. http://www.ncbi.nlm.nih.gov/pubmed/26814298
11. http://www.ncbi.nlm.nih.gov/pubmed/14872506
12. http://www.ncbi.nlm.nih.gov/pubmed/16586062
13. http://www.ncbi.nlm.nih.gov/pubmed/20219398
12. http://www.ncbi.nlm.nih.gov/pubmed/20823782
13.http://www.ncbi.nlm.nih.gov/pubmed/24607845
14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404223/
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16 articles, and yet not one stands for the proposition that all chronic low back pain is central in origin.
Several of your articles discuss how to distinguish nociceptive from neuropathic from central. None dispute the notion that most back pain is initially peripheral, and can subsequently develop central components over time.
No one disputes that SOME patients catastrophize. No one disputes that some patients develop secondary depression. Nobody disputes that a multimodal approach with these patients is better than injections or opioids alone.
However, none of your 16 articles interventions don't work. None of your 16 articles say that chronic low back pain is a somatoform disorder. None of your 16 articles stand for the proposition you claim they do.
Also, next time, at least do us the courtesy of generating a new list of irrelevant articles. Given that your numbers aren't sequential, it's obvious you just cut and pasted this same mishmash of articles from a prior post.
So I congratulate you for providing us with citations. I was naive to assume you understood I was looking for RELEVANT citations.
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ampa, maybe if you take a different context to 101N's words, and instead of assuming that this argument is about all patients...
of those patients that are working aged, that have chronic pain, who are disabled and unable to work - what percentage of those patients do you think do not have central sensitization?
of those patients that are working aged, that have chronic pain, who are disabled and unable to work - what percentage of those patients do you think do not have central sensitization?
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No higher than in the general population.
CS and somatiform disorders are not one and the same.
I do not pretend to know the answer. I acknowledge that some pain patients have a central component to their pain. Not all, some. Those that do may well benefit from a multimodal approach. What I'm not willing to go along with is that their sole etiology is central, and every other approach is a waste of time.
CS and somatiform disorders are not one and the same.
I do not pretend to know the answer. I acknowledge that some pain patients have a central component to their pain. Not all, some. Those that do may well benefit from a multimodal approach. What I'm not willing to go along with is that their sole etiology is central, and every other approach is a waste of time.
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Pain Med. 2016 Aug;17(8):1452-64. doi: 10.1093/pm/pnv074. Epub 2015 Dec 17.
An Examination of Pain Catastrophizing and Endogenous Pain Modulatory Processes in Adults with ChronicLow Back Pain.
Owens MA1, Bulls HW1, Trost Z1, Terry SC1, Gossett EW1, Wesson-Sides KM1, Goodin BR2.
Author information
Abstract
OBJECTIVE:
Research on chronic low back pain (cLBP) has focused heavily on structural abnormalities with emphasis on diagnostic imaging. However, for many cLBP patients, clinical pain and disability are not clearly associated with identifiable pathology of the spine or associated tissues. Therefore, alternative determinants such as psychological factors and dysfunctional pain modulatory processes have been suggested to be important.
METHODS:
This observational study examined differences in pain catastrophizing and endogenous pain modulation between 25 cLBP patients and 25 pain-free controls. Associations among pain catastrophizing, endogenous pain modulatory processes, clinical pain reports, and disability were also examined in cLBP patients. Endogenous pain modulation was examined using temporal summation (TS) of mechanical and heat painstimuli as well as conditioned pain modulation (CPM) with algometry (test stimulus) and the cold pressor task (conditioning stimulus).
RESULTS:
Findings demonstrated significantly greater pain catastrophizing as well as greater TS of mechanical and heat pain for cLBP patients compared with controls. CPM was not present in cLBP patients or controls. Among cLBP patients, pain catastrophizing was significantly associated with disability, while TS of mechanical pain was significantly associated with clinical pain severity and disability.
CONCLUSIONS:
This study suggests that endogenous pain modulatory processes are altered for cLBP patients, particularly TS of mechanical and heat stimuli. Pain catastrophizing and TS of mechanical pain may have important clinical relevance for cLBP, given associations with clinical pain and disability; however, future research is needed to replicate these findings.
An Examination of Pain Catastrophizing and Endogenous Pain Modulatory Processes in Adults with ChronicLow Back Pain.
Owens MA1, Bulls HW1, Trost Z1, Terry SC1, Gossett EW1, Wesson-Sides KM1, Goodin BR2.
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Abstract
OBJECTIVE:
Research on chronic low back pain (cLBP) has focused heavily on structural abnormalities with emphasis on diagnostic imaging. However, for many cLBP patients, clinical pain and disability are not clearly associated with identifiable pathology of the spine or associated tissues. Therefore, alternative determinants such as psychological factors and dysfunctional pain modulatory processes have been suggested to be important.
METHODS:
This observational study examined differences in pain catastrophizing and endogenous pain modulation between 25 cLBP patients and 25 pain-free controls. Associations among pain catastrophizing, endogenous pain modulatory processes, clinical pain reports, and disability were also examined in cLBP patients. Endogenous pain modulation was examined using temporal summation (TS) of mechanical and heat painstimuli as well as conditioned pain modulation (CPM) with algometry (test stimulus) and the cold pressor task (conditioning stimulus).
RESULTS:
Findings demonstrated significantly greater pain catastrophizing as well as greater TS of mechanical and heat pain for cLBP patients compared with controls. CPM was not present in cLBP patients or controls. Among cLBP patients, pain catastrophizing was significantly associated with disability, while TS of mechanical pain was significantly associated with clinical pain severity and disability.
CONCLUSIONS:
This study suggests that endogenous pain modulatory processes are altered for cLBP patients, particularly TS of mechanical and heat stimuli. Pain catastrophizing and TS of mechanical pain may have important clinical relevance for cLBP, given associations with clinical pain and disability; however, future research is needed to replicate these findings.
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Elevated Catastrophizing Predicts Disability:
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Lazy. Malingering. Government teat freeloaders. I bet over half do not have cs, but they have no reason or motivation to get or say they are better. Id like to know how folks stratify under surveillance. I bet the cs folks might do a lot less than the folks who only peesent to office unable to work.
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Maybe CS/FMS is the name a rheumatologist, without any pain psychology exposure, gives to
the patient who catastrophizes about their pain in rheumatology clinic in 1990. Given that there has been
no clear biological basis established for FMS over the past 25yrs it's sure starting to look that way.
Perhaps it was Wolfe himself who got the train off it's tracks.
"I once published an article on psychological issues, I pointed out that psychologists see patients when they are bad, but rheumatologists see them over a life-time over good and bad times, particularly with RA. I said we know more about the psychological lives of our patients than psychologists. In my practice beginning around 1974 I started to collect PE and self-report data in a computer (I wrote the software). So for every patient visit I has pain, global HAQ, fatigue and in the beginning anxiety and depression data. I thought what patients wanted from me was support and an interface to the world as they, as often was the case in those day, progressed to disability and dissolution of plans and often lives. I think we should use psychological skills and do have a part in the existential troubles of the world."
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Agree completely with you here. FMS is a survey patients complete outside the office. SSS/WPI. Treatment is exercise, cbt, non narcotic, non procedural care.
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According to 101N, all FMS=CS. All CLBP=CS. All Catastrophizers=CS.
NONE OF THESE ARE TRUE.
FMS is psychogenic and/or rheumatologic disorder
CLBP is musculoskeletal
Catastrophizers have poor coping skills
CS is a neuroplastic windup phenomenon.
You can have more than one.
NONE OF THESE ARE TRUE.
FMS is psychogenic and/or rheumatologic disorder
CLBP is musculoskeletal
Catastrophizers have poor coping skills
CS is a neuroplastic windup phenomenon.
You can have more than one.
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"You are ignoring an essential part of my argument. I don't debate that a disc can hurt, I've had them myself
and seen many, many patients over the years with an acute HNP and BAD back pain. Given. However, in
the absence of psychological confounders - CS - that pain resolves. Thus, discogenic pain isn't a chronic
condition, it's episodic waxing and waning, not chronic, unrelenting, and not long-term disabling.
Those working-aged individuals with chronic, disabling, back can't have their pain explained by 'discogenic'
label. That is a pseudodiagnosis. Those people at the extreme end of back pain disability, those who go on
to discography, and fusion, or IDET, etc, more often than not have non-specific back pain and CS."
and seen many, many patients over the years with an acute HNP and BAD back pain. Given. However, in
the absence of psychological confounders - CS - that pain resolves. Thus, discogenic pain isn't a chronic
condition, it's episodic waxing and waning, not chronic, unrelenting, and not long-term disabling.
Those working-aged individuals with chronic, disabling, back can't have their pain explained by 'discogenic'
label. That is a pseudodiagnosis. Those people at the extreme end of back pain disability, those who go on
to discography, and fusion, or IDET, etc, more often than not have non-specific back pain and CS."
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Focal fibro.
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So we can agree that there is a role for Interventional pain management. IPM can identify those patients who have specific pain generators, and therefore do not fall into the 'non-specific' group.
This has nothing to do with whether or not the patient is working. This has nothing to do with their age. This is a simple binary, yes we can identify the pain generator, or no we can't.
We still seem to have a problem with taxonomy. 'Discogenic' pain is pain emanating from the disc by we know this because the patient has exhibited concordant pain on provocation discography, using appropriate pressure parameters, and we have identified a control disc.
This has nothing to do with whether or not the patient is working. This has nothing to do with their age. This is a simple binary, yes we can identify the pain generator, or no we can't.
We still seem to have a problem with taxonomy. 'Discogenic' pain is pain emanating from the disc by we know this because the patient has exhibited concordant pain on provocation discography, using appropriate pressure parameters, and we have identified a control disc.
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But who says all pain resolves? Who says all pain waxes and wanes? Who says you can't have acute exacerbations of chronic conditions with minimal injuries? Who says all chronic pain is not legitimate?
Again, these are absolutist positions. Some pain resolves. Some pain waxes and wanes. Some chronic pain is not legitimate.
Likewise, some patients with chronic low back pain also have central sensitization. Not all, some.
Again, these are absolutist positions. Some pain resolves. Some pain waxes and wanes. Some chronic pain is not legitimate.
Likewise, some patients with chronic low back pain also have central sensitization. Not all, some.
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I don't know, I haven't been real impressed with transforaminal epidurals for radiculopathy due to foraminal or lateral recess stenosis.
I've come to the realization, that no matter how technically complex the procedure is made out to be, in the end, it's still just a cortisone shot.
Regarding making plenty of money, it's all relative I suppose. I personally don't think Pediatricians make very much.
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The original post was about market demand. In terms of employed positions, there will be a lower demand for high volume proceduralists, and the earning potential will be less.
Sure, patients may demand procedures, and that's fine so long as you're in a position to have cash practice and charge what you feel to be adequate rates.
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These types of patients often only have very transient relief (couple days or couple weeks only after TFESI with dex).
This where it's important to recognize that the pathophysiology of stenosis is different from radiculopathy caused only from an acute disc herniaton.
While several studies have demonstrated that dex is nearly equal to particulate steroid for duration of relief when treating radiculopathy caused by acute disc herniation, there are no decent studies demonstrating the same for radiculopathy secondary to stenosis.
I would try some fairly lateral ILESI with depo on these patients who failed TFESI with dex for their foraminal and lateral recess stenosis.
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Observational, but my comparison has been particulate transforaminal vs. interlaminar, for the above conditions. Less than a month or two of relief generally, with either.
On average, what proportion of patients referred to "pain clinics" have radicular pain due to spinal stenosis/chronic disc herniation vs. an acute disc herniation?
What I was getting at, in the context of the thread, and the prior posts, is that IPM helps some patients. But, looking at the big picture, chronic pain management for the US population, it doesn't seem to be where the goods are at.
On average, what proportion of patients referred to "pain clinics" have radicular pain due to spinal stenosis/chronic disc herniation vs. an acute disc herniation?
What I was getting at, in the context of the thread, and the prior posts, is that IPM helps some patients. But, looking at the big picture, chronic pain management for the US population, it doesn't seem to be where the goods are at.
