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Pan-Canadian estimates of chronic pain prevalence from 2000 to 2014: A Repeated Cross-Sectional Survey Analysis

The prevalence of chronic pain in Canada increased between 1996 and 2006, from 15.3% to 19.5%.20 This increase parallels changes reported in other western countries, including the United States,9,13 and is of major concern because chronic pain is associated with substantial costs to the individual and society (i.e., decreased quality of life, lost productivity, and increased health care expenses).16,14 However, since 2008, there has been a paucity of information on the prevalence of chronic pain in Canada.

Pan-Canadian estimates of chronic pain prevalence from 2000 to 2014: A Repeated Cross-Sectional Survey Analysis

Orginally Published At: Pain Journal

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Trait perceived injustice is associated with pain intensity and pain behaviour in participants undergoing an experimental pain induction procedure

Over the past decade, numerous investigations have examined the role of justice-related appraisals as determinants of health and mental health outcomes of individuals with chronic pain conditions 40, 41. In the context of pain and pain-related disability, perceived injustice has been conceptualized as an appraisal process characterized by a tendency to construe injury or illness as a violation of justice principles, to view one’s losses as severe and irreparable, and to attribute blame to others for one’s suffering 39.

Trait perceived injustice is associated with pain intensity and pain behaviour in participants undergoing an experimental pain induction procedure

Orginally Published At: Pain Journal

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Biological vulnerabilities: the underestimated x-factors in chronic pain

Biological vulnerability has been on my mind a lot lately.

Imagine the most structural, biomechanical, tissue-in-trouble problems that can cause chronic pain. Things that seem very likely to hurt: A neuroma on a nerve root. A calcified, elongate styloid process stabbing someone in the throat (Eagle’s syndrome). An entrapped cluneal nerve in the butt, being strangled by connective tissue. A substantially degenerated tendon.

All things that seem likely to hurt.

And yet none of these always causes pain. Some people feel them, some people never even know about them. In fact, there is almost no physical problem in the entire world of chronic pain that is consistently symptomatic in everyone. Why is that?

Probably because some people are more vulnerable.


Close-up photograph of hot coals.

[Image caption: Is a fire “caused” by the fuel? Or how dry it is? Or the match? Or the oxygen? Trick question…]

Probably because of biological x-factors, non-structural problems. Biochemistry. Nutrition. Cellular business. Maybe patient X is vulnerable to that cluneal nerve impingement because of a vitamin D or magnesium deficiency. Or a medication side effect. The biological consequences of sleep deprivation, or sleep apnea (blood gases get weird with that condition). Or the chronic stress of social isolation. Or “inflammaging.” Or any one of about ten thousand other possibilities. The list of could-be’s is almost literally endless.

The so-called “problem” is just like kindling for a fire: just inert fuel by itself. That doesn’t mean it’s not a problem — you don’t really want fuel for chronic pain lying around your body just waiting for you to get vulnerable enough for it to burst into flame — but you also don’t blame fuel for a fire. Well, not just the fuel anyway.

This is speculation, of course. It would be difficult indeed to prove causation for even a single example, let alone the whole class of potential vulnerabilities. But I think it’s one plausible explanation for one of the most difficult puzzles in pain science: why physical problems have such inconsistent consequences. (The other big one, of course, is the psychosocial dimension of pain.)

That kindling metaphor

The kindling metaphor came from Greg Lehman, and was the original inspiration for this post:

So perhaps we want to view these structural changes as similar to kindling for a fire.

Kindling is not a fire. Its a precursor and before it can become a fire you need some accelerant or spark. We can view degenerative changes the same way. They aren’t sufficient for pain but perhaps you need some sort of sensitizing agent to create that “spark’ and the “fire” of pain.

Sometimes the accelerant is too much physical loading. Perhaps the accelerant is too much psychological load. Pain is multidimensional and the accelerant come from anywhere…but so can the solution 🙂

Greg has also been thinking and posting about this lately (yesterday): see “Non-specific low back pain exists. You just don’t want to admit it.”

The other thing that fueled this line of thinking was…

Butt nerve entrapment

The cluneal nerves pass from the low back and sacrum into the buttocks. Aota reported on “a case of severe low back pain, which was completely treated by release of the middle cluneal nerve.” Exploratory surgery identified cluneal nerves “entrapped in adhesions.” They cut them free… and that was the ticket. The patient was decisively cured of “non-specific” back pain.




[Image caption: #1 marks the site of the superior cluneal nerves, #2 marks the middle cluneal nerve.]

Seems pretty specific to me. It seems like a vivid example of how the cause of pain can sometimes be completely “mechanical” in nature. Tissue with an issue. Case closed, surely?

But the more I think about it, the more I believe that even here biological vulnerabilities potentially play a major role. Even in a case as “simple” as this. How can they not? We see wide variation in directly analgous conditions like carpal tunnel syndrome: the predicament of the nerve leads to symptoms only in some people, not others. Surely the same applies to a cluneal nerve in trouble.

I’ve now written about the implications of this interesting case in my back pain book, one of my articles about back massage, in my long rants about “structuralism” and fascia. Plus more to come! Sometimes just one tiny case study can spawn many changes to PainScience.com!

[Go to this post on PainScience.com]

Biological vulnerabilities: the underestimated x-factors in chronic pain


Orginally Published At: Pain Science

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Characterizing chronic pain in late adolescence and early adulthood: prescription opioids, marijuana use, obesity, and predictors for greater pain interference

Introduction:
Chronic
pain in late adolescence and young adults is understudied and poorly characterized.
Objectives:
We sought to characterize key variables that may impact pain interference in late adolescents and young adults with chronic pain, including prescription opioid use, marijuana use, psychological symptoms, and obesity.
Methods:
Retrospective, cross-sectional medical chart review for patients aged 17 to 23 years (N = 283; 61% Females) seeking care at a tertiary care pain clinic. Data on pain characteristics, health behaviors, and mental health distress were examined, in addition to self-reported pain intensity and interference.
Results:
Overlapping pain conditions were common in this young adult sample (mean ≥ 2 pain conditions). Back pain was the most commonly cited pain condition, and the majority of pain was of unknown etiology. Results revealed high rates for current opioid prescription, overweight or obese status, and mental health problems. Those using prescription opioids were more likely to endorse tobacco use and had greater pain interference. Importantly, the presence of mental health distress and opioid use were predictive of higher levels of pain-related interference.
Conclusion:
Treatment-seeking adolescents and young adults with chronic pain evidence complex care needs that include pain and mental comorbidities, as well as risky health behaviors. Pain and mental health distress were associated with poorer physical health, opioid prescription and marijuana use, and pain-related interference. Findings underscore the need for additional research on pain, treatment patterns, and health behaviors and their impact on developmental trajectories, as well as the need to develop and apply effective early interventions in this at-risk population.
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.
Corresponding author. Address: Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, 1070 Arastradero Rd, Suite 200, MC5596, Palo Alto, CA 94304. Tel.: (650) 736 5494. E-mail address: mziadni@stanford.edu (M. Ziadni).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received June 18, 2018
Received in revised form September 24, 2018
Accepted October 01, 2018
© 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain.

Characterizing chronic pain in late adolescence and early adulthood: prescription opioids, marijuana use, obesity, and predictors for greater pain interference


Orginally Published At: PAIN Reports

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Alleviation of mechanical allodynia by 14,15-EET in a central post-stroke pain model: possible role of allopregnanolone and δGABAAR

Central post-stroke pain (CPSP) is a neuropathic pain syndrome arising after lesion of the central nervous system (CNS) due to cerebrovascular insult. This syndrome is characterised by somatosensory abnormalities including spontaneous pain, hyperalgesia and allodynia, which localized to body areas corresponding to the injured brain region.2 These conditions are constant and could impair activities of daily living, consequently undermine quality of life and rehabilitation process. However, CPSP is probably the least recognized complication of stroke and the mechanism of which has not been adequately studied to date.

Alleviation of mechanical allodynia by 14,15-EET in a central post-stroke pain model: possible role of allopregnanolone and δGABAAR

Orginally Published At: Pain Journal

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Trait mindfulness is associated with lower pain reactivity and connectivity of the default mode network

Mindfulness training reduces pain in clinical and laboratory settings.10,24,34,41,53,60 Similarly, long term meditative practice mitigates sensory17–19 and emotional8,16,37 components of pain. Several studies have shown that mindfulness attenuates pain by enhancing attentional focus on the present moment and regulating associated emotional responses.4,31,43 A growing body of work documents neural activations associated with the effects of mindfulness training on pain. Decreases in pain following mindfulness-based training are frequently associated with greater activation in brain areas associated with sensory and/or salience processing,16,32,61 alongside decreases in the prefrontal cortical regions linked to evaluative and/or emotional responses.

Trait mindfulness is associated with lower pain reactivity and connectivity of the default mode network

Orginally Published At: Pain Journal

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Preoperative Psychosocial and Psychophysical Phenotypes as Predictors of Acute Pain Outcomes after Breast Surgery

The effective and safe management of postsurgical pain is an important clinical goal, as an estimated 240 million surgeries are performed each year worldwide.60 Despite increased recognition of acute41 and chronic34 postsurgical pain, and much excellent study of the mechanistic underpinnings of postsurgical pain,7 acute postsurgical pain remains a problem21 for a significant minority of patients. In a recent large study in a variety of surgical types, 28% of patients (of 22,000 patients studied) still experienced moderate-severe acute pain after surgery,24 and a sizable number of patients remain on long-term opioids months after orthopedic surgery.

Preoperative Psychosocial and Psychophysical Phenotypes as Predictors of Acute Pain Outcomes after Breast Surgery

Orginally Published At: Pain Journal

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Activation of KCNQ channels prevents paclitaxel-induced peripheral neuropathy and associated neuropathic pain

Paclitaxel is a commonly used chemotherapeutic agent for the treatment of breast and other cancers12. Unfortunately, its use is often associated with significant neurotoxicity, especially resulting in sensory peripheral neuropathies that are often accompanied by neuropathic pain and are frequently severe and resistant to intervention. Paclitaxel-induced peripheral neuropathy (PIPN) results from damage to, or dysfunction of, peripheral nerves, including sensory, autonomic, and motor neurons. The incidence and severity of PIPN is duration- and dose-related, such that more than 60% of patients receiving paclitaxel-based chemotherapy experience peripheral neuropathy in first 3 months58.

Activation of KCNQ channels prevents paclitaxel-induced peripheral neuropathy and associated neuropathic pain

Orginally Published At: Pain Journal

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Incident chronic spinal pain and depressive disorders: Data from the National Comorbidity Survey

Chronic spinal pain and depression are common conditions associated with a good deal of morbidity and healthcare utilization. In the US, low back pain, neck pain, and major depressive disorder comprise three of the top four leading causes of years lived with disability.51 The point-prevalence or past-year prevalence of chronic neck and back pain has been estimated at 8.1%-19% in large population-based studies.15,19,25,49,52 The lifetime prevalence of major depressive disorder (MDD) was 17.1% and 16.2% and dysthymic disorder (DD) was 6.4% and 6.9% in the original National Comorbidity Survey (NCS) and its replication (NCS-R), respectively.

Incident chronic spinal pain and depressive disorders: Data from the National Comorbidity Survey

Orginally Published At: Pain Journal