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AAPT Diagnostic Criteria for Fibromyalgia

Over many decades, there have been efforts to develop diagnostic criteria for the condition we now recognize as fibromyalgia (FM). The multiple symptoms and comorbidities associated with FM make it difficult to diagnose, and FM is still under-diagnosed and under-treated.7,34,79 The diagnosis of FM might take more than 2 years, with patients seeing an average of 3.7 different physicians during this time.34 Many health care providers, particularly in primary care, report unclear diagnostic criteria, a lack of confidence in using existing criteria for diagnosis, insufficient training or skill in diagnosing FM, and a lack of knowledge of treatment options.

AAPT Diagnostic Criteria for Fibromyalgia

Orginally Published At: Pain Journal

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Influence of Abuse History on Concurrent Benzodiazepine and Opioid Use in Chronic Pain Patients

In 2016, more than 42,200 deaths in the United States involved opioids.41 The rate of opioid-related deaths has risen steadily and drastically since 1999. Although public policy has focused on curbing these high rates, the epidemic remains a public health crisis. An important predictor of opioid overdose is the co-use of benzodiazepines.12,22,36 Benzodiazepines are frequently prescribed among patients with chronic pain due to their broad clinical applications, including treatment of anxiety, sleep disorders, and seizures.

Influence of Abuse History on Concurrent Benzodiazepine and Opioid Use in Chronic Pain Patients

Orginally Published At: Pain Journal

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Experimental Pain Decreases Corticomuscular Coherence in a Force- But Not a Position-Control Task

Neural drive to muscles is altered in pain, but this depends on task type. Acute experimental pain reduces the discharge rate of many active motor units during gentle isometric contractions,12,51,54 but this is less pronounced in position- than force-control tasks.44 Even when tasks are identical in mechanical requirements and muscle torques, neuromotor control during position- and force-control tasks differs. Task-specific differences at the spinal cord and descending inputs are thought to explain this difference.

Experimental Pain Decreases Corticomuscular Coherence in a Force- But Not a Position-Control Task

Orginally Published At: Pain Journal

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Is stress inflammatory?

Another “inflammatory” post today. The last one was about tendinopathy.

There are strong but murky links between chronic pain and stress (and all its cousins: anxiety, insomnia, depression, social isolation, etc.) We still don’t know if stress directly causes chronic pain and other health problems — though there are signs that it can (Thompson) — or if it “just” feeds back into it (Elbinoune). It’s possible that low-grade chronic inflammation is one way that stress can become painful. It might even be the way.

Inflammation is immunity’s fingerprint, and we know (or strongly suspect) that “immunity is tuned by one’s emotions, personality, and social status as well as by other life style variables like sleep, nutrition, obesity, or exercise” (Lasselin). We know that nervous-wreck monkeys are inflamed, their immune systems a mess. Dr. Robert Sapolsky, regarding a study of low-status monkeys (Snyder-Mackler), who have really hard lives:

At the end of the day, being a chronically subordinate nonhuman primate and being a human mired at the bottom of the socioeconomic scale are similar in the most fundamental ways. You have remarkably little control and predictability in your life, your outlets for frustration are limited, and it’s relatively hard to access social support. That’s the prescription for chronic, stress-related maladies.

The same thing probably happens in humans. We suspect that rough childhoods may be a risk factor for several disorders that probably share inflammation as a mechanism (Burke).

Aren’t stress hormones anti-inflammatory?

This is all a bit counterintuitive, because we “know” that stress can actually suppress immunity, and that stress hormones — corticosteroids — are impressively anti-inflammatory. But that’s short term stress. It’s insanely complicated, but prolonged stress almost certainly does the opposite: overstimulates the immune system, causing chronic excessive inflammation and likely autoimmune disease risk too.

In the very short term (minutes), stress is indeed an immune stimulator (inflammatory). But then, almost right away, that effect gets reeled in to prevent collateral damage: you don’t want sustained immune stimulation! This suppressive effect is robust, and it’s why stress/steroids suppress inflammation.

In chronic stress, the stimulatory phase keeps happening over and over again, and the suppressive phase never quite catches up, and so overall immune system activation gradually ratchets up … and up … and up. Ergo, long term stress is inflammatory.




Chart showing a sawtooth pattern of immune function increasing and decreasing with repeated stressors, but never quite recovering before increasing again, producing a steady upward trend.

[Image caption: “A schematic representation of how repeated stress increases the risk of autoimmune disease,” adapted from Sapolsky’s Why Zebras Don’t Get Ulcers.]

Sapolsky goes deep on this topic in Why Zebras Don’t Get Ulcers, and I am completely relying on him for this point. I hope I’ve boiled it down to the essentials correctly. His bottom line:

The system apparently did not evolve for dealing with numerous repetitions of coordinating the various on-and-off switches, and ultimately something uncoordinated occurs, increasing the risk that the system becomes autoimmune [inflammatory].

This is an excerpt from an update to my main article about systemic inflammation and pain:

[Go to this post on PainScience.com]

Is stress inflammatory?


Orginally Published At: Pain Science

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Cannabinoid type 2 (CB2) receptor system modulates paclitaxel-induced microglial dysregulation and central sensitization in rats

Chemotherapy-induced peripheral neuropathy (CIPN) occurs in 40 to 60% of patients who receive paclitaxel, which is used clinically to treat breast, lung, and ovarian cancer.12,44 CIPN appears to be a dose-limiting toxicity, especially after multiple treatment courses.49 CIPN may also persist for years after the therapy is stopped; a small percentage of patients experience life-long CIPN.15

Cannabinoid type 2 (CB2) receptor system modulates paclitaxel-induced microglial dysregulation and central sensitization in rats

Orginally Published At: Pain Journal

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Rethinking the causes of pain in herpes zoster and postherpetic neuralgia: the ectopic pacemaker hypothesis

Introduction:
Pain in herpes zoster (HZ) and postherpetic neuralgia (PHN) is traditionally explained in terms of 2 processes: irritable nociceptors in the rash-inflamed skin and, later, deafferentation due to destruction of sensory neurons in one virally infected dorsal root ganglion.
Objectives and methods:
Consideration of the evidence supporting this explanation in light of contemporary understanding of the pain system finds it wanting. An alternative hypothesis is proposed as a replacement.
Results:
This model, the ectopic pacemaker hypothesis of HZ and PHN, proposes that pain in both conditions is driven by hyperexcitable ectopic pacemaker sites at various locations in primary sensory neurons affected by the causative varicella zoster virus infection. This peripheral input is exacerbated by central sensitization induced and maintained by the ectopic activity.
Conclusions:
The shift in perspective regarding the pain mechanism in HZ/PHN has specific implications for clinical management.
This is an open access article distributed under the Creative Commons Attribution-NoDerivatives License 4.0 (CC BY-ND) which allows for redistribution, commercial and non-commercial, as long as it is passed along unchanged and in whole, with credit to the author.
Corresponding author. Address: Department of Cell and Developmental Biology, Institute of Life Sciences 3-533, The Hebrew University of Jerusalem, Jerusalem 91904, Israel. Tel.: +972 2 658-5085; fax: +972 2 658-4480. E-mail address: marshlu@mail.huji.ac.il (M. Devor).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received June 07, 2018
Accepted October 10, 2018
© 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain.

Rethinking the causes of pain in herpes zoster and postherpetic neuralgia: the ectopic pacemaker hypothesis


Orginally Published At: PAIN Reports

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Strange but true: the meaning of “pain science” is controversial

It’s weird for me to see the title “pain science is not a thing.” O rly?! Well, it is my website!

But Dr. Thompson is aware of that. What she’s writing about is the strange fact that “pain science” is controversial — the words themselves, that is. The meaning of that specific pairing of words has somehow become a subject of debate and concern, mainly because a certain type of healthcare professional insists on perceiving it as a method of treating people and/or a clique of believers in a particular way of doing this.

It’s really not. But some people have a hard time imagining healthcare without gurus and workshops, and they see everything through that lens. It must be PainScience™! When all you have is a hammer

It’s much ado about nothing and doesn’t concern me much. But, as the owner of the “PainScience.com” domain, it’s noteworthy and rather surreal. It amazes me that it’s enough of an issue to inspire posts like the one I’m sharing today. And it’s not even the first! This has come up before (see also, “Pain science is not a modality!” by Lars Avemarie). ……I agree with Bronnie and Lars wholeheartedly… but, wow, it’s just so bizarre that there’s any kind of need for it.

For whatever it’s worth, when I chose the domain name (circa 2014), I was thinking exclusively of “pain science” as meaning “pain being examined through multiple scientific lenses.” No other interpretation was even on my radar, and I am rather horrified and baffled by other interpretations that have emerged since then!

What interests me about this is mostly that it’s so painfully obvious that the people systematically abusing the idea of “pain science” see their jobs through a thick lens of methods and techniques, of skills learned from gurus at weekend workshops, ways of “fixing” patients. They have a hard time wrapping their heads around the idea of an abstract perspective/process (AKA “science”) that informs clinical reasoning in a complex, unpredictable way, which can’t be packaged. It is really only the people most blinkered in this way that are systematically oversimplifying and misrepresenting what “pain science” refers to, like thinking astrology is the same as astronomy.

[Go to this post on PainScience.com]

Strange but true: the meaning of “pain science” is controversial


Orginally Published At: Pain Science

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Designing and conducting proof-of-concept chronic pain analgesic clinical trials

Introduction:
The evolution of
pain treatment is dependent on successful development and testing of interventions. Proof-of-concept (POC) studies bridge the gap between identification of a novel target and evaluation of the candidate intervention’s efficacy within a pain model or the intended clinical pain population.
Methods:
This narrative review describes and evaluates clinical trial phases, specific POC pain trials, and approaches to patient profiling.
Results:
We describe common POC trial designs and their value and challenges, a mechanism-based approach, and statistical issues for consideration.
Conclusion:
Proof-of-concept trials provide initial evidence for target use in a specific population, the most appropriate dosing strategy, and duration of treatment. A significant goal in designing an informative and efficient POC study is to ensure that the study is safe and sufficiently sensitive to detect a preliminary efficacy signal (ie, a potentially valuable therapy). Proof-of-concept studies help avoid resources wasted on targets/molecules that are not likely to succeed. As such, the design of a successful POC trial requires careful consideration of the research objective, patient population, the particular intervention, and outcome(s) of interest. These trials provide the basis for future, larger-scale studies confirming efficacy, tolerability, side effects, and other associated risks.
This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Corresponding Author. Address: Department of Psychiatry & Behavioral Sciences, Johns Hopkins University School of Medicine, 5510 Nathan Shock Dr, Suite 100 Baltimore, MD 21224. Tel.: (410) 510-7989; fax: (410) 510-0117. E-mail address: ccampb41@jhmi.edu (C.M. Campbell).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received March 13, 2018
Received in revised form September 24, 2018
Accepted September 26, 2018
© 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain.

Designing and conducting proof-of-concept chronic pain analgesic clinical trials


Orginally Published At: PAIN Reports

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Was that painful or non-painful? The Sensation and Pain Rating Scale (SPARS) performs well in the experimental context

Pain intensity is best assessed by self-report. Clinicians and researchers attempt to capture another’s pain using cross-modality matching tasks in which pain is matched to a rating scale.31 Numerical rating scales (NRS) and visual analogue scales (VAS) anchored at opposite extremes with ‘no pain’ and something akin to ‘most intense pain you can imagine’ are widely used, and have evidence for being robust assessments of pain in clinical and experimental contexts.8 Indeed, for both of these scale types, the stimulus-response relationship has been described by a classical psychophysical power relationship, and the VAS has been said to have ratio properties.

Was that painful or non-painful? The Sensation and Pain Rating Scale (SPARS) performs well in the experimental context

Orginally Published At: Pain Journal

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Stretching as a sign of maturity?

Loud conversation overheard at the gym:

These kids, you know, they workout out like kids, they don’t stretch, they get hurt, they pull a groin, and they’re like, why, how did this happen? Well, maybe if you knew that stretching prevents injury, like a grown up, you wouldn’t have gotten hurt! Adults know that you have to stretch.

I love the implication that stretching to prevent injury is such locked-in wisdom that, in this guy’s mind, it’s synonymous with maturity: to be an adult is to know that stretching prevents injury! I came so close to interjecting: “And adults with more education know that the stretching to prevent injury is based on faith and received wisdom, and the scientific evidence clearly contradicts it.” I doubt that would have resulted in a productive conversation.

[Go to the link featured in this post]

[Go to this post on PainScience.com]

Stretching as a sign of maturity?


Orginally Published At: Pain Science