#painresearchmatters campaign

Yes, I’m on twitter and I’m now posting in Twitterspeak. That’s the hashtag for a little campaign I am starting on twitter to highlight the importance of pain research. The idea is simple, tell the twitter world why you support pain research or why pain research matters to you and use the hashtag #painresearchmatters. I’ll be posting facts about pain and links to interesting papers on pain throughout the coming weeks. I hope you will join me.

This week has not been a good one for pain researchers. Some of our own have come under attack by a publication that is misrepresenting both the purpose and interpretation of their work. This has led to numerous stories around the web resulting in a real firestorm at McGill that has serious potential to spread. I won’t be linking to any of these stories because none of them even bother to describe the purpose of the experiments. If you want to see the story behind the recent fury, read the paper.

It has long been my opinion that us pain researchers do a pretty poor job of educating the public about what we do and why. This is one of the reasons I started the blog. If you’re new here and you want to take a look at some of what I have written about pain and pain research here are some links to start with:

1) What is hyperalgesia and what is allodynia
2) Why does pain become chronic
3) What is central sensitization
4) Why are new classes of analgesics needed
5) Can chronic pain be reversed
If you want to read more, here is an article I co-authored in the popular press. No access? Email me and I’ll send you a PDF.
A wealth of information can also be found at the IASP website

Here are some facts about pain that illustrate why pain research is so important. These are just a taste of what I will be posting on twitter
1) The World Health Organization considers relief from pain to be a universal human right
2) Migraine headache is the most common neurological disorder in the world
3) More people seek medical attention for pain than for any other reason
4) Nearly 50% of people who seek medical treatment for pain report that they do not achieve pain relief with treatment
5) Chronic pain conditions disproportionately affect women

Now that I’ve given you some basic information its time to tell you why pain research is so important to me.
I am a pain researcher. However, I never intended to be one until fairly recently. I went to grad school to study serotonin pharmacology. While I am still fascinated by that topic, the lab I was planning to be in just wasn’t right for me at the time so I switched to studying cannabinoid pharmacology. This was the topic of study for my PhD. I was in a pain lab; however, my focus was almost entirely on cannabinoid ligands and their effects on GPCRs (CB1 and CB2) and TRP channels. My plan, for quite some time, was to move onto another lab for my postdoc that was doing cannabinoid pharmacology in a completely different area. Some interesting circumstances kept me from doing that: 1) the lab I wanted to go to turned me down, 2) I learned to speak Spanish after meeting a beautiful woman who I later married (as you might have guessed, she is latina) and we decided we wanted to move to a Spanish speaking country for awhile and 3) I became enamored with a technique I wanted to learn (in vivo electrophysiology). Hence, I contacted a researcher in Madrid who did that technique, who happened to be in the pain field, and we were all set to go. He ended up moving his lab to McGill and the rest is history…although I do still wish we would have had a chance to live in Madrid, maybe one day.

At McGill 3 very important things happened to me.
1) I was suddenly working in the most dynamic pain research center in the world. The multidisciplinary nature of pain research suddenly became very apparent to me and opportunities to translate basic science findings into clinical results seemed more attainable than in other areas (I’m not saying this is true, just my perception).
2) I started to go to pain clinical rounds. There I finally gained a grasp of the horrific suffering of chronic pain patients. It is one thing to read about it, it is quite another to meet these patients and hear their stories. A consistent story you hear from these people is how they are abused or dismissed by a medical system that all too often does not take pain seriously. This inevitably makes their pain condition worse and by the time they finally start to get relief from their pain they are often out of work, severely depressed and sometimes even suicidal. It is truly heartbreaking.
3) I became a pain patient myself. I suffered a spine injury that forever ended my days of hovering over an electrophys rig (that’s okay, I wasn’t much of an electrophysiologist anyway). Lucky for me, I regained most of the use of my partially paralyzed leg; however, I will likely forever suffer from lowback pain that waxes and wains. There is little question that I am one of the lucky ones, I honestly cannot imagine how I would have been able to live with the horrific, screaming, fire-like pain that lived (that is the correct term, it was not part of me) in my leg (where there was no injury – btw – the injury was at L4) for two weeks between the injury and the surgery. I would also just like to point out that nothing I tried stopped the pain during that period. NSAIDs were a joke and opioids only barely took the edge off.

The culmination of the confluence of these events was that I decided that pain research was the place to be for me. The work we do in the lab is largely aimed at understanding what underlies neuropathic pain on the molecular level and trying to design treatments that target these mechanisms in the hopes of reversing the pathology. We also work on synaptic plasticity and chronic pain. Essentially we are trying to erase the “pain memory” through these efforts. We have also recently started an academic drug discovery effort against a popular pain target that has thus far proven somewhat intractable pharmacologically. Together with an excellent medicinal chemist and a physiologist with some clever approaches to doing high-throughput screening on the cheap (its academia after all) we’ve actually made a lot of progress. We’re not operating at Big Pharma speed but we’re certainly operating. I will write more about this process in the near future. Finally, I started this blog in hopes of educating the public just a bit more about pain. I am going to ramp up that effort even more now that I am back to stay.

So, pain research matters to me because chronic pain is poorly treated, poorly understood and the people that suffer from chronic pain deserve a chance at getting that part of their life that pain sucks out of you back. I hope you’ll join me with tweets #painresearchmatters

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23 responses to “#painresearchmatters campaign

  1. Wow. Back with a bang, my friend. Looking forward to some posts on the science of pain.

  2. Mod Scientist

    Great post. Will do my part to promote this worthy campaign and looking forward to more posts on this topic.

  3. My personal experiences with pain deal mostly with labor (last episode almost 18 years ago) and bad high heels. However, I do collaborate with some neuroscience pain researcher types, and this is a really important area. I look forward to reading your posts so I can understand what the hell my collaborative efforts say!

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  6. Thank you for this great post and for the campaign. And for your work on pain research – from someone who suffers all the time from migraine pain.

  7. As a thirty-five year chronic pain patient, accident right after high school graduation, I send as much of my positive energy to you thru the blog-o’s-fear to aid in your quest to help us. May your grant money never dry up!!

    Thank you from the bottom of my non-unioned sacrum.

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  9. Great post, great idea for an awareness campaign. I have an autoimmune rheumatic disease and a degree in neuroscience, so this is of interest to me. I’ve already started passing the info around. Thanks!

  10. Thank you for this. I’m an MS patient, who also has chronic pain from bulging disks and migraines. It is *very* difficult to get the medical profession to take pain seriously. They treat all patients like “drug seekers” and play a numbers game “X number of Y patients find this sufficient” instead of treating patients like individuals. Where a disease like MS is involved, the amount of pain a particular individual experience is exceedingly variable. Pain & fatigue cause more MS patients to go on disability than anything else.

    A question I have never asked a doctor but probably should is “If I am going to have this pain all my life, and the medication relieves it at least partially, why do you care if I am “dependent” on the medication? The pain isnt going away, why should the medication?”

    • Broce, I have asked that question so many times I can practically lip read it! I await a satisfactory answer from someone who knows about what they speak.

  11. Broce, good point on your question! Hopefully we can eventually come up with disease modifying treatments, not only for MS but for pain in general.

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  13. In looking for reviews on MAPKs I just stumbled across a review about neuropathic pain and TNF alpha. And I remembered our conversation about RAW cells. I was wondering if you had thoughts on the inflammatory connection with some (many? most? basically all?) pain conditions and just thought I’d put a word in for you writing about it. *poke poke* (yeah yeah, I know it’s bad form to tell a blogger what to blog about; but I am curious about your take on it).

  14. Hi Becca, I can do that, no problem. I just posted a review of TNFalpha and neuropathic pain on the twitter feed. Is that the same one you found? Either way, the connection between inflammatory mediators and pain is huge. The issue is that when the inflammation resolves, the pain tend to stick around, sometimes for very long periods of time. We think this happens because the inflammatory mediators cause a long-lasting change in the sensitivity of nociceptors (those pesky pain sensing neurons in the PNS). I’ll likely write a post focused on that issue. Interestingly, nociceptors express receptors for a wide range of inflammatory mediators. They are excellent detectors of inflammation which is good for protecting injured parts of the body but bad for what happens after the injury has healed.

  15. JP,
    Question from the arse end of the pain research effort (channel geek): given the efficacy of brute force strategies like botox for chronic pain conditions, is there a reason that neurolysis hasn’t achieved a broader appeal than merely serving as an absolute last resort for the seriously ill*? How much research is going on at the transitional end towards finding more selective means to just shut the troublesome nociceptors up permanently and be done with it?

    * or am I completely wrong about this, and that it is already utilised more broadly than I thought?

  16. Yay!! Thankee.

    And yep, that’s the review I saw.
    So then, you’d want to look for… HDAC enzymes or histone acetyltransferases that are up/down-regulated in nociceptors after TNF-alpha (or HMGB1 or *insert other inflammatory signal here*) stimulation?
    I was at a talk not too long ago where they talked about CNS mediated signaling controlling all manner of things I wouldn’t expect (in the context of obesity, I believe it was… *pubmeds* AH! something like this: “MyD88 signaling in the CNS is required for development of fatty acid-induced leptin resistance and diet-induced obesity.” http://www.ncbi.nlm.nih.gov/pubmed/19808018)
    Have you given any thought to inflammatory signaling in the CNS causing chronic pain through the periphery in this kind of fashion?

  17. Becca,
    Let’s not talk about HDACs too much lest someone gets scooped :-) Part of the problem with doing this sort of work is that nociceptors exist within a heterogeneous population of sensory neurons that cannot be easily purified. It requires developing methods to look at populations of neurons within the ganglia to get an idea of what is happening specifically in nociceptors. Either that or doing ChIP with genes that are specifically expressed in nociceptors.

    On inflammatory signaling in the CNS, there is an entire field that has sprung up around this and pain. Linda Watkins (at UColorado) and Joyce DeLeo (at Dartmouth) have led the charge for more than a decade. They have basically shown that chronic pain induces a glial phenotype in the dorsal spinal cord that is consistent with chronic neuroinflammation. Whether this will lead to any clinical treatments is still an open question.

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  20. Thank you for this great post and for the campaign. And for your work on pain research – from someone who suffers all the time from migraine pain.

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