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Unexplained pain: "Pain-initiating function of glial cells identified"

Discussion in 'Other Health News and Research' started by natasa778, Nov 16, 2016.

  1. natasa778

    natasa778 Senior Member

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    http://medicalxpress.com/news/2016-11-pain-initiating-function-glial-cells.html

    paper: http://science.sciencemag.org/content/early/2016/11/04/science.aah5715
     
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  2. Woolie

    Woolie Gone now, come see me in my new home at S4ME.info

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    Thanks for posting, @natasa778.

    I just want to point out that we should be cautious about articles that include statements like this (my bolding):
    The reason is that there are a lot of peripheral pain phenomena that have nothing to do with tissue damage. Extremes of cold and heat can be very painful, even without "tissue damage". Local inflammation (for example, when a wound gets infected) is often much more painful that the "tissue damage" that led to it. Labor pains during childbirth and severe period pain are other nice examples. Immune activity can be painful - for example, the muscle aches that accompany severe flu are usually attributed to antibody complexes circulating within the system. Not. tissue damage.

    If anyone tries to claim that all pain that isn't caused by tissue damage must be "central" (ie. generated in the brain), they have set up a false dichotomy.

    At worst, this kind of reasoning can be used to justify a lot of bullshit about how people with chronic pain need psychotherapy.
     
    Last edited: Nov 16, 2016
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  3. Woolie

    Woolie Gone now, come see me in my new home at S4ME.info

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    I just read the paper. I'm pretty much a layperson when it comes to this area, but my reading of it was this. Its about glial cells in the spinal cord, which can "remember" pain for a short while, and even amplify it. The new contribution this study makes is that this memory/amplification effect may have a "spreading" effect, so that the experience of pain appears to "spread" to areas outside the affected site.

    The spread is still narrow, though. And the duration is a couple of hours max, at least from what I can tell. Yet the paper ends with the usual far-flung claims about how this line of research could help us understand chronic pain, and every manner of psychiatric condition under the sun.

    Could others with more expertise perhaps comment?
     
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  4. lansbergen

    lansbergen Senior Member

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    @Woolie as an aside. Did you ever disinfect an open wound with hydrogenperoxide? If so can you imagine how painfull high endogenous hydrogenperoxide can be?
     
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  5. natasa778

    natasa778 Senior Member

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  6. natasa778

    natasa778 Senior Member

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    Also this one

    Glial contributions to visceral pain: implications for disease etiology and the female predominance of persistent pain

    they go on to speculate that female sex hormone modulation of glial reactivity could be contributing to the female predominance of persistent pain ...


    PS note the major role of purinergic receptors/ATP signalling in the above...
     
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  7. Woolie

    Woolie Gone now, come see me in my new home at S4ME.info

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    @natasa778, if you know about this work, maybe you could do an everyman's summary for us?

    I am troubled by it. In the excerpt you quote it states:

    Okay, so these products, on their own can induce pain. That seems like a pretty good explanation on its own for the higher incidence of many pain syndromes in women, right there. Given that women are much more susceptible to autoimmune illnesses. What's left - which consists largely of menstrual syndromes - well those might not occur very often in those without a uterus! There's also no mention of the persistent pain syndromes that are actually more common in men, such as back pain.

    This is the interesting new idea:

    So the idea is, you can also induce pain just by transferring the reactive microglia to another animal. That's a "central" pain phenomenon, if you mean central as anywhere in the CNS. But still not that central. The effect persists for a limited period (couple of months max).

    Okay, so glial cells can enhance and prolong the sensation of peripherally-induced pain. But only for a short time. Then all goes back to normal if there isn't any peripheral pain stimulus.

    One problem is that this mechanism cannot account for relapsing-remitting pain, which is the more common presentation in most of the conditions mentioned.

    But my big problem is that, it doesn't lead anywhere in terms of interventions. Even if you coudl somehow tranpslant glial cells form a healthy indivudal, that might reduce the intensity of the pain experience a bit, for a while. But then the peripheral factors that initially triggered the pain response will still be in place. So the cycle would just start all over again. We need to target those peripheral factors to really relieve the pain.

    Also, one of the subtitles in the article is this:

    (no, we don't know that. They justify this claim on the basis of the false dichotomy error I mentioned earlier: If there's no tissue damage then the pain must be central. Not true, you might have persistent peripheral factors, such as the persistent production of inflammatory cytokines, and these mechanisms might have nothing to do with the CNS).

    I don't think the approach is going to lead to much in the way of help for people with pain, and I also worry that it could be misused by psychosocial advocates to justify all sorts of dodgy claims and treatments
     
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  8. lansbergen

    lansbergen Senior Member

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    For instance: superoxide production as an early immune response and if the agent is hard or impossible to destroy, ongoing production.
     
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