Cort
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: Trends Neurosci. 2009 Sep 23. [Epub ahead of print]
Critical role of nociceptor plasticity in chronic pain. Reichling DB, Levine JD.
http://www.ncbi.nlm.nih.gov/pubmed/19781793?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
They seem to be making quite a bit of progress in understanding chronic pain (and one hopes that this will give them an insight into chronic fatigue as well!).
This is so interesting. The Dubbo group has shown that people who come down with ME/CFS after an infection tend to have abnormally high cytokine levels during the infection.
Here we have a paper stating an 'inflammatory insult' or 'environmental stressor' can trigger 'long-lasting hypersensitivity' of the nerve receptors for pain; they essentially flip on the pain switch in the nerves sending pain signals to the brain.
(This suggests the problem is not in the brain as many have suggested that the nerves sending signals to the brain. Yes, the brains pain producing pathways are overly activated - but they're activated by the problems in the nerves in the body. Interestingly Dr. light somewhat similar thesis for ME/CFS; the receptors for muscle damage are way over sensitized in ME/CFS - they are continuously sending pain and fatigue signals to the brain. )
They even think they know how this happens; protein kinase C. - which controls the signaling pathways - appears to flip the system into a hypersensitive state. Essentially it sounds like a system which should be turned on during an injury -stays on.
This is the biochemistry of chronic pain! When they get down to things like signaling molecules specific pathways you get the feeling that they may be getting close. Very hopeful stuff!
Critical role of nociceptor plasticity in chronic pain. Reichling DB, Levine JD.
http://www.ncbi.nlm.nih.gov/pubmed/19781793?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
They seem to be making quite a bit of progress in understanding chronic pain (and one hopes that this will give them an insight into chronic fatigue as well!).
This is so interesting. The Dubbo group has shown that people who come down with ME/CFS after an infection tend to have abnormally high cytokine levels during the infection.
Here we have a paper stating an 'inflammatory insult' or 'environmental stressor' can trigger 'long-lasting hypersensitivity' of the nerve receptors for pain; they essentially flip on the pain switch in the nerves sending pain signals to the brain.
(This suggests the problem is not in the brain as many have suggested that the nerves sending signals to the brain. Yes, the brains pain producing pathways are overly activated - but they're activated by the problems in the nerves in the body. Interestingly Dr. light somewhat similar thesis for ME/CFS; the receptors for muscle damage are way over sensitized in ME/CFS - they are continuously sending pain and fatigue signals to the brain. )
They even think they know how this happens; protein kinase C. - which controls the signaling pathways - appears to flip the system into a hypersensitive state. Essentially it sounds like a system which should be turned on during an injury -stays on.
This is the biochemistry of chronic pain! When they get down to things like signaling molecules specific pathways you get the feeling that they may be getting close. Very hopeful stuff!