Hi Mike,
The paper posted by Sandel “The origin of all Pain is Inflammation and the Inflammatory Response” appropriately addresses the audience for which it was intended.
To answer your question one simply needs to scroll down to the conclusion.
Quote:
In accordance with our Law of Pain, the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile.
Treatment of pain syndromes should be based on these principles:
1. Determination of the inflammatory profile of the pain syndrome
2. Inhibition or suppression of production of the appropriate
inflammatory mediators e.g. with inflammatory mediator blockers or
surgical intervention where appropriate
3. Inhibition or suppression of neuronal afferent and efferent (motor)
transmission e.g. with anti-seizure drugs or local anesthetic blocks
4. Modulation of neuronal transmission e.g. with opioid medication.
At the L.A. Pain Clinic, we have successfully treated a variety of pain syndromes by utilizing these principles. This unifying theory of the biochemical origin of pain is compatible with, inclusive of, and unifies existing theories and knowledge of the mechanism of pain including the gate control theory, and theories of pre-emptive analgesia, windup and central sensitization. Our current knowledge is rudimentary and but a beachhead in the vast frontier of inflammation and the inflammatory response. We have medications for only a few of these mediators. More research is needed to understand and develop new drugs and interventions to treat inflammation and the inflammatory response and thus to conquer pain.
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As the authors state "Our current knowledge is rudimentary". It has provided some current forward thinking guidelines for treatment based on a set of principles outlined above. It's a broad paper and doesn't address your specific question about the problem of post-cytokine pain with any great depth. I don't believe that is well understood by many practicing doctors let alone many of the researchers.
The problem as I see it is that the science is just now starting to understand chronic pain. Most clinicians still use the surgical pain model to bridge the gap between acute pain and chronic pain. There is little general knowledge among many medical professionals of the fact that it is the persistence of that acute pain that in fact leads to chronic pain although I do believe the tides are changing.
Most people understand acute pain, you break an arm, you set it in a cast give some pain relievers and it heals. It wasn't until most recently that chronic pain began to be accepted by the medical professionals as a disease process in and of itself.
As patients we have all experienced an analgesic gap, a specific time period during pain therapy when our pain is unrelieved. This sets off a whole series of mechanisms, which is where I believe your question is leading.
Unfortunately there is still a huge gap in translating the most recent discoveries of chronic pain research to the bedside and that where most of us wallow in our frustrations.
Hope you are doing well.
MsL