In my last post we looked at the brain science on pain. Among the facts we observed was that there were two distinct pathways associated with pain. I have a couple more thoughts to add on the brain science front before we turn to a consideration of what this means for assessment. A review of the last post would be helpful for reading this one. How Does Our Brain Register Pain?
Purves et al, explain how the increased activity of the NMDA receptor can amplify the pain impulse coming from the periphery. This is known as the “wind-up phenomenon.” (Sandkulher, 2000) The consequence can be central sensitization and hyper-excitability, which may increase the sensitivity to pain impulses in the whole spinal cord. “The result of such modulation can be hyperalgesia (an extreme or heightened reaction to a stimulus that normally provokes pain) and allodynia, which means pain from a stimulus that normally does not lead to the sensation of pain and often occurs after injury to that site.” (Purves et. al, 2004,p.209-228)
What this amounts to is that we cannot link the two phenomena (ie. the lesion/trauma and the degree of perceived pain) in a reliable way. The effect of this discovery is that policy-making criteria for disability needs to become less dismissive of people’s perceived pain. Although we may be able to understand some of the neuronal modulations and pathways, we can only surmise the degree of sensitivity felt, and there is a big gap when it comes to “lesion-proof.” Therapeutically, emphasis on pain-killers may actually miss the mark as there is more to the story.
In my next post, I’ll provide an example to illustrate this point.