Thanks again for another very interesting post Lorimer. I have not read the paper in detail yet, but based on your own summary I think that variations in what we mean when we say “central sensitisation” are important in this regard. We must be careful that we don’t add to the confusion, by focussing on the small areas of controversy between research groups, at the expense of ignoring the vast swathe of literature which is in agreement on the vital role of the CNS in persistent pain. I accept that in terms of fully understanding the phenomenon of pain, differentiating the precise mechanisms involved (homo- v hetero-synaptic, role of descending modulation etc..) is clearly important work. But none of the current controversies or points of confusion on “central sensitisation” weaken the evidence that pain involves a hell of a lot more than a local tissue (joint, disc, muscle, “trigger point” or whatever). It might seem simplistic, but my impression is that wider society (and sadly a majority of healthcare professionals) are still wedded to the predominant role of peripheral tissue “damage” as a cause of pain. Therefore, the message that CNS changes are pivotal in pain needs to be heard loud and clear by the public. In the meantime, we can try to figure out exactly how these CNS changes work (facilitation, inhibition, etc…) and what we can do to address them.