domingo, 1 de maio de 2011

Central Sensitisation


DECADES OF DENIAL

We have known about central sensitisation (CS) for at least 20 years, since Patrick Wall, Clifford Woolf and others published seminal papers suggesting that some pain and altered sensory states may be due to synaptic and membrane excitability changes in the central nervous system and not necessarily due to processes in tissues. This should have been a great relief to health professionals, but attempts to introduce the notion into rehabilitation, especially the manual therapy world (Butler 1994; Gifford and Butler 1997) were met with slow acceptance and often derision. I can recall introducing it in a conference in Scandinavia in the early 90s with the following speaker saying "well that's well and good but we have to get on with the treatment", and so the next session was on muscle stretching. "You are turning into a counsellor" was another comment. Many prominent physiotherapists and anatomists still deny the state and the current level of integration in most undergraduate and postgraduate programmes appears little more than lip service. Central sensitisation underpins modern biopsychosocial holistic management, yet we have a long way to go to integrate it. It deserves core curriculum status. A hot off the press review article by Clifford Woolf (2010) makes me believe that there may be a growing knowledge gap between science and practice.

ADMITTING THAT THERE IS MORE TO THE STORY

For health practitioners to take on central sensitisation, they usually need to accept that the old peripheral story is not complete. A trigger point may have little to do with issues in the soft tissues, the palpably tender C2-3 nothing to do with processes around the joint, and the irritated gut only partly related to the gut, but are now known to be more due to a central nervous system which has lost the ability to "feature extract" from input and defaults quickly to a pain construction. The pathophysiology of this state is now well described. See Latremoliere (2009) and Woolf (2010) for updates. Of course this can be a challenge – many successful practitioners have a lot of clinical mileage at stake and large investments in continuing education. While many readers of these notes will have embraced it, most of the rehabilitation community is yet to integrate it.

A WORD FROM A BIG PICTURE EXPERT

Gordon Waddell (1998) summed it up nicely when defending modern holistic biopsychosocialism "it is all very well to say that we use science and mechanical treatment within a holistic framework, but it is too easy for that framework to dissolve in the starry mists of idealism. We all agree in principle that we should treat people and not spines, but then in daily practice we get on with the
business of mechanics."

"BUT WHAT ABOUT CHRONIC KNEE OA AND OA HIPS THAT RESPOND
TO HIP REPLACEMENT?"

The hard core biomedicalists often bring this out as evidence of the tissue base of chronic pain. Of course, these are peripheral diseases which are often amenable to peripherally directed management. But even here, the degree of pain does not match radiological finding or degree of inflammation, suggesting a central mechanism as well (Bradley, Kersch et al. 2004). In OA knees (Arendt-Nielsen, Nie et al. 2010) and OA hips, there is impaired central inhibitory controls. This key feature of central sensitisation will improve with hip replacement (Kosek and Ordeberg 2000). This and other data summarized by Woolf (2010) strongly suggests central sensitisation should be a consideration in all acute and chronic pain states.
Fonte: NOI Group