Clifford Woolf, who some may know as the ‘father of central sensitisation’, recently wrote a commentary to PAIN.[1] It piqued our interest because it was about the use of the term ‘central sensitisation’, and we suspect we know people who’d insist that the term ‘central sensitisation’ should only be used to describe changes at the dorsal horn, and who’d think of that insistence as being true to the beliefs of the person who first described the phenomenon.
Per Hansson had written a topical review objecting to the frequent, inappropriate use of the term ‘central sensitisation’ (which I shall now call ‘CS’) as though its definition extended beyond that provided by the IASP.[2] Hansson had said that the term is used loosely, and often to name a reason for clinical phenomena that have not been demonstrably linked to CS. His solution was to remove the term from the clinical context entirely, and to restrict its use to the preclinical context, where neural activity can be controlled and measured.
Woolf wrote a concise, pointed objection to Hansson’s essay, nailing his own colours to the mast in a few succinct points.
First, Woolf tackled the IASP’s definition of CS, saying that ‘CS’ should refer to “all forms pain sensitisation that arise within the central nervous system”. This was fundamentally different to Hansson’s ideas, which seemed to restrict CS to describing the phenomenon as it was first discovered: dorsal horn changes induced by peripheral input.
Woolf argued that there is little basis for such a restriction of use, because processes similar to the ‘original CS’ have been identified in other central nervous system locations and with other drivers. The concept of CS is useful principally because it distinguishes between pain problems that are driven by peripheral dysfunction and those driven by central dysfunction.
Hansson had also suggested that ‘CS’ ought to be used with subcategories denoting possible causative mechanisms. Woolf’s rebuttal was that the mechanistic drivers of the sensitisation are often difficult to identify or isolate, and may change with time, and so to limit the use of CS to sensitisation due to a particular cause would not be helpful. However, he said, further qualifying terms could be used in conjunction with the term ‘CS’ where they are known and considered helpful. Woolf’s priority seems to be to reserve the clinical utility of the term. His definition allows it to serve as a useful descriptor which hints at possible causative mechanisms, but does not require recordings of neuronal activity.
At this point we must ask for clarity on the distinction between central sensitisation and a lowered pain threshold to a given stimulus: what is the difference? To me, it seems clear that a lowered pain threshold is a clinical finding, whereas (in Woolf’s view) central sensitisation is one of two mechanisms that could underlie that finding. Peripheral sensitisation is the other option; if that can be ruled out, then the patient’s lowered pain threshold is probably due to central sensitisation.
I find it interesting that Woolf does not distinguish, in his definition of CS, between pain and nociception. Of course, to make it about sensitisation of nociception would require measurement of said nociception, which would drastically limit the clinical utility of the term ‘CS’, and indeed, perhaps the idea. However, sensitisation of pain is tricky, too, because it implies that the usual amount of pain to a given stimulus is both known and reliable. Perhaps, though, this is exactly what we do when we identify hyperalgesia: we assume that we know how much pain the person should be feeling – a questionable assumption in itself.
Hansson had highlighted the paucity of research into what he describes as a patient “setting new criteria for pain reporting as a result of a concomitant pain experience”, and how such shifting criteria might influence clinical findings. He suggests a new term for such a situation: “cognitive-emotional sensitisation”. Woolf objects to this idea by stating the obvious: that teasing apart psychological from neurological drivers is not relevant if psychological drivers influence neuronal activity – these psychological factors would merely represent another driver of CS. And then he tackles an ‘elephant in the room’: the idea that it is acceptable to think that patients are not being truthful when they report experiences that we do not understand. Although I am not convinced that Hansson himself suggested such an idea, it is a helpful and important reminder to us all to listen to the patient.
As a spectator to this particular show of words and arguments, it occurs to me that this conversation seems rather overdue. I have heard the term ‘central sensitisation’ bandied about with all sorts of meanings, and few people seem to be entirely clear about what is meant, or whether everyone is really talking about the same thing. Perhaps this Hansson-Woolf-IASP show will lend greater clarity to those conversations in the future.
Tory Madden
Tory arrived from South Africa to start her PhD at BiM. She is a physiotherapist who worked clinically before turning her focus toward research. She is interested in pretty much anything related to pain and neuroscience, thanks to some particularly inspirational teaching by Romy Parker during her undergraduate training at the University of Cape Town.
Tory’s research looks at classical conditioning and pain. She is also an associate editor for BiM. She tries to spend much of her spare time exercising to compensate for the vast quantity of chocolate that lives in her bottom desk drawer. Luckily, she loves trail running as much as she does food.
References
[1] Woolf CJ (2014). What to call the amplification of nociceptive signals in the central nervous system that contribute to widespread pain? Pain, 155 (10), 1911-2 PMID: 25083929
[2] Hansson P (2014). Translational aspects of central sensitization induced by primary afferent activity: what it is and what it is not. Pain, 155 (10), 1932-4 PMID: 25067835