What’s in a name? Nociception by any other name will hurt, or not hurt, just as much

A while back I wrote a piece about Consciousness and Pain, in which I argued that consciousness might be the key ingredient for pain.  I even tried my hand at a bit of maths, with this little equation (not to be taken too exactly): pain = nociception + consciousness.  I got a great response to this post.  People had some really interesting points to add.  While we all basically agreed that nociception—tissue damage/impending tissue damage—doesn’t necessarily cause pain, we couldn’t quite put a name on that ‘catalyst’, that other something that has to be there in order for pain to result.  Is it consciousness?  Or maybe awareness or attention?

There was one comment in there which I’ve been thinking about ever since, because it made me stop and think about the nociception bit first.  I thought it was worth bringing to the fore and starting another discussion.

Tim (sorry to stick you in the spotlight!) said:

Just as we don’t have ‘pain receptors’, perhaps the notion of nociceptors imparts a judgement on the news of difference too early (that judgement being threat)…

Great point.  What Tim is saying here, correct me if I’m wrong, is that we are already imparting a value on an incoming nociceptive stimulus by its very definition, “tissue threatening stimulus” or “an actual or potentially tissue-damaging event”… i.e. I am already aware, attentive, conscious of the fact that I may feel pain very soon because I just hit my thumb with a hammer!  And we’re supposedly not even onto the second half of my equation yet…

If nociception IS NOT pain, that is if the former is incoming stimulus and the latter instead a complex experience, then why do these peripheral receptors have a special name at all?  Admittedly nociceptors are high threshold; they do not respond to any stimuli that are not close to being dangerous to tissue.  But maybe we should just stick with the tried-and-tested innocuous names—thermal, mechanical, chemical sensory receptors, and perhaps just stick a “high threshold” prefix in there for further clarification.  After all, a lot of thermal, mechanical and chemical stimuli are “tissue threatening” or “actual or potentially tissue-damaging stimuli”.  I guess it comes down the least confusing for all of us, and definitely the least likely to create panic and danger messages, for patients.

About Flavia

Flavia Di PietroFlavia Di Pietro is a PhD student in the Moseley Group investigating the development of Complex Regional Pain Syndrome (CRPS) after wrist fracture. Flavia’s PhD focuses on the early detection of brain changes in CRPS using fMRI.  But get this – Flavia did Physiotherapy Honours degree at Notre Dame and completely cleaned up – Brian Edwards Memorial Award, Physio Research Foundation Award, Dean’s Award. Now, these things mean that she is not only ticking the academic boxes but all the other fluffy stuff too. No surprises that the NHMRC of Australia jumped to support her PhD.  So she has come over from Perth where she has been working as a physiotherapist.  All her achievements, however, pale in comparison to her celebrated status as the best Shoe Salesperson south of Milano, as evidenced by her taking out the 2006 and 2008 Diana Ferrari Golden Boot Award.  Clearly, she did not write this bio.

* One of the awards in Flavia’s bio is fictitious.


Editor’s Selection IconThis post was chosen as an Editor's Selection for ResearchBlogging.org [1] Merksey, H. (1986). Pain terms: a current list with definitions and notes on usage. Pain Suppl. 3 S215-S221

[2] Chalmers, D. (1995). Facing up to the problem of consciousness. J. Consciousness Studies, 2, 200-219.


  1. Lorimer says:

    Nice thoughts. I don’t think the thermal grill illusion does change things re nociception because as far as I know it involves a central disinhibtion or ‘unmasking’. I think the ‘dangerfication’ then, happens spinally. One of many examples of pain without primary nociceptive input. What do you reckon Danny?

  2. Doesn’t the thermal grill illusion cast doubt on the whole idea of an isolated, specialised system to detect danger? This would be an example of a sensory paradox that manifests as pain. No peripheral ‘danger’ signal per se, but a nice example of pain being a multi-systems output.

    The nervous system (body) only ever functions as a whole. Notions of peripheral, central etc are purely agreed sub-divisions that exist for the purposes of teaching, research etc etc A neo-cartesianism if you like.


    David Reply:


    thanks for the “Thermal Grill” concept, hadn’t heard of that. Regarding “neo-cartesianism” I can see the parallels but would acknowledge the practicalities from a reseach perspective.

    I must confess I,m not entirely comfortable with the idea that symptom behaviour which is predictable (including the other typical nociceptive markers) is peripherally mediated and when it doesn’t behave as expected then it’s some class of central mal-processing.

    I guess it comes down to attaching putative biological processes to symptom charactaristics?


  3. lorimer says:

    Flavia et al – this is EXACTLY what BiM is about – great conversations, great respect, considered views. I tend to fall back to wanting a label that is sufficiently within reach for people in pain from where they currently sit. For me, I have found the IDEA of nociceptors to work well in this sense. I call them danger receptors – almost a literal translation – and I think this is a defendable position. I think threshold is important, just as there are thresholds for warm and cold systems, alkali and acid systems, but also, as has been mentioned, the functional characteristics of true nociceptors are different. I can see the legitimacy of the debate however – c fibres and a delta fibres can respond to very small changes in internal states, changes that are not dangerous – Bud Craig talks well about this stuff. Also, c-fibres are probably important in their ectopic functions to almost remind the brain of the body – knock them out and we start getting weird perceptual distortions. My position, however, is probably most influenced by my experience explaining pain biology to patients. I have found that removing all qualitative judgement from the peripheral and spinal system by taking away the idea that receptors detect danger as distinct from non-dangerous changes, invokes a substantial ‘it’s all in your head’ burden, i have to carry and ultimate disengage. I find it easier to avoid that if I endorse nociception, nociceptors and that some things are truly dangerous and that we have a magnificent danger-detection system.
    Thanks for taking the time all of you. L

    David FitzGerald Reply:

    a very pragmatic view to acknowledge both peripheral and central sensitivity events in the patients pain experience without applying a value judgement on mechanism.
    Do you think all nociceptive mechanisms have a central manifestation / signature?

    I think one clinical challenge is to distinguish pure peripheral nociceptive mechanisms (if that is ever possible), centrally enhanced peripheral input mechanisms and defective descending inhibitory syetems.

    Otherwise we are left with a strategy of a “blunderbus” approach where all of the speculative mechanisms involved in the pain experience become legitimate therapeutic targets.Whilst this is an advance on a purely peripheralist approach I do think it still requires refinement.

    I,m around enough to remember short wave diathermy and hydrotherapy as the dumping grounds for resistant musculoskeletal pain. I wouldn’t like to think we are just replacing them with something more cognitively attractive but nonetheless a “catch all” category.


  4. Jason asked, “Beyond threshold, what differences would you cite?”

    Many nociceptors have this suite of characteristics.

    1. They are often polymodal, and respond to the same suite of stimuli: mechanical stimulation, extreme pH, and temperature around around 45°C.
    2. They become sensitized to repeated stimuli, whereas most sensory neurons tend to habituate.
    3. They are often agonized by similar sets of chemicals, like capsaicin.

    These are not present in every single nociceptor, but are examples of strong “family resemblances.” You find sensory neurons with these properties in mammals, fish, and some invertebrates.

    “If the line is arbitrary and threshold based then we are just contributing to the pain/nociception conflation that plagues medicine in general?”

    That is can be difficult to make fine distinctions doesn’t mean that you can’t make coarse distinctions. “Tall” and “short” are useful classifications, even if there is no generally agree upon cut-off as to when someone is “tall” or when someone is “short”. Similarly, that there could be some overlap in classification of some sensory neurons does not mean the classifications are useless.

  5. Tim Cocks says:

    Hi Flavia

    Incredibly honoured to have been quoted on this site!!

    I think you have, in a much more eloquent and succinct manner, reflected my thoughts, from what was a bit of a rambling comment!

    I will happily defer to other commentators with greater knowledge of receptor anatomy and behavior, the essence of my thought was more in the concept and language associated.

    There are various logical levels/types happening here.

    The scientific discussion -valid and highly appropriate on this site, is at a different level than where i was aiming (think Bertrand Russell, set theory, logical inclusion… in terms of hierarchy, not one based on value judgments).

    In reconceptualizing pain and teaching others (patients/clients/public etc) i have found it useful to discuss the reception of stimuli (whatever they may be) as ‘news of difference’ or simply ‘hey, something is happening here’ as the starting point, as opposed to nociception – again simply because nociception implies a value judgement as the stimulus being threatening/harmful.

    If one of the goals of pain education is to de-threaten the whole process, the use of this language, i have found, can be beneficial.

    It puts that class of stimuli that would normally be discussed as being nociceptive, with the other class of stimuli that includes such experiences as light touch, pressure, warmth, electromagnetic radiation….. presence of aromatic molecules etc etc.

    This approach can also highlight further, that it is the mind making a decision about threat (not the tissues and associated receptors) and whether or not to include pain as one of the multi-system outputs in response to the particular context.

    I’ve found this useful to further normalize the experience of pain as a natural and necessary occurrence with beneficial intentions and outcomes of protecting us.

    Again the discussion will, necessarily, occur at various levels, my fascination is with the linguistic aspects, the story, the narrative, that we use with people in pain.

    In my personal opinion, in response to the questions of “what’s in a name?” my answer would be EVERYTHING!!

  6. Bronnie Thompson says:

    I look forward to a discussion about this distinction between Bogduk and friends and yourselves! There are nocifensive behaviours (eg increased heart rate) that occur without consciousness – while I don’t think this equates with pain, it does suggest that ‘something else’ is going on, and you could call this part nociception.
    What you call the receptors that initiate the chain of events leading to nocifensive behaviours is possibly a combination of mechano, thermo, chemo etc receptors, and the addition of high thresold nociceptors.
    My attention is drawn, not to this part of the pain puzzle, but as you’d expect, to the events and structures that are initiated by nocifensive behaviour.

  7. Jason Silvernail says:

    You said, “There are enough common features across many different taxa that indicate that nociceptors are a physiologically and functionally distinct set of sensory neurons.”
    Beyond threshold, what differences would you cite? Perhaps there are morphological or physiological differences here other than threshold that I’m not aware of – and I’d certainly like a knowledge update.

    You said, “Plus, “tissue damage” is not a value judgement. It’s reasonably objective whether a stimulus does, or does not, damage tissue.”
    This is true but doesn’t address the issue of receptor activation. The question I think we’re pondering, or at least the one I’m pondering, is that for a given minimal stimulus that damages tissue, are nociceptors activated? And conversely are they activated for stimuli that don’t damage tissue?

    If the issue is simply one of threshold then I would suppose that we could show at least some noiciceptors activating in the absence of some tissue damaging stimulus and conversely the failure of at least some nociceptors to activate in the presence of tissue damaging stimulus. Of course that’s just speculation on my part but I’m not aware of such a thing every being demonstrated or studied. Maybe a great paper is out there and I just haven’t read it.

    If I read Flavia correctly, she’s wondering about the sort of question I’m asking – that if the difference is just threshold then where are we drawing the line on what’s a “nociceptor” and therefore contributes to nociception and what’s a “mechanoreceptor” and just contributes to a non-nociceptive sensory experience? Because if indeed the issue is just threshold (and my read of your previous comment says maybe I’m wrong about that being the only issue), then where are we drawing the line between “nociceptor” and “not a nociceptor”? If the line is arbitrary and threshold based then we are just contributing to the pain/nociception conflation that plagues medicine in general? If there are real morphological and physiological differences beyond threshold then we need to ask if those differences are relevant to tissue damage or not. And if not, then maybe the issue of nociception and its definition relative to pain needs to be reexamined.

    David Reply:


    one example that springs to mind is neurogenic inflammation initiatiated by antidromic c-fiber activation. If memory serves me correctly the neuropeptide release from synaptic terminals as a consequence of antidromic C-fiber activation initiated a local biochemical cascade inducing peripheral sensitisation in the absence of specific local damage.

    I suppose this could be classed as supra-threshold chemical activation of “silent” nociceptors but not strictly associated with tissue trauma.

    In my NOI faculty days we used to cite this as an example of secondary tissue sensitivity (secondary hyperalgesia I guess) as a consequence of peripheral neuropathic dyfunction (sick nerves), usually of the sub-clinical variety as percieved by clinical neurophysiology, but very clinical for the patient with refactory shoulder capsulitis, lateral epicondylitis, Achilles Tendonopathy, plantar faciatis in the presence of a spinal spondylitic history.

    All speculative and inferred as biologically plauaible rather than certain fact -I hasten to add!!



  8. “(M)aybe we should just stick with the tried-and-tested innocuous names—thermal, mechanical, chemical sensory receptors, and perhaps just stick a “high threshold” prefix in there for further clarification.”

    Too cautious, methinks. There are enough common features across many different taxa that indicate that nociceptors are a physiologically and functionally distinct set of sensory neurons.

    Plus, “tissue damage” is not a value judgement. It’s reasonably objective whether a stimulus does, or does not, damage tissue. I do agree that “potentially damaging if prolonged” is trickier, but definitions always get fuzzy around the edges.

    Luke Parkitny Reply:

    There is an interesting way of tying together the idea of visceral sensations being different and tissue damage being a value judgement. One of my interested (temporarily shelved due to other interests) has been in the field of gastroenterology, in particular disorders including IBS and IBD. There are very fascinating parallels in the gastro literature with all the other pain knowledge. The experiments on rectal distension, for instance, showing very much non-traumatic stimulation of pain in certain people (with positive correlations with non-traumatic factors like a history of sexual abuse for instance).
    In the area of cardiac pain, we’ve been aware for over a century that people can very much become aware of those nociceptors prior to any signficant damage taking place.
    There are certainly differences in the way visceral pain is interpreted and we probably do not understand it as well as non-visceral pain, but there are plenty of fascinating parallels.
    I think calling it a value judgement implies that there is a strong conscious overtone and is more correctly explained as being a complex mixture of sometimes very complex factors; trauma only being one of those factors.
    From evolutionary perspectives it might be logical to think that we would probably recycle as many mechanisms as possible for the different sensations – just change the things that are absolutely required.

    David Reply:

    I would agree with the parallels between visceral and mechanical pain and the role of a “value judgement” with previously experienced sensations.
    I guess we’re dealing hear with the resultant neural output of a combination of sensory (nociceptive) and cognitive processing – with the key ingredient being a comparative scale of previous experience /exposure?

    But to return to Flavia’s thesis regarding nociceptor activation in the absence of tissue pathology we’re still have this conundrum of “unpleasant sensations” without obvious demonstrable pathology as we define it. Neil’s recent post on spinal imaging also addresses this.

    Regarding visceral pathology, if we could rely on sensory feedback (whatever modality we call it) then there would be no need for angiograms to measure cardiac function, colonoscopy for bowel lesions, Ultrasound for liver function, mammography, blood work-ups etc.

    Is the interpretation that demonstrable pathology (by these measures) has not yet become supra-threshold from a nociceptor perspective?


    Luke Parkitny Reply:

    The interpretation should really be that the pathology has either become suprathreshold but maybe (1) has been arrested by inhibitory processes, say DNIC (in that case trauma without significant pain), or maybe (2) has reached threshold and there is excessive pain (central facilitation). I am not sure that we can speak of the nociceptor as a functionally separate entity from the other modulating mechanisms.

  9. Flavia

    your argument assumes that we have conscous awarness of impending tissue dammage. Whilst that model may apply to mechanical pain it is unlikely to with visceral pain.

    I always remember and old saying by David Butler that we never know much about our heart nociceptors until the fateful moment – they merrily function away with other neurochemical homeostatic tasks until needed.

    Now if we survive the nociceptive warning, we may then become the proverbial “cardiac cripple” who equates percieved exertion with impending doom. Indeed becoming aware of nociceptors may be bad for your health! Theres a new public healh slogan.


  10. Flavia-
    Great point. I often try to emphasize when speaking about pain that nociceptors are not coded for any information the other receptors aren’t – its simply a question of threshold. Perhaps our characterization and separate naming for these receptors as linked with actual/potential tissue damage is responsible for a continued conflation in the nociception/pain issue?

    I’d be interested in some basic science that might find the actual threshold of some of these receptors, physiologically, and see if reaching that threshold with mechanical, thermal, or chemical stimuli is linked to any signs of actual tissue damage such as plastic deformation of connective tissue or an inflammatory response. My sense is that it wouldn’t correlate well, but that’s just a guess at this point.

    In the meantime some reading that may shed light on this issue generally: