Interoception and pain – is it better to be ignorant?

I just read a fascinating paper by Pollatos and colleagues[1] in a recent issue of Pain. This paper evaluated the relationship between interoception (ie, the ability to consciously perceive signals from the body) and pain perception. This study was based on the theory that emotive stimuli initiate changes in physiological and bodily processes and that it is the perception of these reactions that defines the emotional component of that experience.[2] As pain is arguably made up of both sensory and emotional components, the authors were interested in the relationship between pain and the ability to perceive physiological changes.

To evaluate interoception, participants estimated their own heart rate and compared this estimation to actual heart rate count (evaluated by electrocardiography). Participants were split into two groups: high interoceptive sensitivity (high IS; very accurate estimation) and low interoceptive sensitivity (low IS; more error in estimation). Then using a pressure algometer, pain threshold and tolerance levels were determined (with perceived pain unpleasantness and intensity also measured). Importantly, during the application of the pressure pain tests, heart rate (HR), respiration rate, sympathetic function, and sympathovagal balance were also measured.

Interestingly, high IS participants had lower pain threshold and tolerance scores than low IS participants and they also rated threshold level stimuli as significantly more unpleasant. High IS participants also had greater increases in HR during the pain assessments and more autonomic reactivity (ie, greater decrease in parasympathetic function; greater increase in sympathetic influence on sympathovagal balance). Sympathovagal balance was positively correlated with IS level (ie, the better you are at perceiving HR, the greater the increase in sympathetic function in response to pain). Last, regression analyses demonstrated that IS level was the main factor that explained variability in pain threshold and tolerance. This led the authors to conclude that “better detection of internal signals and evoked bodily changes seems to increase pain perception for pressure pain”. That autonomic reactivity (ie, change in sympathovagal balance) was not significant in the regression analysis (outcome pain tolerance) was used by the authors to suggest that it is actually interoceptive sensitivity that is the key to guiding one’s individual responses to noxious stimuli.

I wondered about the alternative conclusion – that people who have heightened bodily responses to painful stimuli are better able to detect bodily responses in general.  Is it not possible that people who find pressure stimuli more painful have greater physiological responses to noxious stimuli in general (ie, greater changes in sympathetic function and thus heart rate)? And if they have greater changes in heart rate to noxious stimuli in general, would that not be easier to detect and wouldn’t they get good at it (ie, high initial IS)? What if autonomic reactivity (ie, how sensitive your ‘system’ is to stimuli) was the most important factor to guide response to noxious stimuli (ie, pain tolerance and unpleasantness)?

So I thought for sure that interoceptive sensitivity would actually be a mediator of the relationship between autonomic reactivity and pain threshold. Just a bit of background: in order to be a mediator, four things must be present.[3]

1) There must be a relationship between the potential mediator (interoceptive sensitivity) and the outcome of interest (pain tolerance), when the independent variable (autonomic sensitivity) is controlled for. Yes there was!

2) There must also be a relationship between the mediator (IS) and the independent variable (autonomic sensitivity). Yes there was!

3) When both the mediator (IS) and the independent variable (autonomic sensitivity) are in the regression model, the independent variable must no longer be significantly related to the outcome of interest (pain tolerance). Yes there was!

4) There must be a relationship between the independent variable (autonomic sensitivity) and the outcome of interest (pain tolerance). But there wasn’t!

So my theory was totally wrong! However, interoceptive sensitivity definitely seems to be a measure worth following up in future studies. And if interoceptive sensitivity is the key issue, could this be a possible mechanism behind pain reduction with meditation? Fascinating indeed.

Tasha Stanton

Tasha Stanton 1 150x150 Interoception and pain – is it better to be ignorant?  Tasha Stanton is a postdoctoral research fellow working with the Body in Mind Research Group both in Adelaide (at University of South Australia) and in Sydney (at Neuroscience Research Australia). Tash has done a bit of hopping around in her career, from studying physio in her undergrad, to spinal biomechanics in her Master’s, to clinical epidemiology in her PhD, and now to clinical neuroscience in her postdoc. Amazingly, there has been a common thread through all this hopping and that common thread is pain. What is pain? Why do we have it? And why doesn’t it go away?  Tasha got herself one of the very competitive Canadian IHR post-doctoral fellowships and is establishing her own line of very interesting investigations.  Her research interests lie in understanding the neuroscience behind pain and its clinical implications. She also really likes nifty experiments that may have no clinical value yet, but whose coolness factor tops the charts. Last, Tash is a bit mad about running, enjoying a good red with friends and organizing theme parties. Tasha, aka Stanton Deliver, was the all round best performer at the Inaugural BiM Table Tennis Comp.

Here is Tasha talking more about what she does and a link to her published research.


[1] Pollatos O, Füstös J, & Critchley HD (2012). On the generalised embodiment of pain: how interoceptive sensitivity modulates cutaneous pain perception. Pain, 153 (8), 1680-6 PMID: 22658270

[2] James W. (1984). What is an emotion? Mind 9:188-205.

[3] Baron RM, & Kenny DA (1986). The moderator-mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations. J Pers Soc Psychol, 51 (6), 1173-82 PMID: 3806354



  1. I have always wondered if the ability to percieve pain were normally distributed like other physiological things. If it were then high potential individuals would have high capacity to feel pain and then it would give them the life experiences – introversion due to negative feedback from experiences and anxiety as a learned behaviour in response to all this pain. This would give us the answer to the chicken and egg. Pain or personality. Purely academic because we treat who we see and accept who they are. Just nice to know a bit about how they got there and that it is not in anyway their fault.
    Good to have another way in which mindfullness can work at a neuro level. The more the merrier.


  2. Thanks for the insight. It was interesting that they used heart rate as a measure of interoception. If they used detection of respiration rate, would this potentially have a reverse relationship ? When looking at the insular cortex and ‘awareness’ of visceral sensations, it seems perception is geared towards threat. Hypervigilance is invariably bad – heart rate seems linked with fear response (? James-Lang hypothesis) and activating the parasympathetic system seems to come most easily through the breath. There are studies of FMS in which patients went into ‘remission’ when they started to pay attention to some of their symptoms, equate it with increased stressors in their life and then proactively took steps to manage their stressors. Interoception with interception after introspection !


  3. Very interesting. Something missing here though in the path from sensation to pain. I can see how more sensativity/awareness can lead to more pain (or more pleasure depending on the stimulas and context). However, with improved self-awareness the reaction to the stimulus can be changed. Just as we can train ourselves to not punch someone out when they are aggresive toward us, we can also change our reaction to potentially painful stimuli. As well as being sensative to a stimulus, I can be sensative to my reaction to stimulus and use that to learn to control that reaction. That could lead the sensative individual to actually having less pain/reaction.


  4. Psychologically flexible people may be able to modify their neuromatrix output. And may do it better if they are clued up with helpful neurophysiological understanding.
    People who are not or folk who have maladaptive coping behaviours or the wrong context to understand this stuff in. The spouse chipping away. All the BPS reasons we see associating with persisting pain.
    At the end of the day they could have an equivalent of a 100Mbps broadband pipe from body to brain where the next person has 10Mbps. And the next 1Mbps – is it possible to know? Is it safe to assume we are all ther same in this regard? I think not from my clinical experience. It could be about information rate of flow. Or how that flow is filtered. As well as how it is processed. As well as what is know in the brain by the mind. And all the stuff yet unknown in science!
    Happy Mondays.


  5. Hi Tasha, I was wondering if you could provide a clear explanation of the conjoint relationship between the anterior insular cortex and the anterior cingulate with respect to interoceptive sensitivity as outlined above. Without the relationship between autonomic sensitivity and pain tolerance – when dealing with complex pain (such as CRPS) is there a clear understanding why there are sympathetic independent and dependent variants ? Why does dealing with those that are sympathetically mediated (SG blocks) temporarily reduce their pain ? The neurogenic inflammation bit in CRPS is tough to explain to patients. Finally, slightly off topic, why is there a noted increase in thickness (or gyrification) in the insular cortex in meditators ? It makes sense that meditators are better able to shift away from DMN (default mode) and stay in the moment but why is there so much increased activity in the AIC (and ACC) with persistent pain states ? – simply heightened awareness again (but in a negative sense) ? Sorry, I know you shouldn’t look at parts of the brain in isolation but I’m hoping for more clarity. If you could recommend an article, that would be great ! Thanks.


  6. Stuart. There is an interesting article going into Pain soon – Functional Connections Between Self-Referential Thought and Chronic Pain:
    A Dysfunctional Relationship by Fadel Zeidan, Robert C. Coghill. Also there is Returning from Oblivion: Imaging the Neural Core of
    Consciousness from The Journal of Neuroscience, April 4, 2012 • 32(14):4935– 4943 • 4935.
    There is so much coming through and all roads seem to lead to the ACC at the moment.
    Thanks Tasha for starting this thread off – I have been using this as part of the neurophysiological education of FMS patients since I read it here :)


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