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 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.
References
[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