Facial pain displays: systematic analyses of variations in encoding patterns, their underlying mechanisms and their impact on decoding performance
Final Report Abstract
The facial expression of pain is an important pain indicator that plays a significant role in social interactions and is also of great clinical relevance since it affects pain diagnostics and pain treatment. Against this background, is seems alarming that many individuals use this communication channel insufficiently by showing reduced or even no facial expression (“facial silence”) although they report to be experiencing pain. It is believed that based on social display rule we learn in early childhood to inhibit the facial expression of negative affective states, including pain. However, even individuals from the same cultural background differ immensely with regard to the degree to which they facially express pain. So far, we know very little about (i) how the degree of facial expressiveness of pain is regulated in the brain and (ii) which factors – besides social learning - underlie the regulation of facial expressiveness. (i) Within the present project we could show that the medial prefrontal cortex (mPFC) is one of the key structures involved in the regulation of facial expressiveness during noxious stimulation. Using rTMS to disrupt the activity of the mPFC led to increased facial expressiveness (without changing self-report ratings of pain), or in other words to a disinhibition of facial responses to pain. Thus, the activity of the mPFC might reflect the implementation of learnt social display rules, which are regulating when and how one should express pain via the face. (ii) Moreover, we found that the tendency to facially express pain was closely associated with the ability to inhibit automatic motor responses. The better an individual was in inhibiting automatic motor responses (as assessed with the anitisaccade task) the more facially stoic the individual responded to noxious stimulation. Interestingly, this association between the degree of facial expressiveness and inhibitory functioning was only true for the specific form of “automatic motor inhibition”, given that no correlations were found with the performance in the Stroop task or with self-evaluated impulse control. Accordingly, the degree of facial expressiveness in response to pain is specifically regulated by motor inhibitory mechanisms, but is not regulated by inhibitory mechanisms in general. We also tried to investigate whether the tendency to facially express pain is regulated by serotonergic pathways. The role of serotonin was investigated using a genetic approach (assessing variations in the promoter region (5-HTTLPR) of the serotonin transporter gene) as well as acute tryptophan depletion. The findings were somewhat inconsistent. However, they seem to suggest that serotonin does not seem to play a crucial role in the learnt downregulation of facial expressiveness during noxious stimulation. However, more research is needed to really know which role serotonergic pathways play in the regulation of facial expressiveness.
Publications
- (2015). The role of inhibitory mechanisms in the regulation of facial expressiveness during pain. Biological Psychology, 104, 82-89
Karmann, A. J., Lautenbacher, S., & Kunz, M.
(See online at https://doi.org/10.1016/j.biopsycho.2014.11.016) - The role of prefrontal inhibition in regulating facial expressions of pain: a Repetitive Transcranial Magnetic Stimulation Study. The Journal of Pain, Volume 17, Issue 3, March 2016, Pages 383-391
Karmann, A. J., Maihöfner, C., Lautenbacher, S., Sperling, W., Kornhuber, J., & Kunz, M.
(See online at https://doi.org/10.1016/j.jpain.2015.12.002)
