Psychophysiological responses to visceral and somatic pain in functional chest pain identify clinically relevant pain clusters
Version of Record online: 18 OCT 2013
© 2013 John Wiley & Sons Ltd
Neurogastroenterology & Motility
Volume 26, Issue 1, pages 139–148, January 2014
How to Cite
Farmer, A. D., Coen, S. J., Kano, M., Naqvi, H., Paine, P. A., Scott, S. M., Furlong, P. L., Lightman, S. L., Knowles, C. H. and Aziz, Q. (2014), Psychophysiological responses to visceral and somatic pain in functional chest pain identify clinically relevant pain clusters. Neurogastroenterology & Motility, 26: 139–148. doi: 10.1111/nmo.12245
- Issue online: 13 DEC 2013
- Version of Record online: 18 OCT 2013
- Manuscript Accepted: 15 SEP 2013
- Manuscript Received: 27 JUL 2013
- Medical Research Council. Grant Number: MGAB1A1R
- Functional chest pain of presumed esophageal origin;
- pain clusters;
Despite chronic pain being a feature of functional chest pain (FCP) its experience is variable. The factors responsible for this variability remain unresolved. We aimed to address these knowledge gaps, hypothesizing that the psychophysiological profiles of FCP patients will be distinct from healthy subjects.
20 Rome III defined FCP patients (nine males, mean age 38.7 years, range 28–59 years) and 20 healthy age-, sex-, and ethnicity-matched controls (nine males, mean 38.2 years, range 24–49) had anxiety, depression, and personality traits measured. Subjects had sympathetic and parasympathetic nervous system parameters measured at baseline and continuously thereafter. Subjects received standardized somatic (nail bed pressure) and visceral (esophageal balloon distension) stimuli to pain tolerance. Venous blood was sampled for cortisol at baseline, post somatic pain and post visceral pain.
Patients had higher neuroticism, state and trait anxiety, and depression scores but lower extroversion scores vs controls (all p < 0.005). Patients tolerated less somatic (p < 0.0001) and visceral stimulus (p = 0.009) and had a higher cortisol at baseline, and following pain (all p < 0.001). At baseline, patients had a higher sympathetic tone (p = 0.04), whereas in response to pain they increased their parasympathetic tone (p ≤ 0.008). The amalgamating the data, we identified two psychophysiologically distinct ‘pain clusters’. Patients were overrepresented in the cluster characterized by high neuroticism, trait anxiety, baseline cortisol, pain hypersensitivity, and parasympathetic response to pain (all p < 0.03).
Conclusions & Inferences
In future, such delineations in FCP populations may facilitate individualization of treatment based on psychophysiological profiling.