Citation

Wollgarten-Hadamek I, Hohmeister J, Zohsel K, Flor H, Hermann C. Eur. J. Pain 2011; 15(4): 423.e1-4210.

Affiliation

Department of Clinical and Cognitive Neuroscience, Ruprecht-Karls-University Heidelberg, Central Institute of Mental Health, Mannheim, Germany.

Copyright

(Copyright © 2011, Elsevier Publishing)

DOI

10.1016/j.ejpain.2010.09.001

PMID

20934358

Abstract

There is evidence in humans and animals that neonatal and early infant pain and stress may sensitize excitatory pain pathways. Possibly such experiences may result in long-term diminished activation of phasic endogenous pain inhibitory mechanisms. We studied stress-induced activation of endogenous pain inhibitory mechanisms in school-aged children (10-16years) who had suffered moderate (N= =12) or severe (N=10) burn injuries in infancy (6-24months of age) and 20 controls. Before and after the stress phase, pain threshold and pain tolerance (heat, pressure, ischemic pain) were assessed. Stress was successfully induced in all children as reflected by increases in heart rate, blood pressure and perceived stress. In the controls, there was evidence for stress-induced hypoalgesia as reflected by significant increases in heat pain threshold, heat pain tolerance and pressure pain tolerance. Pressure pain thresholds were not significantly altered. A similar pattern was observed in the moderately burned children. By contrast, children with severe burn injuries failed to show significant stress-related changes in heat and pressure pain sensitivity. In all groups, ischemic pain sensitivity was elevated post stress. The children reported being more distressed by the perceived loss of strength than by pain and had difficulties differentiating between the two. It is possible that ischemic pain may be less suitable for measuring pain sensitivity in children. The present study provides first evidence that pain and stress exposure due to severe burns in infancy may be associated with an attenuated stress-induced activation of phasic endogenous pain inhibitory mechanisms later in childhood and adolescence.

Language: en