Department of Clinical and Cognitive Neuroscience, Ruprecht-Karls-University Heidelberg, Central Institute of Mental Health, Mannheim, Germany.
Eur J Pain. 2011 Apr;15(4):423.e1-10. doi: 10.1016/j.ejpain.2010.09.001. Epub 2010 Oct 12.
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 (10-16 years) who had suffered moderate (N= =12) or severe (N=10) burn injuries in infancy (6-24 months 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.
有证据表明，新生儿和婴儿期的疼痛和压力可能会使兴奋性疼痛通路敏感。这种经历可能会导致短期相位内源性疼痛抑制机制的长期激活减少。我们研究了在婴儿期（6-24 个月大）中度（N=12）或重度（N=10）烧伤的学龄儿童（10-16 岁）中，应激诱导的内源性疼痛抑制机制的激活情况，以及 20 名对照儿童。在应激前和应激后，评估了疼痛阈值和疼痛耐受力（热、压、缺血性疼痛）。所有儿童的心率、血压和感知压力均增加，表明应激成功诱导。在对照组中，热痛阈值、热痛耐受力和压痛耐受力显著增加，表明存在应激诱导的痛觉过敏。压痛阈值没有明显改变。中度烧伤儿童也观察到类似的模式。相比之下，严重烧伤儿童的热和压痛敏感性没有明显的应激相关变化。在所有组中，缺血性疼痛敏感性在应激后升高。儿童报告说，与疼痛相比，他们更担心感知到的力量丧失，并且难以区分两者。因此，缺血性疼痛可能不太适合测量儿童的疼痛敏感性。本研究首次提供证据表明，婴儿期严重烧伤引起的疼痛和压力暴露可能与儿童后期和青少年期短暂内源性疼痛抑制机制的应激诱导激活减弱有关。
