Karmann A J, Kundermann B, Lautenbacher S
Physiologische Psychologie, Otto-Friedrich-Universität Bamberg, Markusplatz 3, 96045, Bamberg, Deutschland,
Schmerz. 2014 Apr;28(2):141-6. doi: 10.1007/s00482-014-1394-6.
It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?
现已证实，睡眠剥夺或睡眠碎片化会导致痛觉过敏，而这无法通过躯体感觉知觉的总体变化来解释。然而，尚未明确哪个睡眠阶段对此效应最为关键。睡眠剥夺一方面对疼痛诱发的脑电位产生看似矛盾的影响，另一方面对主观疼痛报告也有影响，这表明门控机制发生了复杂变化。由于对疼痛和情感的影响可以分离，因此似乎不太可能存在共同的作用机制。动物研究数据表明，在先前存在神经病变的情况下，睡眠剥夺引起的痛觉过敏可能尤为强烈。结合动物研究结果，内源性疼痛调制（CPM）受睡眠剥夺损害这一发现表明，血清素能系统介导了睡眠剥夺对疼痛感知的影响。然而，其他神经递质和神经调节剂仍需考虑。临床上出现了一个相关问题，即为什么睡眠剥夺在某些个体中比在其他个体中更容易诱发痛觉过敏，以及为什么这种效应持续时间更长？
