Center for Human Sleep Science, Department of Psychology, University of California, Berkeley, California 94720-1650.
Department of Psychiatry, University of California, San Francisco, California 94103.
J Neurosci. 2019 Mar 20;39(12):2291-2300. doi: 10.1523/JNEUROSCI.2408-18.2018. Epub 2019 Jan 28.
Sleep loss increases the experience of pain. However, the brain mechanisms underlying altered pain processing following sleep deprivation are unknown. Moreover, it remains unclear whether ecologically modest night-to-night changes in sleep, within an individual, confer consequential day-to-day changes in experienced pain. Here, we demonstrate that acute sleep deprivation amplifies pain reactivity within human (male and female) primary somatosensory cortex yet blunts pain reactivity in higher-order valuation and decision-making regions of the striatum and insula cortex. Consistent with this altered neural signature, we further show that sleep deprivation expands the temperature range for classifying a stimulus as painful, specifically through a lowering of pain thresholds. Moreover, the degree of amplified reactivity within somatosensory cortex following sleep deprivation significantly predicts this expansion of experienced pain across individuals. Finally, outside of the laboratory setting, we similarly show that even modest nightly changes in sleep quality (increases and decreases) within an individual determine consequential day-to-day changes in experienced pain (decreases and increases, respectively). Together, these data provide a novel framework underlying the impact of sleep loss on pain and, furthermore, establish that the association between sleep and pain is expressed in a night-to-day, bidirectional relationship within a sample of the general population. More broadly, our findings highlight sleep as a novel therapeutic target for pain management within and outside the clinic, including circumstances where sleep is frequently short yet pain is abundant (e.g., the hospital setting). Are you experiencing pain? Did you have a bad night of sleep? This study provides underlying brain and behavioral mechanisms explaining this common co-occurrence. We show that sleep deprivation enhances pain responsivity within the primary sensing regions of the brain's cortex yet blunts activity in other regions that modulate pain processing, the striatum and insula. We further establish that even subtle night-to-night changes in sleep in a sample of the general population predict consequential day-to-day changes in pain (bidirectionally). Considering the societal rise in chronic pain conditions in lock-step with the decline in sleep time through the industrial world, our data support the hypothesis that these two trends may not simply be co-occurring but are significantly interrelated.
睡眠不足会增加疼痛体验。然而，睡眠剥夺后疼痛处理改变的大脑机制尚不清楚。此外，个体夜间睡眠的微小变化是否会导致日常疼痛体验的相应变化也尚不清楚。在这里，我们证明急性睡眠剥夺会放大人类（男性和女性）初级体感皮层的疼痛反应，但会使纹状体和岛叶皮层的高级评估和决策区域的疼痛反应迟钝。与这种改变的神经特征一致，我们进一步表明，睡眠剥夺会扩大温度范围，从而将刺激分类为疼痛，具体来说，是通过降低疼痛阈值。此外，睡眠剥夺后体感皮层的反应性增强程度显著预测了个体之间疼痛体验的扩大。最后，在实验室环境之外，我们同样表明，个体夜间睡眠质量的微小变化（增加和减少）会导致日常疼痛体验的相应变化（分别减少和增加）。总之，这些数据为睡眠不足对疼痛的影响提供了一个新的框架，并进一步表明，睡眠与疼痛之间的关联在一般人群样本中以一种昼夜双向的关系表达。更广泛地说，我们的发现强调了睡眠作为一种新的治疗靶点，用于诊所内外的疼痛管理，包括在睡眠经常不足但疼痛普遍存在的情况下（例如，医院环境）。你感到疼痛吗？昨晚没睡好？这项研究提供了一个潜在的大脑和行为机制来解释这种常见的共同发生。我们发现，睡眠剥夺会增强大脑皮层初级感知区域的疼痛反应，但会使调节疼痛处理的纹状体和岛叶等其他区域的活动减弱。我们进一步确定，一般人群样本中即使是夜间睡眠的微小变化也可以预测日常疼痛的变化（双向）。考虑到慢性疼痛在整个工业世界中随着睡眠时间的减少而普遍增加，我们的数据支持这样一种假设，即这两个趋势可能不仅仅是同时发生的，而且还存在显著的相互关系。
