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首页> 外文期刊>Pain. >Disturbances in slow-wave sleep are induced by models of bilateral inflammation, neuropathic, and postoperative pain, but not osteoarthritic pain in rats
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Disturbances in slow-wave sleep are induced by models of bilateral inflammation, neuropathic, and postoperative pain, but not osteoarthritic pain in rats

机译：慢波睡眠障碍是由大鼠的双侧炎症，神经性和术后疼痛模型引起的，而非骨关节炎性疼痛模型

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Preclinical assessment of pain has typically relied on measuring animal responses to evoked stimulation. Because of inherent limitations of these assays, there is a need to develop measures of animal pain/discomfort that are objective, not experimentally evoked, and mimic the human condition. Patients with chronic pain manifest a variety of co-morbidities, one of which is disturbances in sleep. We used electroencephalography to objectively assess 4 rat models of pain (inflammatory/complete Freund's adjuvant [CFA], neuropathic/chronic constriction injury [CCI], postoperative/skin incision, osteoarthritis/monosodium iodoacetate [MIA]) for the occurrence of sleep disturbances. Four different measures of slow-wave sleep (SWS) were examined: amplitude of 1- to 4-Hz waves, total time spent in SWS, time spent in SWS-1, and time spent in SWS-2. Bilateral injuries were more likely to induce a sleep disturbance than unilateral injuries in the CFA, CCI, and skin incision assays. Sleep disturbances occurred in the deeper stage of SWS, as the amplitude of 1- to 4-Hz waves and time spent in SWS-2 were significantly decreased in all models except the osteoarthritis model. Sleep disturbances lasted for approximately 3 to 14 days, depending on the model, and were resolved despite continued hypersensitivity to evoked stimulation. Morphine, gabapentin, diclofenac, and ABT-102 (TRPV1 antagonist) all improved sleep in the bilateral CFA assay at doses that did not significantly alter SWS in uninjured rats. Preclinical assessment of compounds should follow the path of clinical studies and take into account diverse aspects of the "pain condition." This would include evaluating nociceptive thresholds as well as other endpoints, such as cognition and sleep, that may be affected by the pathological state.
机译：临床上对疼痛的评估通常依赖于测量动物对诱发刺激的反应。由于这些测定法的固有局限性，因此需要开发客观的，不是实验诱发的并且模仿人类状况的客观的动物疼痛/不适的测定方法。患有慢性疼痛的患者表现出多种合并症，其中之一是睡眠障碍。我们使用脑电图客观评估了4种大鼠疼痛模型（炎症/完全弗氏佐剂[CFA]，神经性/慢性收缩损伤[CCI]，术后/皮肤切口，骨关节炎/碘乙酸单钠[MIA]），以评估睡眠障碍的发生。检查了四种不同的慢波睡眠（SWS）量度：1-Hz到4-Hz波的振幅，在SWS中花费的总时间，在SWS-1中花费的时间以及在SWS-2中花费的时间。在CFA，CCI和皮肤切口试验中，单侧受伤比双侧受伤更容易引起睡眠障碍。睡眠障碍发生在SWS的较深阶段，因为除了骨关节炎模型外，所有模型中1-Hz到4Hz的波幅和SWS-2所花费的时间都显着减少。视模型而定，睡眠障碍持续约3至14天，尽管对诱发的刺激持续过敏，但仍可解决。吗啡，加巴喷丁，双氯芬酸和ABT-102（TRPV1拮抗剂）在不显着改变未受伤大鼠SWS的剂量下，在双边CFA分析中均改善了睡眠。化合物的临床前评估应遵循临床研究的路径，并考虑“疼痛状况”的各个方面。这将包括评估伤害性阈值以及可能受病理状态影响的其他终点，例如认知和睡眠。

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