Huber Felicitas A, Kell Parker A, Shadlow Joanna O, Rhudy Jamie L
Department of Psychology, The University of Tulsa, Tulsa, OK, United States.
Washington University Pain Center, Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO, United States.
Neurobiol Pain. 2025 Feb 28;18:100180. doi: 10.1016/j.ynpai.2025.100180. eCollection 2025 Jul-Dec.
Chronic pain is highly prevalent in the U.S. and leads to myriad negative sequalae and suffering. One way to address chronic pain is to identify who is at risk and intervene prior to symptom onset. Research suggests resting peak alpha frequency (PAF), the speed of alpha oscillations at rest, is slower in healthy individuals with greater pain sensitivity and in chronic pain patients. Thus, slower PAF may denote chronic pain vulnerability. Other research has shown that individuals at higher risk of chronic pain exhibit disrupted pain modulation, i.e., less efficient pain inhibition and increased pain facilitation. Currently, the ability of PAF to predict chronic pain and its relation to pain modulation is under-researched. This investigation aimed to address this gap by characterizing associations between PAF, onset of chronic pain, and pain modulation. Using archival data from three independent studies, this investigation assessed whether slower PAF is associated with prospectively-determined chronic pain onset, decreased pain inhibition (i.e., impaired conditioned pain modulation, impaired erotica-induced pain inhibition), and increased pain facilitation (i.e., increased temporal summation of pain, augmented mutilation-induced pain facilitation). Results show that slower PAF was associated with greater facilitation of spinal (i.e., nociceptive flexion reflex) and supraspinal (i.e., N2 potential) nociception in response to unpleasant pictures (i.e., human injury images). This suggests that slower PAF is associated with threat-enhanced spinal and supraspinal nociception and may be relevant for chronic pain conditions with disrupted threat systems. Slower PAF was not associated with any other pain outcome, including prospectively determined chronic pain onset. However, chronic pain onset could only be assessed in one study with a mixed eyes open/eyes closed recording, limiting the significance of this finding.
慢性疼痛在美国极为普遍，会导致无数负面后果和痛苦。解决慢性疼痛的一种方法是确定谁处于风险之中，并在症状出现之前进行干预。研究表明，静息峰值阿尔法频率（PAF），即静息时阿尔法振荡的速度，在疼痛敏感性较高的健康个体和慢性疼痛患者中较慢。因此，较慢的PAF可能表示慢性疼痛易感性。其他研究表明，慢性疼痛风险较高的个体表现出疼痛调制紊乱，即疼痛抑制效率较低和疼痛易化增加。目前，PAF预测慢性疼痛的能力及其与疼痛调制的关系研究不足。本研究旨在通过描述PAF、慢性疼痛发作和疼痛调制之间的关联来填补这一空白。利用来自三项独立研究的存档数据，本研究评估了较慢的PAF是否与前瞻性确定的慢性疼痛发作、疼痛抑制降低（即条件性疼痛调制受损、色情诱导的疼痛抑制受损）和疼痛易化增加（即疼痛的时间总和增加、截肢诱导的疼痛易化增强）相关。结果表明，较慢的PAF与对不愉快图片（即人体受伤图像）的脊髓（即伤害性屈曲反射）和脊髓上（即N2电位）伤害感受的更大易化相关。这表明较慢的PAF与威胁增强的脊髓和脊髓上伤害感受相关，可能与威胁系统受损的慢性疼痛状况有关。较慢的PAF与任何其他疼痛结果均无关联，包括前瞻性确定的慢性疼痛发作。然而，慢性疼痛发作只能在一项采用睁眼/闭眼混合记录的研究中进行评估，这限制了这一发现的重要性。
