Chang Wei-Ju, Jenkins Luke C, Humburg Peter, Schabrun Siobhan M
Centre for Pain IMPACT, Neuroscience Research Australia (NeuRA), Randwick, New South Wales, Australia.
School of Health Sciences, Faculty of Health and Medicine, University of New South Wales, UNSW Sydney, New South Wales, Australia.
Pain Rep. 2025 Apr 24;10(3):e1269. doi: 10.1097/PR9.0000000000001269. eCollection 2025 Jun.
Sensory cortex activity differs between acute and chronic low back pain (LBP) with decreased activity in acute LBP but increased activity in chronic LBP. However, it is unknown how and when sensory cortex activity changes during the transition from acute to chronic LBP and whether fluctuations in sensory cortex activity are associated with pain sensitivity.
To examine (1) the trajectory of changes in sensory cortex activity over a period of six months from the onset of acute LBP; (2) the assoication between sesnory cortex activity and pain pain sensitivity.
In a prospective cohort study (N = 120), sensory evoked potentials (SEPs) were recorded using electroencephalography within 6 weeks of LBP onset (baseline) and at 3- and 6-month follow-up. Pain sensitivity was assessed using quantitative sensory testing (QST).
At baseline, individuals who developed chronic pain at 6-month follow-up exhibited less nonnoxious sensory processing (smaller area of N, N, and P SEP components) compared with those who recovered. In individuals who recovered, SEP measures did not change over time. In individuals who developed chronic pain, N and N SEP area increased between baseline and 3 months, while P SEP area increased between baseline and 6 months, reaching values consistent with those of recovered individuals. Sensory evoked potential measures showed no relationship with QST, except for a larger P SEP area correlating with higher 6-month heat pain threshold at the site of LBP.
Nonnoxious sensory processing in acute LBP was less in those who developed chronic pain than those who recovered. Nonnoxious sensory processing increased over time in those who developed chronic pain but was unchanged in those who recovered. In the transition from acute to chronic LBP, nonnoxious sensory processing in the sensory cortex was not associated with pain sensitivity.
急性和慢性下腰痛（LBP）患者的感觉皮层活动存在差异，急性LBP患者的活动减少，而慢性LBP患者的活动增加。然而，在从急性LBP转变为慢性LBP的过程中，感觉皮层活动如何以及何时发生变化，以及感觉皮层活动的波动是否与疼痛敏感性相关尚不清楚。
研究（1）从急性LBP发作开始的六个月内感觉皮层活动的变化轨迹；（2）感觉皮层活动与疼痛敏感性之间的关联。
在一项前瞻性队列研究（N = 120）中，在LBP发作后6周内（基线）以及3个月和6个月随访时，使用脑电图记录感觉诱发电位（SEP）。使用定量感觉测试（QST）评估疼痛敏感性。
在基线时，与康复者相比，在6个月随访时出现慢性疼痛的个体表现出较少的无害感觉处理（N、N和P SEP成分的面积较小）。在康复者中，SEP测量值随时间没有变化。在出现慢性疼痛的个体中，N和N SEP面积在基线和3个月之间增加，而P SEP面积在基线和6个月之间增加，达到与康复个体一致的值。感觉诱发电位测量值与QST没有关系，除了较大的P SEP面积与LBP部位较高的6个月热痛阈值相关。
与康复者相比，出现慢性疼痛的急性LBP患者的无害感觉处理较少。出现慢性疼痛的个体中，无害感觉处理随时间增加，但康复者中则无变化。在从急性LBP转变为慢性LBP的过程中，感觉皮层中的无害感觉处理与疼痛敏感性无关。
