PDF(Pubmed)
Abstract：
Past cross-sectional chronic pain studies have revealed aberrant resting-state brain activity in regions involved in pain processing and affect regulation. However, there is a paucity of longitudinal research examining links of resting-state activity and pain resilience with changes in chronic pain outcomes over time. In this prospective study, we assessed the status of baseline (T1) resting-state brain activity as a biomarker of later impairment from chronic pain and a mediator of the relation between pain resilience and impairment at follow-up. One hundred forty-two adults with chronic musculoskeletal pain completed a T1 assessment comprising a resting-state functional magnetic resonance imaging scan based on regional homogeneity (ReHo) and self-report measures of demographics, pain characteristics, psychological status, pain resilience, pain severity, and pain impairment. Subsequently, pain impairment was reassessed at a 6-month follow-up (T2). Hierarchical multiple regression and mediation analyses assessed relations of T1 ReHo and pain resilience scores with changes in pain impairment. Higher T1 ReHo values in the right caudate nucleus were associated with increased pain impairment at T2, after controlling for all other statistically significant self-report measures. ReHo also partially mediated associations of T1 pain resilience dimensions with T2 pain impairment. T1 right caudate nucleus ReHo emerged as a possible biomarker of later impairment from chronic musculoskeletal pain and a neural mechanism that may help to explain why pain resilience is related to lower levels of later chronic pain impairment. Findings provide empirical foundations for prospective extensions that assess the status of ReHo activity and self-reported pain resilience as markers for later impairment from chronic pain and targets for interventions to reduce impairment. PRACTITIONER POINTS: Resting-state markers of impairment: Higher baseline (T1) regional homogeneity (ReHo) values, localized in the right caudate nucleus, were associated with exacerbations in impairment from chronic musculoskeletal pain at a 6-month follow-up, independent of T1 demographics, pain experiences, and psychological factors. Mediating role of ReHo values: ReHo values in the right caudate nucleus also mediated the relationship between baseline pain resilience levels and later pain impairment among participants. Therapeutic implications: Findings provide empirical foundations for research extensions that evaluate (1) the use of resting-state activity in assessment to identify people at risk for later impairment from pain and (2) changes in resting-state activity as biomarkers for the efficacy of treatments designed to improve resilience and reduce impairment among those in need.
摘要：
过去的横断面慢性疼痛研究表明，参与疼痛处理和影响调节的区域存在异常的静息状态大脑活动。然而,缺乏纵向研究来检验静息状态活动和疼痛韧性与慢性疼痛结局随时间变化之间的联系.在这项前瞻性研究中，我们评估了基线(T1)静息态脑活动状态,作为慢性疼痛后期损害的生物标志物,以及随访时疼痛复原力和损害之间关系的中介.142名患有慢性肌肉骨骼疼痛的成年人完成了T1评估，其中包括基于区域均匀性（ReHo）和自我报告的人口统计学指标的静息状态功能磁共振成像扫描，疼痛的特点，心理状态,疼痛恢复力，疼痛严重程度，和疼痛障碍。随后，在6个月随访(T2)时重新评估疼痛损害.分层多元回归和中介分析评估了T1ReHo和疼痛韧性评分与疼痛损害变化的关系。在控制所有其他具有统计学意义的自我报告指标后，右尾状核中较高的T1ReHo值与T2时疼痛损害增加有关。ReHo还部分介导T1疼痛韧性维度与T2疼痛损伤的关联。T1右尾状核ReHo是慢性肌肉骨骼疼痛后期损害的可能生物标志物，也是一种神经机制，可能有助于解释为什么疼痛弹性与后期慢性疼痛损害的较低水平相关。研究结果为前瞻性扩展提供了经验基础，该扩展评估了ReHo活性和自我报告的疼痛弹性的状态，作为慢性疼痛后期损害的标志物和减少损害的干预措施的目标。实践点：损伤的静息状态标记：较高的基线（T1）区域同质性（ReHo）值，位于右侧尾状核,在6个月的随访中，与慢性肌肉骨骼疼痛的损害加重有关，独立于T1人口统计学，痛苦的经历，和心理因素。ReHo值的中介作用：右尾状核中的ReHo值也介导了基线疼痛弹性水平与参与者后期疼痛损害之间的关系。治疗意义：研究结果为研究扩展提供了经验基础，这些研究扩展评估（1）在评估中使用静息状态活动以识别有以后疼痛受损风险的人，以及（2）静息状态活动的变化作为生物标志物，用于改善有需要的人的弹性和减少损害。
