Human Affect and Pain Neuroscience Laboratory, Center for Translational Pain Medicine, Department of Anesthesiology, Duke University School of Medicine, Durham, North Carolina, USA.
UiS Biopsychology Research Group, Department of Social Studies, Stavanger University, Stavanger, Norway; Department of Clinical Neuroscience, Karolinska Institute, Solna, Sweden.
Physiol Behav. 2023 Nov 1;271:114358. doi: 10.1016/j.physbeh.2023.114358. Epub 2023 Sep 26.
Urological chronic pelvic pain syndrome (UCPPS) is a debilitating painful condition with unclear etiology. Prior researchers have indicated that compared to healthy controls, patients with UCPPS demonstrated altered brain activity. Researchers have also shown that in UCPPS, several blood inflammatory markers relate to clinical variables of pain, fatigue, and pain widespreadness. However, how altered brain function in patients with UCPPS relates to blood inflammation remains unknown. To extend and connect prior findings of altered brain function and inflammatory factors in UCPPS, we conducted a secondary analysis of data from a cohort of UCPPS patients (N = 29) and healthy controls (N = 31) who provided both neuroimaging and blood data (National Institute of Health MAPP Research Network publicly available dataset). In our present study, we aimed to evaluate relationships between a priori-defined brain neuroimaging markers and inflammatory factors of interest and their relationships to pain-psychological variables. We hypothesized that two brain alterations of interest (i.e., PCC - left hippocampus functional connectivity and PCC - bilateral amygdala functional connectivity) would be correlated with four cytokine markers of interest: interleukin (IL) - 6, tumor necrosis factor-alpha (TNF-a), IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF). In the UCPPS cohort, we identified a significant PCC - left hippocampus functional connectivity relationship with IL-6 (p = 0.0044). Additionally, in the UCPPS cohort, we identified a PCC - amygdala functional connectivity relationship with GM-CSF which did not meet our model's threshold for statistical significance (p = 0.0665). While these data are preliminary and cross-sectional, our findings suggest connections between brain function and levels of low-grade systemic inflammation in UCPPS. Thus, while further study is needed, our data indicate the potential for advancing the understanding of how brain functional circuits may relate to clinical symptoms and systemic inflammation.
泌尿科慢性盆腔疼痛综合征 (UCPPS) 是一种衰弱性疼痛疾病，其病因尚不清楚。先前的研究人员表明，与健康对照组相比，UCPPS 患者表现出大脑活动改变。研究人员还表明，在 UCPPS 中，几种血液炎症标志物与疼痛、疲劳和疼痛广泛性的临床变量相关。然而，UCPPS 患者大脑功能改变与血液炎症之间的关系尚不清楚。为了扩展和连接先前关于 UCPPS 中大脑功能和炎症因子改变的发现，我们对 UCPPS 患者队列（N=29）和健康对照组（N=31）的神经影像学和血液数据进行了二次分析（国立卫生研究院 MAPP 研究网络公开数据集）。在我们目前的研究中，我们旨在评估预先定义的大脑神经影像学标志物与感兴趣的炎症因子之间的关系及其与疼痛心理变量的关系。我们假设两个感兴趣的大脑改变（即 PCC-左侧海马体功能连接和 PCC-双侧杏仁核功能连接）将与四个感兴趣的细胞因子标志物相关：白细胞介素 (IL)-6、肿瘤坏死因子-α (TNF-a)、IL-8 和粒细胞-巨噬细胞集落刺激因子 (GM-CSF)。在 UCPPS 队列中，我们发现 PCC-左侧海马体功能连接与 IL-6 之间存在显著相关性（p=0.0044）。此外，在 UCPPS 队列中，我们发现 PCC-杏仁核功能连接与 GM-CSF 之间存在相关性，但未达到我们模型的统计学显著性阈值（p=0.0665）。虽然这些数据是初步的和横断面的，但我们的发现表明 UCPPS 中大脑功能与低度系统性炎症之间存在联系。因此，虽然需要进一步研究，但我们的数据表明，大脑功能回路可能与临床症状和系统性炎症相关的理解有潜在的进展。
