Department of Obstetrics and Gynecology, NorthShore University HealthSystem, Evanston, IL, USA.
Pritzker School of Medicine, Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL, USA.
BJOG. 2017 Jan;124(2):283-291. doi: 10.1111/1471-0528.14433.
To compare bladder sensitivity between patients with pelvic pain and patients who were pain free, undergoing noninvasive, controlled bladder distension via diuresis. We also sought to measure potential mechanisms underlying bladder sensitivity.
Prospective observational study.
Community teaching hospital.
Reproductive-age women with non-bladder chronic pelvic pain (CPP, n = 23), painful bladder syndrome (PBS, n = 23), and pelvic pain-free controls (n = 42) METHODS: Participants were compared on cystometric capacity, pelvic floor pressure-pain thresholds (PPTs), pelvic muscle function, O'Leary-Sant bladder questionnaire, and psychosocial instruments using Wilcoxon rank-sum tests. Multivariate regression was used to identify factors underlying bladder pain phenotypes.
Pelvic floor pain thresholds; self-reported bladder distension pain.
Participants with PBS exhibited higher bladder distension pain than those with CPP, with both groups reporting higher pain levels than controls (P < 0.05). No significant associations were found between bladder distension pain and pelvic muscle structure or pain sensitivity measures; however, bladder distension pain positively correlates with both vaginal PPTs adjacent to the bladder (r = 0.46) and pain with transvaginal bladder palpation (r = 0.56). Pain at maximal distension was less influenced by somatic sensitivity than bladder symptoms (r = 0.35 versus r = 0.59; P < 0.05). Multivariate regression identified three independent components of bladder symptoms in PBS: bladder distension pain, bladder sensation, and somatic symptoms.
Diuresis-induced bladder pain differentiates CPP from PBS. Experimental bladder pain is not predicted by pelvic floor sensitivity. Compared with patient-reported outcomes it appears less influenced by psychological factors. Further study is needed to determine whether screening for experimental bladder pain sensitivity could predict future risk of PBS.
Controlled, water ingestion-provoked bladder pain can objectively identify visceral pain sensitivity.
比较接受非侵入性、控制性膀胱扩张（通过利尿）的盆腔疼痛患者与无痛患者之间的膀胱敏感性。我们还试图测量膀胱敏感性的潜在机制。
前瞻性观察性研究。
社区教学医院。
患有非膀胱慢性盆腔疼痛（CPP，n=23）、膀胱疼痛综合征（PBS，n=23）和盆腔无痛对照（n=42）的育龄妇女。
采用 Wilcoxon 秩和检验比较参与者的膀胱容量、盆底压力-疼痛阈值（PPT）、盆底肌肉功能、O'Leary-Sant 膀胱问卷和社会心理工具。采用多元回归分析确定膀胱疼痛表型的潜在因素。
盆底疼痛阈值；自我报告的膀胱扩张疼痛。
与 CPP 患者相比，PBS 患者的膀胱扩张疼痛更高，两组报告的疼痛水平均高于对照组（P<0.05）。膀胱扩张疼痛与盆底肌肉结构或疼痛敏感性测量之间无显著相关性；然而，膀胱扩张疼痛与膀胱附近阴道 PPT（r=0.46）和经阴道膀胱触诊疼痛（r=0.56）呈正相关。最大扩张时的疼痛受躯体敏感性的影响小于膀胱症状（r=0.35 与 r=0.59；P<0.05）。多元回归分析确定了 PBS 中膀胱症状的三个独立成分：膀胱扩张疼痛、膀胱感觉和躯体症状。
利尿引起的膀胱疼痛可将 CPP 与 PBS 区分开来。盆腔底部敏感性不能预测实验性膀胱疼痛。与患者报告的结果相比，它似乎较少受心理因素的影响。需要进一步研究来确定是否筛查实验性膀胱疼痛敏感性可预测未来 PBS 的风险。
受控的、饮水引起的膀胱疼痛可以客观地识别内脏疼痛敏感性。
