Interstitial Cystitis/Painful Bladder Syndrome and Irritable Bowel Syndrome

间质性膀胱炎(1C)和肠易激综合征(IBS)总是影响15%-30%的美国人口 女性，以慢性盆腔疼痛、尿路和肠道疼痛重叠症状为特征 功能障碍。人们对它们的病理生理学知之甚少。它们损害了生活质量，并造成了严重的健康问题 护理负担。大多数患者对目前的治疗方法不满意。IBS&1C疗法失败是因为他们没有 解决根本问题。我们的目标是研究导致1C和 IBS。我们对IBS的初步研究揭示了中央和中枢神经再生不良的改变 周围神经系统，但IC/IBS患者的盆底-脑神经肌轴尚未被检测到 检查过了。我们假设脑-盆底/肠轴的双向信号在IC/IBS中是错乱的 病人。我们将通过使用一种新的、非侵入性的、有效的研究脑-盆底的方法来测试这一点。 轴心。 我们提出了四个具体的目标：1)检测大鼠盆底传入-脑轴的超兴奋性。 对66例1C患者、66例1C合并IBS患者和30例健康对照进行皮层诱发电位测定 直肠和肛门电刺激后的电位(CEP)和感觉阈值。2)研究 通过经颅磁刺激刺激大脑皮质传出脑-盆底轴，记录 肛门和直肠运动诱发电位(MEP)。3)确定神经元调制的位置，即 中枢或外周神经元敏感化或两者兼而有之引起的神经肠道变化，通过诱发肛门和直肠 选择性刺激双侧腰、骶神经后的MEP，并与节段性 经颅脑诱发的MEP。4)评估IC/IBS患者出现肠道症状的原因 肛门直肠感觉和感觉运动功能以及肠和膀胱症状与肛门直肠症状的相关性 过敏、直肠顺应性和盆底功能障碍。 我们的多学科、综合方法将研究慢性阻塞性肺疾病的神经生物学机制。 IC/IBS的盆腔疼痛及其与1C的不同之处。我们的研究将提供新的机械论见解 关于这些重叠疼痛综合征的病理生物学，这可能对 我们对1C/IBS的理解，并为基于机械的治疗铺平了道路。

Interstitial cystitis (1C) and Irritable bowel syndrome (IBS) affect 15-30% of the US population, invariably women, and are characterized by overlapping symptoms of chronic pelvic pain, urinary and bowel dysfunction. Their pathophysiology is poorly understood. They impair quality of life and impose major health care burden. Most patients are dissatisfied with current therapies. IBS & 1C therapy fail because they do not remedy the underlying problem. Our goal is to investigate the neurobiologic mechanisms that cause 1C and IBS. Our preliminary studies in IBS reveal maladaptive neuroplastic changes within the central and peripheral nervous system, but the pelvic floor-brain neuromuscular axis in IC/IBS patients has not been examined. We hypothesize that bidirectional signaling in the brain-pelvic floor/gut axis is deranged in IC/IBS patients. We will test this by using a new, noninvasive and validated method of studying the brain-pelvic floor axis. We propose four specific aims: 1) Examine the hyperexcitability of the afferent-pelvic floor-brain axis in 66 patients with 1C, 66 patients with 1C and IBS and 30 healthy controls by measuring the cortical evoked potentials (CEP) and sensory thresholds after electrical stimulation of the rectum and anus. 2) Study the efferent brain-pelvic floor axis by stimulating the cortex with transcranial magnetic stimulation and record the anal and rectal motor evoked potentials (MEP). 3) Determine the locus for neuronal modulation i.e are the neuroenteric changes due to central or peripheral neuronal sensitization or both, by evoking anal and rectal MEPs after selectively stimulating the lumbar and sacral nerves bilaterally, and by comparing segmental with transcranial-induced MEPs. 4) Evaluate why IC/IBS patients experience bowel symptoms by assessing anorectal sensation and sensori-motor function and correlating bowel and bladder symptoms with anorectal hypersensitivity, rectal compliance and pelvic floor dysfunction. Our multidisciplinary, comprehensive approach will investigate the neurobiologic mechanisms of chronic pelvic pain in IC/IBS, and how they differ from 1C. Our studies will provide novel mechanistic insights regarding the pathobiology of these overlapping pain syndromes, which could have a significant impact on our understanding of 1C/IBS, and pave the way for mechanistic-based therapies.