NOCICEPTION IN BULIMIA NERVOSA

神经性贪食症的伤害感受

• 批准号: 7605970
• 负责人: PATRICIA L FARIS
• 金额: $ 0.19万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-01 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7605970
• 关键词: Behavior; Binge Eating; Bulimia; Chronic; Clinical Data; Clinical Pharmacology; Clinical Treatment; Cognitive Therapy; Computer Retrieval of Information on Scientific Projects Database; Condition; Detection; Disease; Double-Blind Method; Drops; Eating Disorders; Evaluation; Functional disorder; Funding; Grant; Hyperactive behavior; Institution; Methods; Nociception; Ondansetron; Pain; Pain Threshold; Patients; Physiological; Placebo Control; Placebos; Production; Psychophysiology; Randomized; Recruitment Activity; Research; Research Personnel; Resources; Role; Satiation; Severities; Severity of illness; Source; Symptoms; Testing; Therapeutic; United States National Institutes of Health; Vagus nerve structure; Vomiting; Week; afferent nerve; base; indexing; neurotransmission; pill

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This research (funded by R01 DK 42291-06-09) proposes to further study the role of vagal afferents in the perpetuation of binge-eatinig and vomiting. We previously proposed that the pathophysiology of bulimia nervosa involves dysregulation of the afferent vagus nerve. To date, we have evaluated vagal involvement in this eating disorder using two main strategies: (1) the use of somatic pain detection as a physiological marker of vagal afferent activity; and (2) the use of ondansetron(a 5 HT3 antagonist known to reduce vagal neurotransmission) as a pharmacological challenge test of vagal modulation of both the bulimic behaviors and on elevated pain detection thresholds. The principle findings from these studies are:(1) pain detection thresholds rise dynamically across the interval between bulimic binge/vomit episodes, apparently reaching their zenith as the next bulimic episode is approached and dropping to their nadir in close temporal association with having recently engaged in a bulimic episode; and (2) ondansetron treatment was associated with a significant moderation in both the cyclic fluctuations in pain detection thresholds and the primary disorder symptom of binge/vomit episodes per week in a group of patients with severe and chronic bulimia nervosa under randomized, placebo controlled, double-blind conditions. Collectively, the above summarized physiological and clinical data have led to the refined hypothesis that the pathophysiology of bulimia nervosa involves a cyclic hyperactivity in vagal afferent nerves. The present research proposes to test the hypothesis that cyclic increases in vagal activity drive the binge eating and vomiting through an interactive combination of clinical pharmacology and psychophysiological approaches. The primary aim of the clinical treatment study is to compare the efficacy of ondansetron to cognitive behavioral therapy (CBT) as a function of illness severity. Subjects will be recruitted into two groupsbased on symptom severity (2-<7 episodes per week; 7 or more episodes per week). Within a severity group, patients will be randomly assigned o one of four treatment groups: cognitive behavioral therapy (CBT) plus pill placebe (CBT+Placebo), ondansetron alone (ONDAN), CBT with concomitant ondansetron (CBT+ONDAN) and pill placebo (PLAC) alone. We propose to utilize the gCRC facilities for conducting the initial evaluation of patients being recruited into this study. The primary aim of the psychophysiological study is to investigate the effect of CBT versus ondansetron treatment on physiological indices of vagal activity, namely thresholds for pain detection and induction of satiety. The approach of this Aim is based on the idea that if vagal hyperactivity represents the critical factor involved in symptom production, then any therapeutic method resulting in a decrease in symptoms would be predicted to be accompanied by a demonstrable correction in vagal function. We propose to utilize the gCRC facilities to conduct tests of meal-induced satiety.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 这项研究（由 R01 DK 42291-06-09 资助）建议进一步研究迷走神经传入在暴食和呕吐持续中的作用。我们之前提出神经性贪食症的病理生理学涉及传入迷走神经的失调。迄今为止，我们已经使用两种主要策略评估了迷走神经对这种饮食失调的影响：（1）使用躯体疼痛检测作为迷走神经传入活动的生理标志； (2) 使用昂丹司琼（一种 5-HT3 拮抗剂，已知可减少迷走神经传递）作为迷走神经调节暴食行为和升高的疼痛检测阈值的药理学挑战测试。这些研究的主要发现是：（1）疼痛检测阈值在暴食/呕吐发作之间的时间间隔内动态上升，显然在下一次暴食发作时达到顶峰，并在与最近参与的时间密切相关时降至最低点暴食症发作时； (2) 在随机、安慰剂对照的一组患有严重和慢性神经性贪食症的患者中，昂丹司琼治疗与疼痛检测阈值的周期性波动和每周暴食/呕吐发作的主要疾病症状的显着缓解相关。双盲条件。总的来说，上述总结的生理和临床数据得出了一个精确的假设，即神经性贪食症的病理生理学涉及迷走神经传入神经的周期性过度活跃。本研究旨在通过临床药理学和心理生理学方法的交互组合来检验迷走神经活动的周期性增加导致暴食和呕吐的假设。临床治疗研究的主要目的是比较昂丹司琼与认知行为疗法（CBT）的疗效，作为疾病严重程度的函数。根据症状严重程度将受试者招募到两组（每周发作 2-<7 次；每周发作 7 次或更多）。在严重程度组内，患者将被随机分配到四个治疗组之一：认知行为治疗 (CBT) 加安慰剂安慰剂 (CBT+Placebo)、单独昂丹司琼 (ONDAN)、CBT 联合昂丹司琼 (CBT+ONDAN) 和安慰剂安慰剂（PLAC）单独。我们建议利用 gCRC 设施对纳入本研究的患者进行初步评估。心理生理学研究的主要目的是研究 CBT 与昂丹司琼治疗对迷走神经活动生理指标（即疼痛检测阈值和饱腹感诱导）的影响。该目标的方法基于这样的想法：如果迷走神经过度活跃代表了症状产生的关键因素，那么任何导致症状减轻的治疗方法都将被预测伴随着迷走神经功能的明显纠正。我们建议利用 gCRC 设施来进行膳食引起的饱腹感测试。