NOCICEPTION IN BULIMIA NERVOSA

神经性贪食症的伤害感受

• 批准号: 2444176
• 负责人: PATRICIA L FARIS
• 金额: $ 23.73万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 1993
• 资助国家: 美国
• 起止时间: 1993-08-01 至 1999-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2444176
• 关键词: analgesia; anorexia nervosa; bulimia nervosa; female; human subject; major depression; mechanical pressure; neural information processing; obesity; pain threshold; personality disorders; satiations; sensory mechanism; sensory thresholds; touch; vagus nerve

The eating disorder bulimia nervosa is characterized by periodic binge- eating usually followed by self-induced vomiting or laxative abuse. These symptoms clearly are related to alterations in meal size and meal patterning. With remarkably few exceptions, information relevant to meal termination is relayed to the central nervous system via the vagus nerve. We therefore hypothesize that an approach to the pathophysiology of bulimia nervosa is through studies of the neurocircuitry and neurochemistry of these satiety mechanisms. In addition to mediating short-term satiety, a rapidly growing body of literature suggests that the vagus Is also involved in modulating nociceptive information. Accordingly, the hypothesis that vagally- activated satiety mechanisms are abnormal in bulimia nervosa would predict that a related alteration in nociception might also be evident in this clinical group. In our initial study of 27 bulimia women and 31 age and sex matched controls, nociceptive thresholds, both pain detection and pain tolerance, were found to be significantly elevated in patients with an active diagnosis of bulimia nervosa compared to controls. Our Initial studies suggest that this effect- may be specific to nociceptive responsivity, since the ability to perceive an innocuous sensory stimulus did not differ between groups. In this application, we propose to further investigate this finding. Sensory processing (both tactile thresholds and pain responsivity) will be characterized in detail in a control population and in patients with either bulimia nervosa or with a psychiatric diagnosis which is frequently co-morbid with bulimia nervosa. We will also study this phenomena over the course of the binge/purge cycle, and in recovered bulimic patients. Regardless of the etiology of bulimia nervosa, we believe that the profound alterations in nutrient intake that characterize this disorder may affect, and in turn be affected by peripheral and central nervous system neurotransmission. Identification of alterations in nervous system function may lead to improved treatment.

饮食失调神经性贪食症的特征是周期性的暴饮暴食 - 饮食通常是自我引起的呕吐或泻药滥用。这些 症状显然与进餐大小和饮食的改变有关 图案。除了很少的例外，与进餐有关的信息 终止通过迷走神经传递到中枢神经系统。 因此，我们假设一种方法 神经性贪食症是通过研究神经记录和 这些饱腹感的神经化学。 除了调解短期饱腹感外， 文献表明迷走神也参与调节 伤害性信息。因此，模糊的假设 激活的饱腹感机制在神经性贪食症中是异常的 预测伤害受伤的相关改变也可能显而易见 在这个临床组中。在我们对27名贪食症妇女和31位的最初研究中 年龄和性别匹配的对照，伤害感受阈值，两个疼痛检测 发现患者的疼痛耐受性显着升高 与对照组相比，神经性贪食症的主动诊断。我们的 初步研究表明，这种效果可能针对伤害感受 响应性，因为感知无害的感觉刺激的能力 两组之间没有差异。在此应用程序中，我们建议进一步 调查这一发现。感官处理（触觉阈值和 疼痛反应性）将在控制中详细描述 人口和神经性贪食症患者或患者 精神病诊断经常与神经性贪食症合并。 我们还将在狂欢/清除过程中研究这种现象 循环，并在恢复的脂肪患者中。 不管神经性贪食症的病因如何 特征这种疾病的营养摄入量的深刻变化 可能会影响，进而受到周围和中枢神经的影响 系统神经传递。识别神经系统的改变 功能可能会导致治疗的改善。