PAIN AND HYPERALGESIA--MICRONEUROGRAPHY IN PATIENTS

慢性神经病理性疼痛的神经机制异常， 将在患者中探索痛觉过敏，利用一系列新的 严格的神经生理学技术现在可用于人类研究， 在我们的实验室里使用。 从拟议的实验结果是 有望改善诊断和管理的科学基础 在这些患者中，许多人目前正在接受构思不良的临床治疗， 调查或接受无效治疗。 实验计划将检验以下假设： 1.异常敏感（或视觉兴奋）的初级放射性 伤害感受器是自发性疼痛和痛觉过敏的基础。 2.低阈值有髓鞘机械感受器的活动异常兴奋 敏感的脊髓神经元引起自发性疼痛和痛觉过敏。 3.交感传出活动，通过低阈值的激发 初级机械感受器或致敏的伤害感受器，触发异常的 负责自发性疼痛和痛觉过敏的机制。 这些有科学根据的假设现在可以直接检验， 患者，消除了从动物中推断结果的必要性 research. 通过我们的专家， 神经感觉单元将接受定量感觉测试， 在引入对照实验之前和期间的显微神经造影术 变量旨在：a）选择性地激活，自然地或电地， 初级感觉单位的亚群; B）机械地选择性阻断 或E1，初级传入纤维亚群; c） 选择性地刺激或抑制，反射，交感神经的亚群， 传出神经元; d）阻断神经元的全部或部分， 交感神经流出 从我们的初步研究结果出现承诺显着产量 在基础科学和应用层面上的研究。

Abnormal neuronal mechanisms underlying chronic neuropathic pain and hyperalgesia will be explored in patients, making use of a novel array of rigorous neurophysiological techniques now available for human studies and in use in our laboratory. Results from the proposed experiments are expected to improve the scientific foundation for diagnosis and management of these patients, many of whom presently undergo ill conceived clinical investigation or receive ineffectual treatment. The experimental plan will test the following hypotheses: 1. Activity in abnormally sensitive (or ephaptically excited) primary nociceptors underlies spontaneous pain and hyperalgesia. 2. Activity in low-threshold myelinated mechanoreceptors excites abnormally sensitive spinal neurons to cause the spontaneous pain and hyperalgesia. 3. Sympathetic efferent activity, through excitation of low-threshold primary mechanoreceptors or sensitized nociceptors, triggers the abnormal mechanisms responsible for spontaneous pain and hyperalgesia. These scientifically based hypotheses are now amenable to direct testing in patients, eliminating the necessity of extrapolating results from animal research. Consenting patients, personally examined and preselected through our Neurosensory Unit, will undergo quantitative sensory testing and microneurography before and during introduction of controlled experimental variables intended to: a) selectively activate, naturally or electrically, subpopulations of primary sensory units; b) selectively block, mechanically or pharmacologically, subpopulations of primary afferent fibers; c) selectively excite or depress, reflexly, subpopulations of sympathetic efferent neurons; d) block pharmacologically the whole or part of the sympathetic outflow. Results emerging from our preliminary studies promise significant yield from this research at both basic scientific and applied levels.