PAIN AND PARESTHESIAS IN DIABETIC NEUROPATHY

描述：在糖尿病中， 神经病性起源的感觉症状的影响，例如感觉异常， 皮肤和肌肉的自发性疼痛和痛觉过敏，挑战 临床科学家更新病理生理学研究 这些异常的基础。 在过去的十年里，基础科学和临床研究导致， 发现异常的外周和中枢神经生理 能够在神经病中引起痛苦感觉的机制。 还有最近的知识过程，连接感觉功能 交感神经活动， 伤害感受器介导的神经血管控制事件。 这类研究 启发了对人类进行研究的强大新方法的设计： 其中包括： * 显微神经造影术;神经内微刺激;测量 纠正神经兴奋性的生物物理因素;定量模态- 具体的心理物理体感测试;药理学和 交感神经介导疼痛的电生理学试验，以及 神经源性炎症当量的测量。 通过应用一系列的这些方法，我们建议调查， 糖尿病痛性神经病变的存在及方式 新识别的初级外周和次级中心的操作 异常的感觉机制，已经显示，由其他人和 我们自己，在神经病动物或实验人类中操作， 科目 其中包括： * 神经源性炎症和疼痛感受器敏感化;异常 生物物理整流和外周异位放电 轴突;不平衡传入纤维的中枢分布;次级 中枢神经系统回路的崩溃和过度兴奋，以及交感神经系统 感觉释放的调节。 疼痛性糖尿病神经病变的当代医学范式已经准备就绪 一个概念和方法的转变。 预期结果来自 目前研究计划将重新调整目前的调查路线 和糖尿病神经病变感觉功能障碍的管理协议。 新的原发性或继发性神经病变机制发现在 一般糖尿病神经病变将提交给科学家， 制药业作为开发药理学或其他 治疗方式。 个别患者将免于治疗 有时会在有问题的机制中解决， 定制化的治疗模式。

DESCRIPTION: In diabetes, the high prevalence, chronicity and crippling impact of sensory symptoms of neuropathic origin, such as parasthesias, spontaneous pains and hyperalgesias from skin and muscle, challenge the clinical scientist to update investigation of the pathophysiological bases of those anomalies. Basic scientific and clinical research have led, over the past decade, to discovery of abnormal peripheral and central neurophysiological mechanisms capable of inducing distressing sensations in neuropathy. There is also recent knowledge on processes which link sensory function with sympathetic nervous activity and also with sympathetic and nociceptor-mediated neurovascular control events. Such research has inspired the design of powerful new methods of investigation in humans: Among them are: *microneurography; intraneural microstimulation; measurement of biophysical factors that rectify nerve excitability; quantitate modality- specific psychophysical somatosensory tests; pharmacological and electrophysiologicaltests for sympathetic mediation of pain, and measurement of equivalents of neurogenic inflammation. Through applying a range of those methods we propose to investigate in patients with painful diabetic neuropathy the existence and mode of operation of newly recognized primary peripheral and secondary central abnormal sensory mechanisms which have been shown, by others and ourselves, to operate in neuropathic animals or in experimental human subjects. These include: *neurogenic inflammation and sensitization of pain receptors; abnormal biophysical rectification and ectopic electrical discharges in peripheral axons; central distribution of imbalanced afferent input; secondary breakdown and hyperexcitability of CNS circuits, and sympathetic mediation of sensory discharge. The contemporary medical paradigm on painful diabetic neuropathy is ready for a conceptual and methodological shift. The results anticipated from the present research plan would resteer current lines of investigation and management protocols for sensory dysfunction in diabetic neuropathy. Novel primary or secondary neuropathic mechanisms found to operate in general in diabetic neuropathy will be presented to scientists and to the industry as priorities for development of pharmacological or other treatment modalities. Individual patients will be spared therapies sometimes addressed at questionable mechanisms, and will be directed towards customized modalities of treatment.