...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Pharmacological modulation of pain-related brain activity during normal and central sensitization states in humans.
【24h】

Pharmacological modulation of pain-related brain activity during normal and central sensitization states in humans.

机译：人体正常和中枢敏化状态下与疼痛相关的大脑活动的药理调节。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abnormal processing of somatosensory inputs in the central nervous system (central sensitization) is the mechanism accounting for the enhanced pain sensitivity in the skin surrounding tissue injury (secondary hyperalgesia). Secondary hyperalgesia shares clinical characteristics with neurogenic hyperalgesia in patients with neuropathic pain. Abnormal brain responses to somatosensory stimuli have been found in patients with hyperalgesia as well as in normal subjects during experimental central sensitization. The aim of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patients, on brain processing of nociceptive information in normal and central sensitization states. Using functional magnetic resonance imaging (fMRI) in normal volunteers, we studied the gabapentin-induced modulation of brain activity in response to nociceptive mechanical stimulation of normal skin and capsaicin-induced secondary hyperalgesia. The dose of gabapentin was 1,800 mg per os, in a single administration. We found that (i) gabapentin reduced the activations in the bilateral operculoinsular cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimulus-induced deactivations, only during central sensitization; this effect was more robust than the effect on brain activation. The observed drug-induced effects were not due to changes in the baseline fMRI signal. These findings indicate that gabapentin has a measurable antinociceptive effect and a stronger antihyperalgesic effect most evident in the brain areas undergoing deactivation, thus supporting the concept that gabapentin is more effective in modulating nociceptive transmission when central sensitization is present.
机译：中枢神经系统中体感输入的异常处理（中枢敏化）是导致周围组织损伤（继发性痛觉过敏）周围皮肤疼痛敏感性增强的机制。继发性痛觉过敏与神经性痛患者的神经源性痛觉过敏具有共同的临床特征。在痛觉过敏患者以及实验中枢敏化过程中的正常受试者中，发现了对体感刺激的异常大脑反应。这项研究的目的是评估加巴喷丁（一种对神经性疼痛患者有效的药物）对正常和中枢敏化状态下伤害感受信息的大脑处理的影响。在正常志愿者中使用功能磁共振成像（fMRI），我们研究了加巴喷丁对正常皮肤的伤害性机械刺激和辣椒素引起的继发性痛觉过敏反应引起的大脑活动的调节。加巴喷丁的剂量为单次口服1,800 mg。我们发现（i）加巴喷丁与中枢敏化作用无关地降低了双侧oper突皮质的激活。 （ii）加巴喷丁仅在中枢敏化过程中才降低脑干的激活； （iii）加巴喷丁仅在中枢敏化过程中抑制刺激诱导的失活；这种作用比对大脑激活的作用更强。观察到的药物诱导的作用不是由于基线fMRI信号的变化。这些发现表明加巴喷丁具有可测量的抗伤害感受作用和更强的抗痛觉过敏作用，这在经历失活的大脑区域最为明显，因此支持了加巴喷丁在存在中枢敏化作用时更有效地调节伤害感受传递的概念。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号