A search for activation of C nociceptors by sympathetic fibers in complex regional pain syndrome.

A search for activation of C nociceptors by sympathetic fibers in complex regional pain syndrome.
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DOI:
10.1016/j.clinph.2009.12.038
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发表时间:
2010-07
期刊:
Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
影响因子:
--
通讯作者:
Ochoa JL
Ochoa JL
中科院分区:
其他
文献类型:
--
作者:
Campero M;Bostock H;Baumann TK;Ochoa JL

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虽然术语“反射性交感神经营养不良”已被“复杂区域疼痛综合征”(CRPS)I型所取代,但仍然存在广泛的假设,即交感神经系统积极参与介导慢性神经性疼痛[“交感神经维持性疼痛”(SMP)],即使在缺乏可检测的神经病理生理学的情况下。我们已经使用显微神经造影术,以评估可能的电生理相互作用,在24例患者诊断为CRPS I(n=13),或CRPS II(n=11),同时记录从单一识别的交感神经传出纤维和C伤害感受器,同时激发交感神经放电的皮肤神经。我们评估了交感神经活动对35个多模态伤害感受器和19个机械不敏感伤害感受器的潜在影响,记录在CRPS I(26个伤害感受器)和CRPS II患者(28个伤害感受器)中。没有证据表明激活的伤害感受器相关的交感神经放电,虽然伤害感受器在6 CRPS II患者表现出无关的自发病理性神经冲动活动。我们的结论是,激活交感神经传出放电的伤害性感受器是不是一个主要的致病事件,无论是CRPS I或CRPS II患者。这项研究表明,交感神经伤害感受器的相互作用,如果他们存在于慢性神经性疼痛的患者沟通,必须是例外。
Although the term ‘reflex sympathetic dystrophy’ has been replaced by ‘complex regional pain syndrome’ (CRPS) type I, there remains a widespread presumption that the sympathetic nervous system is actively involved in mediating chronic neuropathic pain [“sympathetically maintained pain” (SMP)], even in the absence of detectable neuropathophysiology. We have used microneurography to evaluate possible electrophysiological interactions in 24 patients diagnosed with CRPS I (n=13), or CRPS II (n=11) by simultaneously recording from single identified sympathetic efferent fibers and C nociceptors, while provoking sympathetic neural discharges in cutaneous nerves. We assessed potential effects of sympathetic activity upon 35 polymodal nociceptors and 19 mechano-insensitive nociceptors, recorded in CRPS I (26 nociceptors) and CRPS II patients (28 nociceptors). No evidence of activation of nociceptors related to sympathetic discharge was found, although nociceptors in 6 CRPS II patients exhibited unrelated spontaneous pathological nerve impulse activity. We conclude that activation of nociceptors by sympathetic efferent discharges is not a cardinal pathogenic event in either CRPS I or CRPS II patients. This study shows that sympathetic-nociceptor interactions, if they exist in patients communicating chronic neuropathic pain, must be the exception.
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