Mechanisms of causalgia and related clinical conditions. The role of the central and of the sympathetic nervous systems.
Mechanisms of causalgia and related clinical conditions. The role of the central and of the sympathetic nervous systems.
复制标题
灼痛机制和相关临床状况。
DOI：
10.1093/brain/109.4.717
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
G. Schott
中科院分区：
文献类型：
--
作者：
G. Schott
自从世纪前Weir Mitchell提出了这个术语以来，将头痛定义为周围神经损伤后的疼痛状态已被接受。在本文中，命名和疾病分类学的问题进行了讨论，并提请注意的事实是，相同的临床特征可以自发发生，在非创伤性神经病变，在没有一个部分，在幻肢状态，并在疾病局限于中枢神经系统。还应注意的是，疼痛与交感神经系统中儿茶酚胺介导的作用以及对交感神经阻滞的反应缺乏相关性。关于机制，一些外围机制已被假定。这些审查，虽然他们可能是正确的，当causogia引起周围神经损伤，他们不能提供足够的解释，至少在某些情况下causogia。神经瘤作为一般慢性疼痛和头痛模型的相关性受到质疑。也质疑的是这样一种观点，即头痛是一种依赖于外周参与交感神经供应的状态。某些作者在过去认为，中枢神经系统（CNS）发挥了重要作用，在头痛，目前的证据支持这一观点进行了评估。中枢神经系统的参与是由以下因素引起的：在局限于中枢神经系统的疾病和幻痛状态中出现的头痛;有时经历的疼痛的不寻常分布;交感神经系统损伤后可能发生的广泛疼痛的矛盾发展;即使是中枢原因，外周交感神经阻滞的影响;以及中枢与运动、感觉和心理现象的相互作用。保留有关的作用，儿茶酚胺在causogia概述，并认为可能性，非肾上腺素能物质可能有牵连。
The definition of causalgia as a pain state following peripheral nerve injury has been accepted since the term was introduced by Weir Mitchell over a century ago. In the present paper, problems of nomenclature and nosology are discussed, and attention is drawn to the fact that the same clinical features can occur spontaneously, in nontraumatic nerve lesions, in the absence of a part as in phantom limb states, and in diseases confined to the central nervous system. Attention is also drawn to the lack of correlation of pain with the effects mediated by catecholamines in the sympathetic nervous system and with the response to sympathetic blockade. Concerning mechanisms, a number of peripheral mechanisms have been postulated. These are reviewed, and while they might be correct when causalgia arises from peripheral nerve damage, they cannot provide adequate explanation for at least some instances of causalgia. The relevance of the neuroma as a model for chronic pain in general, and causalgia, is questioned. Also questioned is the view that causalgia is a state that depends on peripheral involvement of the sympathetic nerve supply. Certain authors in the past considered that the central nervous system (CNS) played an important part in causalgia, and current evidence supporting this view is assessed. Involvement of the CNS is suggested by the development of causalgia in diseases confined to the CNS and in phantom pain states; the unusual distribution of pain sometimes experienced; the paradoxical development of widespread pain that can occur after damage to the sympathetic nervous system; the effects of peripheral sympathetic blockade even when the cause lies centrally; and central interactions with motor, sensory and psychological phenomena. Reservations concerning the role of catecholamines in causalgia are outlined, and the possibility is considered that nonadrenergic substances may be implicated.