Casale R, Elam M
Service of Clinical Neurophysiology, Foundation Clinica del Lavoro IRCCS-Pavia, Montescano, Italy.
J Auton Nerv Syst. 1992 Dec;41(3):215-9. doi: 10.1016/0165-1838(92)90061-k.
Intraneural recording in skin fascicles of the left ulnar nerve was performed in a 51 year old patient with reflex sympathetic dystrophy (allodynia, marked vasoconstriction in the ulnar part of the left hand) following Vth finger amputation. Skin sympathetic activity showed normal characteristics with a weak discharge at rest whereas bursts of impulses could be evoked by sympatho-excitatory stimuli. Sympathetic bursts induced by painful stimuli were few, also during long-lasting allodynic pain. Sympathetic bursts induced by inspiratory gasps were not associated with excacerbation of pain. The discrepancy between the marked skin vasoconstriction and the low resting sympathetic discharge underlines the fact that sympathetic effector organ hyperactivity (i.e. vasoconstriction and/or hyperhidrosis) cannot be taken as evidence for increased sympathetic discharge. In the present case, the neuropathic pain syndrome cannot be considered as maintained by an increased sympathetic neural discharge to the symptomatic limb.
对一名51岁的患者进行了左侧尺神经皮肤束内记录，该患者在小指截肢后患有反射性交感神经营养不良（异常性疼痛，左手尺侧明显血管收缩）。皮肤交感神经活动表现出正常特征，静息时放电微弱，而交感神经兴奋刺激可诱发冲动爆发。疼痛刺激诱发的交感神经爆发很少，即使在长期的异常性疼痛期间也是如此。吸气喘息诱发的交感神经爆发与疼痛加剧无关。明显的皮肤血管收缩与低静息交感神经放电之间的差异突出了这样一个事实，即交感神经效应器器官的活动亢进（即血管收缩和/或多汗）不能被视为交感神经放电增加的证据。在本病例中，神经性疼痛综合征不能被认为是由对有症状肢体的交感神经放电增加所维持的。
