Kurvers H A, Jacobs M J, Beuk R J, van den Wildenberg F A, Kitslaar P J, Slaaf D W, Reneman R S
Department of Surgery, University Hospital Maastricht, The Netherlands.
Arch Neurol. 1996 Jan;53(1):58-65. doi: 10.1001/archneur.1996.00550010076019.
To determine whether the mechanisms of reflex sympathetic dystrophy, a neuropathic pain syndrome characterized by skin blood flow abnormalities associated with sympathetic vasoconstrictor and antidromic vasodilator mechanisms, are solely of peripheral origin or have an additional spinal component and act exclusively through neural or also involve humoral pathways.
The 54 patients with unilateral reflex sympathetic dystrophy were divided into the following three stages according to their perception of skin temperature in the clinically affected hand: stage I, stationary warmth sensation; stage II, intermittent warmth and cold sensation; and stage III, stationary cold sensation.
Investigation of basal skin blood flow and vasoconstrictive response to dependency of skin microvessels in the clinically unaffected hand and the clinically affected hand of patients with reflex sympathetic dystrophy and the left hand of 16 control subjects. Microcirculation was investigated at the predominantly neurally controlled thermoregulatory level (Doppler laser flowmetry) and at the predominantly humorally controlled nutritive level (capillary microscopy).
In the clinically unaffected hand, at the thermoregulatory level of the microcirculation: (1) basal skin blood flow was increased at stage I compared with the control subjects, whereas no differences could be observed at this stage compared with the clinically affected hand; (2) the vasoconstrictive response to dependency (defined as skin blood flow at heart level divided by skin blood flow in the dependent position) was attenuated at stage I compared with the control subjects, whereas no differences could be observed at this stage compared with the clinically affected hand; and (3) basal skin blood flow and the vasoconstrictive response to dependency did not differ from the control subjects at stages II and III. In the clinically unaffected hand, at the nutritive level, no differences could be observed at any stage of the syndrome compared with the control subjects.
This study indicates that there is a spinal component to microcirculatory abnormalities at stage I of the reflex sympathetic dystrophy syndrome that most likely acts through neural (antidromic vasodilator) mechanisms and that may be initiated by traumatic excitation of a peripheral nerve on the clinically affected side.
确定反射性交感神经营养不良（一种以与交感神经血管收缩及逆行性血管舒张机制相关的皮肤血流异常为特征的神经病理性疼痛综合征）的机制是否仅源于外周，还是具有额外的脊髓成分，并且仅通过神经途径起作用，还是也涉及体液途径。
54例单侧反射性交感神经营养不良患者根据其对临床受累手部皮肤温度的感知分为以下三个阶段：I期，静止性温热感；II期，间歇性温热与寒冷感；III期，静止性寒冷感。
对反射性交感神经营养不良患者临床未受累手和临床受累手以及16名对照受试者左手的基础皮肤血流及皮肤微血管对体位依赖性的血管收缩反应进行研究。在主要由神经控制的体温调节水平（多普勒激光血流仪）和主要由体液控制的营养水平（毛细血管显微镜检查）对微循环进行研究。
在临床未受累手，在微循环的体温调节水平：（1）I期基础皮肤血流较对照受试者增加，而此阶段与临床受累手相比未观察到差异；（2）I期对体位依赖性的血管收缩反应（定义为心脏水平的皮肤血流除以垂位的皮肤血流）较对照受试者减弱，而此阶段与临床受累手相比未观察到差异；（3）II期和III期基础皮肤血流及对体位依赖性的血管收缩反应与对照受试者无差异。在临床未受累手，在营养水平，该综合征任何阶段与对照受试者相比均未观察到差异。
本研究表明，反射性交感神经营养不良综合征I期的微循环异常存在脊髓成分，极有可能通过神经（逆行性血管舒张）机制起作用，且可能由临床受累侧外周神经的创伤性兴奋引发。
