Schattschneider Jörn, Binder Andreas, Siebrecht Dieter, Wasner Gunnar, Baron Ralf
Klinik für Neurologie, Sektion für Schmerzforschung und therapie, Univeritätsklinikum Schleswig-Holstein, Campus Kiel, Germany.
Clin J Pain. 2006 Mar-Apr;22(3):240-4. doi: 10.1097/01.ajp.0000169672.49438.67.
Complex regional pain syndromes (CRPS) can be relieved by sympathetic blockade. Different sympathetic efferent output channels innervate distinct effector organs (ie, cutaneous vasoconstrictor, muscle vasoconstrictor. and sudomotor neurons, as well as neurons innervating deep somatic tissues like bone, joints, and tendons). The aim of the present study was to elucidate in CRPS patients the sympathetically maintained pain (SMP) component that exclusively depends on cutaneous sympathetic activity compared with the SMP depending on the sympathetic innervation of deep somatic tissues.
The sympathetic outflow to the painful skin was modulated selectively in awake humans. High and low cutaneous vasoconstrictor activity was produced in 12 CRPS type 1 patients by whole-body cooling and warming (thermal suit). Spontaneous pain was quantified during high and low cutaneous vasoconstrictor activity. By comparing the cutaneous SMP component with the change in pain that was achieved by modulation of the entire sympathetic outflow (sympathetic ganglion block), the SMP component originating in deep somatic structures was estimated.
The relief of spontaneous pain after sympathetic blockade was more pronounced than changes in spontaneous pain that could be induced by selective sympathetic cutaneous modulation. The entire SMP component (cutaneous and deep) changes considerably over time. It is most prominent in the acute stages of CRPS.
Sympathetic afferent coupling takes place in the skin and in the deep somatic tissues, but especially in the acute stages of CRPS, the pain component that is influenced by the sympathetic innervation of deep somatic structures is more important than the cutaneous activation. The entire sympathetic maintained pain component is not constant in the course of the disease but decreases over time.
复杂性区域疼痛综合征(CRPS)可通过交感神经阻滞得到缓解。不同的交感传出通路支配不同的效应器官(即皮肤血管收缩肌、肌肉血管收缩肌、汗腺运动神经元,以及支配骨骼、关节和肌腱等深部躯体组织的神经元)。本研究的目的是在CRPS患者中阐明仅依赖皮肤交感神经活动的交感神经维持性疼痛(SMP)成分,并与依赖深部躯体组织交感神经支配的SMP进行比较。
在清醒的人体中选择性地调节通向疼痛皮肤的交感神经输出。通过全身冷却和加热(热服)在12例1型CRPS患者中产生高、低皮肤血管收缩活动。在高、低皮肤血管收缩活动期间对自发痛进行量化。通过将皮肤SMP成分与通过调节整个交感神经输出(交感神经节阻滞)所实现的疼痛变化进行比较,估计源自深部躯体结构的SMP成分。
交感神经阻滞后自发痛的缓解比选择性交感神经皮肤调节所诱发的自发痛变化更为明显。整个SMP成分(皮肤和深部)随时间变化很大。它在CRPS的急性期最为突出。
交感神经传入耦合发生在皮肤和深部躯体组织中,但特别是在CRPS的急性期,受深部躯体结构交感神经支配影响的疼痛成分比皮肤激活更为重要。整个交感神经维持性疼痛成分在疾病过程中并非恒定不变,而是随时间降低。