Nordin M, Fagius J, Waldenlind E
Department of Clinical Neurophysiology, University Hospital, Uppsala, Sweden.
Headache. 1997 Jun;37(6):358-67. doi: 10.1046/j.1526-4610.1997.3706358.x.
To search for evidence of sympathetic dysregulation during cluster headache attacks, microneurographic recordings of muscle nerve sympathetic activity (MSA) were obtained from the peroneal nerve. In three recordings commenced after the onset of spontaneous attacks, MSA was about twice as high during the attack as afterwards. In four nitroglycerin-induced attacks, MSA showed a rise paralleling the pain, preceded by an initial peak. The latter accompanied hypotension, whereas the rise coinciding with cluster headache was associated with rising blood pressure. The normal baroreflex-governed pulse synchrony of MSA was preserved both during spontaneous and provoked attacks. In seven cluster headache patients in whom nitroglycerin did not cause an attack, only an initial peak in MSA occurred. Nor was any late nitroglycerin-induced rise in MSA observed in nine healthy subjects; the initial peak in MSA and heart rate was followed by a rapid return to normal despite a falling blood pressure. It is concluded that cluster headache attacks are associated with an increase in MSA that elevates blood pressure by causing vasoconstriction, and that this increase, rather than indicating sympathetic dysregulation, is a normal pain-evoked secondary phenomenon. The findings in healthy subjects support the notion that nitroglycerin has a central sympatho-inhibitory effect.
为了寻找丛集性头痛发作期间交感神经调节异常的证据，从腓神经获取了肌肉神经交感神经活动（MSA）的微神经图记录。在自发发作开始后开始的三次记录中，发作期间的MSA约为发作后两倍。在四次硝酸甘油诱发的发作中，MSA显示出与疼痛平行的升高，之前有一个初始峰值。后者伴有低血压，而与丛集性头痛同时出现的升高与血压升高有关。在自发发作和诱发发作期间，MSA正常的压力反射调节的脉搏同步性均得以保留。在七名硝酸甘油未诱发发作的丛集性头痛患者中，仅出现了MSA的初始峰值。在九名健康受试者中也未观察到硝酸甘油诱发的MSA后期升高；尽管血压下降，但MSA和心率的初始峰值之后迅速恢复正常。得出的结论是，丛集性头痛发作与MSA增加有关，MSA通过引起血管收缩来升高血压，并且这种增加并非表明交感神经调节异常，而是一种正常的疼痛诱发的继发现象。健康受试者的研究结果支持硝酸甘油具有中枢交感神经抑制作用这一观点。
