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Low frequency activation of the sphenopalatine ganglion does not induce migraine-like attacks in migraine patients.
Cephalalgia ( IF 4.9 ) Pub Date : 2020-04-22 , DOI: 10.1177/0333102420921156
Song Guo 1 , Katrine Falkenberg 1 , Henrik Winther Schytz 1 , Anthony Caparso 2 , Rigmor Højland Jensen 1 , Messoud Ashina 1
Affiliation  

Introduction

Cephalic autonomic symptoms occur in 27‒73% of migraine patients during attacks. The role of parasympathetic activation in migraine attack initiation remains elusive. Low frequency stimulation of the sphenopalatine ganglion increases parasympathetic outflow. In this study, we hypothesized that low frequency stimulation of the sphenopalatine ganglion would provoke migraine-like attacks in migraine patients.

Methods

In a double-blind randomized sham-controlled crossover study, 12 migraine patients with a sphenopalatine ganglion neurostimulator received low frequency or sham stimulation for 30 min on two separate days. We recorded headache characteristics, cephalic autonomic symptoms, ipsilateral mechanical perception and pain thresholds, mean blood flow velocity in the middle cerebral artery (VMCA) and diameter of the superficial temporal artery during and after stimulation.

Results

Five patients (42%) reported a migraine-like attack after low frequency stimulation compared to six patients (50%) after sham (p = 1.000). We found a significant increase in mechanical detection thresholds during low frequency stimulation compared to baseline (p = 0.007). Occurrence of cephalic autonomic symptoms and changes in mechanical perception thresholds, VMCA and diameter of the superficial temporal artery showed no difference between low frequency stimulation compared to sham (p = 0.533).

Conclusion

Low frequency stimulation of the sphenopalatine ganglion did not induce migraine-like attacks or autonomic symptoms in migraine patients. These data suggest that increased parasympathetic outflow by the sphenopalatine ganglion neurostimulator does not initiate migraine-like attacks.

Study protocol: ClinicalTrials.gov registration number NCT02510742



中文翻译:

蝶腭神经节的低频激活不会在偏头痛患者中诱发偏头痛样发作。

介绍

27-73% 的偏头痛患者在发作期间会出现头部自主神经症状。副交感神经激活在偏头痛发作中的作用仍然难以捉摸。蝶腭神经节的低频刺激增加副交感神经流出。在这项研究中,我们假设蝶腭神经节的低频刺激会引起偏头痛患者的偏头痛样发作。

方法

在一项双盲随机假对照交叉研究中,12 名使用蝶腭神经节神经刺激器的偏头痛患者在两天内分别接受了 30 分钟的低频或假刺激。我们记录了头痛特征、头部自主神经症状、同侧机械知觉和疼痛阈值、大脑中动脉 (V MCA ) 的平均血流速度和刺激期间和之后的颞浅动脉直径。

结果

5 名患者 (42%) 报告低频刺激后出现偏头痛样发作,而假手术后有 6 名患者 (50%) ( p  = 1.000)。我们发现与基线相比,低频刺激期间的机械检测阈值显着增加(p  = 0.007)。头部自主神经症状的发生和机械感知阈值、V MCA和颞浅动脉直径的变化显示低频刺激与假手术相比没有差异 ( p  = 0.533)。

结论

蝶腭神经节的低频刺激不会在偏头痛患者中诱发偏头痛样发作或自主神经症状。这些数据表明蝶腭神经节神经刺激器增加的副交感神经流出不会引发偏头痛样发作。

研究方案: ClinicalTrials.gov 注册号 NCT02510742

更新日期:2020-04-23
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