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实验性诱导紧张型头痛的起始机制。

Initiating mechanisms of experimentally induced tension-type headache.

作者信息

Jensen R, Olesen J

机构信息

Department of Neurology, Glostrup Hospital, University of Copenhagen, Denmark.

出版信息

Cephalalgia. 1996 May;16(3):175-82; discussion 138-9. doi: 10.1046/j.1468-2982.1996.1603175.x.

DOI:10.1046/j.1468-2982.1996.1603175.x
PMID:8734769
Abstract

To elucidate possible myofascial mechanisms of tension-type headache, the effect of 30 min of sustained tooth clenching (10% of maximal EMG-signal) was studied in 58 patients with tension-type headache and in 30 age- and sex-matched controls. Pericranial tenderness, mechanical and thermal pain detection and tolerance thresholds and EMG levels were recorded before and after the clenching procedure. Within 24 h, 69% of patients and 17% of controls developed a tension-type headache. Shortly after clenching, tenderness was increased in the group who subsequently developed headache, whereas tenderness was stable in the group of patients who remained headache free. Mechanical pain thresholds evaluated by pressure algometry remained unchanged in the group which developed headache, whereas thresholds increased in the group which did not develop headache. Thermal pain detection and tolerance thresholds remained unchanged in both groups. These findings indicate that, although there may be several different mechanisms of tension-type headache, one of them is sustained muscle contraction. A peripheral mechanism of tension-type headache is therefore possible, whereas a secondary segmental central sensitization seems to be involved in subjects with frequent tension-type headache. Finally, the increase in pressure pain thresholds in patients who did not develop headache suggested that clenching activated their antinociceptive system, whereas those developing headache were unable to do so.

摘要

为阐明紧张型头痛可能的肌筋膜机制,对58例紧张型头痛患者及30例年龄和性别匹配的对照者进行了研究,观察持续30分钟紧咬牙(最大肌电图信号的10%)的影响。在紧咬牙程序前后记录颅周压痛、机械性和热痛检测及耐受阈值以及肌电图水平。在24小时内,69%的患者和17%的对照者出现了紧张型头痛。紧咬牙后不久,随后出现头痛的组压痛增加,而未出现头痛的患者组压痛稳定。通过压力痛觉测定法评估的机械性疼痛阈值在出现头痛的组中保持不变,而在未出现头痛的组中阈值升高。两组的热痛检测和耐受阈值均保持不变。这些发现表明,尽管紧张型头痛可能有几种不同的机制,但其中之一是肌肉持续收缩。因此,紧张型头痛的外周机制是可能的,而继发性节段性中枢敏化似乎与频繁发作紧张型头痛的患者有关。最后,未出现头痛的患者压力痛阈值升高表明,紧咬牙激活了他们的抗伤害感受系统,而出现头痛的患者则无法做到这一点。

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