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慢性紧张型头痛与运动学习受损有关。

Chronic tension-type headache is associated with impaired motor learning.

机构信息

The Robinson Institute, School of Paediatrics and Reproductive Health, University of Adelaide, Australia.

出版信息

Cephalalgia. 2013 Sep;33(12):1048-54. doi: 10.1177/0333102413483932. Epub 2013 Apr 18.

Abstract

BACKGROUND

Supraspinal activity-dependent neuroplasticity may be important in the transition from acute to chronic pain. We examined neuroplasticity in a cortical region not considered to be a primary component of the central pain matrix in chronic tension-type headache (CTTH) patients. We hypothesised that neuroplasticity would be exaggerated in CTTH patients compared to healthy controls, which might explain (in part) the development of chronic pain in these individuals.

METHODS

Neuroplasticity was examined following a ballistic motor training task in CTTH patients and control subjects (CS). Changes in peak acceleration (motor learning) and motor-evoked potential (MEP) amplitude evoked by single-pulse transcranial magnetic stimulation were compared.

RESULTS

CTTH patients showed significantly less motor learning on the training task than CS (mean acceleration increase 87% CTTH, 204% CS, P  < .05), and CS but not CTTH patients showed a significant increased MEP amplitude following training (CS: F  = 2.9, P  < .05; CTTH: F  = 1.6, P  > .05).

CONCLUSIONS

These findings suggest a deficit in use-dependent neuroplasticity within networks responsible for task performance in CTTH patients which might reflect reciprocal influences between primary motor cortex and interconnected pain processing networks. These findings may help explain the positive effects of facilitatory non-invasive brain stimulation targeting motor areas on chronic pain and help elucidate the mechanisms mediating chronic pain.

摘要

背景

脊髓上活动依赖性神经可塑性可能在急性疼痛向慢性疼痛转变中起重要作用。我们在慢性紧张型头痛(CTTH)患者中检查了一个皮质区域的神经可塑性,该区域不被认为是中央疼痛矩阵的主要组成部分。我们假设 CTTH 患者的神经可塑性会比健康对照组更明显,这可能部分解释了这些个体慢性疼痛的发展。

方法

在 CTTH 患者和对照受试者(CS)中进行了一项弹道运动训练任务,以检查神经可塑性。比较了单次经颅磁刺激诱发的峰值加速度(运动学习)和运动诱发电位(MEP)幅度的变化。

结果

CTTH 患者在训练任务中的运动学习明显少于 CS(平均加速度增加 87% CTTH,204% CS,P<.05),而 CS 而非 CTTH 患者在训练后 MEP 幅度显著增加(CS:F=2.9,P<.05;CTTH:F=1.6,P>.05)。

结论

这些发现表明 CTTH 患者负责任务表现的网络中存在使用依赖性神经可塑性缺陷,这可能反映了初级运动皮层和相互连接的疼痛处理网络之间的相互影响。这些发现可能有助于解释针对运动区的促进性非侵入性脑刺激对慢性疼痛的积极影响,并有助于阐明介导慢性疼痛的机制。

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