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首页> 外文期刊>The European Journal of Neuroscience >Motor cortex plasticity induced by theta burst stimulation is impaired in patients with obstructive sleep apnoea
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Motor cortex plasticity induced by theta burst stimulation is impaired in patients with obstructive sleep apnoea

机译：θ爆发刺激诱发的运动皮层可塑性在阻塞性睡眠呼吸暂停患者中受损

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摘要

Obstructive sleep apnoea (OSA) is a respiratory condition occurring during sleep characterised by repeated collapse of the upper airway. Patients with OSA show altered brain structure and function that may manifest as impaired neuroplasticity. We assessed this hypothesis in 13 patients with moderate-to-severe OSA and 11 healthy control subjects. Transcranial magnetic stimulation was used to induce and measure neuroplastic changes in the motor cortex by assessing changes in motor-evoked potentials (MEPs) in a hand muscle. Baseline measurements of cortical excitability included active (AMT) and resting motor thresholds (RMT), and the maximal stimulator output producing a 1-mV MEP. Intracortical inhibition (ICI) was investigated with short- and long-interval ICI paradigms (SICI and LICI, respectively), and neuroplastic changes were induced using continuous theta burst stimulation (cTBS). At baseline, differences were found between groups for RMT (9.5% maximal stimulator output higher in OSA) and 1-mV MEPs (10.3% maximal stimulator output higher in OSA), but not AMT. No differences were found between groups for SICI or LICI. The response to cTBS was different between groups, with control subjects showing an expected reduction in MEP amplitude after cTBS, whereas the MEPs in patients with OSA did not change. The lack of response to cTBS suggests impaired long-term depression-like neuroplasticity in patients with OSA, which may be a consequence of sleep fragmentation or chronic blood gas disturbance in sleep. This reduced neuroplastic capacity may have implications for the learning, retention or consolidation of motor skills in patients with OSA.
机译：阻塞性睡眠呼吸暂停（OSA）是一种睡眠期间发生的呼吸系统疾病，其特征是上呼吸道反复塌陷。 OSA患者显示大脑结构和功能改变，可能表现为神经可塑性受损。我们在13名中度至重度OSA患者和11名健康对照者中评估了这一假设。经颅磁刺激用于通过评估手部肌肉的运动诱发电位（MEP）的变化来诱导和测量运动皮层的神经塑性变化。皮质兴奋性的基线测量包括活动（AMT）和静止运动阈值（RMT），以及产生1-mV MEP的最大刺激器输出。使用短间隔和长间隔ICI范式（分别为SICI和LICI）研究了皮层内抑制（ICI），并使用连续θ爆裂刺激（cTBS）诱导了神经塑性改变。在基线时，在RMT组（OSA中最大刺激物输出高9.5％）和1-mV MEP（OSA中中最大刺激物输出10.3％）之间发现了差异，但AMT没有差异。 SICI或LICI组之间没有发现差异。两组之间对cTBS的反应不同，对照组显示cTBS后MEP振幅有望降低，而OSA患者的MEP则没有变化。对cTBS的缺乏反应表明OSA患者长期抑郁样神经可塑性受损，这可能是睡眠破碎或睡眠中慢性血气紊乱的结果。神经塑形能力的降低可能对O​​SA患者的学习，保留或巩固运动技能有影响。

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