Huynh Nelly, Lavigne Gilles J, Lanfranchi Paola A, Montplaisir Jacques Y, de Champlain Jacques
Faculte de médecine, Université de Montréal, Québec, Canada.
Sleep. 2006 Mar;29(3):307-16. doi: 10.1093/sleep/29.3.307.
To examine whether 2 sympatholytic medications decrease sleep bruxism and prevent the rise in sympathetic activity preceding the onset of sleep bruxism: propranolol, a nonselective adrenergic beta-blocker, and clonidine, a selective alpha2-agonist.
Experimental randomized controlled crossover studies with placebo and active treatments (propranolol 120 mg; clonidine 0.3 mg).
Hospital-based sleep research laboratory.
Twenty-five subjects with a history and diagnosis of SLEEP BRUXISM (11 men, 14 women; age range, 21 to 31 years).
Polygraphic study.
Polygraphic sleep laboratory recordings were done for 4 nights: the first night was habituation, the second, sleep bruxism diagnosis; and 3 and 4 were study nights. The sleep bruxism index was estimated using masseter muscle activity. Heart rate variability was estimated with spectral analysis of RR intervals. Sleep and sleep bruxism variables were not significantly influenced by propranolol. A reduction of the mean RR intervals and of the sympathetic dominance (p < .05) was seen. Under clonidine, duration of sleep stage 2 was prolonged, whereas REM sleep was suppressed in 14 of 16 subjects with sleep bruxism. The sleep bruxism index was reduced by 61% (p < .05). Under clonidine, a reduction in heart rate and sympathetic dominance was observed in stable sleep and in the minute preceding the onset of sleep bruxism (p < .05).
Although propranolol did not affect sleep bruxism, clonidine decreased sympathetic tone in the minute preceding the onset of sleep bruxism, thus reducing sleep bruxism by preventing the sequence of autonomic to motor activation of sleep bruxism. This further supports the role of sympathetic activity in the pathophysiology of sleep bruxism. Because morning hypotension was seen in 19% of patients, further dose-dependant research is required to assess the safety of clonidine for the management of sleep bruxism.
探讨两种抗交感神经药物是否能减少磨牙症并预防磨牙症发作前交感神经活动的增加,这两种药物分别是普萘洛尔(一种非选择性肾上腺素β受体阻滞剂)和可乐定(一种选择性α2激动剂)。
采用安慰剂和活性治疗(普萘洛尔120毫克;可乐定0.3毫克)进行实验性随机对照交叉研究。
医院睡眠研究实验室。
25名有磨牙症病史且经诊断患有磨牙症的受试者(11名男性,14名女性;年龄范围21至31岁)。
多导睡眠图研究。
进行了4晚的多导睡眠实验室记录:第一晚为适应期,第二晚用于磨牙症诊断,第3晚和第4晚为研究夜。使用咬肌活动来评估磨牙症指数。通过RR间期的频谱分析来评估心率变异性。普萘洛尔对睡眠和磨牙症变量没有显著影响,但观察到平均RR间期和交感神经优势降低(p < 0.05)。在可乐定作用下,2期睡眠持续时间延长,而16名磨牙症受试者中有14名的快速眼动睡眠受到抑制。磨牙症指数降低了61%(p < 0.05)。在可乐定作用下,在稳定睡眠期以及磨牙症发作前一分钟观察到心率和交感神经优势降低(p < 0.05)。
虽然普萘洛尔不影响磨牙症,但可乐定在磨牙症发作前一分钟降低了交感神经张力,从而通过防止自主神经到磨牙症运动激活的序列来减少磨牙症。这进一步支持了交感神经活动在磨牙症病理生理学中的作用。由于19%的患者出现晨起低血压现象,因此需要进一步进行剂量依赖性研究以评估可乐定治疗磨牙症的安全性。