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1.
目的:观察睡眠状态下阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者上气道扩张肌肌电活性的变化,探讨其在OSAHS中的作用及意义。方法:对中、重度OSAHS患者69例(OSAHS组)及健康志愿者20例(对照组)于诱导睡眠后分别行颏舌肌、腭帆张肌和腭帆提肌等上气道扩张肌肌电图的检测并与诱导睡眠前比较。结果:(1)清醒状态下OSAHS组上气道扩张肌肌电水平较对照组高(均P〈0.01);②与清醒状态比较,睡眠状态下OSAHS组上气道扩张肌肌电水平显著下降(均P〈0.01);③从清醒状态到睡眠状态,OSAHS组上气道扩张肌肌电水平下降幅度明显大于对照组(均P〈0.01)。结论:OSAHS患者清醒状态下上气道扩张肌肌电活性代偿性升高及睡眠状态下失代偿是该病发生的重要病理生理机制。  相似文献   

2.
目的利用口外表面电极定量测量下颌肌电活性,验证是否能基本反应上气道扩张肌(主要指颏舌肌)活性的变化趋势,即有效性的研究;验证不同时间重复测量两次的结果是否一致,即稳定性的研究。方法利用口外表面电极测量下颌肌电,且和整夜多道睡眠监测(polysomnography,PSG)同步,对10例阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)患者整夜睡眠阶段的下颌肌电的活性变化给予分析;比较清醒期、非快眼动(non rapid eye movement,NREM)期睡眠和快眼动(rapid eye movement,REM)期睡眠不同阶段的肌电变化;分析呼吸暂停事件期间肌电活性的变化;将下颌肌电活性的变化趋势和口内表面电极测量的颏舌肌活性的变化趋势做一比较,验证其有效性;1周后重新行PSG和下颌肌电检查,比较两次的结果是否一致,验证其稳定性。结果10例OSAHS患者不同睡眠阶段下颌肌电的变化及呼吸暂停事件期间下颌肌电的变化是和口内表面电极反应的颏舌肌肌电的变化趋势一致;口外表面电极1周前、后两次测量的下颌肌电活性变化规律基本一致。结论利用口外表面电极测量下颌肌电,其变化规律能基本反应上气道扩张肌(主要指颏舌肌)活性的变化规律,是有效的,且有很好的稳定性。  相似文献   

3.
阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hyponea syndrome,OSAHS)是一种普遍的睡眠相关呼吸障碍疾病,主要表现为睡眠期间上呼吸道反复塌陷阻塞引起的呼吸暂停和低通气。而慢性间歇性低氧(chronic intermittent hypoxia,CIH)作为OSAHS最具代表性的病理生理特征,常引发机体低氧血症,高碳酸血症等一系列不良后果,是机体代谢性障碍及心血管疾病的潜在高危因素。研究证实上呼吸道扩张肌,尤其是颏舌肌功能异常是OSAHS的重要致病诱因,而CIH又进一步加重了颏舌肌功能损伤。本文就CIH引起颏舌肌损伤的机制做一综述。  相似文献   

4.
目的研究在兔颏舌肌内注射肉毒杆菌毒素(botulinum toxin,BTX)能否建立舌根后气道狭窄的阻塞性睡眠呼吸暂停低通气综合征(OSAHS)动物模型。方法以24只新西兰大白兔为实验动物,建立实验组和两组对照组,实验组行颏舌肌内注射BTX,第一对照组行颏舌肌注射生理盐水,第二对照组行股二头肌注射BTX。用药后均行动脉血氧饱和度(SaO2)监测,人工计算氧减饱和度指数(ODI4),采用配对样本t检验,以P〈0.05作为动物模型成功建立的标准。结果实验组颏舌肌内注射BTX后动物出现明显缺氧症状,SaO2监测显示睡眠状态下出现间歇性低氧,其ODI4与对照组进行统计学分析具有显著性差异。结论运用颏舌肌注射BTX能够成功的建立兔舌根后气道阻塞的OSAHS动物模型,这一模型更符合OSAHS患者发病原因和自然病程。  相似文献   

5.
关于睡眠呼吸暂停(OSA)的发病机理,各界说法不一。有人以肌电图测定睡眠时颏舌肌的功能,发现吸气期颏舌肌轻度外突以保持气道通畅,因此设想OSA可能是颏舌肌功能受损、吸气时舌根脱垂,与咽后壁抵触之故。也有人通过实验,发现在出现呼吸道阻塞症状之前,呼吸的神经冲动和膈肌运动均见减退,因此认为OSA的发生与神经和肌肉等因素有关。OSA亦可能是吸气时咽部负压大大超过使上呼吸道扩张的肌肉的张力的结果;也有认为鼻阻塞可增加呼吸道之阻力,使吸气费力,并因负压而使气道萎陷遂  相似文献   

6.
目的观察一氧化氮(NO)供体二乙胺一氧化氮水合钠盐(diethylamine NONOate sodium salthydrate,DEA)作用在舌下神经核(hypoglossal motornucleus,HMN)对颏舌肌(genioglossus,GG)活动的影响并初步探讨其机制。方法雄性成年wistar大鼠,微透析探针持续给予不同浓度DEA到HMN,观测GG及膈肌电活动、动脉血压的变化。结果 DEA作用于HMN使GG肌电活动增加,低浓度时以时相性成分为主,高浓度时以紧张性成分为主。对呼吸频率、膈肌活动和血压无明显影响。结论 NO供体DEA作用于HMN,对其产生兴奋作用,使颏舌肌活动增强。NO作为HMN的神经递质,可能参与了维持上气道开放的神经机制。  相似文献   

7.
吞咽反射是由咽喉粘膜受刺激而引起,需要很多神经肌肉高度配合。关于以延髓吞咽中枢为主的高级中枢参与问题有待基础和临床医学密切配合研究才有可能解决。本文研究正常吞咽运动和吞咽障碍机理。与吞咽有关的神经肌肉包括:三叉神经支配的颞肌、嚼肌、翼内肌、翼外肌、二腹肌前腹、颏舌肌,面神经支配的面肌、二腹肌后腹、茎突舌骨肌,迷走神经支配的喉内肌、腭帆提肌、腭舌肌、咽肌、咽鼓管咽肌、上咽缩肌、中咽缩肌及下咽缩肌、食管肌;舌下神经支配的舌肌、舌骨舌肌、茎突舌肌、甲状舌骨肌等。  相似文献   

8.
目的建立一种无创的颏舌肌(genioglossus,GG)肌电活性的检查方法,对阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep hypopnea apnea sy nd rome,OSAHS)患者各睡眠阶段的GG肌电活性变化进行分析,探讨GG在OSAHS发病中的地位及其发病机理。方法①采用GG肌电活性测量与夜间多导睡眠监测(polysomnography,PSG)同步进行的方法,对符合OSAHS诊断标准的15例男性患者进行研究,分析比较清醒期、慢动眼睡眠期(non rapidey emovement,NREM)、快动眼睡眠期(rapideye movement,REM)GG肌电活性的差异;②分析呼吸暂停期间GG肌电活性的变化规律。结果①清醒期大于NREM期GG肌电指数,NREM期大于REM期GG肌电指数,差异均有统计学意义;②睡眠呼吸暂停期间GG肌电活性呈周期性改变。结论①氯化银球形表面电极可以准确测定GG肌电活性;②OSAHS患者NREM期、REM期GG肌电活性明显下降,是OSAHS发病因素之一;③睡眠呼吸呼吸暂停发作期间GG肌电活性呈规律性变化,是其与上气道负压相互作用的结果。  相似文献   

9.
阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的外科治疗技术主要包括UPPP、颏舌肌前移、舌骨悬吊、上下颌骨前移术等。多数OSAHS患者存在腭咽、舌咽等多平面阻塞或塌陷。同期行UPPP、颏舌肌前移及舌骨悬吊术,可以解除腭咽、舌咽平面阻塞或塌陷,并可明显提高疗效。  相似文献   

10.
目的 探讨慢性间歇性缺氧(chronic intermittent hypoxia,CIH)对颏舌肌肌电、超微结构及血清脂联素水平的影响,并观察补充脂联素后有无干预效果.方法 健康雄性Wistar大鼠42只,随机数字表法分为健康对照组(A组)、慢性间歇性缺氧组(B组)和脂联素干预组(C组),每组14只.对B组、C组大鼠间歇缺氧(每日8 h,连续5周);同时C组大鼠给予注射用脂联素10μg/次,A组与B组给予无菌生理盐水0.5 ml/次,颈静脉注射,每周2次,持续5周.第5周末采用插入式双极针电极引导大鼠颏舌肌肌电,检测各组动物颏舌肌肌电电压基线及低氧刺激和低氧刺激终止后各时间段平均肌电电压;透射电镜观察颏舌肌肌细胞超微结构的改变.电生理检测后抽血检测脂联素水平.结果 B组大鼠的血清脂联素质量浓度(1226.0±112.0)ng/ml((-)x±s,下同)显著低于A组(2491.8±117.9)ng/ml,q=38.2,P<0.01;C组大鼠的血清脂联素质量浓度(1988.3±114.7)ng/ml较B组显著增高(q=23.0,P<0.01).在低氧刺激前的基线状态时,B组颏舌肌肌电电压水平明显低于A组和C组(P值均<0.01);低氧刺激5 min,A、B、C三组颏舌肌肌电电压较基线时明显增高(P值均<0.01),其增高幅度A组最高,B组最低,C组居中,差异均有统计学意义(P值均<0.01);低氧刺激终止后的15 min、30 min及45 min,A、C两组颏舌肌电压仍维持在较高的水平,显著高于B组(P值均<0.01).CIH还造成颏舌肌结构的变性,使B组大鼠肌原纤维结构紊乱,肌丝溶解、消失,线粒体水肿、嵴断裂,部分线粒体空泡改变或溶解消失,而脂联素注射组病理改变较轻.结论 CIH可引起颏舌肌病理改变及肌电活动下降,该变化可能与CIH所致的低脂联素血症有关.  相似文献   

11.
Recent studies have shown that neuromuscular stimulation of the genioglossus muscle and direct stimulation of the hypoglossal nerve can be performed selectively and safely. Such stimulation, delivered below the arousal threshold, can modulate airflow during sleep in patients with OSA. The feasibility and potential of upper airway stimulation for the treatment of OSA have been demonstrated. Further studies and stimulation-system refinements are presently underway, with hopes of establishing upper airway stimulation as a therapeutic option for this challenging disorder.  相似文献   

12.
OBJECTIVES: To determine the effects of neuromuscular stimulation (NS) of the genioglossus muscle on hypopharyngeal airway size. STUDY DESIGN: Fourteen consecutively recruited healthy volunteers underwent percutaneous electrical NS of the genioglossus muscle. METHODS: Bipolar hooked wires were inserted percutaneously into the genioglossus muscle and used for NS. The anterior--posterior diameter of the hypopharynx was measured at the level of the superior edge of the epiglottis at baseline and during NS from recorded video endoscopic examinations. RESULTS: NS of the genioglossus muscle resulted in a significant increase in the diameter of the hypopharyngeal airway (P =.002) compared with baseline, ranging from a 33% to 284% increase in airway diameter. Three of the 14 patients demonstrated modest decreases in airway diameter, likely the result of faulty electrode placement in surrounding tongue retrusive muscles. CONCLUSIONS: NS of the genioglossus muscle was effective in increasing the hypopharyngeal airway and may provide a useful alternative to direct stimulation of the hypoglossal nerve with a nerve cuff electrode in the development of neuroprosthetic treatments for obstructive sleep apnea.  相似文献   

13.
Hypoglossal nerve stimulation was investigated as a method to relieve an induced upper airway obstruction. Six dogs were implanted with a cuff electrode applied to each hypoglossal nerve and a pulse generator. After 4 weeks, the hypoglossal nerve was stimulated (50% duty cycle) for up to 8 weeks. At 12 weeks a double tracheotomy was placed, with a negative pressure intermittently applied to the upper limb, simulating inspiratory airway pressure. Unilateral hypoglossal nerve stimulation improved peak upper airway flow from an average of 0.1 L/s to 1.6 L/s (P = 0.0001). Seventy-seven percent of the maximum possible flow(explanted tracheotomy tube) was obtained with unilateral stimulation. Histopathological evaluation revealed no nerve damage secondary to chronic stimulation. This study provides support for clinical trials of hypoglossal stimulation for obstructive sleep apnea.  相似文献   

14.
BACKGROUND: Hypoglossal nerve stimulation has been demonstrated to relieve upper airway obstruction acutely, but its effect on obstructive sleep apnea is not known. OBJECTIVE: To determine the response in obstructive sleep apnea to electrical stimulation of the hypoglossal nerve. METHODS: Eight patients with obstructive sleep apnea were implanted with a device that stimulated the hypoglossal nerve unilaterally during inspiration. Sleep and breathing patterns were examined at baseline before implantation and after implantation at 1, 3, and 6 months and last follow-up. RESULTS: Unilateral hypoglossal nerve stimulation decreased the severity of obstructive sleep apnea throughout the entire study period. Specifically, stimulation significantly reduced the mean apnea-hypopnea indices in non-rapid eye movement (mean +/- SD episodes per hour, 52.0 +/- 20.4 for baseline nights and 22.6 +/- 12.1 for stimulation nights; P<.001) and rapid eye movement (48.2 +/- 30.5 and 16.6 +/- 17.1, respectively; P<.001) sleep and reduced the severity of oxyhemoglobin desaturations. With improvement in sleep apnea, a trend toward deeper stages of non-rapid eye movement sleep was observed. Moreover, all patients tolerated long-term stimulation at night and did not experience any adverse effects from stimulation. Even after completing the study protocol, the 3 patients who remained free from stimulator malfunction continued to use this device as primary treatment. CONCLUSION: The findings demonstrate the feasibility and therapeutic potential for hypoglossal nerve stimulation in obstructive sleep apnea.  相似文献   

15.
The objective of this communication is to describe our preliminary results in upper airway stimulation surgery via hypoglossal nerve stimulation implantation for obstructive sleep apnoea. We describe 4 cases and the outcomes of the surgery were analysed using the Epworth scale, apnoea-hypopnoea index, minimal O2 Sat, average O2 Sat and snoring intensity. In all cases a significant reduction in Epworth scale values and apnoea-hypopnoea index were obtained (P<.05). The minimum and average oxygen saturation had better values after the surgery, however, there was no statistically significant difference. The snoring severity measured subjectively changed from «intense» to «absent» in all cases. The preliminary results obtained with the upper airway stimulation surgery via hypoglossal nerve stimulation showed objective and subjective improvement after the implant activation.  相似文献   

16.
目的观察耳穴与舌下神经针刺治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的疗效。方法60例OSAHS患者,随机分为治疗组和对照组。治疗组39例,采用耳穴与舌下神经针刺治疗;对照组21例,采用调整睡眠姿势和减肥措施治尹氕比较分析治疗前后的临床症状改变。结果与对照组比较,治疗组临床症状改善明显。结论耳穴与舌下神经针蒯治疗OSAHS疗效显著,是一种方便、经济、无副作用的早期预防和治疗方法。  相似文献   

17.
The following report presents a case of two late embedded hypoglossus branches during implantation of an upper airway stimulation device that caused a mixed activation of the tongue when included in the stimulation cuff. In the end, correct cuff placement could be achieved by careful examination of the hypoglossal nerve anatomy, precise nerve dissection, tongue motion analysis and intraoperative nerve monitoring.  相似文献   

18.
目的:探讨诱导睡眠下电子喉镜在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)定位诊断中的应用价值.方法:将经PSG确诊的132例OSAHS患者随机分成A、B 2组:A组61例为实验组,术前给予咪唑安定诱导睡眠后用电子喉镜对上呼吸道进行动态观察,以确定阻塞部位;B组71例作为对照组,术前清醒状态下行常规上呼吸道检查和电子喉镜检查.所有患者均根据定位诊断结果进行针对性手术治疗.结果:A组存在多部位阻塞者达72.1%,而B组仅为33.8%,2组差异有统计学意义(P<0.05).患者术后均随访6个月以上,A组总有效率达91.8%,B组仅为64.8%.A、B 2组的治愈率、显效率、总有效率均差异有统计学意义(均P<0.05).结论:诱导睡眠状态下大部分OSAHS患者上呼吸道存在多部位的解剖性狭窄,术前在诱导睡眠下应用电子喉镜进行OSAHS患者上呼吸道阻塞部位的定位诊断,并据此进行针对性的手术治疗,可以显著提高OSAHS手术治疗的效果.  相似文献   

19.
The patient is a 62‐year‐old man with continuous positive airway pressure‐intolerant obstructive sleep apnea who was enrolled in a study for a hypoglossal nerve upper airway stimulation device (UAS). Nearly 2.5 years later, he was admitted to the hospital for unstable angina. Diagnostic workup revealed a prior myocardial infarction, an ejection fraction of 30% on maximal medical therapy, and episodes of nonsustained ventricular tachycardia. During hospitalization, the patient received an implantable cardioverter defibrillator (ICD). This is the first reported case of simultaneous use of a UAS and an ICD, and we report no untoward device interference between the two implantable devices. Laryngoscope, 126:E86–E89, 2016  相似文献   

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