强短声诱发的咬肌肌源性电位的起源及其解剖基础的初步研究

发布时间：2018-09-07 07:04

【摘要】： 尽管声音不是前庭自然的生理刺激，但研究者发现高强度声对前庭有作用，动物及人体实验表明，球囊斑是前庭系统中对声最敏感的部分。已知前庭系统在许多脑干和姿态运动系统的运动控制中起重要作用，其输入通过调制眼肌和颈肌以及躯干和四肢伸肌的活动，为头-眼协调活动和头-颈系统提供反馈信息。Colebatch最早记录到强短声在紧张性收缩的胸锁乳突肌上诱发的肌源性电位，该电位依赖于前庭传入神经的完整性，因此被称为前庭诱发的肌源性电位(Vestibular-evoked myogenic potentials，VEMP)，目前VEMP已成为临床评估球囊和前庭下神经功能的重要工具，并在前庭神经炎、梅尼埃病、听神经瘤、上半规管裂综合征、双侧前庭病、多发性脑硬化等疾病的诊断中得到广泛应用。由于VEMP的检测需要保持较大的胸锁乳突肌紧张性收缩，一些颈肌肌力较弱的老年人和颈椎病患者不能耐受，无法完成检测，因此，人们开始寻找在其他肌肉上记录VEMP的新方法，例如斜方肌和颈伸肌都曾被用作记录区，都获得了与胸锁乳突肌记录相似的VEMP发现。近来Deriu等发现前庭电刺激会诱发短潜伏期的、短持续时间的咬肌反射(咬肌肌源性电位)，其短潜伏期的特性决定其脑干神经通路不超过3个突触(前庭感受器—前庭核—三叉神经运动核—神经肌肉接头)。但不知道强短声刺激是否会在咬肌上诱发相似的肌源性电位，该电位是否来源于前庭，该电位的存在是否具有其解剖基础——是否存在支配咬肌的前庭三叉运动神经通路，这些问题就是本课题要解决的目标，因此本研究分以下三部分实验：第一部分健康人强短声诱发的短潜伏期咬肌肌源性电位目的观察健康人强短声诱发的短潜伏期咬肌肌源性电位，并初步确定其起源。方法21名健康志愿者，给予单侧或双侧强短声刺激(0.1 ms、5Hz、70～100 dB nHL)，在稳定收缩的双侧咬肌表面，记录咬肌肌源性电位，观察头左右倾斜30°对双侧强短声(100 dB nHL)诱发的咬肌肌源性电位的影响，并对强短声在咬肌和在胸锁乳突肌(SCM)上诱发的肌源性电位的刺激阈值进行比较。1名传导性耳聋患者及2名单侧重度感音性耳聋患者也进行强短声诱发的短潜伏期咬肌肌源性电位检测，以初步确定该电位的起源。结果健康人单侧短声刺激可诱发双侧短潜伏期的咬肌肌源性电位，根据其潜伏期、阈值和波形可有三种反应模式：在较低阈值(70-80 dB nHL)时为p16／n21，在高强度(90-100 dB nHL)刺激时表现为p11／n15或p11／n21波。p11幅度受头左右30°倾斜的不对称性调制。咬肌p11波的阈值和短声在SCM上诱发的p13／n23波的阈值相同。传导性耳聋患者强短声刺激患耳不能诱发出咬肌p11电位，而重度感音性耳聋患者单侧或双侧强短声刺激均可诱发出双侧咬肌p11肌源性电位。结论强短声可以诱发健康人体双侧咬肌p11肌源性电位，该肌源性电位可能源于前庭，特别是球囊斑，三叉神经运动系统受到前庭刺激的影响。第二部分在清醒豚鼠上记录的强短声诱发的咬肌肌源性电位目的建立强短声诱发的咬肌肌源性电位的豚鼠模型，并确定该电位的起源。方法20只豚鼠随机分成3组，正常组5只，阿米卡星处理组：5只豚鼠以450 mg／kg剂量每天肌注阿米卡星1次，持续注射18 d，以选择性药物破坏耳蜗，庆大霉素处理组：10只豚鼠左侧圆窗区滴注庆大霉素0.05 ml(40mg／ml)以选择性破坏左侧前庭。3组动物运用冷热实验、听性脑干反应(ABR)测试进行电生理检测，对正常组豚鼠和选择性内耳破坏造模成功的豚鼠进行强短声诱发的咬肌肌源性电位测试。完成测试后，为进一步证实动物药物选择性破坏内耳的效果，每组动物选取2只处死进行内耳的扫描电镜观察。结果正常组豚鼠，120、110、100和90 dB单耳声刺激，单侧记录到的豚鼠咬肌肌源性电位的反应率分别为100％、90％、70％和0％。120，110和100 dB声刺激诱发的肌源性电位的正负波的潜伏期分别为6.73±0.59 ms和8.84±0.56 ms、6.80±0.43 ms和8.92±0.48 ms，以及6.94±0.49 ms和9.00±0.51 ms。平均峰间幅度分别为6.23±2.37μV、6.12±2.24μV和6.36±3.13μV，刺激强度对豚鼠的咬肌肌源性电位的平均潜伏期或峰间幅度无显著影响。10只采用庆大霉素单侧处理的豚鼠，损伤侧的冷热反应均缺失，其中3只豚鼠处理侧ABR阈值增高，其余7只ABR阈值正常，这7只豚鼠损伤同侧声刺激诱发的咬肌肌源性电位缺失。阿米卡星处理组5只豚鼠冷热实验均正常，双侧ABR阈值显著增加，但短声诱发的咬肌肌源性电位均存在。扫描电镜检查显示阿米卡星处理组豚鼠的耳蜗明显损害，而前庭未有明显损害，庆大霉素听泡内给药组豚鼠耳蜗无明显损害，仅第一转有少量散在外毛细胞缺失，而前庭出现严重的损害。结论豚鼠强短声诱发的咬肌肌源性电位来源于前庭而非耳蜗。第三部分强短声诱发的咬肌肌源性电位的解剖基础—支配豚鼠咬肌的前庭-三叉通路的HRP逆行追踪研究目的以前的研究报告支配咬肌的三叉神经运动神经元的活动受前庭输入的调制。本研究为这些生理学上的观察提供解剖基础。方法21只豚鼠，随机分成3组，每组7只，实验组采用跨突触的逆行追踪剂HRP，注射进豚鼠左侧咬肌浅层下1／3的多个区域，咬肌神经切除组豚鼠在HRP注射前进行左侧咬肌神经切除，对照组豚鼠用生理盐水代替HRP进行咬肌注射，，所有动物在72小时存活期后处死，采用组织化学染色方法观察HRP阳性标记细胞在脑干的分布。结果在72小时的存活期后，许多跨突触标记的神经元出现在双侧前庭内侧核(MVN)、舌下前置核(PH)以及同侧三叉神经运动核(Mo5)。而咬肌神经切除组、对照组豚鼠的双侧前庭内侧核(MVN)、舌下前置核(PH)以及三叉神经运动核(Mo5)均未见阳性标记的神经元。结论MVN和PH中的神经元双侧投射至支配豚鼠咬肌浅层下1／3的运动神经元群。MVN，PH似乎在产生前庭—三叉反应中起主要的整合作用。
[Abstract]:Although sound is not a natural vestibular stimulus, researchers have found that high intensity sound acts on the vestibule. Animal and human experiments have shown that the vestibular plaque is the most sensitive part of the vestibular system to sound. Colebatch was the first to record myogenic potentials evoked by short and strong sounds on the tensely contracting sternocleidomastoid muscle, which depend on the integrity of the vestibular afferent nerve and are therefore called vestibular evoked myogenic potentials (Vestibular-ev). Oked myogenic potentials, VEMP, has become an important tool for clinical evaluation of balloon and infravestibular nerve function, and has been widely used in the diagnosis of vestibular neuritis, Meniere's disease, acoustic neuroma, superior canal fissure syndrome, bilateral vestibular disease, multiple cerebral sclerosis and other diseases. The contraction of the clavicle-mastoid muscle tension is intolerable in some elderly patients with weaker cervical muscles and in patients with cervical spondylosis. As a result, new methods for recording VEMP on other muscles, such as trapezius and cervical extensor muscles, have been used as recording areas. Recently, similar VEMP findings have been obtained from the sternocleidomastoid muscle. It was found that vestibular electrical stimulation could induce short latency, short duration masseter reflex (masseter myogenic potential), and its short latency characteristics determined that the brainstem pathway did not exceed three synapses (vestibular receptor-vestibular nucleus-trigeminal motor nucleus-neuromuscular junction). There are three parts in this study, which are: whether the potential originates from the vestibule, whether the potential has its anatomical basis, whether there is a vestibular trigeminal motor nerve pathway that innervates the masseter muscle.
Part one: short latency evoked short latency masseter myogenic potentials in healthy subjects
Objective To observe the short latency masseter myogenic potential (SMP) evoked by strong and short tones in healthy volunteers and determine its origin.Methods 21 healthy volunteers were given unilateral or bilateral strong and short tone stimulation (0.1 ms, 5 Hz, 70-100 dB nHL) to record the masseter myogenic potential on the surface of stable contraction of bilateral masseters. The effects of 100 dB nHL on masseteric myogenic potentials were compared with the stimulation thresholds of myogenic potentials evoked by strong and short tones on masseteric muscle and sternocleidomastoid muscle (SCM). Short latency masseteric myogenic potentials evoked by strong and short tones were also detected in 1 conductive deafness patient and 2 severe sensorineural deafness patients for preliminary purpose. Results Bilateral short latency masseter myogenic potentials were induced by unilateral short-tone stimulation in healthy subjects. According to the latency, threshold and waveform could be divided into three modes: p16/n21 at low threshold (70-80 dB nHL), p11/n15 or p11/n21 at high intensity (90-100 dB nHL). Asymmetric modulation of head tilt at 30 degrees left and right. The threshold of masseter P11 wave is the same as that of short-tone evoked p13/n23 wave on SCM. The myogenic potential of the masseter muscle P11 in healthy volunteers can be induced by strong and short tones. The myogenic potential may originate from the vestibule, especially the balloon plaque. The trigeminal motor system is affected by vestibular stimulation.
The second part is the intense short tone evoked masseter myogenic potentials recorded on conscious guinea pigs.
Methods Twenty guinea pigs were randomly divided into three groups: normal group (5), amikacin treatment group (5). Five guinea pigs were injected with amikacin once a day at a dose of 450 mg/kg for 18 days to destroy the cochlea by selective drugs. Gentamicin treatment group (1): Gentamicin 0.05 ml (40 mg/ml) was injected into the left circular window area of 0 guinea pigs to selectively destroy the left vestibule. Results In normal guinea pigs, 120, 110, 100 and 90 dB monoaural stimulation, the response rates of unilateral recorded masseter muscle-derived potentials were 100%, 90%, 70% and 0%, respectively. The latencies of the positive and negative waves of the myogenic potentials were 6.73 (+ 0.59 ms) and 8.84 (+ 0.56 ms), 6.80 (+ 0.43 ms) and 8.92 (+ 0.48 ms), and 6.94 (+ 0.49 ms) and 9.00 (+ 0.51 ms, respectively. The mean inter-peak amplitudes of the myogenic potentials were 6.23 (+ 2.37 mV), 6.12 (+ 2.24 mV) and 6.36 (+ 3.13 mV), respectively. Ten guinea pigs unilaterally treated with gentamicin showed no significant difference in amplitude. The ABR threshold of 3 guinea pigs was higher than that of 7 other guinea pigs. The masseter muscle-derived potentials of 7 guinea pigs were deleted after ipsilateral acoustic stimulation. Scanning electron microscopy showed that the cochlea of guinea pigs in amikacin treatment group was damaged obviously, but the vestibule was not damaged obviously. The cochlea of guinea pigs in gentamicin intravesicular administration group was not damaged obviously, only a small amount of scattered outer hair cells were missing in the first turn, but the vestibule was serious. Conclusion the guinea pig's strong short tone evoked myogenic potential originates from the vestibule rather than the cochlea.
Part 3 Anatomical basis of masseteric myogenic potentials induced by strong and short sound: retrograde tracing study of vestibular-trigeminal pathway innervating masseteric muscles in guinea pigs
Objective Previous studies have reported that the activity of trigeminal motor neurons innervating the masseter muscle is modulated by vestibular inputs.This study provides anatomical basis for these physiological observations.Methods Twenty-one guinea pigs were randomly divided into three groups, seven in each group. In multiple regions, the masseteric nerve was excised before HRP injection in the masseteric nerve resection group, and the masseteric nerve was injected with normal saline instead of HRP in the control group. All the animals were sacrificed after 72 hours of survival. The distribution of HRP positive labeled cells in the brain stem was observed by histochemical staining. Multisensynaptic labeled neurons were found in bilateral medial vestibular nucleus (MVN), sublingual preposition nucleus (PH) and ipsilateral trigeminal motor nucleus (Mo5). No positive labeled neurons were found in masseter nerve resection group, bilateral medial vestibular nucleus (MVN), sublingual preposition nucleus (PH) and trigeminal motor nucleus (Mo5) in control group. Neurons projected bilaterally to the motor neurons innervating one-third of the superficial layers of the masseter muscle in guinea pigs. MVN and PH seem to play a major role in the integration of vestibular-trigeminal responses.
【学位授予单位】：中国人民解放军军医进修学院
【学位级别】：博士
【学位授予年份】：2007
【分类号】：R764;R322

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