強(qiáng)短聲誘發(fā)的咬肌肌源性電位的起源及其解剖基礎(chǔ)的初步研究
發(fā)布時(shí)間：2018-09-07 07:04
【摘要】： 盡管聲音不是前庭自然的生理刺激，但研究者發(fā)現(xiàn)高強(qiáng)度聲對前庭有作用，動物及人體實(shí)驗(yàn)表明，球囊斑是前庭系統(tǒng)中對聲最敏感的部分。已知前庭系統(tǒng)在許多腦干和姿態(tài)運(yùn)動系統(tǒng)的運(yùn)動控制中起重要作用，其輸入通過調(diào)制眼肌和頸肌以及軀干和四肢伸肌的活動，為頭-眼協(xié)調(diào)活動和頭-頸系統(tǒng)提供反饋信息。Colebatch最早記錄到強(qiáng)短聲在緊張性收縮的胸鎖乳突肌上誘發(fā)的肌源性電位，該電位依賴于前庭傳入神經(jīng)的完整性，因此被稱為前庭誘發(fā)的肌源性電位(Vestibular-evoked myogenic potentials，VEMP)，目前VEMP已成為臨床評估球囊和前庭下神經(jīng)功能的重要工具，并在前庭神經(jīng)炎、梅尼埃病、聽神經(jīng)瘤、上半規(guī)管裂綜合征、雙側(cè)前庭病、多發(fā)性腦硬化等疾病的診斷中得到廣泛應(yīng)用。由于VEMP的檢測需要保持較大的胸鎖乳突肌緊張性收縮，一些頸肌肌力較弱的老年人和頸椎病患者不能耐受，無法完成檢測，因此，人們開始尋找在其他肌肉上記錄VEMP的新方法，例如斜方肌和頸伸肌都曾被用作記錄區(qū)，都獲得了與胸鎖乳突肌記錄相似的VEMP發(fā)現(xiàn)。近來Deriu等發(fā)現(xiàn)前庭電刺激會誘發(fā)短潛伏期的、短持續(xù)時(shí)間的咬肌反射(咬肌肌源性電位)，其短潛伏期的特性決定其腦干神經(jīng)通路不超過3個(gè)突觸(前庭感受器—前庭核—三叉神經(jīng)運(yùn)動核—神經(jīng)肌肉接頭)。但不知道強(qiáng)短聲刺激是否會在咬肌上誘發(fā)相似的肌源性電位，該電位是否來源于前庭，該電位的存在是否具有其解剖基礎(chǔ)——是否存在支配咬肌的前庭三叉運(yùn)動神經(jīng)通路，這些問題就是本課題要解決的目標(biāo)，因此本研究分以下三部分實(shí)驗(yàn)： 第一部分健康人強(qiáng)短聲誘發(fā)的短潛伏期咬肌肌源性電位 目的觀察健康人強(qiáng)短聲誘發(fā)的短潛伏期咬肌肌源性電位，并初步確定其起源。方法21名健康志愿者，給予單側(cè)或雙側(cè)強(qiáng)短聲刺激(0.1 ms、5Hz、70～100 dB nHL)，在穩(wěn)定收縮的雙側(cè)咬肌表面，記錄咬肌肌源性電位，觀察頭左右傾斜30°對雙側(cè)強(qiáng)短聲(100 dB nHL)誘發(fā)的咬肌肌源性電位的影響，并對強(qiáng)短聲在咬肌和在胸鎖乳突肌(SCM)上誘發(fā)的肌源性電位的刺激閾值進(jìn)行比較。1名傳導(dǎo)性耳聾患者及2名單側(cè)重度感音性耳聾患者也進(jìn)行強(qiáng)短聲誘發(fā)的短潛伏期咬肌肌源性電位檢測，以初步確定該電位的起源。結(jié)果健康人單側(cè)短聲刺激可誘發(fā)雙側(cè)短潛伏期的咬肌肌源性電位，根據(jù)其潛伏期、閾值和波形可有三種反應(yīng)模式：在較低閾值(70-80 dB nHL)時(shí)為p16／n21，在高強(qiáng)度(90-100 dB nHL)刺激時(shí)表現(xiàn)為p11／n15或p11／n21波。p11幅度受頭左右30°傾斜的不對稱性調(diào)制。咬肌p11波的閾值和短聲在SCM上誘發(fā)的p13／n23波的閾值相同。傳導(dǎo)性耳聾患者強(qiáng)短聲刺激患耳不能誘發(fā)出咬肌p11電位，而重度感音性耳聾患者單側(cè)或雙側(cè)強(qiáng)短聲刺激均可誘發(fā)出雙側(cè)咬肌p11肌源性電位。結(jié)論強(qiáng)短聲可以誘發(fā)健康人體雙側(cè)咬肌p11肌源性電位，該肌源性電位可能源于前庭，特別是球囊斑，三叉神經(jīng)運(yùn)動系統(tǒng)受到前庭刺激的影響。 第二部分在清醒豚鼠上記錄的強(qiáng)短聲誘發(fā)的咬肌肌源性電位 目的建立強(qiáng)短聲誘發(fā)的咬肌肌源性電位的豚鼠模型，并確定該電位的起源。方法20只豚鼠隨機(jī)分成3組，正常組5只，阿米卡星處理組：5只豚鼠以450 mg／kg劑量每天肌注阿米卡星1次，持續(xù)注射18 d，以選擇性藥物破壞耳蝸，慶大霉素處理組：10只豚鼠左側(cè)圓窗區(qū)滴注慶大霉素0.05 ml(40mg／ml)以選擇性破壞左側(cè)前庭。3組動物運(yùn)用冷熱實(shí)驗(yàn)、聽性腦干反應(yīng)(ABR)測試進(jìn)行電生理檢測，對正常組豚鼠和選擇性內(nèi)耳破壞造模成功的豚鼠進(jìn)行強(qiáng)短聲誘發(fā)的咬肌肌源性電位測試。完成測試后，為進(jìn)一步證實(shí)動物藥物選擇性破壞內(nèi)耳的效果，每組動物選取2只處死進(jìn)行內(nèi)耳的掃描電鏡觀察。結(jié)果正常組豚鼠，120、110、100和90 dB單耳聲刺激，單側(cè)記錄到的豚鼠咬肌肌源性電位的反應(yīng)率分別為100％、90％、70％和0％。120，110和100 dB聲刺激誘發(fā)的肌源性電位的正負(fù)波的潛伏期分別為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。平均峰間幅度分別為6.23±2.37μV、6.12±2.24μV和6.36±3.13μV，刺激強(qiáng)度對豚鼠的咬肌肌源性電位的平均潛伏期或峰間幅度無顯著影響。10只采用慶大霉素單側(cè)處理的豚鼠，損傷側(cè)的冷熱反應(yīng)均缺失，其中3只豚鼠處理側(cè)ABR閾值增高，其余7只ABR閾值正常，這7只豚鼠損傷同側(cè)聲刺激誘發(fā)的咬肌肌源性電位缺失。阿米卡星處理組5只豚鼠冷熱實(shí)驗(yàn)均正常，雙側(cè)ABR閾值顯著增加，但短聲誘發(fā)的咬肌肌源性電位均存在。掃描電鏡檢查顯示阿米卡星處理組豚鼠的耳蝸明顯損害，而前庭未有明顯損害，慶大霉素聽泡內(nèi)給藥組豚鼠耳蝸無明顯損害，僅第一轉(zhuǎn)有少量散在外毛細(xì)胞缺失，而前庭出現(xiàn)嚴(yán)重的損害。結(jié)論豚鼠強(qiáng)短聲誘發(fā)的咬肌肌源性電位來源于前庭而非耳蝸。 第三部分強(qiáng)短聲誘發(fā)的咬肌肌源性電位的解剖基礎(chǔ)—支配豚鼠咬肌的前庭-三叉通路的HRP逆行追蹤研究 目的以前的研究報(bào)告支配咬肌的三叉神經(jīng)運(yùn)動神經(jīng)元的活動受前庭輸入的調(diào)制。本研究為這些生理學(xué)上的觀察提供解剖基礎(chǔ)。方法21只豚鼠，隨機(jī)分成3組，每組7只，實(shí)驗(yàn)組采用跨突觸的逆行追蹤劑HRP，注射進(jìn)豚鼠左側(cè)咬肌淺層下1／3的多個(gè)區(qū)域，咬肌神經(jīng)切除組豚鼠在HRP注射前進(jìn)行左側(cè)咬肌神經(jīng)切除，對照組豚鼠用生理鹽水代替HRP進(jìn)行咬肌注射，，所有動物在72小時(shí)存活期后處死，采用組織化學(xué)染色方法觀察HRP陽性標(biāo)記細(xì)胞在腦干的分布。結(jié)果在72小時(shí)的存活期后，許多跨突觸標(biāo)記的神經(jīng)元出現(xiàn)在雙側(cè)前庭內(nèi)側(cè)核(MVN)、舌下前置核(PH)以及同側(cè)三叉神經(jīng)運(yùn)動核(Mo5)。而咬肌神經(jīng)切除組、對照組豚鼠的雙側(cè)前庭內(nèi)側(cè)核(MVN)、舌下前置核(PH)以及三叉神經(jīng)運(yùn)動核(Mo5)均未見陽性標(biāo)記的神經(jīng)元。結(jié)論MVN和PH中的神經(jīng)元雙側(cè)投射至支配豚鼠咬肌淺層下1／3的運(yùn)動神經(jīng)元群。MVN，PH似乎在產(chǎn)生前庭—三叉反應(yīng)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.
【學(xué)位授予單位】：中國人民解放軍軍醫(yī)進(jìn)修學(xué)院
【學(xué)位級別】：博士
【學(xué)位授予年份】：2007
【分類號】：R764;R322
本文編號：2227547
[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.
【學(xué)位授予單位】：中國人民解放軍軍醫(yī)進(jìn)修學(xué)院
【學(xué)位級別】：博士
【學(xué)位授予年份】：2007
【分類號】：R764;R322
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