前庭学

20050680前庭代偿过程中前庭传出性和传入性神经系统的相互作用/迟放鲁…//中华耳鼻咽喉科杂志·2005,40(2)·111~114目的:通过前庭代偿的动物模型,了解在前庭病变的情况下,前庭传出性和传入性神经系统的相互作用。方法:动物模型:A组(16只)为正常大鼠。B组(15只)左侧前庭损毁术后7d。C组(7只)术后3个月。D组(7只)前庭代偿后。检测两侧头长肌静息状态的肌电图。检测传出性前庭神经系统降钙素基因相关肽免疫组化。检测传出性前庭神经系统胆硷乙酰转移酶(AchT)免疫组化。检测传入性前庭神经系统Na K ATP酶活性。结果:损伤同侧肌群肌电活动…     

外周前庭器官操作后传出性前庭神经系统降钙素基因 …

目的 探讨外周前庭器官损伤后不同时间病理状态下传出性状庭神经系统降钙素基因相关肽（ｃａｌｃｉｔｏｎｉｎ ｇｅｎｅ－ｒｅｌａｔｅｄ ｐｅｐｔｉｄｅ,ＣＧＲＰ）的变化。方法 制作ｗｉｓｔａｒ大鼠单侧外周前庭损伤模型２９只,对照健康动物１６只,取动物脑干切片,用ＡＢＣ法作传出前庭神经系统ＣＧＲＰ免疫组化反应。结果 健康动物传出性前庭神经系统ＣＧＲＰ呈弱阳性反应,单侧前庭损伤后双侧传出性前庭神经系统ＣＧＲ     

外周前庭器官损伤后传出性前庭神经系统降钙素基因相关肽的变化

目的探讨外周前庭器官损伤后不同时间病理状态下传出性前庭神经系统降钙素基因相关肽（ｃａｌｃｉｔｏｎｉｎｇｅｎｅｒｅｌａｔｅｄｐｅｐｔｉｄｅ,ＣＧＲＰ）的变化。方法制作ｗｉｓｔａｒ大鼠单侧外周前庭损伤模型２９只,对照健康动物１６只,取动物脑干切片,用ＡＢＣ法作传出性前庭神经系统ＣＧＲＰ免疫组化反应。结果健康动物传出性前庭神经系统ＣＧＲＰ呈弱阳性反应,单侧前庭损伤后双侧传出性前庭神经系统ＣＧＲＰ反应呈强阳性反应,其阳性反应程度在损伤后１０～１２ｄ达高峰,以后随前庭功能恢复而逐渐减弱,但５个月时阳性反应程度仍高于健康动物。结论传出性前庭神经系统ＣＧＲＰ在外周前庭器官损伤后可能起一定的调节性作用。     

大鼠传出前庭神经元与传入前庭神经核的神经联系

目的阐明传出前庭神经元与传入前庭神经核的神经联系。方法将辣根过氧化物酶注射到大鼠面神经膝内侧传出前庭神经元区，经过48h的逆行轴突运输后用组织化学的方法在脑干中显示被标记的神经元。结果在双侧前庭神经内侧核及外侧核中均发现辣根过氧化物酶阳性标记细胞，以注射示踪剂同侧前庭神经内侧核数量最多。结论传出前庭神经元与前庭神经核间存在神经联系，本试验的结果提示前庭神经系统中可能存在前庭传入-传出反馈调节机制。     

大鼠传出前庭神经元与传入前庭神经核的神经联系

目的 阐明传出前庭神经元与传入前庭神经核的神经联系。方法 将辣根过氧化物酶注射到大鼠面神经膝内侧传出前庭神经元区,经过48 h的逆行轴突运输后用组织化学的方法在脑干中显示被标记的神经元。结果 在双侧前庭神经内侧核及外侧核中均发现辣根过氧化物酶阳性标记细胞,以注射示踪剂同侧前庭神经内侧核数量最多。结论 传出前庭神经元与前庭神经核间存在神经联系,本试验的结果提示前庭神经系统中可能存在前庭传人-传出反馈调节机制。     

胆碱能传出性前庭神经元的分布

目的：观察胆碱能传出性前庭神经元的分布。方法：采用辣根过氧化酶逆行追踪和免疫组化技术观察大鼠碱乙酰转移酶的表达,了解传出性前庭神经元的分布。结果：大鼠胆碱乙酰转移酶阳性传出性前庭神经元分布在面神经膝内侧Ｅ群,背外侧Ｅ九吸脑桥尾侧网状核,以内侧Ｅ群为主。结论：乙酰胆碱分布于各群传出性前庭神经元,并作为神经递质而具有重要的功能。     

前庭损伤后脑干相关神经元C-FOS的表达

目的观察大鼠内耳前庭损伤后，在静止和角加速度刺激状态下双侧前庭神经核C—FOS阳性表达的改变，初步探讨前庭代偿机制。方法将60只SD大鼠分为5组（12只，组）：（1）无手术组；（2）单耳前庭神经切断手术组；（3）单耳前庭神经切断手术对照组；（4）双耳前庭神经切断手术组；（5）双耳前庭神经切断手术对照组，每组一半动物给予角加速度刺激。用免疫组化ABC法观察C—FOS在前庭神经核、舌下神经前置核的神经元表达的改变。结果在静止状态下，正常鼠和手术对照组鼠的双侧前庭神经核、舌下神经前置核无C—FOS阳性神经元；给予旋转刺激后，双侧前庭神经核、舌下神经前置核皆有C—FOS阳性神经元。单耳手术组术后24小时．同侧前庭神经内核、对侧舌下神经前置核有C—FOS阳性神经元，旋转刺激后双侧前庭神经核、舌下神经前置核皆有C—FOS阳性神经元。双耳手术组24小时，在静止状态和角加速度刺激状态下，双侧前庭神经核、舌下神经前置核皆无C—FOS阳性神经元。结论一侧前庭损伤后，同侧前庭神经内核、对侧舌下神经前置核C—FOS阳性神经元在前庭代偿早期可能起启动突触联系的作用。     

眼肌和颈肌前庭诱发肌源性电位在外周性前庭传导通路疾病诊断中的应用

目的:观察外周性前庭损害患者眼肌前庭诱发肌源性电位(oVEMP)和颈肌前庭诱发肌源性电位(cVEMP)的引出情况并探讨其临床诊断价值。方法:选择2011-03-2012-03期间在我院临床诊断为外周前庭损害,并接受门诊和(或)住院治疗的患者13例(14耳),进行双耳气导短纯音诱发的oVEMP和cVEMP检测,观察两种电位的引出情况,分析前庭上成分(椭圆/前庭上神经传入通路)和前庭下成分(球囊/前庭下神经传入通路)机能受损的状况。结果:13例(14耳,双侧1例)外周性眩晕患者包括:耳带状疱疹3例(3耳),听神经瘤3例(4耳),Ⅶ+Ⅷ颅神经牵拉伤1例(1耳),前庭神经炎2例(2耳),梅尼埃病3例(3耳),单侧内听道发育不全1例(1耳)。总体oVEMP正常引出2耳(正常引出率为14.3%),cVEMP正常引出3耳(正常引出率21.4%)。结论:外周性眩晕患者前庭耳石器及其传导通路机能受损的情况可以通过临床oVEMP和cVEMP检测进行客观评价,其表现形式根据病变波及的范围与程度不同各异。     

声刺激诱发麻醉豚鼠前庭咬肌反射及起源的研究

目的 建立声诱发前庭咬肌反射的动物模型,探讨咬肌反射电位的特征及起源.方法 20只豚鼠,随机分为正常对照组(10只)、单侧前庭下神经切断组(5只)、单侧耳蜗神经破坏组(5只).3组动物分别在麻醉下于豚鼠下颌骨及颅顶之间用金属夹夹住,使咬肌保持一定的张力,记录click声诱发的咬肌反射电位,并进行听性脑干反应(ABR)测试.结果正常对照组豚鼠声诱发咬肌反射电位的负波(negative peak,NP)阈值为92±7.68dB nHL.给予100、90、80、70 dB nHL单侧声刺激时,同侧记录咬肌反射NP引出率分别为100%、7O%、40%、0%.给予100、90、80 dB nHL单侧声刺激时,同侧记录咬肌反射NP平均潜伏期分别为6.57±0.26、6.64±0.23、6.69±0.19 ms,不同刺激强度下NP潜伏期差异无统计学意义(P>0.05).ABR的平均反应阈为31±7.88 dBnHL.单侧前庭下神经切断组术侧声诱发咬肌反射消失,ABR反应阈在正常范围内.单侧耳蜗神经破坏组术侧声诱发咬肌反射存在,NP阈值及潜伏期与正常对照组差异无统计学意义(P>0.05),ABR消失.结论 在豚鼠下颌骨及颅顶之间应用金属夹使咬肌保持一定的张力,同时给予click声刺激,可以建立一个理想的声刺激诱发前庭咬肌反射的动物模型;声刺激诱发的豚鼠咬肌反射电位NP来源于前庭,且该反射是肌源性的.     

前庭性偏头痛患者的前庭功能分析北大核心CSCD

目的探讨前庭性偏头痛(vestibular migraine,VM)患者的前庭功能特点。方法对43例确诊为VM的患者(VM组)及30例健康志愿者(对照组)分别进行纯音测听、声导抗、冷热水试验(caloric test)、眼肌前庭诱发肌源性电位(ocular vestibular evoked myogenic potential,oVEMP)、颈肌前庭诱发肌源性电位(cervical vestibular evoked myogenic potential,cVEMP)和视频头脉冲试验(video head impulse test,vHIT),比较分析两组结果。结果VM组患者中纯音测听、冷热水试验、oVEMP及vHIT中的水平增益、代偿性扫视异常例数分别为10例(23.3%)、14例(32.6%)、18例(41.9%)、14例(32.6%)、13例(30.2%),显著高于对照组[分别为0例(0%)、3例(10.0%)、5例(16.7%)、1例(3.3%)、0例(0%)](P<0.05),而声导抗、cVEMP及vHIT中的水平不对称性比异常例数分别为3例(7.0%)、10例(23.3%)、3例(7.0%),与对照组[分别为0例(0%)、7例(23.3%)、2例(6.7%)]差异无统计学意义(P>0.05)。43例VM患者中,oVEMP振幅比(amplitude ratio,AR)及耳间不对称比(interaural asymmetric ratio,IAR)的异常率最高,分别为41.9%及34.9%。结论 VM患者存在一定程度的前庭功能损害,纯音测听、冷热水试验、oVEMP及vHIT中的水平增益、代偿性扫视结果有助于VM患者的诊断及与其他前庭性疾病的鉴别。     

Calcitonin gene-related peptide changes in efferent vestibular system during vestibular compensation]

OBJECTIVE: To investigate the calcitonin gene-related peptide (CGRP) effect on efferent vestibular system during pathological state of vestibular afferent system. METHODS: An animal model of vestibular compensation was made by administration of streptomycin to rat vestibular organ to destroy unilateral vestibular function. Change of CGRP in efferent vestibular neurons in all processes from vestibular disorder to vestibular compensation was observed utilizing ABC method of immunohistochemical technique. RESULTS: Efferent vestibular neurons of normal animals showed low immunoreactivity to CGRP. The number of CGRP immunoreactivity neurons and level of CGRP immunoreactivity increased in efferent vestibular system during vestibular disorder, and these changes decreased with vestibular compensation. CONCLUSION: Activity of CGRP in efferent vestibular system plays a regular role on accelerating vestibular compensation.     

Calcitonin gene-related Peptide and choline acetyltransferase colocalization in the human vestibular periphery

Within the vestibular system, calcitonin gene-related peptide (CGRP) has been localized in the efferent terminals and their brainstem neuronal cell bodies in several animal models. Presently, very few studies have verified these findings in the vestibular system in adult primates or humans. CGRP immunoreactivity (CGRPi) and its colocalization with choline acetyltransferase immunoreactivity (ChATi) in human vestibular end organs and Scarpa's ganglion were studied using polyclonal antibodies against CGRP and ChAT, at the light-microscopic level. The CGRPi axons ramified to produce numerous CGRPi terminals throughout the neurosensory epithelium of the maculae and cristae, primarily in the basal and midbasal areas. Numerous CGRPi efferent terminals made contact with both type II vestibular hair cells and the afferent chalices surrounding type I vestibular hair cells. All CGRP immunoreactive fibers also exhibited ChATi. As in the animal models, no CGRPi was found within Scarpa's ganglion. This study provides evidence for CGRPi in the human vestibular periphery and validates the biomedical relevance of the current animal models.     

前庭神经切断术后的前庭代偿观察

目的观察前庭神经切断术后的前庭代偿过程。方法对1998-2005年10例前庭神经切断术后患者．观察自发性眼震和平衡失调的持续时间，并对4例术前、后眼震电图进行对比观察。结果患者术后均出现快相向健侧的水平性眼震，持续4～7天消失，平衡失调恢复时间为一月至一年不等，年龄越大持续时间越长。4例进行眼震电图检查的患者，3例前庭功能均丧失，1例热水试验出现反向眼震。结论前庭代偿是前庭神经切断术后患者康复的必然过程，前庭康复训练可缩短前庭代偿的时间。     

Effects of pre-flocculectomy on Fos expression and NMDA receptor-mediated neural circuits in the central vestibular system after unilateral labyrinthectomy

In this study in order to elucidate the role of the flocculus in the whole process of vestibular compensation from the very early stage to the chronic stage, we first examined unilateral labyrinthectomy (UL)-induced spontaneous nystagmus (SN), a behavioral marker of vestibular compensation, and Fos expression, a marker of neural activity, in the vestibular brainstem in pre-unilateral flocculectomized (pre-UF) rats. UL in pre-UF rats caused more severe vestibulo-ocular deficits at the very early stage than it did in floccular-intact rats. Fos expression occurred in the medial vestibular nucleus contralateral to the UL side (contra-MVe) and the prepositus hypoglossal nucleus ipsilateral to the UL side (ipsi-PrH), whereas Fos expression was never seen after UL in floccular-intact rats. Therefore, these findings suggest the UL in pre-UF rats activates the contra-MVe and ipsi-PrH neurons and causes great imbalance between intervestibular nuclear activities, inducing more severe vestibular symptoms at the very early stage than those in floccular-intact rats. Next, we observed MK801 (a specific antagonist on the NMDA receptor)-induced SN in pre-UF rats at the chronic stage after UL. MK801 administration to pre-UL rats caused reappearance of SN even 14 days after UL, while administration to floccular-intact rats at a post-UL interval of 14 days never induced decompensation. Therefore, these findings suggest that the flocculus takes part in NMDA receptor-mediated neural circuits involved in vestibular compensation and modifies the neural interactions at the chronic stage after UL. Taken together, those results suggest that the flocculus plays important roles in the restoration of a balance between intervestibular nuclear activities, to reduce vestibular symptoms during the very early stage, and thereafter in the modification of NMDA receptor-mediated neural interactions in the central vestibular system at the chronic stage.     

CGRP expression in the vestibular periphery after transient blockage of bilateral vestibular input

This study aimed to establish an animal model of reversible bilateral vestibular disorders that is suitable for examining the mechanisms of vestibular plasticity, and to observe the changes in the plasticity of vestibular efferent systems. Tetrodotoxin (TTX) was infused continuously for 7 days into the bilateral perilymph of guinea pig cochlea. We assessed the vestibulo-ocular reflex (VOR) for evaluating the vestibular function. We also investigated the changes in calcitonin gene-related peptide (CGRP) immunoreactivity in vestibular end organs to observe the changes in the plasticity of vestibular systems. The VOR was completely eliminated by TTX administration and returned to the preoperative levels within 120 h after TTX discontinuation. An obvious increase in the number of CGRP-immunoreactive fibers was observed within the neurosensory epithelia of the maculae and cristae. An animal model of reversible bilateral vestibular disorders was established and used for investigating the plasticity of the vestibular nervous system.     

Electronystagmographic characteristics of peripheral vestibular asymmetries in compensation development stage II

Spontaneous and reflex nystagmus of 10 patients with peripheral lesions of the vestibular system at one of the stages of vestibular dysfunction compensation development were examined. Spontaneous nystagmus (recovery) toward the sound side and asymmetry of reflex nystagmus in the form of DP toward the affected side were revealed. The period of disease characterized by the development of spontaneous and reflex nystagmus is termed compensation development stage II. This stage develops when central and peripheral compensation of vestibular dysfunction is realized simultaneously. Analysis of compensation development stage II helps to identify the compensation lesion level, side and degree of lesion of peripheral vestibular structures.     

Early rehabilitation for unilateral peripheral vestibular disorders: a prospective, randomized investigation using computerized posturography

Patients with unilateral vestibular lesions have a set of deficits requiring compensation based on the inherent plasticity of the central nervous system. In the 1940s, it was reported that patients with unilateral vestibular dysfunctions who exercised recovered faster than those who did not. The present prospective, randomized investigation aimed to assess the role of a computerized posturography-assisted early vestibular rehabilitation protocol combined with a home-based exercise program in the treatment of patients with unilateral peripheral vestibular disorders occurring 2 weeks previously. Fifteen patients were randomly assigned to a 5-week posturography-assisted vestibular rehabilitation protocol and a home-based exercise program (Group A), while 15 simply awaited spontaneous compensation (Group B). All patients underwent computerized posturography approximately 2 weeks after their vestibular disorder was diagnosed and again after 6 weeks. Ten healthy volunteers were also studied (Group C). After rehabilitation, Group A patients improved significantly in most sensory measures [modified clinical test of sensory organization and balance (mCTSIB)] and motor parameters [limits of stability (LOS)] by comparison with preliminary outcomes, and there were no significant differences in sensory (mCTSIB) and motor (LOS) findings between Group A and the healthy volunteers. At the same time point, several motor (LOS) parameters were still altered in Group B by comparison with the healthy volunteers. These preliminary outcomes support the hypothesis that the compensation achievable after 6 weeks with a customized program of posturography-assisted vestibular rehabilitation and home-based exercises is superior to the results of physiological spontaneous compensation.