锁孔入路颅神经血管减压术诊治前庭阵发症的临床观察

目的　探讨局部麻醉下锁孔入路颅神经血管减压术对前庭阵发症的诊断价值及疗效评估。方法　40例三叉神经痛、面肌痉挛及舌咽神经痛患者中,8例合并前庭阵发症患者采用局麻下经乙状窦后锁孔入路探查听神经根血管压迫情况,并进行神经血管减压治疗。运用症状卡,评价术后眩晕情况,随访期为36～61个月。结果　术中8例前庭 阵发症患者前庭神经根部均可见责任血管压迫,7例患者可诱发血管压迫性眩晕,术后眩晕均消失;1例患者未诱发出血管压迫性眩晕,术后眩晕无明显改善。平均随访57个月,8例前庭阵发症患者中,7例前庭阵发症患者无血管压迫性眩晕复发,眩晕有效控制率为87.5%。结论　局麻下听神经根血管减压术是治疗前庭阵发症、控制血管压迫性眩晕的有效治疗方法,同时该方法对明确诊断前庭阵发症也具有一定的临床意义。     

前庭性偏头痛与几种常见周围性眩晕的鉴别诊断

前庭性偏头痛（VM）是一种伴有前庭症状的偏头痛,有报道该病占耳鼻咽喉科眩晕门诊16%,被列为所谓“难治性眩晕”的重要病因之一,也是近年来眩晕方面的研究“热点”之一。VM的发病机制目前尚不明确,其临床表现多样,不仅某些表现与耳源性眩晕类似,而且甚至共存于同一患者。加之随着临床前庭功能检查和评估方法的迅速发展,能够对半规管、耳石器以及前庭神经功能进行初步评估。介绍了VM发病机制以及与梅尼埃病、前庭神经炎、良性阵发性位置性眩晕、前庭阵发症等临床常见的耳源性眩晕的鉴别诊断。     

急性前庭病

急性前庭病的特点是：急性或亚急性出现眩晕或平衡障碍，可以由于前庭外周各部或中枢前庭结构的功能低下或各种原因的刺激引起。本文着重于对前庭急性外周病变，如BPPV、前庭神经元炎、上半规管裂隙综合征及前庭阵发症；前庭中枢急性病变如前庭性偏头痛及一些新近认识的文献进行综述。     

外周性眩晕的手术治疗

外周性眩晕疾病如迷路瘘管、梅尼埃病及迟发性膜迷路积水、上半规管裂综合征、良性阵发性位置性眩晕、前庭阵发症等保守治疗效果欠佳的,可行外科治疗.根据眩晕的不同类型,相应的选择不同的手术方式,随着临床实践的深入和相关理论的更新,现代眩晕外科治疗提倡在控制眩晕的基础上同时改善听力及耳鸣.当前眩晕患者中能用外科治疗的比例不高,但...     

临床常见眩晕病的诊治

眩晕症是临床常见病，因其涉及到多个学科，该病的诊断与治疗一直令许多医生感到困惑。导致这种现状主要有三个因素：1．内耳位置深，体积小以及实验方法的限制，前庭病变实质的研究发展缓慢；2．前庭疾病的检查手段是间接的，需要依靠眼动、脊髓反射反映前庭功能状态；3．病因和发病机制不明，前庭疾病治疗多限于对症^[1]。因此很多眩晕患者经常在临床的多个科室之间辗转，     

前庭系疾病研究的临床与基础研究进展

眩晕症是临床的常见病，涉及临床多学科，该症的诊断与治疗一直是令许多医生困惑。导致这种现状主要有三个因素：1、前庭器官是高度分化的器官，许多神经通路及发病机理不明，目前限于动物试验和推理阶段，病因研究不够深入；2、前庭疾病的检查手段间接，依靠第二器官眼动、脊髓反射反映前庭功能状态，不能像听力学的诊断手段那样直接；3、因病因、发病机制不清，前庭疾病治疗多限于对症。由于这些原因很多眩晕患者得不到适当的诊断与治疗。     

前庭阵发症

前庭阵发症(vestibular paroxysmia,VP)又名致残性位置性眩晕(disabling positional vertigo,DPV),是引起眩晕的疾病之一,主要表现为短暂性的眩晕发作,可能是桥小脑角池段第Ⅷ颅神经根受到血管压迫所致,致病机制类似三叉神经痛(trigeminal neuralgia,TN)[1]。VP在头晕门诊中占     

基层医院前庭康复现状及思考

前庭康复是治疗眩晕和平衡障碍的一种安全有效的方法,适用于外周性、中枢性和混合性病变引起的非进行性前庭病变及老年人平衡功能障碍.基层医院需要进行前庭康复的头晕和眩晕患者众多,但目前尚无专业前庭康复师,而侧重神经康复的康复师有广泛基础,通过编写专业教材,对其进行继续教育培训,与三甲医院形成转诊联动、借助互联网平台及虚拟现实...     

伴或不伴眩晕的突发性聋的比较

目的探讨伴或不伴眩晕突发性聋的听力学和前庭功能检查结果的不同.方法25例突发性聋按伴或不伴眩晕分为两组,同时进行听力学、前庭功能等检查,包括纯音测听、听性脑干反应(ABR)、耳蜗电图、视频眼震电图(VNG)等,比较其检查结果的不同.结果突发性聋伴眩晕者发病时即多为重度或极重度感音神经性聋,耳蜗电图多表现为-SP/AP≥0.4,提示有膜迷路积水,与VNG表现出来的单侧减弱及优势偏向相对应,且可合并有耳石症.     

前庭康复在眩晕治疗中的应用

眩晕是平衡系统 (视觉、本体感觉和前庭系统 )功能障碍所致的常见临床综合征,药物治疗和外科手术治疗是目前国内治疗眩晕的主要手段。但 2种方法都存在自身缺陷,如药物毒副作用、手术创伤及术后并发症、治疗费用昂贵等,而且有相当一部分患者无法通过药物或手术达到缓解症状的目的。在这种背景下,基于前庭代偿机制的前庭康复治疗(vestibularrehabilitationtherapy,VRT),因其无创、廉价和肯定的疗效应运而生,并逐渐成为治疗眩晕的第三大主要治疗手段。我们回顾了国内外文献,对VRT在眩晕治疗中的应用做简要综述。VRT的概念及生理学理论…     

MRI of the vestibular nerve after selective vestibular neurectomy

CONCLUSION: In patients with Ménière's disease and persisting vertigo attacks after vestibular neurectomy (VNx) MRI of the vestibulocochlear nerve can identify residual vestibular nerve fibres that could be responsible for the vertigo attacks. OBJECTIVE: To test if MRI of the vestibulocochlear nerve can corroborate the presence of residual vestibular nerve fibres in patients with persisting vertigo attacks and residual vestibular function after VNx. MATERIALS AND METHODS: Vestibulocochlear nerve bundles of seven post-VNx unilateral Ménière's patients were imaged using 1.5 Tesla MRI with steady state free precession (SSFP) sequences. Reformatted MR images orthogonal to the vestibulocochlear nerve axis in internal auditory canal were compared on the VNx and intact sides. Vestibular function was assessed with caloric tests, three-dimensional head impulse tests and vestibular evoked myogenic potentials. Of the seven patients only one was asymptomatic (totally free of vertigo); six had continued to experience vertigo attacks, albeit not as long or as severe as before VNx. RESULTS: On the VNx side, MRI showed intact facial and cochlear nerves in all seven patients. In the six symptomatic patients, although superior and inferior vestibular nerve bulk and signal were reduced, residual bulk suggestive of inferior vestibular nerve was evident, correlating with evidence of residual posterior canal function on impulsive testing in all six symptomatic patients. In the asymptomatic patient, superior and inferior vestibular nerves were absent on MRI and impulsive testing revealed no residual posterior canal function.     

MRI of the vestibular nerve after selective vestibular neurectomy

Conclusion. In patients with Ménière's disease and persisting vertigo attacks after vestibular neurectomy (VNx) MRI of the vestibulocochlear nerve can identify residual vestibular nerve fibres that could be responsible for the vertigo attacks. Objective. To test if MRI of the vestibulocochlear nerve can corroborate the presence of residual vestibular nerve fibres in patients with persisting vertigo attacks and residual vestibular function after VNx. Materials and methods. Vestibulocochlear nerve bundles of seven post-VNx unilateral Ménière's patients were imaged using 1.5 Tesla MRI with steady state free precession (SSFP) sequences. Reformatted MR images orthogonal to the vestibulocochlear nerve axis in internal auditory canal were compared on the VNx and intact sides. Vestibular function was assessed with caloric tests, three-dimensional head impulse tests and vestibular evoked myogenic potentials. Of the seven patients only one was asymptomatic (totally free of vertigo); six had continued to experience vertigo attacks, albeit not as long or as severe as before VNx. Results. On the VNx side, MRI showed intact facial and cochlear nerves in all seven patients. In the six symptomatic patients, although superior and inferior vestibular nerve bulk and signal were reduced, residual bulk suggestive of inferior vestibular nerve was evident, correlating with evidence of residual posterior canal function on impulsive testing in all six symptomatic patients. In the asymptomatic patient, superior and inferior vestibular nerves were absent on MRI and impulsive testing revealed no residual posterior canal function.     

Does vestibular damage cause cognitive dysfunction in humans?

For more than a decade, evidence from animal studies has suggested that damage to the vestibular system leads to deficits in spatial navigation which are indicative of impaired spatial learning and memory. More recently, direct evidence has emerged to demonstrate that humans with vestibular disorders exhibit a range of cognitive deficits that are not just spatial in nature, but also include non-spatial functions such as object recognition memory. Vestibular dysfunction has been shown to adversely affect attentional processes and increased attentional demands can worsen the postural sway associated with vestibular disorders. Recent MRI studies also show that humans with bilateral vestibular damage undergo atrophy of the hippocampus which correlates with their degree of impairment on spatial memory tasks. These results are consistent with those from animal studies and, together, suggest that humans with vestibular disorders are likely to experience cognitive dysfunction which is not necessarily related to any particular episode of vertigo or dizziness, and therefore may occur even in patients who are otherwise well compensated. These findings may be related to the observation that patients with vestibular deficits experience a high incidence of depression and anxiety disorders.     

Vertebrobasilar ischaemia presenting as recurrent isolated vertigo

Chronic recurrent isolated vertigo is an uncommon manifestation of vertebrobasilar ischaemia. We report a 43-year-old female with 12-month history of recurrent attacks of isolated vertigo who presented with acute pontine infarctions. Clinical examination and vestibular function testing showed bilateral vestibular hypofunction affecting the horizontal and posterior semicircular canals and right saccule. Diffusion-weighted magnetic resonance imaging (MRI) demonstrated acute bilateral pontine infarcts and significant vertebrobasilar stenoses. The findings of recurrent isolated vertigo and bilateral vestibular hypofunction should not prevent a search for vertebrobasilar ischaemia, particularly in the presence of vascular risk factors.     

Vestibular neuritis: etiopathogenesis

Vestibular neuritis presents as sudden unilateral vertigo in the absence of hearing loss or neurologic involvement and is thought to be due to neurotropic viruses. Its morbidity is unknown and it affects both sexes equally, with the highest incidence at 40-50 years of age. The etiology of this condition has been ascribed to viral, bacterial and protozoan infections, as well as allergic and auto-immune causes. Inflammation of the vestibular nerve is followed by demyelination and loss of function, which is not always reversible. Higher plasma fibrinogen and CRP levels in the acute phase, longer BERA latency and I-III interval and increased gadolinium uptake in the vestibular nerve and Scarpa's ganglion on enhanced MRI confirm the inflammatory nature of the process. An animal model of vestibular neuritis using retroauricular inoculation of herpes simplex virus in mice, histologic findings in the temporal bone of individuals who had vestibular neuritis, and influenza A virus infection in cultured Schwann's cells suggest viral infection as the main aetiologic cause.     

Changes in endolymphatic hydrops after vestibular neurectomy observed in magnetic resonance imaging – A pilot study

ObjectivesThe aim was to evaluate endolymphatic hydrops in patients with Ménière's disease before and after vestibular neurectomy to verify if the endolymphatic space dilatation, observed in magnetic resonance imaging, regressed within several months after surgery.MethodsMagnetic resonance imaging was performed after intravenous gadolinium injection in four patients with unilateral definite Ménière's disease before and eight months after vestibular neurectomy. Clinical symptoms, audiovestibular tests, and endolymphatic hydrops in magnetic resonance imaging were evaluated.ResultsEndolymphatic hydrops was visualized in preoperative magnetic resonance imaging in three out of four analyzed patients. In the remaining one, an asymmetrical contrast enhancement in the affected ear was found. After the vestibular neurectomy, all four patients presented a complete resolution of vertigo episodes and improved functional level. Significant postoperative hearing deterioration was found in two patients. In the follow-up magnetic resonance imaging, no reduction of the endolymphatic hydrops was visualized. A reduction of asymmetrical contrast enhancement in one patient was found.ConclusionsMagnetic resonance imaging of the inner ear is a helpful diagnostic tool for Menière's disease. Vestibular neurectomy is an effective treatment for intractable vertigo; however, there is no endolymphatic hydrops regression evidence within several months after the surgery. Therefore, further studies with a long follow-up period and repeated magnetic resonance imaging are needed to assess the vestibular neurectomy's impact on endolymphatic hydrops. Nevertheless, magnetic resonance imaging supports the clinical diagnosis of Ménière's disease and may help understand its pathophysiology.     

Bilateral multicanal benign paroxysmal positional vertigo coexisting with a vestibular schwannoma: case report

We describe a rarely encountered case of coexisting bilateral multicanal benign paroxysmal positional vertigo (BPPV) and vestibular schwannoma in a 56-year-old woman. The patient had presented with a 10-year history of dizziness and imbalance, and her vestibular findings were perplexing. We decided on a working diagnosis of BPPV and began treatment. After several months of canalith repositioning maneuvers had failed to resolve her symptoms, we obtained magnetic resonance imaging, which revealed the presence of the vestibular schwannoma. This case serves as a reminder of the importance of differentiating between central and peripheral vestibular disorders, as well as central and anterior canal BPPV-induced down-beating nystagmus in order to establish the correct diagnosis and initiate appropriate treatment.     

Ultrastructure of the vestibular sensory organs in delayed endolymphatic hydrops

Vestibular sensory organs were examined ultrastructurally in two cases of delayed endolymphatic hydrops. The patients, two women, 27 and 16 years of age, suffered profound sensory hearing loss in childhood and experienced severe, recurrent vertigo. Specimens were obtained by a translabyrinthial vestibular nerve transection. We studied the utricular macula and the lateral and posterior cristae in one case, and the utricular macula, the anterior and posterior cristae, and the vestibular ganglion in the other. The otoconia and the otoconial membrane, the sensory epithelia, and the vestibular ganglion appeared fairly normal. Although the entire vestibular end organs were not studied in these cases, it was surprising that the ultrastructural findings did not conclusively identify vestibular end organ pathology as the cause of the vertigo attacks.