血管源性中枢急性前庭综合征及其眼震形式

急性前庭综合征（acute vestibular syndrome,AVS）是以急性持续性眩晕起病,伴有恶心、呕吐,自发眼震,步态不稳,头动不能耐受等症状的临床综合征,持续时间超过24?h,大多为数天或数周。中枢性AVS以血管源性常见,其中大多数为后循环缺血性卒中,尤其部分脑干、小脑梗死常表现为急性孤立性眩晕,这类患者的诊断极具挑战性。随着前庭及眼动生理机制研究的深入,基于前庭、眼动及姿势平衡系统等方面的床旁检查重要性也日益凸显。眩晕患者的床旁检查,除了常规的神经科及耳科查体外,基于前庭-眼反射的各类眼震的评价极有助于快速诊断、识别中枢性AVS。本文对血管源性中枢性AVS的神经血管解剖基础、脑干和小脑卒中所致AVS的眼震特点等进行了综述归纳。     

眩晕的诊断顺序和分类(附386例临床分析)

按Drachman等的眩晕诊断顺序回顾性审定386例眩晕病人的诊断顺序合理性,发现诊断顺序混乱者有71例(18％)。同时指出问诊,神经系统检查及神经眼、耳科检查是确诊的关键。认为刘道宽氏分类法比较适合神经科诊断的定位和定性。     

不同眼动特征在中枢性孤立性眩晕中的诊断价值

目前研究认为,孤立性眩晕是后循环TIA或脑梗死的常见表现形式,而且当中枢病变患者 以前庭症状发病时,初始的临床表现中,孤立性眩晕较非孤立性眩晕更为常见。长期以来,临床医师 对中枢性眩晕的诊断多基于临床体征的定位诊断,事实上,在脑干和小脑中包含诸多调控眼动的中 枢前庭结构,这些结构受损会导致相应的异常眼动模式。本文综述了中枢性孤立性眩晕的临床表现 及不同眼动特征,并对其中包含的6个中枢前庭结构（前庭神经核、舌下前核、小脑下脚、小结叶、小 脑扁桃体、绒球叶）的病变特点进行了系统介绍,旨在促进临床医师对中枢性孤立性眩晕的认识,提 高鉴别诊断的水平。     

视频眼震电图在后循环缺血性眩晕诊断中的应用

目的探讨视频眼震电图（VNG）在以眩晕为主诉的后循环缺血患者诊断中应用价值。方法运用VNG技术检查68例以眩晕为主诉的后循环缺血患者，观察视眼动系统反应、自发性眼震、冷热试验、位置性眼震，并以40例正常健康老年人为对照。结果后循环缺血性眩晕组中有自发性眼震18例（26．5％），位置性眼震31例（45，6％），显著高于对照组（P〈0.05）。视眼动系统检查共56例（82．3％）出现1项或多项异常，表现为扫视试验32例（47.1％）异常，视跟踪试验Ⅲ型改变24例、Ⅳ型改变5例共29例（42．6％）异常，均显著高于对照组（P〈0．01）。视动试验有8例（11．8％）出现视动性眼震或视动眼震减弱。温度试验单侧减弱异常28例（41．2％），优势偏向异常16例（23.5％），总慢相角速度降低7例（10.3％），均显著高于对照组（P〈0.05）。结论VNG在后循环缺血性眩晕诊断中有重要意义。     

椎基底动脉供血不足性眩晕患者ENG,BAEP与rCBF的对照研究

目的 探讨眼震电图（ＥＮＧ）,脑干听觉诱发电位（ＢＡＥＰ）,局部脑血流（ｒＣＢＦ）地椎基底动脉供血不足（ＶＢＩ）性眩晕的诊断价值,方法 对６０例ＶＢＩ眩晕患者进行ＥＮＧ,ＢＡＥＰ与ｒＣＢＦ检测,结果 本病ＥＮＧ异常率为９８．４％ＢＡＥＰ异常率５８．３％,ｒＣＢＦ异常率国６１％,结论 三项检查均为较理想的非创伤性检查,对ＶＢＩ眩晕的诊断三者相互补充,可提高早期确诊率,并有助于定位诊断。     

前庭中枢性及周围性眩晕患者视频眼震图参数特点分析

目的 探讨前庭中枢性眩晕和前庭周围性眩晕患者视频眼震图（videonystagmography,VNG）的参数特点。 方法 收集2011年3～12月首都医科大学附属北京天坛医院神经内科住院的69例后循环缺血所致前庭中枢性眩晕患者和眩晕会诊中心就诊的108例前庭周围性眩晕（梅尼埃病12例、良性阵发性位置性眩晕96例）患者的临床资料,分析并比较其VNG参数特点和临床特征。 结果 69例前庭中枢性眩晕患者和108例前庭周围性眩晕患者相比,临床特点：男性多见（P<0.001）,年龄更大（P=0.009）,病程更短（P<0.001）,更多出现视物成双（P<0.001）、偏身麻木无力（P<0.001）、言语不利（P<0.001）等症状,较少出现耳蜗症状（P=0.021）,眩晕持续时间更长（P<0.001）,发病多与体位改变无关（P<0.001）;VNG参数特点：视跟踪异常（40.6% vs 0.9%,P<0.001）、定标试验异常（13.0% vs 0.0%,P<0.001）、视动试验异常（10.1% vs 0.0%,P=0.003）、凝视试验异常（10.1% vs 0.0%,P=0.003）、自发性眼震（8.7% vs 0.0%,P=0.007）或位置性眼震（8.7% vs 0.0%,P=0.007）发生比例前庭中枢性眩晕组高于前庭周围性眩晕组;而变位试验阳性（14.5% vs 74.1%,P<0.001）前庭中枢性眩晕组低于前庭周围性眩晕组。 结论 VNG参数特点能客观地反映前庭中枢性眩晕和前庭周围性眩晕患者的眼震情况,结合临床特征有助于前庭系统性眩晕的定位诊断。     

后循环梗死患者的眼动及前庭功能评价

目的   评价眼动及前庭功能检查对后循环梗死（posterior circulation Infarction,PCI）患者的诊断价值。 方法  纳入22例PCI患者,收集其临床基线资料,包括性别、年龄、首发症状、高血压、糖尿病、吸烟、饮酒史及入院体征等相关指标。患者均行眼动检查：包括凝视试验（gaze test,GT）、扫视试验（saccade test,ST）、平滑跟踪试验（smooth pursuit test,SPT）、视动眼震检查（optokinetic nystagmus test,OPK）;前庭功能检查：包括自发眼震（spontaneous nystagmus,SN）、摇头试验（head shaking test,HST）、固视抑制检查,上述检查均应用眼震视图仪（videonystagmograph,VNG）进行记录。 结果  共纳入22例PCI患者,首发症状：15例（68.2%）为头晕/眩晕,7例（31.8%）为肢体无力麻木。眼动检查提示：异常19例（86.4%）,其中GT异常4例（18.2%）,ST异常11例（50.0%）,SPT异常15例（68.2%）,OPK异常12例（54.5%）。前庭功能检查提示：22例完成SN检查,其中SN阳性8例（36.4%）,包括小脑梗死4例,脑桥梗死3例,左侧延髓背外侧、双侧小脑半球及蚓部梗死1例;17例完成HST检查,其中HST阳性6例（35.3%）,包括小脑梗死2例,脑桥梗死2例,小脑及脑桥梗死1例,右侧小脑及延髓上段梗死1例;19例完成固视抑制检查,其中固视抑制失败8例（42.1%）,包括双侧小脑梗死1例,脑桥梗死4例,左侧延髓梗死1例,右侧小脑及延髓上段梗死1例,左侧延髓背外侧、双侧小脑半球及蚓部梗死1例。以头晕/眩晕为首发症状的患者与以肢体无力、麻木为首发症状的患者相比,眼动及固视抑制检查阳性率高（P分别为0.023和0.045）。 结论  小脑、延髓梗死的患者常以头晕/眩晕起病;眼动检查有助于筛查PCI患者;小脑梗死患者的病灶侧别常与自发、摇头眼震的水平成分一致;脑桥梗死患者HST后可诱发下跳眼震;脑桥、延髓梗死患者常固视抑制失败。     

血管源性眩晕的临床与眼震图特征

发作性眩晕是椎基底动脉缺血的常见症状。若眩晕与其它椎基动脉供血不足(VBI)的症状同时出现,或伴脑干和/或小脑梗塞症状时,诊断多无困难。当仅出现孤立性眩晕发作时,往往与累及内耳的良性疾病难以鉴别。作者分析1974至1978年间神经耳科门诊84例血管性眩晕患者的资料,着重探讨孤立性眩晕的发生机理及与梗塞的关系。84例患者均进行神经耳科检查、定量前庭功能试验及限震图检查。部分患者行CT 及MRI 检查。16例进行后循环动脉造影,7例表现为与梗塞相关的     

神经电生理检查对前庭阵发症的诊断意义

前庭阵发症(VP)是一种以短暂、频繁的发作性眩晕为主要表现,伴或不伴耳部症状的外周眩晕疾病。其发病机制尚不明确,缺乏特异性的检查方法,诊断主要依靠典型的临床表现及相关辅助检查。脑干听觉诱发电位(BAEP)是一项反映听神经传导通路上电位变化的电生理检查手段,Ⅰ～Ⅲ波峰间期延长是VP在BAEP上最常见的异常表现。前庭诱发肌源性电位(VEMPs)是反映前庭-眼肌和前庭-颈肌反射通路的电生理测试手段,可准确发现VP损害部位,对前庭系统的微变化更敏感。眼震视图(VNG)是通过红外线摄像头直接记录眼球震颤,反映视动系统和前庭系统功能状态的检查方法,VP的眼震形式多样。本综述总结了VP的BAEP、VEMPs、VNG表现特点及三者在VP诊疗中的应用,以期提高临床医生的诊疗效率和水平,避免漏诊和误诊。     

头脉冲-眼震-眼偏斜试验在急性前庭综合征中的应用价值

眩晕为神经内科和急诊科最常见的主诉之一,其中急性前庭综合征(AVS)的病因诊断对于众多医生一直是个难题。外周性和中枢性的AVS治疗预后相差大,漏诊和误诊甚至可导致严重后果。近几年文献表明头脉冲-眼震-眼偏斜试验(HINTS)在鉴别中枢性AVS中,敏感性可高达100%,特异性可达69%~96%。HINTS是一项易获得、敏感度和特异性均高的床旁检查技术,在神经科门诊和急诊科易于开展。本文将对HINTS试验的最新文献进行综述,为AVS的临床诊治提供参考。     

Bedside Evaluation of Dizzy Patients

In recent decades there has been marked progress in the imaging and laboratory evaluation of dizzy patients. However, detailed history taking and comprehensive bedside neurotological evaluation remain crucial for a diagnosis of dizziness. Bedside neurotological evaluation should include examinations for ocular alignment, spontaneous and gaze-evoked nystagmus, the vestibulo-ocular reflex, saccades, smooth pursuit, and balance. In patients with acute spontaneous vertigo, negative head impulse test, direction-changing nystagmus, and skew deviation mostly indicate central vestibular disorders. In contrast, patients with unilateral peripheral deafferentation invariably have a positive head impulse test and mixed horizontal-torsional nystagmus beating away from the lesion side. Since suppression by visual fixation is the rule in peripheral nystagmus and is frequent even in central nystagmus, removal of visual fixation using Frenzel glasses is required for the proper evaluation of central as well as peripheral nystagmus. Head-shaking, cranial vibration, hyperventilation, pressure to the external auditory canal, and loud sounds may disclose underlying vestibular dysfunction by inducing nystagmus or modulating the spontaneous nystagmus. In patients with positional vertigo, the diagnosis can be made by determining patterns of the nystagmus induced during various positional maneuvers that include straight head hanging, the Dix-Hallpike maneuver, supine head roll, and head turning and bending while sitting. Abnormal smooth pursuit and saccades, and severe imbalance also indicate central pathologies. Physicians should be familiar with bedside neurotological examinations and be aware of the clinical implications of the findings when evaluating dizzy patients.     

Ipsilateral Saccade Hypometria and Contralateral Saccadic Pursuit in a Focal Brainstem Lesion: a Rare Oculomotor Pattern

Eye movement examination may be used to rapidly differentiate peripheral and central vestibular syndromes in patients with acute unsteadiness. The analysis of oculomotor impairments may also support the accurate localization of cerebral lesions, particularly those in the brainstem, that are often loosely defined by cerebral MRIs. Saccades, smooth pursuit, and nystagmus were recorded with video-oculography in a patient who had developed sudden vertigo as a consequence of a focal lesion in the depth of the brachium pontis. The patient had shown a previously unreported pattern of eye movement impairments consisting of (i) ipsilesional hypometric saccades, (ii) contralesional saccadic smooth pursuit, and (iii) unilateral gaze-evoked nystagmus. These symptoms enabled the precise localization of the trajectory of pontocerebellar saccadic tracts in the depth of the brachium pontis. We propose that this rare association resulted from a disruption of cerebellar afferents of saccadic pathways and of cerebellar efferents of horizontal smooth pursuit pathways. This reported case emphasizes the crucial role of careful bedside oculomotor examination in order to discriminate between peripheral and central vestibular syndromes in the diagnosis of sudden vertigo. Moreover, it reveals an exceptional pattern of oculomotor impairments that may allow for the precise localization of the trajectory of cerebellar saccadic afferent pathways in the depth of the brachium pontis.     

Recent advances in central acute vestibular syndrome of a vascular cause

Acute vestibular syndrome (AVS) is characterized by acute onset of spontaneous prolonged vertigo (lasting days), spontaneous nystagmus, postural instability, and autonomic symptoms. Peripheral AVS commonly presents as vestibular neuritis, but may also include other disorders such as Meniere's disease. Vertigo in central AVS due to vertebrobasilar ischemic stroke is usually accompanied by other neurological dysfunction. However it can occur in isolation and mimicking peripheral AVS, particularly with cerebellar strokes. Recent large prospective studies have demonstrated that approximately 11% of patients with isolated cerebellar infarction presented with isolated vertigo mimicking peripheral AVS, and the bedside head impulse test is the most useful tool for differentiating central from peripheral AVS. Herein we review the keys to the diagnosis of central AVS of a vascular cause presenting with isolated vertigo or audiovestibular loss.     

Neuro-otological emergencies

PURPOSE OF THE REVIEW: Physicians find acute vertigo a diagnostic challenge. This article review recent evidence outlining the clinical presentation of acute central and peripheral dizzy syndromes and suggest when clinicians may consider acute neuro-imaging. RECENT FINDINGS: Recent evidence highlights the difficulty that acute vertigo may sometimes pose to the clinician. For example, migrainous vertigo may have oculomotor abnormalities suggestive of either central neurological or peripheral vestibular dysfunction. Furthermore, vertebrobasilar stroke syndromes may mimic peripheral disorders such as vestibular neuritis, or when there is hearing involvement may be misdiagnosed as Meniere's disease. In addition to the need for identifying serious conditions in acute vertigo, recent evidence suggests that early steroid treatment in vestibular neuritis may improve long term outcome. Further trials regarding symptomatic outcome are required, however, before routine use of steroids can be recommended in this condition. SUMMARY: Recent findings have not made the assessment of acute vertigo any easier for the nonspecialist. Although the commonest vertigo syndromes are benign, serious conditions such as stroke may masquerade as a peripheral labyrinthine disorder and conversely benign conditions such as migrainous vertigo may have clinical characteristics of central disorders. These findings re-emphasize the need for a thorough clinical evaluation of the acutely dizzy patient.     

General vestibular testing.

A dysfunction of the vestibular system is commonly characterized by a combination of phenomena involving perceptual, ocular motor, postural, and autonomic manifestations: vertigo/dizziness, nystagmus, ataxia, and nausea. These 4 manifestations correlate with different aspects of vestibular function and emanate from different sites within the central nervous system. The diagnosis of vestibular syndromes always requires interdisciplinary thinking. A detailed history allows early differentiation into 9 categories that serve as a practical guide for differential diagnosis: (1) dizziness and lightheadedness; (2) single or recurrent attacks of vertigo; (3) sustained vertigo; (4) positional/positioning vertigo; (5) oscillopsia; (6) vertigo associated with auditory dysfunction; (7) vertigo associated with brainstem or cerebellar symptoms; (8) vertigo associated with headache; and (9) dizziness or to-and-fro vertigo with postural imbalance. A careful and systematic neuro-ophthalmological and neuro-otological examination is also mandatory, especially to differentiate between central and peripheral vestibular disorders. Important signs are nystagmus, ocular tilt reaction, other central or peripheral ocular motor dysfunctions, or a unilateral or bilateral peripheral vestibular deficit. This deficit can be easily detected by the head-impulse test, the most relevant bedside test for the vestibulo-ocular reflex. Laboratory examinations are used to measure eye movements, to test semicircular canal, otolith, and spatial perceptional function and to determine postural control. It must, however, be kept in mind that all signs and ocular motor and vestibular findings have to be interpreted within the context of the patient's history and a complete neurological examination.     

Vascular vertigo syndromes

Ischemia,hemorrhages, and other vascular disorders can result in various central or peripheral vestibular syndromes with vertigo, oculomotor/balance disturbances, and nausea. The vascular vertigo syndromes listed in Table 1 can however be brought about by other causes such as demyelitizing focuses in multiple sclerosis or space-occupying lesions, so that not only localization of the damaged structure but also the various etiologies are decisive for the choice of therapy. Occasionally, combined functional disturbances of the peripheral and central vestibular system appear, such as an infarction of the inferior anterior cerebellar artery, which supplies the labyrinth and parts of the brainstem and cerebellum. In rare cases, a central lesion can have the same signs as a peripheral-vertibular disturbance: a lacunar infarct at the root entry zone of the eighth nerve can mimic a unilateral partial loss of labyrinth function as it occurs in vestibular neuritis, thus named "pseudoneuritis". Differential diagnosis between vestibular migraine, vestibular paroxysmia, transient ischemic brainstem attacks, and Meniere's disease is sometimes so difficult that only trial therapies such as prophylaxis with beta blockers, carbamazepine, thrombocyte aggregation inhibitors, antiplatelet drugs, or betahistin can clarify the issue.     

Isolated vestibular nuclear infarction: report of two cases and review of the literature

Cerebral infarction presenting with isolated vertigo remains a diagnostic challenge. To define the clinical characteristics of unilateral infarctions restricted to the vestibular nuclei, two patients with isolated unilateral vestibular nuclear infarction had bedside and laboratory evaluation of the ocular motor and vestibular function, including video-oculography, bithermal caloric irrigation, the head impulse test (HIT) using magnetic scleral coils, and cervical and ocular vestibular-evoked myogenic potentials (VEMPs). We also reviewed the literature on isolated vertigo from lesions restricted to the vestibular nuclei, and analyzed the clinical features of seven additional patients. Both patients showed spontaneous torsional-horizontal nystagmus that beat away from the lesion side, and direction-changing gaze-evoked nystagmus. Recording of HIT using a magnetic search coil system documented decreased gains of the vestibular-ocular reflex for the horizontal and posterior semicircular canals on both sides, but more for the ipsilesional canals. Bithermal caloric tests showed ipsilesional canal paresis in both patients. Cervical and ocular VEMPs showed decreased or absent responses during stimulation of the ipsilesional ear. Initial MRIs including diffusion-weighted images were normal or equivocal, but follow-up imaging disclosed a circumscribed acute infarction in the area of the vestibular nuclei. Infarctions restricted to the vestibular nuclei may present with isolated vertigo with features of both peripheral and central vestibulopathies. Central signs should be sought even in patients with spontaneous horizontal–torsional nystagmus and positive HIT. In patients with combined peripheral and central vestibulopathy, a vestibular nuclear lesion should be considered especially when hearing is preserved.     

Predictors of vertigo in the emergency department: The preved study

Background and PurposeAcute vertigo (sense of motion) can be the sole manifestation of a posterior circulation stroke, and often gets missed in the emergency department (ED). The studies for evaluation of central vertigo have focused on physical exam findings, which require expertise and may not be suitable for rapid triage by a nurse in ED or by paramedics.MethodsThis cross sectional study included retrospective chart review of patients 18 years of age and older who presented to the Adult ED with acute dizziness or vertigo during the calendar year 2017. All the patients with a diagnosis of central or peripheral vertigo were included in the final analysis. Sensitivity, specificity, Likelihood Ratio of positive result (LR (+)) and Likelihood Ratio of negative result (LR (-)) for central and peripheral vertigo were calculated for risk factors, symptoms and physical examination features. Chi-squared test and univariate logistic regression were used to evaluate statistical correlation and to calculate the prevalence odds ratio (POR).ResultsTwo hundred and forty nine out of 505 (49.3%) patients presenting with dizziness had vertigo. Of these, 14 had central vertigo and 163 had peripheral vertigo. Statistically significant variables were: constant symptoms of vertigo (p 0.000- POR 8.7, 95% confidence interval (CI) 2.3-33.1), no change in symptoms with head movement (p 0.000- POR 10.2, 95% CI 3.0-35.4), dysmetria (p 0.000- POR 56.8, 95% CI 5.8-557.1), and unsteady gait (p 0.000- POR 13.3, 95% CI 3.3-54.3). The sensitivity and specificity to detect central vertigo were 100% and 66.4% respectively if the patient had either unsteady gait, constant symptoms, or no change in symptoms with head movement, [VAIN triad (Vertigo- Ataxia, Incessant, or Non-positional)].ConclusionsWe suggest that triage with VAIN triad can be used to design prospective studies to develop a triage algorithm for the detection of central vertigo in the ED.     

Multiple sclerosis as a cause of the acute vestibular syndrome

Multiple sclerosis (MS) causes dizziness and vertigo. Reports suggest responsible lesions are often in the intra-pontine 8th nerve fascicle. We sought to determine frequency and clinical features of demyelinating acute vestibular syndrome (AVS). This is a prospective observational study (1999–2011). Consecutive AVS patients (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with a risk for central localization underwent structured bedside examination and neuroimaging. When applicable, we identified MS based on clinical, imaging, and laboratory features. Of 170 AVS presentations, 4 % (n = 7) were due to demyelinating disease. Five had an acute MS plaque likely responsible for the clinical syndrome. Lesion location varied—1 medulla; 1 inferior cerebellar peduncle; 1 middle cerebellar peduncle; 1 posterior pontine tegmentum; 1 in the intrapontine 8th nerve fascicle; 1 superior cerebellar peduncle; 1 midbrain. Only two had a lesion in or near the intra-pontine 8th nerve fascicle. Three were first presentations (i.e., clinically isolated demyelinating syndrome), while the others were known MS. All had central oculomotor signs. In two patients, the only central sign was a normal horizontal head impulse test (h-HIT) of vestibular function. All patients improved with steroid therapy. Demyelinating disease was an uncommon cause of AVS in our series. Symptomatic lesions were not restricted to the 8th nerve fascicle. Five patients had relatively obvious oculomotor signs, making differentiation from vestibular neuritis straightforward. Two patients had unidirectional, horizontal nystagmus that followed Alexander’s law and was suppressed with fixation (true pseudoneuritis). The presence of a normal h-HIT in these suggested central localization.