阿米三嗪-萝巴新对缺血性卒中恢复期患者的疗效

目的　评估阿米三嗪 萝巴新对缺血性卒中后功能恢复的疗效。方法　采用多中心、随机、双盲、安慰剂对照研究。缺血性卒中后 1个月患者 ,随机服用阿米三嗪 萝巴新或安慰剂每日 2片 ,共服 3个月。每个月随诊 1次 ,以巴氏指数 (BI) ,神经功能缺损量表 (NFDS)和长谷川痴呆量表(HDS)作为疗效评估指标。结果　 74例最终完成了 3个月随访 ,其中药物组 38例 ,安慰剂组 36例。巴氏指数在治疗后 1、2、3个月药物组均优于安慰剂组 (P <0 0 5 ) ;神经功能缺损量表分在治疗第 1个月药物组 (6 7± 4 7)优于安慰剂组 (9 6± 6 8,P =0 0 34<0 0 5 ) ,第 2、3个月两组无显著性差异 ;长谷川痴呆量表分在治疗 1、2、3个月均无显著性差异。阿米三嗪 萝巴新的不良反应发生率为 7 9% ,安慰剂组为 2 7% ,主要表现为头晕、失眠 ,并不影响患者继续治疗。结论　阿米三嗪 萝巴新在一定程度上加快缺血性卒中后患者神经功能恢复 ,不良反应少     

都可喜治疗发作性眩晕66例疗效观察

发作性眩晕是以眩晕、平衡障碍、眼震 ,严重时伴恶心、呕吐 ,可伴或不伴有耳鸣 ,听力障碍为主要临床表现的一组综合征〔1〕;是神经内科和五官科临床上的一种常见病 ,其主要病因为耳蜗前庭功能紊乱所致〔2〕。比较传统的治疗方法有应用前庭功能抑制剂、血管扩张药及对症支持治疗等〔3〕;但疗效并不肯定。我院门诊自 2 0 0 1 0 3～ 2 0 0 3 0 3期间用都可喜口服治疗发作性眩晕 6 6例 ,并随机选择同期常规治疗者 33例 ,进行对照分析 ,现将其结果报告如下。1　对象与方法1 1　对象　 (1)门诊病例 ,年龄 >18岁 ;(2 )主诉眩晕、伴或不伴有耳鸣、听…     

阿米三嗪-萝巴新治疗轻度血管性痴呆的疗效和安全性

目的评价阿米三嗪．萝巴新治疗轻度血管性痴呆（VD）的疗效和安全性。方法采用多中心、开放、自身对照试验研究方法，对128例临床诊断为轻度可能的VD患者，给予口服阿米三嗪-萝巴新，每日2片，早晚各1片。分别于服药前及服药后6周和12周，采用简易精神状态（MMSE）量表、AD评估量表-认知部分、Mattis痴呆评价（CDR）量表、日常生活能力（ADL）量表等神经心理分析工具对轻度VD患者的记忆力、注意力、定向力、语言能力、执行能力及生活能力进行评价，并观察有无恶心、头晕等副作用，进行安全性评估。结果经过3个月阿米三嗪-萝巴新治疗，轻度VD患者的MMSE评分（治疗前16．98，治疗后17．97，P〈0．05），CDR评分（治疗前1．43，治疗后1．21，P〈0．01），ADAS总分（治疗前35．12，治疗后33．08，P〈0．05）以及ADAS因子分中的记忆力和定向力评分、语言能力评分、实践能力评分和ADL评分（治疗前45．55，治疗后43．41，P〈0．01）均有明显改善。阿米三嗪-萝巴新的安全性和依从性良好，在研究期间，3例患者出现皮疹，1例患者因药物作用不明显退出研究，不良事件发生率为2．3％。结论阿米三嗪-萝巴新可以改善轻度VD的认知功能，提高患者的生活能力，且药物的安全性好。     

阿米三嗪-萝巴新对慢性间断性缺氧大鼠学习记忆能力的改善及相关生化机制的探讨

目的　探讨阿米三嗪 萝巴新 (almitrine raubasine)对慢性间断性缺氧 (chronicepisodichypoxia ,EHYP)大鼠学习记忆能力和脑内胆碱乙酰转移酶 (cholineacetyltransferase ,ChAT)活性的影响 ,为寻找改善阻塞性睡眠呼吸暂停 (OSAS)患者学习记忆障碍的方法提供实验依据。方法　建立EHYP大鼠模型 (EHYP组 ,9只 ) ,并给予阿米三嗪 萝巴新 (0 0 3片 / 2 5 0 g体重 ,每天 2次 )干预(治疗组 ,9只 ) ,并设不行缺氧处理大鼠为对照组 (7只 )。用被动避暗回避反射试验评价大鼠学习记忆能力 ,潜伏期 (STL)越长 ,学习记忆能力越强 ;用放射化学法测定大鼠皮层、海马和纹状体ChAT活性。结果　与对照组相比 ,EHYP组大鼠STL明显短于对照组和治疗组 (P <0 0 1) ,各脑区ChAT活性明显低于对照组和治疗组 (均P <0 0 1)。结论　阿米三嗪 萝巴新可改善EHYP大鼠学习记忆能力并提高其脑内ChAT活性。     

服用都可喜的注意事项

都可喜为一种薄膜包衣片,每片含阿米三嗪（almitrine）30 mg,萝巴新（raubasine）10mg.该药的主要功效是能够增加动脉血氧含量,故临床主要用于治疗因缺氧所导致的各种症状.都可喜增加动脉血氧分压（PaO2）、改善脑缺氧的作用主要是由其活性成分阿米三嗪所致,作用强度和持续时间则由萝巴新所决定.都可喜可以改善老年期认知功能障碍和慢性感觉神经损害所引起的相关症状;血管性听觉损害、眩晕和耳鸣的辅助治疗;以及治疗大脑功能不全所致的智能损害如失忆或注意力减退.都可喜是神经科较为常用的药物,经过多年临床验证,疗效确切,已得到广泛认可.     

血管舒缩功能变化在急性脑梗死发病中的作用及阿米三嗪-萝巴新的干预

急性脑梗死中无疑存在血管功能异常,直接的证据可以从脑梗死的概念中得到。我们选取血管内皮细胞分泌的具有代表性的两种影响血管舒缩功能的细胞因子,观察它们在急性脑梗死中的变化及其相互关系,并给予阿米三嗪 萝巴新干预,以探讨血管舒缩功能变化在脑梗死病因中的作用并寻找相应对策。资料和方法1.研究对象与分组:研究对象分为脑梗死常规治疗组、脑梗死常规加阿米三嗪 萝巴新治疗组、脑梗死高危组和健康对照组。脑梗死组为急性脑梗死住院患者,共收集到10 8例,均为3日内发病的住院患者,平均年龄(6 0 0±6 8)岁,男性6 2例,女性4 6例,利用随…     

前庭神经元炎（附1例报告）

前庭神经元炎 (ｖｅｓｔｉｂｕｌａｒｎｅｕｒｏｎｉｔｉｓ)的病变部位虽有不少研究 ,但影像学检查方面尚未见有价值发现。本院收治 1例头颅ＭＲＩ显示脑干前庭神经核受累患者 ,现报告如下。临床资料患者　女 ,30岁 ,住院号 2 4 5 172 ,因眩晕、呕吐 2ｄ于 2 0 0 1年 10月 2 5日入院。患者 2周前曾患上呼吸道感染 ,入院前日凌晨突然眩晕 ,视物旋转 ,不能起床 ,伴恶心呕吐 ,左侧头胀痛 ,无耳鸣耳聋 ,无发热。主要体征 :眼震Ⅲ°,快相向右 ,呈水平旋转性 ,指鼻试验 (+ ) ,闭目难立征 (+ ) ,向左倾倒。主要辅助检查 :眼震电图自发性眼震Ⅲ°。…     

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。     

复位无效且磁共振成像阴性的位置性眩晕临床特点初探

目的对手法复位无效且MRI阴性的位置性眩晕患者的眼震类型和特点进行分析,并探讨药物治疗及预防方案。方法选择2016年6月至2017年9月共43例位置性眼震患者,随机(随机数字表法)接受氯硝西泮和盐酸氟桂利嗪治疗,通过比较治疗前后最大慢相角速度评价急性期药物疗效;另选择其中21例近2个月发作频繁患者,分为盐酸氟桂利嗪预防治疗组和对照组,随访并记录每月眩晕平均发作天数(单次发作时间×发作次数),分析盐酸氟桂利嗪对眼震发作的预防作用。结果 43例患者中有29例符合确定的和很可能的前庭性偏头痛,其眼震类型分别为水平背地性(23例,53.49%)、水平向地性(3例,6.98%)、垂直下跳性(4例,9.30%)和混合性(13例,30.23%),眼震持续时间长并缺乏渐强渐弱特点。治疗3 d后,氯硝西泮组患者最大慢相角速度[2.40(0.00,17.15)°/s]显著降低,急性期疗效优于氟桂利嗪组[18.85(1.58,35.75)°/s;Z=-2.284,P=0.022)];2个月后预防治疗组患者每月眩晕平均发作天数[1(0,2)d]缩短,与对照组[3.50(1.50,6.50)d]相比差异具有统计学意义(Z=-2.096,P=0.036)。结论手法复位无效且MRI阴性的位置性眩晕可能与中枢功能异常有关,排除相关禁忌证后,急性期予以氯硝西泮治疗具有缓解眩晕和眼震作用,尤以前庭性偏头痛患者疗效更佳;频繁发作者可预防性应用盐酸氟桂利嗪。     

初发梅尼埃病一例

患者男性,26岁.主因突发性左耳听力减退伴发作性眩晕、耳鸣8天,于2018年9月7日入院.患者8天前无明显诱因出现左耳听力下降,伴眩晕、呕吐3小时并持续性左侧耳闷、耳鸣.发作当日于当地医院就诊,纯音电测听检查提示左耳低频听力下降,频率为125 Hz、250 Hz、500 Hz、1 kHz、2 kHz、4 kHz和8 k...     

Migräne und Vestibularapparat

Thirty patients with simple or ophthalmic migraine had an otoneurological examination. 13% complained of vertigo during attacks of migraine, 17% of giddiness and 6.7% of tinnitus. The usual tests for equilibrium were normal. On electronystagmographical examination 17% of the patients showed only pathological spontaneous nystagmus, 33% only disturbances of caloric response and 7% a combination of both. Audiological testing was normal. The incidence of vestibular disturbances, particularly sensitivity differences of the labyrinths, was significantly greater in the group of patients with migraine than in a control group of 30 healthy persons (P less than or equal to 0.025). On the average, the sensitivity differences, in terms of duration of reactive nystagmus, were greater for these than for the healthy persons (P less than or equal to 0.01). Patients with vestibular disturbances did not show a greater frequency of pathological EEG readings than patients with normal vestibular function. Some hypotheses concerning the pathogenesis of vestibular symptoms as found in migrainous patients are mentioned.     

Final diagnosis of patients with clinically suspected vestibular neuritis showing normal caloric response

Vestibular neuritis is one of the most common peripheral causes of acute vestibular syndrome, of which the diagnosis is generally based on a comprehensive interpretation of clinical and laboratory findings following reasonable exclusion of other disorders. This study aimed to investigate the final diagnosis of patients admitted to hospital under the clinical impression of vestibular neuritis who showed no unilateral caloric paresis.Forty-five patients who visited the emergency department with isolated acute spontaneous vertigo were included. Among them, six patients (13%) developed definitive spontaneous vertigo lasting longer than 20 min again after discharge from hospital, accompanied by hearing loss, which was audiometrically documented, leading to a final diagnosis of definite Ménière’s disease. Nine patients (20%) revisited our clinic with recurrent episodic vertigo without any documented hearing loss or auditory symptoms such as hearing loss, tinnitus or ear fullness, which led to a final diagnosis of possible Ménière’s disease. In four patients (9%), initial spontaneous vertigo and nystagmus changed to positional vertigo and nystagmus on the second hospital day. In 26 patients (58%), neither another episode of vertigo nor auditory symptoms developed during follow-up period (7–92 months), a condition to which the authors gave an arbitrary diagnosis of “mild unilateral vestibular deficit”. In conclusion, patients admitted to hospital under clinical impression of vestibular neuritis may have various final diagnoses, and “mild unilateral vestibular deficit” was the most common final diagnosis among patients who did not meet the diagnostic criteria of vestibular neuritis.     

Mastication-induced vertigo and nystagmus

Even though trigeminovestibular connections are well established in animals, mastication-induced dizziness has been described only as a vascular steal phenomenon in humans. We determined induction or modulation of nystagmus in two index patients with mastication-induced vertigo, 12 normal controls, and 52 additional patients with peripheral (n = 38, 26 with vestibular neuritis/labyrinthitis and 12 with Meniere’s disease) or central (n = 14, 11 with Wallenberg syndrome, two with cerebellar infarction, and one with pontine infarction) vestibulopathy during their acute or compensated phase. Both index patients developed mastication-induced vertigo after near complete resolution of the spontaneous vertigo from presumed acute unilateral peripheral vestibulopathy. The nystagmus and vertigo gradually built up during mastication and dissipated slowly after cessation of mastication. Brain MRI and cerebral angiography were normal in these patients. Mastication did not induce nystagmus in normal controls. However, mastication induced nystagmus in five (24 %) of the 21 patients without spontaneous nystagmus (SN) but with a previous history of a vestibular syndrome, and either increased (21/31, 68 %) or decreased (7/31, 23 %) the SN in almost all the patients (28/31, 90 %) with SN. Mastication may induce significant vertigo and nystagmus in patients with a prior history of acute vestibulopathy. The induction or modulation of nystagmus by mastication in both peripheral and central vestibulopathies supports trigeminal modulation of the vestibular system in human. The gradual build-up and dissipation suggest a role of the velocity storage mechanism in the generation of mastication-induced vertigo and nystagmus.     

Deafness associated with vertebrobasilar insufficiency.

The incidence of auditory disturbances in vertebrobasilar insufficiency (VBI) is considered much rarer than vestibular disturbances, but no routine audiometric test results for VBI patients have been published. To determine the incidence of deafness associated with VBI and the sites predominantly involved in deafness, we studied 70 vertiginous patients with VBI using a routine audiological examination and magnetic resonance imaging (MRI). MRI detected a lacunar infarct involving the cochlear nuclei in one patient, but lacunae did not involve central auditory structures in the other patients. Twenty-five patients experienced tinnitus, deafness, or both, during vertigo episodes. Audiological examinations confirmed the development of unilateral deafness in 15 (21%) patients, involving the cochlea in 14 and cochlear nuclei in one. These findings indicate that hearing loss occurs in approximately one-fifth of VBI patients, much less frequently than vestibular disturbances, and that deafness associated with VBI mainly involves the cochlea.     

Simple method of differential diagnosis of peripheral and central vertigo--development of diagnostic method and studies of 178 cases]

In patients who complain of vertigo or who have equilibrium disorders, it is often difficult to determine the etiology of the disorder, that is to determine whether it is dependent on a peripheral or central vestibular disorder. To attempt to determine the etiology in these cases, we divised a new method, the caloric eye tracking pattern test (CETP-Test). Seventeen normal subjects and 161 patients were tested. The latter group included 33 with peripheral disorders such as Meniere's disease, benign paroxysmal positional nystagmus, and others, and 128 with central disorders such as vertebral basilar artery insufficiency, cervical vertigo, and others, were tested. The cases of central disorders were limited to those patients whose eye tracking pattern before the caloric stimulation was normal. In normal subjects and in patients with peripheral disorders, it is well known that caloric nystagmus has little influence on the eye tracking pattern. In contrast, in patients with central vestibular disorders, caloric nystagmus evokes abnormalities on the eye tracking pattern, either superimposed or saccades, despite the fact that the eye tracking pattern before the caloric stimulation is normal. First we administer the eye tracking stimulation test using a target which moves horizontally at 0.3 cycle per second. Next, we perform the caloric test on the right ear, using 20 c.c. of ice water for 10 seconds. During the evoked caloric nystagmus we administer the eye tracking test once again. The eye tracking pattern is recorded for 20 seconds beginning 50 seconds after the start of the ice water injection. The procedure repeated on the left ear. The results on each case are presented as three patterns of ENG-recording. We may stat that in normal subjects and in patients with peripheral vestibular disorders, visual suppression of caloric nystagmus remains functional. Caloric induced nystagmus does not affect the CETP. In patients with central vestibular disorders, visual suppression of caloric nystagmus does not function properly because of defects in the visual suppression mechanism. Therefore, caloric nystagmus greatly influences the CETP. Consequently, the CETP may not be smooth when CETP test is administered to patients with central vestibular disorders. We may say also that the visual suppression to the vestibular nystagmus is evoked more strongly by pursuing a moving visual stimulus than by gazing a stational target. These results allow for a differential diagnosis between peripheral and central disorders.     

Inferior vestibular neuritis

Vestibular neuritis (VN) mostly involves the superior portion of the vestibular nerve and labyrinth. This study aimed to describe the clinical features of VN involving the inferior vestibular labyrinth and its afferents only. Of the 703 patients with a diagnosis of VN or labyrinthitis at Seoul National University Bundang Hospital from 2004 to 2010, we retrospectively recruited 9 patients (6 women, age range 15-75) with a diagnosis of isolated inferior VN. Diagnosis of isolated inferior VN was based on torsional downbeating spontaneous nystagmus, abnormal head-impulse test (HIT) for the posterior semicircular canal (PC), and abnormal cervical vestibular-evoked myogenic potentials (VEMP) in the presence of normally functioning horizontal and anterior semicircular canals, as determined by normal HIT and bithermal caloric tests. All patients presented with acute vertigo with nausea, vomiting, and imbalance. Three patients also had tinnitus and hearing loss in the involved side. The rotation axis of torsional downbeating spontaneous nystagmus was best aligned with that of the involved PC. HIT was also positive only for the involved PC. Cervical VEMP was abnormal in seven patients, and ocular VEMP was normal in all four patients tested. Ocular torsion and subjective visual vertical tests were mostly within the normal range. Since isolated inferior VN lacks the typical findings of much more prevalent superior VN, it may be mistaken for a central vestibular disorder. Recognition of this rare disorder may help avoid unnecessary workups in patients with acute vestibulopathy.     

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.     

Differential diagnosis of tinnitus and vertigo. A review

Tinnitus and vertigo, two common neurological complaints, often challenge the physician's ability with respect to possible etiology. Objective tinnitus can result from an abnormally patent eustachian tube, from tetanic contractions of the muscles of the soft palate, or from vascular abnormalities within the head or neck. Subjective tinnitus refers to lesions involving the external ear canal, tympanic membrane, ossicles, cochlea, auditory nerve, brainstem, and cortex. As many as 50% of patients with tinnitus do not exhibit associated hearing loss; in these patients, the cause of the tinnitus is rarely identified. An illusion of movement is specific for vestibular system disease--a peripheral or central location depending upon associated audiologic and neurologic symptoms, respectively. However, a presyncopal, light-headed sensation is most commonly associated with diffuse cerebral ischemia: in the young patient, this may be caused by a hyperventilation syndrome; in the aged individual, this can result from diffuse atherosclerotic cerebrovascular disease and decreased cardiac output. Postural and gait imbalance associated with acute vertigo indicates a unilateral peripheral vestibular or a central vestibular lesion; if vertigo is absent, either a cerebellar, proprioceptive, or bilateral peripheral vestibular lesion is likely. Transient oscillopsia suggests unilateral peripheral vestibular lesions. Permanent oscillopsia indicates a bilateral peripheral vestibular lesion or--in the absence of severe vertigo--brainstem or cerebellar damage.     

Diagnosis and treatment of the most frequent vestibular syndromes

The aims of this study were to identify the most common vestibular syndromes in a dizziness unit, and to observe their clinical aspects and response to treatment. Five hundred and fifteen patients were studied retrospectively in two institutions. Aspects of anamnesis, physical examination and the response to treatment were evaluated. The most frequent syndromes were: benign paroxysmal positioning vertigo (VPPB) (28.5%), phobic postural vertigo (11.5%), central vertigo (10.1%), vestibular neuritis (9.7%), Meniere disease (8.5%), and migraine (6.4%). A good response to treatment was observed in most patients with migraine (78.8%), VPPB (64%), vestibular neuritis (62%), Meniere disease (54.5%) and vestibular paroxismia (54.5%). On the other hand, patients with downbeat nystagmus and bilateral vestibulopathy had poor response (52.6% and 42.8%, respectively). The diagnosis of these most frequent vestibular syndromes were established through anamnesis and physical examination (with specific clinical tests for evaluation of the vestibular function). The correct diagnosis and adequate treatment are important since these syndromes may have a good prognosis.