不同前庭刺激对人体听觉认知活动的影响

目的观察不同前庭刺激对人体听觉认知活动和脑事件相关电位(ERPs)的影响。方法33名大学生,在前庭刺激为10°/s匀速旋转150s后,分别进行0.6°/s2、0.8°/s2、1.0°/s2和1.2°/s2四种不同角加速度梯形旋转刺激,并完成听觉认知任务:对等概率出现的中文阿拉伯数字信号2～9中的奇数(靶信号,T)进行按键反应,对偶数(非靶信号,NT)不反应。记录受试者脑电图并分析ERPs。结果不同前庭刺激条件下,受试者完成听觉认知任务的反应时和正确率差异均无显著性意义。匀速旋转时,受试者N1P2和N2P3峰峰波幅相对于对照和四种角加速度作用时显著降低,靶信号P3潜伏期显著缩短。结论匀速旋转和恒角加速度前庭刺激对人体听觉认知活动效应明显不同:匀速旋转加快听觉认知活动,而恒角加速度抑制听觉认知活动。     

盐酸苯环壬酯及东莨菪碱对线加速度前庭知觉的影响

目的 观察抗运动病药物盐酸苯环壬酯和东莨菪碱对线加速度前庭知觉的影响,以判定用此类药物防治晕机病时是否影响飞行人员的空间定向知觉。方法 分别测8名受试者服用盐酸苯环壬酯、东莨菪碱和安慰剂1h后,在不同线加速度作用下的前庭知觉。结果 服用盐酸苯环壬酯和东莨菪碱的两个试验组与安慰剂对照组之间的线加速度前庭知觉无显著差别。结论 盐酸苯环壬酯和东莨菪碱对线加速度前庭知觉无明显影响。没有发现对飞行人员空间定向能力的负面影响。     

前庭核H1受体在运动病发生中的作用

目的研究H1受体在大鼠脑干前庭核的表达及其在运动病发生和信号转导过程中的作用。方法24只健康SD大鼠（200g～250g,雌雄各半）依随机数字表法随机分为4组,每组6只。A：对照组,不接受运动刺激和抗运动病药物;B：仅暴露运动刺激组;C：仅接受抗运动病药物组（H,受体阻断剂盐酸异丙嗪,0．25mg／只,腹腔注射）;D：接受运动刺激和抗运动病药物组。通过旋转摆动复合运动刺激诱使大鼠发生运动病,以出现对糖精水的厌饮症状作为运动病发病指标。测定运动刺激后及暴露其他相应实验因素后45min内各组小鼠0．15％糖精水的饮用量。通过免疫荧光染色观察大鼠脑干前庭核H。受体的分布;蛋白印迹法分析大鼠前庭核层面脑干组织H1受体蛋白的表达,并观察运动刺激和异丙嗪对H1受体表达的影响。结果各组大鼠平均糖精水饮用量有明显差异（F=346．82,P〈0．01）。运动刺激组平均糖精水饮用量明显少于对照组,差异有统计学意义（P〈0．01）。异丙嗪组平均糖精水饮用量与对照组相近（P〉O．05）。应用异丙嗪后接受运动刺激组的平均糖精水饮用量多于运动刺激组（P〈O．01）,但仍明显少于对照组及异丙嗪组（P〈0．01）。免疫荧光染色显示,大鼠脑干前庭核表达有H1受体,运动刺激可使其表达增加,但未受到异丙嗪的明显抑制。蛋白印迹法分析显示,大鼠前庭核层面脑干组织有H1受体蛋白的表达,运动刺激亦使其表达增加,异丙嗪对其表达增加不具有明显的抑制作用。结论旋转摆动复合运动刺激可有效地诱发大鼠发生运动病。大鼠脑干前庭核存在有H1受体,运动刺激可使其表达增加。异丙嗪具有一定的抗运动病作用,但对运动刺激所诱发的大鼠脑干前庭核H1受体表达增加没有明显的抑制作用。其作用机制可能是与组胺竞争性地结合H1受体而非通过影响H1受体的表达。     

异丙嗪对人的效能、自主性反应和运动病耐受性的效应

前言 为使我们更多地了解药物治疗改善运动病和航空运动病耐受性的机理及其对认知功能的影响。方法 12名年龄在30岁～40岁的男性参加了这项研究。所有受试者均参加4种实验条件,间隔期为一周无注射的训练日,25mg和50mg异丙嗪(Promethazine)肌肉注射,安慰剂注射。在每一阶段给受试者重复4次     

视觉、前庭觉及其相互作用对视觉认知的动态影响

航天飞行初期,空间运动病、空间定向障碍一直是航天医学界的重要难题,而两者的发生机制均与视觉和前庭觉有着紧密的联系。如今视觉刺激、前庭刺激对脑高级认知功能影响的研究已展开,但视-前庭联合刺激下对脑高级认知功能影响的研究,还处于探索阶段。目前认知有关的研究手段有很多,其中具有毫秒级时间分辨率的脑事件相关电位(event-related potentials,ERPs)是一种较为客观且简便易行的研究方法。本文综述了视觉、前庭觉与脑高级功能联系的解剖学基础,介绍了采用ERP为研究手段的部分视觉认知研究动态以及视-前庭相互作用对脑高级功能影响的研究现状,提出了今后的研究方向,为今后开展该方面研究提供了参考。     

偏心旋转刺激下大鼠前庭核c-fos表达的观察

目的 观察偏心旋转刺激下前庭核早期即刻基因Ｃ－ｆｏｓ的表达特征和抗运动病药物对这种表达的影响。方法 取ＳＤ大鼠１９只分为对照组,旋转组、药物组三组。庄园２组用偏心旋转刺激方式刺激６０ｍｉｎ;药物组在偏心旋转刺激前４５ｍｉｎ腹腔注射抗运动病药物盐酸扁桃桥哌酯（ＰＡＰＭ）,对照组不进行旋转刺激。用免疫组化法和图象分析技术对大鼠脑干前庭神经ｆｏｓ蛋白含量变化进行定量、定位、测定。结果 偏心旋转刺激。用免     

某些抗运动病药物对前庭受刺激时兔脑电功率谱的影响

目的：观察一些抗运动病药物对前庭受刺激时兔脑电功率谱的影响。方法：前庭刺激为持续４５分钟的正弦旋转，峰角速度６０°／ｓ，正弦周期４秒。结果与结论：旋转刺激引起生理盐水对照组动物大脑皮质抑制。哌醋甲酯可逆转这种作用，支持Ｋｏｈｌ提出的该药抗运动病的作用假说。东莨菪碱加深了前庭刺激对大脑皮质的抑制。而山莨菪碱可阻断前庭刺激对大脑皮质的抑制，且文献报道其外周副作用亦小。因此山莨菪碱用于抗运动病比东莨菪碱对机体有利。     

脑益嗪抗运动病时大鼠脑细胞钙离子超微结构定位的变化(论著)

目的：观察脑益嗪抗运动病时脑细胞钙离子（Ｃａ２＋）的变化并探讨其作用机理。方法：采用Ｃａ２＋超微结构定位方法，对ＳＤ大鼠预先给予脑益嗪后，采用正负交变加速度旋转刺激制备运动病模型。观察运动病大鼠和脑益嗪给药组大鼠大脑皮质、小脑皮质和脑干前庭区脑细胞Ｃａ２＋超微结构定位变化。结果：运动病大鼠大脑皮质、小脑皮质和脑干前庭区脑细胞质基质、线粒体和内质网中Ｃａ２＋反应产物增多。预先给予脑益嗪后，大脑皮质、小脑皮质和脑干前庭区脑细胞质Ｃａ２＋反应产物明显下降（Ｐ＜０．０１）。结论：脑益嗪抗运动病的中枢机理之一可能与抑制脑细胞Ｃａ２＋内流有关     

姜素预防犬运动病的效果观察

目的　观察姜素预防犬运动病的效果和对豚鼠视前庭相互作用的影响。　方法　采用随机双盲和安慰剂对照实验设计 ,观察 7 2mg/kg ,3 6mg/kg和 1 8mg/kg 3种剂量姜素及苯海拉明 (乘晕宁 3 2mg/kg)、盐酸苯环壬酯 (飞塞乐 0 2mg/kg)对犬运动病预防效果和对豚鼠视前庭系统的影响。犬运动病采用三角离心摆动方式 (峰速 2 4 0°/s ,频率 0 0 5Hz)诱发 ,以一定时间内犬的呕吐发生率作为犬运动病的观察指标 ;以正弦摆动 (峰速 6 0°/s,频率 0 0 5Hz)加光条刺激方式诱发豚鼠视前庭相互作用眼震 ,以眼震次数、慢相速度和增益作为视前庭相互作用观察指标。　结果　 3种剂量姜素均可显著降低犬呕吐发生率 ,且在 7 2mg/kg和 3 6mg/kg剂量时其效果较苯海拉明、盐酸苯环壬酯显著 ,各种药物对豚鼠VVOR眼震均无显著影响。　结论　姜素用于预防对抗运动病效果显著且不会影响正常的视前庭功能     

新药ST93—1抗运动病效果的试验观察

目的观察新药ＳＴ９３－１对正常人前庭－植物神经反应的影响，比较ＳＴ９３－１与东莨菪碱的抗运动病效果。方法１５名健康男性志愿者，在平行秋千摆动（摆长６ｍ，摆角４５°，频率０．２２Ｈｚ）刺激下诱发出运动病。运动病症状严重程度用Ｇｒａｙｂｉｅｌ运动病症状数字评分法评定；测定心率、皮肤温度。采用自身对照、双盲和安慰剂技术，以３－拉丁方排列顺序服药。在试验前３０ｍｉｎ分别口服ＳＴ９３－１２ｍｇ，东莨菪碱１ｍｇ和乳糖（安慰剂）。二次服药间隔７天～１０天。结果ＳＴ９３－１的保护率８０％，比东莨菪碱保护率高（７３．３％）；从秋千摆动刺激的耐受时间和运动病症状分值看，新药ＳＴ９３－１、东莨菪碱与安慰剂相比较有明显差异（Ｐ＜０．０５）。而ＳＴ９３－１的副作用比东莨菪碱少。ＳＴ９３－１对体温没有明显影响，对心率有调节作用。结论新药ＳＴ９３－１是一种副作用小、有效的抗运动病药。     

Effects of some motion sickness suppressants on static and dynamic tracking performance

Two studies examined the influence of three established antimotion sickness drugs on tracking performance in static (stationary) and dynamic (angular acceleration) conditions and on visual fixation ability during motion. In Study I, 40 young men were randomly assigned in equal numbers to either a control (lactose placebo), dimenhydrinate (50 mg), promethazine hydrochloride (25 mg), or mixture (25 mg promethazine plus 10 mg d-amphetamine) group. Study II used 30 new subjects equally divided into control, dimenhydrinate (100 mg), and promethazine (50 mg) groups. Following practice, tests were conducted prior to, and 1, 2, and 4 h after drug ingestion. The depressant drugs had little effect on static tracking, but impaired dynamic tracking performance and reduced ability to maintain visual fixation on a localizer/glide slope instrument due to increased ocular nystagmus. The mixture of promethazine plus d-amphetamine produced none of these deleterious effects.     

The effects of TTS-scopolamine, dimenhydrinate, lidocaine, and tocainide on motion sickness, vertigo, and nystagmus

The effects of TTS-scopolamine, dimenhydrinate, lidocaine, and tocainide on motion sickness and vertigo and on caloric and postrotatory nystagmus were evaluated in healthy volunteers. TTS-scopolamine was administered transdermally (delivering approximately 10 micrograms X h-1 scopolamine base) and 100 mg dimenhydrinate orally. Lidocaine and tocainide were administered intravenously (average plasma concentration of lidocaine 6 mol X L-1 and of tocainide 20 mol X L-1). TTS-scopolamine and dimenhydrinate significantly reduced vertigo induced by calorization of the ears, nausea provoked with Coriolis maneuvre, and nystagmus in caloric and rotatory tests. During treatment with lidocaine and tocainide no alleviation of vertigo and nausea was observed. Caloric nystagmus was reduced but rotation induced nystagmus was virtually unchanged. Presumably the motion sickness drugs act at the brain stem where TTS-scopolamine and dimenhydrinate have their target cells in the vestibular nuclei. Furthermore, the alleviation of motion sickness was linked to a decline of nystagmus. Lidocaine and tocainide, the action of which in vertigo and nausea in patients is proposed to be on the vestibular end organs and the supratentorial brain structures, consistently failed to alleviate motion sickness.     

Evaluation of antimotion sickness drug side effects on performance

This project has employed a computerized pursuit meter which has a high correlation with operational performance (2) to test the principal antimotion sickness drugs. Proficiency scores on the pursuit meter task were improved over placebo scores in subjects with d-amphetamine 10 mg and 5 mg, the combination of promethazine 25 mg plus scopolamine 0.4 mg with d-amphetamine 10 mg, and the combination of scopolamine 1 mg with d-amphetamine 10 mg. Scores were not significantly different from placebo scores in tests with scopolamine 0.25 mg, 0.5 mg, or 0.6 mg; marezine 50 mg; meclizine 50 mg; or dimenhydrinate 50 mg. This was also true for the combination of scopolamine 1 mg with d-amphetamine 5 mg, and that of promethazine 25 mg with d-amphetamine 10 mg. A statistically significant decrement of performance scores was seen with scopolamine 1 mg or 0.8 mg, and with promethazine 25 mg oral or 25 mg I.M. The combination of promethazine 25 mg with scopolamein 0.4 mg, and that of promethazine 25 mg oral plus 25 mg I.M. with d-amphetamine 10 mg, also gave significant decrements from placebo scores. These results indicate that selected doses and combinations of antimotion sickness drugs can be used without loss of operational proficiency.     

Motion-sickness medications for aircrew: impact on psychomotor performance

INTRODUCTION: Motion sickness remains a significant problem for aircrew both in the flying environment (airsickness) and for aircrew deployed at sea (seasickness). While some anti-motion-sickness medications provide reasonable efficacy, adverse neurocognitive effects limit their use in military personnel engaged in safety-sensitive operational roles such as flying. The purpose of this study was to assess the impact on psychomotor performance of promethazine, meclizine, and dimenhydrinate and to determine if the addition of pseudoephedrine or damphetamine to promethazine would ameliorate its adverse effects. METHODS: There were 21 subjects (11 men, 10 women), aged 22-59, who were assessed for psychomotor performance on 4 tasks as well as with sleepiness and drug side-effects questionnaires. Psychomotor testing was conducted prior to, and for 7 h after, ingestion of a single dose of each of placebo, promethazine 25 mg, meclizine 50 mg, dimenhydrinate 50 mg, promethazine 25 mg plus pseudoephedrine 60 mg, and promethazine 25 mg plus d-amphetamine 10 mg. RESULTS: Relative to placebo, promethazine, meclizine, and promethazine plus pseudoephedrine impaired performance on all four tasks [serial reaction time (SRT), logical reasoning (LRT), serial subraction (SST), and multitask (MT)]. Dimenhydrinate impaired performance on the SRT only. Promethazine plus d-amphetamine did not impair performance on any task nor did it result in increased sleepiness. The times to recovery of normal performance for SRT with promethazine, meclizine, dimenhydrinate, and promethazine plus pseudoephedrine were > 7.25, 7.25, 4.25, and 7.25 h, respectively; for LRT were > 7.25, > 7.25, ns, and 7.25 h; for SST were > 7.25, > 7.25, ns, and 7.25 h; for MT were 7.25, 7.25, ns, and 7.25 h. Recovery times to baseline sleepiness levels for promethazine, meclizine, dimenhydrinate, and promethazine plus pseudoephedrine were 7.25, > 7.25, 6.25, and > 7.25 h. CONCLUSION: Only promethazine plus d-amphetamine was free from impact on psychomotor performance and did not increase sleepiness.     

Calcium antagonists in the prevention of motion sickness

Flunarizine is a calcium antagonist which has proved clinically useful in controlling chronic vertigo. In a double blind crossover trial 10 subjects were used to compare the electronystagmic responses to motion in patients taking flunarizine, prochlorperazine maleate, or placebo. Flunarizine is shown to be a powerful peripherally acting labyrinthine suppressant, with application in the prevention of motion sickness. Flunarizine produces none of the central depressive side effects characteristic of antihistamines and anticholinergics, which are the conventional anti-motion sickness drugs.     

Control of nausea and autonomic dysfunction with terfenadine, a peripherally acting antihistamine.

Terfenadine (Seldane) was administered to 14 male subjects in a randomized, double-blinded, and crossed-over design to assess the efficacy of this peripherally active antihistamine as an anti-motion sickness drug. Terfenadine possesses practically no central side effects. A Staircase Profile Test was administered 4 h following placebo or a single oral dose of terfenadine (300 mg). The study revealed a statistically significant therapeutic effect from terfenadine (p less than 0.05). This led us to conclude that because the drug does not or only poorly crosses the blood-brain barrier, a selective peripheral antihistamine (H1) action may be sufficient in the control of motion sickness induced through cross-coupled accelerative semicircular canal stimulation using a rotating chair. This finding implies that other peripherally acting agents might be found that possess even greater anti-motion sickness efficacy. The present research raises additional questions regarding current theories on the etiology of motion sickness, its associated autonomic system dysfunction, and the validity of assumptions that effective pharmacological agents must act centrally.     

High dose ondansetron for reducing motion sickness in highly susceptible subjects

BACKGROUND: Ondansetron is currently being explored as a treatment for motion sickness due to its proven prophylactic effect on post-operative nausea, the nausea and vomiting associated with chemotherapy, and its lack of side effects. This study sought to compare the effectiveness of placebo, dimenhydrinate, and ondansetron for preventing motion sickness in highly susceptible subjects. METHODS: A total of 63 subjects with a history of frequent motion sickness and positive report of self-treatment of motion sickness with over-the-counter medications were divided into 3 groups of 20 (3 were disqualified). Depending on their group assignment, subjects were given placebo, dimenhydrinate, or ondansetron 1 h before being rotated at 20 rpm while making head movements. Symptoms of motion sickness and electrogastrogram (EGG) data were collected prior to and during rotation. RESULTS: There were no differences between the groups in number of head movements tolerated, time rotating, or symptom questionnaire scores. All groups showed a marginally significant decrease in normal 3 cycle per minute activity [F (1.45) = 3.04, p = 0.088] and a significant increase in gastric tachyarrhythmia [F (1,45) = 9.71, p = 0.003], a pattern typically associated with motion sickness development. CONCLUSION: Neither ondansetron or dimenhydrinate prevented motion sickness in groups of highly susceptible people. Continued development of new treatments is necessary.     

Investigation of the anti-motion sickness effect of 3-hydroxypyridine derivatives]

Experiments with rats showed that three out of 12 3-hydroxypyridine derivatives (ethyl-methyl hyd- roxypyrine succinate, SK-132 and IBCP-2 - had an anti-motion sickness effect stronger than of scopolamine, the reference vestiboloprotector. The anti-motion sickness effect of ethyl-methyl hydroxypyrine was also demonstrated in experiments with cats. Apparent anti-motion sickness effect of ethyl-methyl hydroxypyrine (mexydol) was found in 69% of healthy male volunteers which is comparable with the effect of scopolamine (62%). In experiments with immobilized cats (myorelaxation drugs) the microelectrode technique and microontoiphoresis of physiologically active substances revealed that ethylmethyl hydroxypyrine influences the majority of neurons in the medial vestibular nucleus (61%). Suppression of cell spontaneous activities in more than one half of cases can be stopped completely or attenuated significantly by bicucculine, a specific GABA(A)-receptor antagonist. In 42% of neurons ethyl-methyl hydroxypyrine subdues the response to vestibular stimulation which is likely to underlie the anti-motion sickness effect.     

Motion sickness: advances in pathogenesis, prediction, prevention, and treatment

Motion sickness has a major influence on modern traveling activities and the rapidly spreading engagement in virtual reality immersion. Recent evidence emphasizes the role of the otoliths in the pathogenesis of motion sickness, and several new theories may help explain its occurrence beyond the traditional sensory conflict theory. A promising new direction is the recently reported association of genetic polymorphism of the alpha2-adrenergic receptor with increased autonomic response to stress and motion sickness. Various physiological measures for the evaluation and prediction of motion sickness have been tested. However, no single parameter has yet been found to be of high enough sensitivity and specificity for the diagnosis or prediction of individual motion sickness susceptibility. A number of pharmacological and non-pharmacological countermeasures are used for the prevention and treatment of motion sickness. The non-pharmacological options include all procedures that reduce conflicting sensory input, accelerate the process of multi-sensory adaptation, and promote psychological factors which enable the subject to cope with his/her condition. The most effective anti-motion sickness drugs are central acting anticholinergics and H1 antihistamines; however, adverse effects on psychomotor performance may limit their use in drivers, pilots, and naval crewmembers. Recent studies may be relevant to our understanding of the link between motion sickness, migraine, vertigo, and anxiety. Based on these findings and on recent neurochemical data, the development of new anti-motion sickness agents is a promising field of investigation.