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国外医学（老年医学分册） 1993年第4期14卷 164-168页

作者： baloh RW 李兴武

许多患者使用头晕一词来描述空间定位感觉的改变。由于视觉、本体感觉、躯体感觉及前庭信号确定头部和身体的空间位置, 其中任一系统损伤便可引起头晕。大脑中枢综合这些定位信号的改变也能导致头晕。本文集中讨论老年人头晕的病理生理... 详细信息

许多患者使用头晕一词来描述空间定位感觉的改变。由于视觉、本体感觉、躯体感觉及前庭信号确定头部和身体的空间位置, 其中任一系统损伤便可引起头晕。大脑中枢综合这些定位信号的改变也能导致头晕。本文集中讨论老年人头晕的病理生理学、诊断及常见病因的治疗。

关键词：头晕老年人病理生理学诊断病因

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Dear Diary

Women of China 2008年第5期 66-67页

作者： Kaja.baloh.Jessica Guo Tomoko Miyoshi

Some people-many of us,in fact-have precious memories of picking up and traveling hundreds,even thousands,of miles from our homes and *** landed in strange lands and we began our studies or *** so doing,we learned to exist in a new culture and to enjoy a new lifestyle,one in which we had a lot of freedom,but in which we were alone. Beginning with this issue,we will provide our readers with space to write their diary *** purpose is to provide readers with an opportunity to share their experiences in another land,whether laowai (foreigners) in China or Chinese traveling *** hope you will enjoy this feature of our magazine.

关键词：英文土地

谷氨酸转运蛋白EAAT1突变引起间歇性共济失调、偏瘫及癫痫发作

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世界核心医学期刊文摘（神经病学分册） 2005年第12期1卷 56-57页

作者： Jen J.C. Palos T.P. R.W. baloh 刘凯 Dr. Department of Neurology School of Medicine University of California Los Angeles CA 90095 United States

Background: Transporters, ion pumps, and ion channels are membrane proteins that regulate selective permeability and maintain ionic gradients across cell membranes. Mutations in CACNA1A encoding a neuronal calcium channel and ATP1A2 encoding an ion pump cause episodic ataxia, hemiplegic migraine, and seizures. Mutant gene products of both CACNA1A and ATP1A2 may affect neurotransmission of glutamate, the most abundant excitatory amino acid neurotransmitter. Methods: We examined our patient population with episodic ataxia and hemiplegic migraine but with no mutation in either CACNA1A or ATP1A2. We looked for mutations in SLC1A3, which encodes the glutamate transporter excitatory amino acid transporter (EAAT) 1 that is important in removing glutamate from the synaptic cleft. Results: A patient with episodic ataxia, seizures, migraine, and alternating hemiplegia has a heterozygous mutation in SLC1A3 that is not present in his asymptomatic parents and controls. Expression studies of the mutant EAAT1 showed decreased expression of the protein with a markedly reduced capacity for glutamate uptake. When coexpressed, the mutant EAAT1 decreased the activity of wild-type EAAT1 but not of two other transporters EAAT2 or EAAT3, suggesting that mutant EAAT1 specifically multimerizes with wild-type EAAT1 to exert its dominant negative effect. Conclusion: Our data show that a heterozygous mutation in EAAT1 can lead to decreased glutamate uptake, which can contribute to neuronal hyperexcitability to cause seizures, hemiplegia, and episodic ataxia.

关键词：共济失调 EAAT1 转运蛋白氨基酸神经递质偏头痛患者离子通道通透性离子泵转运体离子梯度

迟发性单纯小脑共济失调:鉴别有和无可识别突变的患者

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世界核心医学期刊文摘（神经病学分册） 2006年第3期2卷 14-15页

作者： Kerber K.A. Jen J.C. Perlman S. baloh R.W. 周永 David Geffen School of Medicine at UCLA Reed Neurological Research Center Box 951769 710 Westwood Plaza Los Angeles CA 90095-1769 United States

Late onset cerebellar ataxia can be caused by several genetic mutations but a large percentage of patients remain undiagnosed. Thirty-eight patients with onset of slowly progressive, pure cerebellar ataxia ≥40 years-of-age were identi fied from a large ataxia database. Their clinical findings and quantitative ocul omotor tests were reviewed; all were screened for SCA1, SCA2, SCA3, SCA6, SCA8, SCA14, and the Fragile X premutation (FMR1). All 47 exons of CACNA1A were screen ed for mutations. Genetic analysis uncovered a mutation in 11 patients. The SCA6 mutation was present in 8 patients (repeats 22-23). Three additional genetic m utations were found: SCA1 (42 repeats), SCA3 (66 repeats), and SCA8 (121 repeats ). Patients without identified genetic mutations were characterized by 1) a late r age of onset, 2) truncal without extremity ataxia, 3) and down beat nystagmus. Although only a third of these idiopathic late onset ataxia patients had a posi tive family history, this homogeneous syndrome probably represents a yet to be i dentified genetic disorder.

关键词：小脑共济失调基因突变回顾研究突变筛查眼球运动眼震试验结果遗传性疾病阳性家族史遗传分

登陆病综合征诊断标准:Bárány协会前庭疾病分类委员会共识

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神经损伤与功能重建 2021年第12期16卷 683-687页

作者：宋宁(译) 李响(译) 张梦露(译) 隋汝波(审校) 杨旭(审校) Yoon-Hee Cha Robert W.baloh Catherine Cho Måns Magnusson Jae-Jin Song Michael Strupp Floris Wuyts Jeffrey P.Staab 航天中心医院(北京大学航天临床医学院)神经内科锦州医科大学附属第一医院神经内科美国明尼苏达大学神经病学系美国加州大学洛杉矶分校神经病学系美国纽约大学格罗斯曼医学院神经内科和耳鼻喉-头颈外科瑞典隆德大学耳鼻喉科韩国首尔大学盆唐医院耳鼻喉-头颈外科德国慕尼黑大学神经内科德国眩晕与平衡疾病中心比利时安特卫普平衡研究与航空航天实验室(LEIA) 美国明尼苏达州罗彻斯特市梅奥诊所精神心理学系和耳鼻喉-头颈外科

我们提出了登陆病综合征(mal de débarquement syndrome,MdDS)的诊断标准,并将其纳入国际前庭疾病分类。这些诊断标准包括:(1)非旋转性眩晕,其特征是持续性或1天中大部分时间都存在振荡感("摇摆"、"摆动"或"晃动");(2)被动运动结束后4... 详细信息

我们提出了登陆病综合征(mal de débarquement syndrome,MdDS)的诊断标准,并将其纳入国际前庭疾病分类。这些诊断标准包括:(1)非旋转性眩晕,其特征是持续性或1天中大部分时间都存在振荡感("摇摆"、"摆动"或"晃动");(2)被动运动结束后48小时内发作;(3)症状在被动运动时(例如驾驶)可暂时减轻;(4)症状持续>48小时。病程不足1月且症状仍持续者,定义为"进展型";如果症状在1个月或1个月内得以缓解,观察期至少延长到缓解点,则为"短暂型";如果症状持续超过1个月不缓解,则为"持续型"。事实上,MdDS患者亦可伴发空间定向障碍、视觉运动不耐受、疲劳以及头痛或焦虑加剧的症状。本文也回顾总结了MdDS与前庭性偏头痛、运动病及持续性姿势-感知性头晕(persistent postural perceptual dizziness,PPPD)的临床鉴别要点。此外,非运动触发、可通过运动缓解的振荡性眩晕在其他前庭疾病、内科疾病、精神紧张加剧或代谢紊乱之后出现,由于其具有MdDS和PPPD这2种疾病的特点,在非运动诱发的表现描述方面多样,因此,进一步研究其现象及生物学与MdDS、PPPD及其他前庭疾病的相关性是非常有必要的。

关键词：登陆病综合征 MdDS 被动运动非运动触发的持续性振荡性眩晕持续性姿势-感知性头晕

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显性遗传的听觉前庭综合征的颞骨组织病理学

世界核心医学期刊文摘（神经病学分册） 2005年第4期1卷 44-44页

作者： Ishiyama A. Ishiyama G. Lopez I. R.W. baloh 夏峰 Department of Neurology UCLA School of Medicine Reed Neurologic Research Center 710 Westwood Los Angeles CA 90095- 1769 United States Dr.

Objective: To describe the clinical and pathologic features of a new dominantly inherited audiovestibular syndrome. Methods: History, examination, and audiometric testing in the proband, brother, and son; quantitative rotational testing in the proband and son; histopathology of the cochlea and vestibular labyrinth in the proband; sequencing candidate genes COCH and MYO7A in the brother and son. Results: Affected family members developed slowly progressive hearing loss beginning in their late 30s and progressive imbalance in their early 70s. Three of four affected had brief (minutes) episodes of vertigo typically occurring a few times per year. Auditory and vestibular function testing documented a slowly progressive loss of auditory and vestibular function. Postmortem examination showed a loss of hair cells in the cochlea and vestibular receptor organs. There were no cellular infiltrates or acidophilic deposits. No mutations were found in the COCH or MYO7A genes. Conclusions: This dominantly inherited audiovestibular syndrome results in a selective loss of hair cells in the auditory and vestibular end organs. Finding the causative gene could have important implications for understanding the pathophysiology of presbycusis and dysequilibrium of aging.

关键词：前庭功能显性遗传组织病理学先证者毛细胞听力减退旋转试验老年性耳聋病理学检查前庭迷路