耳石复位法治疗良性阵发性位置性眩晕42例临床分析

目的 探讨耳石复位法治疗良性阵发性位置性眩晕(BPPV)的效果.方法 应用 Epley管石复位法、 Semont管石解脱法、Barbecue翻滚法治疗良性阵发性位置性眩晕42例.结果 42 例中经耳石复位法治愈36例(85.7%),有效4例(9.5%),复位失败2例(4.8%).失败的2例经前庭功能训练治愈.结论 耳石复位法是BPPV的首选治疗方法,对于复位失败的患者可试行前庭功能训练.     

耳石手法复位、前庭习服训练和单纯药物治疗良性发作性位置性眩晕的疗效观察

良性发作性位置性眩晕(BPPV)用耳石手法复位、前庭习服训练及药物均可治疗。本研究观察耳石手法复位、前庭习服训练和单纯药物治疗对BPPV的效果。现报告如下。1对象与方法1.1对象系2010年1月～2011年5月我院门诊及住院的病程<14 d的BPPV患者163例,均符合BPPV诊断标准[1]。     

联合手法复位治疗后半规管良性发作性位置性眩晕疗效观察

良性发作性位置性眩晕（BPPV）是因特定头位改变而诱发的阵发性短暂眩晕,是最常见的位置性眩晕,约占位置性眩晕患者的90%.BPPV可能涉及到各个半规管,但后半规管良性阵发性位置性眩晕（PC-BPPV）最常见[1].耳石复位法是治疗PC-BPPV的主要方法.现将我科2012-04-2013-02耳石复位法治疗68例PC-BPPV患者资料报告如下.     

良性阵发性位置性眩晕与前庭神经元炎相继发病一例

目的 探讨良性阵发性位置性眩晕(BPPV)、前庭神经元炎(VN)在同一患者相继发病时的临床表现及鉴别诊断,以期提高对这两种疾病的再认识。方法 分析1例BPPV与VN相继发病时的临床表现、诊疗经过。结果 患者最初以“发作性眩晕,发生体位改变时加重”被诊断为“BPPV”,行耳石复位治疗后眩晕症状缓解。3d后头晕症状再次出现,且呈持续性,再次行耳石复位治疗无效,结合病史、症状体征、冷热试验和视频头脉冲试验,诊断为VN。经对症支持治疗、糖皮质激素抗炎治疗和前庭功能康复锻炼,4w后患者痊愈。结论 BPPV与VN均是以眩晕为主要临床表现的两种常见疾病,VN亦可诱发BPPV。两种疾病在同一患者相继出现时,尤其当患者先发生BPPV时,更容易发生误诊或者漏诊。因此提高临床医师对眩晕症状及相关疾病的认识以及熟练运用两种疾病的检查手段,可对患者尽早作出正确诊断并及时治疗。另外,临床医师亦应克服“一元论”的惯性思维模式,综合判断,全面诊断,防止以偏概全。     

Epley耳石复位法结合心理干预对后半规管BPPV的疗效观察

良性发作性位置性眩晕(BPPV)起病急骤,与头位改变有密切关系,持续时间一般为数秒至数10s,是中老年人眩晕最常见的原因,其中后半规管BPPV占90.1%。但此症常常被误诊为椎基底动脉系统的TIA甚至椎动脉供血不足,有86%的BPPV日常生活受到影响,但只有8%的BPPV得到有效的治疗[1]。为此我们采用Epley耳石复位法结合心理干预对后半规管良性阵发性位置性眩晕进行治疗,并分析其疗效。     

Epley耳石复位法结合心理干预对后半规管EPPV的疗效观察

良性发作性位置性眩晕(BPPV)起病急骤,与头位改变有密切关系,持续时间一般为数秒至数10s,是中老年人眩晕最常见的原因,其中后半规管BPPV占90.1%.但此症常常被误诊为椎基底动脉系统的TIA甚至"椎动脉供血不足",有86%的BPPV日常生活受到影响,但只有8%的BPPV得到有效的治疗[1].为此我们采用Epley耳石复位法结合心理干预对后半规管良性阵发性位置性眩晕进行治疗,并分析其疗效.     

从前庭病理生理学角度指导良性阵发性位置性眩晕的诊断与治疗

良性阵发性位置性眩晕是临床最常见的周围性眩晕性疾病,本文旨在从前庭病理生理学角度阐述其临床特点,首先介绍良性阵发性位置性眩晕相关前庭病理生理学,包括耳石和内淋巴比重及其与半规管空间位置关系、Flourens定律、Ewald第二定律、耳石移动致内淋巴动力学改变、半规管耦联作用、半规管与眼外肌的耦联关系和中枢速度储存机制;其次从前庭病理生理学角度剖析眩晕发作特征和眩晕眼震发作机制,水平半规管与后半规管良性阵发性位置性眩晕的差异,手法复位过程中眼震变化规律;最后基于前庭病理生理学,对两种类型耳石的判断、手法复位和前半规管良性阵发性位置性眩晕诊断的注意事项提出观点。     

良性阵发性位置性眩晕的耳石复位治疗

目的探讨良性阵发性位置性眩晕(BPPV)耳石复位法的疗效。方法应用Epley手法、Barbecue翻滚法和Semont手法对12例BPPV患者进行治疗。结果12例患者经上述手法复位治疗48h后眩晕症状均完全消失,无明显不良反应,分别随访3～11个月无再发。结论耳石复位法治疗BPPV有效、简便、安全,可作为BPPV的首选治疗方法。     

良性阵发性位置性眩晕

良性阵发性位置性眩晕(BPPV)的临床特点表现为头部位置变化所引起的短暂性、发作性眩晕和眼球震颤。BP-PV的发病机理有嵴顶石学说和管石学说。BPPV症状的严重程度、持续时间和频率与所累及的半规管及结石碎片的位置有关。不同类型的BPPV可以通过观察体位诱发试验中出现的眼球震颤特点来诊断。BPPV可在保守治疗时自行缓解。管石复位法能将结石碎片从半规管转移到前庭,从而快速消除症状。     

改良式耳石复位法联合益气聪明汤治疗良性阵发性位置性眩晕疗效观察

目的 探讨改良式耳石复位法联合益气聪明汤治疗良性阵发性位置性眩晕(BPPV)的疗效.方法 56例BPPV患者随机分为对照组(耳石复位法)和治疗组(改良式耳石复位法联合益气聪明汤),随访1 a,观察治疗效果.结果 经上述方法治疗后,眩晕症状完全消失或明显改善.对照组治愈率81.5%,有效率100%,复发率22.2%;治疗...     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。