左旋多巴联合恩他卡朋治疗帕金森病疗效观察

目的研究左旋多巴联合恩他卡朋治疗帕金森病(PD)的疗效及对炎症因子、氧化应激指标水平的影响。方法选取132例PD患者为研究对象,随机数字表法分成治疗组和对照组各66例。治疗组给予左旋多巴联合恩他卡朋治疗,对照组给予左旋多巴治疗。3个月后采用帕金森统一评分量表(UPDRS)比较2组临床疗效,记录其治疗前后血清炎症因子[白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)]、血浆氧化应激指标[超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)水平变化情况。结果 2组治疗后UPDRS评分和IL-1β、IL-6、MDA水平均较治疗前显著降低(P0.05),SOD、GSH水平则较治疗前显著升高(P0.05),且治疗组变化幅度大于对照组(P0.05);治疗组总有效率优于对照组(P0.05)。结论左旋多巴联合恩他卡朋方案对PD患者体内炎症因子和氧化应激指标水平有一定调节作用,疗效确切,于病情转归有利。     

金刚烷胺治疗帕金森病异动症的疗效观察

目的探讨金刚烷胺治疗帕金森病(PD)左旋多巴诱导异动症(LID)的临床疗效。方法将42例帕金森病患者随机分为金刚烷胺组与恩托卡朋组,每组21例,每组均应用美多巴和普拉克索作为帕金森病基础治疗。经12 w联合用药治疗后,以统一帕金森病评定量表(UPDRS)各部分评分相对于基线(治疗前评分)的变化为指标评估疗效。同时监测血压,观察患者不良反应,比较两组治疗方案的安全性。结果经12 w治疗后金刚烷胺组UPDRS.IV(治疗的并发症)评分相对基线有显著下降.差异有统计学意义(P<0.05)。金刚烷胺组UPDRS.IV(治疗的并发症)评分较恩托卡朋组评分下降更多,差异有统计学意义(P<0.05)。金刚烷胺组临床总有效率为86%,恩托卡朋组临床总有效率为32%,差异有显著统计学意义(P<0.05)。两组药品不良反应发生率分别为19%和23%。差异无统计学意义(P>0.05)。结论金刚烷胺治疗左旋多巴诱导的帕金森病异动症可获得较显著的近期疗效。     

左旋多巴联合恩他卡朋在帕金森病患者中的应用效果及安全性

目的 分析左旋多巴联合恩他卡朋在帕金森病患者中的应用效果及安全性。方法 选择2018—2019年在河南科技大学第二附属医院治疗的帕金森病患者78例,随机化原则分为2组,各39例。对照组给予左旋多巴治疗,观察组在对照组基础上加用恩他卡朋治疗,比较2组血清指标、帕金森评分量表-Ⅱ(UPDRS-Ⅱ)、UPDRS-Ⅲ评分及不良反应情况。结果 治疗后,观察组白细胞介素-1β(IL-1β)、IL-6、丙二醛(MDA)水平均明显低于对照组,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPx)水平较高,差异有统计学意义(P0.05);与对照组治疗后比较,观察组UPDRS-Ⅱ、UPDRS-Ⅲ评分均较低,差异有统计学意义(P0.05);观察组不良反应发生率(10.25%)与对照组(15.38%)比较,差异无统计学意义(P0.05)。结论 左旋多巴联合恩他卡朋治疗帕金森病效果较好,可有效改善患者血清水平,提高帕金森量表评分,且未增加不良反应发生率。     

恩他卡朋添加治疗症状波动的帕金森病的随机、双盲、安慰剂对照临床研究

目的:探讨添加恩他卡朋治疗PD患者剂末现象的疗效和安全性。方法:40例伴有剂末现象的PD患者进行随机、双盲、安慰剂、平行分组临床对照试验。根据患者日记记录的"开"、"关"期时间、UPDRS各部分评分、研究者总体评估变化量表和左旋多巴每日剂量来评定疗效。结果:恩他卡朋治疗12周时能显著延长"开"期时间、缩短"关"期时间,降低UPDRS评分,减少每日左旋多巴用量,研究者主观感觉65%的患者病情好转,与安慰剂组相比差异有显著意义。不良事件的发生率与安慰剂组相比差异无显著意义。结论:添加恩他卡朋治疗伴有剂末现象的PD患者安全、有效。     

恩他卡朋治疗帕金森病剂末现象的临床观察

目的探讨恩他卡朋对PD患者剂末现象影响。方法选择40例出现剂末现象的PD患者进行相关资料分析,根据不同治疗方案分为普拉克索组和恩他卡朋组,入选患者治疗8周,分析恩他卡朋对PD剂末现象的疗效。结果恩他卡朋组疗效(90%)高于普拉克索组(60%),UPDRSⅡ评分低于普拉克索组,关期时间短于普拉克索组;恩他卡朋组异动症时间(2.3±0.6)h,低于普拉克索组的(2.7±1.0)h,差异均有统计学意义(P0.05)。结论恩他卡朋能够延长患者开期时间,缩短关期时间,改善剂末现象开期运动症状。     

美多芭联合恩他卡朋治疗对帕金森病患者血浆同型半胱氨酸水平的影响

目的探讨美多芭联合恩他卡朋治疗对帕金森病(PD)患者血浆同型半胱氨酸(Hcy)水平的影响。方法选取30名健康体检者作为对照组,20例未服用过左旋多巴(LD)制剂的PD患者为未服药组,63例美多芭治疗的PD患者为美多芭组,49例美多芭联合恩他卡朋治疗的PD患者为联合组。检测患者外周血中的LD稳态峰浓度并进行统一PD评分量表Ⅲ(UPDRSⅢ)的评分。检测所有研究对象的血浆Hcy水平。结果联合组患者LD血浆浓度明显高于美多芭组(P0.05)。美多芭组及联合组患者UPDRSⅢ评分均明显低于未服药组(均P0.05)。与对照组比较,未服药组、美多芭组及联合组患者血浆Hcy水平均明显升高(均P0.05);且美多芭组患者血浆Hcy水平明显高于未服药组及联合组(均P0.05)。结论美多芭联合恩他卡朋能显著降低PD患者血浆Hcy水平,对PD治疗有积极意义。     

恩他卡朋添加治疗对药效减退的帕金森病患者的疗效观察

目的 探讨恩他卡朋添加治疗对药效减退的帕金森病(PD)患者的疗效及安全性.方法 对4l例服用美多芭疗效减退的PD患者添加恩他卡朋治疗.在添加恩他卡朋治疗前和治疗后第1个月、2个月、3个月分别进行"统一PD评定量表(UPDRS)"评分及运动诱发电位(MEP)检查,比较各时间点美多芭的每日服用总量,并观察其不良反应.结果 添加恩他卡朋治疗后第1个月、2个月、3个月UPDRSⅡ和UPDRSⅢ评分均较添加治疗前明显下降,差异有统计学意义(均P＜0.05),美多芭每日服用总量也明显减少,与添加治疗前比较有统计学意义(均P＜0.05);MEP静息阈值(RMT)在治疗后第3个月明显升高(P＜0.05),潜伏期(CL)及皮质静息期(CSP)明显延长(均P＜0.05);无严重不良反应.结论 恩他卡朋添加治疗能有效改善美多芭药效减退PD患者的运动功能,且安全.     

参附注射液对帕金森病临床疗效的影响

目的研究联用参附注射液对帕金森病(PD)的临床疗效及血清炎性因子水平的影响。方法选取PD患者40例,随机分为对照组(19例)和观察组(21例)。入院后对照组给予美多芭治疗,观察组联合使用参附注射液治疗。比较两组的统一PD评定量表(UPDRS)、PD睡眠量表(PDSS)、汉密尔顿抑郁量表(HAMD)、MMSE评分。同时对比两组血清IL-1β、IL-6、TNF-α、核转录因子(NF-κB)-p65水平变化。结果观察组患者治疗后UPDRSⅡ、UPDRSⅢ及总UPDRS评分明显低于治疗前及对照组,差异有统计学意义(均P0.05)。观察组患者治疗后HAMD明显低于治疗前及对照组,差异有统计学意义(均P0.05);而PDSS、MMSE结果差异无统计学意义(均P0.05)。对照组和观察组各项炎症因子水平均显著高于健康组,差异有统计学意义(均P0.01)。观察组患者治疗后IL-1β、IL-6水平明显低于治疗前及对照组,差异有统计学意义(均P0.01);而观察组与对照组患者治疗前后TNF-α、NF-κB-p65结果差异无统计学意义(均P0.05)。结论联合使用参附注射液可以明显改善PD患者的多项评分结果和炎症因子水平,对PD治疗有积极作用。     

美多巴联合恩他卡朋治疗帕金森病的临床研究

目的观察美多巴联合恩他卡朋治疗法对帕金森病的临床疗效。方法选取三门峡第三人民医院收治的80例帕金森病患者纳为研究对象,随机分为对照组与观察组各40例,对照组单纯给予美多巴治疗,观察组采取美多巴联合恩他卡朋治疗,对比2组治疗前与治疗12周后汉密顿抑郁量表(HAMD)评分、生活能力(ADL)评分、副作用(TESS)评分及疗效。结果治疗12周后,观察组HAMD评分(6.58±1.74)分与TESS评分(2.12±0.84)分,明显低于对照组(11.43±2.86)分、(4.75±1.37)分,且ADL评分为(88.25±7.26)分,明显高于对照组(70.54±7.05)分(P0.05);观察组治疗总有效率为95.00%,显著高于对照组的75.00%(P0.05)。结论美多巴联合恩他卡朋治疗帕金森病,能有效改善患者抑郁程度,提高其生活能力,改善不良反应情况,获得显著疗效。     

新疆维吾尔族、汉族帕金森病患者α-突触核蛋白SNCA基因多态性与临床症状的关系

目的探讨新疆维吾尔族、汉族帕金森病(PD)患者α-突触核蛋白SNCA基因多态性与临床症状的关系。方法应用PCR-限制性片段长度多态性分析法对新疆地区的90例维吾尔族和135例汉族PD患者进行SNCA基因rs3822086位点多态性分析。采集相关临床资料;采用H-Y分期法判断PD严重程度;采用统一PD评定量表(UPDRS)、日常生活能力问卷(ADL)、MMSE和神经精神问卷(NPI)进行评分。比较SNCA基因rs3822086位点不同基因型PD患者间临床症状的差异。结果基因检测结果显示,SNCA基因rs3822086位点C/T基因型111例,T/T基因型61例,C/C基因型53例;不同基因型PD患者间年龄、性别、民族及病程的差异均无统计学意义。不同基因型PD患者间H-Y分期的差异无统计学意义(P=0.237);PD严重程度的差异无统计学意义(P=0.068);首发症状的差异无统计学意义(P=0.746);UPDRSⅡ评分的差异无统计学意义(P=0.598);UPDRSⅢ评分的差异无统计学意义(P=0.815);UPDRSⅣ评分的差异无统计学意义(P=0.096);ADL评分的差异无统计学意义(P=0.464);MMSE评分的差异无统计学意义(P=0.475)。SNCA基因rs3822086位点T/T基因型PD患者NPI评分明显高于C/C基因型PD患者(P0.05)。结论新疆维吾尔族、汉族PD患者SNCA基因T/T基因型在神经精神症状方面的风险要高于C/C基因型,其他临床症状与SNCA基因多态性无关。     

视频脑电图在小儿癫痫诊断中的应用

目的评价视频脑电图(video-EEG)在小儿癫诊断中的应用价值。方法对126例具有发作性症状的患儿进行连续8h的包括清醒、睡眠、诱发试验及必要的认知测验的视频脑电图监测。结果经发作期视频脑电图证实,39例初诊为癫性发作的患儿中14例(35%)为非癫性发作;15例其他症状发作中13例(86%)为非癫性发作。64例样放电患儿中51例(80%)确定发作类型,22例(34%)确定癫类型。视频脑电图可发现短暂轻微的癫发作及样放电引起的一过性认知损伤。结论视频脑电图在排除非癫性发作、确定癫性发作的类型、评价脑电-临床关系方面可提供准确可靠的证据,进一步提高癫的临床诊断水平。     

Role of glutathione in repair of free radical damage in hippocampus in vitro.

Depletion of glutathione (GSH), an intrinsic antioxidant, increases vulnerability to free radical damage in a number of cell systems. This study investigates the role of GSH in limiting electrophysiological damage and/or recovery from free radical exposure in slices of guinea pig hippocampus. Synaptic potentials (PSPs) and population spikes (PSs) were recorded from field CA1. Free radicals were generated from 0.006% peroxide through the Fenton reaction. Analysis of the input-output curves showed that peroxide treatment decreased PSPs and impaired ability of the PSPs to generate PSs as previously reported. Recovery was nearly total within a half hour. Treatment with 5 mM buthionine sulfoximine (BSO) for 2 h depleted hippocampal GSH to 79.2% of control values. The extent of free radical damage was not increased. Recovery, however, was only partial. GSH was further depleted by oxidation with diamide or covalent bonding with dimethyl fumarate (DMF) immediately before and during the peroxide treatment. Neither diamide nor DMF treatment in BSO-incubated tissue enhanced peroxide-induced electrophysiological deficits. Following these treatments, however, tissue showed little recovery from free radical damage. We conclude that glutathione is essential for repair processes in hippocampal neurons exposed to oxidative damage.     

Neuroprotective properties of memantine in different in vitro and in vivo models of excitotoxicity

The pathogenesis of stroke, trauma and chronic degenerative diseases, such as Alzheimer's disease (AD), has been linked to excitotoxic processes due to inappropriate stimulation of the N-methyl-D-aspartate receptor (NMDA-R). Attempts to use potent competitive NMDA-R antagonists as neuroprotectants have shown serious side-effects in patients. As an alternative approach, we were interested in the anti-excitotoxic properties of memantine, a well-tolerated low affinity uncompetitive NMDA-R antagonist presently used as an anti-dementia agent. We explored in a series of models of increasing complexity, whether this voltage-dependent channel blocker had neuroprotective properties at clinically relevant concentrations. As expected, memantine protected neurons in organotypic hippocampal slices or dissociated cultures from direct NMDA-induced excitotoxicity. However, low concentrations of memantine were also effective in neuronal (cortical neurons and cerebellar granule cells) stress models dependent on endogenous glutamate stimulation and mitochondrial stress, i.e. exposure to hypoxia, the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) or a nitric oxide (NO) donor. Furthermore, memantine reduced lethality and brain damage in vivo in a model of neonatal hypoxia-ischemia (HI). Finally, we investigated functional rescue (neuronal capacity to migrate along radial glia) by memantine in cerebellar microexplant cultures exposed to the indirect excitotoxin 3-nitropropionic acid (3-NP). Potent NMDA-R antagonists, such as (+)MK-801, are known to block neuronal migration in microexplant cultures. Interestingly, memantine significantly restored the number of neurons able to migrate out of the stressed microexplants. These findings suggest that inhibition of the NMDA-R by memantine is sufficient to block excitotoxicity, while still allowing some degree of signalling.     

Knowledge of management of epilepsy in young adults in Jordan

PURPOSE: Nationwide studies on public knowledge of epilepsy have been undertaken in several countries, but not in Jordan. The purpose of this study was to evaluate knowledge of the management of epilepsy in Jordan. METHODS: A cross-sectional study was performed during the period February-June 2005 on 16,044 individuals selected randomly to represent all regions of Jordan. Respondents were interviewed and asked to complete a five-item questionnaire testing their knowledge of the management of epilepsy. RESULTS: Most of the individuals (77.9%) agreed that patients with epilepsy are best treated in a specialized hospital for neurological diseases. Although the largest percentage of the sample (86.7%) agreed that the best person to treat epilepsy is a neurologist, others believed that a hypnotherapist (25.4%) or a religious healer (22.6%) is. As an immediate measure during an attack of epilepsy, most respondents (82.6%) agreed that protecting the patient's head is most important. During the postseizure period, 45.8% of respondents believed that offering the patient water or a cold or hot drink is appropriate. Two-thirds of the respondents (66.2%) agreed that epilepsy can be treated with drugs. Responses of the participants to the five items significantly differed with respect to age, gender, level of education, and occupation. CONCLUSION: Jordanians are reasonably well informed about most aspects of the management of epilepsy, but there is still a need for public education about this disorder.