丁苯酞软胶囊联合奥拉西坦注射液治疗血管性痴呆的疗效观察

目的探讨丁苯酞软胶囊联合奥拉西坦注射液对血管性痴呆病人认知功能的影响及应用的安全性。方法选择血管性痴呆病人120例,随机分为3组,丁苯酞软胶囊联合奥拉西坦注射液治疗组40例;奥拉西坦注射液治疗组40例;对照组40例,对照组只用胞磷胆碱钠注射液。以1个月为1疗程,3组病人治疗前及治疗1个月后均采用简易智能状态量表(MMSE)和日常生活能力量表(ADL)评价临床疗效。结果治疗后丁苯酞软胶囊联合奥拉西坦注射液治疗组MMSE和ADL评分优于奥拉西坦注射液治疗组(P<0.05),显著优于对照组(P<0.01)。结论丁苯酞软胶囊联合奥拉西坦注射液治疗血管性痴呆有效、安全,能显著改善病人的认知功能,提高生活质量。     

丁苯酞氯化钠注射液用于脑梗死患者治疗对脑梗死后抑郁的预防效果评价

目的探究丁苯酞氯化钠注射液对脑梗死后抑郁患者的预防效果。方法选取2015.12~2016.6之间河北大学附属医院收治的60例急性脑梗死患者,数字表法随机分组,对照组30例进行常规治疗,研究组30例在此基础上应用丁苯酞氯化钠注射液治疗,两组患者均连续治疗14d,采用美国国立卫生研究院卒中量表(NIHSS)评价神经功能缺损状况,并采用汉密尔顿抑郁量表(HAMD)评价抑郁表现情况。结果治疗后两组患者的NIHSS评分均显著改善,但研究组改善程度显著优于对照组(P0.05);治疗后两组患者的HAMD评分均显著改善,但研究组改善程度显著优于对照组(P0.05)。结论丁苯酞氯化钠注射液能够有效改善脑梗死患者的神经功能缺损,同时可减少脑梗死后抑郁的发生。     

丁苯酞氯化钠联合美金刚对肝性脑病致血管性痴呆患者的效果

目的分析肝性脑病致血管性痴呆患者应用丁苯酞氯化钠注射液联合美金刚治疗效果。方法采用随机数字表法将我院85例肝性脑病致血管性痴呆患者分组,对照组42例给予美金刚治疗,观察组43例美金刚联合丁苯酞氯化钠注射液治疗,对比两组患者治疗后认知功能、痴呆程度、氧化应激指标水平、生活质量及临床疗效。结果治疗2、4周后,观察组CDR评分低于对照组,MoCA、MMSE评分高于对照组,治疗4周后,观察组SOD水平、ADL评分及总有效率高于对照组,MDA水平低于对照组(P0.05)。结论丁苯酞氯化钠注射液联合美金刚能够有效改善肝性脑病致血管性痴呆患者认知功能,提升生活质量,其机制与抗氧化应激有关。     

阿加曲班联合丁苯酞对分水岭脑梗死的疗效及神经元特异性烯醇化酶水平的影响

目的 观察阿加曲班联合丁苯酞注射液对分水岭脑梗死的临床疗效及对神经元特异性烯醇化酶(neuron-specific enolase,NSE)水平的影响。方法 将186例发病6～48 h内的分水岭脑梗死患者随机分为对照组、丁苯酞组、阿加曲班联合丁苯酞组(联合组)各62例; 对照组按分水岭脑梗死常规方法治疗2周,丁苯酞组在对照组的基础上加用丁苯酞注射液,联合组在对照组的基础上加用丁苯酞注射液及阿加曲班; 3组治疗前、治疗14 d后神经功能均采用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)及日常生活能力量表(Barthel 指数)评定; 观察3组治疗前、治疗14 d后NSE水平的变化; 治疗3个月后采用改良的Rankin量表(Modified rankin Scale,mRS)评分比较3组神经功能恢复情况; 记录相关不良反应。结果 治疗14 d后3组NIHSS评分、NSE水平均显著降低,Barthel 指数显著升高,联合组、丁苯酞组均明显优于对照组,且联合组优于丁苯酞组(P<0.01); 治疗3个月后各组预后良好率比较,联合组、丁苯酞组明显优于对照组,且联合组优于丁苯酞组(P<0.01),治疗期间无明显不良反应发生。结论 阿加曲班联合丁苯酞注射液治疗分水岭脑梗死安全有效,并能降低NSE水平,有效改善神经功能缺损症状及日常生活能力。     

丁苯酞软胶囊和尼莫地平片治疗轻度血管源性认知功能障碍的疗效比较

目的比较丁苯酞软胶囊和尼莫地平片治疗轻度血管源性认知功能障碍的疗效差异。方法选择我院收治的轻度血管源性认知功能障碍患者80例,随机分为观察组和对照组各40例,分别给予丁苯酞软胶囊和尼莫地平片治疗。2组均在治疗前后采用MoCA(蒙特利尔任职评估)量表对患者认知情况评价。结果观察组治疗后MoCA总评分高于对照组,差异有统计学意义(P0.05)。2组治疗后视空间及执行能力、注意力、语言、延迟记忆、定向力评分分别和本组治疗前比较,差异有统计学意义(P0.05);观察组治疗后视空间及执行能力、注意力、语言、延迟记忆、定向力评分分别和对照组比较,差异有统计学意义(P0.05)。结论丁苯酞软胶囊在改善轻度血管源性认知功能障碍患者的认知功能效果显著,优于尼莫地平片,值得临床借鉴。     

丁苯酞氯化钠注射液治疗前循环进展性脑梗死的疗效观察

目的探讨丁苯酞氯化钠注射液治疗前循环进展性脑梗死的临床效果。方法选取于我院住院的60例急性前循环进展性脑梗死患者,按照随机数字表法分为2组各30例。2组均应用胞二磷胆碱针、肠溶阿司匹林片等治疗,治疗组加用丁苯酞氯化钠注射液治疗。比较2组治疗前后NIHSS及BI评分变化。结果 2组NIHSS及BI指数评分治疗前后差异有统计学意义(P0.05)。结论应用丁苯酞氯化钠注射液可改善患者中枢神经功能的损伤,不良反应少。     

丁苯酞软胶囊对血管性痴呆的临床疗效及对ET-1的影响

目的：观察丁苯酞软胶囊对血管性痴呆患者的临床疗效及对E T-1的影响。方法将94例血管性痴呆患者随机分为丁苯酞软胶囊治疗组和对照组,采用MMSE、ADL评分评价丁苯酞软胶囊的治疗效果,并监测2组治疗前后ET-1的变化。结果治疗组治疗后MMSE、ADL评分均优于对照组,治疗后总有效率高于对照组,治疗后治疗组ET-1水平较对照组明显下降,差异有统计学意义（P＜0·05）。结论丁苯酞软胶囊能够改善血管性痴呆患者的认知功能和日常生活能力,并能降低血管性痴呆患者ET-1水平,促进临床应用。     

早期使用丁苯酞注射液治疗基底节区脑梗死对侧支循环建立及神经功能的影响

目的探讨早期使用丁苯酞注射液治疗基底节区脑梗死对侧支循环建立及神经功能的影响。方法根据治疗方法将121例基底节区脑梗死患者分为丁苯酞组53例和对照组68例。两组患者给予脱水剂,胃黏膜保护剂、抗血小板聚集药、调脂药、扩血管药、活血化瘀中药、脑保护药物及其他对症支持治疗,丁苯酞组于发病24 h内加用丁苯酞注射液100 ml,静脉滴注2次/d。于入院第4~5 d采用CTA检查观察所有患者侧支循环的建立情况。于入院时、第2周及第3个月进行NIHSS评分。结果丁苯酞组37例(69.8%)建立侧支循环,对照组38例(55.9%)建立侧支循环。丁苯酞组侧支循环建立率显著高于对照组(P0.05)。丁苯酞组及对照组入院时NIHSS评分差异无统计学意义(P0.05)。与丁苯酞组比较,对照组第2周及第3个月NIHSS评分显著升高(P0.05~0.01)。结论早期使用丁苯酞注射液治疗的基底节区脑梗死患者可促进脑梗死部位的侧支循环的建立,减轻脑梗死症状,改善预后。     

丁苯酞治疗急性脑梗死患者轻度认知功能障碍的随访研究

目的观察丁苯酞对新发急性脑梗死(acute cerebral infarction,ACI)轻度认知功能障碍(mild cognitive impairment,MCI)患者的防治效果,探讨其在干预早期认知功能损害方面的作用和意义。方法对72例新入院的新发ACI患者(7 d)进行蒙特利尔认知评估认知量表(Montreal cognitive assessment,MoCA)评分,其中合并MCI患者40例,认知评定正常组32例。经患者知情同意,72例患者分为丁苯酞治疗组39例(MCI患者22例),给予丁苯酞0.2 g口服,3次/d;常规治疗组33例(MCI患者18例),茴拉西坦0.2 g口服,3次/d。随访8周,用MoCA再次对所有患者进行认知功能评分。结果丁苯酞组与茴拉西坦组相比,治疗8周后MCI患者MoCA评分有所提高,丁苯酞组14例患者MoCA评分认知功能正常,茴拉西坦组4例,差异有统计学意义(P0.05);初评认知功能正常的ACI患者,治疗8周后MoCA评分丁苯酞组显著高于茴拉西坦组(P0.05);其中丁苯酞组3例转化为MCI,茴拉西坦组7例转为MCI,差异有统计学意义(P0.05)。结论丁苯酞对于新发ACI合并MCI患者的认知功能有一定改善作用,对于认知功能正常的ACI患者,可以防治MCI的发生,为临床使用丁苯酞早期干预血管性认知功能障碍提供了一定依据。     

银杏叶注射液联合丁苯酞注射液高压氧治疗进展性脑梗死临床分析

目的观察银杏叶注射液联合丁苯酞注射液、高压氧治疗进展性脑梗死的临床疗效。方法选取2011-06—2014-08收治的进展性脑梗死患者130例,随机分为观察组与对照组,对照组使用丁苯酞注射液及高压氧治疗,观察组在此基础上联合银杏叶注射液治疗,观察2组临床疗效。结果观察组显效率与总有效率明显高于对照组(P0.05),治疗后2组神经功能缺损评分均明显减少,观察组减少更为明显,差异均有统计学意义(P0.05)。结论银杏叶注射液联合丁苯酞注射液、高压氧治疗进展性脑梗死,可明显改善临床症状,显著促进神经功能缺损的恢复,有效提高治疗效果,值得进一步推广应用。     

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.     

Storage of lipofuscin in neurons in mucopolysaccharidosis

Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.Supported by a grant from the Expressen Prenatal Research Foundation