依达拉奉联合早期高压氧疗对急性缺血性卒中的疗效观察

目的 研究依达拉奉联合早期高压氧疗对急性缺血性卒中(ACI)患者的疗效观察.方法 120例急性脑梗死患者随机分为依达拉奉治疗组60例和常规治疗组60例(予常规抗血小板聚集、改善脑循环、营养脑细胞等治疗),依达拉奉治疗组在常规治疗的基础上予依达拉奉注射液及早期高压氧疗,治疗后7、14、28 d用美国国立卫生院神经功能缺损评分量表(NIHSS)评分并进行疗效评定.结果 2组NIHSS评分在治疗前差异无统计学意义 (P＞0.05);2组NIHSS评分在治疗后均明显低于常规治疗组(P＜0.01).结论 依达拉奉联合早期高压氧疗治疗后NIHSS评分明显低于常规治疗组,疗效明显优于常规治疗对照组.     

依达拉奉治疗进展性缺血性脑卒中的临床观察及对其血清红细胞生成素水平的影响

目的 通过观察进展性缺血性脑卒中患者在使用自由基清除剂依达拉奉治疗后的临床疗效及血清红细胞生成素(EPO)水平的变化,探讨依达拉奉对进展性缺血性脑卒中的神经保护作用.方法 60例发病在12～48h,病情呈进行性加重的进展性缺血性脑卒中患者被随机分为依达拉奉组30例和常规治疗组30例,同时设正常对照组30例;依达拉奉组为常规治疗基础上加用依达拉奉静脉滴注10d;治疗前,治疗后3d、10d,应用美国国立卫生研究院卒中量表(NIHSS)对患者神经功能缺损状况进行标准评分,并用放免法检测患者的血清EPO水平.结果 治疗前依达拉奉组、常规治疗组的NIHSS评分和血清EPO水平均高于对照组(P<0.05),但依达拉奉组与常规治疗组相比无统计学差异(P>0.05);治疗后3d,依达拉奉组NIHSS评分开始降低,血清EPO水平开始升高,而常规治疗组NIHSS评分继续升高,血清EPO水平继续降低;治疗后10d,两组患者临床症状明显改善,NIHSS评分降低,血清EPO水平显著增高,两组相比有统计学差异(P<0.05).结论 依达拉奉能有效改善进展性缺血性脑卒中所致的神经功能障碍,升高患者血清EPO水平,提示依达拉奉能通过促进EPO释放发挥其自由基清除的神经保护作用.     

尤瑞克林与依达拉奉治疗急性颈内动脉系统缺血性卒中的临床对比研究

目的 以依达拉奉作对比,探讨尤瑞克林治疗急性缺血性卒中的疗效及安全性。方法 将178例急性缺血性卒中患者随机分为治疗组和对照组,治疗组88例用尤瑞克林0.15PNA单位加入生理盐水250ml静脉滴注,每日1次,共14d为一疗程。对照组90例用依达拉奉30mg加入生理盐水250ml静脉滴注,每日2次共14d为一疗程。治疗前、治疗后14d进行美国国立卫生研究院卒中量表（the National Institutes of Health Stroke Scale,NIHSS）评分,并监测C反应蛋白（C-reactive protein,C-RP）、神经元烯醇化酶（neuron-specificenolase,NSE）变化,治疗前、治疗后14d、治疗后90d行Barthel指数评分。结果 治疗组和对照组治疗前、后的NIHSS评分比较均有统计学差异（P＜0.01）;而两组间的比较无统计学差异（P=0.5867）。治疗组和对照组治疗后第14d的Barthel评分比较无明显差异,治疗后90d的Barthel指数评分出现差异,治疗组优于对照组（P=0.004）。治疗组和对照组治疗后的血清C-RP及NSE值较治疗前下降,差异具有统计学意义,而两组间的比较差异无统计学意义。结论 尤瑞克林治疗急性缺血性卒中,有效、安全,急性期疗效不亚于依达拉奉,而远期疗效优于依达拉奉。     

依达拉奉治疗中青年急性脑出血的临床疗效观察

目的观察依达拉奉治疗中青年急性脑出血的临床疗效。方法将156例急性脑出血中青年患者分为依达拉奉组和对照组,每组78例,两组患者均在发病24h内给予降颅压、调整血压及血糖等对症治疗。依达拉奉组在上述治疗的基础上,给予依达拉奉注射液(30mg),每日2次,共14d。两组分别于治疗前和治疗后第14天进行神经功能缺损评分和日常生活能力评分。神经功能缺损评分采用美国国立卫生研究院卒中量表(NIHSS),日常生活活动能力评分采用Barthel指数(BI)。结果依达拉奉组NIHSS评分和BI明显优于对照组(P0.05)。依达拉奉组有效率为84.6%,明显高于对照组的62.9%,差异有统计学意义(P0.05)。结论依达拉奉可以明显地改善急性脑出血中青年患者的神经功能损伤,提高患者日常生活活动能力。     

尤瑞克林联合依达拉奉治疗急性缺血性脑卒中的临床对照研究

目的探讨尤瑞克林联合依达拉奉治疗缺血性脑卒中的临床疗效及安全性。方法将40例急性缺血脑卒中患者随机分为联合治疗组和对照组,联合治疗组:尤瑞克林针联合依达拉奉针静滴治疗;对照组:单用依达拉奉针静滴;疗程均为14d;治疗前、治疗后14d分别进行美国国立卫生研究院卒中量表(theNational Institutes of Health Stroke Scale,NIHSS)评分,同时于治疗前、后第14及90d行日常生活活动能力量表(Activities of Daily Living Scale,ADL)评分。结果联合治疗组和对照组治疗前、治疗后14d NIHSS评分组内比较有明显差异(P<0.01),有效率分别为80%及75%,组间比较无差异(P>0.05)。联合治疗组和对照组治疗后第14d的ADL评分组间比较无差异(P>0.05),治疗后第90d的ADL评分组间比较有差异(P<0.01)。结论在缺血性脑卒中的治疗中尤瑞克林联合依达拉奉能有效、安全发挥疗效;其急性期疗效与单用依达拉奉比较无明显差异,但远期疗效及改善患者日常生活活动能力方面明显优于单用依达拉奉。     

依达拉奉早期应用于急性缺血性卒中的临床分析

目的 观察依达拉奉治疗急性缺血性卒中的疗效。方法 选择82例发病时间在6～72 h的急性缺血性卒中患者,随机分为治疗组42例,对照组40例。治疗组在基础治疗的基础上加用依达拉奉30mg加入0.9%氯化钠注射液100 ml静脉滴注,每天2次,连用14 d;对照组仅给予基础治疗和0.9%氯化钠注射液100ml 静脉滴注,每天2次,连用14 d。比较两组治疗前后的患者临床神经功能缺损程度评分和临床疗效。结果 治疗前两组临床神经功能缺损评分无明显差异（21.23±5.64分 vs 20.23±5.14分,P >0.05）。治疗14 d后,治疗组评分低于对照组（9.60±2.50 vs 12.10±2.21,P＝0.027）。治疗组临床疗效总有效率为92.8%,对照组为72.5%,差异有统计学意义（P＝0.016）。结论 依达拉奉治疗急性缺血性卒中有显著疗效。     

尤瑞克林联合依达拉奉治疗急性后循环脑梗死疗效观察

目的观察尤瑞克林联合依达拉奉注射液治疗急性后循环脑梗死的疗效。方法将95例急性后循环脑梗死患者随机分为治疗组(尤瑞克林联合依达拉奉)45例和对照组(单用依达拉奉)40例,分别于入院时和治疗后14 d、28 d进行临床神经功能缺损程度(NIHSS)评分,治疗后90 d进行Barthel指数评分;分别在治疗前后测血液流变学并行经颅多普勒(TCD)检查。结果 2组治疗后14 d及28 d神经功能缺损评分均有明显改善,但治疗组与对照组的NIHSS、Barthel指数、血液流变学、TCD变化等比较差异均有统计学意义(P<0.05或P<0.01)。结论尤瑞克林联合依达拉奉可增加急性后循环脑梗死患者的脑血流,改善微循环,并有助于急性后循环脑梗死患者的神经功能恢复。     

依达拉奉联合血栓通对急性脑梗死患者血流变学的影响

目的分析依达拉奉联合血栓通对急性脑梗死患者血流变学的影响,探讨其临床适用性。方法选择2013-05—2014-05于我院就诊的60例急性脑梗死患者,随机分为试验组30例和对照组30例,对照组采用血栓通治疗,试验组在对照组基础上联合依达拉奉进行治疗。观察2组治疗前后NIHSS评分、血脂水平和凝血指标、血液流变学指标的变化情况及治疗后临床疗效。结果治疗前2组NIHSS评分、血脂水平和凝血情况、血流变学相关指标水平比较无明显差异(P0.05),治疗后2组的NIHSS评分、血脂水平和凝血情况、血流变学相关指标水平均明显降低(P0.05),且试验组改善情况优于对照组(P0.05);试验组总有效率为93.33%(28/30),对照组为73.33%(22/30),差异有统计学意义(χ2=4.320 0,P=0.037 7)。2组治疗过程中未出现明显不良反应。结论依达拉奉联合血栓通治疗急性脑梗死安全有效,可有效改善患者的血脂和血流变,降低病情进展危险因素。     

尤瑞克林联合依达拉奉治疗急性脑梗死的疗效及对炎症介质水平的影响

目的探讨尤瑞克林联合依达拉奉治疗急性脑梗死的临床效果以及治疗前后的炎症介质水平。方法选取2011—2013年我院收治的急性脑梗死患者80例,随机分为2组,分别给予依达拉奉治疗与依达拉奉联合尤瑞克林治疗。结果治疗2周后观察组有效率显著高于对照组,2组治疗后NIHSS评分与血清CRP相比治疗前均明显改善,观察组改善更为显著。结论尤瑞克林联合依达拉奉治疗急性脑梗死效果良好,明显改善患者神经功能,降低血清CRP水平,改善预后。     

丁苯酞联合依达拉奉治疗急性缺血性脑卒中对细胞凋亡的影响

目的探讨丁苯酞注射液联合依达拉奉对急性缺血性脑卒中的临床疗效及对细胞凋亡的影响。方法选择急性脑梗死患者136例,随机分为联合用药组和依达拉奉组,每组68例。依达拉奉组给予依达拉奉注射液治疗,联合用药组在依达拉奉组治疗的基础上加用丁苯酞,共治疗14 d。比较治疗前后NIHSS、ADL评分,测定细胞脂质过氧化水平及抗氧化酶活性及血清Bax、Bcl-2含量。结果联合用药组治疗后NIHSS评分低于依达拉奉组,ADL评分高于依达拉奉组,丙二醛(MDA)、超氧化物歧化酶(SOD)水平低于依达拉奉组(P0.05);联合用药组治疗后血清Bax含量低于依达拉奉组,血清Bcl-2含量高于依达拉奉组(P0.05)。结论丁苯酞注射液联合依达拉奉治疗急性缺血性脑卒中,可减轻缺血再灌注过程中氧化应激反应及细胞凋亡,从而减轻脑缺血再灌注(I/R)所引起的脑损伤。     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

他汀类药物的使用和颅内动脉瘤破裂相关性分析

目的 探讨他汀类药物对颅内动脉瘤破裂的影响。方法 2010年3月至2014年3月收治颅内囊状动脉瘤67例,其中破裂者32例,未破裂者35例。采用多变量Logistic回归评估他汀类药物的使用和颅内动脉瘤破裂的关系。结果 破裂组术前使用他汀类药物4例（12.5%,4/32）,未破裂组16例（45.7%,16/35）。破裂组服用他汀类药物的百分比显著低于未破裂组（P<0.01）。纠正潜在的混杂干扰后（or值: 0.30,95%可信空间:0.12~="" 0.64）显示,颅内动脉瘤破裂与他汀类药物的使用呈显著负相关,也与高血清总胆固醇浓度有关。结论 本结果提示他汀类药物对颅内动脉瘤破裂有一定的预防效果。     

Impact of our understanding of the genetic aetiology of epilepsy

A genetic contribution to aetiology is estimated to be present in up to 40% of patients with epilepsy. It is useful to categorise genetic epilepsies according to the mechanisms of inheritance into Mendelian disorders, non-mendelian or ‘complex’ disorders, and chromosomal disorders. Over 200 Mendelian diseases include epilepsy as part of the phenotype, and the genes for a number of these have been identified recently. These include autosomal recessive progressive myoclonic epilepsies such as Unverricht-Lundborg disease, Lafora disease and the neuronal ceroid lipofuscinoses, and three autosomal dominant idiopathic epilepsies. The last named have been shown to arise from mutations in ion channel genes. Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in CHRNA4, benign familial neonatal convulsions by mutations in KCNQ2 and KCNQ3, and generalised epilepsy with febrile seizures plus by mutations in SCN1B. ‘Complex’, familial epilepsies are more difficult to analyse, but evidence has been obtained for loci predisposing to juvenile myoclonic epilepsy on chromosome 6p and 15q. Lastly, the genes underlying several spike-wave epilepsies in mice have been cloned, and three of these encode sub-units of voltage-gated calcium channels. Received: 29 September 1999/Accepted: 7 December 1999     

肌萎缩侧索硬化三例误诊分析

目的掌握肌萎缩侧索硬化(ALS)的诊断标准,以便早期准确诊断,避免误诊。方法分析3例ALS患者早期被误诊的临床资料。结果 3例患者均以下肢无力发病,逐渐波及上肢或对侧肢体,脊柱MR I示颈部或腰部椎间盘突出压迫硬膜囊,手术治疗后,症状无缓解,病情仍进行性加重,经肌电图检查证实为ALS。结论临床医师应熟知ALS的诊断标准,对患者详细询问病史、认真查体和电生理检查是减少ALS误诊的关键。     

Modelling of movement of the lamprey: Control of oscillators

This article discusses the control methods of the central pattern generator (CPG). First a control model of the CPG is presented using 2 oscillators, and we suggest that phasic modulation to the CPG by means of phasic information is effective for controlling the phase difference between oscillators. Next, two models for controlling the CPG of a lamprey are proposed. One model describes a control system from the brain stem, in which the reticulospinal neurons control the CPG by receiving feedback signals and sending control signals to the neck region of the CPG. The other is a model for learning an localized control system to generate a desired motor pattern. By means of these models, a role of the efference copy is suggested.     

失匹配负波在意识障碍评估中的临床价值探讨

自失匹配负波(MMN)于20世纪70年代被发现以来,我们对规律性声音被打破后所诱发的前注意检测有了进一步认识,而MMN成为了开启认知大门的钥匙。至今为止,MMN的研究范围从产生机制发展到神经精神疾病相关的临床试验,特别是对于急性脑损伤(ABI)昏迷以及进展后的慢性意识障碍(DoC)患者,MMN被认为是一个可靠的预后预测指标。然而,由于MMN难以用于个体评估,目前在临床实践中的应用仍十分有限,广大临床医师对MMN的了解甚少。因此,本文就MMN的产生机制、在意识障碍中的临床意义、判读方法及其影响因素做一综述。