加用姜黄素对脑梗死患者血浆超氧化物歧化酶及丙二醛的影响

研究证实[1,2],自由基和白细胞浸润在脑梗死病理损害中起着重要作用.脑缺血时可造成局部自由基水平增加和白细胞浸润,而自由基和白细胞浸润又可加重脑细胞损害,如此恶性循环.姜黄素(curcumin, Cur)是从姜科植物姜黄中提取的一种酚类物质,具有抗癌变、抗炎、抗氧化等广泛的药理作用[3].我们对33例脑梗死患者应用Cur治疗前后临床神经功能缺损评分及血浆超氧化物歧化酶(SOD)总活力和丙二醛(MDA)含量进行了观察,目的在于探讨Cur治疗脑梗死的效果和机制.

脑梗死和脑出血中西医结合诊断标准(试行)

脑梗死包括动脉粥样硬化性血栓性梗死、脑栓塞和腔隙性脑梗死等;脑出血系指非外伤性原发于脑实质内的出血.无论是脑梗死或脑出血,按其临床表现多属于中医学中风病范畴,统称为脑卒中.本标准系中国中西医结合学会神经科专业委员会依据国内外脑卒中诊断标准,结合临床经验,以及我国对脑梗死、脑出血中西医结合诊断的临床和研究实践制定.

Based on our clinical experience,we formulated Huo Xue Tong Luo Tang(活血通络汤HXTL Decoction),a prescription for treatment of lacunar cerebral infarction.Most of the ingredients are those in the prescriptions of Di Dang Tang(抵当汤)and Gui Gan Long Mu Tang(桂甘龙牡汤)described in the book Treatise of Febrile Diseases(伤寒论)in accordance with the compatible theory of principal,assistant,adjuvant and guiding drugs for improving blood circulation,removing stasis,dispelling endogenous wind and phlegm,inducing resuscitation,removing obstruction in the channels,and balancing the yin and yang.

Cerebrovascular dementia is a common disease in the middle-aged and old people. Its incidence makes up about 10-20% of all kinds of dementia. It is mainly caused by general degeneration of the brain function resulted from cerebral arteriosclerosis and cerebral infarction. The author has treated 32 cases of cerebrovascular dementia with acupuncture in the recent years with satisfactory therapeutic results. A report follows.

Pseudobulbar paralysis is a kind of common clinical syndromes of cerebral vascular diseases, which is manifested as dyslalia, dysphagia and choking. By several-year clinical observations, 36 cases were treated with satisfactory therapeutic effects as reported in the following.Clinical Data Of 36 in-patients, there were 24 males and 12 females, aged from 44 to 81 years, averaging 64.92 years. Of 36 cases, 24 were at the acute stage and 12 at the recovery stage. All the cases were diagnosed as cerebral vascular diseases by cranial CT scan and MRI, of which, 4 were cerebral infarction, 26 lacunar cerebral infarction, 5 cerebral hemorrhage and 1 mixed type. Of 36 cases, 15 were the first attack of wind-stroke, 15 the second attack, 5 the third attack and 1 the forth attack. There were 26 patients with hypertension among 36 cases, of which, 8 patients suffered from hypertension within 10 years, 6 for more than 10 years, 9 for more than 20 years and 3 for more than 30 years. All the 36 cases were associated with dysphagia and agreeable to Standard on Diagnosis and Evaluation of Therapeutic Effects of Wind-stroke issued by the State Scientific Committee 85-919-01-01, 1995.

The aim of this study is to investigate the effect of electro-acupuncture treatment in acute phase of cerebral infarction on the motor functions. In this randomly controlled trial, 86 patients were allocated to two groups, the experimental group given clinical and electro-acupuncture treatments for a period of 4 weeks, and the control group given clinical treatment plus active and/or passive functional exercise. The result showed that the level of impairment and disability in both groups were improvement according to the Chinese Stroke Scale, Brunnstrom-Fugl-Meyer score, and Barthel Index throughout the study and 3 months after. The motor functions and the activities of daily living (ADL) were improved significantly in the electro-acupuncture group as compared with the control group (P<0.05). Also, the results showed greater reduction of neurological deficit in the electro-acupuncture group than in the control group. Conclusion: Early acupuncture treatment for acute stroke patients may improve motor functions, and consequently the activities of daily living.

To study the changes of the expression of growth-associated protein-43 (GAP-43) and pathology in temporal infarction of rats photochemically induced and the effects of batroxobin. Methods: immunohistochemical technique and hematoxylin-eosin stain was used to show the changes of the expression of GAP-43 and pathology. Results: In infarction group, GAP-43 expression was markedly increased on the infarction and surronding tissues at 24h cerebral infarction. The expression reached peak level at 72h after cerebral infarction and was decreased at 7d after cerebral infarction. However, in batroxobin-treated group, GAP-43 expression was increased and the pathological changes were much slight as compared with infarction group. Conclusion: The expression of GAP-43 increases in infarction of temporal neocortex and batroxobin promotes the expression of GAP-43 and ameliorates the pathological changes in infarction of temporal neocortex.

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1, 3, 5 and 7 days after infarction by means of magnetic resonance imaging (MRI), 1H- and 31P- magnetic resonance spectroscopy (MRS). A region of T2 hyperintensity was observed in left temporal neocortex in infarction group and batroxobin group 1, 3, 5 and 7 days after infarction. The volume of the region gradually decreased from 1 day to 7 days after infarction. The ratio of NAA/Cho+Cr in the region of T2 hyperintensity in the infarction group was significantly lower than that in the corresponding region in the sham-operated group 3, 5 and 7 days after infarction respectively (P<0.05). Lac appeared in the region of T2 hyperintensity in the infarction group 1, 3, 5 and 7 days after infarction, but it was not observed in the corresponding region in sham-operated group at all time points. Compared with the sham-operated group, the ratios of bATP/PME+PDE and PCr/PME+PDE of the whole brain in the infarction group were significantly lower 1, 3 and 5 days after infarction respectively (P<0.05), and the ratio of bATP/PCr also was significantly lower 1 day after infarction (P<0.05). Batroxobin significantly decreased the volume of the region of T2 hyperintensity 1 and 3 days after infarction (P<0.05), significantly increased the ratio of NAA/Cho+Cr in the region 5 and 7 days after infarction (P<0.05), significantly decreased the ratios of Lac/Cho+Cr and Lac/NAA in the region 5 and 7 days after infarction (P<0.05), and significantly increased the ratios of bATP/PME+PDE and bATP/PCr in the whole brain 1 day after infarction (P<0.05). The results indicated that the infracted region had severe edema, increased Lac and apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormal changes.

Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1, 3, 5 and 7 days after infarction by means of magnetic resonance imaging (MRI), 1H- and 31P- magnetic resonance spectroscopy (MRS). A region of T2 hyperintensity was observed in left temporal neocortex in infarction group and batroxobin group 1, 3, 5 and 7 days after infarction. The volume of the region gradually decreased from 1 day to 7 days after infarction. The ratio of NAA/Cho+Cr in the region of T2 hyperintensity in the infarction group was significantly lower than that in the corresponding region in the sham-operated group 3, 5 and 7 days after infarction respectively (P<0.05). Lac appeared in the region of T2 hyperintensity in the infarction group 1, 3, 5 and 7 days after infarction, but it was not observed in the corresponding region in sham-operated group at all time points. Compared with the sham-operated group, the ratios of bATP/PME+PDE and PCr/PME+PDE of the whole brain in the infarction group were significantly lower 1, 3 and 5 days after infarction respectively (P<0.05), and the ratio of bATP/PCr also was significantly lower 1 day after infarction (P<0.05). Batroxobin significantly decreased the volume of the region of T2 hyperintensity 1 and 3 days after infarction (P<0.05), significantly increased the ratio of NAA/Cho+Cr in the region 5 and 7 days after infarction (P<0.05), significantly decreased the ratios of Lac/Cho+Cr and Lac/NAA in the region 5 and 7 days after infarction (P<0.05), and significantly increased the ratios of bATP/PME+PDE and bATP/PCr in the whole brain 1 day after infarction (P<0.05). The results indicated that the infracted region had severe edema, increased Lac and apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormal changes.

高压氧对急性脑梗死临床应用分析

Objective:To determine the effect of hyperbaric oxygenation(HBO) on treating acute cerebral infarction(ACI). Methods: We randomly divided 60 patients with acute cerebral infarction into the treatment group and the control group. Hyperbaric oxygenation treatment was applied in the treatment group as routine drug therapy was used. The neurological function, living ability, clinical therapeutic effectiveness and hemorrheology changes of pa tients in the two groups before and after treatment were observed and evaluated. Results: The indexes of treatment were obviously improved one month after treatment (P ＜ 0.05 ). Clinical effective rate was 93.3 % in this group,which was obviously higher than that of the control group(P ＜ 0.05). Conclusion: Hyperbaric oxygenation can accelerate the recovery of neurological function of patients with acute cerebral infarction.

高血压对认知功能的损害及脑功能成像

高血压是引起心脑血管病主要的危险因素,高血压对脑组织的不良影响是一个长期而持续的过程.大量的研究发现高血压在未发生临床脑卒中之前,患者脑形态学和认知功能已经产生一定程度的损害,影像学上表现为无症状脑梗塞(silent cerebral infarction,SCI),脑白质疏松(leukoaraiosis,LA),脑萎缩,即所谓"亚临床改变"[1,2].越来越多的证据显示这些无症状的脑损害在功能上可能引起认知能力的减退,甚至以后发展为痴呆.因此,在高血压患者未发生脑卒中之前,对其脑形态学以及脑功能改变的研究将对患者未来病程的发展起到预测的作用,同时对脑功能神经生物学基础的研究可以从根本上为高血压对某些认知功能影响的研究提供更为有利且直观的证据.近年来逐渐发展的功能磁共振成像(functional magnetic resonance imaging,fMRI)技术,使研究者可以在非侵入性状态下活体检测脑功能,已成为研究人脑高级活动的重要手段.目前,利用fMRI技术对人脑认知活动的研究成为神经心理学和神经影像学所关注的热点.该技术的发展为我们研究疾病状态下脑认知功能改变提供了可靠的方法.本文就高血压所致认知功能减退及其早期神经影像学表现以及脑功能成像综述如下.

急性进展性脑梗死的研究进展

急性进展性脑梗死(acute progressive cerebral infarction,APCI)是指急性脑梗死发生后的一段时间内,神经功能缺损症状继续加重的一种临床过程.进展的时间长短不一,从数小时到十数天不等.本文就其概况、发病机制、影响因素及治疗进行综述.

1例53岁男性多器官衰竭(第1例)

The patient is a man aged 53 yrs old. He had a history of hypertension for ten years, type-2 diabetes for 7 years, fatty liver, lacunar cerebral infarction and prostatic hypertrophy for many years. He had drunk large amounts of alcohol and smoked 50 - 60cigarettes/day for more than 20 years. His parents, sister and son had diabetes.

脑梗死二级预防是否都要用阿司匹林?

贵刊2006年第1期刊登了"缺血性脑血管病阿司匹林规范应用的专家共识[1]".本人对该共识有以下意见,特提出共同讨论.

脑梗死二级预防应该使用阿司匹林

随着社会经济和医学的发展,人口预期寿命明显延长,而同时带来的挑战是脑血管病和痴呆等老龄疾病的增加,而我们对其认识远不如对感染和肿瘤等疾病的认识,当我们对脑血管病的知识和认识不足,还不能完全满足医生和患者的需求时,我们应该怎么办?这里存在着认识论和方法论的问题.

儿童脑梗死的诊治进展

脑血栓形成和脑栓塞都是缺血性脑血管病,临床上统称为脑梗死.儿童脑梗死的发病率为8～13/10万[1-2].随着诊断技术的提高,脑梗死病例在婴儿及儿童中检出率越来越高.脑血栓形成多起病缓慢,常于数十小时或数日内病情达到高峰.

新生儿脑梗死

新生儿脑梗死(neonatal cerebral infarction),又称为新生儿中风(neonatal stroke)、围生期脑梗死(perinatal cere-bml infection)或围生期中风(perinatal stroke),通常指在胎龄28周至生后28 d之间发生于某一或某些脑血管供血区内的脑组织的缺血性坏死,分为出血性脑梗死和缺血性脑梗死.

晚发性维生素K缺乏致出血性脑梗塞11例

外伤性颈动脉夹层致迟发性脑梗死一例及文献复习

患者 男,31岁.因头部外伤后8 d,突发左侧肢体偏瘫4 d,于2007年12月4日收入山东大学齐鲁医院神经外科.患者既往体健.伤后曾于当地医院就诊,神经系统检查无异常,行头部CT未见异常(图1a),胸部CT示双侧肺挫伤,保守治疗后3 d出院,未遗留任何神经系统体征,复查头部CT检查无异常(图1b).伤后第4天,患者突然出现左侧肢体活动不灵活,于伤后第7天行头部CT发现右侧大脑半球大面积脑梗死(图1c),伤后第8天转入我院.体检:意识清楚,语速较慢.左上肢肌力Ⅱ级,左下肢肌力Ⅲ级,肌张力略高,左侧巴宾斯基征(+),左侧躯体浅感觉减退.

脑梗死后锥体束Wallerian变性的影像学研究进展

1850年,Waller首先描述被切断的周围神经远端的组织学改变,称为Wallerian变性(Wallerian degeneration,WD).中枢Wallerian变性可发生于皮质脊髓束、皮质延髓束、皮质脑桥束等神经纤维束中.原发性脑损伤通常位于一侧大脑半球,可以是脑梗死、脑出血、脑外伤、脑肿瘤、脑动静脉畸形、脑手术后、脑白质病等,其中以脑梗死为常见.