急性缺血性脑梗死弥散各项异性的变化规律

目的 探讨急性缺血性脑梗死患者发病24 h内弥散各向异性变化的规律及其临床应用价值.方法 回顾性分析33例次发病24 h内脑梗死病灶的弥散张量成像(DTI)资料,计算病灶和对侧相应部位的平均各向异性分数(FA)和平均弥散系数(ADC).采用配对t检验的方法 分别比较不同发病时间段的梗死病灶与对侧相应部位的FA和ADC值.结果 发病24 h内梗死病灶的ADC值显著低于对侧(P<0.01);而病灶平均FA值与对侧比较差异无统计学意义(P=0.74),6 h内、6～12 h以及12～24 h内病灶与对侧比较差异也无统计学意义(P>0.05).急性期内病灶FA值变化存在显著个体差异,FA升高和保持不变者在三个时间组内发生率差异无统计学意义(P＝0.73).结论 发病24 h内脑梗死病灶弥散各向异性与对侧比较差异无统计学意义,但个体间存在明显差异,这种个体差异有望为脑卒中患者的个体化治疗方案的选择提供依据.     

Alteplase for acute ischemic stroke

Alteplase, an intravenously administered form of recombinant tissue plasminogen activator (rt-PA), remains the only US FDA-approved thrombolytic treatment for acute ischemic stroke within 3 h of symptom onset. Patients treated with intravenous rt-PA are at least 30% more likely to have minimal or no disability at 3 months compared with placebo. Despite an increased risk of symptomatic intracranial hemorrhage, rt-PA does not increase mortality. The benefit achieved with rt-PA is cost effective and sustained 1 year after treatment. Despite its clear benefit, rt-PA remains underutilized. Although the future of acute ischemic stroke treatment will most likely involve a multi-faceted treatment approach, the primary objective remains to establish recanalization of the involved vessel. For patients with acute ischemic stroke within the first 3 h of symptom onset, rt-PA remains the first step in accomplishing this goal.     

Thrombolysis for acute ischemic stroke

Data generated from randomized controlled trials in the last decade have shown that acute intervention can improve neurologic outcome in patients with ischemic stroke. This article reviews recent studies of systemic and intra-arterial thrombolysis for cerebrovascular disease in detail. Important considerations for treating patients with thrombolysis are explored, and theoretic and practical differences in the approach to patients with anterior and posterior circulation disease are highlighted.     

Management of acute ischemic stroke

The treatment of acute ischemic stroke has evolved from observation and the passage of time dictating outcome to an approach that emphasizes time from ictus, rapid response, and a dedicated treatment team. We review the treatment of acute ischemic stroke from the prehospital setting, to the emergency department, to the inpatient hospital setting. We discuss the importance of prehospital assessment and treatment, including the use of elements of the neurologic examination, recognition of symptoms that can mimic those of acute ischemic stroke, and rapid transport of patients who are potential candidates for thrombolytic therapy to hospitals with that capability. Coordinated management of acute ischemic stroke in the emergency department is critical as well, beginning with non-contrast-enhanced computed tomography of the brain. The advantages of a multidisciplinary dedicated stroke team are discussed, as are thrombolytic therapy and other inpatient treatment options. Finally, we cover evolving management strategies, treatments, and tools that could improve patient outcomes.     

急性缺血性脑卒中患者白细胞粘附分子的表达及细胞内[Ca2+]变化的实验研究

目的探讨急性缺血性脑卒中患者外周血白细胞计数和粘附分子表达的变化,以及与中性粒细胞激活密切相关的细胞内游离钙离子浓度[Ca2+]变化,以期为脑卒中的发病机理和治疗提供有价值的理论依据.方法采用流式细胞术(FCM)检测白细胞粘附分子的表达及细胞内[Ca2+]的变化.结果脑卒中急性发作时,患者主要是中性粒细胞数增高明显,外周血白细胞CD11b、CD18的表达在发病24h内升高,同时,脑卒中患者中性粒细胞表面CD62L的表达在急性期明显降低,急性脑卒中患者中性粒细胞内[Ca2+]增加,中性粒细胞表面粘附分子CD11b、CD18的表达与细胞内[Ca2+]具有正相关性,CD62L的表达与[Ca2+]虽无明显的线性相关性,但随着[Ca2+]的增加,CD62L的表达具有下降的趋势.结论急性脑卒中发生时,白细胞被激活,粘附分子CD11b、CD18表达上调,介导白细胞与内皮细胞粘附增强,可能会加重缺血后迟发性神经元死亡的病理生理过程.同时,随着中性粒细胞的激活,细胞表面粘附分子CD62L的表达显著下调,细胞内[Ca2+]增加,在白细胞与内皮细胞的粘附过程中起重要作用.     

Assessment of acute phase proteins in acute ischemic stroke

Acute phase proteins (APPs) have been implicated to play important roles during both acute and chronic inflammatory processes in different diseases including ischemic stroke. Though there are several studies showing the importance of APPs as inflammation markers in acute ischemic stroke (AIS), the time course of these proteins during acute phase of AIS is not well known. Thus, the aim of this study was to show the changes in plasma levels of six APPs (i.e., haptoglobin [Hp], ceruloplasmin [Cp], high-sensitive C-reactive protein [h-CRP], fibrinogen, complement 3 [C3] and complement 4 [C4]) during the first 10 days after acute stroke. The study group consisted of 34 female and 19 male patients (n = 53; mean age 65 +/- 12 years), who had first acute ischemic stroke (AIS). An age-matched control group (n = 53; 32 female and 21 male subjects, mean age 62 +/- 6 years) was also included. To evaluate the plasma levels of six APPs, the blood samples of patients with AIS were withdrawn on admission (day 1), and after 3, 5 and 10 days, whereas only one measurement was performed in the control group. In addition, several cerebrovascular risk factors were determined. The peak levels of APPs were higher in the AIS group than the control group (p < 0.0001). In serial measurements, the levels of h-CRP, Hp, C3 and C4 showed alterations during 10 days after AIS (p < 0.0001, p < 0.05, p < 0.0001, p < 0.0001, respectively). The alterations in levels of fibrinogen and Cp were not statistically significant (p > 0.05). After stroke, h-CRP, C3 and fibrinogen reached their highest values on the third day, Cp and C4 on the fifth day, and Hp on the tenth day. The plasma levels of h-CRP correlated positively with other five APPs studied (p < 0.05). These findings support the importance of inflammation processes after stroke. We suggest that the differences in levels of APPs could be used in predicting the outcome of stroke patients.     

快速波谱成像用于急性缺血性脑卒中

目的评价快速波谱成像(TSI)技术用于急性缺血性脑卒中(AIS)的价值。方法对40例AIS患者行TSI及常规多体素化学位移波谱成像(CSI),采用对应频谱拟合脚本获得N-乙酰天冬氨酸(NAA)、肌酸复合物(Cr)、胆碱复合物(Cho)、乳酸(Lac)峰下面积及NAA、Cho、Lac与Cr的比值;将TSI和CSI拟合后获得的NAA和Lac分布伪彩图分割后与弥散加权成像(DWI)相融合,分析其匹配程度。结果相比周边正常脑组织,梗死边缘区NAA稍降低,梗死核心区NAA降低程度大于梗死边缘区,Lac则呈相反趋势;梗死周边正常脑组织存在少量Lac分布。TSI与CSI数据经拟合的代谢物分布差异无明显统计学意义(P均>0.05)。TSI与CSI分别显示33例及32例NAA伪彩图暗区分布小于DWI高信号区,Lac伪彩图高亮区明显大于DWI高信号区。结论采用TSI可在较短时间内完成采集,并获得与常规CSI基本一致的代谢物分布数据。AIS患者代谢物分布伪彩图可能与DWI高信号区不匹配。     

Thrombolytic therapy for acute ischemic stroke

Current evidence suggests that, in a small subset of acute stroke patients who can be treated within 3 hours of symptom onset, the administration of tissue plasminogen activator (tPA) confers a modest outcome benefit, but that this benefit is associated with an increased risk of intracranial hemorrhage that can be severe or fatal. The data show that tPA therapy must be limited to carefully selected patients within established protocols. Further evidence is necessary to support the widespread application of stroke thrombolysis outside research settings. Until it is clear that the benefits of this therapy outweigh the risks, thrombolytic therapy for acute stroke should be restricted to use within formal research protocols or in monitored practice protocols that adhere to the NINDS (the rt-PA Stroke Study Group trial of the National Institute of Neurological Disorders and Stroke) eligibility criteria. All data on protocol compliance and patient outcomes should be collated in a central Canadian registry for the purposes of tracking safety and efficacy. Stroke thrombolysis should be limited to centers with appropriate neurological and neuro-imaging resources that are capable of administering treatment within 3 hours. In such centres, emergency physicians should identify eligible patients, initiate low risk interventions and facilitate prompt computed tomography. Only physicians with demonstrated expertise in neuroradiology should interpret head CT scans used to determine whether to administer thrombolytic agents to stroke patients. Neurologists should be directly involved prior to the thrombolytic administration.     

Emerging therapies for acute ischemic stroke

Stroke is a major public health problem in the United States and the development of novel therapeutic strategies is an important research priority. Advances in this field are proceeding on several fronts, including the use of next-generation plasminogen activators and glycoprotein IIb/ IIIa inhibitors, refined patient selection with advanced magnetic resonance imaging sequences, endovascular approaches to thrombolysis and thrombectomy, and adjuvant use of ultrasound. There remains no proven therapy for intracerebral hemorrhage, but early results with recombinant activated factor VII look very promising. It is hoped that in the near future, physicians managing patients with acute neurological events will have a robust armamentarium of therapies to bring to bear on both ischemic and hemorrhagic vascular disease.     

Therapeutic hypothermia for acute ischemic stroke

Intravenous recombinant tissue plasminogen activator remains the only US FDA-approved treatment for acute ischemic stroke. However, the very limited time window for its administration restricts its usefulness. Furthermore, it is becoming increasingly clear that, given the numerous pathways via which cerebral ischemia causes cell death, the capacity to inhibit multiple mechanisms simultaneously may provide additive or synergistic beneficial clinical effects for stroke patients. Although no clinical trials have yet investigated the efficacy of therapeutic hypothermia in focal cerebral ischemia, its pleiotropic neuroprotective actions, positive results in preclinical studies, as well as proven enhancement of neurologic outcomes in survivors of cardiac arrest and newborns with hypoxic-ischemic encephalopathy, make this neuroprotective strategy highly promising. This review presents an overview of the potential role of hypothermia in the treatment of acute ischemic stroke and discusses ischemic cell death pathophysiology, neuroprotective mechanisms of hypothermia, methodologies employed for the induction of hypothermia, results from animal models of cerebral ischemia, and finally, currently available clinical trial data. Two valuable lessons learned thus far are that first, rapid induction of hypothermia is key and is best accomplished with a combination of ice-cold saline infusion and the use of endovascular cooling devices, and second, that shivering can be overcome with aggressive anti-shivering protocols including meperidine, buspirone and surface warming. We await the results of clinical trials to determine the utility of therapeutic hypothermia in acute ischemic stroke. If proven efficacious, hypothermia would be a welcome complement to established reperfusion therapies for ischemic stroke patients.     

Thrombolytic treatment of acute ischemic stroke

Intravenous recombinant tissue-type plasminogen activator is approved by the US Food and Drug Administration for treating acute ischemic stroke within 3 hours of onset of symptoms. Initiation of thrombolysis within 90 minutes of onset of symptoms is a treatment goal supported by current studies. Postmarketing data suggest that the risk of intracranial hemorrhage may be unacceptably high when recombinant tissue-type plasminogen activator is given to patients who would not have been eligible for enrollment in the pivotal phase 3 clinical trials. Further studies of local intra-arterial thrombolysis and improved selection of patients with advanced brain imaging are expected in the future, but the emphasis at present should be on rapid identification, evaluation, and treatment of appropriate patients with intravenous therapy.     

Developing therapy for acute ischemic stroke

Currently, the only therapy approved for the treatment of acute ischemic stroke is intravenous recombinant tissue-type plasminogen activator (rt-PA) initiated within 3 hours of symptom onset. This therapy is only used in a very small percentage of stroke patients even in experienced centers. There have been many other clinical trials of thrombolytic drugs beyond the 3-hour time window and neuroprotective drugs, but none of these trials have been positive. There are many potential explanations for these unsuccessful stroke trials and many valuable lessons have been learned. Using imagging technology such as diffusion/perfusion magnetic resonance imaging (MRI) and perfusion computerised tomography (CT) will likely enhance the enhances for success in future acute stroke trials when combined with appropriate trial design and patient selection. Developing new acute stroke therapies will be a difficult but necessary task to meet the large unmet need for this important and under treated disorder.     

卒中后的心肌缺血样损伤

目的　研究卒中后急性期心肌缺血样损伤的发生情况及对预后的影响。方法　以既往无心脏病史的卒中急性期患者为研究对象 ,发病 3d内及 15d后进行心电图 (ECG)检查 ,统计分析ECG出现缺血样改变的发生率及恢复率。以发病 3d内ECG出现缺血样改变患者为缺血组 ,ECG无明显异常者为对照组。统计分析死亡率差别。结果　蛛网膜下腔出血(SAH)后伴有ECG心肌缺血样表现的患者死亡率明显升高 (P <0 0 1)。脑梗死 (CI)或脑出血 (CH)伴有ECG心肌缺血样表现的患者死亡率无明显改变。存活患者中 ,这种ECG心肌缺血样改变短期内恢复的比率较低 ,且SAH的恢复率高于CH和CI(P<0 0 5 )。结论　急性卒中可导致心肌暂时性或长期性损伤 ,这种损伤可导致SAH患者死亡率升高     

Headache associated with acute ischemic stroke

Headache occurs frequently in acute ischemic stroke, but its frequency varies widely among different studies. We have prospectively studied headache features in patients with first-ever ischemic acute stroke and assessed the relationship between headache, stroke location, and etiology. The study included consecutive patients admitted to our Stroke Unit for a first-ever ischemic acute stroke. The study included 154 consecutive patients with ischemic stroke, and 54 of these (35.1%) had headache during stroke onset. Twelve patients (22.2%) with headache during stroke had history of headache; no patients without headache had history of headache. Headache was present in 25.8% (32/124) of the patients with anterior circulation stroke and in 73.3% (22/30) of the patients with posterior circulation stroke (p=0.001). Large artery disease was more frequent with than without headache (40.7% versus 14.0%, p=0.04). Headache was present in more than one-third of the patients with ischemic stroke. All patients with positive history for headache had headache during stroke onset. The cephalic pain was much more common among patients with infarcts in the posterior circulation than in patients in whom the anterior circulation was involved. Headache was more common when the cause of stroke was large artery disease. Received: 5 January 2001 / Accepted in revised form: 6 April 2001     

Critical care of acute ischemic stroke

Stroke is the third leading cause of death and the leading cause of disability in the United States. This article summarizes the critical care of acute ischemic stroke, including conventional and novel therapies. The article provided an overview of the initial management, diagnostic workup, treatment options, and supportive measures that need to be considered in the acute phase of ischemic stroke.     

Pharmacological treatment of acute ischemic stroke

Ischemic stroke is devastating. It is the third leading cause of death in the United States. Each year, 480,000 people fall victim to ischemic stroke, which is estimated to cost 71.8 billion dollars (Hinkle JL, Bowman L. J Neurol Nurs. 2003;35:1-8. New treatment is available. Acute ischemic stroke is no longer considered an accident resulting in damage that must simply be dealt with. Now termed a brain attack, like a heart attack it must be treated immediately. Education is key to improving outcomes. Health care professionals must be trained to recognize early signs and symptoms of stroke. The public must be educated to understand the urgency of early evaluation once symptoms of stroke occur Brown M. Clin Med. 2001; 1:60-65). Television commercials, billboards, and public health lectures can be advantageous in a campaign to educate about stroke and the need to seek help immediately when experiencing symptoms, to halt the ischemic damage Brown M. Clin Med. 2001; 1:60-65.