Therapeutic hypothermia in acute ischemic stroke

Increased body temperatures are common in the acute phase of stroke. Experimental and clinical studies have suggested that increased body temperatures are related to poor outcome. In animal studies of focal cerebral ischemia, early hypothermia consistently reduced infarct volume. Based on these findings, several Phase II clinical trials have been performed to study physical methods to reduce body temperature in patients with acute stroke. The feasibility and safety of these methods have not yet been established with sufficient certainty. Pharmacological lowering of body temperature may be an attractive alternative approach. In guidelines for the treatment of acute stroke, antipyretics are generally recommended to reduce fever, although their effect on functional outcome is unknown. There is currently no evidence from randomized trials to support routine use of physical or pharmacological cooling in acute stroke. Large randomized clinical trials are needed to study the effect of both physical and medical cooling on functional outcome after stroke.     

Therapeutic hypothermia for acute stroke

Experimental evidence and clinical experience show that hypothermia protects the brain from damage during ischaemia. There is a growing hope that the prevention of fever in stroke will improve outcome and that hypothermia may be a therapeutic option for the treatment of stroke. Body temperature is directly related to stroke severity and outcome, and fever after stroke is associated with substantial increases in morbidity and mortality. Normalisation of temperature in acute stroke by antipyretics is generally recommended, although there is no direct evidence to support this treatment. Despite its obvious therapeutic potential, hypothermia as a form of neuroprotection for stroke has been investigated in only a few very small studies. Therapeutic hypothermia is feasible in acute stroke but owing to serious side-effects--such as hypotension, cardiac arrhythmia, and pneumonia--it is still thought of as experimental, and evidence of efficacy from clinical trials is needed.     

The role of ticagrelor in acute ischaemic stroke and high-risk TIA management

Journal of Neurology -     

The role of hyperglycemia in acute stroke

BACKGROUND: Ischemic stroke is a leading cause of death and long-term disability, and hyperglycemia is believed to aggravate cerebral ischemia. OBJECTIVES: To review animal and human studies on the relationship between hyperglycemia and brain ischemia that elucidate some of the mechanisms for the deleterious effect of hyperglycemia. To discuss present and future clinical recommendations for glucose control. METHODS: Computerized data sources and published indexes and articles from 1976 through 2000 were searched for human studies that evaluated the association between stroke and hyperglycemia, and studies focused on experimental models of hyperglycemic animals with focal and global brain ischemia. RESULTS: Most human studies have shown that in acute stroke, admission hyperglycemia in patients with or without diabetes is associated with a worse clinical outcome than in patients without hyperglycemia. This association is more consistent in the nonlacunar type of stroke. Animal studies support these findings by showing both in global and in focal postischemic models that hyperglycemia exaggerates the following damaging processes: intracellular acidosis, accumulation of extracellular glutamate, brain edema formation, blood-brain barrier disruption, and tendency for hemorrhagic transformation. Insulin treatment of hyperglycemic animals was found to have a beneficial effect in focal and global brain ischemia, which may be mediated by the glucose-reduction effect or by a direct neuroprotection. CONCLUSIONS: Most studies show the deleterious effect of early hyperglycemia, especially in patients with nonlacunar focal or global ischemia. Clinical trials of intensive insulin treatment are needed. Meanwhile simple measures to avoid excessive hyperglycemia are recommended.     

The role of MR angiography in the evaluation of acute stroke.

Magnetic resonance angiography is an essential component of the acute stroke MR imaging work-up. Defining the location and extent of vascular compromise greatly aids in the selection of the appropriate therapy. In this article, the most common MR angiography manifestations of acute stroke are illustrated to emphasize the role of MR angiography in the evaluation of patients presenting with symptoms of acute cerebral ischemia.     

中国脑卒中急性期和恢复期管理现状

当前,脑卒中已经成为我国第1位病残性以及第2位病死性疾病。根据卫生部的资料统计显示,我国每年脑卒中新发病例有250万例,而每年死于脑卒中的患者多达150余万例。在幸存下来的脑卒中患者中,大约有四分之三的患者不同程度地丧失了劳动能力,其中重度病残者占到40%。此外,由于脑卒中治疗费用很高,给很多患者造成了沉重的经济负担。近年来,随着中国人口老龄化和经济快     

Perfusion-CT guided acute stroke management.

The easily accessible and available PCT reliably identifies reversible and irreversible ischaemia in acute stroke patients. These knowledge will allow treatment strategies to become more appropriate and individualized. Patients with significant penumbra may be candidates for treatment with dangerous or costly medication, and patients without may not, independently of duration of stroke symptoms. Furthermore, PCT also has the scientific potential to identify appropriate patients for therapeutic trials. Finally, salvage of PCT-defined penumbra could be used as a surrogate marker for effectiveness of interventions.     

The role of hyperglycemia in acute ischemic stroke

Stroke remains a leading cause of death and long-term disability in the developed world. Reperfusion and anti-thrombotic therapies are of limited benefit for the majority of patients following acute ischemic stroke, and increasing interest has focused on therapeutic approaches that seek to modulate infarct evolution. Animal and human studies have linked hyperglycemia in the acute phase of ischemic stroke to worse clinical outcomes regardless of the presence of pre-existing diabetes mellitus. Experimental data suggest that elevated blood glucose may directly contribute to infarct expansion through a number of maladaptive metabolic pathways, and that treatment with insulin may attenuate these adverse effects. In this review, we analyze the relationship between elevated serum glucose and acute cerebrovascular ischemia, and critically appraise the potential of a clinical strategy that targets euglycemia in all acute stroke patients.     

低温治疗急性缺血性卒中的研究进展

脑血管病作为神经系统的常见病及多发病,是目前导致人类死亡的三大主要疾病之一,也是第一大致残性疾病.缺血性卒中是脑血管病最常见的类型,约占脑血管病的70％.在现有的诸多治疗手段中,低温是有效的神经保护措施.自20世纪50年代低温的神经保护作用被发现以来,其已被提出用于外伤性脑损伤、卒中、心脏停搏性脑病、新生儿缺血缺氧性脑病、肝性脑病、脊髓损伤及动脉瘤手术等多个领域.本文根据近年来文献报道,就低温在急性缺血性卒中治疗中的研究进展进行综述,以期为开展低温的临床应用提供依据.     

The neuroprotective role of erythropoietin in the management of acute ischaemic stroke: from bench to bedside

Recombinant human erythropoietin was produced soon after the discovery of the erythropoietin gene in 1985 and since then, it is used in various clinical conditions such as chronic renal failure. Moreover, experimental studies have shown that erythropoietin exerts neuroprotective action as well. Recently, a clinical trial yielded promising results concerning the use of erythropoietin in stroke management. In this review, we summarize the main data which suggest that recombinant human erythropoietin and its analogues may indeed have a role in stroke treatment.     

脑卒中早期康复

国内外的脑卒中康复指南均推荐脑卒中后应尽早进行康复训练,但是尽早康复的时机、强度以及包含的项目尚不明确。脑卒中急性期患者病情稳定后48 h内应召开初次康复评价会,根据患者整体评估和功能障碍评估的结果制定个体化、全面的康复方案和康复目标,并初步判断脑卒中的康复预后。脑卒中患者早期宜进行运动康复、吞咽功能康复及言语功能康复。如康复对象为重症脑卒中患者、大于75岁的老年卒中患者和儿童卒中患者,更需注重个体化的评估及康复方案。     

Thermoregulatory vasococonstriction and shivering impede therapeutic hypothermia in acute ischemic stroke patients.

Objectives. We tested the hypothesis that vasoconstriction and shivering thresholds are sufficiently reduced by acute stroke to permit induction of therapeutic hypothermia without additional pharmacological inhibition of thermoregulatory control. Methods. We studied eight patients 2 +/- 1 days after ischemic stroke. Forced-air cutaneous cooling was administered until the patients shivered continuously or reached a tympanic membrane (ie, core) temperature of 34 degrees C. The tympanic membrane temperatures triggering vasoconstriction and shivering identified the thresholds for each response. Results. Patients had a mean age of 68 +/- 8 years and a mean National Institutes of Health Stroke Scale (NIHSS) score of 5. No patient reached the target core temperature of 34 degrees C. Vasoconstriction and shivering thresholds were 37.1 +/- 0.4 degrees C and 36.6 +/- 0.4 degrees C, respectively. Conclusions. Vasoconstriction and shivering were initiated at roughly normal temperatures in ischemic stroke patients, and these thermoregulatory responses prevented induction of therapeutic hypothermia. Pharmacological reduction of the vasoconstriction and shivering thresholds will be required if therapeutic hypothermia for stroke patients is to be induced easily by surface cooling.     

The emerging role of epigenetics in stroke: III. Neural stem cell biology and regenerative medicine

The transplantation of exogenous stem cells and the activation of endogenous neural stem and progenitor cells (NSPCs) are promising treatments for stroke. These cells can modulate intrinsic responses to ischemic injury and may even integrate directly into damaged neural networks. However, the neuroprotective and neural regenerative effects that can be mediated by these cells are limited and may even be deleterious. Epigenetic reprogramming represents a novel strategy for enhancing the intrinsic potential of the brain to protect and repair itself by modulating pathologic neural gene expression and promoting the recapitulation of seminal neural developmental processes. In fact, recent evidence suggests that emerging epigenetic mechanisms are critical for orchestrating nearly every aspect of neural development and homeostasis, including brain patterning, neural stem cell maintenance, neurogenesis and gliogenesis, neural subtype specification, and synaptic and neural network connectivity and plasticity. In this review, we survey the therapeutic potential of exogenous stem cells and endogenous NSPCs and highlight innovative technological approaches for designing, developing, and delivering epigenetic therapies for targeted reprogramming of endogenous pools of NSPCs, neural cells at risk, and dysfunctional neural networks to rescue and restore neurologic function in the ischemic brain.