RT期刊文章SR电子T1血清生物标志物在缺血性中风早期:Hyperacute检测神经丝重链(S43.006)摩根富林明神经病学神经学乔FD Lippincott Williams &威尔金斯SP S43.006 OP S43.006 VO 78是1补充A1约翰Sellner A1 Amit Patel A1 P首页ooja Dassan A1布朗A1阿克塞尔作品年2012 UL //www.ez-admanager.com/content/78/1_Supplement/S43.006.abstract AB目的:评估脑损伤的早期检测能力三个血清生物标志物在急性中风。背景生物标志物能够决定不可逆neuro-axonal受伤的程度关键中风的早期阶段是必不可少的检查和脑血管疾病的预后。在这方面,血清GFAP、S100B和神经丝重链(NfH)已经被提议作为潜在的脑损伤的标志。设计/方法:22患者承认一个疑似急性脑血管事件和出现症状包括< 24小时和peripheral-venous血液得到上午9点到10点之间到达和日常日时间。16个病人放射缺血的证据和两个脑内出血。22名患者的样本没有神经系统疾病作为控制。GFAP、S100B和NfHSMI35 ELISA测定。结果:神经影像学证实中风患者增加了NfHSMI35水平已经在6小时内出现症状(p < 0.0001)。的增加持续6天课程,达到4。S100B的增加,然而,被推迟,开始3天,在6天中风后达到顶峰。差异没有统计学意义。 GFAP remained below the detection limit in all stroke patients over the entire time course.Conclusions: This study found an extracranial increase of NfHSMI35 in venous blood, a specific marker for axonal injury, degeneration and neuronal loss, already present in the very early course of acute stroke. The data indicate that significant in-vivo information on the pathophysiology of stroke may be obtained by the determination of NfHSMI35. Further studies are required to evaluate whether NfHSMI35 in hyperacute stroke reflects the extent of focal ischaemic injury seen on neuroimaging or is a consequence of more diffuse neuro-axonal damage.Supported by: JS is supported by the Department of Neurology, Technische Universität München and a scientific fellowship from the EFNS.Disclosure: Dr. Sellner has received personal compensation for activities with Novartis, Merck-Serono, and Sanofi-Aventis. Dr. Patel has nothing to disclose. Dr. Dassan has nothing to disclose. Dr. Brown has received research support from Reta Lila Weston Trust for Medical Research. Dr. Petzold has received (royalty or license fee or contractual rights) payments from VUMC.Dr. Petzold has received research support from The Dutch MS Research Foundation.Thursday, April 26 2012, 13:00 pm-14:45 pm