TY - T1的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) JF -神经学乔-神经病学SP - S43.006 LP - S43.006六世- 78 - 1补充AU -约翰·Sellner AU -阿米特·帕特尔盟Pooja Das首页san AU -布朗AU -阿克塞尔作品Y1 - 2012/04/26 UR - //www.ez-admanager.com/content/78/1_Supplement/S43.006.abstract N2 -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患者承认疑似急性脑血管事件和出现症状& lt;包含和peripheral-venous血液得到24小时到达,上午9点到10点之间每天日。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(术中,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 ER -