期刊文献+

亚急性硬化性全脑炎的临床与病理分析(附8例报告) 被引量:3

原文传递
导出
摘要 目的探讨对亚急性硬化性全脑炎(SSPE)的早期临床征象和病理过程。方法分析8例SSPE的首发症状等临床征象,脑脊液丙种球蛋白含量,血清及脑脊液麻疹抗体滴度,脑电图和头部MRI资料;并给活检脑组织以电子显微镜扫描及麻疹病毒分离。结果患者分别以智能障碍(6例)或双眼视觉障碍(2例)为首发症状,并均于病程2月后陆续出现SSPE的典型临床经过;其血及脑脊液的麻疹抗体滴度高,脑脊液丙种球蛋白含量高;脑电图基础节律慢而不规则,伴周期性双侧对称性高波伏棘慢波;头部MRI示弥漫性脑萎缩、灰白质界线模糊及广泛分布的异常信号;电子显微镜扫描显示弥漫性亚急性或慢性脑炎,脑细胞核内嗜酸性包涵体并分离出麻疹病毒。结论SSPE多以亚急性智能障碍或双眼视觉障碍为首发症状,并可在病程2个月后出现SSPE的典型临床经过。
出处 《中国医师杂志》 CAS 2010年第3期370-371,共2页 Journal of Chinese Physician
  • 相关文献

参考文献8

  • 1Garg RK. Snbacnte sclerosing panencephalitis. Jeurol, 2008 255(12) : 1861-1871.
  • 2Zako M, Kataoka T, Ohno-Jinno A, et al. Analysis of progressive ophthalmic lesion in a patient with subacute sclerosing panencephalitis. Eur J Ophthalmol, 2008, 18( 1 ) :155-158.
  • 3刘辉,肖恩华,谭利华,吴小川,范松青.幼儿暴发性亚急性硬化性全脑炎的MRI诊断[J].中华放射学杂志,2006,40(1):60-62. 被引量:7
  • 4徐冰,王树巧,谢广中.亚急性硬化性全脑炎与麻疹免疫[J].中国计划免疫,2003,9(2):120-123. 被引量:3
  • 5Ludlow M, Duprex WP, Cosby SL, et al. Advantages of using recombinant measles viruses expressing a fluorescent reporter gene with vibratome slice technology in experimental measles neuropathogenesis. Neuropathol Appl Neurobiol, 2008, 34 (4);424- 434.
  • 6Babu RB, Biswas J. Bilateral macular retinitis as the presenting feature of subacute sclerosing panencephalitis. J Neuroophthalmol, 2007, 27(4) :288-291.
  • 7Senbil N, Aydin OF, Orer H, et al. Subacute sclerosing anencephalitis: a cause of acute vision loss. Pediatr Neurol, 2004,31 (3) :214-217.
  • 8Berker N, Batman C, Gwen A, et al. Optical atrophy and macular degeneration as initial presentations of subacute sclerosing panencephalitis. Ophthal Mol, 2004, 138(5) :879-881.

二级参考文献40

  • 1戴斌.亚急性硬化性全脑炎一例报告[J].中华儿科杂志,1981,19(4):214-214.
  • 2张宗昊.亚急性硬化性全脑炎(附二例报告)[J].中华医学杂志,1982,62(4):236-236.
  • 3Park S Y, Khol S. Subacute sclerosing panencephalitis in an identical twin[J]. Pediatrics, 1999, 104(6) : 1390 - 1394.
  • 4Lackmarm G M, Hannen M, Madjlessi F, et al.Rapid progressive subacote sclerosing panencephalitis in a 2 - year - old child with congenital athyreosis[ J ]. Clin Infect Dis, 2000, 31( 1 ) : 196 - 199.
  • 5Gascon G G. Subacute sclerosing panencephalitis[ J ]. Semin Pediatr Neurol, 1996, 3 (4) : 260 - 269.
  • 6Anlar B, Kose G, Gurer Y, et al.Changing epldemiological features of subacute sclerosing panencephalitis [ J ]. Infection, 2001, 29 ( 4 ) : 192 - 195.
  • 7Hall W W, Choppin P W. Mealses - virus proteins in the brain tissue of patients with subacute sclerosing panencephalitis: absence of the M protein[J]. N Engl J Med, 1981, 304(19):1152 - 1155.
  • 8Patterson J B, Cornu T I, Redwine J, et al. Evidence that the hypermutated M protein of a suhacute sclerosing panencephalitis measles virus actively contributes to the chronic progressive CNS disease [J]. Virology, 2001,291(2) :215 - 225.
  • 9Cattaneo R, Rose J K.Cell fusion by the envelope glycoproteins of persistent measles viruses, which caused lethal human brain disease[J] .J Virol, 1993, 67(3) : 1493 - 1502.
  • 10Schmid A, Spielhofer P, Cattaneo R, et al, Subacute sclerosing panencephalitis is typically characterized by alterations in the fusion protein cytoplasmic domain of the persisting measles virus[J]. Virology, 1992, 188(2) :910 - 915.

共引文献7

同被引文献68

引证文献3

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部