Abstract:Objective To observe influence of continuous lumbar cistern drainage on levels of amyloid βpeptide (Aβ) subtype (Aβ1-42) in cerebrospinal fluid and plasma in patients with diffuse axonal injury (DAI) and investigate its clinical significance. Methods Eighty-one DAI patients were enrolled and randomized into treatment group (42 cases) and control group (39 cases). Patients in control group received simple conventional therapy, while the patients in treatment group received not only conventional therapy but 14 days of continuous lumbar cistern drainage. Levels of Aβ1-42 in cerebrospinal fluid and plasma were detected by ELISA assay before therapy and at 1, 5, 9, and 14 days after therapy. Prognosis was assessed using GOS at 6 months after therapy. Results Levels of Aβ1-42 in cerebrospinal fluid and plasma showed a decrease in the first place and a gradual decrease afterwards in both groups, but a bigger and earlier drop of Aβ1-42 levels was observed in treatment group. Two groups showed significant difference of Aβ1-42 levels at day 14 (P<0.05). At 6 months after therapy, GOS score between treatment and control groups was (4.1±0.5) and (3.4 ± 0.3) points respectively (P<0.05). Conclusion Continuous lumbar cistern drainage improves the prognosis of DAI and this may relates to the decrease of Aβ1-42 levels in cerebrospinal fluid and plasma.
ZHANG Shu-bao,YIN Su-na,ZHANG Xue-guang et al. Prognosis of patients with diffuse axonal injuries following continuous lumbar cistern drainage[J]. CHINESE JOURNAL OF TRAUMA, 2013, 29(5): 446-450.
[1]Adams JH, Graham DI,Murray LS, et al. Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann Neurol, 1982, 12(6):557-563.
[10]Goldsmith W, Monson KL. The state of head injury biomechanics: past, present, and future part 2: physical experimentation. Crit Rev Biomed Eng, 2005, 33 (2):105-207.
[12]Crossgrove JS, Li GJ, Zheng W. The choroid plexus removes beta-amyloid from brain cerebrospinal fluid. Exp Biol Med (Maywood), 2005, 230(10):771-776.
[13]Bates KA, Verdile G, Li QX, et al. Clearance mechanisms of Alzheimer’s amyloid-beta peptide: implications for therapeutic design and diagnostic tests. Mol Psychiatry, 2009, 14(5):469-486.
[14]Fagan AM, Mintun MA, Mach RH, et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans. Ann Neurol, 2006, 59(3):512-519.
[15]Yan SD, Chen X, Fu J, et al. RAGE and amyloid-beta peptide neurotoxicity in Alzheimers’s disease. Nature, 1996, 382(6593):685-691.
[16]Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science, 2002, 297(5580):353-356.
[17]Wang YJ, Zhou HD, Zhou XF. Clearance of a myloid-beta in Alzheimer’s disease: progress, problems and perspectives. Drug Discov Today, 2006, 11(19-20):931-938.
[19]Lambert MP, Barlow AK, Chromy BA, et al. Diffusible, nonfibrillar ligands derived from Abeta-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA, 1998,95(11):6448-6453.
[20]Dahlgren KN, Manelli AM, Stine WB Jr, et al. Oligomeric and fibrillar species of amyloid-beta peptides differentially affect neuronal viability. J Biol Chem, 2002, 277(35):32046-32053.
[21]Walsh DM, Klyubin I, Fadeeva JV, et al. Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature, 2002, 416(6880):535-539.
[22]Haass C, Selkoe DJ. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat Rev Mol Cell Biol, 2007, 8(2):101-112.