首页> 中文期刊> 《中国实用神经疾病杂志》 >氟西汀对脑卒中后抑郁患者海马磁共振氢质子波谱影响的研究

氟西汀对脑卒中后抑郁患者海马磁共振氢质子波谱影响的研究

         

摘要

目的 探讨氟西汀对脑卒中后抑郁患者海马氢质子磁共振波谱(1H-MRS)影响的特点.方法 以60例脑卒中后抑郁患者为研究组,研究组给予氟西汀抗抑郁治疗8周,以62名脑卒中患者为对照组.采用1H-MRS检测脑卒中后抑郁患者(研究组)治疗前后及脑卒中患者(对照组)双侧海马的N-乙酰基天门冬氨酸(NAA)、胆碱复合物(Cho)与肌酸复合物(Cr),以NAA/Cr值和Cho/Cr值进行统计分析.结果 研究组治疗前后左右侧海马NAA/Cr值(分别为1.22±0.31和1.19±0.42,1.46±0.35和1.43±0.41)均低于对照组(分别为1.69±0.33和1.66±0.47),差异有统计学意义(均P<0.05);研究组治疗前后左右侧海马Cho/Cr值(分别为1.58±0.39和1.59±0.46,1.55±0.43和1.53±0.42)高于对照组(分别为1.26±0.42和1.31±0.47),差异有统计学意义(均P<0.05);研究组治疗后左右侧海马NAA/Cr值(分别为1.46±0.35和1.43±0.41)均高于治疗前(分别为1.22±0.31和1.19±0.42),差异有统计学意义(均P<0.05).结论 氟西汀可能改变脑卒中后抑郁患者海马神经元的代谢异常.%Objective To explore the features of fluoxetine''s effect on hydrogen proton magnetic resonance spectroscopy(1H-MRS) of hippocampus in patients with post-stroke depression.Methods A total of 60 cases with post-stroke depression were collected as research group and were given fluoxetine for 8 weeks,and 62 cases with stroke were selected as control group.The levels of N-asparaginic acid (NAA),choline compound (Cho) and creatine compound (Cr) were detected by using 1H-MRS and then the ratios of NAA to Cr (NAA/Cr) and of Cho to Cr (Cho/Cr) were calculated.Results In left and right hippocampus before and after treatment,the NAA/Cr ratios in the research group (1.22±0.31 and 1.19±0.42,1.46±0.35 and 1.43±0.41) were higher than those in the control group (1.69±0.33 and 1.66±0.47),and the differences were significant (all P<0.05).Similarly,the Cho/Cr ratios of left and right hippocampus before and after treatment in the research group (1.58±0.39 and 1.59±0.46,1.55±0.43 and 1.53±0.42) showed higher ratio than those in the control group (1.26±0.42 and 1.31±0.47),and the differences were significant (all P<0.05).Additionally,in the research group,the NAA/Cr ratios in bilateral hippocampus after treatment (1.46±0.35 and 1.43±0.41) were higher than those before treatment (1.22±0.31 and 1.19±0.42),and the differences were significant (all P<0.05).Conclusion Fluoxetine may change the abnormal metabolism of bilateral hippocampal neurons in post-stroke depression patients.

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