儿童及青少年创伤后应激障碍的杏仁体磁共振波谱研究
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摘要
目的:运用磁共振波谱成像(MRS)探讨儿童及青少年创伤后应激障碍(PTSD)患者双侧杏仁体的神经生化改变。方法:共纳入38例汶川地震幸存者,包括19例PTSD患者[年龄(13.33±1.91)岁]及19例健康人作为对照[年龄(13.11±1.45)岁)]。运用3.0T磁共振仪进行双侧杏仁体单体素MRS采集,采用LC Model测定各代谢物的绝对浓度,比较其组间差异及左右侧差异,并对各代谢物浓度与PCL-C量表评分进行相关性分析。结果:与对照组比较,PTSD患者左侧杏仁体NAA及Glx浓度增高[分别为(9.402±1.033)和(16.865±2.270)mmol/kg],Cr浓度[(7.243±0.945)mmol/kg]降低;右侧杏仁体NAA及Glx浓度亦显著性增高[分别为(9.270±1.555)和(16.081±0.607)mmol/kg]。此外,对照组左侧杏仁体Cr浓度显著高于右侧,而PTSD组左右侧杏仁体Cr浓度无明显差异。PTSD组右侧Glx浓度与PCL-C评分呈显著正相关(r=0.740,P=0.036)。结论:儿童及青少年PTSD患者双侧杏仁体的神经生化均有异常改变,但左侧更明显;其中Glx的改变可能在PTSD病理生理机制中起关键作用。
Objective:This study was designed to evaluate the neuro-chemical changes in bilateral amygdalae of pediatric and adolescent post-traumatic stress disorder(PTSD) patients with MR spectroscopy(MRS).Methods:38 earthquake survivors including 19 PTSD patients with the mean age as(13.33±1.91) years,and 19 healthy controls with the mean age as(13.11±1.45) years.The severity of symptoms was assessed by the PTSD Checklist-Civilian Version(PCL-C).Single-voxel proton magnetic resonance spectroscopy of bilateral amygdalae was performed on a 3.0 Tesla MR scanner.Spectral data were processed with LC model software to measure the absolute concentrations of different metabolites.The differences of each metabolite between patients and controls as well as left and right side were evaluated.Correlation between the concentration of metabolites and PCL-C scores were also studied.Results:Compared with the controls,N-acetylaspartate(NAA) and glutamate/ glutamine(Glx) concentration in the left amygdala increased,which was(9.402±1.033) and(16.865±2.270)mmol/kg respectively,and creatine(Cr) concentration decreased(7.243±0.945)mmol/kg.Similarly,concentration of NAA and Glx was significantly increased in right amygdala,which was(9.270±1.555) and(16.081±0.607)mmol/kg respectively.In addition,creatine level of left amygdala was significantly higher than that of right amygdala in controls,while no significant difference of Cr concentration was existed in bilateral amygdale of PTSD patients.Glx level of the right amygdala in PTSD patients was found to be positively correlated with PCL-C scores(r=0.740,P=0.036).Conclusion:The neurobiochemistry of bilateral amygdalae altered in PTSD patients,while the left side was more significant.Changes of glutamatergic system might be the key factor in the pathogenesis of PTSD.
Objective:This study was designed to evaluate the neuro-chemical changes in bilateral amygdalae of pediatric and adolescent post-traumatic stress disorder(PTSD) patients with MR spectroscopy(MRS).Methods:38 earthquake survivors including 19 PTSD patients with the mean age as(13.33±1.91) years,and 19 healthy controls with the mean age as(13.11±1.45) years.The severity of symptoms was assessed by the PTSD Checklist-Civilian Version(PCL-C).Single-voxel proton magnetic resonance spectroscopy of bilateral amygdalae was performed on a 3.0 Tesla MR scanner.Spectral data were processed with LC model software to measure the absolute concentrations of different metabolites.The differences of each metabolite between patients and controls as well as left and right side were evaluated.Correlation between the concentration of metabolites and PCL-C scores were also studied.Results:Compared with the controls,N-acetylaspartate(NAA) and glutamate/ glutamine(Glx) concentration in the left amygdala increased,which was(9.402±1.033) and(16.865±2.270)mmol/kg respectively,and creatine(Cr) concentration decreased(7.243±0.945)mmol/kg.Similarly,concentration of NAA and Glx was significantly increased in right amygdala,which was(9.270±1.555) and(16.081±0.607)mmol/kg respectively.In addition,creatine level of left amygdala was significantly higher than that of right amygdala in controls,while no significant difference of Cr concentration was existed in bilateral amygdale of PTSD patients.Glx level of the right amygdala in PTSD patients was found to be positively correlated with PCL-C scores(r=0.740,P=0.036).Conclusion:The neurobiochemistry of bilateral amygdalae altered in PTSD patients,while the left side was more significant.Changes of glutamatergic system might be the key factor in the pathogenesis of PTSD.
引文
[1]Shin LM,Liberzon I.The neurocircuitry of fear,stress and anxietydisorders[J].Neuropsychopharmacology,2010,35(1):169-191.
[2]Karl A,Werner A.The use of proton magnetic resonance spec-troscopy in PTSD research-meta-analyses of findings and metho-dological review[J].Neurosci Biobehav Rev,2010,34(1):7-22.
[3]唐鹤菡,月强,陈佳,等.利用空间饱和技术提高杏仁体波谱质量[J].四川大学学报(医学版),2011,42(2):269-272.
[4]Freeman TW,Cardwell D,Karson CN,et al.In vivo proton mag-netic resonance spectroscopy of the medial temporal lobes of sub-jects with combat-related posttraumatic stress disorder[J].MagnReson Med,1998,40(1):66-71.
[5]Rauch SL,Shin LM,Phelps EA.Neurocircuitry models of postt-raumatic stress disorder and extinction:human neuroimaging re-search——past,present and future[J].Biol Psychiatry,2006,60(4):376-382.
[6]Kent JM,Rauch SL.Neurocircuitry of anxiety disorders[J].CurrPsychiatry Rep,2003,5(4):266-273.
[7]Gruber S,Frey R,Mlynarik V,et al.Quantification of metabolicdifferences in the frontal brain of depressive patients and controlsobtained by 1 H-MRS at 3T[J].Invest Radiol,2003,38(7):403-408.
[8]Schuff N,Neylan TC,Fox-Bosetti S,et al.Abnormal N-acetylas-partate in hippocampus and anterior cingulate in posttraumaticstress disorder[J].Psychiatry Res,2008,162(2):147-157.
[9]Castillo M,Kwock L,Mukherji SK.Clinical applications of protonMR spectroscopy[J].AJNR,1996,17(1):1-15.
[10]Brunetti M,Sepede G,Mingoia G,et al.Elevated response of hu-man amygdala to neutral stimuli in mild post traumatic stressdisorder:neural correlates of generalized emotional response[J].Neuroscience,2010,168(3):670-679.
[11]Gabr RW,Birkle DL,Azzaro AJ.Stimulation of the amygdala byglutamate facilitates corticotropin-releasing factor release fromthe median eminence and activation of the hypothalamic-pituita-ry-adrenal axis in stressed rats[J].Neuroendocrinology,1995,62(4):333-339.
[12]Tokarev D,Jezova D.Effect of central administration of the non-NMDA receptor antagonist DNQX on ACTH and corticosteronerelease before and during immobilization stress[J].Methods FindExp Clin Pharmacol,1997,19(5):323-328.
[13]Ziegler DR,Cullinan WE,Herman JP.Organization and regula-tion of paraventricular nucleus glutamate signaling systems:N-methyl-D-aspartate receptors[J].J Comp Neurol,2005,484(1):43-56.
[14]Joca SR,Ferreira FR,Guimaraes FS.Modulation of stress conse-quences by hippocampal monoaminergic,glutamatergic and nit-rergic neurotransmitter systems[J].Stress,2007,10(3):227-249.
[15]Rainnie DG,Bergeron R,Sajdyk TJ,et al.Corticotrophin relea-sing factor-induced synaptic plasticity in the amygdala translatesstress into emotional disorders[J].J Neurosci,2004,24(14):3471-3479.
[16]Hertzberg MA,Butterfield MI,Feldman ME,et al.A preliminarystudy of lamotrigine for the treatment of posttraumatic stressdisorder[J].Biol Psychiatry,1999,45(9):1226-1229.
[17]Horska A,Kaufmann WE,Brant LJ,et al.In vivo quantitativeproton MRSI study of brain development from childhood to ado-lescence[J].JMRI,2002,15(2):137-143.
[18]Raininko R,Mattsson P.Metabolite concentrations in supravent-ricular white matter from teenage to early old age:a short echotime 1 H magnetic resonance spectroscopy(MRS)study[J].ActaRadiologica,2010,51(3):309-315.
[19]Jayasundar R.Human brain:biochemical lateralization in normalsubjects[J].Neurol India,2002,50(3):267-271.
[20]Golden CJ,Graber B,Coffman J,et al.Structural brain deficits inschizophrenia.Identification by computed tomographic scan den-sity measurements[J].Arch Gen Psychiatry,1981,38(9):1014-1017.
[2]Karl A,Werner A.The use of proton magnetic resonance spec-troscopy in PTSD research-meta-analyses of findings and metho-dological review[J].Neurosci Biobehav Rev,2010,34(1):7-22.
[3]唐鹤菡,月强,陈佳,等.利用空间饱和技术提高杏仁体波谱质量[J].四川大学学报(医学版),2011,42(2):269-272.
[4]Freeman TW,Cardwell D,Karson CN,et al.In vivo proton mag-netic resonance spectroscopy of the medial temporal lobes of sub-jects with combat-related posttraumatic stress disorder[J].MagnReson Med,1998,40(1):66-71.
[5]Rauch SL,Shin LM,Phelps EA.Neurocircuitry models of postt-raumatic stress disorder and extinction:human neuroimaging re-search——past,present and future[J].Biol Psychiatry,2006,60(4):376-382.
[6]Kent JM,Rauch SL.Neurocircuitry of anxiety disorders[J].CurrPsychiatry Rep,2003,5(4):266-273.
[7]Gruber S,Frey R,Mlynarik V,et al.Quantification of metabolicdifferences in the frontal brain of depressive patients and controlsobtained by 1 H-MRS at 3T[J].Invest Radiol,2003,38(7):403-408.
[8]Schuff N,Neylan TC,Fox-Bosetti S,et al.Abnormal N-acetylas-partate in hippocampus and anterior cingulate in posttraumaticstress disorder[J].Psychiatry Res,2008,162(2):147-157.
[9]Castillo M,Kwock L,Mukherji SK.Clinical applications of protonMR spectroscopy[J].AJNR,1996,17(1):1-15.
[10]Brunetti M,Sepede G,Mingoia G,et al.Elevated response of hu-man amygdala to neutral stimuli in mild post traumatic stressdisorder:neural correlates of generalized emotional response[J].Neuroscience,2010,168(3):670-679.
[11]Gabr RW,Birkle DL,Azzaro AJ.Stimulation of the amygdala byglutamate facilitates corticotropin-releasing factor release fromthe median eminence and activation of the hypothalamic-pituita-ry-adrenal axis in stressed rats[J].Neuroendocrinology,1995,62(4):333-339.
[12]Tokarev D,Jezova D.Effect of central administration of the non-NMDA receptor antagonist DNQX on ACTH and corticosteronerelease before and during immobilization stress[J].Methods FindExp Clin Pharmacol,1997,19(5):323-328.
[13]Ziegler DR,Cullinan WE,Herman JP.Organization and regula-tion of paraventricular nucleus glutamate signaling systems:N-methyl-D-aspartate receptors[J].J Comp Neurol,2005,484(1):43-56.
[14]Joca SR,Ferreira FR,Guimaraes FS.Modulation of stress conse-quences by hippocampal monoaminergic,glutamatergic and nit-rergic neurotransmitter systems[J].Stress,2007,10(3):227-249.
[15]Rainnie DG,Bergeron R,Sajdyk TJ,et al.Corticotrophin relea-sing factor-induced synaptic plasticity in the amygdala translatesstress into emotional disorders[J].J Neurosci,2004,24(14):3471-3479.
[16]Hertzberg MA,Butterfield MI,Feldman ME,et al.A preliminarystudy of lamotrigine for the treatment of posttraumatic stressdisorder[J].Biol Psychiatry,1999,45(9):1226-1229.
[17]Horska A,Kaufmann WE,Brant LJ,et al.In vivo quantitativeproton MRSI study of brain development from childhood to ado-lescence[J].JMRI,2002,15(2):137-143.
[18]Raininko R,Mattsson P.Metabolite concentrations in supravent-ricular white matter from teenage to early old age:a short echotime 1 H magnetic resonance spectroscopy(MRS)study[J].ActaRadiologica,2010,51(3):309-315.
[19]Jayasundar R.Human brain:biochemical lateralization in normalsubjects[J].Neurol India,2002,50(3):267-271.
[20]Golden CJ,Graber B,Coffman J,et al.Structural brain deficits inschizophrenia.Identification by computed tomographic scan den-sity measurements[J].Arch Gen Psychiatry,1981,38(9):1014-1017.
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