摘要
第一部分梗塞后抑郁症(PSD)的脑形态学研究
目的通过测量梗塞后抑郁(PSD)组、梗塞非抑郁组(CONT)及正常志愿者(NORM)组3组受试者的双侧海马及杏仁核大小以探讨PSD的脑形态学基础，并分析PSD患者梗塞灶部位与抑郁症的关系。
方法研究11例梗塞后抑郁症(PSD)患者及13例脑梗塞无抑郁症(CONT)患者和15例健康志愿(NORM)者，运用容积分析软件测量两侧海马及杏仁核体积。
结果1．各组均显示海马及杏仁核体积左侧＜右侧，其中PSD组与NORM组两侧海马及杏仁核体积差异有显著性，左侧海马：右侧海马(PSD组：t=-3，P=0．013；NORM组：t=-7．46，P=0．000)，左侧杏仁核：右侧杏仁核(PSD组：t=-5．04，P=0．001；NORM组：t=-3．28，P=0．005)，而CONT组两侧海马及杏仁核体积差异没有显著性；2．PSD组中两侧海马及杏仁核体积均明显＜CONT组(海马左右：P=0．001，0．040；杏仁核左右：P=0．000，0．000)，PSD组右侧海马体积明显＜NORM组(P=0．034)；CONT组双侧杏仁核体积均明显＞NORM组(P=0．000，0．000)；3．PSD患者双侧海马及杏仁核体积缩小与HAMD抑郁量表评分均缺乏相关性(P＞0．05)；4．PSD、CONT、NORM 3组杏仁核体积的偏侧化指数(LI)比较有统计学差异(p=0．04)，主要是PSD组与CONT组统计学差异较明显；5．梗塞灶位于额颞顶叶皮质区和脑干及小脑时PSD组与CONT组有显著统计学差异，PSD组双侧梗塞灶部位与额极最短距离均小于CONT组，但无明显统计学差异；6．从相关系数大小来看，各指标与PSD相关性从大到小顺序是脑干及小脑＞左侧杏仁核＞右侧杏仁核＞额颞顶叶皮质区＞左侧海马＞右侧海马＞枕叶皮质区＞左额极距离＞后部＞右额极距离＞左额叶＞基底核区＞海马杏仁核＞前部＞放射冠区＞右额叶。7．同时建立了回代效果好的判别方程。
结论海马及杏仁核体积异常可能构成梗塞后抑郁症的神经生物学基础，脑干、小脑、额颞顶叶皮质区等部位的脑梗塞与双侧杏仁核、海马体积与PSD具有高相关性，说明边缘系统和脑干、小脑、额颞顶叶皮质区梗塞在抑郁症的发病机理中起着重要作用。
第二部分梗塞后抑郁症(PSD)的功能性磁共振成像研究
目的采用功能性磁共振方法研究梗塞后抑郁症(PSD)患者对不同性质情绪图片的差异脑激活反应，以探讨PSD患者的脑活动特征。
方法对11名梗塞后抑郁症(PSD)患者、13例脑梗塞无抑郁症(CONT)患者和15例健康志愿(NORM)者进行国际情绪图片系统中中性-正性-负性三组图片刺激的脑功能磁共振成像(fMRI)扫描，任务为组块设计，用神经功能影像分析(AFNI)软件处理影像数据。
结果1．PSD组、CONT组及NORM组观察中性-正性-负性情绪图片时激活脑区主要有额叶皮层-皮层下网状系统、基底节区(丘脑、苍白球、尾状核)和边缘系统(海马、海马旁回、杏仁核)、岛叶、颞叶、枕叶、脑干及小脑半球，其中负性图片激活脑区面积大于正性图片。2．PSD组组内比较：正性—中性有显著差异的负性激活脑区有双侧额上、中、下回、中央前回、顶上小叶、楔前叶、角回、扣带回压部、岛叶、丘脑、豆状核、海马、海马旁回、颞上、中回、枕叶视皮质区、脑桥、中脑及小脑半球，右侧杏仁核。正性激活脑区有双侧枕叶；负性—中性有显著差异的负性激活脑区有双侧额上、中回、中央前回、楔前叶、角回、缘上回、扣带回前部及压部、胼胝体、岛叶、丘脑、尾状核、豆状核、海马旁回、海马、枕叶视皮质区、脑桥、中脑及小脑半球。正性激活脑区有左侧杏仁核、背侧丘脑及岛叶，双侧枕叶；负性—正性有显著差异的负性激活脑区有双侧额上、中回、豆状核、胼胝体、扣带回前部，左侧岛叶，右侧尾状核。正性激活脑区有双侧额上、中回、中央前回、楔前叶、扣带回压部、岛叶、丘脑、尾状核、豆状核、杏仁核、枕叶视皮质区及小脑半球。3．PSD组减NORM组组间比较：识别中性图像有显着差异的负性激活脑区有双侧顶上小叶、扣带回及胼胝体压部，左额中回、右海马旁回、海马、丘脑、右缘上回。正性激活脑区有右楔叶、枕叶视皮质区，左侧小脑半球。识别正性图像有显着差异的负性激活脑区有双侧海马旁回、海马、背侧丘脑以及顶上小叶、楔前叶、颞中、下回、中脑及小脑半球，右侧额中、下回、豆状核、岛叶。正性激活脑区有双侧小脑半球、枕叶视皮质区及右侧顶叶。识别负性图像有显着差异的激活脑区有双侧海马旁回、丘脑、楔叶、枕叶视皮质区及小脑半球，右侧海马、杏仁核、颞中、下回及顶叶。负性激活脑区有左侧额中、下回、顶上小叶，右顶下小叶。4．PSD组减CONT组组间比较：识别中性图像有显着差异的正性激活脑区有双侧颞上回、颞中回、枕叶视皮质区，左侧额中回、额下回、豆状核、岛叶，右侧海马旁回、海马、顶上小叶。负性激活脑区有左侧额上、中回；识别正性图像有显着差异的正性激活脑区有双侧海马旁回(右侧明显)、额下回、楔叶、颞上、中、下回、梭状回、扣带回压部、枕叶视皮质区，右顶上小叶。负性激活脑区有左侧额上、中回；识别负性图像有显着差异的激活脑区有右海马、海马旁回、顶上小叶，左颞中回、颞下回，正性激活脑区有枕叶视皮质区。
结论PSD与边缘系统(海马、海马旁回、杏仁核)以及额中回、扣带回、丘脑、岛叶、脑干及小脑半球等有密切关系，上述脑区的损害涉及以边缘系统-皮层-纹状体-苍白球-丘脑神经环路为主的多条神经环路的结构和功能异常，可能参与了PSD的病理生理机制。
第三部分梗塞后抑郁症(PSD)的脑白质完整性研究——扩散张量成像(DTI)及其方法学研究
第一节梗塞后抑郁症(PSD)的磁共振扩散张量成像(DTI)研究
目的采用磁共振扩散张量成像(DTI)技术研究梗塞后抑郁症(PSD)的脑白质FA值改变及其意义。
方法采用DTI感兴趣区(ROI)法和基于体素的分析方法(voxelbased measure，VBM)对11名梗塞后抑郁症(PSD)患者、13例脑梗塞无抑郁症(CONT)患者和15例健康志愿(NORM)者进行各部位脑白质FA值测量及脑激活功能区的比较，研究PSD患者的DTI表现特点。
结果1．PSD组与NORM组FA值有显著统计学差异(P＜0．05)的部位有双侧额叶、顶叶、左侧内囊前、后肢、右侧枕叶。PSD组与CONT组FA值有显著统计学差异(P＜0．05)的部位有左侧额叶、顶叶、左侧内囊前、后肢，扣带回前部。CONT组与NORM组FA值有显著统计学差异(P＜0．05)的部位仅右侧丘脑。2．PSD组一CONT组和PSD组—NORM组顶叶及内囊前肢2个部位FA值的偏侧化指数(LI)比较统计学差异较明显(顶叶Pp-c=0．006、Pp-n=0．032；内囊前肢Pp-c=0．014、Pp-n=0．001)。其余部位偏侧化指数(LI)比较无统计学差异。3、PSD组—NORM组FA值有显著差异的激活脑区有双侧额上、中回、顶叶、扣带回前部及体部、胼胝体前部及压部、岛叶、丘脑、豆状核、颞叶、枕叶及小脑半球。以胼胝体、扣带回明显。PSD组—CONT组FA值的有显著差异的激活脑区有双侧额顶叶内侧及扣带回体部交界区，右侧颞叶，左侧枕叶。以双侧额顶叶近中线处及扣带回体部交界区稍明显。CONT组—NORM组FA值有显著差异的激活脑区仅有双侧侧脑室前后角周围少许白质(额叶、顶叶)、岛叶、胼胝体前部、少许颞叶。4．非线性标准化图像要明显比线性标准化图像配伍对位更加准确。
结论PSD组与CONT组、NORM组FA值差异显著的部位主要有左侧额叶、顶叶，左侧内囊前、后肢，扣带回前部及胼胝体、扣带回及额顶叶近中线的脑回，提示这几个部位可能与脑梗塞患者好发PSD有关。DTI为我们活体精确评价PSD脑白质细微结构改变提供了一个较好的平台，从而有望为临床预测、治疗及评估PSD疗效提供新的方法和思路。
第二节磁共振扩散张量成像(DTI)方法学研究——纤维追踪法对脑白质老化的研究初探(90例定量DTI分析)
目的采用DTI纤维追踪法定量比较不同年龄组正常自愿者椎体束从大脑脚到中央前回部分(PRPT)FA值的差别及其意义。
方法将90例正常志愿者(20—83岁)按年龄分为6组进行基于纤维追踪的定量DTI研究，图像标准化后分析各组PRPT的FA值与年龄组老化的关系。
结果各年龄组双侧PRPT的FA值分布相似，最低点在放射冠处，最高峰为内囊后肢；各段FA值随年龄增长呈下降趋势，表明这些部位的纤维随年龄增长发生了老化，其中以额叶老化最为明显；并发现额叶及大脑脚白质老化过程中存在突然变化(P＜0．0001，p=0．0068)。
结论DTI可以作为评价脑组织细微结构变化和老化过程的敏感工具；额叶及大脑脚白质老化过程中存在突变，是否脑生理上老化的标志?，有待进一步研究。
PartⅠThe study the characteristics of brain morphology of patientswith post-stroke depression
Objective To investigate the volume change of the amygdala and hippocampus inpatients with post-stroke depression(PSD) and analyze the relationship of PSD and anatomyposition of infarct lesion using MR imaging.
Methods Quantitative MRI about volumes of the amygdala and hippocampus wasstudied in 11 patients with post-stroke depression and compared with 13 stroke patientswithout depression(CONT) and 15 age-matched controls(NORM).
Results 1.PSD group and NORM group exhisited similar significant hippocampusand amygdala asymmetry(left smaller than right).2.The volume of the bilateralhippocampus and amygdala in PSD group was significantly smaller than that in CONTgroup (P＜0.05).The volume of right hippocampus in PSD group was smaller than that inNORM group(P=0.034);3.There was no correlation between the hippocampus andamygdala volume abnormalities and the score of HAMD in PSD patients (P＞0.05);4.Thedifferences of Laterality Index(LI) of amygdala volume among PSD group、CONT groupand NORM group were statistically difference (p = 0.04),especially in PSD-CONT group.;
5.PSD group and NORM group has a significant statistical difference when infarct lesionswere located in frontal-temporal-parietal cortex and the brain stem and cerebellum.The shortest distance between prefrontal cortex and lesions in PSD group is shorter than thatin CONT group,but no significant statistical difference;6.The size of the correlationcoefficient between all targets and PSD are the brain stem and cerebellum＞the size of leftamygdala＞the size of right amygdala＞frontal-temporal-parietal cortex＞the size of lefthippocampus＞the size of right hippocampus＞occipital cortex＞distance between leftprefrontal cortex and lesion＞posterior cerebral＞distance between right prefrontal cortexand lesion＞left frontal lobe＞basal ganglia area＞hippocampus and amygdale area＞anterior cerebral＞corona radiata district＞right frontal lobe;7.A good discriminantequation was established.
Conclusion Cerebral infarction in brainstem,cerebellum,frontal- temporal-parietalcortex and the volume of amygdale and hippocampus shows well correlation with the PSD,These findings support the hypothesis that the hippocampus and amygdalawithin limbic system-cortical networks may play a crucial role in the pathogenesis ofpost-stroke depression.
PartⅡThe study of brain functional magnetic resonance imaging onpost-stroke depression
Objective To explore the characteristics of brain activity in patients with post-strokedepression (PSD) by probing the differences of neural activation associated with reactivityto different affective stimuli pictures using functional MR imaging (fMRI).
Methods Neural responses to neutral,positive,negative emotional pictures (fromInternational Affective Pictures System,IAPS) stimuli based on block-design weremeasured by functional magnetic resonance imaging(fMRI) in 11 patients with post-strokedepression PSD、13 stroke patients without depression(CONT) and 15 age-matched healthy controls(NORM).the fMRI data were analyzed by using Analysis of FunctionalNeuroimages (AFNI) software.
Results 1.Observing the neutral,positive,negative emotional pictures,All patientsin PSD group、CONT group and NORM group showed mainly activated areas using fMRIinclude the prefrontal cortex - subcortical reticular system、basal ganglia (thalamus,globuspallidus,caudate nucleus) and limbic system (hippocampus,parahippocampal gyrus,amygdale)、insula、temporal lobe、occipital lobe、brain stem and cerebellum.2.PSDgroup Comparison:Positive - neutral showed mainly activated areas include bilateralsuper-,mid- and infer- frontal gyrus,precentral gyrus,superior parietal lobule,precuneus,angular gyrus,splenium cingulate gyrus,insula,thalamus,lentiform nucleus,hippocampus,parahippocampal gyrus,super-,mid- temporal gyrus,occipital visual cortex,pons,midbrain,cerebellar hemispheres,right amygdala.(negative) and bilateral occipitallobe(positive);Negative-neutral showed mainly activated areas include bilateral super-,mid- frontal gyrus,precentral gyrus,superior parietal lobule,precuneus,angular gyrus,,supramarginal gyrus,cingulate gyrus,corpus callosum,insula,thalamus,caudate nucleus,lentiform nucleus,hippocampus,parahippocampal gyrus,occipital visual cortex,pons,midbrain,cerebellar hemisphere.(negative) and left amygdala,dorsal thalamus and insula,bilateral occipital lobe(positive);Negative-positive showed mainly activated areas includebilateral super-,mid- frontal gyrus,lentiform nucleus,corpus caliosum,anterior cingulategyrus,left insula,right caudate nucleus(negative) and bilateral super-,mid- frontal gyrus,precentral gyrus,precuneus,splenium cingulate gyrus,insula,thalamus,caudate nucleus,lentiform nucleus,amygdala,occipital visual cortex and cerebellum(positive).3.PSD-NORM group inter-group comparison:Identify neutral picture showed mainly activatedareas include bilateral superior parietal lobule,cingulate gyrus,corpus callosum,leftmid-frontel gyrus,right parahippo- campal gyrus,hippocampus,thalamus,rightsupramarginal gyrus(negative) and right cuneus,occipital visual cortex,left cerebellarhemisphere(positive).;Identify positive picture showed mainly activated areas include bilateral parahippocampal gyrus,hippocampus,dorsal thalamus,superior parietal lobule,precuneus,,mid-infer-temporal gyrus,midbrain,cerebellar hemisphere,right mid-infer-frontel gyrus,,lentiform nucleus,insular(negative) and bilateral cerebellar hemisphere,occipital visual cortex and right parietal lobe(positive).;Identify negative picture showedmainly activated areas include bilateral parahippocampal gyrus,thalamus,cuneus,occipitalvisual cortex and cerebellar hemisphere,right hippocampus,amygdala,temporal,parietallobe(positive) and left mid-infer- frontal gyrus,superior parietal lobule,right inferiorparietal lobule.(negative).4.PSD-CONT group inter-group comparison:Identify neutralpicture showed mainly activated areas include bilateral super-mid- temporal gyrus,occipital visual cortex,left mid-infer- frontal gyrus,lentiform nucleus,insula,righthippocampaus,parahippocampal gyrus,superior parietal lobule(positive) and leftsuper-mid- frontal gyrus,(negative);Identify positive picture showed mainly activatedareas include bilateral parahippocampal gyrus(right obviously),inferior frontal gyrus,cuneus,super-mid-infer- temporal gyrus,fusiform gyrus,splenium cingulate gyrus,occipital visual cortex,right superior parietal iobule,(positive) and left mid-infer- frontelgyrus(negative);Identify negative picture showed mainly activated areas include righthippocampus,parahippocampal gyrus,superior parietal lobule,left mid-infer- temporalgyrus (negative) and occipital visual cortex (positive).
Conclusion Patients with PSD presented an close relationship with limbic system(hippocampus、parahippocampal gyrus、amygdala)、middle frontal gyrus、superiorparietal lobule、cingulate gyrus、the right dorsal thalamus、insula、the brain stem andcerebellar hemisphere,which may be involved in the mechanism of pathophysiology inPSD by demaging the structure and function of multiple neural loops,primarily in thelimbic system - cortex - the striatum - the globus pallidus - thalamus neural loop.
PartⅢThe research of the integrity of brain white matter in post-stroke depression(PSD) Diffusion tensor imaging (DTI) and its methods
Section 1 The study of magnetic resonance diffusion tensor imaging(DTI) on post-stroke depression(PSD)
Objective To investigate the FA value changes in brain white matter of patients withpost-stroke depression (PSD) using magnetic resonance diffusion tensor imaging (DTI).
Methods Diffusion tensor MR imaging were performed in 11 patients withpost-stroke depression (PSD)、13 stroke patients without depression(CONT) and 15age-matched healthy controls(NORM).The appearances of DTI in patients with PSD wereanalyzed by comparing the FA values of brain white matter and brain activation areasamong three groups based on regions of interest (ROI) methods and voxel-based measuremethods (VBM).
Results 1.The areas of FA values having statistically significant differences (P＜0.05)included both parts of the frontal lobe、parietal lobe、left internal capsule、right occipitallobe in PSD-NORM group,left frontal lobe、left parietal lobe、left internal capsule、theanterior part of cingulate gyrus in PSD-CONT group and only right thalamus inCONT-NORM group.2.The areas of the Laterality Index (LI) of FA values havingstatistically significant differences (P＜0.05) included parietal lobe and internal capsule inPSD-CONT Group and PSD-NORM group (parietal Pp-c = 0.006,Pp-n = 0.032;internalcapsule forelimb Pp-c = 0.014,Pp-n = 0.001).The remaining parts of unilateral index (LI)showed no statistical difference.3.The activated cerebral regions having statisticallysignificant differences included both parts of superior-middle frontal gyrus、parietal lobe、cingulate gyrus、corpus callosum、insula、thalamus、lenticularnucleus、temporal lobe、occipital lobe and cerebellum in PSD-NORM group,bilateral inner parts of frontal lobeand parietal lobe、the body of cingulate gyrus、right temporal lobe、left occipital lobe inPSD-CONT group and a little white matter around lateral cerebral ventricle (frontal lobe, parietal lobe),insula,anterior corpus callosum,temporal lobe in CONT-NORM group.4.The images of nonlinear normalization were more accurate and better than that of linearnormalization.
Conclusion Compared with patients in CONT group and NORM group,Patients withPSD presented an close relationship with the left frontal lobe、parietal lobe、left internalcapsule、cingulate gyms、corpus callosum and bilateral inner parts of frontal lobe andparietal lobe.DTI provides a good platform that can more accurately evaluate themicrostructural changes of brain white matter in vivo,which is expected to offer a newmethod and idea for prediction、treatment and assessment of clinical efficacy in patientswith PSD.
Section 2 The study of methods of magnetic resonance diffusion tensorimaging (DTI)—White matter fiber tracking method for the study ofaging:ninety cases of quantitative diffusion tensor imaging (DTI) analysis
Objective To investigate the difference and significance of Fractional anisotropy (FA)of precentral portion of the pyramidal tract (PRPT,ie from cerebral peduncle to precentralgyrus) in different age-groups health volunteers using quantitative diffusion tensorimaging (DTI) based on fiber tractography.
Methods Quantitative DTI based on fiber tractography were performed in 90 healthvolunteers (20-83years) divided into 6 age groups at a 1.5T MR scanner.Standardizedimages data were analyzed for the relationship between FA values of PRPT and aging.
Results The FA value of bilateral PRPT in each age group distribute similarly,inwhich FA value of corona radiata is the lowest and the posterior limb of the internal capsuleis the highest;The FA values of sections is declining with aging,showed the fibers of these parts had significantly aging and the most obvious aging part is the frontal lobe;we foundthe procedure of aging in the frontal lobe and cerebral peduncle does exist mutationperiod(P＜0.0001,P=0.0068).
Conclusion Diffusion tensor imaging (DTI) is a sensitive method for detecting themicrostructural changes and aging process of brain white matter;Whether the Mutation ofaging in the frontal lobe and cerebral peduncle is the physical signs of aging,it should befurther examined.
引文
1.Whyte EM,Mulsnt BH.Poststroke depression:epideomiology,pathophysiology,and biological treatment[J].Bia Psychiatry 2002;52(3):253-264
2.Tamraz JC,Comair YG..Atlas of regional anatomy of the brain using MRI with functional correlations [M].Berlin:Springer-Verlag,2000.168-181.
3.Watson C,Andemann F,GloorP,etal.Anatomic basis of.amygdaloid and hippocampal volume measurement by magnetic resonance imaging[J].Neurology,1992,42(9):1743-1750
4.Frodl T,Meisenzahl EM,Zetzsche T,et al.Hippocampal changes in patients with a first episode of major depression[J].Am J Psychiatry 2002,159(7):1112-1118
5.Mervaala E,Fohr J,Kononen M,et al.Quantitative MRI of the hippocampus and amygdala in severe depression[J].Psychological Medicine,2000,30(1):117-125
6.Starkstein SE,Robinson RG,Berthier M,et al.Depression disorders following posterior circulationas compared with middle cerebral artery infarects[J].Brain,1998,111(Pt 2):375-387.
7.Robinson RG.Poststroke depression:prevalence,diagnosis,treatment,and disease progression[J].Biol Psychiatry,2003,54(3):376 - 387.
8.Provinciali L,Coccia M.Post-stroke and vascular depression:a critical review[J].Neurol Sci,2002,22(6):417 - 428.
9.Pohjavara T,Leppavuori A,Siira I,et al.Frequency and clinical determinants of post-stoke depression[J].Stroke,1998,29(4):2311-2317.
10.Hsieh LP,Kao HJ.Depressive symptoms following ischemic stroke:a study of 207 patients.Acta Neurol Taiwan.2005 14(4):187-190.
11.Kotila M,Numminen H,Waltimo O,et al Depression after stroke results of the FINNSTROKE Study[ J].Stroke,1998,29(2):368-372
12．龙洁，刘水珍，蔡焯基，等．卒中后抑郁状态的发生率及相关因素研究[J]．中华神经科杂志，2001，34(3)：145-148
13.Williams LS,Ghose SS,Swindle RW.Depression and other mental health diagnoses increase mortality risk after ischemic stroke[J].Am J Psychiatry,2004,.161 (6):1090-1095.
14.Carod-Artal J,Egido JA,Gonz(?)lez JL,et al.Quality of life among stroke survivors evaluated 1 year after stroke[J].Stroke,2000,31(12):2995 - 3000.
15.Larson SL,Owens PL,Ford D,et al.Depressive disorder,dysthymia,and risk of stroke:thirteen-year follow-up from the Baltimore Epidemiological Catchment Area Study[J].Stroke,2001,32(9):1979-1983.
16.Morris PL,Robinson RG,Andrzejewski P,et al.Association of depression with 10- year post- stroke mortality[J].Am J Psychiatry,1993,150(1):124-129
17．汤艳清，谢光荣。抑郁症的脑结构影像学改变及其机制的研究进展[J]。中国临床心理学杂志，2005，13(3)：366-369
18．夏军，陈军，周义成，等。抑郁症患者海马及杏仁核容积异常的MRI研究[J]。中华放射学杂志．2005，39(2)：140-143
19．林明方，李建军，王桂华，等。抑郁症首次发病患者三维磁共振氢质子波谱的分析研究[J]。中华精神科杂志，2006，39：5-8
20.Sheline YI:3D MRI studies of neuroanatomic changes in unipolar major depression:the role of stress and medical comorbidity.Biol Psychiahy,2000;48(8):791-800.
21.Vythilingam M,Heim C,Newport J,et al.Childhood trauma associated with smaller hippocampal volume in women with major depression[J].Am J Psychiatry 2002,159(12):2072-2080
22.Bremner JD.Does stress damage the brain ? (J) .Biolpsychiatry,1999,45(7):797-805
23.Rusch BD,Abercrombie HC,Oakes TR,et al.Hippocampal morphometry in depressed patients and control subjects:relations to anxiety symptoms.Biol Psychiatry,2001;50(12):960-964
24.Rajkowska G..Depression what we can learn from postmortem studies[J].Neuroscientist,2003,9(4):273-284
25.Watanabe Y,Gould E,McEwen BS.Stress induces atrophy of apical dendrite of hippocampal CA3 pyramidal neurons. Brain Res, 1992, 588(2):341-345.
26. Magarinos AM, McEwen BS. Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: comparison of stressors. Neurosci, 1995, 69(1):83-88.
27. Andres MK:Is major depression a neurologic disorder with psychiatric symptoms? [J] Epilepsy & Behavior, 2004;5(5):636-644
28. Perlov E, Philipsen A, Tebartz van Elst L,et al. Hippocampus and amygdala morphology in adults with attention-deficit hyperactivity disorder[J]. J Psychiatry Neurosci. 2008,33(6):509-515.
29. Irwin W, Anderle MJ, Abercrombie HC,et al. Amygdalar interhemispheric functional connectivity differs between the non-depressed and depressed human brain[J]. Neuroimage, 2004, 21(2):674-686.
30. Bowley MP, Drevets WC, Ongur D, et al. Low glial numbers in the amygdala in major depressive disorder[J]. Biol Psychiatry, 2002, 52(5): 404-412
31. Strakowski SM, DelBello MP, Sax KW, et al. Brain magnetic resonance imaging of structural abnormalities in bipolar disorder[J]. Arch. Gen. Psychiatry,1999,56(3):254- 260
32. Robinson RG, Starr LB, Kubos KL, et al. A two-year longitudinal study of post-stroke mood disorders findings during the initial examination[J].Stroke 1983,14:736-741.
33. RobinsonRG. Neuropsychiatric consequences of stroke[J]. Annu Rev Med, 1997, 48(3):217-229.
34. Robinson RG, LipseyJR, Rao K, et al. Two-year longitudinal study of post-stroke mood disorders: comparison of acute onset with delayed-onset depression[J]. Am J Psychiatry, 1996, 143(10):1238-1244.
35. 张庆臣,吴彩云,徐培锡,等.中华神经精神科杂志[J]. 1992, 2(3) :203-210.
36. Vataja R, Pohjasvaara T, Leppavuori A, et al. Magnetic resonance imaging correlates of depression after ischemic stroke[J]. Arch Gen Psychiatry , 2001, 58(10): 925 - 931.
37. Narushima K, Kosier JT, Robinson RG . A reappraisal of post-stroke depression, intra- and inter-hemispheric lesion location using meta-analysis[J].J Neuropsychiatry Clin Neurosci,2003,15(4):422 - 430.
38.Kim JS,Choi-Kwon S.Poststroke depression and emotional incontinence:correlation with lesion location[J].Neurology,2000,54(9):1805 - 1810.
39.Hama S,Yamashita H,Shigenobu M,et al.Post-stroke affective or apathetic depression and lesion location:left frontal lobe and bilateral basal ganglia.Eur Arch Psychiatry Clin Neurosci.2007,257(3):149-152
40．周靖，张涛，李衍滨．老年人脑卒中后发生抑郁症相关因素分析[J]．山东医药，2007．47(31)：29
41．付国惠，张保朝．急性卒中后抑郁症发生与影像学改变临床分析[J]．中国实用神经疾病杂志，2007，(8)：48-49
42 罗汝琴，戴冀斌，王建君，等．脑卒中后抑郁相关因素分析[J]．中国民康医学，2007，19(3)：183-185．
43.Carson AJ,MacHale S,Allen K,et al.Depression after stroke and lesion location:a systematic review.Lancet,2000,356 (9224):122-126.
44.Gainotti G,Azzoni A,Marra C.Frequency,phenomenology and anatomical-clinical correlates of major post-stroke depression.Br J Psychiatry.1999,175(8):163-167.
45.Bhogal SK,Teasell R,Foley N,et al.Lesion location and post-stroke depression:systematic review of the methodological limitation in the literature.Stroke,2004,35 (3):794-802.
46.Strakowski SM,DelBello MP,Adler CM.The functional neuroanatomy of bipolar disorder:a review of neuroimaging findings.Molecular Psychiatry,2005;10(1):105-116.
47.Smith KA,Ploghaus A,Cowen PJ,et al.Cerebellar responses during anticipation of noxious stimuli in subject recovered from depression Functional magnetic resonance imaging study[J].Br J Psychiatry,2002,181 (11):411—415.
48.Fu CH,Williams SC,Cleare AJ,et al.Attenuation of the neural response to sadfaces in major depression by antidepressant treatment:a prospective,event-related functional magnetic resonance imaging study[J]. Arch Gen Psychiatry, 2004,61(9):877-889.
49. Bench CJ,Friston KJ,Brow RG,et al.The anatomy of melancholia: focal abnormalities of cerebral blood flow in major depression. Psychol Med,1992,22(3):607-615
50. Henriques JB, Davidson RJ. Decreased responsiveness to reward in depression. Cogn. Emot, 2000, 14:711-724
51. Soares JC, Mann JJ. The functional neuroanatomy of mood disorders. Journal of Psychiatric Research, 1997, 31(4):393-432
52. Soares JC, Mann JJ. The anatomy of mood disorders: Review of structural neuroimaging studies. Biological Psychiatry, 1997, 41(1): 86-106
1.Whyte EM,Mulsnt BH.Poststroke depression:epideomiology,pathophysiology,and biological treatment[J].Bia Psychiatry 2002;52(3):253-264
2.Wild B,Erb M,Bartels M.Are emotions contagious? Evoked emotions while viewing emotionally expressive faces:quality,quantity,time course and gender differences[J].Psychiatry Res.2001,102(2):109-124
3.Moriguchi Y,Ohnishi T,Kawachi T,et al.Specific brain activation in Japanese and Caucasian people to fearful faces [J].Neuroreport.2005,16(2):133-136.
4.Garc(?)a-Caballero A,Gonz(?)lez-Hermida J,Garc(?)a-Lado I,et al.Impaired facial emotion recognition in a case of right frontotemporal dementia[J].Actas.Esp Psiquiatr.2006,34(6):416-419.
5.Henley SM,Wild E J,Hobbs NZ,et al.Defective emotion recognition in early HD is neuropsychologically and anatomically generic.Neuropsychologia.2008,46(8):2152-2160
6.Posse S.Fitzgerald D.Gao K.et al.Real-time fMRI of temporolimbic regions detects amygdala activation during single-trial self-induced sadness[J].Neuroimage.2003,18(3):760-768
7.Keightley ML,Winocur G Graham S J,et al.An fMRI study investigating cognitive modulation of brain regions associated with emotional processing of visual stimuli[J].Neuropsychologia,2003(41):585-596
8．黄宇霞，罗跃嘉。国际情绪图片系统在中国的试用研究[J]。中国心理卫生杂志，2004，18(9)：631-634
9．杨宏宇，林文娟。国际情感图片系统在中国诱发正性和负性情绪反应的研究[J]。中国行为医学科学， 2005，14(11)：1028-1030
10．王莹、许晶、张炳蔚，等．国际情绪图片系统在116名中国老年人中的试用[J]。中国心理卫生杂志,2008，22(12)：903-907
11.Sonnby-Borgstr(o|¨)m M,J(o|¨)nsson P,Svensson O.Gender differences in facial imitation and verbally reported emotional contagion from spontaneous to emotionally regulated processing levels[J].Scand J Psychol.2008 Apr;49(2):111-122
12.Britton JC,Taylor SF,Sudheimer KD,et al.Facial expressions and complex IAPS pictures:common and differential networks[J].Neuroimage.2006,31 (2):906-919.
13．彭代辉，江开达，徐一蜂，等．IAPS图片诱导首发抑郁症患者的情绪偏向性[J]．中国心理卫生杂志,2007,21(11)：753-755．
14．彭代辉，江开达，徐一蜂，等．抑郁症首次发作患者情绪偏向任务的脑功能磁共振成像研究[J]。中华精神科杂志，2008，41(2)：68-72
15．邵郊．1992．生理心理学．人民教育出版社。431～447
16.George MS,Ketter TA,Parekh PI,et al.Brain activity during transient sadness and happiness in healthy women[J].Am J Psychiatry.1995,152(3):341-351.
17.Strakowski SM,DelBello MP,Adler CM.The functional neuroanatomy of bipolar disorder:a review of neuroimaging findings [J].Molecular Psychiatry,2005 ;10(1):105-116.
18.Turhan C,Heidi S,Moriah E ,et al.Brain activation to emotion words in depressed vs healthy subjects[J].Neuroreport,2004,15(17):2585-2588.
19.Drevets WC.Neuroimaging and neuropathological studies of depression:implication for cognitive-emotion features of mood disorder[J].Curr Opin Neurobiol 2001;11(2):240-249.
20.Kalin NH,Davidson RJ,hwin W,et al.Functional magnetic resonance imaging studies of emotional processing in normal and depressed patients:effects of venlafaxine[J].J CIin Psychiatry,1997,58(Supp 116):32-39
21.Malhi GS,Lagopoulos J,Ward PB,et al.Cognitive generation affect in bipolar depression:an fMRI study[J].European J of Neuroscience.2004,19(3):741-754
22.Ongur D,brevets WC,Price JL.Glial reduction in the subgenual prefrontal cortex in mood disorders[J].Proc Natl Acad Sci U S A 1998;95(22):13290-13295
23.Phan KL,Wager T,Taylor SF,et al.Functional neuroanatomy of emotion:a meta-analysis of emotion activation studies in PET and fMRI[J].Neuroimage,2002,16(2):331-348.
24. Mayberg HS. Limbic-cortical dysregulation: a proposed model of depression[J]. J Neuropsychiatry Clin Neurosci, 1997, 9(3): 471-481.
25. Mega MS, Cummings JL, Salloway S, et al. The limbic system: an anatomic, phylogenetic, and clinical perspective[J]. J Neuropsychiatr Clin Neurosci, 1997, 9(3):315-330.
26. Stuss DT, Levine B, Alexander MP, et al. Wisconsin Card Sorting Test performance in patients with focal frontal and posterior brain damage: effects of lesion location and test structure on separable cognitive processes[J]. Neuropsychologia, 2000, 38(4):388-402.
27. Rajkowska G, Miguel- Hidalgo JJ, Wei J, et al. Morphometric evidence for neuronal and glial prefrontal cell pathology in major depression[J]. Biological Psychiatry, 1999,45 (9):1085-1098
28. Drevets WC, Price JL, Simpson JRJ, et al. Subgenual prefrontal cortex abnormalities in mood disorders[J]. Nature,1997, 386(6627):824- 827
29. Morita Y, Morita K, Yamamoto M. Effects of facial affect recognition on the auditory P300 in healthy subjects[J]. Neuroscience Research, 2001, 41(1): 89-95
30. Adolphs R, Tranel D, Hamann S, et al. Recognition of facial emotion in nine indivi- duals with bilateral amygdala damage[J]. Neuropsychologia, 1999,37(10):1111-1117.
31. Ueda K, Okamoto Y, Okada G,,et al. Brain activity during expectancy of emotional stimuli: an fMRI study[J].Neuroreport,2003,14(1):51-55.
32. Mitterschiffthaler MT, Kumari V, Malhi GS, et a l.Neural response to pleasant stimuli in anhedonia: an fMRI study[J]. Neuroreport ,2003,14(2): 177-182.
33. Davidson RJ, Irwin W, Anderle MJ, et al. The neural substrates of affective processing in depressed patients treated with venlafaxine[J]. Am J Psychiatry, 2003,160(l):64-75.
34. Ramasubbu R, Goodyear BG.Methylphenidate modulates activity within cognitive neural networks of patients with post-stroke major depression: A placebo-controlled fMRI study[J]. Neuropsychiatr Dis Treat. 2008,4(6):1251-1266.
35. Richard J. Davidson , 2002, Annual Review of Psychology.
36. Robinson RG, Starr LB, Kubos KL, et al. A two-year longitudinal study of poststroke mood disorders findings during the initial examination[J].Stroke 1983, 14(5):736-741
37. Vataja R, Pohjasvaara T, Leppavuori A, et al. Magnetic resonance imaging correlates of depression after ischemic stroke[J]. Arch Gen Psychiatry, 2001, 58(10): 925 - 931.
38. Anand A,Li Y,Wang Y,et al. Activity and connectivity of brain mood regulating circuit in depression: a functional magnetic resonance study[J]. BiolPsychiatry, 2005,57(10):1079-1088.
39. Paus T, Tomaiuolo P, otaky N, et al. Human cingulated and Paracingulate sulci: Patten, variability, asymmetry, and Probabilistic map[J]. Cere Cortex, 1996,6(2): 107-214.
40. Austin MP ,Mitchell P, Goodwin GM. Cognitive deficits in depression: Possible implications for functional neuropathology[J]. Br J Psychiatry, 2001,178(3):200-206.
41. Pizzagalli D, Pascual-Marqui RD, Nitschke JB, et al. Anterior cingulate activity as a predictor of degree of treatment response in major depression:evidence from brain electrical tomography analysis[J]. Am J. Psychiatry, 2001,158(3): 405- 415
42. Wu J, Buchsbaum MS, Gillin JC,et al. Prediction of antidepressant effects of sleep deprivation by metabolic rates in the ventral anterior cingulate and medial prefrontal cortex[J]. Am J. Psychiatry, 1999,156(8):1149-1158
43. Lane RD, Fink GR, Chau PM, et al. Neural activation during selective attention to subjective emotional responses[J]. Neuroreport 1997;8(18):3969-3972.
44. Maryberg HS, Liotti M ,Brannan SK, et al .Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness[J]. Am J Pychiatry. 1999;156(5):675-682.
45. Zhao MG,Toyoda H, Lee YS, et al. Roles of NMDA NR2B subtype receptor in prefrontal long-term potentiation and contextual fear memory[J]. Neuron, 2005, 47(6):859-872.
46. Eisenberger NI, Lieberman MD, Williams KD. Does rejection hurt? An fMRI study of social exclusion[J]. Science 2003;302(5643):290-292.
47.Anand A,Li Y,Wang Y,et al.Antidepressant effect on connectivity of the mood-regulating circuit:an FMRI study.Neuropsychopharmacology 2005;30(7):1334-44
48.Rajkowska G.Depression what we can learn from postmortem studies[J].Neuroscientist,2003,9(4):273-284
49.Pittenger C,Kandel E R.In search of general mechanisms for long-lasting plasticity:aplysia and the hippocampus[J].The Royal Society,2003,25(1432):757-763
50.Andres MK.Is major depression a neurologic disorder with psychiatric symptoms? [J]Epilepsy & Behavior,2004;5(5):636-644
51.Cz(?)h B,Michaelis T,Watanabe T,et al.Stress-induced changes in cerebral metabolites hippocampal volume and cell proliferation are prevented by antidepressant treatment with tianeptine.Proceedings of the National Academy of Sciences,2001,23(98):12796-12801
52.Wood G E,Trevor Young L,Reagan L P,et al.Stress-induced structural remodeling in hippocampus:Prevention by lithium treatment.Proceedings of the National Academy of Sciences,2004,101 (11):3973-3978
53．林涛、蔡焯基。抑郁症海马部位的神经可塑性改变及影像学研究[J]。国际精神病学杂志，2005，32(4)：226-229
54．方向军、刘军、朱仁勇等，首发重性抑郁症患者面部表情刺激的脑功能磁共振研究[J]。医学临床研究，2008，25(10)：1736-1743
55.Werner NS,Meindl T,Materne J,et al.Functional MRI study of memory-related brain regions in patients with depressive disorder[J].J Affect Disord.2009 Apr 3.[Epub ahead of print]
56.Rodrigues S M,Schafe G E,LeDou J E.Molecular mechanisms underlying emotional learning and memory in the lateral amygdala[J].Neuron,2004,44(1):75-91
57.Schafe G E,Nadel N V,Sullivan G M,et al.Memory consolidation for contextual and auditory fear conditioning is dependent on protein synthesis,PKA,and MAP kinase[J].Learning and memory,1999,6(2):97-110
58.Ketter T A,Kimbrell T A,George M S,et al.Effects of mood and subtype on cerebral glucose metabolism in treatment-resistant bipolar disorder[J].Biological Psychiatry, 2001, 49(2): 97-109
59. Chen CH, Lennox B, Jacob R, et al Explicit and Implicit Facial Affect Recognition in Manic and Depressed States of Bipolar Disorder: A Functional Magnetic Resonance Imaging Study[J]. Biol Psychiatry 2006, 59(1):31-39
60. Okada G, Okamoto Y, Morinobu S, et al. Attenuated left Prefrontal activation during a verbal flueney task in patients with depression. Neuropsychobiology 2003, 47(1):21-26
61. Bonelli SB, Powell R, Yogarajah M,et al. Preoperative amygdala fMRI in temporal lobe epilepsy[J]. Epilepsia. 2009, 50(2):217-227.
62. Strakowski SM, DelBello MP, Sax KW, et al. Brain magnetic resonance imaging of structural abnormalities in bipolar disorder[J]. Arch. Gen. Psychiatry,1999,56(3):254- 260
63. Bowley MP, Drevets WC, Ongur D, et al. Low glial numbers in the amygdala in major depressive disorder[J]. Biol Psychiatry, 2002, 52(5): 404-412
64. Karolewicz B, Szebeni K, Gilmore T,et al. Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression[J]. Int J Neuropsychopharmacol. 2009,12(2):143-153.
65. Pitkanen A, Pikkarainen M, Nurminen N, et al. Reciprocal Connections between the Amygdala and the Hippocampal Formation, Perirhinal Cortex, and Postrhinal Cortex in Rat:A Review[J]. Ann NY Acad Sci, 2000, 911(6):369-391
66. Richter-Levin G,Akirav I. Amygdala-hippocampus dynamic interaction in relation to memory[J]. Mol Neurobiol, 2000, 22(1-3): 11-20.
67. Blood AJ, Zatorre RJ. Intensely pleasurable responses to music correlate with activity in brain regions implicated in reward and emotion. Proceedings of the National Academy of Sciences of the United States of America, 2001,98 (20): 11818-11823.
68. Rogers MA, Bradshaw JL, Pantelis C,et al. Frontostriatal deficits in unipolar majordepression[J]. Brain Research Bulletin, 1998, 47(4):297- 310
69. Zobel A, Joe A, Freymann N, et al. Changes in regional cerebral blood flow by therapeutic vagus nerve stimulation in depression: an exploratory approach. Psychiatry Res. 2005, 139(3):165-179
70. Davies J, Lloyd KR, Jones IK, et al.. Changes in regional cerebral blood flow with venlafaxine in the treatment of major depression. Am J Psychiatry. 2003; 160(2): 374-376
71. Weisskopf M G, Ledoux J E, LeDoux J E. Distinct populations of NMDA receptors at subcortical and cortical inputs to principal cells of the lateral amygdala[J]. The American Physiological Society, 1999, 81(2): 930-934
72. Young KA, Manaye KF, Liang CL,et al. Reduced number of mediodorsal and anterior thalamic neurons in schizophrenia[J]. Society of Biological Psychiatry, 2000, 47(11): 944-953
73. Smith KA,Ploghaus A,Cowen PJ,et al.Cerebellar response during anticipation of noxious stimuli in subject recovered from depression Functional magnetic resonance imaging study[J]. Br J Psychiatry, 2002,181(11):411-415
74. Fu CH,Williams SC,Cleare AJ,et al. Attenuation of the neural response to sad faces in major depression by antidepressant treatment: a prospective, event-related functional magnetic resonance imaging study[J]. Arch Gen Psychiatry, 2004,61(9):877-889
75. Sui R, Zhang L, Min L,et al. Cerebellar dysfunction may play an important role in post-stroke depression[J]. Med Hypotheses. 2009,72(6):643-646.
76. Schutter DJ, and van Honk J. The cerebellum on the rise in human emotion[J]. Cerebellum 2005, 4(4):290-294
77. Konarski JZ, McIntyre RS, Grupp LA, et al. Is the cerebellum relevant in the circuitry of neuropsychiatric disorders? [J] J Psychiatry Neurosci, 2005,30(3): 178-186
78. Chan SW, Norbury R, Goodwin GM, et al. Risk for depression and neural responses to fearful facial expressions of emotion[J]. Br J Psychiatry. 2009,194(2):139-145.
79. Vasic N, Walter H, Sambataro F,et al. Aberrant functional connectivity of dorsolateral prefrontal and cingulate networks in patients with major depression during working memory processing[J]. Psychol Med. 2008,10(10): 1-11.
80. Liotti M, Mayberg HS, Brannan SK, et al. Differential limbic-cortieal correlates of sadness and anxiety in healthy subjects:implication for affective disorders[J].Biol Psychiatry.2000;48(1 ):30-42,69
81.Leroi I,O'Hearn E,Marsh L,et al.Psychopathology in patients with degenerative cerebellar diseases:a comparison to Huntington's disease[J].Am J Psychiatry.2002;159(8):1306-1314
82．王立，周文琪，旁巨细胞外侧核的解剖联系及可能的生理调控功能概述[J]。昆明医学院学报。2003，24(3)：114-117
83.Flynn FG..Anatomy of the insula functional and clinical correlates[J].Psychology Press,1999,13:55-78.
84.Halari R,Simic M,Pariante CM,et al.Reduced activation in lateral prefrontal cortex and anterior cingulate during attention and cognitive control functions in medication-na(?)ve adolescents with depression compared to controls[J].J Child Psychol Psychiatry.2009,50(3):307-316.
85.Venkatraman TN,Krishnan RR,Steffens DC,et al.Biochemical abnormalities of the medial temporal lobe and medial prefrontal cortex in late-life depression[J].Psychiatry Res.2009,172(1):49-54.
86.Cunningham WA,Raye CL,Johnson MK.Implicit and explicit evaluation:fMRI correlates of valence,emotion intensity,and control in the processing of attitudes[J].J Cogn Neurosci,2004,16(10):1717-1729.
87.Smith APR ,Henson RNA,,Dolan RJ ,et al.fMRI correlates of the episodic retrieval of emotional contexs[J].Neuroimage,2004,22(1):868-878.
88.BensonPJ ,GuoK,HardimanMJ.Cortical evoded potentials due to motion comtrast in the blind hemifield [J].Neuroreport,1999,10(17):3595-3600.
89.Brodtmann A,Puce A,Darby D,et al.Serial functional imaging poststroke reveals visual cortex reorganization[J].Neurorehabil Neural Repair.2009 Feb;23(2):150-159.
90．陈秀琼、阳初玉、徐薇等。急性脑梗死患者抑郁与病灶部位的相关性研究[J]。中国实用神经疾病杂志2008，11(11)：16—18
1 Wieshmann UC,Symms MR,Parker GJ,et al.Diffusion tensor imaging demonstrates deviation of fibres in normal appearing white matter adjacent to a brain tumour[J].Neurol Neurosurg Psychiatry,2000,68(4):501-503.
2 Le Bihan D,Mangin JF,Poupon C,et al.Diffusion Tensor Imaging:concepts and applications[J].J Magn Reson Imaging,2001,13(4):534-546.
3 Lockwood KA,Alexopoulos GS,Kakuma T,et al.Subtypes of cognitive impairment in depressed older adults[J].Am J GeriatrPsychiatry,2000,8(3):201-208.
4 Taylor WD,MacFall JR,Payne ME,et al.Late-life depression and microstructural abnormalities in dorsolateral prefrontal cortex white matter[J].Am J Psychiatry,2004;161(7):1293-1296.
5 Li L,Ma N,Li Z,et al.Prefrontal white matter abnormalities in young adult with major depressive disorder:a diffusion tensor imaging study[J].Brain Res.2007,1168(9):124-128.
6 Yang Q,Huang X,Hong N,White matter microstructural abnormalities in late-life depression[J].Int Psychogeriatr.2007,19(4):757-766.
7 Alexopulos GS,Kiosses DN,Choi S J,et al.Frontal white matter microstructure and treatment response of late-life depression:a preliminary study[J].Am J Psychiatry,2002;159(11):1929-1935.
8 Nobuhara K,Okugawa G,Minami T,et al.Effects of electroconvulsive therapy on frontal white matter in late-life depression:a diffusion tensor imaging study[J].Neuropsychobiology,2004;50(1):50-53.
9 夏军，雷益，徐化剑，等。磁共振扩散张量成像在抑郁症疗效观察中的初步研究[J]。南方医科大学学报，2007，27(12)：1905-1907
10 Taylor WD,Kuchibhatla M,Payne ME,et al.Frontal white matter anisotropy and antidepressant remission in late-life depression[J].PLoS ONE.2008,3(9):e3267.
11 Middleton FA,Strick PL.A revised neuroanatomy of frontal-subcortical circuit,in frontal subcortical circuit in psychiatric and neurological disorders[M].New York:Guilford, 2001:44-58.
12 Kumar A,Thoms A,Laretsky H,et al.Frontal white matter biochemical abnormalities in late-life major depression detected with proton megnetic resonance spectroscopy[J].Am J Psychiatry, 2002,159(4):630-639.
13 Drevets WC. Neuroimaging studies of mood disords[J].Biol Psychiafry, 2000, 48(8):813-829.
14 Macfall JR,Payne ME,Provenzale JE,et al.Medial orbital frontal lesions in late-onset depression[J].Biol Psychiatry,2000,49(9):803-806.
15 Alexopoulos GS,Meyers BS,Young RC,et al. Executive dysfunction and long-term outcomes of geriatric depression[J].Arch Gen Psychiatry,2000,57(3)285-290.
16 Kumar A.Neuroanatomy of late-life mood disorders[J].EconNeurosci,2001,3:44-8
17 Lim KO, Helpern JA. Neuropsychiatric application of DTI-a review[J]. NMR Biomed, 2002,15(7-8):587-593.
18 Raz N, Lindenberger U, Rodrigue, KM., et al. Regional brain changes in aging healthy adults: General trends, individual differences and modifiers[J]. Cerebral Cortex,2005, 15(11):1676-1689.
19 Bronge L, Bogdanovic N, Wahlund LO. Postmortem MRI and histopathology of white matter changes in Alzheimer brains. A quantitative, comparative study[J]. Dement Geriatr CognDisord, 2002,13(4):205-212.
20 Sullivan EV., Pfefferbaum A. Diffusion tensor imaging and aging[J]. Neuroscience and Biobehavioral Reviews, 2006,30(6):749-761.
21 Rademacher J, Burgel U, Geyer S, et al. Variability and asymmetry in the human precentral motor system. A cytoarchitectonic and myeloarchitectonic brain mapping study[J]. Brain, 2001,124(pt11):2232-225
22 Kanaan RA, Shergill SS, Barker GJ, et al. Tract-specific anisotropy measurements in diffusion tensor imaging[J]. Psychiatry Res, 2006,146(1):73-82.
23 Jeffrey IB, Pratik M,Savannah CP,et al. Quantitative diffusion tensor MRI fiber tracto- graphy of sensorimotor white matter development in premature infants[J]. NeuroImage, 2005,27(4);862-871
24 Holodny AI, Watts R, Korneinko VN, et al. Diffusion tensor tractography of the motor white matter tracts in man: Current controversies and future directions[J]. Ann N Y Acad Sci, 2005,1064(12):88-97.
25 Newton JM, Ward NS, Parker GJ,et al. Non-invasive mapping of corticofugal fibres from multiple motor areas-relevance to stroke recovery[J]. Brain, 2006,129(7):1844-1858.
26 Madden DJ, Whiting WL, Huettel SA, et al. Diffusion tensor imaging of adult age differences in cerebral white matter: relation to response time[J]. Neuroimage, 2004,21(3):1174-1181.
27 Ling XY, Huang L, Liu SR, et al. The preliminary diffuse tensor MR imaging study of correlation of white matter anisotropy with age in normal adults[J]. Chin J Geriatr,2005, 9(24):667-669
28 Reich DS, Smith SA, Jones CK, et al. Quantitative characterization of the corticospinal tract at 3T[J]. AJNR Am J Neuroradiol, 2006,27(10):2168-2178.
29 Chepuri NB, Yen YF, Burdette JH,et al. Diffusion anisotropy in the corpus callosum[J]. AJNR Am J Neuroradiol, 2002,23(5):803-808.
30 Moody DM, Bell MA, Challa VR.The corpus callosum, a unique white-matter tract: anatomic features that may explain sparing in Binswanger disease and resistance to flow of fluid masses[J]. Am J Neuroradiol, 1988,9(6): 1051-1059
31 Duong TQ, Sehy JV, Yablonskiy DA, et al. Extracellular apparent diffusion in rat brain[J]. Magn Reson Med, 2001,45(4):801-810.
32 Sullivan EV, Adalsteinsson E, Hedehus M, et al. Equivalent disruption of regional white matter microstructure in ageing healthy men and women[J]. Neuroreport, 2001,12(1): 99-104.
33 Madden DJ, Spaniol J, Whiting WL, et al. Adult age differences in the functional neuroanatomy of visual attention: A combined fMRI and DTI study[J]. Neurobiology of Aging, 2007,28(3): 459-476.
34 Salat D H., Tuch D S, Greve D N, et al. Age-related alterations in white matter microstructure measured by diffusion tensor imaging[J]. Neurobiology of Aging, 2005,26(8):1215-1227.
35 Abe O, Aoki S, Hayashi N, et al. Normal aging in the central nervous system: quantitative MR diffusion-tensor analysis[J]. Neurobiol Aging, 2002,23(3): 433-441.
36 Bartzokis G, Age-related myelin breakdown: a developmental model of cognitive decline and Azheimer's disease. Neurobiol, Aging 2004,25(1): 5-18
37 Salat DH, Tuch DS, Hevelone ND,et al. Age-related changes in prefrontal white matter measured by diffusion tensor imaging. Ann N Y Acad Sci, 2005,1064(4):37-49.
38 Marner L, Nyengaard JR, Tang Y, et al. Marked loss of myelinated nerve fibers in the human brain with age[J]. J Comp Neurol, 2003,462(2): 144-152.
39 Yoon B, Shim YS, Lee KS, et al. Region-specific changes of cerebral white matter during normal aging: A diffusion-tensor analysis[J]. Arch Gerontol Geriatr, 2008,47(1): 129-138.
1.Robinson RG.Poststroke depression:prevalence,diagnosis,treatment,and disease progression[J].Biol Psychiatry,2003,54:376 - 387.
2.Provinciali L,Coccia M.Post-stroke and vascular depression:a critical review[J].Neurol Sci,2002,22:417 - 428.
3.Pohjavara T,Leppavuori A,Siira I,et al.Frequency and clinical determinants of post-stoke depression[J].Stroke,1998,29(4):2311-2317.
4.Hsieh LP,Kao HJ.Depressive symptoms following ischemic stroke:a study of 207 patients.Acta Neurol Taiwan.2005 14(4):187-190.
5.Kotila M,Numminen H,Waltimo O,et al Depression after stroke results of the FINNSTROKE Study[ J].Stroke,1998,29( 2):368-372
6．龙洁，刘水珍，蔡焯基，等．卒中后抑郁状态的发生率及相关因素研究[J]．中华神经科杂志，2001，34(3)：145-148
7.Williams LS,Ghose SS,Swindle RW.Depression and other mental health diagnoses increase mortality risk after ischemic stroke[J].Am J Psychiatry,2004,161:1090-1095.
8.Carod-Artal J,Egido JA,Gonz(?)lez JL,et al.Quality of life among .stroke survivors evaluated 1 year after stroke[J].Stroke,2000,31:2995 - 3000.
9.Larson SL,Owens PL,Ford D,et al.Depressive disorder,dysthymia,and risk of stroke:thirteen-year follow-up from the Baltimore Epidemiological Catchment Area Study[J].Stroke,2001,32:1979-1983.
10.Morris PL,Robinson RG,Andrzejewski P,et al.Association of depression with 10-year post-stroke mortality[J].Am J Psychiatry,1993,150(1):124- 129
11.Robinson RG,Starr LB,Kubos KL,et al.A two-year longitudinal study of post-stroke mood disorders findings during the initial examination[J.Stroke 1983,14:736-741.
12.RobinsonRG.Neuropsychiatric consequences of stroke[J].Annu Rev Med,1997,48(3):217-229.
13.Robinson RG,Lipsey JR,Rao K,et al.Two-year longitudinal study of post-stroke mood disorders:comparison of acute onset with delayed-onset depression[J].Am J Psychiatry,1996,143(10):1238-1244.
14．张庆臣，吴彩云，徐培锡，等．中华神经精神科杂志[J]．1992，2(3)：203-210．
15.Vataja R,Pohjasvaara T,Leppavuori A,et al.Magnetic resonance imaging correlates of depression after ischemic stroke[J].Arch Gen Psychiatry,2001,58:925-931.
16.Narushima K,Kosier JT,Robinson RG.A reappraisal of post-stroke depression,intra and inter-hemispheric lesion location using meta-analysis[J].J Neuropsychiatry Clin Neurosci,2003,15:422 - 430.
17.Kim JS,Choi-Kwon S.Poststroke depression and emotional incon-tinence:correlation with lesion location[J].Neurology,2000,54:1805 - 1810.
18.Hama S,Yamashita H,Shigenobu M,et al.Post-stroke affective or apathetic depression and lesion location:left frontal lobe and bilateral basal ganglia.Eur Arch Psychiatry Clin Neurosci.2007,257(3):149-152
19．周靖，张涛，李衍滨．老年人脑卒中后发生抑郁症相关因素分析[J]．山东医药，2007．47(31)：29
20．付国惠，张保朝．急性卒中后抑郁症发生与影像学改变临床分析[J]．中国实用神经疾病杂志，2007，(8)：48-49
21 罗汝琴，戴冀斌，王建君，等．脑卒中后抑郁相关因素分析[J]．中国民康医学，2007，19(3)：183-185．
22.Gainotti G,Azzoni A,Marra C.Frequency,phenomenology and anatomical-clinical correlates of maj or post-stroke depression.Br J Psychiatry.1999,175:163-167.
23.Carson A J,MacHale S,Allen K,et al.Depression after stroke and lesion location:a systematic review.Lancet,2000,356 (9224):122-126.
24.Bhogal SK,Teasell R,Foley N,et al.Lesion location and post-stroke depression:systematic review of the methodological limitation in the literature.Stroke,2004,35(3):794-802.
25.Starkstein SE,Robinson RG,Berthier M,et al.Depression disorders following posterior circulationas compared with middle cerebral artery infarects[J].Brain,1998,111:375-387.
26．吕路线、宋景贵、卢红，等．卒中后抑郁状态患者的血浆、脑脊液单胺类神经递质测定[J]．中华精神科杂志，2000，33(1)：29-32．
27 Wiart L,Petit H,Joseph PA,et al.Fluxetine in early poststroke depression:A double-blind placebo-controlled study[J].Stroke J,2000,31(10):1829.
28．叶建宁，邓志宽，帅杰，等．脑卒中患者早期血清C反应蛋白含量与脑卒中后抑郁症的关系[J]．中国临床康复杂志,2003，7(28)：3838．
29.Cassidy E,O'Connor R,O'Keane V.Prevalence of post-stroke depression in an Irish sample and its relationship with disability and outcome following inpatient rehabilitation[J].Disabil Rehabil,2004;26(2):71-77.
30.Mayberg HS .Positron emission tomography imaging in depression:aneural system sperspective [J].Neuroimaging Clin N Am,2003,13(4):805-815.
31．张选红，江开达，等首发抑郁症患者局部脑葡萄糖代谢的PET初步研究，上海精神医学,2004；16(3)：129-135
32．徐伊，徐浩，贾艳滨。抑郁症患者局部脑血流变化的SPECT研究。中国神经精神疾病杂志，2005；31(3)：206-209
33.Sargent PA,Kjaer KH,Bench C J,et al.Brain serotonin,a receptor binding measured by positron emission tomography withllC WAY-100635.Effects of depression and antidepressant treatment[J].Arch Gen Psychiatry,2000,57:174-180.
34．林铮，李惠春，龚向阳，等。抑郁症患者前额叶、海马磁共振质子波谱成像的研究。中华精神科杂志，2005；11，38(4)：193-197．
35.Sanacora G,Gueorguieva R,Epperson CN,et al.Subtype-specific alterations of gamma-aminobutyric acid and glutamate in patients with major depression.Arch Gen Psychiatry,2004;61 (7):705-713.
36．夏军，雷益，周义成。抑郁症的~1H-MRS研究。医学影像学杂志．2008；18(7)：697-701．
37.Wieshmann UC,Symms MR,Parker GJ,et al.Diffusion tensor imaging demonstrates deviation of fibres in normal appearing white matter adjacent to a brain tumour.Neurol Neurosurg Psychiatry,2000,68(4):501-503.
38 Taylor WD,MacFall JR,Payne ME.Late-life depression and microstructural abnormal- lities in dorsolateral prefrontal cortex white matter.Am J Psychiatry,2004;161:1293-1296.
39 Li L,Ma N,Li Z,et al.Prefrontal white matter abnormalities in young adult with major depressive disorder:a diffusion tensor imaging study.Brain Res.2007,1168:.124-128.
40 Yang Q,Huang X,Hong N,White matter microstructural abnormalities in late-life depression.Int Psychogeriatr.2007,19(4):757-766.
41 Alexopulos GS,Kiosses DN,Choi SJ,et al.Frontal white matter microstructure and treatment response of late-life depression:a preliminary study.Am J Psychiatry,2002;159:1929-1935.
42 Nobuhara K,Okugawa G,Minami T.Effects of electroconvulsive therapy on frontal white matter in late-life depression:a diffusion tensor imagingstudy.Neuropsychobiology,2004;50:50-53.
43 夏军，雷益，徐化剑，等。磁共振扩散张量成像在抑郁症疗效观察中的初步研究。南方医科大学学报，2007，27(12)：1905-1907
44 Taylor WD,Kuchibhatla M,Payne ME,et al.Frontal white matter anisotropy and antidepressant remission in late-life depression.PLoS ONE.2008,3(9):e3267.
45 Rajkowska G,Miguel- Hidalgo J J,Wei J,et al.Morphometric evidence for neuronal and glial prefrontal cell pathology in major depression.Biological Psychiatry,1999,45 (9):1085-1098
46 Ueda K,Okamoto Y,Okada G,,et al.Brain activity during expectancy of emotional stimuli:an fMRI study[J].Neuroreport,2003,14(1):51-55.
47 Davidson RJ,Irwin W,Anderle M J,et al.The neural substrates of affective processing in depressed patients treated with venlafaxine.Am J Psychiatry,2003,160(1):64-75.
48 Rajkowska G.Depression what we can learn from postmortem studies[J].Neuroscientist,2003,9(4):273-284
49 Bowley MP,Drevets WC,Ongur D,et al.Low glial numbers in the amygdala in major depressive disorder[J].Biol Psychiatry,2002,52(5):404-412
50 Adolphs R, Tranel D, Hamann S, et al. Recognition of facial emotion in nine individuals with bilateral amygdala damage. Neuropsychologia, 1999,37(10): 1111-1117.
51 Chen CH, Lennox B, Jacob R, et al Explicit and Implicit Facial Affect Recognition in Manic and Depressed States of Bipolar Disorder: A Functional Magnetic Resonance Imaging Study. Biol Psychiatry 2006, 59(1):31-39