首发抑郁症患者药物治疗前后的磁共振成像研究
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摘要
第一部分首发抑郁症患者基于体素的形态学MRI研究
目的:探讨首发抑郁症患者基于体素的全脑形态改变特点。方法:采用3.0T磁共振,研究32例抑郁症患者及32例性别、年龄相匹配的正常志愿者。运用SPM2分析软件,采用基于体素的形态学方法,进行全脑比较分析。结果:抑郁症患者右侧海马、右侧杏仁核及右侧枕中回体积较正常对照组缩小(P＜0.05,FDR-corrected)。结论:首发抑郁症患者右侧海马、右侧杏仁核及右侧枕中回体积有明显缩小倾向。
第二部分首发抑郁症患者治疗前后基于体素的DTI研究
目的:应用磁共振弥散张量成像(DTI)技术,探讨首发抑郁症患者的治疗前后脑白质异常的变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行DTI检查。运用SPM2分析软件,采用基于体素的分析方法,比较全脑FA值的差异及变化。结果:首发抑郁症患者的右侧胼胝体膝部、内囊膝部、右侧下纵束所属部分区域FA值明显低于正常对照组(P＜0.001 corrected),经过药物治疗症状缓解后,FA值明显恢复(P＜0.001 corrected)。结论:治疗有效的首发抑郁症患者脑白质微观的病理改变是可逆的;DTI可以动态观察抑郁症患者脑白质微观的病理改变。
第三部分首发抑郁症患者治疗前后悲伤及高兴体验的fMRI研究
目的:应用功能磁共振技术,探讨首发抑郁症患者治疗前后体验悲伤及高兴面部表情的脑功能区变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行fMRI检查。运用SPM2分析软件,比较悲伤及高兴表情(与中性表情对照)体验的脑功能区变化。结果:悲伤体验时,治疗前患者组扣带回前部皮层活动性较正常人增高(P＜0.001,uncorrected),治疗后明显恢复(P＜0.001,uncorrected);高兴体验时,治疗前患者组左侧MDD的额上、中回背外侧皮层活动性较正常人减低(P＜0.001,uncorrected),经过治疗后明显恢复(P＜0.001,uncorrected)。结论:悲伤及高兴体验的fMRI是一项用来动态评价抑郁症患者情感障碍的重要手段,可以作为一项客观评价抗抑郁药物疗效的重要生物学指标。
第四部分首发抑郁症患者治疗前后的静息态fMRI研究
目的:应用低频波幅(ALFF)技术,探讨首发抑郁症患者治疗前后静息态脑功能的变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行静息态fMRI检查,运用REST、SPM2分析软件,进行全脑分析,比较基于ALFF的BOLD信号变化。结果:治疗前患者组“默认模式”神经网络的ALFF较正常对照组普遍性减低(P＜0.001,uncorrected)。经8周有效治疗后,右侧扣带回前部及双侧背外侧额叶、右侧眶额叶、颞叶、双侧楔前叶、扣带回后部皮层、右侧枕叶视区BOLD信号较治疗前增高(P＜0.05,uncorrected)。结论:治疗有效的首发抑郁症患者静息态脑功能区的异常变化是可逆的;基于ALFF的静息态fMRI技术为临床更客观地动态评价抗抑郁药物疗效开辟一条新的思路。
PARTⅠCortical abnormalities in first-onset major depressive disorder investigated with MRI and voxel-based morphometry
Objective To study the structural changes of the whole brains in first onset major depressive disorder(MDD).Material and Methods Thirty-two patients with first onset MDD and 32 the age- and sex-matched control subjects were enrolled in the study.Gray volume differences of the whole brain were assessed using SPM2 to make voxel-based morphometry comparison between patients and the control subjects.Results The volume of the right hippocampus,amygdala and right medial occipital lobule was significantly smaller in the patient group than controls(P＜.05 FDR corrected).
Conclusion Tendency of the reduced volume of the right hippocampus,amygdala and right medial occipital lobule was a characteristic of first onset major depressive disorder.
PARTⅡWhite matter abnormalities and changes in first-onset major depressive disorder by antidepressant treatment investigated with voxel-based diffusion tensor imaging
Objective To detect white matter abnormalities in patients with in first-onset major depressive disorder(MDD) and identify changes by antidepressant treatment.Material and Methods Thirteen patients with first onset MDD and 14 normal age-matched volunteers underwent diffusion tensor imaging(DTI) and patients underwent scanning twice during an 8-week period.Fractional anisotropy(FA) maps were processed using SPM2 to make voxel-wise comparison of anisotropy in whole brain between the two groups.Results Significant reductions in anisotropy were found in the white matter of genu of corpus callosum,genu of the right internal capsule and right inferior longitudinal fasciculus in patients(P＜.001 corrected).Symptomatic improvement after antidepressant was associated with reversion of the FA reductive areas (P＜.001 corrected).Conclusion Changes in FA maps of genu of corpus callosum, genu of the right internal capsule and right inferior longitudinal fasciculus associated with symptomatic improvement indicate that DTI may be a useful surrogate marker of antidepressant treatment response.
PARTⅢNeural responses with emotional processing in first-onset major depressive disorder by antidepressant treatment investigated with functional MRI
Objective To detect Changes of neural response toward sad and happy facial expressions in first-onset major depressive disorder(MDD) by antidepressant treatment investigated with functional magnetic resonance imaging(fMRI).Material and Methods Thirteen patients with with first onset MDD and 14 normal age-matched volunteers underwent fMRI and patients underwent scanning twice during an 8-week period.Blood oxygenation level dependent(BOLD) were processed using SPM2 to compare of function in whole brain between the two groups during exposure to neutral, positive and negative pictures.Results Incresesd activation of anterior cingulate cortex (ACC) during exposure to sad pictures and decreased activation of left laterial superior frontal cortex during exposure happy pictures were found in patients compared with control grougs(P＜.001,uncorrected).Symptomatic improvement after antidepressant was associated with reversion of ACC and left laterial superior frontal cortex(P＜.001, uncorrected).Conclusion Changes in BOLD of fMRI associated with symptomatic improvement indicate that fMRI may be a useful surrogate marker of antidepressant treatment response.
PARTⅣAmplitude of low frequency fluctuation in first-onset major depressive disorder by antidepressant treatment investigated with resting-state functional MRI
Objective To detect amplitude of low frequency fluctuation(ALFF) in patients with in first-onset major depressive disorder and identify changes by antidepressant treatment.Material and Methods Thirteen patients with with first onset major depressive disorder(MDD) and 14 normal age-matched volunteers underwent resting-state functional MRI and patients underwent scanning twice during an 8-week period.ALFF were processed using REST and SPM2 to compare resting-state function in whole brain between the two groups.Results Patients with MDD had decreased ALFF in "default-mode" network compared with control grougs(P＜.001,uncorrected). Symptomatic improvement after antidepressant was associated with reversion of the ALFF decreased areas in the right anterior cingulated cortex,right laterial inferior frontal cortex,right orbital frontal cortex,right temporal lobe,and bilateral posterior cingulated cortex(P＜.05,uncorrected).Conclusion Changes in ALFF maps of resting-state function associated with symptomatic improvement indicate that ALFF may be a useful surrogate marker of antidepressant treatment response.
目的:探讨首发抑郁症患者基于体素的全脑形态改变特点。方法:采用3.0T磁共振,研究32例抑郁症患者及32例性别、年龄相匹配的正常志愿者。运用SPM2分析软件,采用基于体素的形态学方法,进行全脑比较分析。结果:抑郁症患者右侧海马、右侧杏仁核及右侧枕中回体积较正常对照组缩小(P＜0.05,FDR-corrected)。结论:首发抑郁症患者右侧海马、右侧杏仁核及右侧枕中回体积有明显缩小倾向。
第二部分首发抑郁症患者治疗前后基于体素的DTI研究
目的:应用磁共振弥散张量成像(DTI)技术,探讨首发抑郁症患者的治疗前后脑白质异常的变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行DTI检查。运用SPM2分析软件,采用基于体素的分析方法,比较全脑FA值的差异及变化。结果:首发抑郁症患者的右侧胼胝体膝部、内囊膝部、右侧下纵束所属部分区域FA值明显低于正常对照组(P＜0.001 corrected),经过药物治疗症状缓解后,FA值明显恢复(P＜0.001 corrected)。结论:治疗有效的首发抑郁症患者脑白质微观的病理改变是可逆的;DTI可以动态观察抑郁症患者脑白质微观的病理改变。
第三部分首发抑郁症患者治疗前后悲伤及高兴体验的fMRI研究
目的:应用功能磁共振技术,探讨首发抑郁症患者治疗前后体验悲伤及高兴面部表情的脑功能区变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行fMRI检查。运用SPM2分析软件,比较悲伤及高兴表情(与中性表情对照)体验的脑功能区变化。结果:悲伤体验时,治疗前患者组扣带回前部皮层活动性较正常人增高(P＜0.001,uncorrected),治疗后明显恢复(P＜0.001,uncorrected);高兴体验时,治疗前患者组左侧MDD的额上、中回背外侧皮层活动性较正常人减低(P＜0.001,uncorrected),经过治疗后明显恢复(P＜0.001,uncorrected)。结论:悲伤及高兴体验的fMRI是一项用来动态评价抑郁症患者情感障碍的重要手段,可以作为一项客观评价抗抑郁药物疗效的重要生物学指标。
第四部分首发抑郁症患者治疗前后的静息态fMRI研究
目的:应用低频波幅(ALFF)技术,探讨首发抑郁症患者治疗前后静息态脑功能的变化特点。方法:采用3.0T磁共振,对13例首发抑郁症患者(分别于治疗前及抗抑郁药物治疗8周后)和14例性别、年龄相匹配的正常志愿者进行静息态fMRI检查,运用REST、SPM2分析软件,进行全脑分析,比较基于ALFF的BOLD信号变化。结果:治疗前患者组“默认模式”神经网络的ALFF较正常对照组普遍性减低(P＜0.001,uncorrected)。经8周有效治疗后,右侧扣带回前部及双侧背外侧额叶、右侧眶额叶、颞叶、双侧楔前叶、扣带回后部皮层、右侧枕叶视区BOLD信号较治疗前增高(P＜0.05,uncorrected)。结论:治疗有效的首发抑郁症患者静息态脑功能区的异常变化是可逆的;基于ALFF的静息态fMRI技术为临床更客观地动态评价抗抑郁药物疗效开辟一条新的思路。
PARTⅠCortical abnormalities in first-onset major depressive disorder investigated with MRI and voxel-based morphometry
Objective To study the structural changes of the whole brains in first onset major depressive disorder(MDD).Material and Methods Thirty-two patients with first onset MDD and 32 the age- and sex-matched control subjects were enrolled in the study.Gray volume differences of the whole brain were assessed using SPM2 to make voxel-based morphometry comparison between patients and the control subjects.Results The volume of the right hippocampus,amygdala and right medial occipital lobule was significantly smaller in the patient group than controls(P＜.05 FDR corrected).
Conclusion Tendency of the reduced volume of the right hippocampus,amygdala and right medial occipital lobule was a characteristic of first onset major depressive disorder.
PARTⅡWhite matter abnormalities and changes in first-onset major depressive disorder by antidepressant treatment investigated with voxel-based diffusion tensor imaging
Objective To detect white matter abnormalities in patients with in first-onset major depressive disorder(MDD) and identify changes by antidepressant treatment.Material and Methods Thirteen patients with first onset MDD and 14 normal age-matched volunteers underwent diffusion tensor imaging(DTI) and patients underwent scanning twice during an 8-week period.Fractional anisotropy(FA) maps were processed using SPM2 to make voxel-wise comparison of anisotropy in whole brain between the two groups.Results Significant reductions in anisotropy were found in the white matter of genu of corpus callosum,genu of the right internal capsule and right inferior longitudinal fasciculus in patients(P＜.001 corrected).Symptomatic improvement after antidepressant was associated with reversion of the FA reductive areas (P＜.001 corrected).Conclusion Changes in FA maps of genu of corpus callosum, genu of the right internal capsule and right inferior longitudinal fasciculus associated with symptomatic improvement indicate that DTI may be a useful surrogate marker of antidepressant treatment response.
PARTⅢNeural responses with emotional processing in first-onset major depressive disorder by antidepressant treatment investigated with functional MRI
Objective To detect Changes of neural response toward sad and happy facial expressions in first-onset major depressive disorder(MDD) by antidepressant treatment investigated with functional magnetic resonance imaging(fMRI).Material and Methods Thirteen patients with with first onset MDD and 14 normal age-matched volunteers underwent fMRI and patients underwent scanning twice during an 8-week period.Blood oxygenation level dependent(BOLD) were processed using SPM2 to compare of function in whole brain between the two groups during exposure to neutral, positive and negative pictures.Results Incresesd activation of anterior cingulate cortex (ACC) during exposure to sad pictures and decreased activation of left laterial superior frontal cortex during exposure happy pictures were found in patients compared with control grougs(P＜.001,uncorrected).Symptomatic improvement after antidepressant was associated with reversion of ACC and left laterial superior frontal cortex(P＜.001, uncorrected).Conclusion Changes in BOLD of fMRI associated with symptomatic improvement indicate that fMRI may be a useful surrogate marker of antidepressant treatment response.
PARTⅣAmplitude of low frequency fluctuation in first-onset major depressive disorder by antidepressant treatment investigated with resting-state functional MRI
Objective To detect amplitude of low frequency fluctuation(ALFF) in patients with in first-onset major depressive disorder and identify changes by antidepressant treatment.Material and Methods Thirteen patients with with first onset major depressive disorder(MDD) and 14 normal age-matched volunteers underwent resting-state functional MRI and patients underwent scanning twice during an 8-week period.ALFF were processed using REST and SPM2 to compare resting-state function in whole brain between the two groups.Results Patients with MDD had decreased ALFF in "default-mode" network compared with control grougs(P＜.001,uncorrected). Symptomatic improvement after antidepressant was associated with reversion of the ALFF decreased areas in the right anterior cingulated cortex,right laterial inferior frontal cortex,right orbital frontal cortex,right temporal lobe,and bilateral posterior cingulated cortex(P＜.05,uncorrected).Conclusion Changes in ALFF maps of resting-state function associated with symptomatic improvement indicate that ALFF may be a useful surrogate marker of antidepressant treatment response.
引文
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62. Bouhuys AL, Geerts E, GordijnMCM. Depressed patients' perceptions of facial emotions in depressed and remitted states are associated with relapse: A longitudinal study. J Nerv Ment Dis, 1999, 187:595- 602.
63. Ohman A, Mineka S. Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 2001, 108:483-522.
64. Surguladze SA, Young AW, Senior C, Brebion G, Travis MJ, Phillips ML. Recognition accuracy and response bias to happy and sad facial expressions in patients with major depression. Neuropsychology, 2004, 8:212-218.
65. Leppanen JM. Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Curr Opin Psychiatry, 2006, 19):34-9.
66. Suslow T, Junghanns K, Arolt V. Detection of facial expressions of emotions in depression. Percept Mot Skills, 2001, 92:857- 868
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70. Winston JS, O'Doherty J, Dolan RJ. Common and distinct neural responses during direct and incidental processing of multiple facial emotions. Neuroimage, 2003, 20:84-97.
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72. Hoffman, EA, Haxby, JV. Distinct representations of eye gaze and identity in the distributed human neural system for face perception. Nature Neuroscience, 2000, 3:80-84.
73. Kanwisher, N, McDermott, J, Chun, M. M. The fusiform face area: A module in human extrastriate cortex specialized for face perception. The Journal of Neuroscience, 1997, 17:4302-4311.
74. Haxby, JV, Hoffman, EA, Gobbini, M. I. The distributed human neural system for face perception. Trends in Cognition Science, 2000, 4:223-233.
75. George, N, Driver, J, Dolan, R. J. Seen gaze-direction modulates fusiform activity and its coupling with other brain areas during face processing. Neuroimage, 2001, 13:1102-1112.
76. Gorno-Tempini, ML, Price, CJ, Josephs, O, Vandenberghe, R., Cappa, S. F., Kapur, N., et al. The neural systems sustaining face and proper-name processing. Brain, 1998, 121:2103-2118.
77. Friesen CK, Kingstone, A. Abrupt onsets and gaze direction cues trigger independent reflexive attentional effects. Cognition, 2003, 87(1), B1-B10.
78. Gobbini MI, Haxby J. V. Neural systems for recognition of familiar faces. Journal of Neurophysiology, 2007, 45, 32-41.
79. Bruce V, Young A. Understanding Face Recognition. British Journal of Psychology, 1986,77:305-327.
80. Breen N, Caine D, Coltheart M. Models of face recognition and delusional misidentification: A critical review. Cognitive Neuropsychology, 2000, 17:55-71.
81. Kopell BH, Greenberg B, Rezai AR. Deep brain stimulation for psychiatric disorders. J Clin Neurophysiol, 2004,21:51-67
82. Siegle GJ, Carter CS, Thase ME. Use of FMRI to predict recovery from unipolar depression with cognitive behavior therapy. Am J Psychiatry, 2006, 163:735-8.
83. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry, 2006, 59:816-20.
84. Goldapple K, Segal Z, Garson C, et al. Modulation of cortical-limbic pathways in major depression: treatment-specific effects of cognitive behavior therapy. Arch Gen Psychiatry, 2004,61:34-41
85. Mayberg HS. Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment. Br Med Bull, 2003,65:193-207.
86. Davidson RJ, Irwin W, Anderle MJ, et al. The neural substrates of affective processing in depressed patients treated with venlafaxine. Am J Psychiatry, 2003,160:64-75.
87. 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. Arch Gen Psychiatry, 2004, 61:877-89.
88. Kilts C. In vivo neuroimaging correlates of the efficacy of paroxetine in the treatment of mood and anxiety disorders. Psychopharmacol Bull, 2003,37 Suppl 1:19-28.
89. Laufs H, Holt JL, Elfont R, et al. Where the BOLD signal goes when alpha EEG leaves. Neuroimage, 2006, 31:1408-18.
90. Drevets WC, Burton H, Videen TO, et al. Blood flow changes in human somatosensory cortex during anticipated stimulation. Nature, 1995, 373:249-52.
91.Mazoyer B, Zago L, Mellet E, et al. Cortical networks for working memory and executive functions sustain the conscious resting state in man. Brain Res Bull, 2001,54:287-98.
92. Gusnard DA, Raichle ME,Searching for a baseline: functional imaging and the resting human brain. Nat Rev Neurosci 2001 2:685 - 694.
93. Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA,Shulman GL: A default mode of brain function. Proc Natl Acad Sci USA ,2001, 98:676 - 682.
94. Zang Y, Jiang T, Lu Y, et al. Regional homogeneity approach to fMRI data analysis. Neuroimage, 2004,22:394-400
95. Liu H, Liu Z, Liang M, et al. Decreased regional homogeneity in schizophrenia: a resting state functional magnetic resonance imaging study. Neuroreport, 2006, 17:19-22.
96. Michael D. Greicius, Benjamin H. Flores, Vinod Menon, Gary H. Glover, Hugh B. Solvason, Heather Kenna, Allan L. Reiss, and Alan F. Schatzberg Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus. Biol Psychiatry, 2007;62:429-437
97. Anand A, Li Y, Wang Y, et al. Activity and connectivity of brain mood regulating circuit in depression: a functional magnetic resonance study. Biol Psychiatry, 2005, 57:1079-88.
98. Cordes D, Haughton VM, Arfanakis K, et al. Frequencies contributing to functional connectivity in the cerebral cortex in "resting-state" data. AJNR Am J Neuroradiol, 2001,22:1326-33.
99. Lowe MJ, Dzemidzic M, Lurito JT, et al. Correlations in low-frequency BOLD fluctuations reflect cortico-cortical connections. Neuroimage, 2000, 12:582-7.
100. Yang H, Long XY, Yang Y, et al. Amplitude of low frequency fluctuation within visual areas revealed by resting-state functional MRI. Neuroimage, 2007,36:144-52.
101. Newton AT, Morgan VL, Gore JC. Task demand modulation of steady-state functional connectivity to primary motor cortex. Hum Brain Mapp, 2007,28:663-72.
102. Zang YF, He Y, Zhu CZ, et al. Altered baseline brain activity in children with ADHD revealed by resting-state functional MRI. Brain Dev, 2007,29:83-91.
103. American Psychiatric Association (2000): Diagnostic and Statistical Manual of Mental Disorders (4th edition). Washington, DC: American Psychiatric Press.
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105. Pelled G, Goelman G. Different physiological MRI noise between cortical layers. Magn Reson Med. 2004, 52:913-6.
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107. Steriade M, McCormick DA, Sejnowski TJ. Thalamocortical oscillations in the sleeping and aroused brain. Science, 1993;262:679 - 85.
108. Greicius MD, Srivastava G, Reiss AL, Menon V. Default-mode network activity distinguishes Alzheimer' s disease from healthy aging: evidence from functional MRI. Proc Natl Acad Sci USA, 2004; 101:4637 - 42.
109. Biswal, B.B., Yetkin, F.Z., Haughton, V.M., Hyde, J.S., 1995. Functional connectivity in the motor cortex of resting human brain using echoplanar MRI. Magn. Reson. Med. 34, 537-541.
110. Kiviniemi, V., Jauhiainen, J., Tervonen, O., Paakko, E., Oikarinen, J.,Vainionpaa, V., Rantala, H., Biswal, B., 2000. Slow vasomotor fluctuation in fMRI of anesthetized child brain. Magn. Reson. Med. 44, 373 - 378.
111. Logothetis NK, Pauls J, Augath M, Trinath T, Oeltermann A. Neurophysiological investigation of the basis of the fMRI signal. Nature, 2001, 412:150 - 7
112. Drevets WC. Prefrontal cortical-amygdalar metabolism in major depression. Ann N Y Acad Sci, 1999,877:614-37.
113. Mayberg HS, Brannan SK, Tekell JL, Silva JA, Mahurin RK, McGinnis S, et al. Regional metabolic effects of fluoxetine in major depression: Serial changes and relationship to clinical response. Biol Psychiatry, 2000, 48: 830-843.
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42. Ohman, A., & Mineka, S. Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 2001, 108: 483-522.
43. Bouhuys AL, Geerts E, GordijnMCM. Depressed patients' perceptions of facial emotions in depressed and remitted states are associated with relapse: A longitudinal study. J Nerv Ment Dis, 1999, 187:595-602.
44. Surguladze SA, Young AW, Senior C, Brebion G, Travis MJ, Phillips ML. Recognition accuracy and response bias to happy and sad facial expressions in patients with major depression. Neuropsychology, 2004, 8:212-218.
45. Leppanen JM. Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Curr Opin Psychiatry, 2006, 19:34-9.
46. Suslow T, Junghanns K, Arolt V: Detection of facial expressions of emotions in depression. Percept Mot Skills, 2001, 92:857- 868
47. Ekman, P., Friesen, W., 1976. Pictures of Facial Affect. Consulting Psychologists Press, Palo Alto.
48. Gur RC, Schroeder L, Turner T, et al. Brain activation during facial emotion processing. Neuroimage, 2002,16:651-62.
49. Winston JS, O'Doherty J, Dolan RJ. Common and distinct neural responses during direct and incidental processing of multiple facial emotions. Neuroimage, 2003,20:84-97.
50. Kesler-West ML, Andersen AH, Smith CD, et al. Neural substrates of facial emotion processing using fMRI. Brain Res Cogn Brain Res, 2001,11:213-26.
51. Hoffman, E. A., Haxby, J. V. Distinct representations of eye gaze and identity in the distributed human neural system for face perception. Nature Neuroscience, 2000, 3: 80-84.
52. Kanwisher, N., McDermott, J., Chun, M. M. The fusiform face area: A module in human extrastriate cortex specialized for face perception. The Journal of Neuroscience, 1997, 17:4302-4311.
53. Haxby, J. V., Hoffman, E. A., & Gobbini, M. I. The distributed human neural system for face perception. Trends in Cognition Science, 2000, 4: 223-233.
54. George, N., Driver, J., & Dolan, R. J. Seen gaze-direction modulates fusiform activity and its coupling with other brain areas during face processing. Neuroimage, 2001, 13: 1102-1112.
55. Gorno-Tempini, M. L., Price, C. J., Josephs, O., Vandenberghe, R., Cappa, S. F., Kapur, N., et al. The neural systems sustaining face and proper-name processing. Brain, 1998, 121:2103-2118.
56. Friesen, C. K., Kingstone, A. Abrupt onsets and gaze direction cues trigger independent reflexive attentional effects. Cognition, 2003, 87(1), B1-B10.
57. Gobbini, M. I., Haxby, J. V. Neural systems for recognition of familiar faces. Journal of Neurophysiology, 2007,45, 32-41.
58. Bruce V, Young, A. Understanding Face Recognition. British Journal of Psychology, 1986,77:305-327.
59. Breen, N., Caine, D., Coltheart, M. Models of face recognition and delusional misidentification: A critical review. Cognitive Neuropsychology, 2000, 17:55-71.
60. Kopell BH, Greenberg B, Rezai AR. Deep brain stimulation for psychiatric disorders. J Clin Neurophysiol, 2004,21:51-67
61. Siegle GJ, Carter CS, Thase ME. Use of FMRI to predict recovery from unipolar depression with cognitive behavior therapy. Am J Psychiatry, 2006,163:735-8.
62. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry, 2006,59:816-20.
63. Goldapple K, Segal Z, Garson C, et al. Modulation of cortical-limbic pathways in major depression: treatment-specific effects of cognitive behavior therapy. Arch Gen Psychiatry, 2004,61:34-41
64. Mayberg HS. Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment. Br Med Bull, 2003,65:193-207.
65. Davidson RJ, Irwin W, Anderle MJ, et al. The neural substrates of affective processing in depressed patients treated with venlafaxine. Am J Psychiatry, 2003,160:64-75.
66. 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. Arch Gen Psychiatry, 2004, 61:877-89.
67. Kilts C. In vivo neuroimaging correlates of the efficacy of paroxetine in the treatment of mood and anxiety disorders. Psychopharmacol Bull, 2003, 37 Suppl 1:19-28.
68. Drevets WC, Burton H, Videen TO, et al. Blood flow changes in human somatosensory cortex during anticipated stimulation. Nature, 1995, 373:249-52.
69. Mazoyer B, Zago L, Mellet E, et al. Cortical networks for working memory and executive functions sustain the conscious resting state in man. Brain Res Bull, 2001,54:287-98.
70. Gusnard DA, Raichle ME: Searching for a baseline: functional imaging and the resting human brain. Nat Rev Neurosci, 2001, 2:685 - 694.
71. Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA,Shulman GL: A default mode of brain function. Proc Natl Acad Sci USA, 2001, 98:676 - 682.
72. Zang Y, Jiang T, Lu Y, et al. Regional homogeneity approach to fMRI data analysis. Neuroimage, 2004,22:394-400
73. Liu H, Liu Z, Liang M, et al. Decreased regional homogeneity in schizophrenia: a resting state functional magnetic resonance imaging study. Neuroreport, 2006,17:19-22.
74. Michael D. Greicius, Benjamin H. Flores, Vinod Menon, Gary H. Glover, Hugh B. Solvason, Heather Kenna, Allan L. Reiss, and Alan F. Schatzberg Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus BIOL PSYCHIATRY 2007;62:429-437
75. Anand A, Li Y, Wang Y, et al. Activity and connectivity of brain mood regulating circuit in depression: a functional magnetic resonance study. Biol Psychiatry, 2005,57:1079-88.
76. Cordes D, Haughton VM, Arfanakis K, et al. Frequencies contributing to functional connectivity in the cerebral cortex in "resting-state" data. AJNR Am J Neuroradiol, 2001,22:1326-33.
77. Lowe MJ, Dzemidzic M, Lurito JT, et al. Correlations in low-frequency BOLD fluctuations reflect cortico-cortical connections. Neuroimage, 2000,12:582-7.
78. Yang H, Long XY, Yang Y, et al. Amplitude of low frequency fluctuation within visual areas revealed by resting-state functional MRI. Neuroimage, 2007,36:144-52.
79. Newton AT, Morgan VL, Gore JC. Task demand modulation of steady-state functional connectivity to primary motor cortex. Hum Brain Mapp, 2007,28:663-72.
80. Zang YF, He Y, Zhu CZ, et al. Altered baseline brain activity in children with ADHD revealed by resting-state functional MRl. Brain Dev, 2007,29:83-91.
81. American Psychiatric Association (2000): Diagnostic and Statistical Manual of Mental Disorders (4th edition). Washington, DC: American Psychiatric Press.
82. Pelled G, Goelman G. Different physiological MRI noise between cortical layers. Magn Reson Med 2004;52:913 - 6.
83. McCormick DA. Spontaneous activity: signal or noise? Science 1999;285:541 - 3.
84. Steriade M, McCormick DA, Sejnowski TJ. Thalamocortical oscillations in the sleeping and aroused brain. Science 1993;262:679 - 85.
85. Greicius MD, Srivastava G, Reiss AL, Menon V. Default-mode network activity distinguishes Alzheimer' s disease from healthy aging: evidence from functional MRI. Proc Natl Acad Sci USA 2004; 101:4637 - 42.
86. Biswal, B.B., Yetkin, F.Z., Haughton, V.M., Hyde, J.S., 1995. Functional connectivity in the motor cortex of resting human brain using echoplanar MRI. Magn. Reson. Med. 34,537-541.
87. Kiviniemi, V., Jauhiainen, J., Tervonen, O., Paakko, E., Oikarinen, J.,Vainionpaa, V., Rantala, H., Biswal, B., 2000. Slow vasomotor fluctuation in fMRI of anesthetized child brain. Magn. Reson. Med. 44, 373 - 378.
88. Logothetis NK, Pauls J, Augath M, Trinath T, Oeltermann A. Neurophysiological investigation of the basis of the fMRI signal. Nature 2001;412:150 - 7
89. Drevets WC. Prefrontal cortical-amygdalar metabolism in major depression. Ann N Y Acad Sci, 1999,877:614-37.
90. Mayberg HS, Brannan SK, Tekell JL, Silva JA, Mahurin RK, McGinnis S, et al: Regional metabolic effects of fluoxetine in major depression: Serial changes and relationship to clinical response. Biol Psychiatry, 2000, 48: 830-843.
91. Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA,Shulman GL: A default mode of brain function. Proc Natl Acad Sci USA ,2001, 98:676 - 682.
92. Laufs H, Holt JL, Elfont R, et al. Where the BOLD signal goes when alpha EEG leaves. Neuroimage, 2006, 31:1408-18.
2. Belmaker RH, Agam G. Major depressive disorder. N Engl J Med, 2008, 358: 55-68.
3. Monkul ES, Malhi GS, Soares JC. Mood disorders - review of structural MRI studies.Acta Neuropsychiatrica 2003: 15:368-380.
4. Leppanen JM. Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Curr Opin Psychiatry, 2006, 19(1):34-9.
5. Bremner JD, Vythilingam M, Vermetten E et al. Reduced volume of orbitofrontal cortex inmajor depression. Biol Psychiatry 2002, 51:273-9.
6. Lacerda AL, Keshavan MS, Hardan AY, et al. Anatomic evaluation of the orbitofrontal cortex in major depressive disorder. Biol Psychiatry, 2004,55:353-8
7. Caetano SC, Kaur S, Brambilla P, et al. Smaller cingulate volumes in unipolar depressed patients. Biol Psychiatry, 2006, 59:702-6.
8. C M Kipps, A J Duggins, N Mahant, L Gomes, J Ashburner and E A McCusker Progression of structural neuropathology in preclinical Huntington's disease: a tensor based morphometry study J. Neurol. Neurosurg. Psychiatry 2005;76;650-655
9. Nugent AC, Milham MP, Bain EE, et al. Cortical abnormalities in bipolar disorder investigated with MRI and voxel-based morphometry. Neuroimage, 2006, 30:485-97.
10. Teipel SJ, Born C, Ewers M, et al. Multivariate deformation-based analysis of brain atrophy to predict Alzheimer's disease in mild cognitive impairment. Neuroimage, 2007,38:13-24.
11. Good CD, Johnsrude IS, Ashburner J, et al. A voxel-based morphometric study of ageing in 465 normal adult human brains. Neuroimage, 2001, 14:21-36.
12. Rosso IM. Review: hippocampal volume is reduced in people with unipolar depression. Evid Based Ment Health, 2005, 8:45.
13. Bremner JD, Narayan M, Anderson ER et al. Hippocampal volume reduction in major depression. Am J Psychiatry 2000, 157:115-7
14. Frodl T, Meisenzahl EM, Zetzsche T et al. Hippocampal changes in patients with a first episode of major depression. Am J Psychiatry 2002, 159:1112-8.
15. Frodl T, Meisenzahl EM, Zetzsche T et al. Hippocampal and amygdala changes in patients with major depressive disorder and healthy controls during a 1-year follow-up. J Clin Psychiatry 2004, 65:492-9.
16. Hickie I, Naismith S, Ward PB et al. Reduced hippocampal volumes and memory loss in patients with early- and late-onset depression. Br J Psychiatry 2005,186:197-202.
17. MacMaster FP, Kusumakar V. Hippocampal volume in early onset depression. BMC Med 2004, 2:2.
18. Neumeister A, Wood S, Bonne O et al. Reduced hippocampal volume in unmedicated, remitted patients with major depression versus control subjects. Biol Psychiatry 2005, 57:935-7
19. Videbech P, Ravnkilde B. Hippocampal volume and depression: a meta-analysis of MRI studies. Am J Psychiatry, 2004, 161:1957-66.
20. Sheline YI. 3D MRI studies of neuroanatomic changes in unipolar major depression: the role of stress and medical comorbidity. Biol Psychiatry, 2000, 48:791-800.
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18. Young EA, Haskett RF, Grunhaus L. Increased circadian activation of the hypothalamic pituitary adrenal axis in depressed patients in the evening. Arch Gen Psychiatry 1994,51:701-7
19. Starkman MN, Giordani B, Gebarski SS et al. Decrease in cortisol reverses human hippocampal atrophy following treatment of Cushing's Disease. Biol Psychiatry 1999, 46:1595-602.
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21. Diamond DM, Fleshner M, Ingersoll N et al. Psychological stress impairs spatial working memory: Relevance to electrophysiological studies of hippocampal function.Behav Neurosci 1996; 110:661-72
22. Luine V, Villages M, Martinex C et al. Repeated stress causes reversible impairments of spatial memory performance. Brain Res 1994, 639:167-70.
23. Posener JA, Wang L, Price JL et al. High-dimensional mapping of the hippocampus in depression. Am J Psychiatry 2003, 160:83-9.
24. Rosso, IM, Cintron CM, Steingard RJ et al. Amygdala and hippocampus volumes in pediatric major depression. Biol Psychiatry 2005, 57:21-6.
25. Coffey CE, Wilkinson WE, Weiner RD et al. Quantitative cerebral anatomy in depressions controlled magnetic resonance imaging study. Arch Gen Psychiatry 1993,50:7-16.
26. Kumar A, Zin Z, Bilker W et al. Late onset minor and major depression: early evidence for common neuroanatomical substrates detected by using MRI. Proc Natl Acad Sci USA 1998, 95:7654-8.
27. Narayan M, Bremner JD, Kumar A. Neuroanatomical substrates of late-life mental disorders. J Geriatr Psychiatry Neurol 1999;12:95-106.
28. Caetano SC, Kaur S, Brambilla P, et al. Smaller cingulate volumes in unipolar depressed patients. Biol Psychiatry, 2006, 59:702-6.
29. Sheila C. Caetano, Simerjit Kaur, Paolo Brambilla, Mark Nicoletti, John P. Hatch, Roberto B. Sassi,Alan G. Mallinger, Matched S. Keshavan, David J. Kupfer, Ellen Frank, and Jair C. Soares. Smaller Cingulate Volumes in Unipolar Depressed Patients. BIOL PSYCHIATRY 2006, 59:702-706.
30. Filley CM. The behavioral neurology of cerebral white matter. Neurology, 1998, 50:1535-40.
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33. Lenze E, Cross D, McKeel D, et al. White matter hyperintensities and gray matter lesions in physically healthy depressed subjects. Am J Psychiatry, 1999,156:1602-7.
34. Nobuhara K, Okugawa G, Sugimoto T, et al. Frontal white matter anisotropy and symptom severity of late-life depression: a magnetic resonance diffusion tensor imaging study. J Neurol Neurosurg Psychiatry, 2006,77:120-2
35. Gunning-Dixon FM, Hoptman MJ, Lim KO, et al. Macromolecular White Matter Abnormalities in Geriatric Depression: A Magnetization Transfer Imaging Study. Am J Geriatr Psychiatry, 2008.
36. Taylor WD, MacFall JR, Payne ME, et al. Late-life depression and microstructural abnormalities in dorsolateral prefrontal cortex white matter. Am J Psychiatry, 2004,161:1293-6
37. 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. Neuropsychobiology, 2004, 50:48-53.
38. Alexopoulos GS, Kiosses DN, Choi SJ, et al. Frontal white matter microstructure and treatment response of late-life depression: a preliminary study. Am J Psychiatry, 2002,159:1929-32
39. Bae JN, MacFall JR, Krishnan KR, et al. Dorsolateral prefrontal cortex and anterior cingulate cortex white matter alterations in late-life depression. Biol Psychiatry, 2006,60:1356-63
40. Alexopoulos GS, Murphy CF, Gunning-Dixon FM, et al. Microstructural white matter abnormalities and remission of geriatric depression. Am J Psychiatry, 2008,165:238-44
41. Gur RC, Erwin RJ, Gur RE, Zwil AS, Heimberg C, Kraemer HC. Facial emotion discrimination: II. Behavioral findings in depression. Psychiatry Res, 1992, 42: 241-251
42. Ohman, A., & Mineka, S. Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 2001, 108: 483-522.
43. Bouhuys AL, Geerts E, GordijnMCM. Depressed patients' perceptions of facial emotions in depressed and remitted states are associated with relapse: A longitudinal study. J Nerv Ment Dis, 1999, 187:595-602.
44. Surguladze SA, Young AW, Senior C, Brebion G, Travis MJ, Phillips ML. Recognition accuracy and response bias to happy and sad facial expressions in patients with major depression. Neuropsychology, 2004, 8:212-218.
45. Leppanen JM. Emotional information processing in mood disorders: a review of behavioral and neuroimaging findings. Curr Opin Psychiatry, 2006, 19:34-9.
46. Suslow T, Junghanns K, Arolt V: Detection of facial expressions of emotions in depression. Percept Mot Skills, 2001, 92:857- 868
47. Ekman, P., Friesen, W., 1976. Pictures of Facial Affect. Consulting Psychologists Press, Palo Alto.
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49. Winston JS, O'Doherty J, Dolan RJ. Common and distinct neural responses during direct and incidental processing of multiple facial emotions. Neuroimage, 2003,20:84-97.
50. Kesler-West ML, Andersen AH, Smith CD, et al. Neural substrates of facial emotion processing using fMRI. Brain Res Cogn Brain Res, 2001,11:213-26.
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52. Kanwisher, N., McDermott, J., Chun, M. M. The fusiform face area: A module in human extrastriate cortex specialized for face perception. The Journal of Neuroscience, 1997, 17:4302-4311.
53. Haxby, J. V., Hoffman, E. A., & Gobbini, M. I. The distributed human neural system for face perception. Trends in Cognition Science, 2000, 4: 223-233.
54. George, N., Driver, J., & Dolan, R. J. Seen gaze-direction modulates fusiform activity and its coupling with other brain areas during face processing. Neuroimage, 2001, 13: 1102-1112.
55. Gorno-Tempini, M. L., Price, C. J., Josephs, O., Vandenberghe, R., Cappa, S. F., Kapur, N., et al. The neural systems sustaining face and proper-name processing. Brain, 1998, 121:2103-2118.
56. Friesen, C. K., Kingstone, A. Abrupt onsets and gaze direction cues trigger independent reflexive attentional effects. Cognition, 2003, 87(1), B1-B10.
57. Gobbini, M. I., Haxby, J. V. Neural systems for recognition of familiar faces. Journal of Neurophysiology, 2007,45, 32-41.
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60. Kopell BH, Greenberg B, Rezai AR. Deep brain stimulation for psychiatric disorders. J Clin Neurophysiol, 2004,21:51-67
61. Siegle GJ, Carter CS, Thase ME. Use of FMRI to predict recovery from unipolar depression with cognitive behavior therapy. Am J Psychiatry, 2006,163:735-8.
62. Harmer CJ, Mackay CE, Reid CB, et al. Antidepressant drug treatment modifies the neural processing of nonconscious threat cues. Biol Psychiatry, 2006,59:816-20.
63. Goldapple K, Segal Z, Garson C, et al. Modulation of cortical-limbic pathways in major depression: treatment-specific effects of cognitive behavior therapy. Arch Gen Psychiatry, 2004,61:34-41
64. Mayberg HS. Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment. Br Med Bull, 2003,65:193-207.
65. Davidson RJ, Irwin W, Anderle MJ, et al. The neural substrates of affective processing in depressed patients treated with venlafaxine. Am J Psychiatry, 2003,160:64-75.
66. 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. Arch Gen Psychiatry, 2004, 61:877-89.
67. Kilts C. In vivo neuroimaging correlates of the efficacy of paroxetine in the treatment of mood and anxiety disorders. Psychopharmacol Bull, 2003, 37 Suppl 1:19-28.
68. Drevets WC, Burton H, Videen TO, et al. Blood flow changes in human somatosensory cortex during anticipated stimulation. Nature, 1995, 373:249-52.
69. Mazoyer B, Zago L, Mellet E, et al. Cortical networks for working memory and executive functions sustain the conscious resting state in man. Brain Res Bull, 2001,54:287-98.
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