Changes in brain metabolism associated with remission in unipolar major depression

被引:106
作者
Holthoff, VA
Beuthien-Baumann, B
Zündorf, G
Triemer, A
Lüdecke, S
Winiecki, P
Koch, R
Füchtner, F
Herholz, K
机构
[1] Univ Cologne, Dept Psychiat & Psychotherapy, Cologne, Germany
[2] Univ Cologne, Dept Nucl Med, Cologne, Germany
[3] Univ Cologne, PET Ctr, Cologne, Germany
[4] Univ Cologne, Dept Neurol, Cologne, Germany
[5] Max Planck Inst Neurol Res, Cologne, Germany
[6] Tech Univ Dresden, Inst Med Informat & Biometr, D-8027 Dresden, Germany
[7] Res Ctr Rossendorf, PET Ctr, Inst Bioorgan & Radiopharmaceut Chem, Dresden, Germany
关键词
depressive disorder; tomography; emission-computed; limbic system; frontal lobe; cerebellum;
D O I
10.1111/j.1600-0447.2004.00351.x
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objective: Functional brain correlates of remission in patients with major depressive disorder (MDD) are measured with positron emission tomography (PET) and F-18-fluorodeoxyglucose. Method: Glucose metabolism was measured in patients (n = 41) with moderate to severe MDD during acute depression and in the remitted state defined as a period of asymptomatic condition over 12 weeks. Data analyses used a region-of-interest (ROI) approach and statistical parametric mapping (SPM). Results: There were significant decreases in metabolism upon remission with respect to the baseline scan in left prefrontal, anterior temporal and anterior cingulate cortex and bilateral thalamus (SPM analysis) and bilateral putamen and cerebellum (SPM and ROI analyses). There was a significant asymmetry in prefrontal and anterior cingulate cortex metabolism with lower metabolism in the left hemisphere that persisted despite clinical remission. Conclusion: These findings support the hypothesis that selective monoamine reuptake inhibition leads to an attenuation of a brain circuit that mediates depressive symptomatology.
引用
收藏
页码:184 / 194
页数:11
相关论文
共 93 条
[51]  
Manji HK, 2003, BIOL PSYCHIAT, V53, P707, DOI 10.1016/S0006-3223(03)00117-3
[52]   Positron emission tomographic imaging of serotonin activation effects on prefrontal cortex in healthy volunteers [J].
Mann, JJ ;
Malone, KM ;
Diehl, DJ ;
Perel, J ;
Nichols, TE ;
Mintun, MA .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1996, 16 (03) :418-426
[53]  
MARTINOT JL, 1990, AM J PSYCHIAT, V147, P1313
[54]   Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment [J].
Mayberg, HS .
BRITISH MEDICAL BULLETIN, 2003, 65 :193-+
[55]  
Mayberg HS, 1997, J NEUROPSYCH CLIN N, V9, P471
[56]  
Mayberg HS, 1999, AM J PSYCHIAT, V156, P675
[57]   Regional metabolic effects of fluoxetine in major depression: Serial changes and relationship to clinical response [J].
Mayberg, HS ;
Brannan, SK ;
Tekell, JL ;
Silva, JA ;
Mahurin, RK ;
McGinnis, S ;
Jerabek, PA .
BIOLOGICAL PSYCHIATRY, 2000, 48 (08) :830-843
[58]   Cingulate function in depression: A potential predictor of treatment response [J].
Mayberg, HS ;
Brannan, SK ;
Mahurin, RK ;
Jerabek, PA ;
Brickman, JS ;
Tekell, JL ;
Silva, JA ;
McGinnis, S ;
Glass, TG ;
Martin, CC ;
Fox, PT .
NEUROREPORT, 1997, 8 (04) :1057-1061
[59]   QUANTITATION IN POSITRON EMISSION COMPUTED-TOMOGRAPHY .5. PHYSICAL-ANATOMICAL EFFECTS [J].
MAZZIOTTA, JC ;
PHELPS, ME ;
PLUMMER, D ;
KUHL, DE .
JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY, 1981, 5 (05) :734-743
[60]   No effect of depression on [15O]H2O PET response to intravenous d-fenfluramine [J].
Meyer, JH ;
Kennedy, S ;
Brown, GM .
AMERICAN JOURNAL OF PSYCHIATRY, 1998, 155 (09) :1241-1246