Investigation of Cortical Glutamate-Glutamine and γ-Aminobutyric Acid in Obsessive-Compulsive Disorder by Proton Magnetic Resonance Spectroscopy
Investigation of Cortical Glutamate-Glutamine and γ-Aminobutyric Acid in Obsessive-Compulsive Disorder by Proton Magnetic Resonance Spectroscopy
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DOI：
10.1038/npp.2012.132
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发表时间：
2012-11-01
影响因子：
7.6
通讯作者：
Kegeles, Lawrence S.
中科院分区：
文献类型：
--
作者：
Simpson, Helen B.;Shungu, Dikoma C.;Kegeles, Lawrence S.
皮质纹状体脑回路中的谷氨酸能异常被认为是强迫症（OCD）的基础。这些异常是否存在于患有强迫症的成年人中尚不清楚。我们使用质子磁共振波谱（H-1 MRS）来检验我们的假设，即与健康对照组相比，未用药的强迫症成人内侧前额叶皮层（MPFC）中的谷氨酸加谷氨酰胺（Glx）水平降低。还探索了g-氨基丁酸（GABA）的水平。24例未服药的成人强迫症患者和22例匹配的健康对照者在3.0 T下进行了1H MRS扫描。使用标准J编辑技术获得Glx和GABA的共振，并评估为MPFC（感兴趣区域）和背外侧前额叶皮层（DLPFC）中相对于体素组织水（W）的比率，以探索任何发现的区域特异性。在MPFC中，Glx/W在诊断组（p = 0.98）或性别（p = 0.57）之间没有差异。然而，与健康对照组（2.43 +/-0.45 x 10（-3），p = 0.045）相比，强迫症患者（2.16 +/-0.46 x 10（-3））的GABA/W降低;此外，强迫症发病年龄与MPFC GABA/W呈负相关（r =-0.50，p = 0.015）。MPFC GABA/W女性高于男性。在DLPFC中，诊断或性别对Glx/W或GABA/W没有主效应。这些数据表明，未经药物治疗的成人强迫症没有Glx异常的MPFC体素，包括前膝前扣带皮层。然而，它们可能降低了MPFC GABA水平。GABA异常如何导致强迫症患者皮质纹状体功能障碍值得进一步研究。Neuropsychopharmacology（2012）37，2684-2692; doi：10.1038/npp.2012.132; 2012年8月1日在线发表
Glutamatergic abnormalities in corticostriatal brain circuits are thought to underlie obsessive-compulsive disorder (OCD). Whether these abnormalities exist in adults with OCD is not clear. We used proton magnetic resonance spectroscopy (H-1 MRS) to test our hypothesis that unmedicated adults with OCD have reduced glutamate plus glutamine (Glx) levels in the medial prefrontal cortex (MPFC) compared with healthy controls. Levels of g-aminobutyric acid (GABA) were also explored. Twenty-four unmedicated adults with OCD and 22 matched healthy control subjects underwent 1 H MRS scans at 3.0 T. Resonances of both Glx and GABA were obtained using the standard J-editing technique and assessed as ratios relative to voxel tissue water (W) in the MPFC (the region of interest) and the dorsolateral prefrontal cortex (DLPFC) to explore the regional specificity of any finding. In the MPFC, Glx/W did not differ by diagnostic group (p = 0.98) or sex (p = 0.57). However, GABA/W was decreased in OCD (2.16 +/- 0.46 x 10(-3)) compared with healthy controls (2.43 +/- 0.45 x 10(-3), p = 0.045); moreover, age of OCD onset was inversely correlated with MPFC GABA/W (r = -0.50, p = 0.015). MPFC GABA/W was higher in females than in males. In the DLPFC, there were no main effects of diagnosis or gender on Glx/W or GABA/W. These data indicate that unmedicated adults with OCD do not have Glx abnormalities in a MPFC voxel that includes the pregenual anterior cingulate cortex. However, they may have decreased MPFC GABA levels. How GABA abnormalities might contribute to corticostriatal dysfunction in OCD deserves further study. Neuropsychopharmacology (2012) 37, 2684-2692; doi:10.1038/npp.2012.132; published online 1 August 2012