What have we learned from proton magnetic resonance spectroscopy about schizophrenia? A critical update
What have we learned from proton magnetic resonance spectroscopy about schizophrenia? A critical update
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DOI：
10.1097/01.yco.0000214337.29378.cd
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发表时间：
2006-03-01
影响因子：
6.9
通讯作者：
Bustillo, J
中科院分区：
文献类型：
--
作者：
Abbott, C;Bustillo, J
综述的目的本综述讨论了最近的研究调查精神分裂症的质子磁共振波谱，包括第一个荟萃分析[Steen RG，Hamer RM，Lieberman X测量脑代谢物的1 H磁共振波谱在精神分裂症患者：系统性回顾和荟萃分析。神经心理学2005; 30：1949-1962]。我们还强调方法问题，并建议今后的研究模式，以进一步探讨acumamatergic功能障碍在schizophrenia.Recent的研究结果尽管方法的差异，光谱研究与精神分裂症显示减少N-乙酰天冬氨酸在内侧颞叶和前额叶区域。其他区域，如前扣带、顶叶皮质、丘脑和小脑也可能有N-乙酰天冬氨酸减少。质子磁共振波谱研究在较高的领域和较短的回波时间显示异常谷氨酸和谷氨酰胺。动物研究表明，患者和对照组之间代谢物的差异不是由于抗精神病药物暴露，长期暴露于N-甲基-D-天冬氨酸拮抗剂导致颞叶皮层中N-乙酰天冬氨酸减少。人类和动物的研究都支持一个兴奋性毒性amatergically介导的过程，可以解释减少N-乙酰天冬氨酸，体积损失，和精神分裂症的不良结局。摘要使用较高的场强和纵向研究可能会揭示一个渐进的兴奋性毒性amatergic过程，导致N-乙酰天冬氨酸和体积减少。这可能导致神经保护剂的发展，改变精神分裂症的进程。
Purpose of review This review discusses recent studies investigating schizophrenia with proton magnetic resonance spectroscopy including the first meta-analysis [Steen RG, Hamer RM, Lieberman X Measurement of brain metabolites by 1 H magnetic resonance spectroscopy in patients with schizophrenia: a systematic review and meta-analysis. Neuropsychology 2005; 30:1949-1962]. We also highlight methodological issues and suggest a modality for future research to further explore glutamatergic dysfunction in schizophrenia.Recent findings Despite methodological differences, spectroscopy studies with schizophrenia show reductions in N-acetylaspartate in the medial temporal and prefrontal regions. Other areas such as the anterior cingulate, parietal cortex thalamus, and cerebellum may also have N-acetylaspartate reductions. The proton magnetic resonance spectroscopy studies at higher fields and with shorter echo time have revealed abnormalities in glutamate and glutamine. Animal studies have shown that the discrepancies in metabolites between patients and controls are not due to antipsychotic medication exposure, and that chronic exposure to N-methyl-D-aspartate antagonists has produced decreased N-acetylaspartate in the temporal cortex. The human and animal studies both support an excitoxic glutamatergically mediated process that may explain decreased N-acetylaspartate, volume loss, and the poor outcomes of schizophrenia.Summary Use of higher field strengths and longitudinal studies may reveal a progressive excitoxic glutamatergic process that leads to N-acetylaspartate and volume reductions. This may lead to the development of neuroprotective agents that change the course of schizophrenia.