期刊
BIOLOGICAL PSYCHIATRY
卷 68, 期 7, 页码 625-633出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2010.04.013
关键词
Anterior cingulate cortex; functional magnetic resonance imaging; magnetic resonance spectroscopy; adults; N-acetylaspartate; glutamate; schizophrenia
资金
- University of Alabama Health Services Foundation
- Institute of Mental Health [R01 MH081014]
- National Institute of Health (NIH) [R01 NCI141663, R01 NS053998, U01 NS058634]
- Pfizer
Background: Neuroimaging and electrophysiologic studies have consistently provided evidence of impairment in anterior cingulate cortex/medial frontal cortex function in people with schizophrenia. In this study, we sought to clarify the nature of this abnormality by combining proton magnetic resonance spectroscopy (1H-MRS) with functional magnetic resonance imaging (fMRI) at 3T. Methods: We used single-voxel MRS acquired in the dorsal anterior cingulate cortex and fMRI during performance of a Stroop color-naming task to investigate the neurochemistry and functional response of the anterior cingulate cortex/medial frontal cortex in 26 stable, medicated subjects with schizophrenia and 23 matched healthy control subjects. Results: In schizophrenia subjects, we found decreased blood oxygen level dependent signal in the medial frontal wall, with significant clusters restricted to more dorsal regions compared with healthy subjects. In addition, we observed a trend-level decrease in N-acetylaspartate/creatine (NAA/Cr) levels and a significant positive correlation between NAA/Cr level and the blood oxygen level-dependent signal in schizophrenia subjects that did not exist in healthy subjects. Furthermore, in this group of medicated subjects, we did not find evidence of decreased glutamate + glutamine(Glx)/Cr levels, but there was a significant negative correlation between Glx/Cr levels and negative symptoms. Conclusions: Our results suggest that abnormal NAA levels, which may reflect a neuronal dysfunction related to schizophrenia, affect neuronal physiology, as evidenced by reduced blood oxygen level dependent response.
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