REGIONALLY SPECIFIC PATTERN OF NEUROCHEMICAL PATHOLOGY IN SCHIZOPHRENIA AS ASSESSED BY MULTISLICE PROTON MAGNETIC-RESONANCE SPECTROSCOPIC IMAGING

Citation
A. Bertolino et al., REGIONALLY SPECIFIC PATTERN OF NEUROCHEMICAL PATHOLOGY IN SCHIZOPHRENIA AS ASSESSED BY MULTISLICE PROTON MAGNETIC-RESONANCE SPECTROSCOPIC IMAGING, The American journal of psychiatry, 153(12), 1996, pp. 1554-1563
Citations number
55
Categorie Soggetti
Psychiatry,Psychiatry
ISSN journal
0002953X
Volume
153
Issue
12
Year of publication
1996
Pages
1554 - 1563
Database
ISI
SICI code
0002-953X(1996)153:12<1554:RSPONP>2.0.ZU;2-E
Abstract
Objective: Several single-voxel proton magnetic resonance spectroscopy (H-1-MAS) studies of patients with schizophrenia have found evidence of reductions of N-acetyl-aspartate (NAA) concentrations in the tempor al lobes. Multislice proton magnetic resonance spectroscopy imaging (H -1-MRSI) permits simultaneous acquisition and mapping of NAA, choline- containing compounds (CHO), and creatine/phosphocreatine (CRE) signal intensities from multiple whole brain slices consisting of 1.4-ml sing le-volume elements. We have used H-1-MRSI to assess the regional speci ficity of previously reported changes of metabolite signal intensities in schizophrenia. Hippocampal volume was also measured to test the re lationship between H-1-MRSI findings and tissue volume in this region. Method: Ratios of areas under the metabolite peaks of she proton spec tra were determined (i.e., NAA/CRE, NAA/CHO, CHO/CRE) for multiple cor tical and subcortical regions in 10 inpatients with schizophrenia. Res ults: Patients showed significant reductions of NAA/CRE and NAA/CHO bi laterally in the hippocampal region and in the dorsolateral prefrontal cortex. There were no significant changes in CHO/CRE or in NAA ratios in any other area sampled. No significant correlation was found betwe en metabolite ratios in the hippocampal region and its volume. Conclus ions: NAA-relative signal intensity reductions in schizophrenia appear to be remarkably localized, involving primarily she hippocampal regio n and the dorsolateral prefrontal cortex, two regions implicated promi nently in the pathophysiology of this disorder.