Proton magnetic resonance spectroscopic imaging in drug free patients with schizophrenia: Regional neuronal damage

Decreased left frontal lobe N-acetylaspartate in schizophrenia

“…In addition, the absence of choline signal elevation does not support reactive gliosis in the frontal lobe regions examined. Our N-acetylaspartate findings are consistent with two other preliminary investigations of the frontal lobe that used proton MRSI (6,8) as well as one study that used single voxel proton MRSI (7). The discrepancy between these studies and other proton MRSI studies (9, 10) that failed to detect any decrease in left frontal lobe N-acetylaspartate is most likely due to differences in spectroscopy techniques, voxel sizes (ranging from 0.84 ml to 11 ml), voxel positioning within the left frontal lobe, and the heterogeneous nature of the schizophrenic population.…”

“…Preliminary in vivo 1 H-MRSI investigations of the frontal lobes in patients with schizophrenia have yielded conflicting findings; some studies have reported significant decreases in frontal lobe N-acetylaspartate (6)(7)(8), while others have found no differences (9, 10). We conducted a pilot study using 1 H-MRSI to test the hypothesis that frontal lobe N-acetylaspartate would be reduced in schizophrenic patients compared to healthy subjects, implying reduced frontal lobe neuronal density.…”

On Localizing Schizophrenic Neuropathology

“…However, her dramatic results of a 40 percent reduction of cell number and a 25 percent reduction in volume of mediodorsal thalamus seem inconsistent with some negative postmortem (e.g., Lesch and Bogerts 1984) and in vivo imaging studies (e.g., Jernigan et al 1991). We have surveyed the thalamus using our MRI proton spectroscopic imaging method, which is sensitive to neuronal loss, and found no differences between patients and controls (Bertolino et al 1996 a , 1996 b ).…”

“…Our group has been exploring in vivo neurochemical pathology using a magnetic resonance imaging (MRI) proton spectroscopic technique that generates neurochemical maps of multiple brain slices with relatively high resolution (approximately 1 ml voxel size). We have found—in both chronic and never-medicated acute patients—a pattern of relatively reduced concentrations of N -acetyl aspartate (NAA), an intraneuronal marker, exclusively in mesial temporolimbic and dorsolateral prefrontal cortices, bilaterally (Bertolino et al 1996 a , 1996 b ). The neuropathological implications of this finding are uncertain (it does not correlate with hippocampal volume), but the finding does point to the temporolimbic cortex as a pathological site, and it appears to exclude chronicity as a factor.…”