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Proton Magnetic Resonance Spectroscopy (1H MRS) of the Hippocampal Formation in Schizophrenia: A Pilot Study

Published online by Cambridge University Press:  02 January 2018

Henry A. Nasrallah ,
Thomas E. Skinner ,
Petra Schmalbrock  and
Pierre-Marle Robitaille
Henry A. Nasrallah*
Affiliation:
Ohio State University, College of Medicine, Columbus, Ohio, USA
Thomas E. Skinner
Affiliation:
Ohio State University, College of Medicine, Columbus, Ohio, USA
Petra Schmalbrock
Affiliation:
Ohio State University, College of Medicine, Columbus, Ohio, USA
Pierre-Marle Robitaille
Affiliation:
Ohio State University, College of Medicine, Columbus, Ohio, USA
*
Professor Nasrallah, Department of Psychiatry, Ohio State University, College of Medicine, 473 W. 12th Avenue, Columbus, Ohio 43210, USA
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Abstract

Background

Recent post-mortem and magnetic resonance imaging (MRI) studies strongly suggest a decrease in the volume of the hippocampus and other limbic temporal structures in schizophrenia. Therefore, we hypothesised that N-acetyl aspartate (NAA) which is found mainly in neurons and which can be measured by proton magnetic resonance spectroscopy (1H MRS) would be decreased in the limbic temporal region in schizophrenia.

Method

Consenting subjects fulfilling DSM-III-R criteria for schizophrenia (n = 11) and matched healthy volunteers (n = 11) who were recruited in a tertiary university referral centre, participated in a 1H MRS brain study. Proton MRS spectra were obtained from a 12 cm3 voxel (2 × 2 × 3 cm) in the right and left hippocampus/amygdala region. A researcher blind to the source of the spectra, measured the NAA intensity in all subjects, which were then statistically compared across the two groups.

Results

NAA intensities were significantly reduced in the right hippocampus/amygdala region of schizophrenic patients (P = 0.038). The difference of the left side did not reach significance at the 95% confidence level.

Conclusions

The findings of decreased NAA in this study suggest that there may be a decrement in neuronal number or tissue volume of the right hippocampal/amygdala region in schizophrenia. Biochemical alterations in the metabolism of NAA in schizophrenia may be an alternative explanation. The findings are consistent with other types of post-mortem and in vivo evidence for hypoplasia of the limbic temporal structures in schizophrenia, postulated to be of neurodevelopmental pathogenesis.

Type
Papers
Information
The British Journal of Psychiatry , Volume 165 , Issue 4 , October 1994 , pp. 481 - 485
Copyright
Copyright © Royal College of Psychiatrists, 1994 

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References

Bruhn, H., Frahm, J., Gyngell, M. L., et al (1989) Cerebral metabolism in man after acute stroke: new observations using localized proton NMR spectroscopy. Magnetic Resonance in Medicine, 9, 126–131.CrossRefGoogle ScholarPubMed
Conrad, A. J. & Scheibel, A. B. (1987) Schizophrenia and the hippocampus: The embryological hypothesis extended. Schizophrenia Bulletin, 13, 577–587.CrossRefGoogle ScholarPubMed
Deakin, J. F. W., Slater, P., Simpson, M. D. C., et al (1989) Frontal cortical and left temporal glutamatergic dysfunction in schizophrenia. Journal of Neurochemistry, 52, 1781–1786.CrossRefGoogle ScholarPubMed
Haase, A., Frahm, J., Haenicke, W., et al (1985) 1H NMRS chemical shift selective (CHESS) imaging. Physics in Medicine and Biology, 30, 341–344.CrossRefGoogle Scholar
Kerwin, R. W., Patel, S., Meldrum, B. S., et al (1989) Asymmetrical loss of glutamate receptor subtype in left hippocampus in schizophrenia. Lancet, i, 583–584.Google Scholar
Lock, T., Abou-Saleh, M. T. & Edwards, R. H. T. (1990) Psychiatry and the new magnetic resonance era. British Journal of Psychiatry, 157 (suppl. 9), 38–55.CrossRefGoogle Scholar
Mednick, S. A., Cannon, T. D., Barr, C. E., et al (eds) (1991) Developmental Neuropathology of Schizophrenia. New York: Plenum Press.CrossRefGoogle Scholar
Moonen, C. T. & van Zijil, P. C. M. (1990) Highly effective water suppression for in vivo proton NMR spectroscopy (DRYSTEAM). Journal of Magnetic Resonance, 88, 28–41.Google Scholar
Nadler, J. & Cooper, J. (1972) N-acetyl-L-aspartic acid content of human neural tumors and bovine peripheral nervous tissue. Journal of Neurochemistry, 19, 313–319.CrossRefGoogle Scholar
Nasrallah, H. A. (1993) Neurodevelopmental pathogenesis of schizophrenia. Psychiatric Clinics of North America, 16, 269–280.CrossRefGoogle ScholarPubMed
Reynolds, G. P. (1983) Increased concentrations and lateral asymmetry of amygdala dopamine in schizophrenia. Nature, 305, 527–529.CrossRefGoogle ScholarPubMed
Suddath, R. L., Christison, G. W., Torrey, E. F., et al (1990) Anatomical abnormalities in the brains of monozygotic twins discordant for schizophrenia. New England Journal of Medicine, 322, 789–794.CrossRefGoogle ScholarPubMed
Yurgelun-todd, D. A., Renshaw, P., Waternaux, C. M., et al (1993) 1H magnetic resonance spectroscopy (MRS) of the temporal lobes in schizophrenia. Schizophrenia Research, 9, 213.CrossRefGoogle Scholar
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