title: Glutamatergic changes in the cerebral white matter associated with schizophrenic exacerbation.
abstract: OBJECTIVE
  Glutamatergic dysfunction in the brain has been implicated in the pathophysiology of schizophrenia. This study was aimed to examine several brain chemical mediators, including Glx (glutamate + glutamine), using (1)H magnetic resonance spectroscopy (MRS) in medicated patients with schizophrenia, with and without psychotic exacerbation.
  
  
  METHODS
  (1)H MRS was acquired in 24 patients with schizophrenia, with psychotic exacerbation; 22 patients without exacerbation; and 27 age- and sex-matched healthy volunteers. The levels of metabolites were measured in the left frontal and inferior parietal white matter and compared across the three groups.
  
  
  RESULTS
  The Glx level was significantly elevated in the left inferior parietal white matter in the patients with psychotic exacerbation in comparison with that in the healthy volunteers and the patients without exacerbation (P < 0.05). We also detected that there was a significant correlation between Positive and Negative Syndrome Scale-positive scale and Glx level in the left parietal white matter (r = 0.51, P < 0.001).
  
  
  CONCLUSIONS
  Higher than normal Glx levels indicate glutamatergic overactivity in the left inferior parietal white matter with schizophrenic exacerbation, a finding that is in accordance with the glutamatergic hypothesis in schizophrenia. The Glx level measured by (1)H MRS could be a biomarker for exacerbation in schizophrenia.
authors.affiliation: Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. ota@ncnp.go.jp
authors.forename: M
authors.initials: M
authors.lastname: Ota
authors.forename: M
authors.initials: M
authors.lastname: Ishikawa
authors.forename: N
authors.initials: N
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Hori
authors.forename: D
authors.initials: D
authors.lastname: Sasayama
authors.forename: K
authors.initials: K
authors.lastname: Hattori
authors.forename: T
authors.initials: T
authors.lastname: Teraishi
authors.forename: Y
authors.initials: Y
authors.lastname: Nakata
authors.forename: H
authors.initials: H
authors.lastname: Kunugi
mesh_terms: D000328:Adult; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001923:Brain Chemistry / Q000502:physiology*; D016022:Case-Control Studies; D018450:Disease Progression; D018846:Excitatory Amino Acids / Q000378:metabolism / Q000502:physiology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism / Q000502:physiology*; D005973:Glutamine / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D059906:Neuroimaging; D010296:Parietal Lobe / Q000378:metabolism / Q000503:physiopathology; D012559:Schizophrenia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018846:Excitatory Amino Acids; D005973:Glutamine; D018698:Glutamic Acid