title: Neurochemical and structural correlates of executive dysfunction in schizophrenia.
abstract: BACKGROUND
  Executive dysfunction is a core feature of schizophrenia. The neurochemical and structural changes associated with this deficit are, however, largely unclear. This study tested the hypothesis that changes in glutamate, glutamine and N-acetyl-aspartate (NAA) in hippocampal and dorsolateral prefrontal (DLPFC) regions as well as hippocampal, amygdalar and DLPFC volume reductions are associated with executive dysfunction.
  
  
  METHODS
  Twenty-nine subjects with schizophrenia and 31 healthy controls were examined by short-echo single voxel magnetic resonance spectroscopy of the left anterior hippocampus and the left DLPFC. Volumes of the hippocampi, amygdalae and DLPFC were measured bilaterally using manual volumetry. Executive functioning was assessed by the Wisconsin Card Sorting Test (WCST).
  
  
  RESULTS
  Poor WCST performance was associated with increased hippocampal glutamate concentrations among subjects with schizophrenia, not among healthy controls. Glutamate in the DLPFC as well as NAA or glutamine in the hippocampus or the DLPFC were not related to executive functioning in schizophrenia or healthy controls. Reduced amygdalar volume was associated with impaired executive functioning in subjects with schizophrenia (p=.06) and healthy controls (p=.04).
  
  
  CONCLUSIONS
  Altered hippocampal glutamatergic neurotransmission and amygdalar volume loss may be associated with executive dysfunction in schizophrenia.
authors.affiliation: Department of Psychiatry and Psychotherapy, University of Freiburg, Germany.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Rüsch
authors.forename: Ludger
authors.initials: L
authors.lastname: Tebartz van Elst
authors.forename: Gabi
authors.initials: G
authors.lastname: Valerius
authors.forename: Martin
authors.initials: M
authors.lastname: Büchert
authors.forename: Thorsten
authors.initials: T
authors.lastname: Thiel
authors.forename: Dieter
authors.initials: D
authors.lastname: Ebert
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hennig
authors.forename: Hans-Martin
authors.initials: HM
authors.lastname: Olbrich
mesh_terms: D000328:Adult; D000679:Amygdala / Q000473:pathology / Q000503:physiopathology; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001284:Atrophy; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D003072:Cognition Disorders / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology; D004292:Dominance, Cerebral; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009483:Neuropsychological Tests; D017397:Prefrontal Cortex / Q000473:pathology / Q000503:physiopathology; D011340:Problem Solving / Q000502:physiology*; D012563:Schizophrenia, Paranoid / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology
chemical_list: D005973:Glutamine; D001224:Aspartic Acid; D018698:Glutamic Acid; C000179:N-acetylaspartate