title: Thalamocortical disconnection in the orbitofrontal region associated with cortical thinning in schizophrenia.
abstract: BACKGROUND
  Dysfunction of the thalamocortical pathway has been proposed as a putative underlying pathology of schizophrenia. Although the mechanisms involved remain unclear, postmortem studies suggest the involvement of altered neural projections from the thalamus to layers within the prefrontal cortex.
  
  
  OBJECTIVE
  To investigate thalamocortical connectivity in schizophrenia and to examine its possible association with cortical thinning in vivo.
  
  
  METHODS
  Case-control cross-sectional study.
  
  
  METHODS
  Department of Psychiatry at Kyoto University Hospital, Japan.
  
  
  METHODS
  A total of 37 patients with schizophrenia and 36 age-, sex-, and education-matched healthy controls recruited from the local community underwent diffusion-weighted imaging and T1-weighted 3-dimensional magnetic resonance imaging.
  
  
  METHODS
  Probabilistic tractography was performed to investigate thalamocortical pathways. Group differences in mean fractional anisotropy (FA) values were examined in the entire thalamocortical pathway, the thalamolateral prefrontal pathway, the thalamomedial prefrontal pathway, and the thalamo-orbitofrontal pathway. Surface-based analysis was performed to investigate cortical thickness, and the correlation between FA values and cortical thickness was examined.
  
  
  RESULTS
  The patient group exhibited reduced FA values within the right thalamo-orbitofrontal pathway (P < .05 for the 8 group comparisons of FA, Bonferroni correction). In the patient group only, the mean FA value for this pathway was positively correlated with thickness of the right frontal polar and lateral orbitofrontal cortices (P < .05, clusterwise correction).
  
  
  CONCLUSIONS
  These results suggest that, in schizophrenia, regional thalamocortical white matter pathology is specifically associated with cortical pathology in regions where fibers connect.
authors.affiliation: Department of Psychiatry, Graduate School of Medicine, Kyoto University, Japan.
authors.forename: Manabu
authors.initials: M
authors.lastname: Kubota
authors.forename: Jun
authors.initials: J
authors.lastname: Miyata
authors.forename: Akihiko
authors.initials: A
authors.lastname: Sasamoto
authors.forename: Genichi
authors.initials: G
authors.lastname: Sugihara
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Yoshida
authors.forename: Ryosaku
authors.initials: R
authors.lastname: Kawada
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Fujimoto
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Nobukatsu
authors.initials: N
authors.lastname: Sawamoto
authors.forename: Hidenao
authors.initials: H
authors.lastname: Fukuyama
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Takahashi
authors.forename: Toshiya
authors.initials: T
authors.lastname: Murai
mesh_terms: D000328:Adult; D016880:Anisotropy; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D038524:Diffusion Magnetic Resonance Imaging / Q000295:instrumentation / Q000379:methods*; D005260:Female; D006801:Humans; D008297:Male; D009434:Neural Pathways / Q000473:pathology*; D009483:Neuropsychological Tests; D017397:Prefrontal Cortex / Q000473:pathology*; D011569:Psychiatric Status Rating Scales; D012559:Schizophrenia / Q000473:pathology*; D013788:Thalamus / Q000473:pathology*