title: Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia.
abstract: OBJECTIVE
  Deficits in sensory gating are a common feature of schizophrenia. Failure of inhibitory gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, has been previously studied using EEG methods. These methods yield information about the temporal characteristics of sensory gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor sensory gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of sensory gating deficits in schizophrenia.
  
  
  METHODS
  Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a sensory gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects.
  
  
  RESULTS
  Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI sensory gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG sensory gating measure.
  
  
  CONCLUSIONS
  Poor sensory gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.
authors.affiliation: VISN19/MIRECC, Denver VA Medical Center, Denver, Colorado, USA. Jason.Tregellas@UCHSC.edu
authors.forename: Jason R
authors.initials: JR
authors.lastname: Tregellas
authors.forename: Deana B
authors.initials: DB
authors.lastname: Davalos
authors.forename: Donald C
authors.initials: DC
authors.lastname: Rojas
authors.forename: Merilyne C
authors.initials: MC
authors.lastname: Waldo
authors.forename: Linzi
authors.initials: L
authors.lastname: Gibson
authors.forename: Korey
authors.initials: K
authors.lastname: Wylie
authors.forename: Yiping P
authors.initials: YP
authors.lastname: Du
authors.forename: Robert
authors.initials: R
authors.lastname: Freedman
mesh_terms: D000328:Adult; D001303:Auditory Cortex / Q000098:blood supply / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004569:Electroencephalography; D005260:Female; D006624:Hippocampus / Q000098:blood supply* / Q000503:physiopathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D017397:Prefrontal Cortex / Q000098:blood supply* / Q000503:physiopathology*; D012559:Schizophrenia / Q000453:epidemiology* / Q000503:physiopathology*; D012678:Sensation Disorders / Q000453:epidemiology* / Q000503:physiopathology*; D013788:Thalamus / Q000098:blood supply* / Q000503:physiopathology*