title: Thalamic dysfunction in schizophrenia suggested by whole-night deficits in slow and fast spindles.
abstract: OBJECTIVE
  Slow waves and sleep spindles are the two main oscillations occurring during non-REM sleep. While slow oscillations are primarily generated and modulated by the cortex, sleep spindles are initiated by the thalamic reticular nucleus and regulated by thalamo-reticular and thalamo-cortical circuits. In a recent high-density EEG study, the authors found that 18 medicated schizophrenia patients had reduced sleep spindles, compared with healthy and depressed subjects, during the first non-REM episode. In the present study, the authors investigated whether spindle deficits were present in a larger sample of schizophrenia patients, were consistent across the night, were related to antipsychotic medications, and were suggestive of impairments in specific neuronal circuits.
  
  
  METHODS
  Whole-night high-density EEG recordings were performed in 49 schizophrenia patients, 20 nonschizophrenia patients receiving antipsychotic medication, and 44 healthy subjects. In addition to sleep spindles, several parameters of slow waves were assessed.
  
  
  RESULTS
  Schizophrenia patients had whole-night deficits in spindle power (12-16 Hz) and in slow (12-14 Hz) and fast (14-16 Hz) spindle amplitude, duration, number, and integrated activity in the prefrontal, centroparietal, and temporal regions. Integrated spindle activity and spindle number had the largest effect sizes (effect size: ≥ 2.21). In contrast, no slow wave deficits were found in schizophrenia patients.
  
  
  CONCLUSIONS
  These results indicate that spindle deficits can be reliably established in schizophrenia, are stable across the night, are unlikely to be due to antipsychotic medications, and point to deficits in the thalamic reticular nucleus and thalamo-reticular circuits.
authors.affiliation: School of Medicine and Public Health, Department of Psychiatry, University of Wisconsin, Madison, WI 53719, USA.
authors.forename: Fabio
authors.initials: F
authors.lastname: Ferrarelli
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Peterson
authors.forename: Simone
authors.initials: S
authors.lastname: Sarasso
authors.forename: Brady A
authors.initials: BA
authors.lastname: Riedner
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Murphy
authors.forename: Ruth M
authors.initials: RM
authors.lastname: Benca
authors.forename: Pietro
authors.initials: P
authors.lastname: Bria
authors.forename: Ned H
authors.initials: NH
authors.lastname: Kalin
authors.forename: Giulio
authors.initials: G
authors.lastname: Tononi
mesh_terms: D000293:Adolescent; D000328:Adult; D014150:Antipsychotic Agents / Q000009:adverse effects / Q000627:therapeutic use; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D020646:Intralaminar Thalamic Nuclei / Q000187:drug effects / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology; D011569:Psychiatric Status Rating Scales; D012016:Reference Values; D012559:Schizophrenia / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D012815:Signal Processing, Computer-Assisted; D012890:Sleep / Q000502:physiology*; D013788:Thalamus / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D014150:Antipsychotic Agents