Reduced sleep spindle activity in schizophrenia patients.
OBJECTIVE
High-density EEG during sleep represents a powerful new tool to reveal potential abnormalities in rhythm-generating mechanisms while avoiding confounding factors associated with waking activities. As a first step in this direction, the authors employed high-density EEG to explore whether sleep rhythms differ between schizophrenia subjects, healthy individuals, and a psychiatric control group with a history of depression.


METHODS
Healthy comparison subjects (N=17), medicated schizophrenia patients (N=18), and subjects with a history of depression (N=15) were recruited. Subjects were recorded during the first sleep episode of the night with a 256-electrode high-density EEG. Recordings were analyzed for changes in EEG power spectra, power topography, and sleep-specific cortical oscillations.


RESULTS
The authors found that the schizophrenia group had a significant reduction in centroparietal EEG power, from 13.75 to 15.00 Hz, in relation to both the comparison and depression groups. No significant difference in EEG power between the comparison and depression groups was identified. The authors also found a decrease in sleep spindle number, amplitude, duration, and integrated spindle activity in schizophrenia patients. Furthermore, integrated spindle activity had an effect size corresponding to 93.0% or 90.2% separation of the schizophrenia from the comparison or depression group.


CONCLUSIONS
Sleep spindles are generated by the thalamic reticular nucleus in conjunction with specific thalamic nuclei and are modulated by corticothalamic and thalamocortical connections. The deficit in sleep spindles in schizophrenia subjects may reflect dysfunction in thalamic-reticular and thalamocortical mechanisms and could represent a biological marker of illness.
Ferrarelli
Fabio
F
University of Wisconsin, Department of Psychiatry, 6001 Research Park Blvd., Madison, WI 53719, USA.
Huber
Reto
R
Peterson
Michael J
MJ
Massimini
Marcello
M
Murphy
Michael
M
Riedner
Brady A
BA
Watson
Adam
A
Bria
Pietro
P
Tononi
Giulio
G
D000293:Adolescent; D000328:Adult; D015415:Biomarkers; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000502:physiology / Q000503:physiopathology*; D003866:Depressive Disorder / Q000175:diagnosis / Q000503:physiopathology; D003937:Diagnosis, Differential; D004569:Electroencephalography / Q000379:methods / Q000706:statistics & numerical data*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009434:Neural Pathways / Q000502:physiology / Q000503:physiopathology; D010296:Parietal Lobe / Q000502:physiology / Q000503:physiopathology; D012154:Reticular Formation / Q000502:physiology / Q000503:physiopathology; D012559:Schizophrenia / Q000175:diagnosis* / Q000503:physiopathology*; D012890:Sleep / Q000502:physiology*; D012894:Sleep Stages / Q000502:physiology; D013788:Thalamus / Q000502:physiology / Q000503:physiopathology
D015415:Biomarkers