Resting state electroencephalogram oscillatory abnormalities in schizophrenia and psychotic bipolar patients and their relatives from the bipolar and schizophrenia network on intermediate phenotypes study.
BACKGROUND
Abnormal resting state electroencephalogram (EEG) oscillations are reported in schizophrenia (SZ) and bipolar disorder, illnesses with overlapping symptoms and genetic risk. However, less evidence exists on whether similar EEG spectral abnormalities are present in individuals with both disorders or whether these abnormalities are present in first-degree relatives, possibly representing genetic predisposition for these disorders.


METHODS
Investigators examined 64-channel resting state EEGs of 225 SZ probands and 201 first-degree relatives (SZR), 234 psychotic bipolar (PBP) probands and 231 first-degree relatives (PBPR), and 200 healthy control subjects. Eight independent resting state EEG spectral components and associated spatial weights were derived using group independent component analysis. Analysis of covariance was conducted on spatial weights to evaluate group differences. Relative risk estimates and familiality were evaluated on abnormal spectral profiles in probands and relatives.


RESULTS
Both SZ and PBP probands exhibited increased delta, theta, and slow and fast alpha activity. Post-hoc pair-wise comparison revealed increased frontocentral slow beta activity in SZ and PBP probands as well as SZR and PBPR. Augmented frontal delta activity was exhibited by SZ probands and SZR, whereas PBP probands and PBPR showed augmented fast alpha activity.


CONCLUSIONS
Both SZ and PBP probands demonstrated aberrant low-frequency activity. Slow beta activity was abnormal in SZ and PBP probands as well as SZR and PBPR perhaps indicating a common endophenotype for both disorders. Delta and fast alpha activity were unique endophenotypes for SZ and PBP probands, respectively. The EEG spectral activity exhibited moderate relative risk and heritability estimates, serving as intermediate phenotypes in future genetic studies for examining biological mechanisms underlying the pathogenesis of the two disorders.
Olin Neuropsychiatry Research Center, Hartford Hospital (IOL campus), Hartford, Connecticut. Electronic address: Balaji.narayanan@hhchealth.org.
Balaji
B
Narayanan
Olin Neuropsychiatry Research Center, Hartford Hospital (IOL campus), Hartford, Connecticut.
Kasey
K
O'Neil
Olin Neuropsychiatry Research Center, Hartford Hospital (IOL campus), Hartford, Connecticut.
Clifton
C
Berwise
Olin Neuropsychiatry Research Center, Hartford Hospital (IOL campus), Hartford, Connecticut.
Michael C
MC
Stevens
Department of Electrical and Computer Engineering, University of New Mexico, Albuquerque, New Mexico.
Vince D
VD
Calhoun
Department of Psychology, University of Georgia, Athens, Georgia.
Brett A
BA
Clementz
Department of Psychiatry, UT Southwestern Medical School, Dallas, Texas.
Carol A
CA
Tamminga
Department of Psychiatry, UT Southwestern Medical School, Dallas, Texas.
John A
JA
Sweeney
Department of Psychiatry, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Matcheri S
MS
Keshavan
Olin Neuropsychiatry Research Center, Hartford Hospital (IOL campus), Hartford, Connecticut; Department of Psychiatry and Neurobiology, Yale University School of Medicine, New Haven, Connecticut.
Godfrey D
GD
Pearlson
D000328:Adult; D001714:Bipolar Disorder / Q000235:genetics / Q000503:physiopathology*; D058256:Brain Waves; D002540:Cerebral Cortex / Q000503:physiopathology*; D005190:Family; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012559:Schizophrenia / Q000235:genetics / Q000503:physiopathology*
Bipolar disorder; EEG; intermediate phenotypes; psychosis; resting state; schizophrenia