Neural anomalies during sustained attention in first-degree biological relatives of schizophrenia patients

被引:57
作者
Sponheim, Scott R.
McGuire, Kathryn A.
Stanwyck, John J.
机构
[1] Vet Affairs Med Ctr, Minneapolis, MN 55417 USA
[2] Univ Minnesota, Dept Psychiat & Psychol, Minneapolis, MN USA
关键词
schizophrenia; sustained attention; vigilance; electrophysiology; genetic liability; evoked potential;
D O I
10.1016/j.biopsych.2005.11.017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: A deficit in sustained attention might serve as an endophenotype for schizophrenia and therefore be a useful tool in understanding the genetic underpinnings of the disorder. We sought to detail functional brain abnormalities associated with sustained attention (i.e., vigilance) in individuals with genetic liability for schizophrenia. Methods: We gathered electrophysiological data from 23 schizophrenia patients, 28 first-degree biological relatives of schizophrenia patients, and 23 nonpsychiatric control subjects while they performed a degraded-stimulus continuous performance task. Inclusion of sensory control trials allowed separation of target detection and vigilance effects on brain potentials. Results. Schizophrenia patients, but not relatives, showed a behavioral deficit in sustained attention. During target detection, relatives exhibited diminished late positive amplitudes (P3b, i.e., P300) over parietal brain regions and augmented early posterior (Pi) and right frontal (anterior NI) potentials. Electrophysiological anomalies were still evident after the exclusion of three relatives with histories of psychosis. Conclusions: Genetic liability for schizophrenia is associated with augmented early and diminished late brain potentials during sustained attention. Electrophysiological anomalies suggestive of rightfrontal-posteriorparietal dysfunction might represent neural expression ofgenetic liability for schizophrenia. Electrophysiological indices also seem to be more sensitive than behavioral measures in assessing genetic liabilityfor schizophrenia.
引用
收藏
页码:242 / 252
页数:11
相关论文
共 68 条
[1]  
Andreasen N, 1984, SCALE ASSESSMENT POS
[2]   Neurocognitive impairments in nonpsychotic parents of children with schizophrenia and attention-deficit/hyperactivity disorder - The University of California, Los Angeles family study [J].
Asarnow, RF ;
Nuechterlein, KH ;
Subotnik, KL ;
Fogelson, DL ;
Torquato, RD ;
Payne, DL ;
Asamen, J ;
Mintz, J ;
Guthrie, D .
ARCHIVES OF GENERAL PSYCHIATRY, 2002, 59 (11) :1053-1060
[3]  
BLACKWOOD DHR, 1991, ARCH GEN PSYCHIAT, V48, P899
[4]   Schizophrenia and affective disorders - Cosegregation with a translocation at chromosome 1q42 that directly disrupts brain-expressed genes: Clinical and P300 findings in a family [J].
Blackwood, DHR ;
Fordyce, A ;
Walker, MT ;
St Clair, DM ;
Porteous, DJ ;
Muir, WJ .
AMERICAN JOURNAL OF HUMAN GENETICS, 2001, 69 (02) :428-433
[5]  
BROOKER BH, 1986, J CLIN PSYCHOL, V42, P982, DOI 10.1002/1097-4679(198611)42:6<982::AID-JCLP2270420624>3.0.CO
[6]  
2-G
[7]  
BUCHSBAUM MS, 1992, ARCH GEN PSYCHIAT, V49, P935
[8]  
Chen WJ, 2000, AM J MED GENET, V97, P52, DOI 10.1002/(SICI)1096-8628(200021)97:1<52::AID-AJMG7>3.0.CO
[9]  
2-6
[10]   Sustained attention deficit and schizotypal personality features in nonpsychotic relatives of schizophrenic patients [J].
Chen, WJ ;
Liu, SK ;
Chang, CJ ;
Lien, YJ ;
Chang, YH ;
Hwu, HG .
AMERICAN JOURNAL OF PSYCHIATRY, 1998, 155 (09) :1214-1220