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

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.

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.

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 (P1) and right frontal (anterior N1) potentials. Electrophysiological anomalies were still evident after the exclusion of three relatives with histories of psychosis.

Genetic liability for schizophrenia is associated with augmented early and diminished late brain potentials during sustained attention. Electrophysiological anomalies suggestive of right frontal-posterior parietal dysfunction might represent neural expression of genetic liability for schizophrenia. Electrophysiological indices also seem to be more sensitive than behavioral measures in assessing genetic liability for schizophrenia.