Furthermore, it is unknown whether abnormalities in transient GBRs observed in schizophrenia patients predate the onset of psychosis, or co-occur with illness onset. This question can be addressed by studying patients at clinical high risk (CHR) for developing psychosis. Being at “clinical high risk” is defined by the Criteria of Prodromal Syndromes (COPS; Miller et al., 2002) and the similar criteria for At Risk Mental States (ARMS; Yung and McGorry, 1996). The North American Prodromal Longitudinal Study (NAPLS) consortium reported that 35% of patients meeting COPS criteria converted to a psychotic disorder within a 2.5 year follow-up period (Cannon et al., 2008). An increasing number of studies are finding that electrophysiological abnormalities associated with schizophrenia are evident in clinical high risk patients (Bodatsch et al., 2011; Brockhaus-Dumke et al., 2008b; Jahshan et al., 2011; Perez et al., 2011a; Perez et al., 2011b; Shin et al., 2009; van Tricht et al., 2010); however, none has assessed whether GBRs are abnormal in these patients. GBR abnormalities in CHR patients may reflect vulnerability to the disorder and/or abnormal neurodevelopment, particularly in connection with
