VGO phase locking evoked by standard stimuli in an oddball task was reduced in SZ. Previously we reported that Gestalt stimuli evoked the VGO in healthy individuals but not in chronic schizophrenia patients (6
). One possible explanation was that this VGO deficit reflected a specific failure of synchronization to Gestalt stimuli. The present results rule this out because the stimulus used here was a letter.
Another explanation was that the VGO deficit reflected a failure of synchronization to “target-like” stimuli, as the VGO can be influenced by the degree to which a particular stimulus matches the target stimulus in a discrimination task (31
). However, here the VGO was evoked in HC by standard stimuli in an oddball task that were not associated with a manual response, rather than target stimuli as in the Gestalt perception task. Thus, the VGO deficit has been found in two different tasks for different stimuli with differing response requirements. These results suggest that the VGO deficit may be a general phenomenon in schizophrenia, independent of task and stimulus type.
The origin of the VGO deficit is not clear. One possibility is some neural circuitry abnormality in visual cortex that prevents gamma-frequency synchronization from occurring. Another possibility is deficient attentional modulation from the dorsolateral prefrontal cortex (DLPFC) (32
). In healthy individuals the VGO is influenced by attentional demands (33
) and target-match effects (31
), so the failure of an attentional signal to enhance neuronal synchronization in visual cortex could impair the VGO. For instance, Barceló et al (35
) found that attention-sensitive visual evoked potentials were reduced over the hemisphere ipsilateral to a DLPFC lesion. The VGO deficit could represent a similar failure of attentional modulation of sensory processing, given the evidence of DLPFC neural circuitry abnormalities (4
) and attentional dysfunction (38
) in schizophrenia.
The AGO was not abnormal in SZ, consistent with the finding of Gallinat et al. (16
) that AGO evoked power did not differ between healthy individuals and unmedicated, mainly first-episode schizophrenics. Here the patients were chronic and medicated, so together these studies suggest that the AGO is generally not affected in schizophrenia. (Nor was an auditory N1 deficit found; see Supplementary Material
.) The absence of an AGO deficit is surprising given the abundance of structural and functional abnormalities of the auditory system in schizophrenia (17
), especially since the gamma-band auditory steady-state response is reduced in schizophrenia (39
). But since our study and that of Gallinat et al. used oddball tasks with simple tone stimuli, it remains to be determined whether the absence of an AGO deficit is specific to this particular type of task and/or stimuli.
While none of the electrophysiological measures was correlated with antipsychotic medication dosage, possible influences of medication cannot be ruled out, given the inexact nature of chlorpromazine equivalency and the complex effects of atypical antipsychotics on neural activity.