Impairments in frontal cortical γ synchrony and cognitive control in schizophrenia

TLDR

Cognitive control deficits in schizophrenia stem from disrupted prefrontal cortical function, and γ‑band synchrony—linked to many cognitive processes—may underlie these deficits. The study aimed to assess induced γ‑band activity during a cognitive control task to investigate its role in prefrontal cortical function. We recorded induced γ‑band activity while participants performed a cognitive control task, linking it to prefrontal cortical activations observed in imaging studies. Healthy subjects showed increased prefrontal γ‑band activity with higher cognitive control demands, whereas schizophrenia patients lacked this modulation; the γ‑band disturbances correlated with symptoms and predicted performance in controls but not in patients, linking thalamofrontocortical abnormalities to frontal cortical dysfunction and suggesting a role for γ‑band synchrony deficits in cognitive control impairments.

Abstract

A critical component of cognitive impairments in schizophrenia can be characterized as a disturbance in cognitive control, or the ability to guide and adjust cognitive processes and behavior flexibly in accordance with one's intentions and goals. Cognitive control impairments in schizophrenia are consistently linked to specific disturbances in prefrontal cortical functioning, but the underlying neurophysiologic mechanisms are not yet well characterized. Synchronous γ-band oscillations have been associated with a wide range of perceptual and cognitive processes, raising the possibility that they may also help entrain prefrontal cortical circuits in the service of cognitive control processes. In the present study, we measured induced γ-band activity during a task that reliably engages cognitive control processes in association with prefrontal cortical activations in imaging studies. We found that higher cognitive control demands were associated with increases in induced γ-band activity in the prefrontal areas of healthy subjects but that control-related modulation of prefrontal γ-band activity was absent in schizophrenia subjects. Disturbances in γ-band activity in patients correlated with illness symptoms, and γ-band activity correlated positively with performance in control subjects but not in schizophrenia patients. Our findings may provide a link between previously reported postmortem abnormalities in thalamofrontocortical circuitry and alterations in prefrontal activity observed in functional neuroimaging studies. They also suggest that deficits in frontal cortical γ-band synchrony may contribute to the cognitive control impairments in schizophrenia.