Evidence for prefrontal cortex hypofunctioning in schizophrenia through somatosensory evoked potentials.

Patients with schizophrenia (SCZ) exhibit a variety of symptoms related to altered processing of somatosensory information. Little is known, however, about the neural substrates underlying somatosensory impairments in SCZ. This study endeavored to evaluate somatosensory processing in patients with SCZ compared to healthy individuals by generating somatosensory evoked potentials through stimulation of the right median nerve. The median nerve was stimulated by a peripheral nerve stimulator in 34 SCZ and 33 healthy control (HC) participants. The peripheral nerve stimulus (PNS) intensity was adjusted to 300 percent of sensory threshold and delivered at 0.1 Hz. The EEG data were acquired through 64-channels per 10-20 montage. We collected and averaged 100 trials and the recording electrodes of interest were the F3/F5 electrodes representing the dorsolateral prefrontal cortex (DLPFC) and C3/CP3 representing the somatosensory cortex (S1). In response to PNS, SCZ participants experienced over the DLPFC N30 amplitude that was significantly smaller than that of HC participants. By contrast, S1 N20 was of similar amplitude between the two groups. In addition, we found an association between N20 and N30 amplitudes in SCZ but not in HC participants. Our findings suggest that patients with SCZ demonstrate aberrant processing of somatosensory activation by the DLPFC locally and not due to a connectivity disruption between S1 and DLPFC. These results could help to develop a model through which to DLPFC hypofunctioning could be studied. Our findings may also help to identify a potential biological target to treat somatosensory information processing related deficits in SCZ.