of abnormal theta connectivity in subjects at high-risk for psychosis has been reported suggesting that impairment in this frequency band could be a trait of the SCZ/psychosis spectrum (Andreou et al., 2015). Our results are largely in line with these findings. Moreover diffuse hyperconnectivity characterizes both early stage (SDD) and chronic (LDD) disease even if only the latter is characterized by a prefrontal involvement. Animal studies have demonstrated that GABAergic inhibition and disinhibition can directly modulate cortical synchrony especially in low frequencies (Xiao et al., 2012); GABA neurotransmission is altered in prefrontal cortex (Volk and Lewis, 2002) and its impairment plays a key role in schizophrenic disease (Stan and Lewis, 2012; Schmidt and Mirnics, 2015). Bearing in mind the limitations in translating data from animal models, increased EEG-SFC at rest in low frequencies may be explained as a result of inefficient modulation (impaired inhibition), leading to aberrant synchrony.
