Abnormalities of regional brain functional connectivity have been suggested for the syndromes of schizophrenia since the origin of the name using the Greek roots: skhizein (to split) and phren (mind) by Eugen Bleuler in 1908 (Kuhn, 2004). The neuropsychologist Norman Geschwind generalized this pathophysiological concept in his classic papers about what he called the disconnexion syndromes (Geschwind, 1965). He suggested that deficits in higher functions resulted from the disruption of pathways involving the signal relay functions of the association cortices. Discontinuities in white matter observed in diffusion tensor imaging and inferences from fMRI have been interpreted as evidence for cortical network disconnections in patients with schizophrenia (Bullmore et al, 1997).

More dynamical approaches to functional pathophysiological connections between brain regions have assessed their nearly simultaneous mutual similarities in frequency, wavelength, and phase (Uhlhaas and Singer, 2006). In addition, analysis of the envelope of oscillatory activity has yielded additional measures of connectivity. However, the brain does not operate by copying information from one region to another. The more general approach is to observe how broadband electrophysiological activity in one region shares information with other regions. To accomplish this we have expanded on our previous work using nonlinear dynamical measures of complexity for cortical activity (Robinson et al, 2012; Mandell, 2013).

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