A unifying tenet of the ‘connectivity’ theories of schizophrenia is that the disease is ultimately underpinned by abnormal interactions between brain regions, as opposed to abnormal brain regions per se (Friston, 1998). Several ‘connectivity’ theories have emphasized the role of aberrant neural timing in the etiology of schizophrenia (Andreasen et al., 1999; Bartzokis, 2002; Bressler, 2003; Phillips and Silverstein, 2003; Stephan et al., 2009). It has been suggested that this aberrant neural timing could be caused by conduction delays arising from structural damage to the white-matter fasciculi that physically connect spatially disparate populations of neurons (Bartzokis, 2002; Fields, 2008; Whitford et al., 2010a). This suggestion is supported by the facts that a) a primary role of myelin is to increase the speed of neural transmissions (Baumann and Pham-Dinh, 2001), b) damage to the white-matter has consistently been shown to cause conduction delays or even blockages in vivo, such as characteristically occurs in multiple sclerosis patients with optic neuritis (Cuypers et al., 1995), and c) schizophrenia patients have repeatedly been shown to exhibit white-matter abnormalities, both in vitro with microscopy (Uranova
