have consistently been associated with white-matter pathology, including in dysmyelinated mice (Harsan et al., 2006), and patients with the demyelinating disease multiple sclerosis (Roosendaal et al., 2009). Furthermore, such white-matter pathology has consistently been associated with slowed neural transmission velocity, for example in the slowed action potentials observed in dysmyelinated mice in situ (Roy et al., 2007), and in the increased P1 latencies to visually-evoked potentials typically observed in multiple sclerosis patients with optic neuritis (Jones, 1993). Hence our finding of a significant negative correlation between FA and IHTT (i.e., longer transmission times associated with lower FA and reduced white-matter integrity) is consistent with the available literature, and suggests that the established microscopic relationship between white-matter integrity and transmission velocity is observable at the macroscopic scale with neuroimaging. It should be acknowledged, however, that while transcallosal connections between the primary visual cortices have been identified in humans (Clarke and Miklossy, 1990; Saenz and Fine, 2010) and several other mammals including macaques (Kennedy et al., 1986), cats (Payne, 1991) and tree-shrews (Bosking et al., 2000), the extent and topographic organization of these callosal connections remains an ongoing topic of investigation in the neuroscience literature.
