Classical and contemporary research in neuroscience postulates that connectivity is a fundamental component of human brain function. Recently, advances in computational neuroimaging have enabled reconstruction of macroscopic human brain structural connectivity in vivo using diffusion MRI. Studies show that the structural network topology may discriminate between neurological phenotypes or relate to individual brain function. To investigate disease effectively, it is necessary to determine the network methodological and biological variability. Reproducibility was calculated for two state-of-the-art reconstruction pipelines in healthy subjects. High reproducibility of connection weights was observed, which increased with connection strength. A high agreement between pipelines was found across network density thresholds. In addition, a robust core network was identified coinciding with a peak in similarity across thresholds, and replicated with alternative atlases. This study demonstrates the utility of applying multiple structural network pipelines to diffusion data in order to identify the most important connections. Focal epilepsy is characterised by seizures that can spread to contiguous and non-contiguous sites. Diffusion MRI and cortico-cortical evoked potentials were acquired in focal epilepsy patients to reconstruct and correlate their structural and effective brain networks and examine connectivity of the ictal-onset zone and propagative regions. Automated methods are described to reconstruct comparable largescale structural and effective networks. A high overlap and low correlation was observed between network modalities. Low correlation may be due to imperfections in methodology, such as difficulty tracing U-fibers using tractography. Effective connectivity amplitude, baseline fluctuation, and outward connectivity tended to be higher at ictal-onset regions, while higher structural connectivity between ictal-onset regions was observed. Furthermore, a high prevalence of structural and effective connections to sites of non-contiguous seizure spread was found. These results support the concept of highly excitable cortex underlying ictal-onset regions which promotes non-contiguous seizure spread via high outward connectivity
