Tinnitus and the Somatosensory System

Pathological perturbations of the brain are rarely confined to a single locus; instead, they often spread via axonal pathways to influence other regions. Patterns of such disease propagation are constrained by the extraordinarily complex, yet highly organized, topology of the underlying neural architecture; the so-called connectome. Thus, network organization fundamentally influences brain disease, and a connectomic approach grounded in network science is integral to understanding neuropathology. Here, we consider how brain-network topology shapes neural responses to damage, highlighting key maladaptive processes (such as diaschisis, transneuronal degeneration and dedifferentiation), and the resources (including degeneracy and reserve) and processes (such as compensation) that enable adaptation. We then show how knowledge of network topology allows us not only to describe pathological processes but also to generate predictive models of the spread and functional consequences of brain disease.

Modern network science has revealed fundamental aspects of normal brain-network organization, such as small-world and scale-free patterns, hierarchical modularity, hubs and rich clubs. The next challenge is to use this knowledge to gain a better understanding of brain disease. Recent developments in the application of network science to conditions such as Alzheimer's disease, multiple sclerosis, traumatic brain injury and epilepsy have challenged the classical concept of neurological disorders being either 'local' or 'global', and have pointed to the overload and failure of hubs as a possible final common pathway in neurological disorders.

Animal studies have shown that sensory deprivation in one modality can have striking effects on the development of the remaining modalities. Although recent studies of deaf and blind humans have also provided convincing behavioural, electrophysiological and neuroimaging evidence of increased capabilities and altered organization of spared modalities, there is still much debate about the identity of the brain systems that are changed and the mechanisms that mediate these changes. Plastic changes across brain systems and related behaviours vary as a function of the timing and the nature of changes in experience. This specificity must be understood in the context of differences in the maturation rates and timing of the associated critical periods, differences in patterns of transiently existing connections, and differences in molecular factors across brain systems.