This thesis explored common mechanisms of oxidative damage in multiple sclerosis and neurotrauma and encompasses work that has been published in four journal articles. Initially, the effectiveness of a combinatorial ion channel inhibitor treatment was established in models of both disorders. The cuprizone model of demyelinating disease was also optimised, followed by explorations into the relationship between oxidative DNA damage, cell proliferation and blood vessel dysfunction in models of neurotrauma and multiple sclerosis
