This manuscript considers some of the most prominent consequences of traumatic brain injury (TBI), namely vascular and axonal change, and evaluates the role of damaging oxygen radicals in their pathogenesis. To this end, existing as well as new data derived from traumatically injured experimental animals and humans was employed. Experimental animals were subjected to fluid-percussion brain injury. Some animals were equipped with cranial windows to allow for the functional assessment of the pial vasculature, while others received various exogenous tracers to assess blood-brain barrier status. In order to identify traumatically induced axonal change, some animals were also processed for the light and electron microscopic visualization of antibodies targeted to the neurofilament subunits. Similar immunocytochemical strategies were employed in the postmortem study of humans who had sustained severe TBI. Through these approaches, TBI was recognized to result in vascular abnormalities ranging from impaired vascular responsiveness to altered blood-brain barrier status. Typically, these vascular abnormalities continued for several hours postinjury and showed evolution which correlated with the production of damaging oxygen radicals. Importantly, the use of radical scavengers reversed these vascular abnormalities and provided protection. Traumatically induced axonal damage was also associated with evolving posttraumatic change. This involved the continued posttraumatic disassembly and misalignment of the intra-axonal neurofilament subunits which caused impaired axoplasmic transport leading to axonal swelling and detachment. Although these intra-axonal changes did not appear to be directly caused by oxygen radicals, it is suggested that the presence of oxygen radicals may exacerbate the progression of these reactive events.