Oxidative damage after severe head injury and its relationship to neurological outcome

We sought to establish the time course of reactive oxygen species after severe head injuries in humans and to investigate their relationship with clinical outcomes.

Both the markers of oxidative damage-malonylaldehyde (MDA) and the enzymatic and nonenzymatic antioxidant defenses (i.e., superoxide dismutase [SOD] and vitamin E [VE], respectively)-were studied. To assess the time course of MDA, SOD, and VE, jugular bulb (JB) and peripheral venous blood samples were obtained from 30 patients within 8 hours of severe head trauma onset (T(0)) and 6 (T(1)), 12 (T(2)), 24 (T(3)), and 48 hours (T(4)) after trauma onset. Patients were divided into good and poor outcome groups according to their 6-month neurological outcome as determined on the basis of their Glasgow Outcome Scale scores and biochemical profiles.

In JB samples, MDA levels increased significantly at T(1), T(2), T(3), and T(4) as compared with T(0); SOD activity increased significantly at T(2) and T(3) as compared with T(0); and VE levels decreased significantly at T(1), T(2), and T(3) as compared with T(0). The same variables did not change significantly over time in peripheral venous blood samples. Moreover, the MDA levels and SOD activity detected in JB samples were significantly higher in the poor outcome group at T(1) and T(2). No significant difference in VE levels was observed between the two outcome groups.

Reactive oxygen species-mediated oxidative damage can play an important role in determining the prognosis of severe brain injury in humans.