Study design: Cross-sectional study. Objective: To analyze the predictors of severe neurogenic bowel dysfunction (NBD) in persons with spinal cord injury (SCI). Setting: The Kaohsiung Medical University Hospital, Taiwan. Methods: Two questionnairesFthe NBD score and the Beck Depression Inventory second editionFwere sent to 232 persons with SCI by mail. The demographic factors and injury-related factors were recorded to evaluate any relationships with severe NBD. The associations between the severity of NBD and psychological condition were also measured. Results: In all, 39.4% of the respondents suffered from severe NBD. Multiple logistic regression analysis showed that those with a cervical injury (odds ratios (OR) ¼ 10.5, 95% confidence interval (CI) 1.6-67.7) or a thoracic injury (OR ¼ 7.1, 95% CI 1.2-40.3) had a higher risk of severe NBD than those with a lumbar injury. Persons with American Spinal Injury Association (ASIA) A had a 12.8-fold higher risk of severe NBD than persons with ASIA D (OR ¼ 12.8, 95% CI 3.3-50.1). Longer duration of injury (X10 years) was another risk factor of severe NBD. Moderate-to-severe depression was associated with reduced bowel function. Conclusions: This study showed that high level of cord lesion, completeness of cord injury and longer duration of injury (X10 years) could predict the severity of NBD in patients with SCI.

Several events occurring during the secondary damage of traumatic brain injury (TBI) can cause oxidative stress. F(2)-isoprostanes (F(2)-IsoPs) and F(4)-neuroprostanes (F(4)-NPs) are specific lipid peroxidation markers generated from arachidonic acid and docosahexaenoic acid, respectively. In this study, we evaluated oxidative stress in patients with moderate and severe TBI. Since sedatives are routinely used to treat TBI patients and propofol has been considered an antioxidant, TBI patients were randomly treated with propofol or midazolam for 72 h postoperation. We postoperatively collected cerebrospinal fluid (CSF) and plasma from 15 TBI patients for 6-10 d and a single specimen of CSF or plasma from 11 controls. Compared with the controls, the TBI patients exhibited elevated levels of F(2)-IsoPs and F(4)-NPs in CSF throughout the postsurgery period regardless of the sedative used. Compared with the group of patients who received midazolam, those who received propofol exhibited markedly augmented levels of plasma F(2)-IsoPs, which were associated with higher F(4)-NPs levels and lower total nitrate/nitrite levels in CSF early in the postsurgery period. Furthermore, the higher CSF F(2)-IsoPs levels correlated with 6-month and 12-month worse outcomes, which were graded according to the Glasgow Outcome Scale. The results demonstrate enhanced oxidative damage in the brain of TBI patients and the association of higher CSF levels of F(2)-IsoPs with a poor outcome. Moreover, propofol treatment might promote lipid peroxidation in the circulation, despite possibly suppressing nitric oxide or peroxynitrite levels in CSF, because of the increased loading of the lipid components from the propofol infusion.