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Aim: To study the effects of niacin, a water-soluble vitamin, on inflammation, oxidative stress and apoptotic processes observed after mild traumatic brain injury (TBI)., Material and Methods: A total of 25 Wistar albino male rats were randomly divided into control (n=9), TBI + Placebo group (n=9), TBI + niacin (500 mg/kg; n=7) groups. Mild TBI was performed under anesthesia by dropping a 300 g weight from a height of 1 meter onto the skull. Behavioral tests were applied before and 24 hours after TBI. Luminol and lucigenin levels and tissue cytokine levels were measured. Histopathological damage was scored in brain tissue., Results: After mild TBI, luminol and lucigenin levels were increased (p < 0.001), and their levels were decreased with niacin treatment (p < 0.01-p < 0.001). An increased score was obtained with trauma in the tail suspension test (p < 0.01), showing depressive behavior. The number of entries to arms in Y-maze test were decreased in TBI group compared to pre-traumatic values (p < 0.01), while discrimination (p < 0.05) and recognition indices (p < 0.05) in object recognition test were decreased with trauma, but niacin treatment did not change the outcomes in behavioral tests. Levels of the anti-inflammatory cytokine IL-10 were decreased with trauma, and increased with niacin treatment (p < 0.05). The histological damage score was increased with trauma (p < 0.001), and decreased with niacin treatment in the cortex (p < 0.05), and hippocampal dentate gyrus region (p < 0.01)., Conclusion: Niacin treatment after mild TBI inhibited trauma-induced production of reactive oxygen derivatives and elevated the anti-inflammatory IL-10 level. Niacin treatment ameliorated the histopathologically evident damage.

Aim: To investigate the effects of cerebrolysin on inflammation, oxidative stress, apoptosis, and neurologic recovery in the setting of an experimental rabbit model of spinal cord ischemia/reperfusion injury (SCIRI)., Material and Methods: Rabbits were randomly divided into five groups: control, ischemia, vehicle, methylprednisolone (30 mg/kg), and cerebrolysin (5 ml/kg) group. The rabbits in the control group underwent only laparotomy; the other groups underwent spinal cord ischemia and reperfusion injury for 20 minutes. Neurologic examination after 24 hours was based on the Modified Tarlov scale. Myeloperoxidase activities, catalase and malondialdehyde levels, and caspase-3 concentrations were determined in serum and tissue samples. Serum xanthine oxidase levels were studied and histopathological and ultrastructural changes were examined., Results: After SCIRI, serum and tissue myeloperoxidase activities, malondialdehyde levels, caspase-3 concentrations, and serum xanthine oxidase activities were increased (p < 0.01?0.001). Catalase levels were significantly diminished (p < 0.001). Cerebrolysin treatment correlated with reduced myeloperoxidase and xanthine oxidase activities, malondialdehyde levels and caspase-3 concentrations; and with increased catalase levels (p < 0.001, for all). The cerebrolysin group showed improved histopathological, ultrastructural, and neurological outcomes., Conclusion: For the first time in the literature, the current study reports anti-inflammatory, antioxidant, antiapoptotic, and neuroprotective effects of cerebrolysin in a SCIRI rabbit model.

Aim: To investigate the effects of an anti-ischemic agent, mildronate, on subarachnoid hemorrhage-induced vasospasm., Material and Methods: Rabbits were randomly divided into four groups: control, subarachnoid hemorrhage (SAH), vehicle, and mildronate (n=8 animals per group). In the treatment group, 200 mg/kg of mildronate were intraperitoneally administered 5 minutes after the procedure and continued for 3 days as daily administrations of the same dose. At the end of the third day, the cerebrum, cerebellum, and brain stem were perfused, fixated, and removed for histopathological examination. Tissues were examined for arterial wall thickness, luminal area, and hippocampal neuronal degeneration., Results: Mildronate group showed significantly increased luminal area and reduced wall thickness of the basilar artery compared with the subarachnoid hemorrhage group. In addition, the hippocampal cell degeneration score was significantly lower in the mildronate group than in the SAH and vehicle groups., Conclusion: These results show that mildronate exerts protective effects against SAH-induced vasospasm and secondary neural injury.

Aim: The aim of this study was to assess the surgical outcome and the prognostic importance of clinical and radiological data of patients operated emergently for an extraaxial hematoma causing brain herniation., Material and Methods: This retrospective study comprised 108 adult patients who were operated due to herniated traumatic extraaxial hematomas from January 2000 to January 2013., Results: Of 108 patients, 63 patients (58.3%) were diagnosed as subdural hematoma (SDH), and 45 patients (41.7%) as epidural hematoma (EDH). An unfavorable outcome was significantly increased for patients who were diagnosed as SDH (90.4%) compared with EDH patients (33.3%). Mortality rate for herniated SDH patients was 65.1%, and 26.6% for herniated EDH patients. High mortality and unfavorable outcome ratios were associated with Glasgow Coma Scale scores at admission, mean postoperative intracranial pressure (ICP) values, type of the brain herniation, interval from the time of trauma to the time of hematoma decompression, the duration of the brain herniation, intraoperative acute brain swelling, hematoma volume and thickness, degree of the midline shift and the obliteration of the basal cisterns., Conclusion: Our data showed that, postoperative ICP values were one most important predictor of the mortality. We recommended postoperative ICP monitoring for all patients presenting with the brain herniation due to traumatic extraaxial hematoma.

Aim: Bacitracin is one of the most frequently used agents for the topical irrigation of the cerebral cortex. The aim of this study is to investigate whether bacitracin has histopathological and ultrastructural effects when applied topically to the cerebral cortex., Material and Methods: Twenty-eight rats were randomly assigned to four groups. Except the control group, each rat underwent left frontoparietal craniectomy with dural removal. Then, in the sham group a piece of dry absorbable gelatin sponge was placed over the left hemisphere; in the saline group a gelatin sponge soaked in normal saline; and in the bacitracin group a gelatin sponge soaked in 500 units bacitracin was used. After 48 hours, brain tissues were extracted for histopathological and electron microscopic analyses., Results: Among the four groups dark stained neurons were found to be statistically higher in number in the bacitracin group compared with the control, sham and saline groups. Electron microscopic evaluation revealed that, in the bacitracin group, almost all cytoplasmic organelles were poorly preserved., Conclusion: Topical application of the bacitracin on to the cerebral cortex caused histopathological and ultrastructural changes in the neural tissue. These changes may be an evidence for the neurotoxic effects of bacitracin.