Traumatic brain injury (TBI) was induced by a weight-drop device using 300 g–1 m weight-height impact. The study groups were: control, alpha-lipoic acid (LA) (100 mg/kg, po), TBI, and TBI + LA (100 mg/kg, po). Forty-eight hours after the injury, neurological scores were measured and brain samples were taken for histological examination or determination of thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels, myeloperoxidase (MPO) and Na⁺-K⁺ ATPase activities, whereas cytokines (TNF-α, IL-1β) were determined in blood. Brain oedema was evaluated by wet–dry weight method and blood–brain barrier (BBB) permeability was evaluated by Evans Blue (EB) extravasation. As a result, neurological scores mildly increased in trauma groups. Moreover, TBI caused a significant decrease in brain GSH and Na⁺-K⁺ ATPase activity, which was accompanied with significant increases in TBARS level, MPO activity and plasma proinflammatory cytokines. LA treatment reversed all these biochemical indices as well as histopathological alterations. TBI also caused a significant increase in brain water content and EB extravasation which were partially reversed by LA treatment. These findings suggest that LA exerts neuroprotection by preserving BBB permeability and by reducing brain oedema probably by its anti-inflammatory and antioxidant properties in the TBI model.

✓ Brain abscesses are well-known lesions that have been reported from the beginning of the Hippocratic era. They continue, however, to be characterized by problematic and fatal features, even though there have been enormous developments in treatment and diagnostic technologies—especially in the areas of computed tomography (CT), surgery, anesthesia, bacterial isolation techniques, and new antibiotics. The predisposing factors may change according to patient age, geographic location, and socioeconomic conditions of the community, but patients frequently have a contiguous infection such as otitis or mastoiditis. The clinical signs and symptoms of brain abscesses are nonspecific. Patients typically present with signs and symptoms due to mass effects, accompanied by high fever and seizure. The main treatment is surgical, although medical therapy can be used for selected cases. The treatment of choice is aspiration, which may be performed with the aid of an endoscope or free hand, with or without stereotactic or intraoperative ultrasound guidance. Excision is valuable in some cases. The success of the treatment, whether surgical or medical, mostly depends on the success of isolation of the causative organism, which provides essential data for accurate medical treatment. Third-generation cephalosporins and metronidazole are the most commonly used antimicrobial agents in the treatment of brain abscesses. Use of corticosteroids may be acceptable when lesions are accompanied by edema. Prophylactic antiepileptic therapy is strongly recommended. The patient's Glasgow Coma Scale score at presentation is one of the most important factors predicting outcome.

The overproduction of reactive oxygen species and resultant damage to cellular proteins or lipids of cell membranes and DNA by free radicals are the underlying mechanisms of many neuropathologies. Cyclooxygenase-2 (COX-2) inhibitors have been suggested to be neuroprotective by reducing prostanoid and free radical synthesis, or by directing arachidonic acid metabolism through alternate pathways. This study investigated the putative neuroprotective effect of the COX-2 inhibitor, meloxicam, in a rat model of diffuse brain injury. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g(-1) m weight-height impact. The groups were: control, meloxicam (2 mg/kg, i.p.), trauma and trauma + meloxicam (2 mg/kg, i.p.). Forty-eight hours after the injury, neurological examination scores were measured, the animals were decapitated and brain tissues were taken. Brain edema and blood-brain barrier (BBB) permeability were evaluated by wet-dry weight method and Evans blue (EB) extravasation respectively. In brain tissues, malonedialdehyde, glutathione, myeloperoxidase and Na/K-ATPase levels were measured. The neurological examination scores mildly increased in trauma groups 48 hours after the induction of trauma. Meloxicam treatment improved the altered neurological status. The trauma caused a significant increase in brain water content that was partially reversed by meloxicam. Meloxicam also reduced the EB extravasation indicating the preservation of the BBB integrity. Meloxicam treatment also significantly reduced the increase in malondialdehyde and myeloperoxidase levels and restored glutathione content of the brains that had been significantly increased after trauma. Meloxicam exerts neuroprotective effect by preserving BBB permeability and by reducing brain edema (probably by its anti-inflammatory properties) in the diffuse brain injury model.

Background: Nosocomial meningitis is a rare complication following neurosurgical procedures and is associated with high morbidity and mortality. Aim: The aim of this study was to describe the clinical characteristics and the risk factors associated with mortality in patients who developed nosocomial meningitis following neurosurgical operations. Setting and design: Tertiary care hospital and an observational study. Materials and Methods: The study subjects included 2265 patients who underwent various neurosurgical operations during 2003-05. The diagnosis of nosocomial meningitis was based on the Center for Disease Control criteria. Statistical analysis: It was performed by using Statistical Package for Social Sciences for Windows 10.0 program. Results: The incidence of postoperative nosocomial meningitis was 2.7% (62 episodes in 49 patients among 2265 patients operated). Staphylococcus aureus and Acinetobacter spp. were the most frequently isolated pathogens. Of the 49 with meningitis 20 (40.8%) patients died. In the logistic regression analysis model, Glascow coma scale score less than 10 (Odds Ratio (OR): 19.419, 95% Confidence Interval (CI); 1.637-230.41, P = 0.001), and low cerebrospinal fluid glucose level (≤ 30 mg/ dL) (OR: 10.272, 95% CI; 1.273-82.854, P = 0.002), and presence of concurrent nosocomial infection (OR: 28.744, 95% CI;1.647-501.73, P =0.001) were the independent risk factors associated with mortality. Conclusion: The mortality in patients who developed meningitis was high. The high percentage of concurrent nosocomial infections was associated with a high mortality rate which was a serious problem.