A New Approach in the Treatment of Traumatic Brain Injury: The Effects of Levosimendan on Necrosis, Apoptosis, and Oxidative Stress.

OBJECTIVE: Traumatic brain injury (TBI) is an essential and common health problem worldwide. Levosimendan is an inotropic and vasodilator drug used to treat heart failure. Moreover, it exerts pleiotropic effects and, thus, protective effects on many organs. The present study aimed to investigate the effect of levosimendan on necrosis, apoptosis, and reactive oxygen species in rats with TBI. METHODS: The study included 28 female Wistar-Albino rats weighing 200-250 g. The rats were divided into 4 groups with 7 rats each as follows: Group 1: No trauma group (Control), Group 2: Traumatized, untreated group (T), Group 3: Levosimendan was administered at a dose of 12 µg/kg intraperitoneally 1 hour after the trauma (L1), Group 4: Levosimendan was administered at a dose of 12 µg/kg intraperitoneally 2 hours after the concussion (L2). After the experiment, the rats were decapitated, and the brain tissue was removed. Necrosis was assessed with Cresyl violet staining, apoptosis was assessed with immunohistochemical analysis, superoxide dismutase and catalase levels were measured with the spectrophotometric method, and malondialdehyde (MDA) levels were assessed by High-Performance Liquid Chromatography. RESULTS: The number of necrotic cells in the L1 and L2 groups was significantly lower than in the K and T groups (P = 0.015 and P = 0.03, respectively). Although the active caspase-3 level was signified considerably in the T, L1, and L2 groups compared to the K group, no significant difference was found among these 3 groups (P > 0.05). The results of superoxide dismutase levels were similar to those of active caspase-3. catalase level was significantly higher in the K group than in the T and L2 groups (P = 0.045). Malondialdehyde activity was considerably higher in the L1 and L2 groups compared to the K group (P = 0.023). CONCLUSIONS: Our results indicated that levosimendan may exert a neuroprotective effect by reducing necrosis in TBI and that levosimendan does not affect apoptosis and antioxidant levels in TBI. Comprehensive studies are needed to elucidate the effect of levosimendan on TBI fully.

Evaluation of Oxidative Stress Levels and Antioxidant Enzyme Activities in Burst Fractures.

BACKGROUND Spinal burst fractures are pathologies that occur in spinal injuries and cause significant mortality and morbidity as a result. Burst fractures in spinal cord injuries can result in rapid and significant oxidative stress. In addition to the primary injury in severe spinal cord injuries, subsequent secondary lesions are mainly due to inflammatory cascade activation and excessive production of free radicals. This study evaluated oxidative stress and antioxidant enzyme levels in burst fractures. MATERIAL AND METHODS Twenty patients with burst fractures were diagnosed and underwent surgery and 20 healthy control subjects were included in the study. Neurological status was evaluated using the American Spine Injury Association Impairment Scale (ASIA) before and after surgery. Neurological function was scored as ASIA A: complete deficits, ASIA B-D: incomplete deficits, and ASIA E: neurologically intact. Spectrophotometry was performed to measure malondialdehyde (MDA) and low glutathione (GSH), glutathione peroxidase (GPx) levels, which represent lipid peroxide content. Evaluations were performed within 2 days after injury in the patients. RESULTS MDA levels were higher in the burst fracture group (p<0.001), whereas GSH and SOD activities were higher in the control group (both p<0.001). There was no statistically significant difference in GPx levels between the groups (p=0.482). CONCLUSIONS Oxidative stress appears to be related to burst fractures. Considering the importance of burst fractures in spinal cord injuries, a better understanding of these mechanisms may help in defining the role of oxidative stress after burst fractures. Prospective, randomized, controlled trials may reveal new therapeutic approaches that include antioxidants for explosive fractures focusing on oxidative stress.

Relationship between hydrocephalus etiology and ventriculoperitoneal shunt infection in children and review of literature.

OBJECTIVE: The purpose of this retrospective study was to clarify the relationship of shunt infection to childhood hydrocephalus etiology. METHODS: We analyzed 1021 patients with childhood hydrocephalus who underwent V-P shunting over a period of approximately 15 years. The etiology of 1021 patients include myelomeningocele (794 patient), congenital (165 patient) and intraventricular haemorrhage (62 patient). RESULTS: Of the 1021 patients who underwent V-P shunting, 19.32% exhibited shunt infection. Shunt infection developed in 180 (22.67%) of 794 patients with myelomeningocele, 9 (5.45%) of 165 patients with congenital obstructive hydrocephalus, and 9 (14.51%) of 62 patients with intraventricular haemorrhage. Recurrent shunt infection was detected in 54 (27.27%) of 198 patients with a previous shunt infection. CONCLUSIONS: Patients with previous shunt infection as well as those with shunts associated with myelomeningocele were observed to be at a greater risk for shunt infection. Results indicated that patients with congenital obstructive hydrocephalus may be less prone to shunt infections.

Spinal Metastasis of Unknown Primary Accompanied by Neurologic Deficit or Vertebral Instability.

BACKGROUND AND OBJECTIVE: Spinal bone metastases are common. They are mostly localized to the lumbar, thoracic, and cervical spine. The most common primaries to result in spinal metastases include lung, breast, and prostate carcinomas in adults as opposed to leukemia, Ewing sarcoma, rhabdomyosarcoma, and neuroblastoma in children. In patients diagnosed with cancer, bone metastases are found in 40% and spinal metastases in 10%. In this study, we reviewed 25 patients diagnosed with a spinal metastasis of unknown primary who presented with low back pain or acute-onset neurologic deficits and underwent operative treatment. METHODS: The retrospective study included 25 patients with a spinal metastasis of unknown primary who presented to our clinic with acute-onset vertebral fracture or neurologic deficit. Statistical descriptions were obtained for each patient. Survival analysis was performed using the Kaplan-Meier method. RESULTS: The 25 patients included 17 men (68%) and 8 women (32%), with a mean age of 55 years (range, 14-81 years). Eleven patients (44%) presented with varying degrees of motor deficits ranging from flaccid paralysis to paraplegia. Motor deficits were completely reversed in 4 patients postoperatively. The tumors were localized to the upper thoracic spine (T1-4) in 2 patients, in the midthoracic spine (T5-8) in 2 patients, in the lower thoracic spine (T9-12) in 8 patients, in the cervical 7 in 1 patient, and in the lumbar spine in 12 patients. In 10 patients, the tumor affected multiple spinal regions. Nonosseous tumors were not present in 10 patients. Ten patients had an extradural tumor. Costal involvement was detected in 2 patients. The tumors were pathologically identified as lung cancer (n = 3), lymphoma (n = 5), breast cancer (n = 3), gastric cancer (n = 2), liver cancer (n = 2), prostate cancer (n = 2), renal cell carcinoma (n = 2), malignant melanoma (n = 1), plasmacytoma (n = 1), bladder cancer (n = 1), paraganglioma (n = 1), Ewing sarcoma (n = 1), and yolk sac carcinoma (n = 1). Posterior instrumentation was performed in patients with instability. In addition, decompression was performed in patients with neurologic deficit. CONCLUSIONS: Considering that 10% of patients with cancer are diagnosed by vertebral metastasis, presence of malignancy should be suspected and a detailed examination should be performed in patients presenting with vertebral fractures caused by no or minor trauma. Moreover, in patients presenting with neurologic deficit, soft tissue metastases leading to spinal cord compression should be kept in mind and further examinations should be promptly administered.