Blocking VEGF by Bevacizumab Attenuates VEGF-Induced Vasospasm After Experimental Subarachnoid Hemorrhage in Rabbits.

OBJECTIVE: Vasospasm after subarachnoid hemorrhage (SAH) plays a vital role in the development of delayed cerebral ischemia. Anti- vascular endothelial growth factor (VEGF) antibodies, like bevacizumab (BEV), may attenuate VEGF-stimulated angiogenesis, reduced vascular cell proliferation, and improve vasospasm after SAH. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into 4 groups of 8 rabbits in each group: group 1 (control); group 2 (SAH); group 3 (SAH + vehicle); and group 4 (SAH + BEV). BEV (5 mg/kg, intraperitoneally) was administered 5 minutes after the intracisternal blood injection and continued for 72 hours once per day in the same dose for group 4. Animals were sacrificed 72 hours after SAH. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS: VEGF is associated with the narrowing of the basilar artery. Treatment with BEV statistically significantly increased the cross-sectional area of the basilar artery when compared with the SAH and the vehicle groups. Basilar artery wall thicknesses in the BEV group was statistically significant smaller than in the SAH and vehicle groups. The hippocampal degeneration scores for the BEV and control groups were similar and significantly lower than those for the SAH and vehicle groups. CONCLUSIONS: Cellular proliferation and subsequent vessel wall thickening is a reason to delay cerebral ischemia and deterioration of the neurocognitive function. Intraperitoneal administration of BEV was found to attenuate cerebral vasospasm and prevent delayed cerebral ischemia and improve neurocognitive function after SAH in rabbits.

Oval Window Temperature Changes in an Endoscopic Stapedectomy.

OBJECTIVES: Following the initial use of endoscopes in otology, the pros and cons of these instruments have been questioned increasingly. These instruments cause an increase in temperature that needs to be investigated. In this study, the authors aimed to investigate the temperature increase caused by endoscopes and light sources in the perilymph by performing a stapedotomy in an animal model under anesthesia. STUDY DESIGN: The study was performed in a guinea pig model. METHODS: In the animal model, a simulated otologic stapes surgery was performed at room temperature. The body temperatures of the guinea pigs were monitored; the temperature increase caused by the 0-degree rigid endoscopes with diameters of 3 and 4  mm as well as the light sources, including halogen, light-emitting diode (LED), and xenon lamps, were monitored following the stapedotomy to measure and document the continuous temperature increase in the perilymph using sensors placed at the oval window. RESULTS: Rigid endoscopes cause a temperature increase in the tympanum regardless of their diameter when used with xenon and halogen light sources. The LED light caused a relatively small temperature increase. CONCLUSIONS: The endoscopic instruments used in the stapes operation caused a temperature increase in the oval window. The authors concluded that this heat could easily be transmitted to the cochlea by the perilymph, which has obstructed contact with the outer environment following stapedomy, resulting in neurosensorial damage.

Methothrexate attenuates early neutrophil infiltration and the associated lipid peroxidation in the injured spinal cord but does not induce neurotoxicity in the uninjured spinal cord in rats.

BACKGROUND: The goal of most acute therapies for spinal cord injury (SCI) in humans include attenuation of the early inflammatory response and may limit the extent of tissue injury and the consequent disability. OBJECTIVE: The purpose of this study was to investigate the early effects of methothrexate (MTX) treatment on myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and ultrastructural findings in the injured and uninjured spinal cords of rats. The effects of MTX treatment were also compared with methylprednisolone sodium succinate (MPSS) treatment. METHODS: Wistar rats were divided into seven groups: control; trauma alone (50 g/cm weight drop trauma); SCI + MPSS (30 mg/kg); SCI + low-dose (0.5 mg/kg) MTX (LDMTX); SCI + higher-dose (1 mg/kg) MTX (HDMTX); non-trauma + LDMTX; non-trauma + HDMTX. RESULTS: Administration of MTX and MPSS treatments significantly decreased MPO activity (p < 0.05) and MDA level (p < 0.05) in the first 24 h. The MTX treatments, particularly HDMTX, were more effective than MPSS in reducing MPO activity, and MTX treatments were also more effective than MPSS in reducing MDA level (p < 0.05). The MTX treatment was more protective on large- and medium-diameter myelinated axons in minimizing ultrastructural changes in the spinal-cord-injured rats, but did not induce neurotoxicity in normal spinal cord. CONCLUSION: The results of this study indicate that MTX treatment has a beneficial effect by reducing early neutrophil infiltration and the associated lipid peroxidation, and has significantly protective effects on the injured spinal cord tissue in the first 24 h after SCI. Given the anti-inflammatory properties of MTX, a single dose of MTX a week is used for non-neoplastic disease in humans, and MTX may have a beneficial role in the immediate management of acute SCI.

Intradiscal electrothermal treatment for chronic discogenic low back pain: a prospective outcome study of 39 patients with the Oswestry disability index at 18 month follow-up.

OBJECTIVE: The authors evaluate the efficacy of intradiscal electrothermal therapy (IDET) for discogenic pain on outcome of patients using the Oswestry disability index (ODI) after 18 month follow-up. METHODS: Thirty-nine patients with chronic discogenic low back pain who failed to improve following conservative treatment were considered for this study. Inclusion criteria included the presence of one- or two-level symptomatic disk degeneration without evidence of nerve root compression. Patients were excluded if there was severe disk degeneration together with loss of more than 50% disk height. We measured the outcome scores at minimum of 18 month period with the Turkish version of the ODI and compared them with pre-treatment scores. RESULTS: All procedures were considered technically successful and there were no device-related complications. Mean ODI scores of 39 patients pre-operatively and post-operatively 6, 12 and 18 months were 45.7436 +/- 11.6545, 24.7692 +/- 10.7861, 23.0256 +/- 10.6412 and 21.4872 +/- 10.0286, respectively. The effect of treatment was calculated as the difference between the scores before and after treatment. They were 20.9744 +/- 12.5394, 22.7179 +/- 12.5697 and 24.2564 +/- 12.5922 after the same follow-up periods. There was a significant difference (p<0.01) between all the mean scores after treatment (6, 12 and 18 months) compared with the pre-IDET mean ODI. DISCUSSION: Although various alterations in outcome scores have been reported in previous works, we found nearly four in five patients (79.48%) who clearly benefited from this therapy. This procedure may become a middle step for carefully selected group of patients who failed non-operative treatment before surgical intervention.