Migration of a Lumbar Spinal Fusion Rod Into the Posterolateral Knee: A Case Report.

STUDY DESIGN: Case report (level V evidence). OBJECTIVE: We report a case of a 33-year-old man with Marfan syndrome that visited our clinic for left knee pain and stiffness. Radiographs of the left knee and lumbar spine demonstrated a spinal rod in the posterolateral left knee and its origin being a broken rod from his previous unilateral spinal fusion 17 years prior. SUMMARY OF BACKGROUND DATA: Spinal arthrodesis is a common treatment modality for a wide range of spinal pathologies including infection, trauma, congenital and developmental deformities, and degenerative conditions. A rare complication that may arise from said procedure is implant migration, most often a result of pseudoarthrosis. METHODS: Description of the case report. RESULTS: Patient was taken to the operating room 2 weeks later for an uneventful removal of the implant and immediate improvement with pain and range of motion. CONCLUSION: Spinal implant migration is a rare complication most often due to implant failure from pseudoarthrosis. In the case presented, this phenomenon was likely attributed to the use of unilateral instrumentation coupled with Marfan syndrome, shown to lead to insufficient implant stability and poorer fusion rates, respectively.Level of Evidence: 5.

Protection against Experimental Stroke by Ganglioside GM1 Is Associated with the Inhibition of Autophagy.

UNLABELLED: Ganglioside GM1, which is particularly abundant in the central nervous system (CNS), is closely associated with the protection against several CNS disorders. However, controversial findings have been reported on the role of GM1 following ischemic stroke. In the present study, using a rat middle cerebral artery occlusion (MCAO) model, we investigated whether GM1 can protect against ischemic brain injury and whether it targets the autophagy pathway. GM1 was delivered to Sprague-Dawley male rats at 3 doses (25 mg/kg, 50 mg/kg, 100 mg/kg) by intraperitoneal injection soon after reperfusion and then once daily for 2 days. The same volume of saline was given as a control. Tat-Beclin-1, a specific autophagy inducer, was administered by intraperitoneal injection at 24 and 48 hours post-MCAO. Infarction volume, mortality and neurological function were assessed at 72 hours after ischemic insult. Immunofluorescence and Western blotting were performed to determine the expression of autophagy-related proteins P62, LC3 and Beclin-1 in the penumbra area. No significant changes in mortality and physiological variables (heart rate, blood glucose levels and arterial blood gases) were observed between the different groups. However, MCAO resulted in enhanced conversion of LC3-I into LC3-II, P62 degradation, high levels of Beclin-1, a large area infarction (26.3±3.6%) and serious neurobehavioral deficits. GM1 (50 mg/kg) treatment significantly reduced the autophagy activation, neurobehavioral dysfunctions, and infarction volume (from 26.3% to 19.5%) without causing significant adverse side effects. However, this biological function could be abolished by Tat-Beclin-1. IN CONCLUSION: GM1 demonstrated safe and robust neuroprotective effects that are associated with the inhibition of autophagy following experimental stroke.