Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics ...Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics due to deregulated sympathetic outflow. As a result of the reduced sympathetic activity, patients with SCI may experience hypotension, cardiac dysrhythmias, and hypothermia post-injury. In the chronic phase, changes within the CNS and blood vessels lead to orthostatic hypotension and life-threatening autonomic dysreflexia（AD）. AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. The syndrome is often triggered by unpleasant visceral or sensory stimuli below the injury level. Currently the only treatments are palliative - once a stimulus elicits AD, pharmacological vasodilators are administered to help reduce the spike in arterial blood pressure. However, a more effective means would be to mitigate AD development by attenuating contributing mechanisms, such as the reorganization of intraspinal circuits below the level of injury. A better understanding of the neuropathophysiology underlying cardiovascular dysfunction after SCI is essential to better develop novel therapeutic approaches to restore hemodynamic performance.展开更多
BACKGROUND： Propofol combined with ischemic preconditioning （IPC） could prevent spinal ischemia/reperfusion injury. However, the effect of this combination remains poorly understood. OBJECTIVE： To measure neuropro...BACKGROUND： Propofol combined with ischemic preconditioning （IPC） could prevent spinal ischemia/reperfusion injury. However, the effect of this combination remains poorly understood. OBJECTIVE： To measure neuroprotection of IPC in combination with propofol in a rabbit model of aorta occlusion-induced spinal injury. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Anesthesiology, Wuhan University and Central Laboratory of the First Clinical Medical College, China Three Gorges University, from October 2006 to April 2008. MATERIALS： Propofol was purchased from AstraZeneca, UK; malondialdehyde （MDA） and superoxide dismutase （SOD） kits were purchased from Nanjing Jiancheng Bioengineering Institute, China. METHODS： A total of 32 male, Japanese White rabbits, were randomly assigned to model, IPC, propofol, and combination groups, with eight rabbits in each group, using 2×2 factorial experimental design. Spinal ischemiaJreperfusion injury was induced by abdominal aorta occlusion for 40 minutes and reperfusion for 7 days. The IPC group was subjected to IPC treatment for 30 minutes prior to occlusion; the propofol group was treated with propofol for 10 minutes before occlusion; and the combination group underwent IPC treatment for 30 minutes and propofol for 10 minutes prior to occlusion. MAIN OUTCOME MEASURES： Serum MDA levels and SOD activity were detected 35 minutes prior to occlusion, immediately after reperfusion, and 60 minutes and 7 days after reperfusion, respectively. Rabbit hind limb nerve function and spinal pathological changes following injury were observed, and spinal neuronal apoptosis was determined using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling method. RESULTS： Serum MDA levels, spinal neuronal apoptosis, and palsy incidence following injury were greatest in the propofol group, followed by the IPC and combination groups （P 〈 0.01）, while SOD activity and hind limb neurological scores were greatest in the combination group, followed by the IPC and propofol groups. Spinal cord injury in the combination group was slight （P 〈 0.01）. CONCLUSION： IPC and propofol treatment resulted in a synergistic effect for treating spinal ischemia/reperfusion injury. Combined application was superior to IPC or propofol treatment, suggesting that the protection of spinal cord injury may relate with anti-peroxidation.展开更多
目的探讨利妥昔单抗治疗长脊髓损害(LESCL)的临床疗效及安全性。方法收集2010年首都医科大学宣武医院神经内科经糖皮质激素治疗无效的LESCL住院患者2例,治疗前2例患者扩展残疾状态量表(expanded disability status scale,EDSS)评分均为...目的探讨利妥昔单抗治疗长脊髓损害(LESCL)的临床疗效及安全性。方法收集2010年首都医科大学宣武医院神经内科经糖皮质激素治疗无效的LESCL住院患者2例,治疗前2例患者扩展残疾状态量表(expanded disability status scale,EDSS)评分均为8.5分。对两患者均予利妥昔单抗500mg治疗1次,并随访6个月。分别于治疗后1周检测患者的淋巴细胞亚群CD19+CD20+细胞比例,评价治疗后6个月时的EDSS评分,并观察治疗期间(治疗之后至6个月)有无发热、寒战、低血压等不良反应。结果应用利妥昔单抗治疗1周后,两患者淋巴细胞亚群CD19+CD20+细胞比例均为0.00%。6个月后随访,病例1和病例2的EDSS评分分别为6.5分和2.5分,两患者均无明显不良反应。结论利妥昔单抗可能是一种治疗LESCL的有效药物。展开更多
A total of 66 samples （from 27 cases with neuromyelitis optica, 26 cases with multiple sclerosis, aa 13 cases with optic neuritis） were tested for aquaporin-4 antibody by a cell-based immunofluorescence assay and an...A total of 66 samples （from 27 cases with neuromyelitis optica, 26 cases with multiple sclerosis, aa 13 cases with optic neuritis） were tested for aquaporin-4 antibody by a cell-based immunofluorescence assay and an enzyme-linked immunosorbent assay. The sensitivities and specificities of the two assays were similar. We further analyzed an additional 68 patients and 93 healthy controls using the enzyme-linked immunosorbent assay. A Kappa test showed good consistency between the two methods in terms of detection of anti-aquaporin-4 antibody in the se of neuromyelitis optica patients. No significant correlations were identified with onset age or disea duration, suggesting that aquaporin-4 antibody is a good marker for neuromyelitis optica. The enzyme-linked immunosorbent assay can be used for quantifying aquaporin-4 antibody concentrations and may be useful to dynamically monitor changes in the levels of aquaporin-4 antibody during disease duration.展开更多
基金supported by research grants to VJT from the National Institutes of Health(R01 NS085426)the Department of Defense(W81XWH-14-1-060)
文摘Both sensorimotor and autonomic dysfunctions often occur after spinal cord injury（SCI）. Particularly, a high thoracic or cervical SCI interrupts supraspinal vasomotor pathways and results in disordered hemodynamics due to deregulated sympathetic outflow. As a result of the reduced sympathetic activity, patients with SCI may experience hypotension, cardiac dysrhythmias, and hypothermia post-injury. In the chronic phase, changes within the CNS and blood vessels lead to orthostatic hypotension and life-threatening autonomic dysreflexia（AD）. AD is characterized by an episodic, massive sympathetic discharge that causes severe hypertension associated with bradycardia. The syndrome is often triggered by unpleasant visceral or sensory stimuli below the injury level. Currently the only treatments are palliative - once a stimulus elicits AD, pharmacological vasodilators are administered to help reduce the spike in arterial blood pressure. However, a more effective means would be to mitigate AD development by attenuating contributing mechanisms, such as the reorganization of intraspinal circuits below the level of injury. A better understanding of the neuropathophysiology underlying cardiovascular dysfunction after SCI is essential to better develop novel therapeutic approaches to restore hemodynamic performance.
文摘BACKGROUND： Propofol combined with ischemic preconditioning （IPC） could prevent spinal ischemia/reperfusion injury. However, the effect of this combination remains poorly understood. OBJECTIVE： To measure neuroprotection of IPC in combination with propofol in a rabbit model of aorta occlusion-induced spinal injury. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Anesthesiology, Wuhan University and Central Laboratory of the First Clinical Medical College, China Three Gorges University, from October 2006 to April 2008. MATERIALS： Propofol was purchased from AstraZeneca, UK; malondialdehyde （MDA） and superoxide dismutase （SOD） kits were purchased from Nanjing Jiancheng Bioengineering Institute, China. METHODS： A total of 32 male, Japanese White rabbits, were randomly assigned to model, IPC, propofol, and combination groups, with eight rabbits in each group, using 2×2 factorial experimental design. Spinal ischemiaJreperfusion injury was induced by abdominal aorta occlusion for 40 minutes and reperfusion for 7 days. The IPC group was subjected to IPC treatment for 30 minutes prior to occlusion; the propofol group was treated with propofol for 10 minutes before occlusion; and the combination group underwent IPC treatment for 30 minutes and propofol for 10 minutes prior to occlusion. MAIN OUTCOME MEASURES： Serum MDA levels and SOD activity were detected 35 minutes prior to occlusion, immediately after reperfusion, and 60 minutes and 7 days after reperfusion, respectively. Rabbit hind limb nerve function and spinal pathological changes following injury were observed, and spinal neuronal apoptosis was determined using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling method. RESULTS： Serum MDA levels, spinal neuronal apoptosis, and palsy incidence following injury were greatest in the propofol group, followed by the IPC and combination groups （P 〈 0.01）, while SOD activity and hind limb neurological scores were greatest in the combination group, followed by the IPC and propofol groups. Spinal cord injury in the combination group was slight （P 〈 0.01）. CONCLUSION： IPC and propofol treatment resulted in a synergistic effect for treating spinal ischemia/reperfusion injury. Combined application was superior to IPC or propofol treatment, suggesting that the protection of spinal cord injury may relate with anti-peroxidation.
文摘目的探讨利妥昔单抗治疗长脊髓损害(LESCL)的临床疗效及安全性。方法收集2010年首都医科大学宣武医院神经内科经糖皮质激素治疗无效的LESCL住院患者2例,治疗前2例患者扩展残疾状态量表(expanded disability status scale,EDSS)评分均为8.5分。对两患者均予利妥昔单抗500mg治疗1次,并随访6个月。分别于治疗后1周检测患者的淋巴细胞亚群CD19+CD20+细胞比例,评价治疗后6个月时的EDSS评分,并观察治疗期间(治疗之后至6个月)有无发热、寒战、低血压等不良反应。结果应用利妥昔单抗治疗1周后,两患者淋巴细胞亚群CD19+CD20+细胞比例均为0.00%。6个月后随访,病例1和病例2的EDSS评分分别为6.5分和2.5分,两患者均无明显不良反应。结论利妥昔单抗可能是一种治疗LESCL的有效药物。
基金the grants from the Ministry of Sciences and Technology of China, No. 2006AA02A408, 2008ZX09312-014
文摘A total of 66 samples （from 27 cases with neuromyelitis optica, 26 cases with multiple sclerosis, aa 13 cases with optic neuritis） were tested for aquaporin-4 antibody by a cell-based immunofluorescence assay and an enzyme-linked immunosorbent assay. The sensitivities and specificities of the two assays were similar. We further analyzed an additional 68 patients and 93 healthy controls using the enzyme-linked immunosorbent assay. A Kappa test showed good consistency between the two methods in terms of detection of anti-aquaporin-4 antibody in the se of neuromyelitis optica patients. No significant correlations were identified with onset age or disea duration, suggesting that aquaporin-4 antibody is a good marker for neuromyelitis optica. The enzyme-linked immunosorbent assay can be used for quantifying aquaporin-4 antibody concentrations and may be useful to dynamically monitor changes in the levels of aquaporin-4 antibody during disease duration.
