中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2009年
7期
721-724
,共4页
袁芳%胡涛%王艺东%黄穗乔%潘经锐%邱宇%彭英
袁芳%鬍濤%王藝東%黃穗喬%潘經銳%邱宇%彭英
원방%호도%왕예동%황수교%반경예%구우%팽영
血氧水平依赖功能磁共振成像%脑梗死%激肽释放酶
血氧水平依賴功能磁共振成像%腦梗死%激肽釋放酶
혈양수평의뢰공능자공진성상%뇌경사%격태석방매
Functional magnetic resonance imaging,blood oxygen level-dependent%Cerebral infarction%Kallikrein
目的 通过血氧水平依赖功能磁共振成像(BOLD-fMRI)的方法 观察尤瑞克林治疗急性脑梗死的疗效及其作用机制. 方法 将23例急性脑梗死患者按随机数字表法分成对照组(11例)和治疗组(12例),对照组给予常规治疗,治疗组在常规治疗的基础上加用尤瑞克林,疗程均为12~14d.观察治疗前后BOLD-fMRI影像和患侧手食指肌力评分和美国国立卫生研究院卒中量表(NIHSS)评分的变化. 结果 治疗后,治疗组息侧感觉运动皮层(SMC)激活频率和激活体积较治疗前明显增加(11/12 vs 4/12;199.58±169.41 vs 105.17±197.23),且治疗前后激活体积之差明显大于对照组(94.42±51.57 vs 16.09±106.61),差异有统计学意义(P<0.05);治疗后,治疗组患侧食指肌力评分和NIHSS评分较治疗前明显改善(2.67±1.44 vs 1.25±1.48;4.92±2.94 vs 10.42±3.80),且治疗前后NIHSS评分之差明显大于对照组(5.50±1.31 vs 3.18±2.48),差异有统计学意义(P<0.05). 结论 促进脑功能区SMC的激活恢复可能是尤瑞克林治疗脑梗死的一个重要机制.
目的 通過血氧水平依賴功能磁共振成像(BOLD-fMRI)的方法 觀察尤瑞剋林治療急性腦梗死的療效及其作用機製. 方法 將23例急性腦梗死患者按隨機數字錶法分成對照組(11例)和治療組(12例),對照組給予常規治療,治療組在常規治療的基礎上加用尤瑞剋林,療程均為12~14d.觀察治療前後BOLD-fMRI影像和患側手食指肌力評分和美國國立衛生研究院卒中量錶(NIHSS)評分的變化. 結果 治療後,治療組息側感覺運動皮層(SMC)激活頻率和激活體積較治療前明顯增加(11/12 vs 4/12;199.58±169.41 vs 105.17±197.23),且治療前後激活體積之差明顯大于對照組(94.42±51.57 vs 16.09±106.61),差異有統計學意義(P<0.05);治療後,治療組患側食指肌力評分和NIHSS評分較治療前明顯改善(2.67±1.44 vs 1.25±1.48;4.92±2.94 vs 10.42±3.80),且治療前後NIHSS評分之差明顯大于對照組(5.50±1.31 vs 3.18±2.48),差異有統計學意義(P<0.05). 結論 促進腦功能區SMC的激活恢複可能是尤瑞剋林治療腦梗死的一箇重要機製.
목적 통과혈양수평의뢰공능자공진성상(BOLD-fMRI)적방법 관찰우서극림치료급성뇌경사적료효급기작용궤제. 방법 장23례급성뇌경사환자안수궤수자표법분성대조조(11례)화치료조(12례),대조조급여상규치료,치료조재상규치료적기출상가용우서극림,료정균위12~14d.관찰치료전후BOLD-fMRI영상화환측수식지기력평분화미국국립위생연구원졸중량표(NIHSS)평분적변화. 결과 치료후,치료조식측감각운동피층(SMC)격활빈솔화격활체적교치료전명현증가(11/12 vs 4/12;199.58±169.41 vs 105.17±197.23),차치료전후격활체적지차명현대우대조조(94.42±51.57 vs 16.09±106.61),차이유통계학의의(P<0.05);치료후,치료조환측식지기력평분화NIHSS평분교치료전명현개선(2.67±1.44 vs 1.25±1.48;4.92±2.94 vs 10.42±3.80),차치료전후NIHSS평분지차명현대우대조조(5.50±1.31 vs 3.18±2.48),차이유통계학의의(P<0.05). 결론 촉진뇌공능구SMC적격활회복가능시우서극림치료뇌경사적일개중요궤제.
Objective To investigate the therapeutic effect of human urinary kallidinogenase in patients with acute cerebral infarction and explore the mechanism by blood oxygen level dependent functional magnetic resonance imaging (BOLD-fMRI). Methods twenty-three patients with acute cerebral infarction were randomized into control group (n=11) and treatment group (n=12) to receive conventional treatment and additional human urinary kallidinogenase treatment for 12 to 14 days, respectively. BOLD-fMRI was performed, and the affected forefinger muscle strength and NIHSS score were recorded before and after the treatment. Results In the treatment group, the activated frequency and volume in the sensorimotor cortex (SMC) ipsilateral to the infarct increased significantly after the treatment (11/12 vs 4/12; 99.58±169.41 vs 105.17±197.23, P<0.05). The inerernent in the activated volume in the SMC was significantly greater in the treatment group than in the control group (94.42±51.57 vs 16.09±106.61, P<0.05). The forefinger muscle strength and NIHSS score in the treatment group improved significantly after treatment (2.67±1.44 vs 1.25±1.48; 4.92±2.94 vs 10.42±3.80, P<0.05), and the improvement in NIHSS score was significantly greater in the treatment group than in the control group (5.50±1.31 vs 3.18±2.48, P<0.05). Conclusion The therapeutic effect of human urinary kallidinogenase on acute cerebral infarction is mediated essentially by promoting the activation in the SMC in the functional area of the brain.