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背景:随着镁离子对缺血性脑损伤治疗的研究进展,人们越来越重视镁对缺血性脑损伤的神经保护作用。镁对缺血性脑血管病的治疗已有报道,但对脑梗死患者诱发电位的研究国内外报道较少。目的:通过研究镁剂对脑梗死患者体感诱发电位的影响,证实镁剂的脑保护作用。设计:以诊断为依据的病例对照研究。地点和对象:选择2000-01/2001-12在聊城市第三人民医院神经内科确诊脑梗死患者60例,分为治疗组30例,男16例,女14例;年龄36～72岁,平均(62±4)岁。病变部位:基底核区18例,放射冠区8例,大脑半球4例。对照组30例,男15例,女15例;年龄37～75岁,平均(63±5)岁。病变部位:基底核区16例,放射冠区9例,大脑半球5例。方法:治疗组均在12h内应用250g/L硫酸镁20mL静滴,1次/d,连用7d,14d后进行前后体感诱发电位的比较。对照组除不用硫酸镁外,其余治疗均同治疗组。主要观察指标:体感诱发电位反应形式,神经功能缺损评分。结果:治疗组体感诱发电位治疗前后变化显著且逐渐好转。治疗组治疗前神经功能缺损评分12.60±5.31,治疗后神经功能缺损评分7.41±4.35,差异有显著意义(t=4.141,P<0.01);对照组治疗前神经功能缺损评分12.80±7.01,治疗后神经功能缺损评分12.80±5.37,差异有显著意义(t=2.99,P<0.05)。两组治疗前后神经功能缺损评分
BACKGROUND: With the development of magnesium ion in the treatment of ischemic brain injury, more and more attention is paid to the neuroprotective effect of magnesium on ischemic brain injury. Magnesium treatment of ischemic cerebrovascular disease has been reported, but the study of evoked potentials in patients with cerebral infarction less reported at home and abroad. Objective: To study the effect of magnesium on somatosensory evoked potentials in patients with cerebral infarction and to confirm the neuroprotective effects of magnesium. Design: A case-control study based on diagnosis. Location and Subjects: A total of 60 patients with cerebral infarction diagnosed in Department of Neurology, Third People’s Hospital of Liaocheng City from January 2000 to December 2001 were selected and divided into treatment group (30 cases), 16 males and 14 females, aged from 36 to 72 years (62 ± 4) years old. Lesions: 18 cases of basal ganglia, 8 cases of corneal irradiation, 4 cases of cerebral hemispheres. Control group, 30 cases, 15 males and 15 females; aged 37 to 75 years, mean (63 ± 5) years. Lesions: 16 cases of basal ganglia, 9 cases of corneal irradiation, 5 cases of cerebral hemisphere. Methods: The treatment group were treated with 250g / L magnesium sulfate 20mL intravenously, once daily for 12h, and then for 7d, 14d after the somatosensory evoked potentials were compared. In addition to the control group without magnesium sulfate, the rest of the treatment with the treatment group. MAIN OUTCOME MEASURES: Somatosensory evoked potential response form, neurological deficit score. Results: Before and after treatment, somatosensory evoked potentials changed significantly and gradually improved. The score of neurological deficit in treatment group before treatment was 12.60 ± 5.31, and the score of neurological deficit in treatment group was 7.41 ± 4.35 (t = 4.141, P <0.01). The score of neurological deficit in control group before treatment was 12.80 ± 7.01. After treatment, Neurological deficit score 12.80 ± 5.37, the difference was significant (t = 2.99, P <0.05). Two groups before and after treatment neurological deficit score