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背景:神经元特异性烯醇酶是γ型同工酶特异地存在于神经元和神经内分泌细胞的胞浆内,是神经元损伤较敏感的标志物。目的:观察短暂性脑缺血发作患者血清神经元特异性烯醇酶的变化,探讨其与疾病的神经损伤程度的关系。设计:病例-对照观察。单位:济南市第四人民医院神经内科。对象:选择2002-03/2004-05在济南市第四人民医院神经内科入院的短暂性脑缺血发作患者29例(均为起病后6h的急诊观察患者)。男18例,女11例。平均(60.36±11.67)岁。根据神经功能缺失症状持续时间分为两组:短症状组(≤6h)19例,长症状组(>6h)10例。同期选取健康体检者为对照组,共25人。男15人,女10人。平均(62.34±9.65)岁。方法:对照组只取1次空腹肘静脉血1mL,短暂性脑缺血组在入院即时,第2,3,4,5天分别采空腹肘静脉血1mL。采用罗氏Elecsys2010免疫测定分析仪检测血清神经元特异性烯醇酶。用神经功能缺损程度量表(基本痊愈为评分减少90%-100%;显著进步为评分减少46%-89%;进步为评分减少18%-45%;无效为评分减少17%以下或病情恶化)评定患者的神经损伤程度。主要观察指标:观察患者血清神经元特异性烯醇酶的每天变化情况。结果:检测者54例均进入结果分析。①神经元特异性烯醇酶浓度的比较:短暂性脑缺血发作组明显高于对照组[(23.53±12.35,14.29±6.83)μg/L,t=2.678,P<0.01]。②急性期内神经元特异性烯醇酶变化曲线:早期增高,次日达高峰,后趋向逐渐下降,四五天基本恢复正常。③神经功能缺失症状持续时间不同的两组血清神经元特异性烯醇酶:短症状组明显高于对照组[(19.24±8.95,14.29±6.83)μg/L,t=1.893,P<0.05],长症状组高于对照组[(28.87±13.15,14.29±6.83)μg/L,t=4.367,P<0.001]。④神经元特异性烯醇酶值的大小与神经功能缺损时间呈正相关(r=0.815,P<0.01)。结论:短暂性脑缺血发作患者短期内血清神经元特异性烯醇增高,24～36h达到高峰,提示检测短暂性脑缺血发作患者血清神经元特异性烯醇酶浓度。对判断病情严重程度有指导意义。
BACKGROUND: Neuron-specific enolase is a type of isozyme that specifically exists in the cytoplasm of neurons and neuroendocrine cells and is a more sensitive marker of neuronal damage. Objective: To observe the changes of serum neuron-specific enolase in patients with transient ischemic attack and to explore its relationship with the severity of neurological damage. Design: Case-control observation. Unit: Jinan Fourth People ’s Hospital Department of Neurology. PARTICIPANTS: Twenty - nine patients with transient ischemic attack admitted to the Fourth People ’s Hospital of Jinan City from March 2002 to May 2004 were enrolled in this study. 18 males and 11 females. Average (60.36 ± 11.67) years old. According to the duration of neurological deficit symptoms were divided into two groups: 19 cases of short symptoms (≤ 6h), 10 cases of long symptoms (> 6h). In the same period, healthy people were selected as the control group, a total of 25 people. 15 men and 10 women. Average (62.34 ± 9.65) years old. Methods: The control group received only 1 mL of fasting cubital vein blood. The transient ischemic group was admitted immediately and 1 mL of fasting and elbow venous blood was collected on the 2nd, 3rd, 4th and 5th days respectively. Serum neuron-specific enolase was detected using a Roche Elecsys 2010 immunoassay analyzer. The scale of neurologic impairment (basic recovery score decreased by 90% -100%; marked improvement by 46% -89%; progressive score decreased by 18% -45%; ineffective score decreased by 17% or worsened ) To assess the patient’s degree of nerve damage. MAIN OUTCOME MEASURES: Daily changes of serum neuron-specific enolase in patients were observed. Results: All the 54 cases were involved in the result analysis. ① Comparison of neuron-specific enolase concentrations: TIA group was significantly higher than that of the control group [(23.53 ± 12.35, 14.29 ± 6.83) μg / L, t = 2.678, P <0.01]. ② During the acute phase neuron-specific enolase curve: increased early, peaked the next day, after the trend gradually decreased, four or five days basically returned to normal. ③ Serum neuron-specific enolase in two groups with different durations of neurological deficit: the short symptom group was significantly higher than that in the control group [(19.24 ± 8.95, 14.29 ± 6.83) μg / L, t = 1.893, P <0.05] (28.87 ± 13.15, 14.29 ± 6.83) μg / L, t = 4.367, P <0.001] in the long symptom group. ④ The value of neuron-specific enolase was positively correlated with the time of neurological deficit (r = 0.815, P <0.01). CONCLUSIONS: In transient ischemic attack, serum neuron-specific enolase is increased in the short term, reaching a peak at 24-36h, suggesting the detection of serum neuron-specific enolase concentration in patients with transient ischemic attack. To determine the severity of the disease is instructive.