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目的观察静脉推注丙泊酚对皮层脑电图(electrocorticography,ECoG)波形的影响,探究其对幕上肿瘤伴癫痫患者致痫灶脑电活动的激化作用。方法选择2011年4月至2012年2月我院神经外科60例幕上肿瘤伴癫痫发作患者为试验组,不伴癫痫发作的无皮质侵犯的深部肿瘤及动脉瘤患者40例为对照组。所有患者行常规静吸复合麻醉,硬脑膜切开后,停用丙泊酚10～15 min,最低肺泡有效浓度(minimum alveolar concentration,MAC)控制在0.3～0.4,脑电双频指数(bispectral index,BIS)控制在40～60,于术区行ECoG监测,于癫痫波明显处做标记,待脑电背景恢复后推注丙泊酚(0.1 mg/kg),以丙泊酚推注前2 min(时段A)与推注后至暴发抑制现象前(时段B)之间为自身对照比较的2个时间段,定量、定性比较各组ECoG癫痫波的变化。病灶切除后,术中麻醉重复上述过程,对试验组非功能区致痫灶行皮层切除或热凝癫痫波(处理组),对功能区致痫灶暂不处理(非处理组)。术后随访20～24个月,比较术后早期癫痫发生率、晚期癫痫控制率。结果①硬脑膜切开后,试验组推注丙泊酚前后(时段A与B)棘波定量分析:棘波波幅分别为(347±30)、(479±27)μV,波幅增长幅度为1.2～1.6倍;棘波频率分别为(31±6)、(44±7)Hz,频率增加1.0～2.0倍;经配对t检验,差异有统计学意义(P<0.05)。对照组棘波量化分析无统计学差异(P>0.05)。试验组与对照组棘波定性比较:静推丙泊酚后,试验组棘波增强率为95.00%(57/60),对照组仅为10.00%(4/40),两组差异有统计学意义(χ2=72.89,P<0.05)。②随访结果:处理组术后早期癫痫发作5例(13.89%,5/36),非处理组术后早期癫痫发作9例(42.86%,9/21)。差异有统计学意义(χ2=6.01,P<0.05)。晚期癫痫控制率:处理组与非处理组分别为88.89%(EngelⅠ～Ⅱ级,32/36)及61.90%(EngelⅠ～Ⅱ级,13/21),差异有统计学意义(χ2=4.30,P<0.05)。结论小剂量静推丙泊酚对幕上肿瘤伴癫痫发作患者病灶周围皮层癫痫波有激化作用,可辅助定位致痫灶,指导术中致痫灶的有效处理,有利于提高晚期癫痫控制率。
Objective To observe the effect of intravenous propofol on the waveform of cortical electrocorticography (ECoG), and to explore its potentiation on the electroencephalogram (EEG) activity of epileptic focus in patients with supratentorial tumor with epilepsy. Methods From April 2011 to February 2012, 60 patients with supratentorial tumor with epilepsy in our department of neurosurgery were selected as the experimental group. 40 patients with deep tumor and aneurysm without cortical invasion without epileptic seizures were selected as the control group. All patients underwent routine static inhalation combined anesthesia. After dural incision, propofol was discontinued for 10-15 min, minimum alveolar concentration (MAC) was 0.3-0.4, Bispectral index , BIS) was controlled at 40-60. ECoG monitoring was performed in the surgical field and markedly marked in the epileptic wave. After propofol (0.1 mg / kg) was injected after the background restoration of the electroencephalogram, propofol min (period A) and the period from post-injection to before suppression (period B) compared with self-control. The changes of ECoG epilepsy wave in each group were quantitatively and qualitatively compared. After the resection of the lesion, intraoperative anesthesia was repeated the above process, the experimental group of non-functional area induced epileptogenic lesions cortex or thermal coagulation epilepsy wave (treatment group), the functional area of epileptic foci temporary treatment (non-treatment group). The patients were followed up for 20-24 months. The incidence of early postoperative epilepsy and late epilepsy control rate were compared. Results ① After the dural incision, the experimental group before and after the injection of propofol (period A and B) spike quantitative analysis: Spike wave amplitude (347 ± 30), (479 ± 27) μV, the amplitude of the amplitude of 1.2 ~ 1.6 times; spike wave frequency was (31 ± 6), (44 ± 7) Hz, frequency increased 1.0 to 2.0 times; by paired t test, the difference was statistically significant (P <0.05). There was no significant difference in the spike wave quantification in the control group (P> 0.05). In the test group and the control group, the spikes were qualitatively compared. After the propofol was bolted, the spike enhancement rate was 95.00% (57/60) in the test group and only 10.00% (4/40) in the control group. The difference between the two groups was statistically significant Significance (χ2 = 72.89, P <0.05). ② The follow-up results: In the treatment group, 5 cases (13.89%, 5/36) of early epileptic seizures and 9 cases of early epileptic seizures (42.86%, 9/21) in the untreated group. The difference was statistically significant (χ2 = 6.01, P <0.05). The rate of control of advanced epilepsy was 88.89% (EngelⅠ-Ⅱ, 32/36) and 61.90% (EngelⅠ-Ⅱ, 13/21) respectively, the difference was statistically significant (χ2 = 4.30, P <0.05). Conclusions Low-dose intravenous propofol can stimulate the epilepsy waves in the cortex around the supratentorial tumor with seizure. It can help to locate the epileptogenic zone and guide the effective treatment of the epileptogenic zone. It is helpful to improve the control rate of advanced epilepsy.