脑电监测在癫痫患者间期皮层和皮层下高代谢灶的判读中的应用

目的　探讨癫痫患者无临床发作情况下18F氟脱氧葡萄糖(18Ffluorodeoxyglucose,18FFDG)正电子发射计算机断层 (positron emission tomography, PET)脑显像呈现高代谢时脑电监测的应用价值。 方法　对北京协和医院2008年1月至2014年3月共3例无临床发作的间期情况下18FFDG PET脑显像呈现皮层或皮层下高代谢的癫痫患者, 静脉注射安定抑制皮层放电，在脑电监测确认无皮层异常放电时复查18FFDG PET脑显像，并对比两次显像结果。结果　病例1为颞叶癫痫患者，在无临床发作时18FFDG PET显像除发现右颞低代谢外，右额部分皮层及同侧基底节、丘脑及左侧小脑局灶代谢增高。脑电监测下抑制皮层放电后的18FFDG PET显像示原额叶皮层及同侧基底节、丘脑、对侧小脑高代谢灶消失。表明该患者上述高代谢灶为颞叶外皮层潜在致痫灶亚临床放电所致，同时证实了致痫灶与同侧基底节丘脑、对侧小脑之间的神经传导。此例改变了先前单纯前颞叶切除术的临床决策。病例2的间期18FFDG PET显像发现右侧大片额叶皮层高代谢，脑电监测下抑制临床下放电后，原皮层高代谢仍存在，原同侧基底节、对侧小脑的高代谢已不明显,证实皮层存在高代谢的基础病变(炎症)，而基底节丘脑为继发功能改变，确定了病变性质及范围。病例3为颞叶癫痫患者，临床及脑电无法确定癫痫起源部位，磁共振成像未见明显异常。18FFDG PET显像在无临床发作的情况下左侧海马区呈高代谢，脑电监测下在明确的间期状态复查18FFDG PET脑显像，左侧海马区仍为高代谢。提示该部位存在基础病变(肿瘤),帮助临床确定手术部位。 结论　癫痫患者无临床发作情况下18FFDG PET显像呈现高代谢图像时，在脑电监测下确认绝对的间期状态时复查18FFDG PET显像，有助于分析高代谢的病因及明确病变范围，帮助作出临床决策。

Videoelectroencephalography Applied in Interpretation of Cortical and SubcorticalHypermetabolic Foci in Interictal 18Ffluorodeoxyglucose Positron EmissionTomography Imaging in Patients with Epilepsy

Objective　To evaluate the role of vedioelectroencehpalography (VEEG) monitoring in interpreting the cortical and subcortical hypermetabolic foci in interictal 18Ffluorodeoxyglucose(18FFDG) positron emission tomography (PET) imaging in patients with epilepsy. Methods　From January 2008 to March 2014 in Peking Union Medical College Hospital, 3 epileptic patients whose first 18FFDG PET scan showed unexplained hypermetabolic foci without seizure underwent repeated 18FFDG PET scan in the interictal status proved by VEEG monitoring after discharge suppression by intravenous diazepam. Then compared the first and second scan images. Results　For case 1 who suffered from epilepsy originating from medial right temporal lobe, unexplainable hypermetabolic foci in right frontal lobe, basal ganglia, thalamus, and left cerebellum were present in interictal 18FFDG PET scan. After suppressing cortical discharge under VEEG monitoring, the second 18FFDG PET scan showed that the cortical and subcortical hypermetabolism disappeared, indicating that the hypermetabolic foci in the first scan was due to the subclinical discharge in a potential extratemporal seizure origin site, and the existence of efferent network activity from that origin site to ipsilateral basal ganglia and thalamus and contralateral cerebellum. The original clinical decision of simple anterior temporal lobectomy was altered based on the findings. For case 2，hypermtabolism was present in a large part of right frontal lobe, which persisted after suppressing discharge under VEEG monitoring. While the hypermetabolic foci in ipsilateral basal ganglia and contralateral cerebellum became less obvious in the second 18FFDG PET scan, proving that the original lesion (inflammation) with hypermetabolism existed in the cortex, and the hypermetabolic foci in basal ganglia and thalamus were due to secondary functional change. Case 3 suffered from temporal lobe epilepsy with origin undeterminable with clinical information, electroencephalogram, or magnetic resonance imaging. Hypermtabolic left hippocampus was shown in both the first 18FFDG PET scan and the second PET scan under definite interictal status with VEEG monitoring, suggested the existence of a hypermetabolic lesion (tumor), facilitating the clinical decision on surgical site. Conclusions　For the epileptic patients with hypermetabolic foci in 18FFDG PET without seizure, repeated 18FFDG PET imaging in definite interictal status under VEEG monitoring can help interpret the etiology and define the extent of lesions for better clinical decisionmaking.