Glucose and [11C]flumazenil positron emission tomography abnormalities of thalamic nuclei in temporal lobe epilepsy
Glucose and [11C]flumazenil positron emission tomography abnormalities of thalamic nuclei in temporal lobe epilepsy
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DOI：
10.1212/wnl.53.9.2037
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发表时间：
1999-12-10
期刊：
影响因子：
9.9
通讯作者：
Chugani, HT
中科院分区：
文献类型：
--
作者：
Juhász, C;Nagy, F;Chugani, HT
目的：使用高分辨率 2-脱氧-2[F-18]氟-D-葡萄糖 (FDG) 和 [C-11]氟马西尼 (FMZ) PET 分析难治性颞叶癫痫 (TLE) 患者丘脑核葡萄糖代谢和苯二氮卓受体结合的发作间期模式。背景：丘脑的结构和葡萄糖代谢异常被认为在 TLE 的病理生理学中很重要。人类各种丘脑核团的不同参与尚不清楚。方法：12 名 TLE 患者接受了体积 MRI、FDG 和 FMZ PET 以及长时间的视频脑电图监测。在 MRI 上定义的三个丘脑区域（背内侧核 [DMN]、枕丘和外侧丘脑 [LAT]）获得了葡萄糖代谢和 FMZ 结合的标准化值和不对称性，并将其复制到配准、部分体积校正的 FDG 和 FMZ PET 图像中。还测量了海马和杏仁核 FMZ 结合不对称性和丘脑体积。结果：DMN 显示癫痫病灶一侧的葡萄糖代谢和 FMZ 结合显着降低。 LAT 显示双侧代谢亢进和 FMZ 结合增加。 DMN 和杏仁核的 FMZ 结合不对称性之间存在显着相关性。 PET 异常与癫痫病灶同侧丘脑体积明显减少有关。结论：背内侧核（DMN）的[C-11]氟马西尼（FMZ）结合和葡萄糖代谢降低是常见的，并且对人类颞叶癫痫的癫痫病灶具有很强的偏侧化价值。苯二氮卓受体结合减少可能是由于神经元损失所致，如容量损失所表明的那样，但也可能表明DMN中的γ-氨基丁酸（GABA）能传递受损，DMN与边缘系统的其他部分有很强的相互联系。外侧丘脑中葡萄糖代谢和 FMZ 结合的增加可能代表 GABA 介导的抑制回路的上调。
Objectives: To analyze interictal patterns of thalamic nuclei glucose metabolism and benzodiazepine receptor binding in patients with medically intractable temporal lobe epilepsy (TLE) using high-resolution 2-deoxy-2[F-18]fluoro-D-glucose (FDG) and [C-11]flumazenil (FMZ) PET. Background: Structural and glucose metabolic abnormalities of the thalamus are considered important in the pathophysiology of TLE. The differential involvement of various thalamic nuclei in humans is not known. Methods: Twelve patients with TLE underwent volumetric MRI, FDG and FMZ PET, and prolonged video-EEG monitoring. Normalized values and asymmetries of glucose metabolism and FMZ binding were obtained in three thalamic regions (dorsomedial nucleus [DMN], pulvinar, and lateral thalamus [LAT]) defined on MRI and copied to coregistered, partial-volume-corrected FDG and FMZ PET images. Hippocampal and amygdaloid FMZ binding asymmetries and thalamic volumes also were measured. Results: The DMN showed significantly lower glucose metabolism and FMZ binding on the side of the epileptic focus. The LAT showed bilateral hypermetabolism and increased FMZ binding. There was a significant correlation between the FMZ binding asymmetries of the DMN and amygdala. The PET abnormalities were associated with a significant volume loss of the thalamus ipsilateral to the seizure focus. Conclusions: Decreased [C-11]flumazenil (FMZ) binding and glucose metabolism of the dorsomedial nucleus (DMN) are common and have strong lateralization Value for the seizure focus in human temporal lobe epilepsy. Decreased benzodiazepine receptor binding can be due to neuronal loss, as suggested by volume loss, but also may indicate impaired gamma-aminobutyric acid (GABA)ergic transmission in the DMN, which has strong reciprocal connections with other parts of the limbic system. Increased glucose metabolism and FMZ binding in the lateral thalamus could represent an upregulation of GABA-mediated inhibitory circuits.