不同诱发因素下抗N-甲基-D-天冬氨酸受体脑炎患者的脑葡萄糖代谢特征

Characteristics of brain glucose metabolism in patients with anti-N-methyl-D-aspartate receptor encephalitis underlying different inducing factors

目的从抗体不同诱发因素的角度探讨抗N-甲基-D-天冬氨酸受体(NMDAR)脑炎患者脑部葡萄糖代谢特征和差异。方法回顾性纳入2016年1月至2019年1月间复旦大学附属华山医院15例抗NMDAR脑炎确诊患者[男8例、女7例,年龄(30.5±17.7)岁],所有患者行静息状态下^(18)F-FDG PET脑显像,分析其脑部葡萄糖代谢特征,并与12名健康者[HS;男7名、女5名,年龄(51.5±9.6)岁]进行SUV比值(SUVR)半定量分析组间比较。采用两独立样本t检验分析数据。结果15例抗NMDAR脑炎患者中,病毒性脑炎源性5例,^(18)F-FDG PET显像表现为单侧颞叶或基底节区局灶性代谢减低(SUVR:患者:0.659±0.219;HS:1.754±0.203;t=-9.58,P<0.001)伴对侧颞叶或基底节区代谢增高(SUVR:患者:2.275±0.244;HS:1.960±0.227;t=2.55,P=0.022);隐源性6例,^(18)F-FDG PET显像表现为非对称性的额叶、颞叶、顶叶及基底节区代谢增高(SUVR:患者:2.482±0.395;HS:1.754±0.203;t=5.23,P<0.001)伴双侧枕叶代谢轻度减低;副肿瘤源性4例,均合并畸胎瘤,^(18)F-FDG PET显像表现为双侧颞叶和基底节区代谢增高(SUVR:患者:2.359±0.181;HS:1.960±0.227;t=3.16,P=0.007)伴双侧枕叶代谢轻度减低。结论抗NMDAR脑炎患者脑部存在葡萄糖代谢异常改变,根据不同诱发因素可分为至少3种模式。全面认识其特征性代谢改变有助于对抗NMDAR脑炎的识别,还对提示病因有一定价值。

Objective To investigate characteristics and differences of cerebral glucose metabolism in patients with anti-N-methyl-D-aspartate receptor(NMDAR)encephalitis from the perspective of different trigger factors of antibodies.Methods A total of 15 patients(8 males,7 females,age(30.5±17.7)years)with anti-NMDAR encephalitis between January 2016 and January 2019 in Huashan Hospital,Fudan University were recruited retrospectively.All patients underwent resting state cerebral ^(18)F-FDG PET imaging.The characteristics of brain glucose metabolism were analyzed,and the SUV ratio(SUVR)was semi-quantitatively compared with that in 12 healthy subjects(HS;7 males,5 females,age(51.5±9.6)years).Independent-sample t test was used to analyze the data.Results Among 15 patients,5 patients were viral encephalitis-related anti-NMDAR encephalitis,showing focal decreased metabolism in unilateral temporal lobe or basal ganglia(SUVR:patients:0.659±0.219;HS:1.754±0.203;t=-9.58,P<0.001),with increased metabolism in contralateral temporal lobe or basal ganglia(SUVR:patients:2.275±0.244;HS:1.960±0.227;t=2.55,P=0.022)in ^(18)F-FDG PET imaging.Six patients were cryptogenic anti-NMDAR encephalitis,showing asymmetric increased metabolism in frontal,temporal,parietal and basal ganglia(SUVR:patients:2.482±0.395;HS:1.754±0.203;t=5.23,P<0.001),with decreased metabolism in bilateral occipital lobes.The remaining 4 cases were paraneoplastic origin accompanied by teratoma,showing increased metabolism in bilateral temporal and basal ganglia(SUVR:patient:2.359±0.181;HS:1.960±0.227;t=3.16,P=0.007),with mild decreased metabolism in bilateral occipital lobe.Conclusions The abnormal changes of cerebral glucose metabolism in patients with anti-NMDAR encephalitis can be divided into at least three patterns according to different trigger factors.A comprehensive understanding of these characteristic metabolic changes is helpful for detecting disease,and may provide potential value in indicating different causes.