抗LGI1抗体相关边缘性脑炎临床分析
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摘要
目的探讨抗富亮氨酸胶质瘤失活基因1 (LGI1)抗体相关边缘性脑炎临床特点。方法与结果2016年6月至2017年10月共诊断与治疗7例抗LGI1抗体相关边缘性脑炎病例,平均发病年龄为(48.29±15.09)岁。呈急性(4例)或亚急性(3例)发病,以癫(?)发作和记忆障碍为主要表现,可伴有面-臂肌张力障碍发作(5例)、精神行为异常或性格改变(4例),或合并难治性低钠血症(2例)、胸腺瘤(1例);脑脊液(6例)或血清(7例)抗LGI1抗体呈阳性;头部MRI检查单侧或双侧颞叶内侧异常信号(6例),脑电图呈连续棘慢复合波和慢波(1例)。大剂量糖皮质激素序贯治疗(6例)有效。7例患者中2例失访,余5例遗留远期记忆障碍(3例)或近期与远期记忆障碍并存(2例),其中1例出院6个月后复发。结论依据特异性临床表现如面-臂肌张力障碍发作、记忆障碍等,结合影像学及脑脊液检查结果可明确诊断;免疫抑制剂可有效改善临床症状与预后。
Objective To investigate the clinical characteristics of anti-leucine-rich glioma-inactivated 1(LGI1) antibody-associated encephalitis. Methods and Results From June 2016 to October2017, a total of 7 patients with anti-LGI1 antibody-associated limbic encephalitis were diagnosed and treated, with an average age at onset(48.29 ± 15.09) years. Patients presented acute(4 cases) or subacute onset(3 cases), with seizures and memory dysfunction as the main manifestations. It may be accompanied by faciobrachial dystonic seizures(FBDS, 5 cases), mental and behavioral abnormalities or personality changes(4 cases), or even combined with intractable hyponatremia(2 cases) or thymoma(one case). Serum anti-LGI1 antibody tests showed positive results in 7 cases, and cerebrospinal fluid(CSF) anti-LGI1 antibody tests showed positive results in 6 cases. MRI showed unilateral or bilateral medial temporal lobe abnormal signals(6 cases), and EEG showed continuous spike-slow waves or slow waves(one case). Highdose glucocorticoid sequential therapy was effective in 6 cases. During the follow-up period, 2 cases were lost, and the other 5 cases presented long-term memory disorder(3 cases) or long-term and short-term memory disorders(2 cases). Among them, one case relapsed 6 months after discharge. Conclusions According to specific clinical manifestations of patients(such as onset of FBDS, memory disorders, etc.),combined with imaging and CSF examination results, this disease can be clearly diagnosed.Immunosuppressive agents can effectively improve the clinical symptoms and prognosis.
Objective To investigate the clinical characteristics of anti-leucine-rich glioma-inactivated 1(LGI1) antibody-associated encephalitis. Methods and Results From June 2016 to October2017, a total of 7 patients with anti-LGI1 antibody-associated limbic encephalitis were diagnosed and treated, with an average age at onset(48.29 ± 15.09) years. Patients presented acute(4 cases) or subacute onset(3 cases), with seizures and memory dysfunction as the main manifestations. It may be accompanied by faciobrachial dystonic seizures(FBDS, 5 cases), mental and behavioral abnormalities or personality changes(4 cases), or even combined with intractable hyponatremia(2 cases) or thymoma(one case). Serum anti-LGI1 antibody tests showed positive results in 7 cases, and cerebrospinal fluid(CSF) anti-LGI1 antibody tests showed positive results in 6 cases. MRI showed unilateral or bilateral medial temporal lobe abnormal signals(6 cases), and EEG showed continuous spike-slow waves or slow waves(one case). Highdose glucocorticoid sequential therapy was effective in 6 cases. During the follow-up period, 2 cases were lost, and the other 5 cases presented long-term memory disorder(3 cases) or long-term and short-term memory disorders(2 cases). Among them, one case relapsed 6 months after discharge. Conclusions According to specific clinical manifestations of patients(such as onset of FBDS, memory disorders, etc.),combined with imaging and CSF examination results, this disease can be clearly diagnosed.Immunosuppressive agents can effectively improve the clinical symptoms and prognosis.
引文
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[22] Wennberg R, Steriade C, Chen R, Andrade D. Frontal infraslow activity marks the motor spasms of anti-LGI1 encephalitis[J].Clin Neurophysiol, 2018, 129:59-68.
[23] Malter MP, Helmstaedter C, Urbach H, Vincent A, Bien CG.Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis[J]. Ann Neurol, 2010, 67:470-478.
[24] Finke C, Priiss H, Heine J, Reuter S, Kopp UA, Wegner F,Then Bergh F, Koch S, Jansen O, Münte T, Deuschl G,Ruprecht K, Stocker W, Wandinger KP, Paul F, Bartsch T.Evaluation of cognitive deficits and structural hippocampal damage in encephalitis with leucine-rich glioma-inactivated 1antibodies[J]. JAMA Neurol, 2017, 74:50-59.
[25] McQuillan RF, Bargman JM. Hyponatraemia caused by LGI1-associated limbic encephalitis[J]. NDT Plus, 2011, 4:424-426.
[26] Murata Y, Watanabe O, Taniguchi G, Sone D, Fujioka M,Okazaki M, Nakagawa E, Watanabe Y, Watanabe M. A case of autoimmune epilepsy associated with anti-leucine-rich glioma inactivated subunit 1 antibodies manifesting electrical shocklike sensations and transparent sadness[J]. Epilepsy Behav Case Rep, 2015, 4:91-93.
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[29] Nilsson AC, Blaabjerg M. More evidence of a neurocardiac prodrome in anti-LGI1 encephalitis[J]. J Neurol Sci, 357(1/2):310-311.
[30] Tumminelli G, Battisti C, Cioni C, Mignarri A, Annunziata P,Federico A. Demyelinating polyneuropathy in a case of antiLGI1 encephalitis[J]. Muscle Nerve, 2017, 56:E2-3.
[31] Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, BaliceGordon R, Cowell JK, Dalmau J. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels:a case series[J]. Lancet Neurol, 2010, 9:776-785.
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[33] Wang SJ, Zhao YY, Wang QZ, Guo B, Liu YM, Yan CZ. Pearls&Oy-sters:limbic encephalitis associated with positive antiLGI1 and antithyroid antibodies[J]. Neurology, 2016, 86:E16-18.
[34] Yu J, Yu X, Fang S, Zhang Y, Lin W. The treatment and followup of anti-LGIl limbic encephalitis[J]. Eur Neurol, 2016, 75(1/2):5-11.
[35] van Sonderen A, Petit-Pedrol M, Dalmau J, Titulaer MJ. The value of LGI1, Caspr2 and voltage-gate potassium channel antibodies in encephalitis[J]. Nat Rev Neurol, 2017, 13:290-301.
[36] Park S, Choi H, Cheon GJ, Wook Kang K, Lee DS.~(18)F-FDG PET/CT in anti-LGIl encephalitis:initial and follow-up finding[J]. Clin Nucl Med, 2015, 40:156-158.
[37] Wegner F, Wilke F, Raab P, Tayeb SB, Boeck AL, Haense C,Trebst C, Voss E, Schrader C, Logemann F, Ahrens J, Leffler A, Rodriguez-Raecke R, Dengler R, Geworski L, Bengel FM,Berding G, Stangel M, Nabavi E. Anti-leucine rich glioma inactivated 1 protein and anti-N-methyl-D-aspartate receptor encephalitis show distinct patterns of brain glucose metabolism in~(18)F-fluoro-2-Deoxy-d-glucose positron emission tomography[J]. BMC Neurol, 2014, 14:136.
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[2] Malter MP, Frisch C, Schoene-Bake JC, Helmstaedter C,Wandinger KP, Stoecker W, Urbach H, Surges R, Elger CE,Vincent AV, Bien CG. Outcome of limbic encephalitis with VGKC-complex antibodies:relation to antigenic specificity[J].J Neurol, 2014, 261:1695-1705.
[3] Irani SR, Vincent A. The expanding spectrum of clinicallydistinctive, immunotherapy-responsive autoimmune encephalopathies[J]. Arq Neuropsiquiatr, 2012, 70:300-304.
[4] Jin LR, Liu Q, Ren HT, Guan HZ, Zheng JB, Cui RX, Wu LW,Yang YC, Cui LY. Clinical characteristics of one patient with leucine-rich glioma inactivated-1 antibody positive limbic encephalitis[J]. Zhonghua Shen Jing Ke Za Zhi, 2013, 46:461-464.[金丽日,柳青,任海涛,关鸿志,郑建彪,崔瑞雪,吴立文,杨荫昌,崔丽英.富亮氨酸胶质瘤失活1蛋白抗体阳性边缘系统脑炎一例临床特点[J].中华神经科杂志,2013, 46:461-464.]
[5] Irani SR, Alexander S, Waters P, Kleopa KA, Pettingill P,Zuliani L, Peles E, Buckley C, Lang B, Vincent A. Antibodies to Kvl potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan's syndrome and acquired neuromyotonia[J]. Brain, 2010, 133:2734-2748.
[6] Sagane K, Ishihama Y, Sugimoto H. LGI1 and LGI4 bind to ADAM22, ADAM23 and ADAM11[J]. Int J Biol Sci, 2008, 4:387-396.
[7] Zhou YD, Lee S, Jin Z, Wright M, Smith SE, Anderson MP.Arrested maturation of excitatory synapses in autosomal dominant lateral temporal lobe epilepsy[J]. Nat Med, 2009, 15:1208-1214.
[8] Kim TJ, Lee ST, Moon J, Sunwoo JS, Byun JI, Lim JA, Shin YW, Jun JS, Lee HS, Lee WJ, Yang AR, Choi Y, Park KI, Jung KH, Jung KY, Kim M, Lee SK, Chu K. Anti-LGI1 encephalitis is associated with unique HLA subtypes[J]. Ann Ncurol, 2016,81:183-192.
[9] van Sonderen A, Roelen DL, Stoop JA, Verdijk RM, Haasnoot GW, Thijs RD, Wirtz PW, Schreurs MW, Claas FH, Sillevis Smitt PA, Titulaer MJ. Anti-LGI1 encephalitis is strongly associated with HLA-DR7 and HLA-DRB4[J]. Ann Neurol,2017, 81:193-198.
[10] van Sonderen A, Thijs RD, Coenders EC, Jiskoot LC, Sanchez E, de Bruijn MA, van Coevorden-Hameete MH,Wirtz PW,Schreurs MW, Sillevis Smitt PA, Titulaer MJ. Anti-LGI1encephalitis:clinical syndrome and long-term follow-up[J].Neurology, 2016, 87:1449-1456.
[11] Bastiaansen AE, van Sonderen A, Titulaer MJ. Autoimmune encephalitis with anti-leucine-rich-glioma-inactivated 1 or anticontactin-associated-protein-like 2 antibodies(formerly called voltage-gated potassium channel-complex antibodies)[J]. Curr Opin Neurol, 2017, 30:302-309.
[12] Arino H, Armangue T, Petit-PedrolM, Sabater L, MartinezHernandez E, Hara M, Lancaster E, Saiz A, Dalmau J, Graus F.Anti-LGI1-associated cognitive impairment:presentation and long-term outcome[J]. Neurology, 2016, 87:759-765.
[13] Celicanin M, Blaabjerg M, Maersk-Moller C, Beniczky S,Marner L, Thomsen C, Bach FW, Kondziella D, Andersen H,Somnier F, Illes Z, Pinborg LH. Autoimmune encephalitis associated with voltage-gated potassium channels-complex and leucine-rich glioma-inactivated 1 antibodies:a national cohortstudy[J]. Eur J Neurol, 2017, 24:999-1005.
[14] Yang XL, Lu QC. Anti-LGI1 limbic encephalitis presenting as faciobrachial dystonic seizures:a report of three cases and literature review[J]. Shen Jing Bing Xue Yu Shen Jing Kang Fu Xue Za Zhi,2017,13:186-196.[杨晓岚,陆钦池.以面-臂肌张力障碍发作为主要表现的抗LGI1抗体相关边缘性脑炎:3例报告及文献复习[J].神经病学与神经康复学杂志,2017,13:186-196.]
[15] Shin YW, Lee ST, Shin JW, Moon J, Lim JA, Byun JI, Kim TJ,Lee KJ, Kim YS, Park KI, Jung KH, Lee SK, Chu K. VGKCcomplex/LGI1-antibody encephalitis:clinical manifestations and response to immunotherapy[J]. J Neuroimmunol, 2013, 265(1/2):75-81.
[16] Irani SR, Gelfand JM, Bettcher BM, Singhal NS, Geschwind MD. Effect of rituximab in patients with leucine-rich, gliomainactivated 1 antibody associated encephalopathy[J]. JAMA Neurol, 2014, 71:896-900.
[17] Sen A, Wang J, Laue-Gizzi H, Lee T, Ghougassian D,Somerville ER. Pathognomonic seizures in limbic encephalitis associated with anti-LGI1 antibodies[J]. Lancet, 2014, 383:2018.
[18] Irani SR, Michell AW, Lang B, Pettingill P, Waters P, Johnson MR,Schott JM, Armstrong RJ, S Zagami A, Bleasel A,Somerville ER, Smith SM, Vincent A. Faciobrachial dystonic seizures precede LGI1 antibody limbic encephalitis[J]. Ann Neurol, 2011, 69:892-900.
[19] Isnard J, Guenot M, Sindou M, Mauguière F. Clinical manifestations of insular lobe seizures:a stereoelectroencephalographic study[J]. Epilepsia, 2004, 45:1079-1090.
[20] Proserpio P, Cossu M, Francione S, Tassi L, Mai R, Didato G,Castana L, Cardinale F, Sartori I, Gozzo F, Citterio A, Schiariti M, Lo Russo G, Nobili L. Insular-opercular seizures manifesting with sleep-related paroxysmal motor behaviors:a stereo-EEG study[J]. Epilepsia, 2011, 52:1781-1791.
[21] Gao L, Liu A, Zhan S, Wang L, Li L, Guan L, Zhao X, Zhang X,Wang Y. Clinical characterization of autoimmune LGI1 antibody limbic encephalitis[J]. Epilepsy Behav, 2016, 56:165-169.
[22] Wennberg R, Steriade C, Chen R, Andrade D. Frontal infraslow activity marks the motor spasms of anti-LGI1 encephalitis[J].Clin Neurophysiol, 2018, 129:59-68.
[23] Malter MP, Helmstaedter C, Urbach H, Vincent A, Bien CG.Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis[J]. Ann Neurol, 2010, 67:470-478.
[24] Finke C, Priiss H, Heine J, Reuter S, Kopp UA, Wegner F,Then Bergh F, Koch S, Jansen O, Münte T, Deuschl G,Ruprecht K, Stocker W, Wandinger KP, Paul F, Bartsch T.Evaluation of cognitive deficits and structural hippocampal damage in encephalitis with leucine-rich glioma-inactivated 1antibodies[J]. JAMA Neurol, 2017, 74:50-59.
[25] McQuillan RF, Bargman JM. Hyponatraemia caused by LGI1-associated limbic encephalitis[J]. NDT Plus, 2011, 4:424-426.
[26] Murata Y, Watanabe O, Taniguchi G, Sone D, Fujioka M,Okazaki M, Nakagawa E, Watanabe Y, Watanabe M. A case of autoimmune epilepsy associated with anti-leucine-rich glioma inactivated subunit 1 antibodies manifesting electrical shocklike sensations and transparent sadness[J]. Epilepsy Behav Case Rep, 2015, 4:91-93.
[27] Liu J, Li M, Li G, Zhou C, Zhang R. Anti-leucine-rich gliomainactivated 1 limbic encephalitis:a case report and literature review[J]. Exp Ther Med, 2016, 11:315-317.
[28] Naasan G, Irani SR, Bettcher BM, Geschwind MD, Gelfand JM.Episodic bradycardia as neurocardiac prodrome to voltage-gatedpotassium channel complex/leucine-rich, glioma inactivated 1antibody encephalitis[J]. JAMA Neurol, 2014, 71:1300-1304.
[29] Nilsson AC, Blaabjerg M. More evidence of a neurocardiac prodrome in anti-LGI1 encephalitis[J]. J Neurol Sci, 357(1/2):310-311.
[30] Tumminelli G, Battisti C, Cioni C, Mignarri A, Annunziata P,Federico A. Demyelinating polyneuropathy in a case of antiLGI1 encephalitis[J]. Muscle Nerve, 2017, 56:E2-3.
[31] Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, BaliceGordon R, Cowell JK, Dalmau J. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels:a case series[J]. Lancet Neurol, 2010, 9:776-785.
[32] Haitao R, Huiqin L, Tao Q, Xunzhe Y, Xiaoqiu S, Wei L,Jiewen Z, Liying C, Hongzhi G. Autoimmune encephalitis associated with vitiligo[J]? J Neuroimmunol, 2017, 310:14-16.
[33] Wang SJ, Zhao YY, Wang QZ, Guo B, Liu YM, Yan CZ. Pearls&Oy-sters:limbic encephalitis associated with positive antiLGI1 and antithyroid antibodies[J]. Neurology, 2016, 86:E16-18.
[34] Yu J, Yu X, Fang S, Zhang Y, Lin W. The treatment and followup of anti-LGIl limbic encephalitis[J]. Eur Neurol, 2016, 75(1/2):5-11.
[35] van Sonderen A, Petit-Pedrol M, Dalmau J, Titulaer MJ. The value of LGI1, Caspr2 and voltage-gate potassium channel antibodies in encephalitis[J]. Nat Rev Neurol, 2017, 13:290-301.
[36] Park S, Choi H, Cheon GJ, Wook Kang K, Lee DS.~(18)F-FDG PET/CT in anti-LGIl encephalitis:initial and follow-up finding[J]. Clin Nucl Med, 2015, 40:156-158.
[37] Wegner F, Wilke F, Raab P, Tayeb SB, Boeck AL, Haense C,Trebst C, Voss E, Schrader C, Logemann F, Ahrens J, Leffler A, Rodriguez-Raecke R, Dengler R, Geworski L, Bengel FM,Berding G, Stangel M, Nabavi E. Anti-leucine rich glioma inactivated 1 protein and anti-N-methyl-D-aspartate receptor encephalitis show distinct patterns of brain glucose metabolism in~(18)F-fluoro-2-Deoxy-d-glucose positron emission tomography[J]. BMC Neurol, 2014, 14:136.
[38] Szots M, Blaabjerg M, Orsi G, Iversen P, Kondziella D, Madsen CG, Garde E, Magnusson PO, Barsi P, Nagy F, Siebner HR,Illes Z. Global brain atrophy and metabolic dysfunction in LGI1encephalitis:a prospective multimodal MRI study[J]. J Neurol Sci, 2017, 376:159-165.
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